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                    <text>IV:

10/113/60

Experieeutel Peyehietrie Presreue et niiieide neepitni
A

The

Review

veeieue prostate in the Department at Experineetei

W

Psychiatry have been devoted to en undereiending e: the node at

W‘iherepiu
“tie:
or

thrush undies or hreiu

taxation. the principal techniieel have been edepted tree deeoriptive
peyehieiry, uenrepeyehoiexy, electreeeeeyheiecrephy, linguietiee,
phereeeelour, end eeeielecy.
In

initial etudiee It

reaction were round

cenvuleive iterepy. ehenzee in brain

it reiete beth to

iepreveuent retinge end to

pro-treatment peyuhelecic variables. in our enderetendin; e:
ceevuieive therepy develeped, e centre: neerephyeieiezio-edeptive
view

e: eaeetie therepiee eeerted

(

). In this

Suuka»

view psychiatric

treeteente ereﬁtherepeutieeiir exteetive to the degree that brein
function in nee-trebly’eitered. While ehense in brein tenetien
neeeeeery

to: behavioral

change, the irpe

e: edeptetiee,

it

however,

veriee depending upon pre-treeinent peyoheleuiigend eeeieiecieag

charecterietiee er the subject. Thee, the node at eotien ie not eeen
ee

eiiher 'ercenic' er 'peyehelexie' bet tether ee the intereotion at

both eepeete in the individeel. further, while behevierei change in

�-2-

ralatad to chanson in brain function;

and the adaptiva

pattarn to

paynhologiéﬂoharaatariatic!t
praotraatnant
avalaationa at 'inprovaaant';
baing spacial typan at avalnatian or ahanga, ara darivativa Jadgnanta
baaad an

start

and

tanily anpaatatiana

and

talarannaa.

Thin hypothaaia was dovalapad and anatainad

in a aariaa at

atudiaa at onnvulaiva therapy. concurrant atndiaa of insulin tuna

indicatad that behavioral changa hora, too. van ralatnd to tha anaat
and dacraa o: prolancad cana

a: rapaatad aaiauraa - than. bainx tho

nanraphyaialogiélnhanaa
nanixantatiana
at
principal
prolansnd
in

thin thanany.
Tho node

at action of tha

nan paychetroyic asanta

anpraaaad within thin hypothaaia (

aganta would

III all.

). It ran anxgaatad that thaaa

b. attactiva to the dasraa that tho: indnaad paraiatant

chanxaa in brain

fanaticn'

and

that tha typa a: bahavioral raaponaa

vanld ha ralatad to tha type at brain nhanza, and to pranorbid

pnyehaloxigﬁ(para¢nality) pattarna. rho praaant proxrann in tha
Bogart-ant an. danisnnd to atndy than. ralatianahipa in datail.
Canvnlaiva Tharazz Prooana

or variaua anaanraa at brain tnnatian, tha anannt of slow

vat. activity in tho alantronncnphalacran

and cantabnlatory and

�-3H

dontal languago pottorno attor aaohorbital

(

)

oonottivo indiooo in oonvaloivo thorany oohaoeto.

voro tho aoot

In tho

firot

oxporioont, improvooont ratings ooro round to ho oorrolatod

dirootly with tho appoaranoo or high dogrooo o: ohango
indicoo (

).

1n thoao

rhooo oboorvationo woro tootod in a douhlo-hlind

study in which pationto rotorrod for olootroohock woro randoaly ao~
aignod to coorooo or oithor oonvuloivo or auboonvoloivo thorapy undo:

poutothal pronodioation. nigh dogrooo o: nourophyoiologie ohango
ooro oboorvod only in tho aonvoloivo group; improvonont ratoo

significantly highor in this group;

'02.

and than oubconvnloivo oohjooto

uoro ro-troatod by convuloivo appliaationo, tho improvoaont rota was

oinilar to tho original convaloivo group.
In tho oihconvnloivo troatod oahjoota, oonoidorahlo anonnto

o: oloetrieol corront paoaod hotwooh tho hitouporal oloetrodoo.

It woo

ooncludod, thorotoro, that tho thoropoutio agont

total oloctrioal curront,

or no, but an

all

woo

not tho

or nono quality

aahitootod by tho grand nal ooiouro. rho otgniticaneo or tho grand

nal ooiouro

was

turthor olahoratod

1n otudioo of tho

inhalant

convuloont, hoxatluorodtothylothor (Indoklon). 31-11ar dogrooo

o: olootrographio ohaugo, iayrovoaont ratoo, typo: o: bohavtoral

�‘hV,

change and ohanxee

in neuropeyohologio teak behavior were obaerved

in the inhalant and in electrically treated :ronpa.

It nae

anon apparent, however,

that not all anbjeote aaniteetin;

high decreea of physiologic ohanga were rated on 'inproved'.

In a

deeoriptive typelogio atndy, rive patterne were doeoribed,

eaperioally teraed ‘enphorio', 'hypoaanio', 'eoaatiaetien’,

’paraneid-Iithdraval',

and

'panio'.

While the

tirat

adaptive aedea were ratod ae 'nnoh inproved', the
aeen ae ‘uniapreved' or 'verae‘

(

two or

latter

theae

two were

).

In etndiee of peyoholegio variablea,

it nae

reported that

patiente rated ae 'anoh inproved' and ’reoevered' frequently
aanireeted peraenality patterne similar to that deeoribod by
Heinatein and

Kenn (

) an

the explicit verbal denial personality.

In language patterna, they expreeeed the language of denial,

when

dittnae brain change

denial,

was indnoed,

exhibiting anoh aepeote

an

niniaiaation, diaplaoenent, oliohee,|g§g. aere treqnontly than
unimproved enhaeote.

high

I Stale

eoore (

Other indioee related to favorable ontoeae were

),

and Rorschach deterninante or color,

abeent aoreaent and abaent torn-oeler (

).

alao, :avorable ontoeae nae aaaooiated

tith lea

In thin population,

educationalaohieveaont

�and

revels: birth

).

(

Antlehellner lea and Convalelve there
Seeking a way
EEG

slew wave

eae given

te eucaent the degree at peet-oeaveleive

activity,

an

inn-anneal: at

antlehelinercle cenpoand, diethaaine,
vex-1e“

“sea at

the eemalelve therapy

preeeee. Contrary to expectatlene, diethaaiae eaueed an iaaedlate
and entrained decreaee

in

EEG

alerting. Patleitl with dental

language patterae rellnxqalehed than; Instead of euphoria and well

being, the eibjeete were irritable, anxieue and expreeelve a:

nre-treateeet patterne. In eubjeete prior to cenvuleive or drug
therapy, elethaalne induced exciteaent, tenelen, anxiety and

lllaeery eeaeatlene.
Sabaeqeent etadlee with ether eentral antlohelinerglo
oeapeeade (VII-2299, JB-318,336, beeaetyaine) abated behavleral and

electrezraphle patterns alaalar te diethaelae. Stellar deeynohrenieatien
a! peet-eenvulelve

EEG

aleeing

wee

aleo noted with central

eynpathealaetie hallucinogene (euphetaaine, aeeoallne, LSD-25). and
baa been reported

re: antihietaainee (dephanlydraalne).

Theee

obeervatlene led to the eaageetlea that an increaee in central

ehellnergie activity eae a biocheaieal haste tor the eenvalelve

�therapy process

(

).

Pszshotrogic Drugs and
During

EEO

this period,the

drugs aroused

interest.

node of action of newer psychotropic

Following the concepts derived from

convulsive therapy, the neurophysiologis ohenges induced by drugs
were

tested within the

experi-ents in an

EEG

Ill.

experimental setting or acute

setting. It

was observed

that phenothiasines

(shlorprolasine, pronssine, triflnepronasine) induced

isation

and a

shitting o: the spectra: to the

ERG

synchron-

slow frequencies;

leprobanate and barbiturates , en increased synchronisation and a shift
of spectra: to

fast frequencies; reserpine,

an

inoreased slowing with

synchronisation at low dosages, and desynchronisatien at higher

levels. Inipraaine induced desynohrenisation with

a

shift of

frequencies to the slow bands.
Other experinental oonpounds tested included

phenyltoloxaline (Bristol), Deaner and

(liker),

wx-21h9 (Wyeth) and

its vsrions

BL-HlBB and

oongeners

trenquel (nerrill). For eaoh, no

consistent electrographis.patterns energed.

It
teens

use suggested that psychopharnaoelogio agents provide a

‘lr eliciting a variety

or nenrephysielogio patterns in

�.7contreet to the eingle pattern of induced oonvuleione. Furthermore,
the typo of neurophysiologie alteration, ee reflected in
synchrony and Iroquoooy

petterns,

or hehoviorel edoptetion.
elow :roqnonoieo

wee

Inoreoein;

EEG

related to epooirio types
EEG

eynohrony and e

shift to

or. oeeooieted with trenquillisetion, eedetion

deoreeeiog ogitotion; while deeynohronisetion and e

end

shift to test

frequencies in eeeooieted with oxoitenent, illusions, end delnlionol

idoetion. These observations orooeaeietont with hypotheeoo or
Hikler

(

).

The

merit of such teohaiqoeo for the eeeey or

psychotropic agents hoe been doeorihod

(

).

new

�-8Pszchcpharaacologz Evaluation Prograa
The

present pregraa, instituted in October 1959, is based

these studies and

is

on

designed to answer the following questions:

Is there s relation between aeasurable alteration in brain function
and behavioral change with

psychotropic drugs

on

chronic administra-

tion? Are there pre-treatasnt clusters of psychiatric, physiologic
and psychologic

variables related to the type of behavioral adanptation?

- to the type and degree of physiologic change?
Method:

is

an

initial approxiaation,

fixed

a double-blind,

dosage rendoa assignment drug study was undertaken.

Based on

clinical

experiences with various psychotropic coapounds, three classes were

selected

on

the basis of their patterns of :30 response.

‘The

selected agents were those eith predoainent desynchronicing patterns;
synchronising and slowing; or niniaal or no effect.

Patients

referred for drug therapy, after medical examination, and after

all other medications

have been discontinued are randoaly assigned

to one of three classes of compounds.

Patients are predoainantly middle class, urban, with high
educational attainment. Hillside Hospital is a non-profit,

philanthropic supported psychiatric institution, admitting voluntary

�.9patients for extensive psychotherapentic treatment.
of stay

is

seven months.

are prescribed by

Kean

duration

Convulsive and psychotropic drug therapies

star! psychiatrists

on

referral to the Department.

All treatment is adninistered by Departaental

start,

so

that the

experinentsl variables or drug dosage, route of administration,
assignsent to groups, 333. are readily controlled. All patients
in the hospital are available for study.

all patients receive

After a testing period,

ho cc of

medication daily tron individually labelled bottles.

increased in fixed weeﬂy etepe until a nsxiaua at

date,

1&amp;0

the study period.

Dosages are

After

weeks.

reotestinz occurs.

two weeks on maximum dosage,
To

h

liquid

subjects have been referred, and

110 have completed

Preliainary analyses of the data are

new

in

progress 0

avieral

Chan e5

In a survey or the behavioral adaptations of patients receiving

phenothiazines er iaipranine, various clusters at behaviors were
developed.

The typology was based on

the pre~treatasnt psychiatric

the treatnent reepenee and

profile. In the present study,

various measures of behavioral change are under study. Therapist

referral questionnaires

and

six

week

evaluatione; therapist and

�-10-

patient
two

Clyde Heed Scales; Lorr Scale evaluations in interview by

research psychiatrist, and Lorr ward scales; patient eelta

ratings including the Johns Hopkins synpten check

list

and the

Chicago Attitude Scalee are ancnget the neaenres being explored.

lenropezchelcgz: Paychelcgic tasks are viewed both as change

variables and predictive variablee. In convulaive therapy, changee

), tactile perception

in aencry tasks (

), crr

(

(

or figuree (

), rignre ground tasks
)

have been

(

), Recheler«3ellevne

(

and
tachietcecopic recogniﬂcn
,

)

related to the degree of induced neuro-

For each task, the degree or decrement in

physiologic change.

taek pertornance has been positively correlated with the amount of
EEG

slowing.

lollcwing treatnent completion, with the return of

physiologic indicee to pre-treatnent levels, performance in these
peychclcgic taaka also returns to prewtreatnent levels, or higher a

betternent of performance ascribed to practice eitect. Denial

scores

on

interview

(

), Rorechack deterninante

),

1

), auditory feedback

(

),and perception of the visual upright

(

)

have been viewed ae

predictive indices of the behavioral changes following nor.
various tasks are

new ﬁbeing

Scale scores

), language patterns after ancbarbital

(

(

(

Theee

asseeeed with paychctrcpic agents.

�.11.
In the convulsive therapy studies; the

lieetreencezhalogrsghzs
degree of

EEG

slowing was measured by counting the consecutive waves

in selected samples.
were

studied,

it was

When

the more subtle changes or druggeftects

necessary to apply less tediens techniques.

Electronic frequency analysis

was

introduced in August 1959.

By

asasurenent e! the pen deflection for various frequencies free
3

to

33 cps

in ten second epochs, rapid aeasnreaent of apparently

saall changes in total activity
and

and frequency

spectra are not obtained

applied.
Other physiologic variables include the response of £30 to

intravenous chlerprcnasine; blood pressure response to sechelyl;
EKG;

radioactive iodine uptake, and analyses or various blood and

urine element ordinarily conceived ac protective of the patient'e
welfare.

�Pnzghuliggualtion:

rollcving thy studios at syntgotio Iguanas. pattorns
(

)

in oonvnlntvo thnrspy, 0th.: anpoctu or Innguagc

cﬁndind for

worn

their ralatiou as 1361... st «hung. in intrnporlonll

with
nonltdurabln
nun:
.xplarctlou
attnr
bcinvior. attic,
(1T3)
thn‘
typewtokoa-rutio
augxoltod
11:;«1-t19 nounurOI,

or connoautivo 33-pin: a: dyldic apcoch

1.:

bu

A

useful lunar.

tppliud to writing toxta or tho

Hull. ran

had previously buon

hung.

nmlu ¢ individuals,

Jute intuit-d ﬂat

the two

index
(dyad)
at
a
ounnunieutioa
an:
sicniriuant
not.
portal

tho

ltttc

at tho intaraction than snnlytcn or

ltplrt‘.

Innplnn

or the participantl.

tpplytn; ‘htv technique to couralsivo tiara»: pntiunta,
august: in ran nonn and atnndnrd deviation worn rclntod both to

tn.

dogroo 0: induced use slow vuvo

nctivity

and to

lyutaatic

lan‘unxa puttorns obtained in indop-ndoat structurod iutcrvicvnc
Bpocch

boa...

new.

rupctttivc (lovarod nag:

223) and Iowa

vurttblc in connocutivo canplou (inoronnod standurd dovistion)

(

).

�In tnttrvidvt tutor.

&amp;nd

aft-r 8h. intravunoul administration

of coutrully .ctivo ngcnta, 11-11;: chtnguu rare obaorvtd.
Axtntu with a prcdauinnnt lynehronisatiou

ptttorn

tn.

on

EEG

uxhibttod n docroaao tn tutu 218 and inarcuao in Itnndtrd

deviation or soorcs,vh11n ataynchroniliag

compounds

olicitcd

grnttnr variability in apooch pa‘torus (lﬂOrOll. in
and

accrual:

13

varidbility at conntnntivo

133 noun)

neuron (doeronlo 1n

It;adnrd dcvistion).

0th.: 1:33:33. nasuuroo under study includu dintronln
r0110: quottontl, colt-rotoronco, tad

potion.

It

1- aucxoutod

are potont tuchaxquos to:
and poyuholusie

ultorttioa

1n

tuna. and

that than. paycholinsutstte nut-urns
ﬁho

operational unnlyiun a: phylialogta

crises: at payohopharnuoologic acunta

C

).

�aotiolg‘io Studio:
2h. cuncral prdbiun 0: tbs rolatiuu at

liaitl tautarl

to choico tad rocuitu o: parchiatrio troutucnt. and tho Ipoeitic
prdblun at tho rolnticn at

it... taatars

pittcrnn, within tun instieutioa.

and

to a cutie: at population

), uduoatiun, ago. place a: birth

In on: tinny (

utmdioa.

13d

ta in. rorcrrul

learn .3 tau California I nail. var. nixnitieuntly rciatod

to thc type .1 thnripr roe-iv'd ind tho utiliuntion o! ndaunctiv.

hoapittl nitric...
ndnantod hid

paiinntl uh. var. old-r, poorly

Than,

night: I

acorou und warn

tar.i;n-horn, pnrtieuinrly

Einicrn lnropo, utro ngat 11301: to be rotorrtd fur oloctro—
shook.

Thou.

rnlntianahipl were pro-nail: iudupondcut a:

diagnnlol. within tho crunp at cloctrolhock putiontl,

rottrrnl {or
In

rclltod to

36? vac .100

g cocond Iﬁuuy

at this

tin. tor

in... factora.

group (

). durstioa or

hospituliaation, dilohurxu ovuluutina and dincnoa¢n wars :0lniod to the can. 000111 taetcru. Fur «suspic, patiunta
hoapituliuod tar Sh. Ihnrtolt patina var. oidoat, had thi

icast oducution, war. nest likely to hivc
and had

in.

high

I

again

boon tornign born

scar... titular, nativoaborn, str-

�uduoatod, lunar 1

real. Ilﬁrl pttiontn v'ro hospltnllscd

tho

lnagost. Inn's rolttsonuhipl bald trnu within tronincnt
typo and
had thn

rithln

diutunaﬁao 31330.

On

allohurxo, .14.: pttttutu

not! tavurubli rttlngo. In not, valiant. rutad

ti

rooovcrod or IIOh luprovnd htd thq hlxhott F scarce, lunat
odnuuttou :ad

var. acct likaly to

ho rarclxn born.

In a study at patlont rtrulal a: 30!, 01:11.: ro-

lutlonlhtpu wort obncrvcd

(

). that. rolgtlounhlpi If.

no! undo: ntndr in tho out-pttlantxdopartnoat, sad in a trlw

hospital cunpnrattvc Itaay. In tn. lnttor Itudr. th- population!
or thrco hunptlalc in which :11

thrupltu are equally arullnbla

to all p¢tluata, - sonniugor roundatlau

lllplttl (Ippir-cltll,

Protoltant), nascaohau-ttn unnttl Xcslth

c ntnr (lavdroclnao

Catholla) and 3311314. noopltll (nlddln-clnnn Jalluh)

boin; alaoaacd.

It

but Etna postulntod that lhunc rcl:t1¢ulhlpl

rctlact tho tntlncncu at

.00131 bunksround on plynhologlcnl

pronoun, nah u hubltul
undo:

at axprcsslon.

tho putt-tn a: nontal

action

tr.

undo:

Ir.

”turn

or

Th. onutwibution

emulation

um

0: than. tactorc to

antaru
tho
tad
patsont-thtrnpttt
lllnsal,

atlﬁr.

�Exporinuutal Plyohiatrio Progr;ul nt Hillside ﬁespitnls
A

Max

Review

rink,

H.D.

the Depurtneut of Experimental Psychiatry, Kill-id.
Hospital, Glen Oaks, 1.1., l.I.

From

V:

11/60

�v: 11/22/50
Experimental Psychiatric Prograns at Hillside hospital:
A

Review

various programs in the Department of Experimental
Psychiatry have been devoted to an understanding or the node of
action or psychiatric therapies through studies or brain function.
The prin(ipnl techniques have been adapted tron descriptive
psychiatry, nenropeychelcgy, electroencephalography, linguistics,
pharaacology, and sociology.
In initial studies of convulsive therapy, changes in brain
function were found to relate both to evaluations of improvement
and to pro-treatment peyohologic variables. is our understanding
or convulsive therapy developed, a general neurophysiologicadaptive view of soaatic therapies emerged ( l ). In this view
psychiatric treataents are therapeutically effective to the degree
that brain tnnction in measurably altered. While change in brain
function is necessary for behavioral change, the type of adaptation,
however, varies depending upon pro-treatment psycholozic and
sociologic characteristics of the subject (2). Thus, the node of
action is not seen as either 'orgenic’ or "psychologic' but rather
as the interaction of diffuse neurophysiologic changes and
adaptive mechanisms. further, while behavioral change is related
to changes in brain function, and the adaptive pattern to
pre-treatnent psychologic characteristics, evaluations of
'inprovenent', being special types of evaluation of change, are
derivative Judgments based on start and {anily expectations and
tolerances (2).
The

�-2...

amine

series "or
studies of convulsive therapy. concurrent etudiee of ineulin ccna
indicated that behavioral change here, too, was related to the
onset and degree e: prolonged cone or repeated seizures - these
being the principal aanitestatiens or prolonged neurophysiologic
change in thie therapy (3,h).
The node of action or the new psychotropic agente was also
expressed within this hypothesis (5,6). It use suggested that
these agents weuld be effective to the degree that they induced
persistent changes in brain function and that the type or behavioral
response would be related to the type of brain change, and to
preeorhid peycholegic (personality) patterns. the present prograne
in the Department are designed to study these relationships in
"""""'m. hypS‘iEiSii‘ﬁ; a.‘+‘¢i3§.ia'gua‘
.. .. «'WIfahlr‘ehnebtn

”1.5";

detail.
GOHVVLSIvg IBERAP! PROCESS

or various neaeuree of brain function, the aecuut or slow
wave actiéity in the electroencephhlcgraa (7,8) and contahulatcry
and denial language

patterns atter anoberhital (9,10) were the
sensitive
nest
indices (11) in convulsive therapy subjects. In
one experieent, improvement ratings were correlated with the
appearance of high degrees or change in these indices (7,10).
These observations were thsted in a double-blind etudy in
which patients referred for electrcehcck were randomly assigned
te ceureee of either convulsive or subccnvuleive therapy under
pentothal prenedication. High degrees of neurophyeiclcgic change
were observed only in the cenvuleive group; improvement rates were
significantly higher in this grog); and when snbconvulsive subjects

�-3-

epplicetiene, the inprevcnent rete
wee sieiler tn the originel convulsive group (2).
In the enbccnvnleive treeted subjects, ceneiderehle emanate
er electric current pessed between the bitenperel electrodes.
It sppeered that the therepeutic egent use not the totel electrical
current, ger es, but en e11 or none quelity eenitested by the
grend eel seizure (8,12). the significsnce cf the grend eel
seizure wee exenined in studies of the inhalant ccnvnleent,
hexetlnorodiethylether (Indoklon). Sieiler degrees at electrogrephic cheese, iepreveeent retes, types at hehevicrel change
end cheeses in nenrepsychclegic tesk behevier were observed in
the inhelent end in electricelly treated groups (13).
It wee seen epperent thet net ell subjects lenitccting
high degrees 0: physielegic chenge were reted es 'iepreved'. In
e descriptive typelegic etndy, rive petterns were described,
eepirieelly tereed 'enphcric', 'hypeeenic', 'seeetieetien',
bereneidovithdreeel', end 'penic'. While the first tee of these
edeptive nodes were reted es 'nuch inpreved', the letter two were
seen es 'uniepreved' er 'ecrse' (It).
In stndiee of psychelcgic veriebles, it wee reported thet
peticnts reted es 'ench improved' end ’reccvered' frequently
menitested perecnelity petterns siniler to thet described by
Heinetsin end Kehn es the explicit verbel deniel personelity.
In lengnege petterns, petients expressed the 'lengnege or deniel',
when diffuse brein chenge wee induced, exhibiting such aspects es
explicit deniel, nininisetien, displeceeent, cliches, etc. eere
frequently then nniepreved subjects. Other indices releted to revereble
were

re-treeted

by convulsive

�4,ontooae were high 1 Scale ecore (15), and Rorechach deterrinante or

color, absent movement and abeent torn-color (16,17). In thie
population, also, favorable outcome wee aeeociated with low
educational echievenent and foreign birth (18).
ilfICXOLIEERGIO courovlnc one GGIVVLSIVE 2323‘?!

Seeking a way to augment the degree of poetoconvnleive

activity,

EEG

anticholinergic compound, diethasine, was
given intravenously at variene stages of the convulsive therapy
proceee (19). Contrary to expectations, dietharine caused an
innediate and sustained decrease in EEG slowing. Patiente with
denial language patterns relinquished then. Inetead of euphoria

nelow wave

and well being, tho

on

ethecte

irritable,

anxione and expreeeive
of pre-troataent patterne. In subjects prior to convulsive or
drug therapy, diethaoine induced excitement, tension, anxiety and
were

illusory sensations.
Snbeequeht etndiee with other central anticholinergic
coapounde (WIH-2299, JB-318,336, benactycinc) ehoued behavioral

electrographic patterne eiailar to dicthasine. Similar
deaynchrenination of poetaoonvuleive EEG cloning wee also noted with
central eyapathoniaetic hallucinogene (amphetamine, neecaline, LSD-2S),
been
and hae
reported for antihietaainoe (diphenylhydraaine).
These obeervatiene led to the suggeetion that an increaee in central
cholinergic activity wae a biochemical basic for the convulsive
therapy proccoe (20).
and

PSIOROERGPIG DRUGS AND EEG

this period, the node of action of newer psychotropic
aroused interest. Following the concept: derived from

During

drnge

convuleive therapy, the nenrephyeiologic changes induced by drnge

�-5-

tested within the sane acute experimental franework of the
EEG setting.
It was observed that phencthiacinee (chlcrpronazine,
proaasine, triftuopronanine) induced EEG synchronisation and a
shifting of the spectra: to the slow frequencies; neprebanate and
barbiturates, an increased synchronization and a shift of spectrum
to fast frequencies; reserpine, an increased slowing with synchrono
isatien at low dosages, and desynchronizaticn at higher levels (5,6).
Inipraaine induced desynchronisatien vith a shift of frequencies
to the slow bands (21).
Other experinental oerponnds tested included BL-H188 and
phenyltolexaaine (Bristol), Deaner and its various cengeners
(hiker), wr~21h9 (Wyeth) and frenqnel (Merrill). For each, no
consistent electrographic pattern was recorded.
It was suggested that psychepharnacclogic egents provide a
means for eliciting a variety of neorophysiclogic patterns in
contrast to the single pattern of induced convulsions. Furthernore, the type of neurophysiologic alteration, as reflected in
EEG synchrony and frequency
oatterns, was related to specified
types of behavioral adaptation. Increasing EEG synchrony and a shift
to slow frequencies were associated with tranquillisaticn, sedation
and decreasing agitation; while desynchronieation and a shift to
fast frequencies was associated with excitement, illusions, and
delusional ideaticn (6,20). These observations are consistent with
hypotheses of Wikler. The advantages of EEG techniques for the
assay of new psychotropic agents have already been reported (6).
were

V

�-6PSYCHOPHARHACOLOGI EVALUATION PROGRAM

besed on

present progree, instituted in October 1959, is
these studies end is designed to ensver the following questions:
Is there e reletion between eeesureble elteretien
in brsin function end behevierel chenge with psychotropic drugs on chronic edninistretion?
Are there pre-treetnent clusters of psychietric,
physiologic end psychologic veriehles releted to the
type of behevierel edsptetien?
And, ere such clusters related to the type end
degree of physiologic ohenge?Method: is en initiel epproxinetion, e double-blind, fixed
dosege rendon eseignnent drug study wes underteken. Besed on our
clinicel experiences with verious psychotropic coeponnds tree
195k to 1959, three clessss were selected on the besis of their
patterns of EEG response.' the egents selected were those with
either predoeinent desynohronising petterns, synchronising end
slowing, or mini-e1 or no effect. Petients referred for drug
therepy, etter nedicel exeeination, end etter ell other eedicetions
heve been discontinued ere rendonly essigned to e conpennd in one
of these three cleeses.
Petients ere predominently middle eless, urhen, with high
eduoetionel etteinnent. Hillside Hospitel is e nonnprﬂtit,
philenthropie supported psychietric institution, ednitting volantery
petients for extensive psychetherepentic treatment. The noen
duration or stey for petients is seven months. Convulsive end
psychotropic drug therepies ere prescribed by stetf psychietrists
The

�.7.
referral to the Departaent. All treatment is administered by
Departaental start, so that the experimental variables of drug
dosage, route of adainistration, assignment to groups, 232' are

on

readily controlled. All patients in the hospital are available
for study.
After a testing period, all patients receive he so of liquid
aediestion daily tron individually labelled bottles. Dosages are
increased in fixed weekly steps until a aaxiaua at h weeks. After
two weeks on maxiaua dosage, ro~testing oeeurs.
Io date, 1&amp;0 subjects have been referred, and 110 have eonpletod
the study period. Preliainary analyses of the data are new in
progress.
Behavioral Change: In a survey of the behavioral adaptations
of patients reeeiving phenothiasines or iaipraaine during 1958-59,
various clusters of behaviors were developed. The typologies were based
on the treataent response and on pre—treatnent psychiatric profiles.
In the present study, the typologies are being tested, and various
measures of behavioral change are being studied. These include
therapist referral questionnaires and six week evaluations, therapist
and patient Clyde Hood Scales; Lorr Scale evaluations in interview
by two research psychiatrists, and Lorr Ward Scales; and patient
sel£~ratings including the Johns Hopkins syaptoa check list and the
Chicago Attitude Scales.
lenrogszehelegx: Psycholozie tasks have been viewed both as
ehanze variables and predictive variables. In convulsive therapy,
changes in aenory tasks (22), tactile perception (23,2h), WeehslerBollevne (13), CF! (13), figureagronnd tasks (25): and taehistoseopie
recognition of figures (26) were related to the degree or induced

0%

�.8neurophyeiolegic change. for each task, the degree of decrement in
tank portornance was found to be positively correlated with the
enount of EEG cloning. Following treatnent completion, with the
return or phyeiologic indicee to pre-treatnent levelo, performance
in these paychologic tacks aloe returned to pro-treatment levels, or
higher - e hetternent of performance ascribed to prectice effect.
Denial ecoree on interview (27), Rorschach determinante (16,17),
I Scale coerce (15,17), language patterne after anoberhital (28),
auditory teedheck end perception of the vienal upright have been
viewed as predictive indicee of the behavioral chengee following
36!.
Thole veriene tasks are now being eeeeeeed with psychotropic
egente, for their capacity to chenge with verione agents, or their

capacity to predict change.
Electroencephelogrephze In the convnleive therepy etndiee,
the degree of RIG cloning nae neaenred by counting the consecutive
waves in selected eenplee (7). When the more subtle changes or
drug effect- are etndied, it ie neoeeeary to apply leee tedious
techniques. Electronic frequency enelyeie wee introduced in inguet
1959. By neaenrenent of the pen deflection for vaﬁione frequenciea
from 3 to 33 ope in ten eecond epoche, repid eeeenreeent of
apparently
enall chengee in total activity and frequency epectra are new obtained
and epplied.
Other phyeiologic variablee etndied in thie progren include the
reepenee er era to intravenous ohlorprenaeine; bleed preeeure reeponee
to neoholyl; the EKG, radioactive iodine npteke, end analyeee o:
varioue blood and urine elenente.

E 5

�PSIGROLIHGBISIIGS

series of studies in the Departnent have been devoted
to ternal lenguege patterns.
Following the etudies of syntactic lenguage petterns (28)
in convuleive therepy, other espects of lenguage were studied for
their relation es indicee or chenge in interpersonal behavior.
darts; otter considerable exploretion with verious linguistic
neesures, nuggested thet typeutoken-retioe (2!!) of consecutive
senplos or dyadic speech nay be e enetnl index (29,30). While
213 hed previously been applied to written texts or the language
senples of indiriduels, Jeffe indicated that the two pereon eonnunicetion (dyed) wee e acre significent index of the etete of
the interaction then enelysee or concrete eenples of the participants.
Ayplying this technique to convulsive therapy petionte,
changes in 21! neon end etenderd deviations were releted both to
the degree of induced ERG slow ueve ectivity end to syntactic
lenguege petterne obteined in independent structured interviews.
Speech heeene more repetitive (lowered nean 113) and nkre verieble
in consecutive eenplee (increesed etenderd devistion)§(31). In
Another

interviews hetero end otter the intrevenous edeinistretion or
centrelly ective egente, einiler chengee were observed. Agente
with e predominent synchronization pettern on the EEG exhibited e
decreese in mean or: and increase in standard deviation of scores,
while deeynchronieing conpounde elicited greater variability in
speech petterne (increase in TTR neon) end decreeee in veriehility
of consecutive eoorss (decreeee in etenderd devietion) (32).
Other lengnege neeeures studied included dietrese~relie£
quotients, self—reference, and elteretion in tense end person.

�«10-

It

was luggontod

that then. psycholingukatic nonsuroa

tr.

techniques for the opcrational annlyaoa or physidlagic and
psychologic ctr-eta of psychopharuteologic ugcnts (32).

potent

�.11 .3001030910 STUDIES

In the course or these psychiatric programs, considerable
interest wee engendered in the tenily organization to which patients

returning. Also, the general problem of the relation of social
factors to choice and results of psychiatric treatment, and the
specific problem of the relation of these factors to the referral
patterns led to a eeriee of pepnletion studies. In one study (33),
education, ego, place or birth and score on the California I scale
were significantly related to the type or therapy received and the
utilization of addonotive hospital services; Thus, patients who
were older, poorly educated, had higher P scores and were foreignhorn, particularly Eastern Europe, were most likely to he referred
for electroshock. These relationships were present independent of
diagnoses. Within the group o: electroshock patients, the tire for
referral for BC! was also related to these factors;
In a second study (18), duration of hospitalization, discharge
evaluation and diagnoses were related to the eaae social factors.
For example, patients hospitalized for the shortest period were
oldeet, had the least education, were most likely to have been foreign»
born and had the higher 1 Scale scores. Younger, native-born, more
educated, lower 1 Scale score patients were hospitalized the longest.
these relationships held true within treatment type and within
diagnostic close. On discharge, older patients had the nest favorable
ratings. In 30?, patients rated as recovered or much improved had the
highest 1 scores, least education and were most likely to he foresighorn. In another study or patient refusal of nor, similar relationships knee observed (3h).
were

�Theee

reletionehipe ere

new

under etudy in the Out-Petient

Depertnent, end in e tri—hoepitel conperetive study. In the letter
etudy, the population: or three hoepitele with preveiling differing
cliente, in which e11 therepiee ere equally eveileble to e11 petiente,
- Kenninger Peundetion Hoepitel (upper-ollee, Proteetent), Hheeeehueette lentel ﬂeelth Center (leverceleee, Getholio) end Hilleide
noepitel (niddle-eleee, Jewieh) ere being eeeeeeed. It hee been
postulated that theee reletionehipe reflect the influence of eociel
beckgrouud on peychologicel processes, such ee hebituel petterne
of eennunieetien and nodes of expreeeion. The contribution of these

factors to the pattern or mental illneee, end the petient-therepiet
interaction ere under etudy.

�-13SEHMAB!

.

on. Dopartnontal programs are a clustor of intsrrslatsd
studios toonssod about common population sonplos. Within Hillside
Hospital, rosoaroh laboratories in Bioohonistry, and in Hsdieino
are aotiro; and other laboratorios in psychodynanic psychiatry aro
boing dovolopod. In this Dopartaont, various disciplinos aro

participants,rsprssonting a gradual growth of six ysars. Furthsr
growth and tho dirsotions o: ensuing studios sro dopondsnt on tho
results of tho studios doscribod bars; as wall as tho growing
institutional avaronsss that roooaroh is an intogral part or the
hospital's operation and budgots - as such as troatnont and staff
training.

�”lh‘
Reterenaea
Authors at the {alleving references include the following
staff nenbere: Hex Pink, Hex Pollack, Robert L. Kuhn, Joseph Jette,
xertin 3. Green, Eric Kerp, Hyman Karin, Doneld F. Klein,
George Ireuthener, Arnold G. Blnnberg, Ittheniel S.
siegel,
Abrehen Keplen end Henry

1. J. Hillside Reap.
113, 19583

3.

J.

lééa 18h6, 1958)
A

Go., 325, 19593

J. Letkewite.

2. Die. Harv. 8:1. 12:
Eilleide Heepitel‘gt 13h, 1955) h. J.A.H.A.
Q}

197, 19571

5. Pszehozhernecolegz Frontiers, Little, Brown
6. Heuregazehozherneeologz, Eleerier, hhl, 1960;

7. A.H.A. Arch. Neural.

Psychiet. 1Q: 516, 19573 8. Die. Kerr.
5:3. 12: 227,19583 9. J. Hillside Heep. g. 3, 1955; 10. Arch.
lenrol &amp; Peychiet. 1g. 23, 1956.
11. First Int'l can . leurol. Sc1., Pergenon, 613, 1959:
12. Jeur. Herr. Kent. Die. $29: 117. 19603 13. A.H.A. Arch. Gen.Paychiet. (in press); lh. Unpublished nenneerﬁﬁtg 13. Jenr. Herr.
&amp;

'

Bent. Die. ggg: 187, 1960; 16. J. leurepeyehiet. 1: 2&amp;2, 19603
1?. Jour. lerv. Kent. Die. ggg. 2h3, 19593 18. A.H.A. Arch. Gen.
Psychiet. 1; S65, 1959: 19. A.H.A. Arch. laurel. &amp; Peychiet. ﬁg:
20. EEG Clin. Neurophyeiel. 15¢ 359, 1960.
380, 19583
21. Gened. Psych. Aeeee.

J.

A: 1668, 19591

22. Cent. Neural.

23. J. Hillside Hoep.‘§: 2&amp;1, 1957;
1g: 88, 19563
2k. Am. J.
Psychol. 13: 38h, 19593 25. A.H.A. Arch. Neural g: 5&amp;7, 19601
26. Free. 1?

Int.

Pezehel., lerth-Hellend, 238, 1959;
1%. J. Heuropeyohiet. 1} hS. 19593
28. Pezehezethelegz of
Guaranieetien, Grnne &amp; Stretton, 126, 19583 29. J. Hillside Heep.
g; 207, 1957; 30. Psyehiet. 3;. 2&amp;9, 1958.
Gong.

�.1531. Jour.

lorv. Hunt.

D13. 120: 235, 19603

Pazchiutric Drug Thorazz, 0.6. that‘s, 29, 19603
3b. Unpublished Hannueript.
Boap. g: 216, 195?)

32. ngnnieu at
33. J. Hillsid-

�lap-rtnaltal Fuyuhtutrac 2701:... at 3:11:14. luapitcls
A

title:

In: fink,

Fran tau ntpnrtuaut

”’F‘ul. 91“ “kl.

7!:
U

I,

1;!50

K.B.

a: sxpurtnuutnl Psychiatry, 1111.14.
10.1.;

'0’.

�/
[,

‘e

VI

//y

11/22/60

layoviunntal ruyuhtutrto Procrnnn u‘ [1113140 loapltnlu
A Icvtou

It. Virtoun

program: 1: an. nupartnant of xxpcrtnantal
Payoh‘airy 531‘ but: dcvutod to an underttnndtn: of tho sad. at
ﬂl‘itl at payuh1n$r1¢ thnruptta through studina at brtiu tunetiun.
rho principal inshnign¢¢ invo boon adapted {ran doneriptiv.

plyuilutry.vnanrapiyuhology, oloetronnotphnlocrnphy. lingututtcl,
phuruaaolﬂtyg and socinlocy.
1n
chungoa
brats
convululvu
thcrtpy,
at
initial attain:
functian nova round ta rtlatc both to ovuluution- o: inpruvaucnt

In

ptywholaciéﬁznrinblca.
Al 0‘? undarnttudtnu
and to pru~tr¢3tncut
or eonvulaivw thcrupy dovelupad, a genera: nouroyhynialozic1
(
usergnd
slanttw
). In this via:
thorapxos
a!
vita
udtpttvc
uiif‘i‘rxplnttonlly
thy
dogtoo
to
ottactivo
troutueutn
payihtntrtu
this brain function 13 uncuurahly nl‘nrnd. will. Chung. in brain
function 1- noatnsary tar bchuvtorul ch:u¢o, the twp. or nd:p$¢tton,
paywhologiédnna
hurtvnr, vnrtoo «avoiding upon pro-‘rontncnt
Itoiuloxliﬂcharactnrtutio: 02 sh. cuhdoot (2). Thus, tho use. or
uotlcn 1. not soon as ulthar 'oralnle' or *poynhologic' but rathcr
and
chaugua
of
nourophyaiologio
distant
tan
lattruaticn
a.
adnptivo 3008331.... turthcr, uh$lo bohtvtirtl chins. 1a rnluted
to ohnngns in brain ttnottaa,‘nnd the nanptivt patio!» t0
prt-triatuont psychologte thirtetcricttot, 07:1nat10nu a:
’1Iprovcunat', but»: npuottl $79.! or uvlzuntiou or chnnxo, arc
atrtvutivs stagnant. hated an :tatt and £1.11: oxpootutions and
inlcrtaonu (2).

�n2-

?hiu hypothuain Ill dovulopca and nuntstncd an a £021.! a!
ntuditl qt cunvulstvn thnrnpy. ctncurrcnt aﬁudios a: tuuulia can.
tnd1¢utod taut hohsvtor¢1 chant. horn. too, wua.r¢1ntod to tn.
lutot ind accrue or piniongut can: a: ropaatod stature. - that.
b.1uc tho prinaxpul manifestations at proloncod nonrcrhysioloctcaﬂ

an that»: (ink).

chm: in

It:

made

if

aoStoa of tho new pcyahotropio «goat; vac also

nithta thin hypothesis (5,6). It nan ouggontod that
ﬁhouo tgan%a would ho affectivc to tho 403:0. that ghoy induced
paratatant ch:ugau 1a brgtn fanatian and that the typo at bchaviur;l
rampaano Inuld to rolttud to tho typo or brain ohaagc, and to
prcaorbtd payohologit (paruunultﬁr) patturnt. Tho prisont pruxruan
in tin Btpartltat ‘20 4331¢u§d to study th.ue volitianuhipt in
unprosuud

_d¢tti1.
E

E

III

13‘ £88

a: turtou: nanutrnn at brain tunusiaa, thc alount a:

slaw

var. atttvity ta ta. cinctrcunoupphagzrin (1,8) tad contcbulutary
and 60.1.1 Inasmuch pattora: nttur unobarbital (9.10) not. thu
unit uoaca‘:vc that... (11) 1a .0I7‘101VD thorny: subjects. In
on. naportnont, tapruvclnnt ratings wire ctrruxttod with the
upponrnacc .1 itch dgcrooa or change in thou. inexact (7.10).
dtnbin-bltnd
1a
1n
abnorvntiana
tkntot
a
a‘udy
”‘2.
it...
Itiuh patiohta rotorrod for clootrguhock var. rand-n1: nustgncd
to court‘s o: otthor ocnvulutvu 0r aubconvulttvo therapy under
anurophytlologiénchaagt
pqntothnl prcnodtonttal. nigh dugrtul or
v!ra obuarvod only in tun convulitvn grnupg inprcvon-nt rutct varnixuitiouutly higher in this ﬁriﬁtj and vhaa subconvuluiv: nubjoeto

�U).

*

v.20 ru-trontad by couVIInivo upyliuutiona, ﬁlo tuprovcnnnt rut.
um: lintzsr to the orictual convtlaivt group (2).
In the anboouvulaivo treated Inhannta, uuuutdar;b1¢ Quaint.
or altntria «arrout yauaca hotuocu tho hitanporul cluotrodoc.
It Ipptﬂrtd that the thorupautic taunt wan not tho total cloatrle.1
currunt, aggugg, but an :11 or non. quality nan££.ctnd by thc
grand In: lotuuru (8,12). Th. algnittenuao at ﬁhc grand In!
I'liir. van~cxan1uod in etudiat of tho inhalant aouvnlsnnt,
insurlugrodtothylcth¢r (13692105). ﬁinilur 4.3!... of alsetro~
graphic ehsngc, ﬁngvovwnaut tutti, typos or bghgviortl ahtugo
and changes In nourvysyuholoxtiﬂgatk bahavivr nﬁro observcd in

tic tnhallnt

tn ulcatrieally treatud groups (13).
It at. anon npyaroat $hat act :11 tubjaats Ianiroatins
high tugraou or physiologxc chnngo warn rttod ts '1npravod'. Ia
a dcsaripttva typolngtn study, :31. ptttarna wire doacrihad,
impartcnlly turned 'ouphnrlu', 'hypounnio', 'sonlttnatiuu',
$0!!ﬂ.1£¢'1‘hdtlﬂl1'. and 'punlo‘. ﬁhtlo the ttrat tun of than.
udnpt11¢ .04.: nor: rttud I. 'nugh taprovod', ¢ho latter two were
noun as 'Iuinprovvd' or 'uoraa' (1%).
In station a: ysyuh01031£#VIrinb1on, it run vaportod that
pctxnnta rntcd as 'I‘ch improvud* and 'reaovurad' frequently
ltnituntcd puruonnltky puttcrut liuillr ta that diaeribod by
ﬁctuutnin and Ink: is ﬁhu laplacit vorbal 4.31.1 pornonality.
'In 1!:zunxo ynﬁtoras, patiantn capraastd thu 'lnazuugu a: doninl',
than ditthln brain ohnagc In: Indueca, txhiblttus anon napocﬁa an
txpltctt dintsl, Izaiuisataun, ditylne¢noat, cliches, g§g&amp;_uorc
traqu.ntly thug untuwravcd cubaoctu. Other 134130: taint-d to tnvorsblo
and

�.3.
hash I 5341. acct. (15), and Roruuhaeh dotarnintnts
«Olav, nbsaut novunaat and nbaont t-rn-calor (16,17). In thia
popu1&amp;tttn, also, :avurablo outatuu at. taaoctntod with 10v
uduaattgnnl uahxuvannnt tad {truism birth (18).

tutu... it?!

at

sitting a way to nuancat tun digit. of pentatonvulitvu :39
$1.! utvu nitzvity, ta anttahozanorciu coupltnd, «totEutzno, was
giro: tutrnvonoualy at various :tngos or tht ccavulutvc thor‘py
-

proutll (19). doa$r¢ry to oxyaetntiaal, ditthnlinc

eaunod In

lunadiatd and «attained ¢aer¢aan in EEG cloning. Patiunta with
donstl lagging. putt'ruu rulaaqntshad than. Inttcud or atphorin
aha wall hasng, thc lubjoota vat. irritqblc, anxious and prrO181V.
or pramtrnatnnnt patterns. In aubaastv prior ta eonvulaiva a:
drug thnrapy, diothantnu andueod uxaitanont, tan-ion, anxiety and
illusory nontatsunc.
ﬁuhaoqncht ntndica with 9th.: «antral antioholinurutc
ae-paunda (VII-8299. 33-318,336g hanaotyttno) aboucd behavioral
sad cloctrogruvhlc pattarau elitist to daoth‘xino. atnilnr
datynahrontnnttau o: postuconvulaivt 330 niacin; was ‘10. notod with
«Mt-'11 amnion-tutu: hunuinnuo (nphounno, «suntan, nan-as).
Ind ht: been rcpur‘od for tatihiatantnoa (diphunyihylrauinc).
that. thiarvaticnu 10d $a tut mugxultion thtt «a incrtano 1n coutrnl
ottltnargia activiiy VQI a btoahouscal haul: for thy convulaivc
ttorapr greats: (26).

rsmgonauo nma an no
During this parted, tho mod. 0: sctlaa cf ucv¢r psychotrepic
drug. trout-d intnrnst. rollcving tho caaouptc doravca tron
'

J2

otavulntvu ‘harupr, thu nc‘rophgwiologio outage: inanood by drug.

�.5...
f

tutti!

I1th1n tun 3.x. aautc oxpcrinautu1 trunnuork at th.
E39 usttinx. It It: thaurvod thtt phonothitslnos (ohlorpronasiac,

any.

prangnlnc, tritanaprolaaxna) :nduood axe ayauhrontauttou and a
oh£tt1ng of tho upcetrun to tho .10! frequaaotts; Improbaghtc cad
barbiturates, an incrouuud IyuchrnaxsatSOB and a shirt 0: spoctrnn
to inst (recitation; roanrpiuo, an Inorouood ulcvtns with Iyaohrouw

inattua at

.

dying... and douynchronisatioa at night! 10'010 (5,6).
2.133.313. tainted ﬁctynohrtnisnttua with a ah1:% ct :rcquauaicu
fa the a!” but: (21).
”‘ng
Gina: expirtnnatal annpounda tul‘cd inaludod nz~uxaa and
phtnyaioltlslino (ariatol), nectar tad its variant aoneaaors
(33:99), wtatlh9 (37"h) and trﬁnquol (lorrill). tor cash, an
I0|tiutcut olnctrucraphia putters it. recordta.
psyuhoyhnrtnollaciéwazoats
wgu
that
staccatod
It
pruvtd. u
nearaphyuiolotiéﬂpat§cran
u
for
of
1a
nasal
eliciting varicty
ctutraat t¢ tho sags}: psttura or induced scavalnionu. furthtrnouroyhyntolugidJtlttrttion,
sh.
a!
type
.02.,
I: rotlon$ad in
as: aynohrcny and IFC‘ICRGI ynttcrna, nun rolnt.‘ to apoottiud
typo: a: behavioral stuptntsdn. InorOtttuc nae aynchrony tad a shirt
GO aluu fvnqncactou aura nauoatttud with
trangutlltzn‘tua, notation
uni docrnﬁatng agitatious stilt angynohraatua£tua and a shirt tn
tu't tragucncloa It: antacxntta with excitouaut, tlluuionu. tad
dolnntcntl ilcatton (6.20). than: aha-trutionu are conclt‘aut with
hypothaloa o: Hitler. 2h. advantagon at are tuchntquco tn: the
300.7 or not payuhntropzc ugcntu haw. nlroady b¢0u reportcd (6).
low

�2h. presuut progrnn, instttnﬁod in Outabcr 1959. 1a banal an
sh... attitua and in 6.113304 £0 .3380? $8. I’llavinc quantlultu
In £3.90 t rolutlon hotutcn Innuurublo altovtttua
in 53:13 tunc‘ian and bohnvtoral «hung. with payuho-

airbus. unnaatatrttian?
120 that. proeﬁrtntnoatfqlua§oru gt paynhxatrao,
ptyctulcciéinnd ptyuhmlc¢1£&amp;variahzoa rolgtud to in.
tropic drugs

an

typa 0: hohnviornl adiptntttn?
And, art such cluntora rolntod to the typo and
403200 at phyutologle ohuuxo?#
‘gggaggs AI ua.1n1t1n1 ayproxinattcn, a doublnuhlind, sized
Gonna. random Isntgnncnt drug study

clinical

In. undertnktn. luccd

on our

varitu' piyuhctropto coup-sud; tron
195k to 1959, thrco clan... unto 0.100%04 an tho 5‘31! or that:
patﬁnrun or 310 ro‘ponao. tho slant. scloutnd wit. that. rich
oxpcrzoncoa with

caﬁhcr proloninan‘ dunynuhrouiutax pattcrnu, Irhahrontutng and

nlyvinc, or nintnal or no errant. Pattoutu r-rorrud in: drug
therapy, IItOf nudist: tun-auntaon. and art-r :11 other nodicntiouu
hay. boon diucoattuucd are randomly usutgacd to ‘ compound.1n an.
or that. ‘hrio «lacs...
Pa‘icnto are pvodonlnnuﬁly Ilddlo eluot, urban, utﬁh high
oiiontaonnl :t‘linlont. 1111.14. 80-pita1 1a a nou-pritit,
philanthtopie supported psychiatric tnutttutton, .duitttng voluntary
pattoutn {or txtonntvn puyuhothurcpoutie troitntut. fin loan
duration or its: fer patients in novon months. convuiaivc and
puychotropao drug thnrnpics It. pronortbud by star: payuhxntriota

�.1.
A11
thc
trlatnnut in aduluintorad by
to
naparﬁutu‘.
rottrrll
Da’artniatul stuff, no that the axpcraanutal vartthlta or drag
daoaco, rant. 0! adutaictrnttua, aaotguunut to groupu, 333, &amp;r¢
roadtly controllod. 111 patiantu in thc hoapttal arc «v.113blu
for titty.
Attor‘a tutti»: ptrtod, 111 puticnt: rocuivc he so or liquid
‘nndtogttoa daily tron 1nd:vtd:ally inhallcd bettlco. Dos;¢o: at:
incrcnscd in ttxnd tOIIII atop: tutti a u.x:uun at h ucnku. Artur
tun wank: on nixtnau 4.111., ro—tnatlnx ¢o¢ura.
to dn‘o, 1&amp;0 vuhjaoto but. hon: rtturtod, and 110 have outplatod
tn. study period. Proltniunry analyst: of tho data At. an: in

on

prozroau.
Ichuvigral GhlI‘Oi In a tutti: u: tho bnhnviorul adnptnstonu
of pt‘tuuta rcaoiviag pitucthiasiutl or inipruutua during 1958-59,
variauc clustorn at bchnvtora var. duvolopad. 1h. typalocton wore but-d
on tho trontatut rcapiaat and on pr0~trlntauut ptyuh1&amp;tr1c protilus.
In $3. pruncut sitar, tho typoloxint at. being tested, and variant
scalarot at behavtoral ahtug. at. being atudtod. It... inaluac

thorlyitt ritorrnl quortiouuairoc

I1:

cvaluntiono) therapiat
tad puts-at Glyn. Road s¢nlang burr aoglu .valuntiona 1n int¢rviov
by two rnutnrch psychiatrtnta. and Lorr Hard Scale.) and puttout
unit—ratings 15013413: ‘ho Johan toutinl symptul about lint and the
stints. Attstnda 50:10:.
boon
both
vtcvod
I‘Vl
tank.
as
Psycholnglc
lutrggangglogzg
thing: vsrtnhlou sud pradlcttvo variablou. In convulsivo thorgpy,
chingo¢ in Inner: tanks (22), tactile paraoption (23,2h), wcohnlcro
Bolltvu‘ (13). err (13). flatro‘3rocnd talk. (25). ‘nd tachlntQUQOptu
recognition a! figure: (26) war. relatcd to thy Court. or induocd
and

ﬂ‘Ok

am

�neurophyutczogaggihnngu.

In: 9.03 tack, tn. dcxroo at docruuont tn
rouui ta b. poatttvny ocrr'lutod with the

‘llk vortoruuncn nus
assist a! :36 closing. lollewaac trout-oat aonalation, with the
rotur: a: phybitloxialiaaauca t. prootroatnnnt lovnln, performing.

payahologidﬁkasku
in than:
also raturnud to pro-trontnont lcvuln, or
higher ~ a buttarntnt 02 purrornnnco ascribed to practi¢o afloat.
Donia: start. on interviﬁw (27), aoroohach dotorl1nuntn (16,17),

r 8.11. Idﬂvit (15,17),

ltngunzu pntﬁarns attnr tnobnrbttal (28),
andatary toodbuck and porcuption if the 11:ua1 Iyrscht have bcan
v10v0d a: prcdlattvu attains at tho hchavioral outages following
362.
fhauo vurinuo tank. are at: being Isa-anon with paychctropio

:.£?:1.1p
agon$s,
alpncxty

capacity to prudiot chaago.

t. cling.

wl‘h vurtona anout319igfﬁhotr

§;I¢§ronniqggg;o‘gughzg In tn. convulttvn therapy ntndlnt.
the intro. of as» slaving was latsurod by counting tho oonncauttv.
wave- 1» lolcotad :unpi:a (7). lab.» ta. not. nubtlchohuazoo at

uttoetl arc ltudiod, it in uooclaury to gyply lula'ttdionn
toohntquoa. Iltctroulc Iroqutncy nnnlrlia wt: introduacd 1h Angint
1959. 8y nauaurounat 0: th. pun doticetion for vaﬁﬂoal rrnquoneius
Iran 3 ta 33 8?! 1n ttn ataoaa epochs, rapid nanuurcnnat o: upptrintly
nlnll august. in total activity nnd troguoncy aptctrl arc new obtatnnd
drug

tad applied.
ethn- play-1.1.316"
in thin program include tha
rtlpautn I: :36 to iatrnvontua chlorpronnsinzj blood protauro reapnunu
to
the nut, pullout!" 1041” mute, and
a:
turtouv blo.d and urin. elegantl.

man" “at“

”any”

“an“

w:

9!

115‘

8

�tho
atadlco
in
napnrtuont hurt beta dovctoa
.:
to torn;1 1.33133: puﬁtcruu.
iylzoving it. stutits ct syntactic lung‘tgu pattern: (:8)
tn asavulitvo ihsrapy, uﬁhor capogts at 11:51:30 vuru Ituaxod for
tkcir r01:$£on an iudSQIa of change in intovpornonnl bohtvtor.
.Jattc, urtnr oonoiiertblc omnlorutian with Various linguistic
consecutivn
or
that
suggcitaa
typo~tokoa~rtttol
(I?!)
lilltrit,
ho t
1nd»: (19.30). man.
«mm: at and“ apneh
it! hid prtvionoly §ncn npplicd tn urittua $311: or en. 1:ngungo
nanplou of indivﬁdulil, 3.1!. indicated that the two pcrnou cou~
nuatcttton (47") was 1 nor. liznitignnt indox at tho itttn at
tho interacting than auulylou or i¢paratu snnpxoa of tho ptrtitiplutl.
tpplying than toohutque ﬁt convulltvu shtrnyy patients.
chanson 13‘!!! noun and atundnrd «aviation. var. r01¢tnd both to
in. deavco or induced 3:3 ulot wire aat1viti and to uyutnet1c
lunxttxo pattern. ob$ttnca 1n indopondtut atruatnral interviouu.
apauah 5.01:. no»: rupo‘tttvc (lowered noun If!) and nor. vartnhlo
in coautcutivu nunplon (in-ruaI04 utnndurd d¢v1at10n) (31). In
intarvtawl but-r. and alter tho mutrtvvaonu aduanlatrtttoa at
ecutrally activa astutu, 31:11:: Ihlngil Int. obnurvod. taint.
with n yrcdouinant lynchruatxgtion pnttorn on tn. £86 oxhibitcd a
4.120ntt in net: 191 cud inﬂfilti tn itandnrd duvxatioa o: necros,
viii. dotynchrouising ealputuda 01101106 groatcr variability in
tyccch pattcrus (1:090... in RI! Inna) tad dtcrunan in v.r1ub111%y
of coauoeutiva scorn. (duorouun 1n ntandnrd deviatian) (32).
6th.: languaga notnnrnl atudiod includod diatroccurolior
quttt¢ata, uclt-rutcruncc, and alttrntion 1n tunnu and paracn.
Antﬁhar 30:10.

m

tutu

�.19.

nu: sagsoaﬁcd that ﬁt... yuywhcltnxutstta Inaiurcs tgo pa‘cat
incantqutl for sh: operational unnlytns o: phyaiologig%und
yi:¢h¢1¢¢1€?£ttactn a: ycychopharanaolugse taunt: (32).

It

�aggggaggzc $233133

It ta. court. at

‘

thou. plyuhta%r1e protraaa, comaidartblo
InﬁnrOtt Ian unguudarcd in at. tantly organisation to which pttttnto
turn rcturntnc. Also, its ginornl problem at tho ralntiou or stein!
M chase. and
a: pnychutric treat-out, and the
Ipttifia prathn a! the rnlutiau of thtli factor. in tht rarogrul
puttarna lad to a aortic at papulatian studsus. In on: study (33).
ﬁduaattua. ﬂgi, plus: ct birth cud score on tho Galltarnia r Iallc
wort ticnttioaatly ralctad to the may. at therapy rocoivod und the
utilatniton at adainottva hotpttnl aortic... rhui, pgttont; aha
var. older, pearl! uduantcd, had hishar I neuron And aura tarnishhnru, ptrtiuularlyranstnrn invent. wart neat ltkuly to be 90:0rfﬂd
tar ¢ls¢trouhooh. that. rclationahlpl worn proaont indopiadont or
atlxntnoa. within tic sunny 3: cluo‘ronhack patiuntu, $3. tins for
rotttrnl for 3a: 3:: ulna rolntnd to ﬁhoau factora.
In t nocand ntud: (18), dnru‘ton a! harpitnliantion, discharge
uvnluattan and asucnoun: vova rolniod ta tho Ian. social flotara.
fur uxauplo, patient: harpitlltuna for it. uhortcnt ported EOE.
oldest, had in. lcaaﬁ education, v¢ro punt llkcly ta hnvc baou farcicaioru and had the hiahﬁr t ﬁnal. user‘s. Younger, uttivowborn, not.
nénuatod, lava: ! 89.10 a¢oro yuttonta worn hospit.11sod thu taunt-t.
I)... rnlntinanhipl htld trnc within troutlant typt and within
diagnoatic 0131!. on dinohargt, 014.: patients had tan unit tavorablc
ratings. In :61, patients rated as renovated or sunk improvod had tho
highoat r 3.0!... lasat aduantion and war. moat 113.1: ta b. rurattg*
born. In anoﬁhcr study or p;t1cat textual a: new, 01.11;: rolattun~
ships tutu obsorvad (3h).

an».

nun:

�.12“

‘

thc
under
antarctiout
in
study
not
volatiiauh1pa
If.
It...
Dtpnrtutnt, and in I triuhtnpttnl coupura‘tvo study. In tho 133%.:
utuﬂy, tho pcpn1n%1ona at ﬁbre. haupttclu uttk provatltac dittcvtng
$0
.11 pttaoutt,
:11
wits!
aquully
in
thoruptcs
arc
I'lillhlt
cltuutu,

- Ionian:- muauw Iowan (mu-«nu, run-mu, hunk»
nottn lontil ﬂunl‘h cantor (lowiroclnns, ctthnlta) ‘34 ltllllio

loaptt&amp;1 (naddzcvcliuu, icwioh)

It.

ﬁning tanouacd.

It ha.

bcon

thy
rotlooﬁ
antlntnco
.2 social
rolutiandhtpt
it...
ha011ruund on payth.lo¢1all prrcanuou, such ll habitual pnttnraa
or contagiouttun and gods: of «sproutioa. {ha cantrthlﬁton 0! than.
tnotara to tho patﬁorn o: ncaﬁal 111303., and thy ptticIt-thnrtpiot
intoruottou are undo: atnﬁy.

postultttd that

�.13-

may;
it. nipnr$uoat:1 99032.3:

are a oluutar a! interrolntod
studios tocuunod about cannon pnpulntauu annplcu. within ltllltdo
Iblpttnl, restart! ltboratoricu 1a niaehauiltry, and in nadtctno
if. aattVQ; and 0th.: inbnrntorina 1a puyuhodyulnto puynhtntry Ar.hmaac aqvolcpud. In tat; Dtpnrtnont, various diacipllnoo tr.
vartttayaats,roprtuoatzn: a gradual cravth a: :1: 33.3.. tartan:
grcuth and t8. ﬂirtation. a: tanning 31341.. tr. dapoudont .a tau
rostlta at tho attain. dotcrahtﬁ hart; no will a: th§ (rowing
£Il$1titt¢ll1.nilrin031 that ruaonrch in an tutogral part of thy
httpitul't opcrnttcu and budgu‘n . II that ll trcntnnat and otutt

training.

�~13:-

kahuna”

fauna: uni-cue“ that“ m £0.11.ng
rut: hum" m rink, ﬂu hunk. “but 1.. tum, Jinnah um,
Int-u I. Erna, 3”,. Km, In" mu, ma: 3'. £1.13.
Guru Imam, ”and a. auburn. “that“ 8. 33.301,
abun- Inn: at! nary J. Mint“...
Aim" at

tho

J. “11.1“ lap. 93 197, 1957;
.3. J. mun. Hospital at
1958;

2. Ms.

3..

.113.

In".

81..

3:2:

h. 4.1.11.1.
1.1m... Iron

131;. 1955;

h
5.
ms
h “mule 1min”,
a c... .325. 1339; 6.
¢h02m00§2u. naval". Mal, 19603
7. Add. not. loan)... a 1-31.31». ﬂ: $16, 1957: 0. Mn. In".
an. '33: ”7.19563 9. J. i111.“- llup. g: 3, 1955: 19. Arab.
18116,

1958;

”my;

1.956.
:3,
rennin.
t
ﬁt
11. nm In“). 3” In“ 1. Sci. , Penman, 613.
u. “an Em. that. 31!. 122' 117. 19691 13. 1.3.1:.

Int-.1

Mm“.

1959)

arch.

Gun.

pan);
ﬁnalist“ autumn 15. Jar. low.
but. ml. ms 15?, 1960: 16. a. lunpuehut. 3,: an, 1960;
1?. am. it". lat. M... m; 11:). 1959: 18. Mid. Arch. on.
”want. .13 555. 1959; 19. Add. Auk. Int-1. I: "youth £9:
no.

1958;

21.

g:

(in

1h.

can“.

8!, 1,563.

usual.

can Emlyn“. 9,3: 359.
uni. Anna. 3. A: 1668, 1959:

to. no

13. 3.

Hanna. luv. g:

1950.

2:.

21:1, 1957:

car. lmol.
2h.

a. J.

luau: g: Shh 1m;
8&amp;.
17.19%:
Gong.
238,
1959]
901350;”
law-mama,
m,
335.
4.
28.
19593
lmopoychiu.
u.
chhgzﬂhclaa at
y
«1-. 35.11.14. Buy.
5
1953;
126,
Gun
29.
Mutton,
cwuuia,
g: 207. 19573 30. urchin. 3.2») 2139, 1958.
1?} 381:. 19593

25. MILL. Arch.

�.

«150

‘1-..

O

3'1.

:"9:

‘.".¢ "”‘o ﬁt‘t

&gt;
‘

‘

hip.

g: 216, 195'!)

g

31:.

w!

”5’

1,69}

M',
uranium-a Mnuonph
3.6;

2’. 196°,

3!.

W

33. ‘¢ 31.11.14.

�Experimental Psychiatric Programs at Hillside Hospital:
A

Max

Review

Fink,

MnD.

the Department of Experimental Psychiatry, Hillside Hospital,
Glen Oaks, L.I., N.Y.
From

VI: 1/61

�Experimental Psychiatric Programs at Hillside Hospital
A

Review

various programs in the Department of EXperimental
Psychiatry have been devoted to an understanding of the mode of
action of psychiatric therapies through studies of brain function.
The

principal techniques have been adapted from descriptive
psychiatry, neuropsychology, electroencephalography, linguistics,
The

pharmacology, and sociology.
In initial studies of convulsive therapy, changes in brain
function were found to relate both to evaluations of improvement
and to pre~treatment

psychological variables. As our understanding
of convulsive therapy developed, a general neurophysiologicadaptive view of somatic therapies emerged (1). In this view
psychiatric treatments are seen as therapeutically effective to
the degree that brain function is measurably altered. While change
in brain function is necessary for behavioral change, the type of
adaptation, however, varies depending upon pre—treatment psychological and sociological characteristics of the subject (2). Thus,
the mode of action is not seen as either "organic" or "psychologic"
but rather as the interaction of diffuse neurophysiologic changes
and adaptive mechanisms. Further, while behavioral change is
related to changes in brain function, and the adaptive pattern to
pre-treatment psychologic characteristics, evaluations of
'improvement’, being special types of evaluation of change, are
derivative Judgements based on staff and family expectations and
tolerances (2).

�-2This hypothesis was developed and sustained in a series of
studies of convulsive therapy. Concurrent studies of insulin coma

indicated that behavioral change here, too, was related to the
onset and degree of prolonged coma or repeated seizures - these
being the principal manifestations of prolonged neurophysiological
change in this therapy (3,h).
The mode of action of the new
psychotropic agents was also
eXpressed within this hypothesis (5,6). It was suggested that
these agents would be effective to the degree that they induced

premorbid psychologic (personality) patterns. The present
programs
in the Department are designed to study these
relationships in

detail.

CONVULSIVE THERAPY PROCESS

0f various measures of brain function, the amount of slow

activity in the electroencephalogram (7,8) and confabulatory
and denial language patterns after amobarbital (9,10)
were the
most sensitive indices (11) in convulsive
therapy subjects. In
wave

one experiment, improvement

ratings

correlated with the
appearance of high degrees of change in these indices (7,10).
These observations were tested in a double-blind
study in
which patients referred for electroshock were
randomly assigned
to courses of either convulsive or subconvulsive therapy under
pentothal premedication. High degrees of neurophysiological change
were observed only in the convulsive group; improvement rates were
were

�-3-

significantly higher in this group; and when subconvulsive subjects
were rc-treated by convulsive applications, the improvement rate .was similar to the original convulsive group (2).
In the subconvulsive treated subjects, considerable amounts
of electric current passed between the bitemporal electrodes.
It appeared that the therapeutic agent was not the total electrical
current, per sez but an all or none quality manifested by the
grand mal seizure (8,12)o

significance of the grand mal
seizure was examined in studies of the inhalant convulsant,
hexafluorodiethylether (Indoklon). Similar degrees of electroThe

graphic change, improvement rates, types of behavioral change
and changes in neuropsychological task behavior were observed in
the inhalant and in electrically treated groups (13).

It

apparent that not all subjects manifesting
high degrees of physiologic change were rated as 'improved’. In
a descriptive typologic study, five patterns were described,
empirically termed 'euphoric', 'hypomanic', 'somatization',
'paranoid-withdrawal', and ‘panic'. While the first two of these
adaptive modes were rated as 'much improved', the latter two were
was soon

seen as *unimproved' or 'worse' (1h).

variables, it was reported that
patients rated as 'much improved' and 'recovered' frequently
manifested personality patterns similar to that described by
Weinstein and Kahn as the explicit verbal denial personality.
In language patterns, patients expressed the 'language of denial',
when diffuse brain change was induced, exhibiting such aspects as
In studies of psychological

�-h-

explicit denial, minimization, displacement, cliches, 222. more
frequently than unimproved subjects. Other indices related to
favorable outcome were high F Scale score (15), and Rorschach
determinants of color, absent movement and absent form-color (16,17).
In this population, also, favorable outcome was associated with low
educational achievement and foreign birth (18).
ANTICHOLINERGIC COMPOUNDS AND CONVULSIVE THERAPY

Seeking a way to augment the degree of post-convulsive
slow wave

activity,

an

anticholinergic

compound,

diethazine,

EEG

was

given intravenously at various stages of the convulsive therapy
process (19). Contrary to expectations, diethazine caused an
immediate and sustained decrease in EEG slowing. Patients with

denial language patterns relinquished them. Instead of euphoria
and well being, the subjects were irritable, anxious and expressive
of pre-treatment patterns. In subjects prior to convulsive or
drug therapy, diethazine induced excitement, tension, anxiety and
illusory sensations.
Subsequent studies with other central anticholinergic
compounds (WIN-2299, JB-318,336, benactyzine) showed behavioral
and electrographic patterns similar to diethazine. Similar
desynchronization of post-convulsive EEG slowing was also noted with
central sympathomimetic hallucinogens (amphetamine, mescaline,
LSD-25), and has been reported for antihistamines (diphenylhydraminc)
These observations led to the suggestion that an increase in central
cholinergic activity was a biochemical basis for the convulsive
therapy process (20).

�PSYCHOTROPIC DRUGS AND EEG

During

this period, the

drugs aroused

mode

of action of newer psychotropic

interest. Following the concepts derived

from

convulsive therapy, the neurophysiological changes induced by drugs
were tested within the same acute experimental framework of the
EEG setting.
It was observed that phenothiazines (chlorpromazine,
promazine, trifluopromazine) induced EEG synchronization and a
shifting of the spectrum to the slow frequencies; meprobamate and

barbiturates, an increased synchronization and a shift of spectrum
to fast frequencies; reserpine, an increased slowing with synchronization at low dosages, and desynchronization at higher levels
(5,6). Imipramine induced desynchronization with a shift of
frequencies to the slow bands (21).
Other experimental compounds tested included BL-M188 and
phenyltoloxamine (Bristol), Deaner and its various congeners
(Biker), WY-21h9 (Wyeth) and frenquel (Merrill). For each, no
consistent electrographic pattern was recorded.
It was suggested that psychopharmacological agents provide a
means for eliciting a variety of neurophysiological patterns in
contrast to the single pattern of induced convulsions. Furthermore, the type of neurophysiological alteration, as reflected in
EEG synchrony and frequency
patterns, was related to specified
types of behavioral adaptation. Increasing EEG synchrony and a
shift to slow frequencies were associated with tranquillization,
sedation and decreasing agitation; while desynchronization and a
shift to fast frequencies was associated with excitement, illusions,

�and

delusional ideation (6,20).

These observations are

consistent
with hypotheses of Wikler. The advantages of EEG techniques for
the assay of new psychotropic agents have already been reported
(6).

�97PSYCHOPHARMACOLOGY EVALUATION PROGRAM

_______an.._________.__u~m._______.

present program, instituted in October 1959, is based on
these studies and is designed to answer the following
questions:
Is there a relation between measurable
alteration in brain function and behavioral
change with psychotropic drugs on chronic
administration?
Are there pre-treatment clusters of
The

psychiatric, physiological and psychological
variables related to the type of behavioral
adaptation?
And,

Method:

As an

are such clusters related to the

initial

approximation, a double-blind, fixed
dosage random assignment drug study was undertaken. Based on
our
clinical experiences with various psychotropic compounds from
l9Sh to 1959, three classes were selected on the basis of
their
patterns of EEG response. The agents selected were those with

either predominant desynchronizing patterns, synchronizing and
slowing, or minimal or no effect. Patients referred for drug
therapy, after medical examination, and after all other medications

have been discontinued are randomly assigned to a
compound in one

of these three classes.

Patients are predominantly middle class, urban, with high
educational attainment. Hillside Hospital is a non-profit,

�-8-

philanthropic supported psychiatric institution, admitting voluntary
patients for extensive psychotherapeutic treatment. The mean
duration of stay for patients is seven months. Convulsive and
psychotropic drug therapies are prescribed by staff psychiatrists
on referral to the Department. All treatment is administered by
Departmental staff, so that the experimental variables of drug
dosage, route of administration, assignment to groups, 323. are
readily controlled. All patients in the hospital are available
for study.
After a testing period, all patients receive no cc of liquid
medication daily from individually labelled bottles. Dosages are
increased in fixed weekly steps until a maximum at h weeks. After
two weeks on maximum dosage, re-testing occurs.
To date, 1ho subjects have been
referred, and 110 have completed the study period. Preliminary analyses of the data are now
in progress.
Behavioral Change: In a survey of the behavioral adaptations
of patients receiving phenothiazines or imipramine during 1958-59,
various clusters of behaviors were developed. The typologies were
based on the treatment response and on pre-treatment psychiatric
profiles. In the present study, the typologies are being tested,
and various measures of behavioral change are being studied. These
include therapist referral questionnaires and six week evaluations;
therapist and patient Clyde Mood Scales; Lorr Scale evaluations in
interview by two research psychiatrists, and Lorr Ward Scales;
and patient self-retina including the Johns Hopkins symptom check

�-9-

list

the Chicago Attitude Scales.
Neuropsychology: Psychologic tasks have been viewed both as
change variables and predictive variables. In convulsive therapy,
changes in memory tasks (22), tactile perception (23,2h), WechslerBellevue (13), OFF (13), figure-ground tasks (25), and tachistoscopic recognition of figures (26) were related to the degree of
induced neurophysiological change. For each task, the degree of
decrement in task performance was found to be positively correlated
with the amount of EEG slowing. Following treatment completion,
with the return of physiologic indices to pre-treatment levels,
performance in these psychological tasks also returned to pretreatment levels, or higher - a betterment of performance ascribed
and

to practice effect.
Denial scores on interview (27), Rorschach determinants (16,17),
F Scale scores (15,17), language patterns after amobarbital (28),
auditory feedback and perception of the visual upright have been
viewed as predictive indices of the behavioral changes following
ECT.

These various tasks are now being assessed with psychotropic

agents, for both their capacity to change with various agents and
their capacity ts predict change.
Electroencephalography: In the convulsive therapy studies,
the degree of EEG slowing was measured by counting the consecutive
waves in selected samples (7). When the more subtle changes of
drug effects are studied, it is necessary to apply less tedious
techniques. Electronic frequency analysis was introduced in

�August 1959.

By

measurement of the pen deflection for various

frequencies from 3 to 33 cps in ten second epochs, rapid measurement of apparently small changes in total activity and frequency
spectra are now obtained and applied.
Other physiological variables studied in this program include
the response of EEG to intravenous chlorpromazine, blood pressure
reaponse to mecholyl, the EKG, radioactive iodine uptake, and
analyses of various blood and urine elements.

�-11PSYCHOLINGUISTICS

series of studies in the Department have been devoted
to formal language patterns.
Following the studies of syntactic language patterns (28)
Another

in convulsive therapy, other aspects of language were studied for
their relation as indices of change in interpersonal behavior}.
Jaffe, after considerable exploration with various linguistic
measures, suggested that type-token-ratios (TTR) of consecutive
samples of dyadic speech may be a useful index (29,30). While
TTR had previously been applied to written texts or the language

individuals, Jaffe indicated that the two person communication (dyad) was a more significant index of the state of
the interaction than analyses of separate samples of the
participants.
Applying this technique to convulsive therapy patients,
changes in TTR mean and standard deviations were related both to
the degree of induced EEG slow wave activity and to syntactic
language patterns obtained in independent struuctured interviews.
Speech became more repetitive (lowered mean TTR) and more variable
in consecutive samples (increased standard deviation) (31). In
interviews before and after the intravenous administration of
centrally active agents, similar changes were observed. Agents
with a predominant synchronization pattern on the EEG exhibited a
decrease in mean TTR and increase in standard deviation of scores,
while desynchronizing compounds elicited greater variability in
samples of

speech patterns (increase in

TTR

mean) and

decrease in variability

�-12-

of consecutive scores (decrease in standard deviation) (32).

other language measures studied included distress-relief
quotients, self-reference, and alteration in tense and person.
It was suggested that these psycholinguistic measures are potent
techniques for the operational analyses of physiological and
psychological effects of psychopharmacologic agents (32);

�SOCIOLOGIC STUDIEE

In the course of these psychiatric programs, considerable
interest was engendered in the family organization to which patients

returning. Also, the general Problem of the relation of social
factors to choice and results of psychiatric treatment, and the
specific prohlem of the relation of these factors to the referral
patterns led to a series of population studies. In one study (33),
education, age, place of birth and score on the California F scale
were significantly related to the type of therapy received and the
utilization of adjunctive hospital services. Thus, patients who
were older, poorly educated, had higher F scores and were foreignborn, particularly in Eastern Europe, were most likely to be referred for electroshock. These relationships were present independent of diagnoses. Within the group of electroshock patients, the
time for referral for ECT was also related to these factors.
In a second study (18), duration of heapitalization, discharge
evaluation and diagnoses were related to the same social factors.
For example, patients hospitalized for the shortest period were
oldest, had the least education, were most likely to have been
foreign-born and had the higher P Scale scores. Younger, nativeborn, more educated, lower F Scale score patients were hospitalized
the longest. These relationships held true within treatment type
and within diagnostic class. On discharge, older patients had the
most favorable ratings. In ECT, patients rated as recovered or
much improved had the highest F scores, least education and were
most likely to be foreign-born. In another study of patient
were

�refusal of

similar relationships were observed (3h).
These relationships are now under study in the Out-Patient
Department, and in a tri-hospital comparative study. In the
latter study, the populations of three hospitals with prevailing
differing clients, in which all therapies areenually available to
all patients, - Menninger Foundation Hospital (upper-class,
Protestant), Massachusetts Mental Health Center (lower-class,
Catholic) and Hillside Hospital (middle-class, Jewish) are being
assessed. It has been “postulated that these relationships reflect
the influence of social background on psychological processes,
such as habitual patterns of communication and modes of expression.
The contribution of these factors to the pattern of mental illness,
and the patient-therapist interaction are under study.
ECT,

�SUMMARY

Departmental programs are a cluster of interrelated
studies focussed about common population samples. Within Hillside
The

HOSpital, research laboratories in Biochemistry, and in Medicine
are active; and other laboratories in psychodynamic psychiatry are
being developed.

In

this Department, various disciplines are

participants, representing a gradual growth of six years. Further
growth and the directions of ensuing studies are dependent on the
results of the studies described here; as well as the growing
institutional awareness that research is an integral part of the
hospital's operation and budgets - as much as treatment and staff
training.

�~16-

References
Authors of the following references include the following
staff members: Max Fink, Max Pollack, Robert L. Kahn, Joseph Jaffe,
Martin A. Green, Eric Karp,

Korin, Donald F. Klein,
George Krauthamer, Arnold G. Blumberg, Nathaniel S. Siegel,
Abraham Kaplan and Henry

Hyman

J. Lefkowits.

1. J. Hillside Hosp. 6: 197, 1957;
2. Dis. Nerv. Sys. 12:
3. J. Hillside Hospital h: 13h, 1955;
113, 1958;
h. J.A.M.A.
166: 18h6, 1958;
5. Psychopharmacology Frontiers, Little, Brown
6. Neuropsychopharmacology, Elsevier, hhl, 1960;
7. A.M.A. Arch. Neurol. &amp; Psychiat. 18: 516, 1957;
8. Dis. Nerv.
Sys. 12: 227, 1958;
9. J. Hillside Hosp. A: 3, 1955;
10. Arch.
Neurol &amp; Psychiat. 16: 23, 1956.
&amp;

Co., 325, 19593

11.

First Int'l

Cong. Neurol.

Sci.,

Pergamon, 613, 1959;

12. Jour. Nerv. Ment. Dis. 129: 117, 1960;
13. A.M.A. Arch. Gen.
Psychiat. (in press); 1h. Unpublished manuscript; 15. Jour. Nerv.
Ment. Dis. 129: 187, 1960;

16.

J. Neuropsychiat.

l:

2h2, 1960;

17. Jour. Nerv. Ment. Dis. 128: 2h3, 1959;
18. A.M.A. Arch. Gen.
Psychiat. l: 565, 1959; 19. A.M.A. Arch. Neurol. &amp; Psychiat. 82:
20. EEG Clin. Neurophysiol. 13: 359, 1960.
380, 1958;

J. g: 1663, 1959; 22.
J. Hillside Hosp. 6: 2hl, 1957;

21. Canad. Psych. Assoc.

16: 88, 1956;

23.

Conf. Neurol.
2h.

Am.

J.

25. A.M.A. Arch. Neurol. g: 5&amp;7, 1960;
Psychol. 13: 38h, 1959;
26. Proc. XV Int. Cong. Psychol., North-Holland, 238, 1959;
27. J. Neuropsychiat. l: h5, 1959;
28. Psychopathologx of

�-17-

m
Communication, Grune

'

&amp;

Stratton, 126,

19583

29.

J. Hillside

Hosp.

6: 207, 1957;

30. Psychiat. g3: 2&amp;9, 1958.
31. Jour. Nerv. Ment. Dis. 130: 235, 1960;

Psychiatric

HOSp.

Drug Therapy, C.C. Thomas, 29, 1960;

6: 216, 1957;

3h. Unpublished Manuscript.

32. ngamics of
33. J. Hillside

�EXPERIMENTAL PSYCHIATRIC RESEARCH
AT HILLSIDE
Review and Prospect
MAX FINK, M.D.

Reprinted from
JOURNAL OF THE
HILLSIDE HOSPITAL
Volume X ' Nos. 3-4 ° July-Oct. 1961
.

�EXPERIMENTAL PSYCHIATRIC RESEARCH
AT HILLSIDE
Review and Prospect
MAX FINK,

MD.

The dedication of Hillside Hospital as a Research Institute
has been a dream of many of its students—a dream that may
achieve realization in this decade. Dr. Tarachow was an early
proponent of this view; and both in his sponsorship of the Journal, and in his encouragement of research studies, he presaged
this development. He was also the inadvertent sire of the research studies in experimental psychiatry. While I was a resident in psychiatry in 1952, we collaborated in a study of the
relation of the early separation of child from a parent to the
adult choice of neurosis. Reviewing the hospital records of ﬁve
previous years we concluded that there was, indeed, a relation—
neurotic patients with obsessional neuroses had a signiﬁcantly,
greater incidence of separation than patients with hysterical
neuroses (2). This report was the beginning of the patient population studies described here.
Since 1954 the various programs in experimental psychiatry have
been devoted to an understanding of the mode of action of the psy-

chiatric therapies of the hospital. The techniques have been adapted
from descriptive and dynamic psychiatry, neuropsychology, electro—
encephalography, linguistics, pharmacology, and sociology. This report reviews these studies and presents support for the creation of
a Research Institute at Hillside.
PAST STUDIES

In our early studies of convulsive therapy, instituted with the
1

From the Department of Experimental Psychiatry, Hillside Hospital, Glen

Oaks, N. Y.

The studies reported here have been aided by the Board of Directors Research

Fund; the National Institute of Mental Health (Grants M-927; MY-2092,-27l5,
~4798; MF-12,033); Foundations Fund for Research in Psychiatry (FFRP 56-151);
Kaufmann, and Dazian Foundations; and numerous pharmaceutical concerns including Geigy, Bristol, Wyeth and Smith, Kline 8: French Laboratories.
159

�160

MAX FINK

aid of a grant award of the National Institute of Mental Health,
evaluations of patient improvement were shown to be dependent
both on changes in brain function and on psychological factors. As
our understanding of convulsive therapy developed, a general neurophysiologic-adaptive view of somatic therapies emerged (6).
A change in brain function was seen as a necessary condition for
behavioral change, with the type of change varying, depending upon
psychological and sociological characteristics of the subject (22, 25).
Thus, the mode of action was not seen as either ”organic” or “psychological” but rather as the interaction of neurophysiological
changes and individual patterns of response and behavior.
This hypothesis was sustained in studies of convulsive and insulin coma therapies (21, 22); and the mode of action of the new
psychotropic agents was expressed within this hypothesis. It was suggested that psychotropic drugs would be effective to the extent that
persistent changes in brain function were induced; and that the type
of behavioral response would be related to the type of brain change,
and to individual premorbid psychologic (personality) patterns (6,
28, 40).

l. Convulsive Therapy Process: Seeking a measure of altered
neurophysiological change that was sensitive and suitable for repeated retests, various measures were studied including changes in
the face-hand test (1, 10, 13, 35), memory tests (17, 35), amount of
slow-wave activity in the EEG (16, 23) and confabulatory and denial
language patterns after amobarbital (3, 15). The latter two, EEG
and amobarbital tests, were the most sensitive indices of change in
convulsive therapy subjects. In one experiment, clinical ratings of
improvement were correlated with high degrees of change in these

indices (15, 16).
These observations were tested in a double-blind study in which
patients referred for electroshock were randomly assigned to either
convulsive or subconvulsive therapy. High degrees of electrographic
slow-wave activity and positive amobarbital tests were observed only
in the convulsive group; improvement rates were signiﬁcantly higher
in this group, and when subconvulsive subjects were retreated by
convulsive applications, the improvement rate was similar to the
convulsive group (22).
In subconvulsive applications, considerable electric current passes
between the electrodes. It was postulated that the therapeutic agent
was not the total electrical current per se, but the “all or none”
quality manifested by the grand-mal seizure (9, 23, 42). The signiﬁ-

�EXPERIMENTAL PSYCHIATRIC RESEARCH

161

cance of the grand-mal seizure was examined in a comparative study
of the inhalant convulsant, hexaﬂuorodiethylether (Indoklon), and
electrically induced seizures. Similar degrees of electrographic change,
improvement rates, types of behavioral adaptations, and changes in
neuropsychological task behavior were observed in both the inhalant
and in the electrically treated groups (49).
However, not all subjects manifesting high degrees of physiological change were evaluated as “improved.” In a descriptive typologic
study, ﬁve adaptive modes were described, empirically termed “euH H
phoric,” “hypomanic,” “somatization, paranoid-withdrawal,” and
“panic.” While the ﬁrst two patterns were rated as “much improved,”
the latter two were seen as “unimproved” or “worse” (50).
In studies of psychological variables, it was reported that patients
rated “much improved” and “recovered" frequently manifested
personality patterns akin to the explicit verbal denial personality type
(37). These patients expressed the “language of denial” more frequently than unimproved subjects, exhibiting such aspects as explicit
denial, minimization, displacement and clichés (27). Other psychological indices also related to favorable outcome included high F
Scale score (42), Rorschach determinants of color, absent movement
and absent form-color (30, 45), and low educational achievement and
foreign birth (31).
2. Anticholinergz'c Compounds and Convulsz've
Therapy: Seeking a way to augment the degree of postconvulsive EEG slow-wave
activity, an anticholinergic compound diethazine, was given intravenously at various stages of the convulsive therapy process (20, 24).
Unexpectedly, diethazine caused an immediate and sustained decrease in EEG slowing, which was associated with marked changes
in language and mood. In patients with denial language
patterns
(27), these could no longer be elicited. Instead of euphoria and wellbeing, the subjects became irritable, anxious, and complaining. In
subjects prior to convulsive or drug therapy, diethazine induced excitement, tension, anxiety, and illusory sensations.
Subsequent studies with other central anticholinergic compounds
and sympathomimetic hallucinogens showed behavior and electrographic patterns similar to diethazine. These observations led to the
suggestion that an increase in the cholinergic activity of the central
nervous system was the biochemical basis for the convulsive therapy
process (38).
3. Psychotropic Drugs and EEG: Following these studies, the
neurophysiological changes induced by drugs were tested within an

�162

MAX FINK

acute experimental EEG setting. It was observed that phenothiazines
induced EEG synchronization and a shifting of the frequency spectrum to the slow frequencies; meprobamate and barbiturates, an
increased synchronization and a shift of the spectrum to fast frequencies; reserpine, an increased slowing with synchronization at low
dosages, and desynchronization at higher levels (18, 26, 28, 40). Imipramine induced desynchronization with a shift of frequencies to
the slow bands (33, 34). Each active psychotropic compound was thus
shown to have a characteristic frequency pattern.
Various other experimental compounds were also tested, and for
these no consistent electrographic pattern was recorded. These compounds have since been shown to have either no or very limited clinical psychotropic activity. The absence of behavioral change with these
compounds lent further support to the assumption that brain change
is a necessary condition for the action of psychotropic drugs.
These observations suggested that psychopharmacological agents
provide a means for eliciting various types of altered brain function
in contrast to the single pattern following convulsive therapy. Furthermore, the type of neurophysiological alteration, as reﬂected in
EEG synchrony and frequency patterns, was found to be related to
speciﬁed types of behavioral adaptation. The advantage of EEG techniques for the assay of new psychotropic agents and the technical
merits of electronic frequency analysis were assayed and described
(47, 52).
4. Insulin Coma Therapy:

In our insulin coma studies we con-

firmed earlier observations that persistent alterations of brain function were related to prolonged coma and spontaneous seizures; and
saw in this relationship support for a neurophysiologic-adaptive hypothesis. With the availability of the new psychotropic agent chlorpromazine, a controlled chlorpromazine-insulin coma study was undertaken in September, 1955. As patients were referred for insulin coma
they were randomly assigned to courses of either oral chlorpromazine
for at least three months in doses adjusted to fall short of toxicity;
or insulin coma, induced by a standard technique at least ﬁfty times
in each patient. While a number of minor differences were noted
in comparing the two therapies, the results at time of discharge
showed no statistical difference in the effectiveness of both treatments.
Neither treatment seemed to affect the basic schizophrenic process,
but chlorpromazine had the advantage of being safer, easier to administer, and better suited to long-term management (21). Concurrently, following the suggestion by the Creedmoor workers that

�EXPERIMENTAL PSYCHIATRIC RESEARCH

163

divided insulin doses were superior to single insulin doses, Blumberg
and Laderman (39) essayed this problem and demonstrated no signiﬁcant merit to the multiple-dose technique. (In 1958, following the
general conﬁrmation of these observations, insulin coma therapy was
discontinued at Hillside).
5. Neuropsychology: Various psychophysical tests were adapted
from neuropsychology, where their signiﬁcance in brain-damaged
subjects had been demonstrated. The early studies assessed these tasks
as indices of altered brain function (35), and measured the range of
performances of psychiatric patients, who are generally assumed not
to be brain-damaged. Thus, memory function was assessed on immediate recall, after various interpolated learning tasks (17, 35),
as well as during convulsive therapy (17). Tactile perceptual tasks
were ﬁrst examined in the clinical population (1). Later, with more
sensitive electrical tactile stimuli, Korin (10) observed the range of
thresholds in different body parts, the changes with altered brain
function (10), and the inﬂuence of set (instruction) on performance
(36). We also studied the perception of embedded geometric ﬁgures
(43), tachistoscopic presentation of embedded color ﬁgures (55), perception of the visual upright (55), critical ﬂicker frequency (49), and
interference in reading time by delayed auditory feedback (55). For
each task, the degree of decrement in task performance was found to
be positively correlated with the amount of EEG slowing. Following
treatment completion, with the return of physiological indices to pretreatment levels, performance in these psychological tasks also returned to pretreatment levels, or higher—a betterment of performance ascribed to practice effect.
Concurrently, assessment of various psychological measures as
indices predictive of behavioral change during convulsive and drug
therapies led to studies of the Rorschach determinants (30, 45), California F Scale scores (30, 42), language patterns after amobarbital
(27), denial scores on interview (37), and the perception of the visual
upright and auditory feedback (55).
6. Psycholinguistics: Concurrent with the syntactic language
studies (27), analyses of other language patterns were undertaken,
both in a search for more objective indices of behavioral change and
to gain experience in the technical problems of tape analysis for psychotherapy research. An index of variability in the vocabulary of
speech, the type-token ratio (TTR) of consecutive samples of dyadic
speech, was extensively studied (7,41, 44, 46, 56, 57).
In convulsive therapy patients, signiﬁcant changes in TTR mean

�164

MAX FINK

and standard deviations were related both to the degree of induced
EEG slow-wave activity and to syntactic language patterns obtained
in independent structured interviews. It was noted that speech became more repetitive (lowered mean TTR) and more variable in
consecutive samples (41). In interviews before and after the intravenous administration of centrally active agents, similar changes were
observed. Agents which produced predominant synchronization patterns on the EEG were related to a decrease in mean TTR and an
increase in the standard deviation of scores, while desynchronizing
compounds elicited greater variability in speech patterns and decrease in variability of consecutive scores (44).
Other language measures studied included distress-relief quotients,
self-reference, and alterations in tense and person. It was suggested
that these psycholinguistic measures are useful techniques for the
operational analyses of physiological and psychological effects of
psychopharmacological agents (44, 46).
7. Brain Damage and Schizophrenia: Following his studies at
Ittleson Center, Pollack reviewed the relationship between age of
hospitalization, intellectual functioning and prognosis in schizophrenic children and adults. He noted that initial hospitalization in
childhood and adolescence was related to I. Q. scores in the subnor—
mal range, deviant performance on psychomotor tasks, and more frequent ratings of “unimproved” at hospital discharge than was initial
hospitalization as an adult. The early and insidious onset of the behavioral syndrome “schizophrenia” was thus related to brain dysfunction (54). Findings suggest that different subgroups of schizophrenia may be classiﬁed on the basis of neuropsychological deviancy.
8. Sociological Studies: Considerable interest in the family organization to which discharged patients were returning, the relation
of social factors to choice and results of psychiatric treatment, and the
specific problem of the relation of these factors to treatment referral
patterns led to a series of population studies. In one study (8), education, age, place of birth, and score on the California F Scale were
signiﬁcantly related to the type of therapy received and the utilization of adjunctive hospital services. In a second study (31), duration
of hospitalization, discharge evaluation, and diagnosis were related
to the same social factors, while in a study of patient refusal of ECT,
similar relationships were observed (51).
These observations suggested a comparative interinstitution study,
and among three hospitals the relationships between social class and
other demographic variables (age, sex, education) to the clinical

�EXPERIMENTAL PSYCHIATRIC RESEARCH

165

variables of patient classiﬁcation (diagnosis), duration of hospitalization, selection of therapy, and discharge evaluation have been assessed.
Three teaching institutions were selected in which all therapies are
equally available to all patients—Menninger Foundation Hospital
(upper-class, Protestant), Massachusetts Mental Health Center (lowerclass, Catholic), and Hillside Hospital (middle-class, Jewish). In such
a comparison we have found the differences in designations of treatment, diagnosis, and discharge evaluation so marked as to make comparisons difﬁcult. While many relationships between social variables
and clinical variables were observed in each hospital, no social variable was found related to the clinical variables in every hospital
(53).

In an outpatient department study, sex, age, and marital status
were found to be related to the acceptance and rejection of patients
and failure to complete the application process (55).
These observations in population samples led to concurrent
studies of staff attitudes in the selection of therapy (ll, 12). In a
series of ward observation studies, Kaplan and Lefkowits indicated
the signiﬁcant role of staff attitudes (especially nursing personnel)
in the referral for subjects for somatic therapies, and in the transfer
of patients from one ward to another. (To study the inﬂuence of
staﬂ attitude on patient selection for drug therapy, we requested one
ward be designated as a “no-movement” unit. This was adopted in
September, 1959 and shortly thereafter by the whole hospital.)
PRESENT STUDIES

During the period of the convulsive therapy studies, many new
psychotropic compounds were assessed clinically (5, 21), electrographically (34, 40, 48), and psychophysically (48). The present psychopharmacology evaluation program, based on these studies, was
designed to answer the following questions:
1.

Is there a relation between measurable alteration in brain

function and behavioral change with psychotropic drugs on
chronic administration?
2. Are there pretreatment clusters of psychiatric, physiological,
and psychological variables which are related to the type of
behavioral adaptation?
3. Are such clusters related to the type and degree of physiologi-

cal change?

As an initial approximation, a double-blind, ﬁxed dosage, ran-

�166

MAX FINK

dom assignment drug study was undertaken. Based on our clinical
experiences three types of compounds were selected on the basis of
their EEG patterns. In this study, 203 subjects were referred, and 149
have completed the testing program, from October, 1959 to July,
1961.

l. Behavioral Change: In a survey of the behavioral adaptations
of patients receiving various psychotropic compounds during 195859, a behavioral typology based on the treatment response and on
pretreatment psychiatric profiles was developed (55). In the present study, the typologies are being tested, and various measures of
behavioral change studied, including therapist ratings, self-ratings,
and various ward observation scales.
2. Neuropsychology: Psychological tasks have been viewed both
as indices of behavioral change and as predictive guides in convulsive
therapy. Each of these tasks and a selected group of motor tasks are
now being assessed for both their capacity to reveal change with
various drugs and their capacity to predict change with the drugs
in this program (48).
3. Electroencephalography: In the convulsive therapy studies,
the degree of EEG slowing was measured by counting the consecutive
waves in selected samples (16). When the more subtle changes of
drug effects are studied, it is necessary to apply less tedious techniques
(48), and electronic frequency analysis was introduced in August,
1959. By measurement of the pen deﬂection for various frequencies
from 3 to 33 cps in ten-second epochs, rapid measurement of apparently small changes in total activity and frequency spectra are
obtained (52).
Other physiological variables studied in this program include the
response of EEG to intravenous chlorpromazine, blood pressure response to mecholyl, the EKG, radioactive iodine uptake, and analyses
of various blood and urine elements.
4. Data Analysis: To analyze the data generated in this study,
we have sought the aid of complex statistical methods and computational facilities. Analyses of covariance, correlation matrices, factor
analyses, and discriminant function analyses are computations now
in progress with these data at the NIMH Psychopharmacology Service Center’s Biometric Laboratory in Washington.
THE NEXT STEPS

Favored by a national research climate and a cooperative hospital
staff, these studies have proceeded vigorously. The assets for research
in this setting have been great—a selected, intelligent patient popula-

�EXPERIMENTAL PSYCHIATRIC RESEARCH

167

tion resident from six to twelve months, without individual economic
limitation of hospital stay; a sophisticated administration tolerant of
controlled studies; and approval of a Board of Directors who desire
“research” as an institutional function.
As Dr. Lewis Robbins noted in his ﬁrst hospital
report in 1959,
a specialty hospital can make little impact on the mental illness
problems of the community by treatment alone. The successful treatment of 350 patients a year is but little comfort to the 40,000 resident
patients in the state hospitals of Long Island. Nor will the annual
training of twenty or thirty physicians in the arts of psychotherapy
do much to help these unfortunates or the
many thousands of ambulatory mentally ill resident in the nation. No, a therapeutic goal
alone is salutary but inadequate to our needs. As he proposed, the
answer may lie in the dedication of a “research hospital,” as it is
here that a specialty hospital can truly excel.
The charter has been written in the Board’s assertion of research
as a hospital goal. With the assets of an exemplary therapeutic facility,
such rededication can provide the stimulus for the continuous
study
of the cause of mental illness and of methods of therapy.
Such dedication would provide the stimulus for comparative and
controlled assessments of different therapeutic techniques. Continued
study is urgently required of the selection of patients for various therapies; the application and mode of action of the therapies; and the
role of social and milieu factors in supporting the effects of our therapies.
Assessments require a meaningful classiﬁcation of subjects. The
behavioral variables alone, which are the basis of our
present diagnostic schemata, are unsatisfactory. Study is urgently required of the
applicability of social and demographic variables; psychological task
performance proﬁles; typologies based on behavioral response to deﬁned stresses or drugs; and physiological reactivity measures. Such
classiﬁcations are also essential for any biochemical, physiological,
or evaluative study to provide homogeneous samples and comparable
controls.
Assessments also require meaningful indices of evaluating change.
Present global “improvement” ratings and socialization measures are
inadequate. Whether the intervening variable be milieu therapy,
psychotherapy, drug therapy, or time, the criteria of behavioral
change require deﬁnition. The applicability of rating scales, language
tasks, self~ratings, psychophysical change scores, family assessments,
etc., require study and evaluation.
Recent studies of psychotic subjects have provided the suggestion

�MAX FINK

168

that there is a neurologic factor in a group of the schizophrenias.
The high incidence of electrographic and neurologic dysfunction, the
lack of behavioral response to all therapies, and the relentless course
of the illness suggest an “organic” involvement in this cluster. Such
a substrate must be clearly sought by the application of biochemical,
neurophysiological, and epidemiological techniques to various clusters of young psychotic subjects.
These are broader views of some of the questions studied in the
programs in experimental psychiatry of the past seven years. These

programs, and the contemporary projects in biochemistry and in
medicine, provide models of bootstrap studies undertaken with
limited support. A dedication of Hillside Hospital as a Research
Institute will provide the needed focus and impetus for the scientiﬁc
and humanitarian forces of the community to join in a common endeavor to resolve the problems of the mentally ill.
Acknowledgment: Participants in these programs include the
present members of the Department of Experimental Psychiatry:
Ira Belmont, Martin A. Green, Abraham Kaplan, Eric Karp, Donald F. Klein, John C. Kramer, Max Pollack, and Arthur Willner.
Former associates included Karl Andermann, Joseph Jaffe, Robert
L. Kahn, Hyman Korin, George Krauthamer, Nathaniel Siegel;
and Research Fellows Barre Alan, Fred Coleman, Harold Esecover,
Stanley Friedman, Henry J. Lefkowits, and Robert Shaw. The
cooperation of Arnold G. Blumberg of the Department of Medicine in the present program is gratefully acknowledged. The reports listed here are the result of the collaboration of these workers
and the professional staffs of the hospital who gave unstintingly of
their time and their good-will.
REFERENCES
(1)

'

This Journal, 1:21, 1952; (2) ibid., 2:67, 1953; (3) ibid., 4:3, 1955; (4)
ibid., 4:134, 1955; (5) ibid., 5:67, 1956; (6) ibid., 6:197, 1957; (7) ibid.,
6:207, 1957; (8) ibid., 6:216, 1957; (9) ibid., 6:229, 1957; (10) ibid., 6:241,
1957.

(13) Neurology, 4:211,
(15) ibid., 76:23, 1956;
1956; (18) EEG Clin.
(20) ibid., 10:207, 1958.
(21) ]. Am. Med. Assn., 166:1846, 1958; (22) Dis. Nero. Sys., 192113, 1958; (23)
ibid., 19:227, 1958; (24) Arch. Neurol., Psychiat., 80:380, 1958; (25) ibid.,
80:73, 1958; (26) Neurology, 8:682, 1958; (27) Psychopathology of Communication, New York: Grune 8c Stratton, 126, 1958; (28) Psychopharmacology Frontiers, New York: Little, Brown, 325, 1959; (29) Proc. XV Int. Cong.
Psychol, North Holland Publ., 238, 1959; (30) J. Nero. Ment. Dis., 128:243,
1959.
(31) Arch. Gen. Psychiat., 1:565, 1959; (32) EEG Clin. Neurophysiol., 11:398,

(11)

This Journal, 10:84, 1961; (12) ibid., 10:97, 1961;
1954; (14) Arch. Neurol., Psychiat, 72:233, 1954;
(16) ibid., 78:516, 1957; (17) Conf. Neurol., 16:88,
Neurophysiol.,9:180,1957; (19) ibid., 10:162, 1958;

�EXPERIMENTAL PSYCHIATRIC RESEARCH

169

1959; (33) ibid., 12:243, 1960; (34) Canad. Psychiat. Assn. ]., 4:1668, 1959;
(35) Proc. Int. Cong. Neurol. Sci., Pergamon, 613, 1959; (36) Am. J. Psychol., 72:384, 1959; (37) J. Neuropsychiat., 1:45, 1959; (38) EEG Clin.
Neurophysiol., 12:359. 1960; (39) Am. ]. Psychiat., 116:839, 1960; (40)
Neuro-Psychopharmacol., 1:441, Elsevier, 1960.
(41) J. Nerv. Ment. Dis., 130:235, 1960; (42) ibid., 1302187, 1960; (43) Arch.
Neurol., 2:547, 1960; (44) Dynamics of Psychiatric Drug Therapy, Springﬁeld: Thomas, 29, 1960; (45) J. Neuropsychiat., 1:242, 1960; (46) Am. J.
Psychother., 15:46, 1961; (47) Neuro-Psychopharmacol., 2:30, Elsevier, 1961;
(48) ibid., 2:381, 1961; (49) Arch. Gen. Psychiat., 4:259, 1961; (50) ibid.,
5:30, 1961.
(51) ]. Nerv. Ment. Dis., 132:153, 1961; (52) Medicina Experimentalis (in press);
(53) VA Conf. Psychopharmacology (in press); (54) Arch. Gen. Psychiat.,
2:652, 1960;
(55) Unpublished manuscript; (56) Psychiatry, 21:249, 1958;
(57) Comparative Psycholinguistic Analysis of Two Psychotherapeutic Interviews. New York: Int. Univ. Press, 1961.
° Due to the length of this Bibliography, it is presented in an abbreviated form.

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�\

PUBLICATIONS OF DR.

MAX

FINK

1950

1.
2a.

Subdural Hematoma Developing During Hospitalization, Amer. J.
M.
1950
Dr.
(With
Green).
107:
381-383,
Pszchiat.
Patterns in Perception of Simultaneous Tests of Face and
Hand, Trans. Amer. Neurol Assoc. 72: 250, 1950 (with Drs.

_'
Ereeni.
&amp;
Arch.
Neurol.
ibid,
Pszchiat. ﬁg: 355-362, 1951.

M.B. Bender and M.

....
3.

1952

Test as a Diagnostic Sign of Organic Mental
Syndrome, Neurologz, 2: h6-58, 1952 (with Drs. M.B. Bender
and M. Green}.
Tactile Perceptual Tests in the Differential Diagnosis of
1952
21-31,
Hillside
J.
Hosp.
1:
Disorders,
Psychiatric
(with Dr. M.B. Bender).
A Clinical Evaluation of Carotid Angiography, Conf. Neurol.
13: 181-195, 1952 (with Dr. J.M. Stein).
Exosomesthesia, or Displacement of Cutaneous Sensation into
1952
Amer.
Assoc.
1Q:
Neurol.
Trans.
Space,
Extra-personal
.B. Ben er .
(with Drs. M.F. Shapiro an
&amp;
1952.
h81-h90,
Neurol.
Arch.
éﬁ:
ibid,
Pszchiat.
....
Order of Dominance in Cutaneous Perception, Trans. Amer.
Neurol. Assoc. 7h: 238-2h0, 1952 (with Drs. M.B. Bender and
M. Green}.
Patterns of Perceptual Organization with Simultaneous Stimuli,
Arch. Neurol. &amp; Ps chiat. 13: 233-255, l95h (with Drs. M.B.
The Face-Hand

'-

Bender and

M.

areani.

1953

8.

9.

HeDeielopment of Perception of Simultaneous Tactile Stimuli in
1953 (with Dr. M.B.
27-3h,
3:
Neurologz
Normal)Chi1dren,
Bender .

Perception of Simultaneous Tactile Stimuli by Mentally
Retarded Adults, J. Nerv. Ment. Dis. 117: h3-h9, 1953
(with Drs. M.B. Bender and M. Green).

�-210.
11.

Spinal Fluid Findings Following Cerebral Angiography, Neurol—
(
1953
with Dr. J.M. Stein).
137,
ogz'g:
A Statistical Study of a Psychoanalytic Hypothesis:
Absence
of a Parent as a Specific Factor Determining Choice of
Neurosis J. Hillside Hosp. 3: 67-71, 1953 (with Dr. S.
Tarachows.

12.
13.

Effects of Barbiturates

on

Perception, Trans. Amer. Neurol.

Assoc. 15: 1953 (with Drs. M.B. Bender, P. Bergman and
M. Nathanson).

Homosexuality with Panic and Paranoid States (Case Report)
J. Hillside Hosp. 3: 16h-19o, 1953.
l95u

Standardization of the Face-Hand Test, Neurology, h: 211-217,
l95h (with Dr.

M.

Green).

1955

Test in Patients with Mental Illness, J. Hillside
Hosp. 3: 3-13, 1955 (with Drs. R.L. Kahn and E.A. Weinstein}.
Delusional Reduplication of Parts of Body after Insulin Coma
Therapy, J. Hillside Hosp. A: 13h-1h7, 1955 (with Drs.
R.L. Kahn and D. Graubert).
The Amytal

16.

195 O\

17.

18.
19.

Relation of Amobarbital Test to Clinical Improvement in
Electroshock, Arch. Neurol. &amp; Ps chiat. 16: 23—29, 1956
(with Drs. R.L. Kahn and E.A. Weinstein).
Evaluation of High-Dose Reserpine Therapy for the Relief of
Anxiety, J. Hillside Hos . g: 67-77 (April) 1956, (with Drs.
M. Wachspress, 1.5. Blumberg and J.S.A. Miller).
Relation of Changes in Memory and Learning to Improvement in
Electroshock, Conf. Neurol. lé’ 88-96, 1956 (with Drs.
H.

20.

Korin and S. Kwalwasser).

Denial of Blindness Following Cerebral Angiography, J. Hillside Hosp. 5: 238-2h5, 1956.

�-321a.

Quantitative Studies of Slow Wave Activity Following Electroshock, EEG. Clin. Neuro hysiol. 8: 158 (abst) web.) 1956
(with Dr. §.E. Kahn).
Relation of EEG Delta Activity to Behavioral Response in
Electroshock: Quantitative Serial Studies, A.M.A. Arch.
Neurol. &amp; Psychiat. 18: 516-525, 1957 (with Dr. 5.5. Kahn).
1957

22a.

Clinical Response to Megimide, EEG. Clin. Neurophysiol. 2: 180, 1957 (with Dr. M. Green).
Clinical and Electroencephalographic Effects of Megimide in
Patients without Cerebral Disease, Neurology 8: 682-685,
EEG

and

1958, (with Dr.

A

Green).

Unified Theory of the Action of Physiodynamic Therapies,

J. Hillside

26.

M.

Hosp.

é:

197-206, 1957.

Perception of Embedded Figures After Induced Altered Brain
Function, Amer. Psychol. lg: 361, 1957 (with Dr. R.L. Kahn).
Social Factors in Selection of Therapy in a Voluntary Mental
Hos . g: 216-228, 1957 (with Drs.
Hospital, J. Hillside
R.L. Kahn and M. Pollacﬁ}.
Role of Stimulus Intensity in Perception of Simultaneous
Cutaneous Electrical Stimuli, J. Hillside Hosp. é: 2h1-250,
1957 (with Dr. H. Korin).
1958

27.

Changes

atholo
grune
&amp;

28.

29a.

in Language During Electroshock Therapy, in Psycho-

of Communication, Ed. Hoch, P. and Zubin,
gtratton, 1958, {with Dr. R.L. Kahn).

J.,

Lateral Gaze Nystagmus as an Index of the Sedation Threshold,
EEG. Clin. Neurophysiol. 12: 162-163, 1958.
Effect of Diethazine on EEG and Significance for Theory of
EEG. Clin. Neurophysiol. 19: 207-208,
Therapy,
Coggulsive
19

.

Effect of Anticholinergic Agent, Diethazine, on EEG and
Behavior: Significance for Theory of Convulsive Therapy,
A.M.A. Arch. Neurol. &amp; Psychiat. 82: 380-387, 1958.

�-uidem, Biol. Psvchiatr
THE-195.

29c.

New

30.
31.

‘

32.

33a.

b.
Bha.

b.

YorE,

ed.
Masserman,
,

J.,

Grune

&amp;

Stratton,

Experimental Studies of the Electroshock Process, Dis. Nerv.
Sys.. 12: 113-118, 1958, (with Drs. Kahn and Green}.
Comparative Study of Chlorpromazine and Insulin Coma in the
Therapy of Psychosis, J. Amer. Med. Assoc. 166: 18h6-1850,1958
(with Drs. R. Shaw, G. Gross, and E.§. Coleman).

Electroencephalographic Correlates of the Electroshock
M.
1958
Green).
Dr.
Nerv.
(with
Dis.
227,
Bye. l2:
Process,
Experimental Studies of Convulsive and Drug Therapies in
Theoretical Implications, A.M.A. Arch. Neurol.
Psychiatry:
&amp;
1958 (ﬁEtE‘ﬁ?§T'§TE?'EEEE‘
80:
733-73h
(abst.),
PSﬁchiat.
an
. . reEK).

Alteration of Brain Function in Therapy, in Ps
&amp;
N.
Brown
Co.,
Ed.,
Frontiers, Kline,
Little,

cho harmacolo y
BosEon, 1958,

Pp. 325‘3320
Effect of Anticholinergic Compounds on Post-Convulsive

EEG

Behavior, EEG. Clin. Neurophysiol. lg: 776 (abst.).
Effect of Anticholinergic Compounds on Post-Convulsive EEG
and Behavior of Psychiatric Patients, EEG. Clin. Neurophysiol. 13: 359-369, 1960.
and

1959

35.
36.

37a.

b.

Effects of Diffuse Altered Brain Function on Perception, in
Proc. XV Int. Con . Psychol., North Holland Publ., Amsterdam,
[959, PP. 238-259 (with ﬁrs. R.L. Kahn and H. Kojéﬁ)..lk~u-Al
Diff rences in
Psychological Factors Affecting Individual Jwﬁfgvﬁt
Behavioral Response to Convulsive Therapy,
2h3-2h8, 1959 (with Drs. R.L. Kahn and M. Po ac

128:

Significance of EEG Pattern Changes in Psychopharmacology,
EEG. Clin. Neurophysiol. 11: 398 (abst.) 1959.
EEG and Behavioral Effects of Psychopharmacologic Agents,
Neuro-Ps cho harmacolo y, ed. Bradley, P., Elsevier,
REE-HES, T950.
Amsterdam,

38ayr

/

Electroencephalographic and Behavioral Effects of Tofranil:
Canad. Psych. Assoc. J. h: 1668-1713., 1959.

v.9w.

�-5;

(abst.),

38b.

Idem, EEG. Clin. Neurophysiol. 13: 2h3-hh

39.

Relation of Tests of Altered Brain Function to Behavioral
Change Following Induced Convulsions, The First International
Con ress of Neurolo ical Sciences (III: EEG, Clinical Neuro—
and EEIIepsyi, Pergamon,‘fondon, 1959, pp. STE-519
physiology
W
a n and H. Korin).
ran

1960.

.

a

of Set in the Perception of Simultaneous Tactile
Stimuli, Am. Jour. Psychol. 13: 38h-392, 1959 (with Dr. H.
The Role

Korin).

Personality Factors in Behavioral Reaponse to Electroshock

l:

J. Neuropsychiatrz

Therapy,
Kahn .

h5-h9, 1959 (with Dr. R.L.

Wm:

Sociopsychologic Aspects of Psychiatric Treatment in A
Voluntary Mental HOSpital: Duration of Hospitalization,
Discharge Ratings and Diagnosis, A.M.A. Arch. Gen. Ps chiat.
"""
_1_: 565-571., 1959 (with Drs. R.L.
and M. Pol ac .
1960

h3.

Efficacy of Divided and Single Dose Schedules in Insulin
Therapy,

Coma

J.

Am.

P8

Drs. A.G. BlumEerg and
hh.
h5.

h7.

h8.

1960 (with

Eaderman).

in Verbal Transactions with Induced Altered Brain
Function, JNMB-IBO: 235—239, 1960 (with Drs. J. Jaffe and
R.L. Kahn).: S;uw.UUub‘Jua'but
Drug Induced Changes in Intervi w Patterns: Linguistic and
Neurophysiologic Indices, in ‘__Dynamics of Psychiatric
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Withdrawal Symptoms Following Discontinuation of Imipramine Therapy, Amer. J. Psychiat. 118: 5h9-SSO (with
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and Prospect, J. Hillside HOSEital 19: 159-169, 1961.
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h: 259- 266, (with R. L. Kahn, E. Karp, M. Pollack,
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53. Behavioral Patterns in Convulsive Therapy, A.M.A. Arch.
Gen. Psychiat. E: 30-36, (with R.L. Kahn).
5h. Sociopsychological Characteristics of Patients Who
Refuse Convulsive Therapy, Jour. Nerv. Ment. Dis. 132:
153-157, (with M. Pollack).
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Techniques in Study of Psychotropic Drugs, Acta of
Int’l Meeting on Techniques for Study of Psychotro ic
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                    <text>January 8, 1960.
KIHORAIDUH

1803:

20:

SUBJECT:

Medical Director
DOpartnent of Experimental Psychiatry
Salary Scales for Professional Staff

Over the

past few years we have attenpted to establish
reasonable salary scales based upon the conception of full tine
work at the institution, without outside professional activity.
By adninistrative pressures, a policy of equating Job positions
both within the institution and between institutions has been
grafted onto the full tine concept. This latter has been nade
an integral part of the salary scales despite the awareness that

so-called equivalent workers within the institution were not
"full tine,’I and that institutional salaries are often different
because of the nador.fringo benefits.
Continuation of these fictions lakes further growth of
this unit extrenely difficult. we are severely handicapped
in recruitment; and the staff is restive, considering the
opportunities they have elsewhere. We cannot provide university
affiliation with graduate students as a source of new personnel;
nor have we established an identification for staff persons with
I

the

institution.

For these reasons, among others, the following revisions
of salary scale and work standards are reconnended for this Department, to be effective July 1, 1960.
A. General

Principles.

1. All appointments in Associate or Senior Associate
categories are to be node on a full tine basis.

�-22. All income tron ancillary eorvicee to accrue to
the aeeeoroh Fund of the Hillside Hospital.
3. For Aoaooioto and Senior iseociate stat: neoboro
‘

aro in apeoial training toward graduate degree or oertitioatee,
no
enae
to 83000 per anon: tor tour yoare lay bo approved by the
Hadioal Director on roooaaondation o: the Director or the Dopartwho

loot.

h.

aebbotioala Salary nay be paid up to .1: loathe
after (it. years service and up to one year after oight yearoerrioa in the Dopartnont for etudy at another laboratory or
ioatitotien. In the event that ouch eabbatioal in approved,

travel and relocation expeneaa up to 3 looo
nay be reqneetod.
5. Mentorohip in proteeaiooal eeoietiee and malpractice
insurance oorerago to to providod by the Departnont.
B. azeoifio Soolea
1e Pchhiﬂt’ye
o. For accredited Alerioan Board or
Peyohiatry, recent $13,000 - $20,000
with $1000 inoreaent, to 827,500;
b. For :raduetoe, eligible for exaninatiooe,
.16'000 ‘ .18,000a
o. tor lellove (hth or 5th year) $12,000 “
;

’1h3000

2.

Payohelegy.

a. Senior Reeearoh atatf ~ 31h,000 - $20,000
Ph.D. and ten or lore yoare orperienoe.
.b. Pazaoaroh Aeaoeiate - $10,000 - $15,000 .D.

o. Roeearoh iseietanae - $8,000
Phono

G‘ndid.t..o

~

$10,000

�ca.
4. Roooorch Follow - $5,000 - $7,000
a. Job Sgociticotioa.
1. For itou la, b, ond to, b, o, tho doooriptiono
in monotondun or ootobor 30. 1958, opply.
i

2. For itolo 1n ond 24:
ohoonto
In tho
or groduoto oohool otriliotion,
tho troininc or our oqn otorr 1o Iondotory. With tho potontiol
oupport of (routing ooonoioo oloo dooirono or providing troiaing
tundo, thooo rongoo oro onggootod,'ond itouo oiil bo roquootod
‘in tho noxt budgot.
10.

Poychiotriota Cooplotion or throo
yooro in psychiatric rooidoacy, ond dooirono or otndyiatdhring
hth ond 5th yoor.
2d. Ph.D. oondidoto or H.A. ooudidoto. Eorly
in coroor, without thooio, would roquoot tnndo to pornit ouch
oooiotont to oporoto within tho loborotorioo.
\

Roopoettully onbnittod,
IX

‘n, oo

�\

Departaent of Experimental Psychiatry

«

April It, 1950.

Director
SUBJECT: Salary Scales fer Pretessienal Start.
Correction of acne dated January 8, 1960.
Here stands except for specified revisiens receanended:

HEEORLIDUH

Page 1.

Page 2.

T0: Medical

General Princigles.
1. All appeiutsents er presetiens te senior
Research Associate are made en a 'full'~tell-tiae
basis. Appeintaents in ether categeriee are "fellotine"
according to established standards of the Hospital.
2. All inceae Irea ancillary services of "full"
full-tine start to accrue to the Research Fund of

A.

Eillsids Hospital.
3’ h, 5.
B.

'tCte

Sgecitic Scales
1. Psychiatry
(a) Sr. Research Asaeciate: en agreeaent
with the Medical Directer
(b) Research Associates for accredited
Aaerican Beard or Psychiatry, recent $18,000 . $20,000,
with $1,000 increaent, to $27,500; for greauates,
eligible for exasiuatiens, $16,000 - $18,000.
(0) tellers: (hth &amp; 5th year) - $12,000 - $1h,000
2.

Psychology
(a) Sr. Research Asseciate: stat.
(b) Research Associate: Ph.D. and esperinental ,»
experience $9,000 - $1h,000
(c) as. Research Assistant: x.i. or equivalent,
three years experience, and candidate for
Ph.D. at accredited university - $7,000 - 39,000
—

(d) Research Assistant er Pelbw: H.i. or one
year experience - $5,000 - $7,000

�Pug.

3

0.

Job Sgociticatiana:

while specificatians at 10/30/58 would apply,
following changes arc rnqnvatnd.
In original docignntion,
Rcuoarch Lsaociata in Psychology was limited to Ph.D. and thrus
ynnra or oxporicnec. this in hurdansonn, and :11 Ph.D. appointinbo designated 'Aaaociatc.' Assistant dasignation be subdividad
to Sonia: Rnaonreh tall-tint and Roacurch Aaaintaut, as abovo
pornittinx tho nmploynont or trainees 1nd aundidat-a, with

origiu;1 cpcoificutiona applying.

Roapodlully submitted,

‘EE§“FIEEI"HTET”~’"'

31:13

�����Pg. 1

Dr. Fink

To:

Director, Research in Emerimental Psychiatry

Prom:

Accounting Dept.

Re:

Report of Expenditures
.131; 1 - October 21: 1960

HOSPITAL SUBSIDIZED RESEARCH

1960-61

Ebcperience
To Date

25, We

8, 331e
3,167.
363.

Dudet

Salaries
BC

Assoc.

8c

arises:

Fink

in Social Psychology

Siegel

Psycholinguistic Technician
Secretary

Medical Equipment
Office Equipment
Travel

Supplies

Social Security

Director's

Kolodny

Podrid

118.

'

Blue Cross
Expense Account
&amp;

Income from Nassau County

Net Expenses

cc: Hr. Bachrach

h85.

1,500.

Total Expenses
Less:

3,120.
2 ,172.
2 , 890.

3,1t00o
3.1100.

(67.)

920.
600.

119.
161.
237.

10,120.

12,796.

3,120.

1214.

h0,000.

12 ,672.

�Dr. Fink

Director, Research in Experimental Psychiatry

Pg. 2

GRANT

biz-2115

5%

to 12/31/61 Grant approved for $65,886.
to 12/31/61 Supplemental Grant
16 2 O.
approved for

Amount

applicable to 1960-61

6

151%:
h1,058.*

1960-61
Budget

quaerience

Grant Balance 6/30/60

32,105-

3h,699.

Additions:
Amount applicable to 1960-61

1.12158 .*

m,

_

Starting Balance

Salaries

&amp;

Additions

8.

nses:

ese
ssoc. n sychiatry
Sr. Assoc. in Ehtp. Psychology
Assoc. in Exp. Psychology

Asst. in Exp. Psychology

Assoc.

in

Exp. Psychology

Psycholinguistic Technician
E.E.G. Technician

Secretary
Secretary

Klein
Pollock
(Gittelman
(Bel-"nut
Karp

(Krauthaner
(Andermnn
Kclodny
Mosquera
Bowie

Podrid

To Date

73,1463.

3h,699.

16,1416.

5,667.

10, 92°.
7,500.

2 ’ 500.
2 ,500.

8,500.

2,931.

h.l.10.

1,1426.

7,333.

3,360-

291.

1,123.

1.80.

MM
Supplies

Iviedical Equipment
Office Equipment

Social Security

8:

Overhead

Blue Cross

Travel

Total Eutpenses

Unexpended Balance

cc :

Mr. Bachrach

2,500.
382.
1,928.

101.

1196.

9,681..

2,7hh.
563.

72,9330

20,8270

13,372.

�1“
Director, Research in Experimm Psychiatry

Dre

mm

Pg. 3

181-2092

Great. terminates 12/31/60; expenditurepicked up by Great III—2715 Supplement.

mm

m0

Starting Behnce 5 Additions

We:PWIC"

Salaries &amp;
Sr. Assoc. in Me

Repairs to quipnent

800111 Security
Overhead

Tom

&amp;

Blue Crone

WW3

Wed

We

6,&amp;7e

7,h35e

To Date

0

Additions

Behave

cc! Hr. Mhrech

Wk

be

1960-61

Bidet
" 6/30/60

te

6,667.

7,h35.

5,667e

11,333.

130.
870.

1:3.

628.

6,667.

5,7080

0

7014.

1,727.

�Pg. 1

”MaDr. Fink

To:

Director, Research in kperimental Psychiatry

Fran:

Accounting Dept.

Re:

Report of Expenditures

.1an

3

.. 393mm; 30, 1260

HOSPITAL SUBSIDIZED RESEARCH

1960-61

W'Lec
Salaries

nses:

&amp;

Assoc. in Social Psychology

Psycholinguistic Technician
Secretary

Medical Equipment
Office Equipment
'l‘revel

Supplies

Social Security

Director's

Blue Cross
Expense Account
&amp;

Total Expenses
Less: Income from Nassau County
Net

muses

cc: Mr. Bachrach

Experience

Bidet

Fink
Siege).

Kolodny

Podrid

25,000.

3,120.
2 ,172.
2,890.

To Date

.

10, 338.

3,958.
5&amp;6.

730.

1,500.

118-

3,h00-

3,1400.

920.
600.

(55a)
173.
22h.
290.

10,120.

16,2014.

3,120,.

177.

130,000.

16,027.

gm

�M
Director, Research in Experimental Psychiatry

Dr.
(

'

GRANT

Pg. 2

111-27};

1/1/61 to 12/31/61 Grant approved for $65,886.
1/1/61 to 12/31/61 Supplemental Grant
approved for

Amount

applicable to 1960-61

W

Grant Balance 6/30/60

Additions:
Amount applicable to 1960-61

Starting Balance
Salaries

8:

ese

uses:

ssoc. n sychiatry

Sr. Assoc. in Eng). Psychology
Assoc. in up. Psychology
Asst. in

Assoc.

Psychology
Exp. Psychology

Ebcp.

in

Psycholingzistic Technician
E.E.G. Technician
Secretary
Secretary

Klein
Pollock
(Gittelman

Social Security

a:

Overhead

1960-61
Budget

Experience

32,1105.

3h,699.

311,699.

16 ,hlé.

7,083.

(Belmont
Karp
(Krauthamer

10,920.
7,500.

3,500,,

(Andaman

8.500.

3,6140.

Kolodny
Hosquera

h.h10.

1,783.
1,h06.

3 , 360.

Bowie

2.500.
382.
1,928.

Blue Cross

Total Expenses

Balance

5
d

.-

cc:

n

.n

ﬁ.w

,...,..—

I

I

Illll

291.

1:80.

165.
607.

3,130.

72,933.

26,185.

675:

-IIIM'
530.

,.
-Nv
“A.

3,125...

9.681;.

Travel

"I'fn'expended

To Date

73.h63.

7,333.

Podrid

Supplies
Medical Equipnent
Office Equipmnt

h1,058.*

1413958 .*

Additions

8.

l
"851%?
6 2 O.

8,51)»

�..o~’

Drcl'ink
Director, Research in

mm

Psychietry

mm

Pg. 3

III-2092

«when:

12/31/60; «podium» to be
picked up by Great 141-2715 Suppl-lent

Went

1960-61

Met
Great Balance

- 6/30/60

6.667.

Belem.

&amp;

mm»

W

Selene: I: Expense”
8r. Assoc. in Exp. Psychology
S plies
‘greee

Social Security
Overhead

Total

To

DI“

7,105,

0

Additions

mm

Experience

a Blue

heme

Wed

Behme

Pollock

6.661.

7,155,

5.567.

S,h17.

130-

SS.

725.

870.

785.

6,667.

6,982.

0

1:53.

�'

To:

Dr. Fink

Director, Research in
Prom

Accounting Dept.

Re:

Report of

119

Pg. 1

M

mm

herinentel Psychiatry

nditures

to

December 31, 1960.

A

-._A

-4tm

,.._

Assoc. in Social Psychol
Paycholinguietic Technician

Secretary

Medical Equipment

Office Equipment
Travel
Supplies

Social Security

ctor'e

Tom

Blue Croce
Expense Account
a:

mews

Less: Income from Nassau
County
Net Expenses

Pink

Siege].
Kolodnv
Podrid

25, 000.

3,120.
2,172.
2,890.

112.3335.

14,750.

739.

”5.

1 500.

,118.

(SS“ )

3 ,hOO.

3,hoo.

920.
600.

233°
290’

1‘3ng

”’566.

3.129..

265.

130,000.

'

‘

'

�Dr. Fink

Director, Research in Experimental Psychiatry
GRANT

Pg. 2

111-2715

approved for $65, 886.
1/1/61 to 12/31/61 Supplemental Grant
approved for

1/1/61 to 12/31/61 Grant

1’20.
ﬁg.

Amount

applicable to 1960-61
1960-61
Budget

quaerience

Grant Balance 6/30/60

32,105.

313,699.

Additions:
Amount applicable to 1960-61

1413958.!-

‘

Starting Balance
Salaries

&amp;

nses:

Asst. in Exp. Psychology

Assoc.

in

Exp. Psychology

Psycholinguistic Technician
E.E.G. Technician

Klein
Pollock

16,h16.
7,333.

8,500.

Karp

10,920.
7,500.

h,soo.

8,500.

31,3338.

h.h10.

2,”.0.

(61th
(Belmont
(Krauthaner
(Aniormann
Kolodny

Hosquera

3,350-

Podrid

Supplies
Medical Equipmnt
Office Equipmnt

Social Security

3h,699,

Bowie

Secretary
Secretary

8:

Overhead

2,500.
382.
1,928.

Blue Cross

Trml

Total kpenses

Unexpended Balance

_

I

cc :

Hr. Bachrach

To Date

73,h63.

Additions

&amp;

ese
ssoc. n sychiatry
Sr. Assoc. in Exp. Psychology
Assoc. in Exp. Psychology

_

hl,058.*

'

I

II.

3,750,.

291.

1,689.

EEO.

278.
697,

9,68,4-

31,116.

72.933.

31,1170.

631.

My
530-

3,229,

Mum

�Dr. Fink

Director, Roam): in Experimental Psychiatry

mm

Pg. 3

31-2092

mus

12/31/60;
Grunt
picked up by Grant 141—2715

Wt.

exp-Mite": to he

1960-61

that Balance - 6/30/60

'

6,667.

3mm. 6 Additions

W
Salute: &amp; Enema:

$‘o

To Date

71:35.

0

Additions

Starting

Met

We

“3°C. in

m. won-m
Supplies

Social Security

Overhead

&amp;

311:.

Total. Expenses

Unmanned Balance

cc: Hr. Bum-ad:

areas

Wk

6,667.

71:35.

5,6670

6

Q

a

130.
870.

63‘.
91-2.

6,667.

8,2138.

0

(813.)

�W
P80 1

W

Dr. Fink

To:

‘

Director, Research in Experimental Psychiatry

Fran:

Accmnting Dept.

Re:

Report of Menditures

1961

HOSPITAL SIBSIDIZED RESEARCH

Salaries

ec
Assoc.

&amp;

uses :

in Social Psychology

Psycholingulatic 'Dechnicien

Secretary

Medical Equipment

Office Equipmnt
Travel
Supplies
Social Security 8: Blue Cross

Director's Expense Account
Total Expenses
Leas:

Income from Nassau County

Fink

Siegel

Kolodny

Podrid

25,000.

3,120.
2,172.

2’890’

lb

181
5,5112.

l

'

’912'
D

220.0
_

1,500.

118.

3,)400o

3,h00.
920.

(SS )

2714'

600.

397‘
387:

10,120.

22,858.

34L

265.

.

l

__________________________________._____———-——--——--—Net Expenses

cc :

Mr. Bachrach

h0,000.

22,593

�Dr. Fink
‘

_..

.,

Director, Research in 'hcperimental Psychiatry
GRANT

Pg. 2

IKE-2715

1/1/61 to 12/31/61 Grant approved for $65 ,886.
1/1/61 to 12/31/61 Supplemental Grant
16 2 0.
approved for

‘B'iﬁi'ﬁ

Mount applicable to

Grant Balance 6/30/60

1960—61

.m

Additions:
Amount applicable to 1960-61

Starting Balance

Salaries

&amp;

Additions

nses:
ReseF-ch Issac. In Psychiatry
Sr. Assoc. in Exp. Psychology
Assoc. in Exp. Psychology

.

1960-61
Budggt

Experience

32,1105.

3h.699.

ulzostm

20,529.

73,h63.

55,228.

16,h16.
7,333.

9 ,917.

1,083.

10,920.
7:500-

5,500,
h,375.

8,500.

5,056.,
291.

To Date

8:

Asst. in Ebcp. Psychology
Assoc. in Exp. Psychology

Psycholinguistic Technician

W

E.E.G. Technician

Secretary
Secretary

Supplies
Medical Equipment
Office Equipment

Social Security a Blue Cross

Overhead

Klein
Pollock
(Gittelman

(Belmont
Karp
(Krauthamer

(Ardemenn
Kolodny
Hosquera

me
Podrid

14,1th3 9 360.
‘

Total Ehcpenses

Unexpended Balance

Mr. Bachrach

2 ,517.

1, 972 ¢
1:80.

Cartolano

13s

2 ,500.

382.
1.928-

99681“

Travel

cc :

b1,058 .*

281;.

920.

5,009.
979.

72:933-

38,396.

530-

16 ,832.

.

�Pg. 1

Dr. Fink

To:

Director, Research in Experimental Psychiatry

From

Accounting Dept.

Re:

Report of Ehcpenditures
1: 1260 - Februagz 28I 1961

ng

HOSPITAL SUBSIDIZED RESEARCH

Salaries

&amp;

80

menses:

Social Psychology
Psycholinguistic Technician
Secretary

Assoc.

111

Medical Equipment
Office Equipment
Travel

Supplies

Social Security

Director's

Blue Cross
Expense Account
8:

Total Memes

less:

Income from Nassau County

Net mpenses

cc: Mr. Bachrach

Fm

Siegel

Kolodny

Podrid

25, m0

3,120.
2,172.
2,890.

1 500.

,118.
3,h00.
3,h00.

12,33:
1’09;

,, J

£1455:

180'
13h.
61.
525.

920.
600.

1:17.

53:12“

26,238.

3,120.

“3,955.

10,000.

2 3 ,283.

"

;

4-;

A

3*)

7’

.

�\

Dre Fink

Director, Research in ﬁrperimental Psychiatry
GRANT

Pg.

2

PIX-273:5

1/1/61 to 12/31/61 Grant approved for $65,886.
1/1/61 to 12/31/61 Supplemental Grant
approved

Amount

Grant Balance 6/30/60

Salaries

&amp;

Eggnses:

ese
esoc.
sychiatry
Sr. Assoc. in Exp. Psychology
Assoc. in Earp. Psychology

Asst. in Ech. Psychology

Assoc.

in

Earp.

Psychology

Psycholinguistic Technician
E.E.G. Technician

Secretary
Secretary
Electronics Technician
Supplies
Medical Equipnent
Office Equipment

Social Security

8:

m

Overhead

Klein
Pollock
(Gittshnan
(Belmont

(Krauthamer
(Andermann
Kolodny
Mosquera

Podrid
Cartolano

Unexpended Balance

cc : Hr. Bachrach

Experience
To Date

3h,699.

M*

203529.

73,1163-

55,223.

16 hlbe
71333-

11

o

3:333.

10 920.

6 500.

3500-

5,765.

7:500-

5:000.

291.

hyhloe

2.895.
2,255.

3’36“

2480.

ho.

\a
’38:.
500.

295.

1,92 e\~\...1
9’68hN-h 5,3533..

Travel

Total Ebnpenses

111,058.?!-

32’h05-

2

Blue Cross

11:15:

1960-61
Budget

Additions

8:

16 230.

applicable to 1960-61

Additions:
Amount applicable to 1960-61

Starting Balance

for

15029.
72,9330

[6,852.

�Pg. 1

W

MEMORANWH

Dre Fink

To:

Director, Research in

Merinontal Psychiatry

From

Accounting Dept.

Re:

Report of Ebcpenditnres
195]
3]
12m
lamb
1.
3
Jul:

W

RESEARCH
SUBSIDIZED
HOSPITAL

Salaries
Assoc.

uses:

6:

in Social Psychology

Psycholinguiatic Technician

Siegel

m

Kolodny

Secretary

Medical Equipment
Office Equipment
Travel

Supplies

Blue Cross
Expense Account

Social Security

Director's

.

Total Expenses

less:

Net Expenses

7’125'

1 500.

180'

3,1400.

151:

1’ 335‘

1:681:

’118.
920.
600.

.

Income from Nassau County
Donation of Paychiatropic Drugs

3,120.
2,172.
2,890.

3,h00.

8:

Experience
To Date

1960-61
Budget

»»

~

x... ,,

.

110‘
626.

1117:

10,120.

2951.0.

3 ,120.

2,955.
2
:295:

h0,000.

21:390.

to Hospital

______________________________...——————————---

cc :

Hr. Bachrach

�Dre Fink

Director, Research in farperimental Psychiatry
GRANT

Pg. 2

m~271§

1/1/61 to 12/31/61 Grant. approved for $65,886.
1/1/61 to 12/31/61 Supplemental Grant
16 2 0.
approved for
T511137
Amount

applicable to 1960-61

1_‘_‘_____

Grant Balance 6/30/60

Additions:
Amount applicable to

Starting Balance

Salaries

Essen

1960—61

Additions

3.

nses:
Issac. In Psychiatry

Assoc.

hp.

in

Psychology

Exp. Psycholog

Psycholinguistic Technician
E.E.G. Technician

Bud eet

Experience
To Date

32,1105.

3h,699.

hl,058.*

20.5293

73,h63.

55,228.

16 ,h16.

12,750.
M327.

(Belmont
Karp
(Krauthamer

10, 920.
7,500.

7 , 5142 ..

(Amiermann

8,500.

6,1173,

Kolodny
Mosquera

,

7,333.

h,h10.
3,360.

&amp;

Overhead

Blue Cross

Travel
Total Expenses

Unexpended Balance

Hr. Bachrach

5,625.
291.
3,272,,

2,592.
1:80.

93.

Castolano

Supplies
Medical Emaipment
Office Equipment

Social Security

Klein
Pollock
(Gittelman

Em;
Podrid

Secretary
Secretary

cc :

1960-61

8c

Sr. Assoc. in Exp. Psychology
Assoc. in Exp. Psychology
Asst. in

h1,058.*

2,500.
382.
1,928.

9.968140"

3760

1,376.

6,1173n

14100"

72,933.

52,770.»

530.

2,158.

�P30 1

Dr. Fink

To:

Director, Research in Emoriuontd Psychiatry

W1

Fran:

Accmnting Dept.

Re:

Report. of Expenditures

w—WW
m
HOSPITAL

wnsmxzm

RESEARCH

M
Salaries

ac
Assoc.

&amp;

gases:

Fink

in Social Psychology

Siegel

Psycholinguistic Technician
Secretary

Kolodmr

Mics]. Equipusnt

1960-61

merience

25gme

19,7950

1,500.

180.

33’4me

5939

3,120.
2,172.
2,890.
118.

Office Equipmnt
bIVOI
Supplies
Social Security &amp; Blue Cross

7,917.
1,57h.
1,906.
711,

3shme
920.
600.

163689.

Total Expenses

1.3.120.

33, 308.

less: Incaus

3,120.

2 ,955.

Director's Expense Account

from Nassau County
Donation of Psychotropic Drugs to Hospital

Net

kpenses

~

41;]

cc: Hr. Backrest:

1417.

2: 295:

150,000.

28 ,058.

�Dre Fink

Pg. 2

Director, Research in "apex-mental Psychiatry
GRANT

'

a...

141-271;

.

$65,886.
for
Grant.
approved
12/31/61
1/1/61 to
1/1/61 to 12/31/61 Supplemental Grant
2
0
6
1
.
for
approved

121115:

Mat

applicable to

1960-61

1960-61
Budget

...

’41, 058 .*

Experience
To Date

Grant Balance 6/30/60

32,)405.

314,699

Additions:
Amount applicable to 1960-61

glIOSBJ

111,058s

73,1163.

75,757.

Klein
Pollock

16,2116.

lh,167.

(30130111:

10,920.
7,500.

8,583.
6,250.

8 ,500.

7 , 181.

Starting Balance

&amp;

Additions

Salaries &amp;ﬁsoc.uses:
In Psychiatry
Sr. Assoc. in Exp. Psychology

Hem

Assoc. in hp. Psychology
Asst. in Exp. Psychology
Assoc. in Exp. Psychology

Psycholinguistic Technician
EOEOG.

WWW

Secretary
Secretary

7,333.

(Gittelmn
Karp
(Krauthatner

(moment:
Kolodny

m
W

ughloe
3,360.

HOWE

5,1111.

291.
3,6509
2,353..
LBO.

93o

Oastslano

'

Supplies

pursuant
Office Equipnnt

2.500.
382.
1,928.

Medical

Social Security

8:

Overhead

Blue Cross

9.681;.

Travel

Total MEMOS

Unexpended Balance

cc: Mr. Bechrach

.

169.
1,5711.

7,366.

$139.91

72,9330

593,458:

530.

16 ,299.

'

�I

[1W

W

Iu' [44/

:

~--—;

I
C.

I

/

1/

/
’W
W

K4444”

'

LI“I

X

{

~//‘/.
/

I/L/
I I

/

1

I,

d
—

/

/
7’
'V e

-

‘1

.__

�2.7

f

444/

Ms/
,1.
r

a

M
dv

//'.

/
.4

—

’

M1

h.

1

a...

/
41%;»! /
’,

[14,.”

I If:/- (I t».

AI'VA‘;_727

44'

w

W
/

.4

/

/

4’15]

/

5;!

1%
’

/

{i
I

440/

a

a/

”M7142:

72ﬁ;4h.&amp;¢ igv

M

(A I»
r],

«Ac/47%

’

3

I

/
(5300

if

1’

C

II»

a»

W

ﬁwm)
72.

13/

/

one
53¢:

39 ace

�5—0

90¢

�1/3/61
Dopartnont or lxpsriaantal Psychiatry
1961-62 Bndgot, Propoood

I.

1960-61 Indgst (-ovsrhsad)

$118,882

a. Inorsasos in salariss, annual
inorsnsnts
b. Additions in prograns:
1. Psycholingnist - to ba aotivatsd
2. Sociologist to tho proxraa
3, £80 technician

Statistical
tsohnioian,
g.. Elootronio oqnipnsnt

é.
o.

s.

Status rslatinx to lndgst
John [razors Irt. tron fallowship
status to Rasaaroh Associats 9/1/61;
snbjoot to approval of g. or‘g.
Donald Klein: continnss as Isa. Assoc.
but is to ba grant (Kh798) supported.
that tho dittorsncs in
It is axpsctod
salary iton on grant and an lsvsl nay
ha up to $7500. Grant providss 85000
additional for sscrotaria1 and othar
sxpansss.
Sabbatieal ~ lax link: 9/15/61-8/1/62
Visiting Soiantist support is roqnsstad.
rhara is no salary ohangs during yaar.
Amount is $15,000 par annnn.
Expanss

III.

W
%,650
1 000

Changas in

0.

Souroas of Support (-ovsrhoad)
a. Approved:
1961-62
1. HI2715
.

ha P01161118:
2, nh798

rotal

0 12,000

170,732
12,000
182,732

72,231

-

(323,000) out.

3. Visiting Soiontist
c. To bs Raqnastads
h. Snpplonantary H12715

126,282

10,000
10,000
6'800

tins
tins

llaetronios spacialist,

II.

7.300

“17,000
13,500
30,000

r¢/~

gh,g§o

�$0,000
a. Board or Daroetorl
1. it would Ilk the Board to
apprevo I grant 0: $h0,000 to:
{var ytara; with an lpyortunity
to carry tarvnrd unoxpondod can:
far 2 yn;rs.
2. WI wanld also ask for a credit
tranltor tron operating budget
funds of value of psychotropic
drugs (to $10,000) roecivod in
the progran. In 1959. the
'

vulno was ontinntod as O11,000.
Inconn Eutinato: 182,731
Exponae

Estinatcs 182,732

��V

WWW—WM...‘

r
L

///~/

5

”A Z

3%”

'

IBKOO
&gt;3, W?

+

'
————-'_f"——'

I

23, We
’3 ’ (00

‘

2.00

..——

I

~

I

I

v

’

2“
3f?”
=

���May

5, 1961

Hrs. Croghan
Departnent of Experieental Psychiatry

Heme:

Iron:

Subject:

Budget

'1. In reviewing
find

budgetery expenses to date, I
the following in the Beapitelised Subsidized Research:
Expenditures 7/1/60 ¢ 3/31/61
$29,5h0
Less

my

credits (Nassau County)

5,250

(Drugs)

Estimated Expenses

nets
sonths

3

$2h,290
I

Salaries (3&amp;00 x 3)
Social Secutity
Travel
Other

10,200
300

1,000

_

200

net:
Less

credit for teeching

900

Research Associete in Psychiatry (Klein) app.

Secretary

I!

(Podrid) app.

hSOO

82g

$5,325
my

calculations are in error, please call as.

Thank yen.

a

Sincerely yours,
HTzOP

11,100
35,990

ax

n ,

.

�5. 1961

May
HOIO!

Mrs. Croghan

Irons Dapartaont of Expsriaantal Psychiatry
Subdaota

Budxat

1. In roviaviag a: budgstory oxpsusaa to data, I
find tho following in tho lospitalisad Subaidisad Rasaaroh:
nxpandituras 7/1/60 ~ 3/31/61
$29,5h0
Lass credits (lasoau county)
5,250
(Drug-v)

__.______

not:

$2h,290

lotiaatad xxoonsos 3 months
salarios (JhOO x 3)

10,200

Social secuoity
Traval
ethar

300

1,000
200

not:
Lass oradit for teaching
2.

11.100
35,990
200

I: this
is
iha

approxiaatsly
would you
oorraot,
ploasa assign
following sxpandituras to this account,
tron Grant l1-2715, attentiva April 1?
nosoaroh Associats in Psychiatry (Ilain) app. ASOO
Saoratary
(Podrid) app. “33:

I:

ay calculations aro in
Thank you.

85,325

error, ploaso call as.
Sinosraly yours,

IIsOP

ax

n ,

. .

�Prcptlod ltdgot 1961-6!
nevi-ad 5/22/61

Doparinont

.: tsp-rtnonttl Plyuhtltry

annuity:
Exponloo 1961-62

$156,hh0

Inoolo
warns

_

Eonpttal eruditl

108,870
1.510

116.;50

lot

Unuubcidisod

ltloarch

8

ko,ooo

�5/22/61

Bspcrt-sct ct lxpssissntsl Psychistry
Prcpcscd 1961-62 ludxst (lsvtssd 5/22/61)
Exp-uses:

1. Blrsctcr
2. Assoc. 1n rsychistry
.AQE‘o/B. Assoc. 1n Psychistry
h. is. Assoc. Expos. Psychology
5. Assoc. in lxpsr. Psychslcgy
6. Assist. in Expos. Psychslcgy
,rswo'7. Assist. in lxpsr. Psychc1cxy
8. Assoc. in Sosisl rsychclcgy

1960-61

1961-62

Apprsvsd

hsqusst

(3. link) 25,000

25.000

16,h16

17'500

Sllcta)
lrsnsr)

.

13.000
Pcllsck;
lslncnt 10.920
1.500
Ksrp)

.

Villas!)

2'004'

b‘;

1h,000
11,000
8.100

73200 (9)

9,500

10,000 (d)

I,$oo

1,h20 (s)

Elbsqusrs)
lss)

h:h10

k,aoo
3.600 (I)

)
12. rsychslingsistis rsshntc1sn élslcdn
Psdridg
13. soot-tar:
(Ibssclnsn)
1h. alcrkotyptst

1,172
3,360
2,890

2.300

-

2.700
3:500

16. [quip-cut (attics, nsdicsl
11. frsvsl
18. acrylics
19. nircctsr's Prstcsstscsl lxysnsss

b.5oo
3,h00
3,hoo

3.000
3,600
3.000

3,31h

3.500

9. Assoc. 1s lxpcr. Psychology 33:6)
Andsrssan)

8:.
”Eu/11. no lcchsicisn, Jr.
10. ans fschnicisn,

AﬂE‘VlSs

fcchnicsl Assistant

20. Social Bcccrisy/llns Gross

(lcs)

(sst.)

21. msrhssd

«-

600

11.01;].

20211

$129,923

33h80

(t)

600

11,200 kg
2,8h0 1
$156,hho

�-2.
Bopartnont

at lxporincutal Prychiatry

lxyoulon 1961~62
lacunae

0&amp;56ikk0‘

ﬂ?{5.3,qzelo

1. warns 31.2115
(62) - 1/1/61»12/61
(1/2)
Iroaght toﬁvurd (03%.)
(1/2)
(ca) - 1/1/62o12/62

h1,oso
k,oeo
32.000

w

87,059

2. warns x.h795

natinutod 8.1.2:

1k,26h
n.710

pr.
0701‘.

2.8!!6

21,820 (a)

3. 2cc¢htn¢ (But. he hrs. .181!!!)
h. Bra: rrnnlror (13%.)

'

1,000 (k)
3,570 (1)

4E=4HHhIHHap6Iadtﬁ-GIaI-é-otalG~9010htt§rttt+jhﬂﬁﬂy4hér

W

”3 Vs'ro

lot

lxpouaoa (Haunt-111104 lcncuroh) 3 ha,ooo

�lgtoot
Sagportod, in art, by l~h798, aa Garcon Iavoaticator,
otfoctivo 1/1 61. Bixtoroaoc in inooao will to
aooignod tron l1-27159
(b) loplncoo 3.). [loin in nx-avzs. In continuing onporvioion of la! prozroa would roqnoot continuation of
clinical onpyott a! l/h otat: poychiatriot iton.
low appointacnt, ottoctivo 9/1/61 at $8,500 for air
nontho, $9,000 thoroottor.
loo appointaont, to ho aado 9/1/61, at oatinatod
$12,600 pot annna.
ippointnont onco 9/1/61. Will not ho roplacod onlooBiroctor rocoivoa II! Vioiting acioatiat award.

(t)

(a)
(h)
(1)
(3)

(k)

(1)

Ion aypointnont to porait hoopital~uido onrvoyw
plannod attor 9/1/61.
low poaition to: ototiotioal ani onporviaory :nnotiono.
lollovo a roooanondatioa at Aaoiotont idniniotrator,
Hr. Bavio, tollowinc a Job convoy Icy 1961.
evorhoad allcvoaoo on l1-2715.
avorhood allowanoo on l-h798.
n~h198 allowo $18,!1h for oalary ani roooarch cooto;
$2,0h6 for ovorhood. rho-o'itoao aro applicablo to tho
prograa. It aloo allovo Oh.838 opooitiod oo training
cooto. Ihilo Dr. Kloin nay not ntilioo tho on: in tho
conin; yoar, it nay not to nood for othor pnrpoooa
without oxprooo provioion. It ia onticipatod that thio
on: will to rotnrnod to tho warns.
Incono ootinato boood on continuation of coarooo in
Biological Paychiotry and in noooarch lothcdology.
lininal oatiaato balod on 1959-60 and 1960.61
oxporionco.
loqnoot continuation ot clinical crodit-tor clinical
oorvicoo, followingll960-6l oxporionco.
‘

�5/!!I61

a.“

nupnrtuont at prorannatal Parnhtu‘vy
ttovonod 19§1~62 nudgit (3011804 5/22/61)
196o~61

lupus-0.:
1. Blrootor
H. fink)
2. assoc. 1a rnynhxntry
x1013)
J. Assoc. in Ptyuhtutvy
tranor)
Assoc.
8!.
8390!.
Psycholtcy
(Pollack)
g. A‘s... in super. Psyuhnlocy (not-oat)
.
6. Acoiut. 1n Savor. Puyehalogy Earp)
7. Alutlt. 1a
Payah01n¢7* Willa-r)
or.
8. Autos. 1: 3.0 :1 Payuholocy
luv;
9. Assoc. in Expor. Psyuholncy Ila

Ap’rovod

8:.

Inna

'

15.133131»,
m
330 ruahaictna,

Andlrllll)

on)

25.000
15.h16

-

13.000
10,9:0
7.500

-

.

8,500

10.
11.
1!.
13.
1h.
15.

47.
ll!
Pﬂytholtsgutattc rochniotna {301.43 )
50ar¢$ary
roarid
Clark. 10%
ftnuatlnan)
rlahnie Lnatutaat
30v)

.
2,112

16.
11.
18.
19.

Equtpuunt (otttc..n¢di¢n1)
traval
Suppltca
Dtruator‘c !rottultonnl lap-anon
800131 80¢n31$7llluo 0:03: (00‘)

h.500
3.h00
3,hoo

to.

no:

21. Ovarhoau

"f
ﬁg?!

{VFW
4‘

anf‘ &lt;\
\J,

a\.

iﬂﬂﬂt

3,360
2,890

-

$00

3.31h
11.0h1

$129,923

‘155 0500

�“531.1190

Inna-0i

1.

um

::::

um

'mzz-wzzx
.

_

W
,

01.059

I. um: MM

“mm am

“.000
10.850

3. latching (83%.)
h.
um.)
S.

m Wu-

clilttti crolit

(xerox/h

500

5.00.0 (a)

Itttr plyth$n3rtnt1;‘ggg

lit lliilill

(I)

(lhlniltltsod tinnitus)

(a)

\

W
W

‘

1505000

�(o)

(d)
(o)

(f)
(s)
(h)

sappurtod, in part, by u~h198. ll carter Invoc‘tcntcr.
ottaottvt 7/1/61. Dittoronco in incon- v111 be
assigned S!!! IY~2715.
Inpltaoa 5.1. Xi'an in ur~2715. In contanuzn; unparttnion a: no: progran would mounts: aonttnuttton at
tho 1/8 nt‘tt poynhxntrtlt.
lav appcxntunut. «rtagtavo 9/1/61 at :0.500 for at:
nontha, $9,000 ‘hnrunttur.
lav appatatnnnt, t- be and. 9/1/61, nﬁ outiuttad
$12,000 par gonna.
Appointncnt and. 9/1/61. 3111 not he rnplnood talus:
ntvactnr rﬁcctvbl III Vitittuc Scientiut award.
luv appointuant.to pcrult hoapxtllavado survey:
planatd utter 9/1/61.
New position for azntintloni and aupnrviaurr tunotlcnt.
Fallout 3 risen-audition of Assistant idlinistr¢‘ar.
pr. navio, (allowing a Job I‘TVII law 1961.
on continuation or court.- in
Inc... ontinnto bland and
non-arch nothodoloay.
Bioloctonl Payohtutry

(1) Kin1nnl catiunto based

anti-stat.

on 1959~60 and 1960~61

'

(3) noqscnt continuation or clinical credit for 01131301
suvvtauu. failurtuc 1960~61 o:pnr1¢n¢¢.

�HILLSIDE HOSEFRHL
WEGE &amp; SALARY SCALES

Scale
#

HIRING
RATE

SERVICE-MERIT INCREMENTS

"‘if""‘i?“”"“"§""

MERIT INCREMENTS

“ﬁf“"“‘3¢‘”"‘

l

185

193

201

209

217

225

2

205

21h

223

232

2&amp;1

250

3

225

235

225

255

265

275

,h

250

‘261

272

283‘

29h

305

5

275

2877

233'

311f

323‘

335

6

305

318

331'

324,

357

370

T

320

355

320

385

hoo

215

385

200

his

h30

nus

8

376

�9113 TITLES

ﬁrm

GRADES AND HOURLLRATES

F0 a JON-PROFESSIONAL PERSONNEE

#h

#5

$250-$305

$275-$33é

GRADE
MONTHLY RANGE

myTITLES ﬂed hr

A

JOB

- $l¢55hr

Accounting Clerk

Busboy

File Clerk
§_; $1.32 hr

Cook‘s Helper

Housekeeping

Dictaphone
Operator II

Asst. Gardener

Counter Aide

Leadman (days)

Dishwasher

'Linen
Asst.

DriYBr

[Store Keeper

Haniyman

Kitchen

Man

Maid

C

Room

" $1.032

:Cook IV

hr

Clerk Iypist

Mimeographer

Receptionist
Stenographer
Telephone

Operator
B

'Porter
Potwasher

- $l.h5 hr

Housekeeping
Leadman(Nights)

"Night Cook

Linen
Clerk

watchman

Painter

N.B, All hourlz

rates

Room

A

- $1.71 hr

Chief Telephone
Operator
Dictaphone
Operator
OPD

Receptionist
CaShier

Seoretary,IIj
Cashier
B "'

$1960 hI‘

Cook
C

III

- $1.50 hr

Licensed

Practical

Nurse

Psychiatric

Aide

Maintenance
Mechanic
include 1 me§l_p§rﬂggz_§t_the rate of $10.00 per month

I

A

- $1.8833

Jr.

Laboratory
Technician

�SUPERVISORY
&amp;
EWIEESSIONAL
PERSOBYlé
FOR
RATES
HOURLY
AND
GRALEE
WITHIN
TITLES
JOB

#6

GRADES

,

$37

$3110

-

$h15§

$370

MONTHLY RANGE

$05 -

JOB TITLES

A- $2.080

A- $2.31

Asst. Office Manager

Bookkeeper

Pay Master

B- $2.02

Assistant Bookkeeper

Registered Nurses

‘

hr
hr

A

-

Charge Nurse

Supervisor

$1.9h hr

Asst. Superintendent
Grounds

Asst. Dietitian
Gardener
Housekeeping Supervisor

0- $1.82 hr
Dental Hygienist
N.B.

All hourlz rates include

1 meal

per day

at the rate of $10.00 per

(Nursing)

Chef

.

Psycholinguistic Technician

8:

§h10 ~ $510

$2.h2 hr

Sr. Laboratory Technician

Bldgs

$1M

$2.19 hr

Executive Secretary

B"

#9

#8

#7

month

�JOB TITLES WITHIN GRADES

#2

#1

$15 -

$235

,

$1.20 hr.

HOURLY RATE

Ass't

AND HOURLY RATES FOR NON—PROFESSIONAL PERSONNFL

m

$215

1§g§g

Cook IV

Gardener

Busboy

Counter

Cleaner,

File Clerk

Housekeeping

Cook's Helper
Counter Aide

II

_

Man

I

Housekeeping
Leadman

Cashier

Clerk-Typist

Boiler

Dictaphone Operator

Chief Telephone
Operator

(days)

Ass't.

Leadman

(nights)

Maintenance Mechanic

Dishwasher

Linen

Driver

Psychiatric Aide II Painter

Handyman

Storekeeper

Receptionist

KitchenvMan

ward Clerk

Stenographer

Maid

Room

II

Mimeographer

linen

Attd‘t

Room

Room

Supervisor

Psychiatric Aide I
Secretary II
Cook

III

Dictaphone Operator

Senior

Telephone Operator

Night Cook

Porter
Poiwasher

*(Licensed Practical
Nurses at_one

incresent higher)

*Watchman

N.P. All rates include one meal per day at the rate of $10.00 per month.
* Not included in Schedule A
'

$235

-

$31.5

Assistant Chef

Accounting Clerk

Housekeeping

*Gateman

.

-,

BET??? :. 9‘19? .51 s- 39.5.}

Secretary I

Jr. Laboratory.

Technician

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                    <text>$57”
4’13

/?é,/~(22
‘

may

JUN

HILLSIDE HOSPITAL

Glen Oaks

New

21

1961

York

June 12, 1961
MEMORANDUM

Victor Leventritt, Chairman, Medical Affairs Committee

TO

k

Mr. M.

FROM

:

Maurice Bachrach, Administrator

WWW”
SUBJECT:

Proposed Research Request Budget for

July'l,

1961

to June 30, 1962

income
and
the
of
proposed
expenses
Attached hereto is a presentation
been
has
carefully
Each
1961/62.
request
departmental
research
for
for
each
schedule
for
There
a
is
Robbins
well
myself.
as
reviewed by Dr.
as
Research Department. After the expenses are given for each department,
we have Shown applicable and potential income from various sources that
each
of
end
At
departmental
the
each
department.
for
have been designated
This
the
is
"net
deficit".
shown
the
have
department's
we
schedule,
income
that
for
designated
less
the
for
department,
expenditure
total

department.

will find the entire deficit picture which gives the
from
various
income
estimated
each
the
of
departments,
for
net deficit
research
the
total
to
which
Trustees
applicable
are
the
than
sources other
The
research
net
departments".
all
and
research
"net
deficit,
program
actual
$53,250;
our
at
was
projected
the
for
present
year
deficit
Budget
Research
1961/62
Request
The
$58,12h.
estimated
at
expenditure is
from
this
$h,250
of
decrease
net
$h9,000,
of
a
net
deficit
a
projects
actual
from
this
year‘s
decrease
and
$9,12h
a
Budget
year's Request
On

page h you

experience.

�-2-

June 12, 1961
HILLSIDE 1109131111,

M
wwnwm‘m
001. I
Col. II
- 1961/62

TENTATIVE REQEARCH BUDGET

1960/51
Budget

I.

001. III
1951752"

1950731

Request
Budget

Experience

est.)

(2 mos.

001. IV
Overage
001

III

over 001.

RE§EARCH IN EXPERIMENTAL
PSYCHIATRY

EXPEN§ES:

l2
3

.
.

.

1 .

Director

.

7 .
8 .
9 .

1o.
11.
12.
13.
11.
19.
16.
17.
18.
19.
20.
21.
22.

1,500
3,100
3,100

3,113
2,163

600

600

600

3,311
11,011

2,817
10,126

25,000
17,000

3r. Assoc. Exper. Psychology 13,000

10,920
7,500

13,000
10,667
7,500

9,500
8,500
1,110

9,500
8,597
1,105

2,172
3,360
2,890

2,251
3,127
2,356

Assoc. in Psychiatry
v

-

n

n

Assoc. EXPer- Psychology
6 . ‘Asst. Exper. Psychology

S

25,000
17,500
9,000
11,000
13,331
8,100
7,218
10,000
1,120
1,800
3,600
2,185
3,192
2,710
1,500
3,000
3,600
3,000

25,000
16,116

u

n

(NEW)

11

Assoc. in Social Psychology
Assoc. Exper. Psychology
E.E.G. Technician, Sr.
E.E.G. Technician Jr. (NEW)
Psycholinguistic Technician

Secretary
Clerk Typist
Technical Ass't.

Equipment

Travel
supplies

(office

(NEW)
&amp;

Medical)

Director's Professional

Expenses
Training Expenses

gocial security

Overhead

&amp;

Blue Cross

Research in
enses115351%§%151'9§23515177'7“'

Total

-

-

-

-

-

—

251

1,838
3,500
11,010

-

1,081
9,000
1,000
2,111

(A)
(B)

(0)

(B)
600 (C
7,218 (E)

500 (F)

(7,080)(G)
390 (c)
3,600 (H)

313 (C)
132 (C)

(150)
1,500 (I)
(1,500)
200

(100)

1,838 (J)
186

2,999

'

129,923

licable &amp; Potential Income
Researcﬁ in ExperimenEEI Psychiatry

122,839

7

159,797

29,871

A

23.'ﬁ?§7”565113 ﬁSEIEE‘EEFFTEE“"‘72,101
21. Drugs
25. Nassau County
26. Potential Income

Total Applicable
PotentiEI Income

-

3,120
11,102

&amp;

Net Deficit, Research in
EggerimenEEI PsycHIatry

78,000
1,800

-

111,708
5,089

-

.

12,307 (K)
5,089 (L)
(3,120)(M)
(11,102)(N)

89,923

82,800

119,797

29,871

10,000

10,039

10,000

0

I

�Memorandum

re: preposed Research Budget

June 12, 1961

ans-u.

II.

RESEARCH IN BIOCHEMISTRY

001.

EXPEN‘EES:

I

1960/61
Budget
27.
28.
29.
30.
31.
32.
33.
3h.
.35 .
36.
3?.
38.
39.
80.

Director
3r. Biochemist

3r. Biochemist
Biochemist
Biochemist
Jr. Biochemist
Jr. Biochemist

13,500
8,786

8,hlh

5,000
21, 500

8,168
h,000
gecretary (%)
1,680
Diener
1, 250
Laboratory Equipment
2,000
§upplies
7,000
Travel
1,000
3ocial Security &amp; Blue Cross 2,h80
Overhead
2,h75

Col. II
I96076I
Experience
(2 mos.

13,500
8,783
8,820
5,000
21,170

8,131;

3,972
1,692
1, 250
1,677
7,89h
1,000
1,776
h,2Bh

est.)

001.

III

I96I752
Request
Budget

13,500
9,883
1,816
5,300
8,600
8,868
h,h00
1,7h8

Col. IV
Everage
Col

III

over 001. I
697 (0)

(6,998)
300
100
308
800
68

(o)
(0)
(0)

5,800
6,200
1,000
2,000
3,200

3,800

(Q)

300

(950)

(800)
725

66,289

67,152

63,815

(2,83h)

Applicable &amp; Potential Income
Research in Biocﬁemist
MET—‘41::
13"".9.
Hea th service
ET
82. Potential Income

18,162
26,087

111,317

-

37,900
6,515

19,738

hh,2h9

h1,317

hh,815

22,000

25,835

19,000

7,000

2,066
1,000
3,000

PatentiaI

(19,572)

&amp;

Woe
Income

h3. Net Deficit- Research in

ems ry

III.

166

(3,000)(R)

MEDICAL DEPARTMENT RESEARCH

EXPENQEE:

88.
85.
86.
87.
88.

1:9.

Research Assoc in Medicine
Research Associate
Nurse-Technician

supplies
Travel &amp; Publications
3ocial 3ecurity &amp; Blue Cross

w

-

3,000

900
800

1160

-

h,000
3,108

(7,000)
8,000
108
100

139

1,000

245

I425

(200)
(35)

6,250

8,733

(3,027)

-

200

Total Expenses - Medical Dept

Research

(0)

(h80)

Total E enses - Research in
Biocﬁemlstry

Total Applicable

(O)

11,760

�Memorandum

-h-

re: proposed Research Budget
£31. I
1960/61
Budget

Applicable

,0.

&amp;

Potential

Income

June 12, 1961

Col.

II

I95575I"
Experience
(2 mos.

Est.)

Col.

III

I§5I752
Request
Budget

Col. IV
Overage

III

Col

over 001.

1,510
5,000

u,000

8,733

h,223
(5,000)

_2,510

h,000

8,733

(777)

2,250

2,250

-

Net Deficits Forwarded
§E§earc 1n
. syc iatry
Research in Biochemistry
Medical Dept. Research

h0,000
22,000
2,250

h0,039
25,835
2,250

h0,000
19,000

-

(3,000)
(2,250)

Total Deficits

6h,250

68,12h

59,000

(5,250)

1,000
2,000

1,000
2,000

1,000
1,000

8,000

7,000

8,000

10,000

10,000

(1,000)

58912::

Egauw

(E: 250)

51.

1c
Potential Income
. .

Total Applicable

PotentIaI Income

.ervzce

-

&amp;

52. Net Deficit Medical.
Dept. ﬁesearcﬁ

Unrestricted Research Income

Henry Kaﬁfmann MemoriaI Funa
scheuer Research Fund

Contributions - Other than
Trustees

Total Unrestricted Research Income 11,000
NET RESEARCH

-

I

DEFICIT;

III‘DEEERTMENT§"‘“‘

53, 250

(2,2SO)(31,_

-

-

(1,000)

-

_

�-Memorandum

- -

re: proposed Research Budget

ane

1

1961

BUDGET COMMENTS

I.

RESEARCH IN EXPERIMENTAL PQYCHEgTRY

EXPENSEB:

projects total expenditures of $159,797, an increase of
$29,87h over the approved budget for 1960/61. This increase is made up of the
The Request Budget

following items:
Note A:

Line 2-Associate in Psychiatry (Dr. Donald Klein)--Increase-----------—-—--$l,08h
This increase represents tﬁo factors:
a. Annual increment of $500 as of July 1, 1961 in accordance
with stated increment plan.
b. Salary adjustment made during the year in order to accurately

reflect

Dr.

Klein's actual qualifications and experience.

Note B:

Zine §--Associate in Psychiatry (Dr. John Kramer)--Increase—---------------$9,000
During the current budget year Dr. Kramer divided his time
between the research and clinical programs, being in charge
of the Electro Shock Therapy services on the clinical side.
He received part of his remuneration from the Operating
Budget and the remainder of his salary was made up by a
United 3tates Public Health Service Fellowship. His
Fellowship terminates geptember, 1961 so that $9,000 of his
total salary of $13,826 should be charged to the Research
Budget.
Note C:

Line 5-- Senior Associate in Experimental Ps hole

---------------------------

ncrease---~---------—-—-$1,000

Line 6--Assistant in Experimental Psychology (Eric Karp)—-Increase --------- $ 600
Line 10--EEG Technician Senior

....................

Increase

.................

$

390

£§§§_}2--PS cholinguistic Technician -------------- Increase ----------------- $

313

Line 13--‘Secretary-------------------------------- Increase----------—------$ 132
These repreEEnt regular increments for these positions.
Note

D:

fine 5--Associate in Experimental Psycholo (Dr. Ira Belmont)--Increase---$2,hlh
This increase represents two factors: Full year
employment for 1961/62 against part year employment
for 1960/61; increment from $12,500 to $13,500 as
of September 1, 1961.

�"Memorandum

-6-

re: prOposed Research

Note E:
Line 7--Assistant

Budget

June 12, 1961

erimental Psychology (NEW)--increase --------------- $7,2h8
personne? itEm grows out of two related factors

in

E

This new
in the program.
1. The volume of work in Experimental Psychology during
the current year has risen to a point where it places
a great strain on the two incumbents. In order to
complete the number of psychological tests and
experiments essential to the program it is necessary
to add personnel able to do this work. This however
would not require a full time worker.
2. This factor is related to the information given below in
Line 11 which states that we have made a definite policy
decision to make encephalographic studies of every
patient admitted to the Hoapital instead of a selected
sample of patients. This program of encephalography
for each patient necessitates a corresponding increase

in the number of associated psychological tests which
are made concurrently with each encephalograph in order
to complete the picture which we are seeking.

These two added work loads

qualified psychologist.

will

amply use the

full

time of a

Note F:

$
500
Kelman)----increase
(Dr.
8--Associate
-----------in roial Psycholo
Line
or y the fact that the
e 1 erence is accoun e
new incumbent has higher qualifications than the
present incumbent.

Note G:
Lin' e §--Associate in
ppo n ment en 3

erimental Psycholo

ugus

,

.

w

(Dr. Karl Anderman)-decrease--$7,080

Note H:

fine IluEEG Technician Junior (NEW) -------------- increase ----------------- $3,600
The purpose of this new position is to enable the department to
make complete encephalographic and associated psychological
examinations of every admitted patient.
At the present time we are making encephalograph studies on only
a portion of the population related to our drug investigations.
much
found
have
we
a
however,
these
of
studies,
In the course
been
have
we
than
abnormal
of
encephalograms
incidence
higher

It has

therefore
been decided that it would be valuable and informative to make
of
instead
each
on
patient
study
encephalographic
a full
selected patients in order to learn whether this high incidence
of abnormal encephalograms will hold for the total patient
population.
In order to achieve this, it is necessary to add this position
in
to
referred
services
additional
psychological
the
well
as
as
led to expect for our patient population.

Line

7

above.

�“memorandum

-7-

Note

re: proposed Research

Budget

June 12, 1961

I:

fine IS--Teohnical Assistant (NEW) ---------------- increase ----------------- $h,500
This positioﬁ‘is Being added in order to relieve higher paid
professionals, psychiatrists and psychologists from statistical
work and to provide a coordinating function in the department
in the development of more efficient methods. This will give
the top professionals more time and opportunity for the use
of their higher skills.
Note J:
Eine 50~~Training Expenses ------------------------ increase ----------------- $h,838

Cost for didactic psychoanalysis, special courses, etc., for
Dr. Donald Klein (Line 2 of budget); this expenditure is
covered in full by United gtates Public Health Service‘Grant.

Note K:

line

Income------ ------------~--~--a_~--increase—-------—--------$h2,307
Represents approximately $16,000 of additional funds for a con—
tinuation grant from the United States Public Health
3ervice and $26,000 from the same source for a Career
Investigation Grant to cover Lines 2 and 20 of the budget.
23--USEHS

Note L:

fine 25--Drugs ------------------------------------increase ----------------- $ 5,089
This {tam is for psychotropic drugs which the Hospital
receives free of charge due to our extensive research
studies. The cost of these drugs which the Hospital
would normally purchase are charged to the Operating
Budget and credited to the Experimental Psychiatry
.

Budget.

Note

M:

Line 2S—-Nassau County---------------------------- decrease----------------- $ 3,120
Research projects supported by Nassau County have been
completed and not renewed.
Note N:

Line 26--Potential Income ------------------------- decrease ----------------- $1h,h02
For I96I752 there are no pending grants or any other sources of
potential income to be noted.

II.

REiEARCH IN BIOCHEMISTRY

EXPENSES:

Note 0:

EIﬁes 58 and 30 through 3h------------------------ increase ----------------- $1,869
AII these increases totalling $1,869 are in accordance with the

stated increment policy of the Hospital.

the
Line

P:

29--§enior Biochemist------------------------decrease ----------------- $6,998

Kppointment ends August 31, 1961

�{Memorandum

-8-

Note

re: prOposed Researdh Budget

June 12, 1961

Q:

ITEE‘36--Laboratory Equipment ------------------ ---increase ----------------- $3, 800
This expenditure is Toor one item of equipment covered
Uhited States PUblic Health Service
in full by
Grant.

a

Note R:
TEEE-E3--Net

Deficit: Research in Biochemist ----decrease --------- - ------- $3,000
The decrease shown is the difference between the current year's
budget and the budget for 1961/62. It should be noted
that there is a decrease of $6,835 from our actual experience

III.

MEDICAL RESEARCH

Note 3:

Line §§--Net Deficit: Medical De
Research-~decrease ---------------- $2,250
ent
¥or
E?
accountéd
This decrease is
the fact that Dr. Arnold
Blumberg's full salary is carried in the Operating Budget
as Hospital Internist and Employee Physician. All other
expenses of this project are covered by a Federal Grant.

�Memorandum
OFFICE 01" 113E

Frm

The

Mlmm
June 30, 1961

Dr. Fink

To:

1961-62 Mdget

Re:

is

etateunt of the budget allowance for your
departnnt for 1961—62; this is sent to you for your guidance
The

attached

a

during the coming year.

If

you have any queationa whatsoever, please feel free to see me
about this femlation;
I do not hear
you I will assure
that all of the figures and procedures are accepted by you.

1133130

Mel.

if

Ira

�”7;” a
Q

ray—o“

meE
1961-62

WEARCH IN

WTAL

Salaries and
Director
Assoc.
"

nses

"

Sr. Assoc. Exper. Psycholoy
Assoc. Exper. Psycholoy
Asst. Exper. Psycholog
I
(new)
I
Assoc. in Social Psychology
Assoc. Exper. Psycholog

'

E.E.G. Technician, Sr.
15.3.0. Technician Jr. (new)

Psycholinguistic Technician
Secretary
Clerk Typist

1961-62
Reguest

(Kramer)

25,000.
17,500.
9,000.

25,000.
17,500.
9,000.

(Belmont)
(Karp)

13,33h.
8,100.

(Fink)
(Klein)

(Pollock)
"’

(Kellen)
(Andersen)

(Hosquera)

(Kolo

(Podrid

Director's Professional Expenses
Training Expenses
Social Security &amp; Blue Cross
Overhead

Research in
Total
nses
ZﬁﬁeriggnEEE

Egichiatii
Potential Income

licable &amp;
Research in EggngESEtal Pszghiatgz
3. Public Health Service

Drugs
Hess au County
Potential Income

Total

tent

Net

licable

Deficit Research in

ﬁrﬁntg

111,000.

114,000.

7,2148.

7:2h80

Psichiat'i

1

r

,Afyc ﬂy}.

‘3

..

jar

~M"
Deferred*

13, 33h.
8,100.

10,000.

10,000.

h,800.
3,600.
2, h85.
3,h92.

h,800.
3,600.
2,h85.
3,192.
2,710.

1,1120.

2,7110.
11,500.

1,1120.

11,500.

3,000.
3,600.
3,000.
600.

3,000.
3,600.
3,000.
600.
h,838.
3.500.
1h,0h0.

3.500.
1h,oho.

159.797.

159,797.

11h,708.

11h,708.

119.797.

119.797.

,

240,000.

110,000.

.

5,0890

&amp;

ncome

"?

\

Approved
1961-62
Budget

Technical Ass't (new)
Equipnent (office &amp; medical)
Travel
Supplies

U.

BUDGET

\\\

{Lu

[7/1,

PSICHIATRI

in" Psychiatry

A

HOSPITAL

/'

:1

11,838.

5,0890

cc: Dr. Fink
Dr. Robbins
Acctg. Dep .
*These items requested may be restored to the budget during 1961-62
additional funds become available.

if

�Duﬂelmh C1707

9L“!

v714x14

C

5.

/£j&gt;ur5r‘pf

~

"‘50 zaﬁ/
"‘.’U.'&gt;V'“
,I‘

June 12, 1961

HILLSIDE HOSPETAL
TENTATIVE REsEARCH BUDGET

Col.

I.

I

- 1961/62

C01. II
1960761

1960/61
Budget

Experience
(2 mos.

est.

Col. III
195I75§*
Request
Budget

)

Col. IV

Overage

7001

III

over Col.

I

RESEARCH IN EXPERDMENTAL
PSYCHIATRY

EXPENgES:

1 .
2 .

Director
Assoc. in Psychiatry

25,000
16,116

25,000
17,000

1 .

9r. Assoc. Exper. Psychology 13,000
7,500

13,000
10,667
7,500

9,500
8,500
1,110

9,500
8,597
1,105

n

.

3

5 .
6 .

7 .
8 .

u

Assoc. Exper. Psychology
“Asst. Exper. Psychology
"

(NEW)

Assoc. in aocial Psychology
Assoc. Exper. Psychology
1.13.0. Technician, Sr.
E.E.G. Technician Jr. (NEW)
Psycholinguistic Technician

9 .

10.
11.
12.
13.

9ecretary
Clerk Typist

'.
15.

Technical Ass't.

16.
17.
18.
19.

Equipment

Travel
supplies

(office

-

&amp;

Medical)

enses- Research in
Ezgerzmeniéz Psychiagry

licable

&amp;

Potential

2'3.
21. Drugs
25. Nassau County
26. Potential Income

Total Applicable

FofenEIaI Income

PS 0

rvice

3,113
2,163
600

600

-

1, 500
3,100
3,100

251

-

-

1,838
3,500
11,010

2,817
10,126

.

1,081
9,000
1,000
2,111

(0)

(D)
600 (C)
7,2118 (E)

500 (F)

(7,080)(G)
390 (c)
3,600 (H)
313 (C)
132 (C)

(150)

1,500 (I)
(1,500)
200

(100)

1,838 (J)
186

2,999

129,923

atry

72,101

-

122,839

78,000
1,800

-

159,797

111,708
5,089

29,871

12,307 (K)
5,089 (L)
(3,120)(M)
(11,102)(N)

-

-

89,923

82,800

119,797

29,871

10,000

10,039

10,000

0

3,120
11,102

&amp;

Net Deficit, Research in
EggsrimenfEI Psychiatry

(A)
(B)

'

“Fawn

.n
erimen
esearc
U:.:S:.::m%c§

Income

7,2113

10,000
1,120
1,800
3,600
2,185
3,192
2,710
1,500
3,000
3,600
3,000

2,251
3,127
2,356

600
Expenses
Training Expenses
30cia1 Security &amp; Blue Cross 3, 311
Overhead
11,011

Total

-

2,172
3,360
2,890

-

(NEW)

Director's Professional

20.
21.
22.

An

10 920

25,000
17,500
9,000
11,000
13,331
8,100

‘

�WWW
Memorandum

~S-

re: proposed Research

Budget

June 12, 1961

BUDGET COMMENTS

I.

RESEARCH IN EXPERIMENTAL PQYCHIATRY

EXPENSEB:

projects total expenditures of $159,797, an increase of
$29,87h over the approved budget for 1960/61. This increase is made up of the
The Request Budget

following items:
Note A:

Line 2-Assgciate in Psychiatry (Dr. Donald Klein)--Increase-~~---—---—-~---$l,08b
This‘fhcrease represen s we ac ors:
a. Annual increment of $500 as of July 1, 1961 in accordance
with stated increment plan.
b. Salary adjustment made during the year in order to accurately

reflect

Dr.

Klein's actual qualifications and experience,

Note B:

tine §--Associate in Psychiatry

(Dr. John Kramer)~-Increase----------------$9,000
During the current budget year Dr. Kramer divided his time
between the research and clinical programs, being in charge
of the Electra Shock Therapy services on the clinical side.
He received part of his remuneration from the Operating
Budget and the remainder of his salary was made up by a
Uhited States Public Health Service Fellowship. His
Fellowship terminates September, 1961 so that $9,000 of his
total salary of $13,826 should be charged to the Research
Budget.

Note 0:

Line ﬁ~~§enior Associate in Experimgital Psycholo
Drtéﬂax PoIIaCE--—-------------------—-::— ncrease ----------------- $1,000
Line 6--As§istant in;§§perimental Psychology (Eric Karp)--Increase
600
$
---------

Line lO--EEG Technician Senior-------------------- Increase ----------------- $ 390

Line 12--Psycholinguistic Technician -------------- Increase ----------------- $ 313

Eine 13--Secretagy -------------------------------- Increase--------~------~-$ 132
These repres§nt regular increments for these positions.
Note

D:

fine §--Associate in Experimental Psychology (Dr. Ira Belmont)--Increase---$2,hlh
This increase represents two factors: Full ytar
employment for 1961/62 against part year employment
for 1960/61; increment from $12,500 to $13,500 as
of 3eptember

l,

1961.

�Memorandum

-6-

re: proposed ?esearch

Budget

June 12, 1961
Un-

Note E:
Line 7--Assistant

erimental Psychology (NEw)--increase--------------- $7,2h8
personne§ item grows out of two related factors

in

E

This new
in the program.
1. The volume of work in Experimental Psychology during
the current year has risen to a point where it places
a great strain on the two incumbents. In order to
complete the number of psychological tests and
experiments essential to the program it is necessary
to add personnel able to do this work. This however
would not require a full time worker.
2. This factor is related to the information given below in
Line 11 which states that we have made a definite policy
decision to make encephalographic studies of every
patient admitted to the Hospital instead of a selected
sample of patients. This program of encephalography
for each patient necessitates a corresponding increase

in the number of associated psychological tests which
are made concurrently with each encephalograph in order
to complete the picture which we are seeking.

These two added work loads

qualified psychologist.

Note F:

will

Line 8-~Associate in gocial Psycholc
The difference is
new incumbent has

present incumbent.

amply use the

(Dr.

full

time of a

Kelman)----increase--------~---$
at the
iac

accounts or y e
higher qualifications than the

500

Note G:

fine §--Associate in §%perimental Psychology (Dr. Karl Andermagl—decrease--$7,080
Kppointment en s ugus
, /a .

the

H:
Line I1--EEG Technician Junior (NEW) -------------- increase ----------------- $3,600
The purpose of this new position is to enable the department to
make complete encephalographic and associated psychological

examinations of every admitted patient.

At the present time we are making encephalograph studies on only
a portion of the population related to our drug investigations.
In the course of these studies, however, we have found a much
higher incidence of abnormal encephalograms than we have been

led to expect for our patient population. It has therefore
been decided that it would be valuable and informative to make
a full encephalographic study on each patient instead of
selected patients in order to learn whether this high incidence
of abnormal encephalograms will hold for the total patient
population.

In order to achieve this, it is necessary to add this position
as well as the additional psychological services referred to in
Line

7

above.

�Memorandum

-7-

Note

re: proposed Research

Budget

June 12, 1961

I:

EEEE'I§--Technical Assistant (NEW) ---------------- increase ----------------- $h,500
This position is Being added in order to relieve higher paid

professionals, psychiatrists and psychologists from statistical
work and to provide a coordinating function in the department
in the development of more efficient methods. This will give
the top professionals more time and opportunity for the use
of their higher skills.

Note

J:

Tine 20--Training Expenses ------------------------- increase ----------------- $b,838
Cost for aiHEE'icfEEychoanalysis, special courses, etc., for
Dr. Donald Klein (Line 2 of budget); this expenditure is
covered in full by United §tates Fublic Health Service‘Grant.
Note K:

Line 23"‘USH‘I9 In00me-----n-m-'~~—--——---ou—-~-.._..-a-increase—-—---—-—--------$b2,30'?
Represents approximately $16,000 of additional funds for a continuation grant from the united States Public Health
3ervice and $26,000 from the same source for a Career
Investigation Grant to cover Lines 2 and 20 of the budget.
Note L:
Line §E--Drugs ------------------------------------ increase ----------------- 3 5,089
This item is for psychotropic drugs which the Hospital
receives free of charge due to our extensive research
studies. The cost of these drugs which the Hospital
would normally purchase are charged to the Operating
Budget and credited to the Experimental Psychiatry

Budget.

Note M:

Line §S--Nassau County---------------------------- decrease----------------- $ 3,120
Research projects supported by Nassau County have been
completed and not renewed.
Note N:

Line 26-—Potential Income ------------------------- decrease ----------------- $lh,h02
For I95I752 there are no pending grants or any other sources of
potential income to be noted.

�T’Heﬁo

ﬁranluh desk of

'L.ING.BE
‘

L

Jun 21, 1961

to: Dr. Fink:
of June 30, 1961, the
changes you requested will be
reflected in your net expenses.
As

will

net expenditure
of h0,000. at that time.

we

114%

show a

M

”(M

(L/ao/o/

6’35?

�Pg. 1

To:

I

Dr. Fink

Director, Research in Experimental Psychiatry

Fran:

Accounting Dept.

Re:

Report of Expenditures
1 60

-

H

31 1961

HOSPITAL 50331012110

”Lac

Fink
Siege],

Secretary

Podrid

Salaries 0

uses :

Assoc. in Social Psychology
Psycholinguistic Technician

maize}!

Kolodny

Medical Equipment

113.

Expense Account

Total Expenses
1333:

Income from Nassau County
'
Donat i on of Psych 0 room Dru g s

Net Expenses

cc: Mr. Bachrach

t

3,120.
2,172.
2,890.

1,500,

Office Equipment
Travel
Supplies
Social Security &amp; Blue Cross

Director's

25,000.

to Hospital
.

23,753'
$33.?-

:1
12, 3 .
18%.

ES.

3’1“».
3 , hog.
920.
600.

1,0 .
2 38 .

143,120,

37,109-

3,120.

3:35;9 .

{5%.
7

'

W,
0.

ho,ooo,

31,859.

�.1

Dr. Fink

Pg.

Director, Research in hcperhnental Psychiatry
GRANT

2

141-2715

1/1/61 to 12/31/61 Grant. approved for $65,886.
1/1/61 to 12/31/61 Supplemental Grant
16 2 0 .
approved for

with:

Amount

hl,058.*

1960.61
to
applicable

hperience

1960-61
Budget

.

To Date

,.

Grant. Balance 6/30/60

32,1105.

311,599-

Additions:
Amount applicable to 1960-61

1431053 -*

bl 053.

Starting Balance

Salaries

&amp;

ese

nses:
ssoc. n sychiatry

Sr. Assoc. in Exp. Psychology
Assoc. in Em. Psychology
Asst. in Exp. Psychology

Assoc.

in

73,u63.

Additions

&amp;

Exp. Psychology

Psycholinguistic Technician
E.E.G. Technician

Secretary
Secretary

16 ,h16.~- \

Klein
Pollock
(Gittehnan

675.

6’8?”
’ 9’

8,500.

7 ’ 890.

291.

luhlo.

3,360. mm»...

RM
V

.

h 028
9,8112.
" ’
7'93:

106.

'

Sspplies

2:5“).

Medical Equipment

Office Equipmnt

Social Security

9

.

7.500.

(Andermann
Kolodny
Mosquera

Castalano

’

10,920.-~r

(Krauthamer

%

15 583
6,1914.’

7,333.

(Belmont
Karp

v-1...

75 , 797 .

8:

Overhead

382.

1,928.

Blue Cross

9,681»

"

1-1519‘

,1 729.
3’ 259

1:100.

“Iravel

”933'

Total Expenses

Unexpended Balance

530'

-

is 3!“an

cc: Hr. Bachrach

"

Em

66,085.

9,672.

if)?

w,

a

5,

X“

I

3

41.3

6

7

3"?

�Pg. 1

W

m
Director, Research in Ehperimsntsl Psychiatry

To:

Dr.

From:

Accounting Dept.

Re:

Report of Menditures

J1EE}. HQ] .. 5323 39 mm

HOSPITAL SUBSDIZED RESEARCH

Experience
To Date

1961-62
Budget

SALARIES

Fink

Kramr

2%

6’25°

Equipment

Travel
supplies
3. S. &amp; Blue Cross
Director‘s Expert“ Accmmt

TOTAL EXPENSES

IESS

Donation of Psychotropic Drugs

NET EXPENSES

CC:

Hr. Baohroch

$313“

'
3
233‘
5 350

“65

5,089.

5 335

h0,000.

1

g

�Pg. 2
To:

Dr. Fink

Director, Research in hperinantal Psychiatry

cam 141—2715
Mariana
To
Date

Grant Balance 6-30-61

’

Addition:

Starting Balance and Additions
_S__ALARIES

Klein
Pollock

Belmont
Karp
Andermann
Kolodmr
Mosquera

Zoller &amp; Schniman

Cartolano

xrlmr

EXPENSES

Winner

Goldaclmidt

Supplies

Equipmant

Travel
S. S. 8: Blue Cross
Overhead

TOTAL EXPENSES

UNEZPENDED BALANCE

00: Hr. Bachrach

Sept. 30, 196;

6,810 .57
20 529,
2

72 ..

1,000.
3 ,500,
3,203,
2,025.
1, 771.
619.

1,133.
625.
ho.

2 ’2500

610.
263.
133,

1,01h.

301.

2 ,676,

21,168.
6,201,,

.,

..

__

..__..

._....

�av~

ﬂh

T6:

Dr. Fink

Director, Research in

Mammal Psychiatry

W

Experience
to Date

3.21;. 302 1961

Grant Balance 6-30-61

Additions

-’\

Starting Balance and Additions
SALARIES

Klein
Podrid

3,500,

861.

EIPENSES

8.8.

8:

Blue Cross

W

@1135
0

Supplies

row. Emmszs

mm

,.

8,166.

p.500.)

BALANCE

«

W
00: Hr. Bachrach

5"

64“

”‘5
27’?
6‘

ﬂex/4’"

ﬁb

(I

M

/
.

�d
To:

.

.‘Dr.

Fink

Director, Research in Experimental Psychiatry
(RANT

HI-hl98

to Date

Sept. 30, 1961

Grant Balance 6-30-61

Additions

___6.ééé..________.____..___

Starting Balance and Additions

M

Klein
Podrid

6.666.

3.500.
861.

EXPENSES

S.S. &amp; Blue Cross
Supplies

Overhead
TOTAL EXPENSES

UNEXPENDED BALANCE

CC:

Mr. Bachrach

78.

_______7_13‘_____________________

�"\

Pg. 1

x

To

W

Dr. Fink

Director, Research in Marianna]. Psychiatry

From: Accounting Dept.

Re:

Report of Expenditures

July

1

- October 31:

1961

HOSPITAL SUBSIDIZED RESEARCH

Ebcperience

'

To

Date

1961-62
Budget

SALARIES

Fink

Kramer

8.331..

EXPENSES

Equipment

Travel
Supplies

Blue Cross
Director's Expense Account

S. S.

&amp;

TOTAL EXPENSES

IESS

Donation of Psychotropic Drugs

NET EXPENSES

00: Hr. Bachrach

221;.

116.
13.

8,990.
1 “55

5,089.

I 525.

140,000.

�Pg. 2
To: Dr. Fink

Director, Research in hperimental Psychiatry
GRANT

141-2715

Experience
To Date Oct. 31, 1961
Grant. Balance 6-30-61

July

Oct.

Additions
. Starting Balance and Additions
§5_LARIES

""‘""""

Klein
Pollock
Belmnt
Karp

Andermann
Kolodny
Mosquera

Zoller- Schnirmn

Cartolano
Kramer

Winner

GOIdBChEidt

EXPENSES

6,810.57
20,529.
20,529.
147,901.57

1, 333.

14,666.

M333,
2,700.
1,771.
906.
1, 510.
879.

ho.
3,000.
1, 277 .
550.

Supplies

we“
3'“
S. S.

Blue Cross
Overhead
&amp;

'7

215.
6 .
l’iog.

3,568.

TOTAL EXPENSES

2Q

UNEXPENDI BALANCE

19.,hﬂs.._______________

00: we

mach

mg.

_...

�.M
W
Pg. 3

Dr. Fink

To:

Director, Research in Experimental Psychiatry

W

herience
to Date

-

Grant Balance 6-30-61

July

Additions

Oct.

Starting Balance and Additions

W

October 31, 1961

6 666.

6:66h.

13,330.

Klein
Pcdrid

h,667.
1,280.

Travel

111;.

EXPENSES

8.5.

&amp;

Blue Cross

Supplies

Overhead

TOTAL

WSES

UNEXPENDED BALANCE

CC:

Hr. Bachrach

10?.
15.
950.

7 ,133.

6,197.

_

��Pg. 1
‘

EEEQEEEEE!

To:

Dr. Fink

Director, Research in Emerimental Psychiatry

From:

Accounting Dept.

Re :

Report of Ehcpenditures

July

1

to

November 30: 1961

HOSPITAL SJBSIDIZED RESEARCH

Experience
To Date

1961-62
Budget

SALARIES

Fink

Kramer

10,u16.

EXPENSES

Equipment

Travel
Supplies

808.
205.
53.

Blue Cross
Director's Expense Account

S. S.

8:

TOTAL EXPENSES

LESS

Donation of Psychotropic Drugs

NET EXPHWSES

CC 3

“re BacmaCh

235

11,767 .

hég,

5,089.

10 302,

130,000.

1

__
,

�Pg.
To:

2

Dr. Fink

Director, Research in Khmerﬂwntal PSyChiatry
GRANT

141-2715

Merience
To

Grant Balance 6-30-61

July

Additions

Oct.

Starting Balance and Additions
SALARIES

Klein
Pollock

Belmont
Karp
Andermann
Kclodny
Mosquera
Zoller- Schnirman

Cartolano

Kramer

EXPENSES

Willner

Gold schmidt

6,816.57
20,529.
20,529.
h7,901.57

1,666.
5,333.
5,1633,375.

1 , 771 ,

1,117.
1 , 888 .
1,111.
ho,
2 ,250.

1 , 9&amp;3 .
83 7 .

Supplies

108.

Equipment

Travel
S. S. G: Blue Cross
Overhead

TOTAL EXPENSES

UNEXPENDED BALANCE

CC 3

Mr. Bacmactl

Date

1

.
’2?“

11,1160-

3h

0h]

13,352..

‘

___-.-

�To:

Dr. Fink

Director, Research in maximum Paychiotry
mum HI-h

98

Exporience
to Date
Grant

July
Oct.

Edam. 6-30-61

6 666.
61661;.

Additions

Starting Balmco and Additions

p.330.

SALARIES

Klein
Podrid

5,833.
1,575.

Travel

209.
138.

EXPENSES

5.3.

a:

Blue Gross

mm:
Overhead
MAL

MSES

mm

MCE

00: Mr. Bachrach

2?.
1,181.
8,969.

5361.

�Pg. 1

To:

Dr. Fink

Director, Research in Experimental Psychiatry

From:

Accmmting Dept.

Re:

Report of icpenditmrea

Jug:

1

to December 31I 1961

HOSPITAL SUBSIDIZED RESEARCH

Experience
To Date

--__

1961—62

Budget

SALARIES

Fink

12, 500.

Kramer

w

Equipment

Travel
Supplies

629.

318

Blue Cross
Director's Expense Account

S. S.

8:

2683,

13,797.

TOTAL EXPENSES

IESS

Donation of Psychotropic Drugs

NET EXPENSES

.

5,089.

2 ,295.

11,502.

ho,ooo
/

2K

CC:

Mr. Bachrach

;

1'

a.)

,7“.
‘
.1

"

..

�Pg. 2
To:

Dr. Fink

Director, Research in Experimental Psychiatry
GRANT

tax-2715

Experience
Tb Date
Grant Balance 6-30b61

July
Oct.

Additions

Starting Balance and Additions
SALARIES

Klein
Pollock

20 ,529 .

20,529.

WI

901.

2

, 000.

7,000.
6,583.

Belmont
Karp
Andermann
Kolodny
Mbsqnera
Zoller - Schnirman

1,771.
1, 327 .
2,255.
1, 310.

Kramer

3,000.

Cartolano

Willner
EXPENSES

6,8h3.57

Gold schmidt

Supplies

those.

hO.

2 ,652 .

1 , 1214 ,
1108 .

Equipment

Traﬂel
S. S. 8: Blue Cross
Overhead

1

.
’23;

5,352.

TOTAL EXPENSES

1 000

UNEXPENDED BALANCE

ﬁIQQ],

CC:

Mr. Bachrach

_

�To:

Dr. Fink

Director, Research in Experiments]. Psychiatry
GRANT

“1:5198

Meme
to Date
Grant Balance 6-30-61

July

Oct.

Additions

Starting Balance and Additions

W
MNSES

my)

BALANCE

cc: Mr. Bschrsch

13,330,

7,000.
1,870.

Travel

350.
171.

Overhead

“FUSES

6,6611.

Klein
Podrid
S.S. &amp; Blue Cross
Supplies

TOTAL

6,666.

.

ho.
____J_’),L2)J_.________________,__
102855.

2.2.15,

�Pg. 1

Dr. Fink

To:

Director, Research

Wu“).

1!:

From: Accounting Dept.

W62

Psychiatry

Report of Expemﬂtures

Re:
.

HOSPITAL

w

SUBSIDI-

RESEARCH

Experience
To Date

Fink

11bit”-

Kramer

750.
21h.
333.

Schnimn

W"

chin

Equipment

Travel
Supplies
S. S.

gig"
1
,1h9.

Blue Cross
Director's Ehpense Account
&amp;

359.

TOTAL EXPENSES

mss

Donation of Psychotropic Drugs

NET EXPENSES

CC:

Mr. Bachrach

1961-62
Budget

m
,

213

2 225

5,089.

15 213

1.0.000.

�Pg.
To:

Dr. Fink

Director, Research in Emperimental PsyChiatry
GRANT

MY-2715

Experience
Tb Date

W

6 ,8h3. 57

Grant Balance 6-30b61

Oct.

Additions

Starting Balance

Jan.
and Additions

68,906.

Klein
Pollock

2,000.
8 ,083.

SALARIES

Belmont
Karp
Andermann
Kolodny
Mosquera

Zoller

Cartolano
Kramer

EXPENSES

Uillnnr

Goldldhnidt
Supplies

Equipment

Travel
S. S. &amp; Blue Cross
Overhead

TOTAL EXPENSES

UNEXPENDED BALANCE

CC:

20,529.
20,32 3.

Mr. Bachrach

7, 628.

h:6730

1,771.
1,522.
2,633.
1’3h3.
3,000.
3. 3061,389.
938.

3,315.

1,h37o
839.

6,100.
50 0h}.

2

�Pg. 3
To:

Dr. Fink

Director, Research in Mex-mental Psychiatry
GRANT

DIX-£1798

Experience
to Date

Additions

July

6,666.

Jan.

6,66h.

Starting Balance and Additions

19

.

8

8.

SALARIES

EXPENSES

Klein
Podrid

21%;,

Travel

350.

Bur

SOS. &amp; Blue

Supplies

Overhead
TOTAL EXPENSES

UNEXPENDED BALANCE

CC :

Mr. Bachrach

60.
Cross

2%.
0.
1, 3,
12 555,

Lugs»,

�Pg. 1

To:

Dr. Fink

Director, Research in Experimental Psychiatry

From:

Accounting Dept.

Re:

Report of Ehcpenditures

July 1, 1961 to February 28, 1962

HOSPITAL NBSIDIZED RESEARCH

Experience
To Date

1961—62

Budget

SALARIES

Fink

Kramer

Schnimn

2%

Klein

Equipment

Travel
Supplies

Blue Cross
Director's Expense Account

S. S.

&amp;

TOTAL EXPENSES

LESS

Donation of Psychotropic Drugs

NET EXPENSES

CC :

Mr. Bachrach

15,371.
1,500.
1428.

666.

M0.
1,329.

232.
['22

21,858.
2 1225

5,039.

19 5§2°

h0,000.

_

_.

�Pg. 2
To:

Dr. Fink

Director, Research in Experimental Psychiatry
GRANT

141.2715

Merience
Date

To

Grant Balance 6-30-61

Additions

6,810.57

July - Jan.

62 ,062.

Starting Balance and Additions
SALARIES

"" '

68,906.

Klein
Pollock

2,000.
9,166.
8,673.
5,296.
1,771.
1,716.
3,000.
1,316.
66.
3,000.
1,694.

Belmont.

Karp

.

Andermann
Kolodny
Moequera
Schnirman

mm
Cartohno

Dramer

Goldachmidt

EXPENSES

Willner
Supplies
Trave1

s. s.

a.

Overhead

TOTAL EXPENSES

UNEXPENDED BALANCE

cc: Mr. Bachrach

3 , i460 .

h, 2 95 .

t

1

)

1:353’1‘..

Blue Cross

7,01h.
‘4

’

9.

13,},62.

�To:

Dr. Fink

Director, Research in Ewerimental Psychiatry
GRANT

DIX-M98

Mama
to Date
Grant Balance 6-30-61

Additions

July - Jan.

.

-—————l9-,991+.——-——————————————.

.___J.2;22L_.____.____.____..

Starting Balance and Additions
SALARIES

Klain
Podrid
EXPENSES

9 11 .
falls»

2

Baer

212 .

Travel

5.8.

&amp;

Blue Cross

Supplies

TOTAL EXPENSES

UNEXPENDED BALANCE

CC:

Mr. Bachrach

350-

319.
11h.

1h,h22.

__§,_S7_g_._________________

�Pg. 1
MEMORANDUM

To 3

Dr 0 Fink

Director, Research in Experimental Psychiatry

From: Accounting Dept.

Re:

Report of Expenditures

Jnl3Al..l£ﬁl.tn.laznh.31,—1262

HOSPITAL SUBSIDIZED RESEARCH

__

...____~_._.._w-.

__

Iii“
hramer
Schnirnan
Klein

Experience
To Date

1961-62
Budget

18,307.
2,250.
6h2.
1,000.

EXPENSES

Equipment

Travel
Supplies

Blue Cross
Director's Expense Account

S. S.

LESS

r

CC:

&amp;

Donation of Psychotropic Drugs

4...:

Mr. Bachrach

1 052.

1:971.

302.
509

‘__~.w_____

2'
““2

23 713.

5,0§3:~*WWM

.

513,960.

�Pg. 2
To

Dr. Fink

Director, Research in Experinental Psychiatry
GRANT

Mir-2715

Merience
To

6,813.57

Grant Balance 6-30-61

Additions

July - Jan.

§2 m2

Starting Balance and Additions
SALARIES

68 Qgé

Klein
Pollock

13:33:

gm“
A”?

ndermam

Kolodm'
Mosquera

w!
Krmr

Ichnirnn

Cartolano

Winner
EXPENSES

Goldachmidt

Supplies

Eq‘li

t

Travel
S. S. 8: Blue Cross
Overhead

TOTAL EXPENSES

UNEXPENDED BALANCE

CC 0

Mr. Bachrach

Date

9,718.
5,919.

1 771.

1:911.
3,353.
1,310.

66
000:
ﬁz6Sg.
1’36 .
h,326o ,

i’gﬁ’
,
0

7,927.

E]

555

‘

�PSe 3

To:

Dr. Fink

Director, Research in herimental Psychiatry
GRANT

MI-h798

aperience
to Date
Chant Balame 6-30-61

Additions

July to Jan.

Starting Balance and Additions

w
EIPENSES

1‘1““
Podrid
Baer

Travel
S.S. &amp; Blue Cross
Supplies

Overhead
TOTAL

MSES

UNEXPENDED BALANCE

CC:

Hr. Bachrach

__J.9..22lL.__.__._.—_______
:2

22!:

10,173.
2,686.
352.
I495.

397,
188.

_____2.135.______________.
16,136.

3

68.

�M
Pg. 1

To:

Dr. Fink

Director, Research in Ehcpermental Psychiatry

From:

Accounting Dept.

Re:

Report of Ebcperaditures

__EﬂaLJg—lﬁél_tn_hp=il_30,—1962

HOSPITAL

sussmxzm

RESEARCH

Experience
To Date

_.._...._.__.

1961—62

Budget

SHARES

Fink

20,2m4.

Kramer
Schnirman

3,000.

81h.

1, 308..

Klein

§§E§E§§§

Equipment

Travel

Supplies

S. S.

&amp;

Blue Cross

Director's Manse

i’éﬁi:
3%

Account

$99.

TOTAL EXPENSES

LESS

Donation of Psychotropic Drugs

NET EXPENSES

CC 3

29

Hr. Bacm‘aCh

‘

.

2

8]

2 295

22 186

5,089.

140,000.

__

_

�Pg. 2
To: Dr. Fink

Director, Research in Experimental Psychiatry
GRANT

Mir-2715

Emerience
To

Grant Balance 6-30-61

Additions

6,816.57

July - April

Starting Balance and Additions
SALARIES

Klein
P°11°°k

29%“
”P
Andaman
KOlOdW

Mosquera

MmSchnirman
Kramer

Willner

Gold schmidt

EXPENSES
-

Supplies

Egamt
8“].

So So &amp; Blue Cross

overhead

TOTAL EXPENSES

UNEXPENDED BALANCE

00: Mr. Bachrach

Date

8 3 , 065 .

_.__...__..__.

52 292

1%???
10,762.
6 , suz .
1 ’ 7 71 .
2 ’ 105 .
3 ’ 736 o

13%;:
3 , 000 .

S
.
3%;
2 o7 .

,

1 12 O

3,315.
2 1468
1,h23.
’

O

8 ’ 8h0 .

52 212
22

5

3?

.

�Pg. 3

Dr. Fink

'Mmqum—‘m
To:

Director, Research in Ebzperimental Psychiatry
GRANT

PIX-M98

Experience
to Date
Grant Balance 6-30-61

Addiu‘ms

July to April

‘

Starting Balance and Additions

—-4515S8~————————————26 658

SALARIES

K331“

1.
2:9g9.

11 2

PM?“

EXPENSES

Baer
T

371“
1

Sgt“;

Blue Cross

Supplies

Overhead
TOTAL EXPENSES

UNEXPENDED BALANCE

CC :

Mr. Bachrach

ﬂit
.

188 .
2 312

18,072.
8 ~86

�’

To:

Pg. 1

Dr. Fink

Director, Research in Experimental Psychiatry

From: Accounting Dept.

Re:

Report of Ebcpenditmrea
Jugs! 1I 1961

-

Max 2]“ 1262

HOSPITAL SIBSIDIZED RESEARCH

Emerience
To

-.....___

Date

1961-62
Budget

SALARIES

Fink

22,179.
3,750.

Kramer
Schnirman

W

1 , 028 .

Klein

1,558.

Equipment

Travel
supplies
8. S. &amp; Blue Cross

Director's

Ishcpense Account

TOTAL EXPENSES

IESS

Donation of Psychotropic Drugs

NET EXPENSES

U4872,032.
356.
519

22

262.

Mr. Bachrach

ho,ooo.

30.6%;

* Transfers from Grants MY 2715 and MY 1:798 as per your
to be entered on books as of June 30, 1962.

CC:

5,089.

2 225

memo

of 5/23/62

-

�Pg. 2
To:

Dr. Fink

Director, Research it:

Write;
GRANT

Psychiatry
rib-2755

Ehcperience
To

We

Grant

Additions

6-30-61
LPN-1;!

~

.

April

"""""

89,909 .

Klein
Pollock

2,000
12,h16.
11,808.

Behnont
Kerp

Andemm
Kolodny

Mos

ere

my:
Certoleno

Schnirman

ramer

1mm.

Travel
S. S. 8: Blue Cross

2,601.
1,600.
9,753.

Overhead

UNEXPDJDED BALANCE

00:

he

WW

92.

Supplies

Gold schmidt

EXPENS$

MOMS.
1,3}43 .

Willner

Equipment

TOTAL

7,165.
1,771.
2,330.

3 ’ 000 ,
6 , O36 .

K

EXPENSES

6,810.57
£33,063.

Starting Balance and Additions
SALARIES

Date

2 A1; ,

72 120,

11.112

.

�To:

Dr. Fink

Director, Research in Mex-mental Psychiatry
GRANT

PIE-M98

Emerience

to Data

Grant Balance

him

Additions

.

Starting Balance and Additions

_

26,658 .

26,658,

SALARIES

Klein
Podrid
EXPENSES

B8

er

12 ,36".

3,2h2_
37h .

Travel

h9h.

S.S. &amp; Blue Cross
Supplies

Overhead
TOTAL EXPENSES

UNEXPENDED BALANCE

00: Hr. Bachrach

2481;.

188.
g

692

12 256

g

202

�July 10, 1961

H830

re:

ﬁre. Groghan
Front Dr. Pollaak
nleaae aet aaide the annual increaent
approved for July 1, 1961 for retirement or other
annuity pnrpneee attentive Jnly 1, 1961. I understand
that the neniea withheld rill be nade available to me
at my raqneet.
Thank ynn.
Would ynn

Sincerely yours,

Hrszp

33E

FoIIacE, 55.5.

�July 10, 1961
HERO

To:

Mrs. Croghan

From:

Dr. Klein

please set aside tho annual increment
approved for July 1, 1961 for retirement or other
annuity purposes effective July 1, 1961. I understand
that the monies withhold will be made available to no
Would you

at

my

requoab.

Thank you.

Sincerely yours,

Drtgp

I

on

.

o

n,

.

�g

.I

Wm

[bur/m. a;

!‘

ll

L~O-h-b-C-* .0i

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“wt
6

?

0

u-'
......... "

ﬁ
WW

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n

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ll

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Q.

�July 13,

1961

HERO

To:

Era. Dorothy Groghan

Front Dr.

rink

Max

Subject: Aaaignaout of salary Itaaa, 1961-62
Plaaao aaoign tho salary itaaa in tho Departaont of
Exporirontal Psychiatry aa tolloval
(a) lon-Govoroaant

1. Director
8. Social Psychologist
15. Toohnioal Aaaiatant
(b)

Dr.

Fink To ho appointad
To be appointod:
H.

NY-2115

2.
3.
h.
5.
7.
9.
10.

Payohiatriot (shooo)
Lazoc.
8r.
Expar. Psychology Aoaoo.
Aoaiataut_ '”
*
'
-

0.1. Kloih

John Kranar

Pollack
Dal-out
Ira
V
Eric Earp
Arthur Willnorﬁ
streettvum9f6t-w
Assoc. Expor.'Payoho1ogy
Karl Andoraanui
Ends 9/1/61
EEG Technician
Hrs. Haaaah-Hooquora
EEG
Taohnioian
ll.
- Hrl. Ilano Goldoohaidtr
Bagino 9/61
12. Poyoholinguiotio Toohoioian - Hrs. Joan Koloday
1h. Clark Typiat
- 32f. fygiawzollor
Max

‘

.

(o)

NI-h128

y

2. Payohiatriat
13. Soorotary
.

- D.F. Klltn
- Hrs. Gloria Podrid
Sinooroly youro,

ﬁtter

-

ﬂax FIBEI

3.5?“

�July 19, 1961

HERO

To:

Hre. Croghen

From:

Dr. Ire Beleont

pleeee set eeide the annual increment
approved for Sept. 1, 1961 for retirement or other
ennuity purposes effective July 1, 1961. I understand
that the monies withheld will be made available to me
Would you

at

my

toque-t.

Thank you.

Sincerely yours,

1331p

Ire

EeImonE,

55.5.

�Novenber 27, 1961
MEMO

To:

Mrs. Dorothy Groghan

From:

Dr.

Max

rink

Subject: Revision of Salary Assignments,
1961-1962 Budgot.

2nd

half,

Please assign tho following salary itoms in tho
Department of Exporinontal Psychiatry offectivo Jan. 1,
1962 to Juno 30, 1962 as follows:
(a) Nen-Govornmont
1. Director
- Dr. H. Pink
3. Psychiatrist
,- John Kronor (O$9000/annlb
8. Social Psychologist
- To be appointod
1h. clerk Typist
”Us Do schnirlm
'15. Technical Assistant
- To be appointed
(b) HI-2712
7

'

-21rPoychtatrist7**“‘““m“““‘””m““““”3“DTFT“ttetn“tO$kooo/annuo
8r. Assoc. lxper. Psychology - ﬂax Pollack
5. Assoc.
I
I
- Ira Bolnont

Assistant
I

'I

3

I
Assoc. Expor. Psychology
EEG Technician
EEG Technician
Psycholinguistic Technician

(c) HI-h798
C}. Psychiatrist
13. Socrotary

-

Eric tarp
Arthur Willner
To be appointed
Hrs. Hannah Hosquera
Hrs. Ilana Goldsohnidt
Hrs. Joan Kolodny

- D.F. Klein (Total loss
$h000)
- Hrs. Gloria Podrid

Sincerely yours,
Mllgp

HIE'TIEEI'HTET'

�MIMOIANDA
,“

�[13/

Memorandum From The
OFFICE OF THE ADMINISTRATOR

December 20, 1961

To:

Dr. Arnold Blumberg
v’Dr. Max Fink
Dr. Harry Goldenberg
1962-63 Budget

Re:

I

am

working on the budget

for the fiscal year -

July 1, 1962 to June 30, 1963.
Attached please find budget'forms with expense categories pertinent
to your department. The first column shows the budgetary allowance

for the current fiscal year; in the second column, kindly indicate
the appropriation you feel will be needed for the 1962-63 fiscal year.
You may append any data or schedules which you feel will be of assistance.
For each item of salary and expense contemplated for 1962-63, kindly
indicate in the appropriate column the source of support for the

expenditure.

Before you make your

please confer with
for next year.
Thank you

MB:DC

Enclosure

M:-

7254'

final determinations for purposes of this budget,

Dre Rebbins

for your cooperation.

as to your plans and budget prospectives

�~T0:

DEPARTWNT 0F MERIMENTAL PSYCHIATRY

HILLSIDE HOSPITAL

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1962—63

Salaries
Director

&amp;

Budget

-

Research in Experimental Psychiatry

Assoc. Exper. Psychology
Asst. Exper. Psychology

.

Kramer

.

’Pollock

»

Belmont

'

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Assoc. in Social Psychology
Assoc. Exper. Psychology
E.E10. Technician, 3r.
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4ﬁdhlﬂr
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Jr.

,(L14‘.ALaQ»‘

(office

and Medical)

Training Expenses (Dr. Klein)
Social Security &amp; Blue Cross

thioaw

Total Expenses

Anglicable &amp; Potential Inca-o
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«Mr—“whoa”,

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Budget

.37

Klein

Nil/Mr

Overhead
$1.1¢¢1Lc.z

1962-63

Egggnees

Associate in Psychiatry
n.
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1961-62

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�H.’ 23’ 1962

\.,

HERO

To:

Mr. H. Bachrach

Front

H.

Fink, H.D.

Subject: Adjustment of Expenditures HI

to

MY

2715 and

KY

h798

1.

Pleaao aeaeeign following expenditurae aaeigned
2715 to "non~government".

a. Salary of
lolodny, Jean

Jan. 1, 1962 - June 30, 1962
Goldechnidt, Ilene
Jan. 1, 1962-May 31, 1962
2. Pleaee reaeaign expenditures charged HY h798 by
transfer to "non-government” of the following items:
a. Gloria Podrid
Charge 2/5 to MY h793
7/1/51
‘
dtto
BIS/to
Ron-Govt.
'
b. Mrs. Gertrude Baer
Charge

o.

all salary to

Non-Govt.

Requiaitione dated:
11/61 ﬂax rink - expenaee
12/61 Max Fink - expenses
12/20/61 Max naailton
2/8/62 L.I. stenotape Co.
(Royal Typita)
2/8/62 Joint Purchasing (aupplies)

9.75
b0.61
50.00
53.20
h6.55

W.

."'

�oemnmtm or:

arm» mcmm
HﬂLﬂDEPKNFgﬂL

Gumcnﬂhl99'

May

23, 1962

MEMO

To:

Mr. M. ﬁachrach

From:

N.

Subject:

to

MY

Pink,

M.D.

Adjustment of Expenditures MY 2715 and
July 1, 1961 - June 30, 1962

MI L798

Please reassign following expenditures assigned
2715 to “non-government”.

1.

a.

Salary of

Jan. 1, 1962 - June 30, 1962
Jen. 1, 1962-Mey 31, 1962
Goldschmidt, Ilene
2. Please reassign expenditures charged HY h798 by
transfer to “non—government" of the following items:
a. Gloria Podrid
Charge 2/5 to MY h798
7/1/61 - data

lolodny, Jeen

"

3/S/to Non-Govt.

b. Mrs. Gertrude Beer
Charge

ell salary to

Non-Govt.

c. Requieitione dated:
Fink - expenses
Fink - expenses
12/20/61 Hex Hamilton

11/61
12/61

Mex
Max

9.75
h0.61
50.00
53.20

2/8/62 L.I. Stenotape Co.
(Royal Typite)
2/8/62 Joint Purchasing (supplies h6.55

Hex FInE, M.D.

�6/11/62
Brain Function and Bohavior Rososrch Progoct
Bud‘otagz Rocoonggggtiono

--

1262

~

62

- Rovisod 6/11/62

Following discussions or 5/22 and 23, a hudgst rooosnondation for oightoon months support was prosontod which
did not lost tho Radical Diroctor's approval. In ossonco,

it provided

for

an oxponditurs or $53.h10

for the

first

six months; $63,183 for tho next twolvo; and of those suns,
325.750 from Hillsido Hospital and $90,8h3 (including $9583
ovorhsod) from tho u.s.9.n.s. In lino with tho discussion
of 6/11/62, tho following rovissd budgot is prosontcd for
consideration.
1. It is tho intsntion of tho Director of tho Dopartnont
or Exporioontal Psychiatry to resign fro- hia prsaont pooition'
on July 1, 1962 to continue os Principal Invsstigator
(Consultant) of tho Brain Function and Bohavior Rosoarch
ProJoct (H! 2715) to Doc. 31, 1962.
For this poriod, to Doconhor 31, 1962 his ssrvicos
will ho conponsasod on a consultant stipond basis, tron
funds providod by tho Board of Directors of Hillsido Hospital.
2. It is roconnondod that Dr. Belmont, boginning 10/1/62,
bo continuod on a flat too stipond basic at an ostblishod
rats oqnivalont in ootivity to ono day pot wash.
3. It is roconnondsd that tho following adjustnonts ho
nadc in Dcpartnontal hudgsts to accomplish tho rsquostod
soparation of tho Dopartaont into constituont unite.

�-2-

s.

the expenses and activities of
Dr. Donald Klein he continued under the direct supervision
of Dr. Robbins, providing such secretarial and data processing services as his project may require.
b. in EEG technician salary be provided by the
hospital at a rate of $5,000/annuu for full tile. 1 would
suggest 2/5 tine; but this should be based on s reconaendation of tho hospital Neurologist. For the period that
Dr. Kramer is available, he will continue to read the
records; but provision should be node for others to do this.
0. Dr. Kroner to continue in the sane relationship
to end or 1962 continuing supervision or 30!, at Dr. Robbins'
K! h798 and

pleasure.
0.

Present budgets (to 6/30/62) he re-ellocated to show
estimated expenditure of approximately $30,000 in Board support,
allowing the following a
a) Estinsted balance 6/30/69 nr 2715
2000
Incone 2nd half 1962

h2001

stupoo
5.

Budgets for six nonths 1962 and 12 nonths 1963,

corrected for social security, blue cross and statistical
expenses are shown on next page. These provide, exclusive or
principal investigators
7/1/62 - 12/31/63
3h,260
Overhead

1/1/63 - 12/31/63

5,100
$38,960
50.500

�-36. Requeet 0.8.P.H.S.t
$hh,000
a. 196? Income
Expendituree 38.960
5.000 app. - carried forward

b. 1963

50,500

-._.£&amp;99_
hS.Soo

Overhead

6.8gg
$52,325

7.

With theee

adjust-cute, the budget ie reconnended

inclueingt
a. Continuation request or I! 2715 be aubaitted to
U.S.P.R.s., requeeting the aaount of 52,325 to retain at
Hillaide ﬁoapital for 1963 and the balance (app. 31.000) he
made available for application of continuation at the Mieeouri
Iuetitute or Paychiatry.
b. iproval for transfer of EEG analyser and tape
eyeten ee requeeted h/l/62 be approved.
6. Board of Directors approval tormfunde or 12,500
for period 7/1/62 - 12/31/62 aa continued aupport of Principal
Investigator (Coneultant) on baeis outlined above. In the
event coneultent tine 1- required in 1963, expenses and
ccnaultation teee are to be paid by Hilleide Hoopital through
{undo provided by the Board of Directore. A contingency fund
in the amount of 86000 ie eugteeted for thia activity.
a. U.3.P.H.s. be requested to approve Dr. Hex Pollack
ea oouinveetigator.

�7/1/62 - 12/31/62

1/63 - 12/63

1. Staff

Psychiatrist
I. Pollack, 8:. Res. Assoc.
taper. Peychol.

John Kroner,

3,956

-

I. Bel-out

7,500
3,582

15,000

'Earn,

Consultant

750

Res. Ass't.
Expor. Fsychol.
A. "illner, Res. Assoc.
Expos. Psychol.
B. Hosquereﬂ, EEO Technician

3.

b.350
h,700
1,000
1,700
1,h57
1,315

0. Podrid, secretary
Dr. schnirnanhe, secretsry
J. Xolodny, technician
351

BC

(OPP)

3,000
8,700
,

9,h00
2,000
3,800
~
2,600

950

Travel
Supplies
Conputaticn c Consultation

‘

Carried forward
Net

Overhead

u.s.r.n.s.

Total

'

Board support

Total Budgets: 18 nos.
uspns
Board

500

600
900
1;560&amp;

1,200
1,800
1,500

3h,260

50,500

3h,260

5,000
u5,500

5.100
38,960

6,822
$2,325

12,599

16,000)

$109,785

91,285
12,500 (¢ $6000 contingency).

Notes
0

H. Hosquere:

tins s 380 resesrch
i
and
as
ties
statistician,
clinicel
EEO services
recouaended by

Allows one

es Secretary-typistc Prograa

(it
sill

Neurologist).

not require second typist 1963.

�6/11/62

I!

Brain Function and Behavior Research Proaect
Budgetarz Reconnendetions

--

1962 - 63

- Revised 6/11/62

Following discussions or 5/22 and 23, a budget reconnendation for eighteen months support was presented which
did not nest the Medical Director's approval. In essence,

it provided

expenditure of $53,h10 for the first
six nonths; $63,183 for the next twelve; and of these suns,
$25,750 from Hillside hospital and $90,8b3 (including $9583
overhead) from the U.3.P.H.3. In line with the discussion
of 6/11/62, the following revised budget is presented for

for

an

consideration.
1. It is the intention of the Director of the Department
of Experimental Psychiatry to resign from his present position
on July 1, 1962 to continue as Principal lnvestigator
(Consultent) or the Brain function and Behavior Research
Project (M! 2715) to Dec. 31, 1962.
1962
December
to
31.
his services
period,
this
will be cenpensaeed on a consultant stipend basis, tron
funds provided by the Board of Directors or Hillside Hospital.
2. It is recon-ended that Dr. Belmont, beginning 10/1/62,
be continued on-e flat fee stipend basis at an estblished
rate equivalent in activity to one day per week.
3. It is recommended that the following adjustnente be
node in Departmental budgets to accomplish the requested
sepsraticn or the Departnent into constituent units.

For

�-2-

a.

activities of
Dr. Donald Klein he continued under the direct supervision
or Dr. Robbins, providing such secretarial and data processH! h798 and the expenses end

ing services as his project

require.
b. in EEG technician salary be provided by the
hospital at a rats of $5.000/annuu for full time. I would
suggest 2/5 time; but this should be based on a reconnendation of the hospital Neurologist. For the period that
Dr. Kramer is available, he will continue to read the
records; but provision should be made for others to do this.
c. Dr. Kramer to continue in the same relationship
to end of 1962 continuing supervision of ICT, at Dr. Rohbins'
pleasure.
h. Present budgets (to 6/30/62) he re-allocated to show
may

estimated expenditure of approximately $30,000 in Board support,
allowing the following:
a) Estimated balance 6/30/6? NY 2715
2000
Income 2nd

5.

half

1962

h2°?Z,
thhpoo

Budgets for six uonths 1962 and 12 months 1963,

corrected for social security, blue cross and statistical
expcnaes are shown on next page. These provide, exclusive of

principal investigator:
7/1/62 - 12/31/63
Overhead

1/1/63 - 12/31/63

3h,260
-

3.100
838,960
50.500

�-36.

Request U.S.P.H.s.s

s.

1962
-

Income

Expenditures

$bh,000
38.960

5,000 spp. - csrried forward

b. 1963

*

50,500
§IOOO

hS’SOO

Overhead

6:825
$52,325

7.

With

these sdJustsents, the budget is recossended

inelusing:

s. Continustion request of I!

2715 be submitted

to

J.S.P.H.S., requesting the ssount or 52,325 to rensin st
Hillside Hospitsl tor 1963 end the bslence (spp. 31,000) be
nsde evsilsble for spplicstion of continuation at the Missouri
Institute of Psychiatry.
b. Aprovsl for transfer of EEG snslyser end tspe
system so requested

h/l/é?

be approved.

0. Bosrd of Directors spprovsl forfﬂunds or 12,500
for period 7/1/62 - 12/31/62 ss continued support of Principal
luvsstigstor (Consultsnt) on basis outlined above. In the
event cousultsnt tine is required in 1963, expenses end

oonsultstion tees sre to be psid by Hillside Hospitel through
funds provided by the Bosrd of Directors. A contingency fund
in the slount or 36000 is suggested for this sotirity.
d. 0.8.9.3.8. be requested to spprove Dr. Hex Pollock
ss eo-investigstor.

�7/1/62 - 12/31/62
1.

1/63 - 12/63

Staff
John Kraser,

Psychiatrist

Pollack, Sr. Res. Assoc.
Bxper. Psychol.
1. Belmont
Consultant
I. tarp, Res. Ass't.
Exper. Psychol.
A. "illner, Ree. Assoc.
Bxper. Psychol.
H. Hosquerae, EEG Technician
0. Podrid, aecretary
at. Schnirneneﬁ, secretary
J. Kolodny, technician
as, no (app)
Travel
Supplies
Computation &amp; Consultation
H.

'

’

3,956

-

7.500
3.582

15,000

750

3.000

b.350

8,700

h.7oo
1,000
1,700
1,h57
1,315

9,hoo
2,000
3,800

950

1,500

600

1,200
1.800
1,200

11500?

Carried forward

,,

Net
'
.

Board Support

03935
Board

50,500.
5,000

_.,

3h,260

hS.Soo

h,zoo

6,825

38,960

52,325

12,500

$6,000)

51,h60

58,325

Overhead

Total Budgets: 18 nos.

9,600

900

3h,260

Total U.8.P.R.S.

-

$109,785

91.285

12,500 (+ $6000 contingency).

Notes

e

i

tine as

research
and i time as clinical
statistician,
EEG services (if reconaanded by Neurologist).
so Secretary-typist: Prograa will not require second typiet 1963.
H. Hosqueras

Allows one

EEG

�Juno 12, 1962
Dr. Lowis L. Robbins, Hodioal Diractor
Hr. Horbsrt Bookind, Prosidsnt, Board or Dirootors

ﬁillsido Hospital
Olon Oaks,

!.!.

Dsar Dr. Robbins and Hr. Bookind:

It is

with rogrst and with tondnsos for my
stimulating and exciting ysars at ﬂillsids that I
submit this lattsr of rosignation as Dirsotor of tho
Dopartssnt or Exporiasntal Psychiatry stractivo
Doooubor 31, 1962. I an aura you will ho ploaosd to
know that tho prograss hora havo lad to tho invitation
to ostahlish a rosoaroh and training program in a now
cantor, tho Missouri Instituto of Psychiatry at
St. Louis; as wsll as my appoint-ant as Rsssarch
Protoosor of Psychiatry at Washington Unirsrsity School
of Hodicino.

I look back at thoss ysara with ploasurs, for I
havo loarnod such and hats round snthusiastio and
dodioatod co-worksrs. I as aratotul to tho contidonoo
sxprosssd in my initial appointasnt by Dr. Israol strauss,
and to tho Board or Diroctor's support during thoso yoars.
During tho nsxt tow aonths, I should liko tho
opportunity to coaplots as such o: my progras as possiblo
hora, and for this roason hays askod to continua as
projaot dirsotor or ths USPH3 grant H12715. is soon as
tho studios hora psrait, I shall lsavs to ossuas my now
dutiss in St. Louis.
with my boot porsonal rogards, and assurancos of
loyalty, I roaain.
Rospoctfully yours,
Hrsgp

.

ﬂax

M

IInE, 5.5.

�HEHORAHDUH

June 12, 1962

to:

Dr. L. Robbins

FROM:

Hex

Pink,

M.D.

With the disapproval of the proposed 18 nonth budget
for the Brein Function and Behavior Project, and without a
to submit the
satisfactory alternative, I an conetreined
enclosed letter of reeignation, dated Deco-her 31, with a
recommended budget for the expenditures under HI-2715
during the renainder ot the grant period. I an dating
the roaignation as of this time to permit the oonpletion
of e major port or the progren. It in my intention to
continue thie program of studies or the relation of brain
function to behevior et the Hieaonri Institute of Poy‘
ehiatry, beginning early in September. For e treneition
period or e few nonthe, while aone onelyeeo end write-up
are in progress here, the continuation progrene will be

eetabliehed there. AI noon on my tine is predoninantly
in St. Louie, I will resign fully from the program here.
I truet this is satisfactory to you.
Roapeotfnlly yonre,

Krzdto
one.

or

M
n

,

. .

�June 12, 1962
Proposed Budget, Brain Function and Behavior Research Project
Jnly 1, 1962 - December 31, 1962

Estimated Balance, 6/30/62 MY2715
Income 6/30-12/31

12,000
h2,007
$Sh,000

Expenditures

l.2.

Prin. Investigator
Psychiatrist (Kramer)
3. Psychologist (Pollack)

h.
5.
6.

-7.

8.
9.
10.
11.
12.
13.

lb.

15.

”

EEG

12,500
3,956
7,500
3,582

(Belmont)

750

(Karp)
''
(Willner)
Technician (Moequara)

Secretary (Podrid)
(Schnirnan)
Technician (Kolodny)
Soc. Sec., Blue Cross
Travel
Supplies
Cowputation and Consultation

0,350
h,700
2,000
1,700
1, h57
1, 315K

'

Overhead

950
600
900

,

’

1,500
h,700

$52,h60
Balance carried forward 1963

$

1,5h0

�June 12, 1962
Proposed Budget, Brain Function and Behavior Research Project
July 1, 196? - December 31, 1962

Estimated Balance, 6/30/62 H12715
Income 6/30-12/31

12,000
h2,oo7
$5h,000

Expenditures

l.2.

Prin. Investigator
Psychiatrist (Kramer)
3. Psychologist (Pollack)

h.
So

6.
7.
a.
9.
10.
11.
12.
13.

lb.

15.

(Belnont)
'I
I
.
(Earp)
(willner)
'
£30 Technician (lacquers)
Secretary (Podrid)
(Schnirnan)
'
Technician (Kolodny)

Soc. Seo., Blue Cross

Travel
Supplies

12,500
3,956
7,500
3,582
750
13,350

‘

h,700
2,000
1,700
1.h57
1,3155
.

'

‘

Computation end Consultation
Overhead

950
600
900

1,500

ht7°°

3 2 h60

Balance carried forward 1963

'

3

1,5h0

�June 1?, 1962
Propoeed Budget, Brein Function end Behevior Reeeeroh Project
July 1, 196? - necenber 31, 196?
V

Settleted Belence, 6/30/62

HYZTIS

Income 6/30-12/31

.

12,000
g2.oov
$5h,000

Expenditures
1. Prin. Inveetigetor
2. Paychietriet (Ire-er)
3. Psychologist (Pelleok)
*
L.
(Beleont)
R
S.

6.

7.
8.
9.
10.
11.
12.

13.
1b.
15.

''

I
(Earp)

(willner)

Technicien (Hoequere)
Secretary (Podrid)
(Schnireen)
\
Technicien (Koladny)
Soc. Sec., Blue Cross
Trevel
Supplies
Coeputetion end Consultetion
EEG

'

Overheed

12,500
3.956
7.500
3.582
750

h,350
h.700
2,000
1,700
1.h57
1.315f
950
600
900

1,500

5&amp;12Q
2

Belence carried toruerd 1963

h60

a 1,5h0

�glidilibﬂl
Jan. 12,
To.

1962

Dr. In Robbins

---.~-- -----”.-.-.with tho disapproval at the prchIod 18 nouth budget
fur the Brain function and lohnvlnr Proaout, and without a
tntlntuatory altornativc, I am eenstrainod to submit the
with a
Isolated lattar at rculznatlon, datod noun-bowII~5115
Jl
roast-andod budgot for the Impoudlturuu and-r
during tho ronnlndor or the grist porlud. I :m attlng
rollcu:tlan In of ﬁhln #1:. to paralt the ounplo‘lon
of a IIJOr part at in. progral. It 1- Iy intanllon to
uoatlano tutubotavlor
proxruu of It‘dlou of tho ralatlon or brain
Pay—
I1UIOIF1
tho
or
functlun $0
InstitutIt
ohlntrr. bout-nan; early in Boptunhor. It: a truulttlou
902106 at I ran monthl, will. aqua analyacn and write-up
are in prograan bars, the oonﬁlnnntlou prouru-l will be
octablilhnd tiara. At noon an my tin. la produuiu:ntly
1a 3%. L§!1l. I will route: tall: from the progrum hcrc.
I ‘rlnt til: 1. natiltlctozr to you.
BprQoSShlly yours,

ti.

nmu
“.0

n

, .

.

�MEMORANDUM

DEPARTMENT OF EXPERIMENTAL PSYCHIATRY

June 1h, 1962

To:

Mr. Bechrsch

FROM:

Dr. Hex Fink

..‘.~.“‘..--.-.“enclosed budget dated June 12, 1962 for
6 months under project support by MY-2715 is contingent upon the adjustments euthorised in my
memorandum of 5/23/62, 3 copy or which is enclosed.
The estineted belence or $12,000 for 6/30/62 may
be in error by 10%, and if so, can be corrected by
using the belenoe, or adjusting expenditures to
conform with reality. Also, it is probable thst
lines 1, 2 ere overestimeted. I have also indented
this grent fully for Mrs. Mosquere (line 7).
After Hrs. Croghen hes made the adjustments of
5/23/62, if she will give me e true balance, I will
revise this budget statement.
The

Thenk you

HFsdts

for your cooperation.
Sincerely yours,

ﬁe: Fink, 5.5.

�MEMORANDUM

DEPARTMENT OF EXPERIMENTAL ?SYCHIATRY

June 1h, 1962

T0:

Mr. Bachrach

FROM:

Dr.

Max

Fink

enclosed budget dated June 12, 1962 for
6 months under project support by MY-2715 is con—
tingent upon the adjustments authorized in my
memorandum of 5/23/62, a copy of which is enclosed.
The estimated balance of $12,000 for 6/30/62 may
be in error by 10%, and if so, can be corrected by
using the balance, or adjusting expenditures to
conform with reality. .Also, it is probable that
lines 1, 2 are overestimated. I have also indented
this grant fully for Mrs. Mosquera (line 7).
After Mrs. Croghan has made the adjustments of
5/23/62, if she will give me a true balance, I will
revise this budget statement.
Thank you for your cooperation.
The

Sincerely yours,

ﬂaw
MF:dts

Max

Fink, M.D.'

�MEMORANDUM

DEPARTMENT OF EXPERIMENTAL PSYCHIATRY

July 20, 1962
Pollack
Co-Investigator
M. Fink, M.D.

T0:

Max

FROM:

MI-2715

Project

In answer to your question of 7/19, I plan to complete
my active participation at Hillside on September 15 and shall
request “vacation” time as terminal leave. For the past year
I have accrued 16 days as of 9/1/62, and have carried forward
15 days from 1960-61. If my calculations are correct, my
salary should be paid to October 26.

Effective on your return from Europe in September, I
believe you should assume full responsibility for the expenditures
and management of MY-27lS. Until I leave for Europe, and in
your absence, I shall continue to carry out these responsibities.
I shall notify NIMH as to the transfer of responsibility as of
September 15, and have notified Mr. Bachrach as attached memo
indicates.
In the event that you balieve my consultation will be of
service to you, I shall be pleased to come to N.Y. However,
reimbursement for expenses should be borne by the grant here.
Good

Hrtdts

luck!

Max

Fink,

M.D.

�do

’

MEMORANDUM

k

DEPARTMENT OF EXPERIMENTAL PSYCHIATRY

July 20, 1962
T0:

Mr. Bachrach

FROM:

Max

Fink, H.D.

Principal Investigator,
permit you to

MI-2715

Project

exact budget estimate for
MI-2715 for 1962-1963, I should like to bring the following
to your attention.
At the completion of my duties in Europe I shall return
to Hillside and complete such reports as may be necessary.
This should be done by September 15. I shall ask that I
complete my service on these programs as of that date, subject
to reimbursement for accrued leave. is of September 1, 1962
accumulated leave time will be 31 days, which will be requested
as terminal leave.
Until September 15 I shall continue to exercise responsibility for the project activities, but shall relinquish these
To

make a more

that date.
Parenthetically, I would suggest a prudent bookkeeping
measure for your consideration. is you know, the office of
Director of the Department has never been supported by
government funds. It is prudent to combine this course
until the final termination of the office. As a record

fully

as of

matter, if you exercise the prerogatives of your position
you could so reassign items in MI-2715, and non-government
for 1961-62 as to "carry forward” in non-government a sum
necessary for the position. In the revised budget estimate
you are planning to submit to NIMH, the item of principal
investigator need no longer appear.
Thank you for your cooperation.

HF:dts

ﬁax Fink, H.D.

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                    <text>Seventy Years an Experimentalist in Neurology and
Psychiatry

Max Fink, M.D.

Professor of Psychiatry and Neurology Emeritus,
State University of New York at Stony Brook.
First Publication in Archives: May 28, 2017
Updated April 18, 2021
11 Buttonfield Lane
South Hadley, MA 01075
Tel.

631.637.1730

fink.max@gmail.com
maxfink55@gmail.com
max.fink@stonybrook.edu
max.fink@stonybrookmedicine.edu
max.fink@sunysb.edu
max.fink@optimum.net
Metrics: April 18, 2021
Pages: 100
Words: 38,107

The ultimate court of appeal is observation and experiment, and not authority.
Thomas H. Huxley

1

�Introduction
Inducing seizures to relieve severe behavior disorders-- electroshock, ECT -is a much prejudiced treatment that is undergoing a renaissance after eight decades
of experience. Usage is increased to varying degrees worldwide. But raucous
attacks by public critics and psychologists claiming treatments cause brain damage
and memory losses are ever common. But assured safety and remarkable efficacy,
even guides to specificity in illnesses, brings the intervention within a successful
medical tent. Introduced for the relief of the imagined Kraepelinian diagnosis of
schizophrenia, recent decades has defined catatonia (and its varieties of mutisms,
manias, motor rigidities) and melancholia (depressive psychoses) as more specific
systemic disorders that are rapidly and effectively relieved.
How was the treatment discovered? And why was it rejected by the
professions? Why the public stigma in the face of efficacy and specificity? How has
the practice and the science of the treatment evolved?

The author, well on his way for full training in conventional neurology and
psychiatry is asked to oversee the seizure therapies in hospitalized severely
psychiatric ill. He takes on the task of improving the science and increasing public
and professional acceptance are highlighted in this personal story of an
experimentalist physician.

These pages cite my education as a physician with qualifications in
neurology, psychiatry and psychoanalysis. From the beginning, I studied patients,
their physiology and symptoms, and applied different interventions, often in a
Random Controlled Trial. When I entered the profession, research studies in man
was an accepted practice. In recent decades, bars to such studies have been
increasingly applied, leading to focus on studies in animals and other surrogates.
Over my professional career my interests focused on the treatment of induced
seizures (electroshock, ECT), the effects of substances that altered brain functions
(psychopharmacology, EEG), and the systemic behavior syndromes of catatonia and
melancholia. The records of my studies are archived at the Stony Brook University
Library. 1

2

�Contents
Introduction for Readers
Book One: Inducing Seizures as Treatments

2

Ending Insulin Coma
Optimizing ECT Procedures
The EEG as Index of Efficacy
Modifying seizures: Muscle relaxants and sedatives
Are subconvulsive treatments effective?
Are chemical induced seizures as effective as electrical?
Is Isoflurane anesthesia a replacement?
Acetylcholine and Anticholinergic Drugs
Neuropsychological Tests and EEG Slowing

9

11
13
15
16
17
17
18

The differences Electrode Placements make, Again
Multiple ECT. MMECT
ECT in Systemic Medical Illnesses
Optimizing Treatments
ECT in Schizophrenia
Clozapine and ECT
Seizures and Brain Fluphenazine
CORE Study: ECT in Depressed Inpatients
Persisting Stigma: Memory Loss and ECT

19
20
21
23
24
25
26
26
28

Creation of Induced Seizures as Therapy
Immediate Rejection by the Profession
First APA Task Force onECT
Out-Patient ECT Commission
Stigma persists: Public Joins Attack
Church of Scientology and Malpractice Legal Suits
Media Attacks: Madness with Jonathan Miller
Active Defense: A Beautiful Mind

30
31
34
34
35
36
36
38

Book Two: After ECT Research Hiatus, Renewed Studies

Book Three: Electroshock in the Public Eye

3

�Book Four: The Enigma: How do Seizures Affect Behavior?
Seizures as systemic reflexes
Neurophysiologic adaptive theory
Cholinergic theory
Neuroendocrine hypothesis
Conferring in the search for mechanism

40
41
42
43
46

The Teaching Case
Catatonia as a type of Schizophrenia?
But Catatonia is not Schizophrenia
In contrast, Catatonia is Treatable
Is NMS a Form of Catatonia?
The Drive to Official Definition
Sedative Verification Test
Many Faces of Catatonia
Delirious mania
Toxic serotonin syndrome
Pervasive Refusal Syndrome
Toxic encephalitis: NMDAR Receptor
Self-injurious behavior in Autism
DSM Classification Debates
Catatonia Textbook, ACTA Supplement

50
51
52
53
54
56
56
57
57
59
59
60
62
62
64

What is next?
Dexamethasons Suppression Test
Melancholia Textbook, History

66
66
67

EEG Introduced to Hillside Hospital
EEG in Psychopharmacology
Grey Walter Analyzer
Digital Computer analysis of EEG
IBM 1800 analysis system
Lessons learned: Putative Drugs Classified
Association-Dissociation Controversy
Pharmaco-EEG Paradigm

69
71
71
71
73
74
76
78

Book Five: The Road to Catatonia

Book Six: Melancholia: Medical Model of Diagnosis

Book Seven: Studies in Electroencephalography

4

�Book Eight: A Medical experimentalist is Created
Medical School Experiences 1942-1945
Neurosyphilis and CSF
Osteomyelitis, Barbiturates
Interneship
Penicillin in Empyema
Residency
Percutaneous Carotid Angiography
Face-Hand Test

79
79
80

Early Life
Family Affairs
Dalliance with Psychoanalysis
Military Career, Ship's Surgeon
Perigrinations
Books Published, Edited

85
87
87
89
93
93

Book Nine: Biography

Appendices

81
82
83

94

5

�Book One: Inducing Seizures as Treatments
My academic arc in electroconvulsive therapy began unexpectedly on
January 2, 1952 as I enrolled for the fifth year of residency training in neurology and
psychiatry at a hospital reputed to use classic psychoanalytic principles to treat
hospitalized severely ill. I arrived on a clear winter day with another new recruit, to
meet the Directors of this 170-bed multi-building Hillside Hospital caring for
voluntary psychiatric in-patients, for up to a year, mainly at public cost.
That morning I was assigned to the electroshock and insulin coma treatment
services. In my previous years, I had no experience with either treatment.

I received my M.D. degree from New York University School of Medicine on
June 12, 1945, followed by nine-month interneship and 20 months service in the US
Army Medical Corps. During the succeeding four years I studied in neurology and
psychiatry residencies, attended a school of psychoanalysis, and sought a final year
in psychoanalytic psychotherapy at an inpatient hospital in the Long Island
farmland, with accredited training psychoanalysts on its faculty.

I accompanied the Associate Medical director to a 2-story building that
housed the electroconvulsive (ECT) treatment unit. One by one, five patients lying
on a wheeled stretcher under sheet restraints were brought into a treatment room,
a rubber bite-bloc placed between their teeth, two stimulating electrodes applied at
the temples, protected by two aides, a seizure induced with currents delivered from
a Medcraft alternating or a Reiter polyrhythm current device with the energy set
according to estimates of what was needed to induce a full grand mal seizure.

As the electric currents were applied, the neck and back arched, the body
became rigid, followed by rhythmic muscle movements and breath holding. The
patient became cyanotic with light blue lips. After a minute, the muscles relaxed,
deep breathing followed, cyanosis waned, and color returned as the patient was
moved to a recovery room, cared for by aides for 15 to 20 minutes until able to get
off the stretcher and walk to the ward for shower, dressing and breakfast. Durations
of the elicited seizures varied in length from 30 seconds to a few minutes,
occasionally requiring termination by intravenous injections of amobarbital.

Observing a full grand mal seizure in each patient jarred me. The previous
week and for years before I had been taught by my neurologist teachers that
seizures were dangerous to patients and must be stamped out. Every teacher had
emphasized the need to fully inhibit seizures to avoid tooth, limb, and spine
fractures, tongue-biting, confusion, injury from falls, and death. Much was made of
the newly developed anticonvulsant phenytoin (Dilantin).

6

�And now, we were deliberately inducing grand mal seizures! This antithesis
has plagued my professional life and the lives of neurologists who, to this day, are
unable to accept the evidence that benefits in behavior accrue to repeated induced
seizures in severely depressed, manic, catatonic, delirious, and psychotic patients.
As I learned how to treat patients safely I realized the remarkable benefits of
inducing seizures, and such treatments became an interest for the remainder of my
professional life.
After introduction to ECT that first morning, we crossed the hall to the
insulin coma treatment unit, a well-lit air-conditioned suite with a large nursing
staff. Filled with cries, coughs, grunts, and groans of patients in various stages of
stupor, coma, drowsiness and confusion, and some suffering a seizure.

They had come to the treatment unit in loose-fitting pajamas at 6 in the
morning and had been injected subcutaneously or intravenously with measured
doses of insulin. For the next three to five hours they were repeatedly tested for
vigilance and response to commands as they lost consciousness; their tendon and
pupillary reflexes disappeared, breathing became stertorous, and intense sweating
soaked the bedsheets. After a measured hour, the stupors were ended by 10%
glucose solution administered either by nasogastric tube or by intravenous injection.
The change from unconsciousness to consciousness and to talking with the aides
occurred rapidly, within 10 to 30 minutes. On awakening, each patient was taken to
shower, dress, and within an hour was eating breakfast. Most were famished and
ate everything put before them.
Insulin coma treatments, like the ECT sessions at the time, were unsafe.
Fractures of teeth and limbs occurred and confusion persisted for hours after
treatment. During 1/5 of the ICT treatments, at least one unscheduled seizure
emergency occurred each morning. For the patients who had shown little change in
behavior during the course of insulin comas, seizures were induced electrically in
the midst of the coma. This combination of ECT and coma was common for the
severely psychotic patients, an implicit recognition that the seizure was the
therapeutic feature of the coma treatments.

Occasionally, consciousness did not return despite repeated doses of glucose.
Stupor persisted with sweating, fever, elevated blood pressure, and rapid heart
rates. We had no understanding of why a state of persistent coma occasionally
occurred nor how to relieve it. Many experimental means were tried. Relief from
the stupor occurred slowly over days of intensive nursing care. Two patients died in
stuporous coma during the six years that I managed the service.

By early afternoon, the ICT and ECT treated patients were in individual and
group treatment sessions, participating in occupational activities, playing musical
instruments and games, and meeting with relatives. I frequently tested their skills
in chess and checkers, finding the skills of many better than my own despite their
morning seizure or coma. It was remarkable to see a patient in coma, unresponsive
7

�to verbal, sensory, or painful stimulation and an hour later chatting with staff,
drawing, and playing games. Older patients, though, were more often confused and
fatigued, spending a good part of their post-treatment day in their rooms or their
beds.

For the next three months, I supervised both the ECT and ICT services, with
ECT three times weekly and ICT every morning. My afternoons were spent in
individual therapy sessions with patients, meeting families, attending staff
conferences about individual patients and classes with attending physicians.

By mid-year I had learned that ECT effectively reduced suicide thoughts,
relieved negativism, aggression, depressed and manic moods. Of the hospital
populations, the patients treated with electroshock improved the most. They
became more cooperative and responsive, no longer expressing morbid thoughts
and threats of self-harm, sleeping and eating better, and interacting more normally
with their families, other patients, and staff. The outcomes with insulin coma were
less well defined, and the risks much greater, but yet, greater percentages of
patients so treated were rated improved than after psychotherapy.

ECT treated patients typically improved rapidly; many returned home, with
few transferred to the local Creedmoor State Hospital for lack of improvement. By
contrast, few insulin coma treated patients returned home after a year's residence;
most continued in chronic care. A 5-year follow-up study of 314 patients admitted
to the hospital in 1950 reported a mean hospital duration for ECT-treated patients
of 5.0 months, for psychotherapy-treated patients 6 months, and for ICT-treat
patients 6.5 months. With ECT, 76% were rated as recovered or much improved
compared to 53% for psychotherapy and 33% with ICT. Admittedly, the selection of
treatments and the diagnostic labels were not random but dictated by the opinions
and beliefs of the Attending physicians and by the preference for trials of
psychotherapy before assignment for ECT or ICT. 2
The teachers used social and symptom guidelines for diagnosis and
treatment. The younger, more literate, and better educated patients with phobias,
obsessions, compulsive rituals, and anxiety states were assigned a diagnosis of
psychoneurosis and valued as participants in psychotherapy; the more aggressive,
over-active, and psychotic patients were labeled schizophrenic, with ICT or ECT the
recommended treatments; while the elderly, poorly educated patients, often
immigrants, were seen as depressed and referred for ECT.

8

�Ending Insulin Coma Therapy
The introduction of Largactil (chlorpromazine) to Hillside Hospital in the fall
of 1954 set in motion the demise of insulin coma therapy. Developed in France as a
sedative, to reduce excitement and psychosis of the psychiatric ill, it first underwent
safety and efficacy trials at various New York State hospitals. At an open meeting
organized at Creedmoor State Hospital in Queens in 1954, I heard one researcher
after another -- Herman Denber, Nathan S. Kline, Sidney Malitz, Sidney Merlis,
Anthony Sainz, and John Whittier -- report reduced excitement, aggression, and
mania, lesser disorders in thought, fewer injuries to patients and staff members,
fewer fires set, fewer mattresses trashed, and fewer windows broken with
chlorpromazine use. At the end of the sessions representatives of the Smith, Kline
and French pharmaceutical company offered 25mg samples for clinical trials and I
enrolled.
As the dosing and risks of chlorpromazine were poorly known, the Hillside
hospital administration decided that referrals for this experimental treatment were
best prescribed and supervised by the ECT/ICT physicians. For the first trials we
selected the most disturbed and least cooperative patients in one study unit.
Patients became more responsive, less aggressive, less manic, and more cooperative.
Soon, nurses from other units asked to enroll their patients. Initial reluctant staff
attitudes changed quickly and our enthusiasm for chlorpromazine added to the
voices encouraging its use from France and Canada.
But soon one patient and then another developed jaundice. Other study
centers reported similar toxicities. Our patients were examined for systemic liver
disease, but no explanation for the jaundice was found. Our initial enthusiasm for
chlorpromazine trials was inhibited, but the strength of the benefits encouraged
continued trials. Within a year, such toxic reports became less frequent (there had
been a contaminant in the initial batch, it turned out) and soon motor rigidity,
tremors, and then tardive dyskinesia (delayed abnormal rhythmic movements of
mouth, tongue and facial muscles) dominated discussions of its risks.

These motor signs were the fore-runners of the Parkinsonism and tardive
dyskinesia that are hallmarks of chronic chlorpromazine use. Similar motor effects
were soon reported for successor neuroleptic drugs and motor inhibition became a
marker of these agents. Decades later, the "atypical neuroleptics" were developed
and promoted for their lesser motor effects with disregard for their lesser clinical
efficacy. The NIMH-sponsored large clinical trial known as CATIE (Clinical
Antipsychotic Trials of Intervention Effectiveness) undertaken in the 1990s
randomly assigned ambulatory out-patients either to the atypical neuroleptics
olanzapine, quetiapine, risperidone, ziprasidone or to the typical neuroleptic
perphenazine. The atypicals did not match the beneficial effects or costeffectiveness of perphenazine.
9

�The EEG profile of chlorpromazine showed dose-related changes of reduced
beta fast frequencies, increased theta slow frequencies, and occasional bursts of
slow waves and spike activity. These rhythms heralded the seizures that became an
acknowledged risk of the drug’s use.

We had begun with 50mg doses but rapidly increased single dosing to 200mg
and daily dosing to 1800mg. We learned that 1200 mg daily was effective and well
tolerated in 80% of our subjects. These experiences led us to undertake two
random controlled trials, one compared chlorpromazine to insulin coma and
another comparing the effects of chlorpromazine, imipramine, and placebo in
patients with a broad range of behaviors.

The Random Controlled Trial: A compelling motive for the comparison of
chlorpromazine and insulin coma was the risks posed by the high doses of insulin.
Seizures occurred in more than 10% of the sessions, and delayed spontaneous
(“tardive”) seizures often occurred late in the day or night, requiring additional
intravenous or gavage dosing with glucose. For patients whose psychosis was
responding slowly, electrically induced seizures were added at the height of the
comas to augment the changes in behavior.

A prolonged coma was a much feared risk, the patient not becoming alert and
oriented for many hours despite extensive dosing with intravenous and gavaged
glucose. Many explanations were considered and many interventions tested, but we
did not find an effective treatment or method of prevention. We depended on
intensive nursing care, repeated dosing with glucose, and monitoring until recovery.
Two deaths in prolonged coma occurred in the five years that I supervised ICT, a 2%
mortality rate.

Sixty patients referred for ICT were randomized to receive either 50 insulin
coma treatments or oral chlorpromazine (0.3 to 2.0 Gm/day; median 0.8 Gm/day)
with both treatments given for a minimum of three months. Chlorpromazine
treatment was as effective as insulin coma but with greater ease of use, greater
patient comfort, lesser risks, and lesser expense— clearly favoring chlorpromazine
as a replacement for ICT. More than half of each sample improved sufficiently to
return to their homes. 3

These findings led to the closing of the Hillside Hospital's insulin coma unit in
1958, followed swiftly by the closing of other units throughout the nation. Within a
decade the treatment had disappeared from American hospitals. A few units
continued to treat patients with ICT as exemplified by the report that the 1994
Nobelist John Nash had received ICT in 1961 at Trenton State Hospital. 4

The treatment also persisted for decades in Russia and China, and was
brought to Israel by Russian emigres. My review in 2003 of what was known about
insulin coma treatment, the lesser efficacy of ICT in treating psychosis and its
10

�increased efficacy with augmented electrical seizures led me to conclude that the
spontaneous random seizures were the basis for ICT’s reported efficacy in relieving
psychosis. ICT, to the extent it had therapeutic value, was best considered a less
efficient and more riskful form of induced seizure therapy. 5

Optimizing ECT Procedures
The EEG as Index of Seizure Efficacy
Since seizures were the core process in both ECT and ICT how can one
record and understand the brain events that were central to the treatments? The
answer seemed to lie in electroencephalography, but such was not available at the
hospital.
In 1771 the Bolognese physician Luigi Galvani had demonstrated that an
electric stimulus caused a living frog muscle to twitch and contract. He observed
electric currents from living muscles by the movements of a magnetized
“galvanometer” needle. His experiments connected the newly discovered
phenomena of electricity to living tissues. Similar reports by Giovanni Aldini and
Benjamin Franklin strengthened the conviction of electricity in living tissues. 6

A century later, in 1875, the physiologist Richard Caton recorded electric
oscillations from the exposed brain of a living animal, securing the connection
between brain functions and electricity. But these currents were too small to be
recorded through the skull and could only be demonstrated in an exposed brain.
Then, in 1929 Hans Berger, a Jewish hospital psychiatrist in Jena Germany adapted
the device that was developed to record the electrical activity of the heart to record
electric oscillations from electrodes on the intact human scalp. Rhythms varied with
changes in vigilance, sleep, body physiology, and the effects of systemic drugs. In his
third report Berger described changes in the EEG under the influence of cocaine,
scopolamine, morphine, chloroform, and sleep. The electrical changes associated
with insulin-induced hypoglycemia (as in insulin coma therapy) and the chemical
and electrical induction of seizures were next charted, as these treatments were
increasingly applied in the severe mentally ill.
Hillside Hospital lacked an EEG laboratory. I sought training in recording and
interpreting the EEG at the Mount Sinai Hospital in New York City supported by a
fellowship of the National Foundation for Infantile Paralysis. 7 By the end of 1953
an EEG technician had been trained, a laboratory established, and developed a
protocol for the study of the changes in EEG associated with ECT. An application to
the National Institute of Mental Health funded a five-year study under Grant
MH-927 "Altered Brain Function Following Electroshock" in the summer of 1954. The
support established a team of researchers to study the treatments. For the next
11

�decade, the physicians, psychologists, and technical staff were centered in a
Department of Experimental Psychiatry. 8

The EEG brain rhythms in alert normal adults are filled with 8-to-12 Hz
(alpha) frequencies with amplitudes of 40 to 80 microvolts (µv). Patterns vary
with age, during day and night, and are altered by drugs and disease. After head
injury and intracranial bleedings, the rhythms slow with increasing amounts of
theta (4.5 -7 Hz) and delta (2-4 Hz) frequencies and the amplitudes increase from 50
µv often to 150 and 200 µv. As brain pathology improves, normal EEG rhythms
return.
During my EEG education I was shown records with high voltage slow waves
with “spikes” appearing in one-to-three second bursts with longer runs of lower
voltage slow waves as evidence of an epileptic seizure. We found similar records on
inter-treatment days during the course of ECT. The pre-treatment records of our
psychiatric ill did not differ from those of healthy individuals, with older patients
showing slower rhythms than did the younger. In the minutes and first hours
immediately after a seizure, EEG voltages increase, frequencies slow, and burst
patterns appear. In ensuing days, the changes after each treatment persist for
longer periods. After 4 to 10 treatments, slow waves persist throughout the day,
then for many days and in some patients for weeks thereafter.
It was technically unfeasible to record the actual seizure as our instruments
became "blocked" by the electrical stimulus. 9 But we could examine the
“interseizure” record, the changes in the resting EEG record on days between
treatments.

Brain electrical rhythms slowed and amplitudes increased during the ECT
course. After treatment ends, more rhythmic, regularized alpha frequencies return.
The changes induced induced by electricity and by the chemicals Metrazol or
flurothyl are not distinguishable, arguing that the EEG records during treatment are
related to the seizure and not to the seizure-inducing agent.
We concluded that progressive slowing of inter-seizure frequencies was
necessary for beneficial behavior effects. The patients whose inter-treatment
rhythms changed very little did not recover from their illness. 10

Although it was customary to describe the rhythms in non-quantitative
descriptive terms, I sought more reliable indices, measuring the frequencies and
amplitudes by height and width of each wave, using calipers and ruler, one wave
after another, in 10-second epochs , up to 60 seconds for each sample, with an
average of 600 waves measured at baseline and 350 to 450 waves at the end of a
course of treatment. By comparing numbers of treatments and degree of slowing
for each patient, slowing occurred earlier and to a greater degree in patients
exhibiting symptom relief than in the patients whose behavior changed slowly or
failed to improve. EEG frequency slowing and amplitude increases became markers
12

�of the brain changes that underlie behavioral improvement. The rate and amount of
change varied with electrical dosing and the number and frequency of treatments.
We concluded that EEG change was necessary for the clinical changes to take place
and marked the physiological changes that are the basis for the treatment response.
This lesson became the critical observation of the ECT process and became the core
of my studies to optimize and understand the convulsive therapy process.
That the changes in EEG rhythms with ECT were similar to those in epilepsy
and after head trauma was often used to justify an anti-ECT prejudice voiced by the
public, by patients, and by psychiatrists and psychologists encouraging beliefs that
seizures “damaged the brain.” We thought otherwise, concluding that the EEG
changes induced by the seizures were necessary markers for the clinical benefits -without persistent EEG slowing, recovery of illness did not occur.

The patients referred to hospital for ECT are very ill, unable to function at
home or at work, sad and unhappy, expressing thoughts of suicide, strange ideation,
and occasionally with aggressive manic behaviors. 11 Almost all have been treated
by a cascade of medicines, psychotherapies, vacations, diets, and much else before
the patient was exposed to electroshock, widely conceived as hazardous and life
threatening. The patients met today’s diagnostic criteria for major depression,
bipolar disorder, and schizophrenia. The quickest resolutions of illness occurred in
the severely depressed, suicidal, catatonic, manic, melancholic, and delirious
patients. The least benefits, were in the withdrawn, apathetic, poorly motivated,
thought-disordered patients who today meet the criteria in the standard diagnostic
system for schizophrenia or bipolar disorder. 12

Modifying Seizures: Muscle Relaxants and Sedatives

Electroshock treatments were “unmodified” -- without sedation or muscle
paralysis, allowing the full grand mal seizure to develop in each treatment. For
anxious patients, amobarbital was injected to sedate and relax. We also interrupted
the longer seizures by injections of amobarbital.
The body movements, EEG seizure patterns, and changes in physiology are
similar for each treatment. Indeed, the “seizure” has the same form and is readily
recognizable in all mammals. It is an inherent pattern that occurs both
spontaneously and when stimulated by electricity, by chemicals, and by disease.
What is the function of such a universal response? In natural environments a
seizure puts the subject at undue risk of predators and one would expect that after
generations the behavior would be extinguished by natural selection. But the
biology persists. Does the seizure serve a useful purpose? What is it? 13

Fractures of teeth, vertebrae, and long bones were unfortunately common.
Many forms of physical restraint and chemical inhibition were tested. Curare,
extracted from South American plants, prevented both the tonic (increased
muscular tone, stiffening of the body muscles) and the clonic movements (rhythmic
13

�movements of the stiffened musces) of the seizure. 14 But curare was unstable. In
some patients curare effectively blocked the motor movements and in others, the
effects were small and a full seizure occurred. A dose on one occasion might
effectively modify the seizure, but in the next, the same dose would fail to relax the
patient. On occasion, paralysis persisted after the seizure and it was necessary to
ventilate oxygen through a mask until natural breathing returned. We discontinued
curare use and depended on sheet restraints alone to prevent fractures.
Spine x-rays were taken in 50 patients before unmodified seizures and
repeated in the week after the last treatment. In seventeen patients a compression
fracture of lumbar vertebrae 4 or 5 or both was recorded. Surprisingly, these
fractures elicited little complaint from the affected patients. Such compression
fractures were accepted as a cost of the treatments.

In the spring of 1953 a new synthetic muscle relaxant suxamethonium
chloride (succinylcholine) was introduced. Limb paralysis occurred within 30 to 60
seconds of intravenous injection, dissipating within a few minutes of its application,
making it an ideal agent for ECT. In our first experience we had not pre-sedated the
patient, succinylcholine was injected, and when muscular twitchings (fasciculations)
and a weakened knee jerk were seen, the seizure was induced. Tonic arching and
clonic movements were much weakened. Spontaneous breathing returned quickly
and the patient was moved to the recovery room. We injected our second patient,
induced a seizure, and then we heard cries of “I cannot breathe, I cannot breathe”
coming from the recovery room. Oxygen was administered by mask only to have
the same experience with the next patient.
Thereafter, we induced amnesia in every patient with amobarbital or
thiopental before the succinylcholine injection. As more physicians studied this
method of muscle relaxation, “modified ECT” was broadly accepted -- sedation by
barbiturate, oxygenation by mask, injection of succinylcholine, and seizure induced
when motor fasciculations and diminished ankle or knee jerk were recognized.
Although my initial experience was in a hospital setting, most treatments were
administered in office settings, such as in my office in Great Neck, where I treated
patients in the early evening hours assisted by a nurse.

“Modified ECT” raised questions. What was the role of the preliminary
sedative -- to induce sleep, reduce anxiety, or block memory of the procedure?
After the 1960s and 1970s, as “anesthesia” became the province of organized
anesthesiologists, psychiatrists administering a sedative and the muscle relaxant
were no longer tolerated, effectively ending ECT in independent psychiatrists' office
settings.
New sedation agents were studied. Benzodiazepines raised seizure
thresholds, reducing treatment efficacy and outcomes. Methohexital offered short
duration of action, safety and efficacy. New anesthetic agents – propofol, etomidate,
14

�ketamine, isoflurane –were tested. Propofol raised seizure thresholds, and the
enthusiasm among some practitioners for minimal energies to induce seizures led to
ineffective treatments and poor outcomes. Etomidate became fashionable for a time
but the sedation was slow in onset and injection sites often became inflamed. Intramuscular ketamine usefully sedated excited delirious patients. An intramuscular
injection in a patient restrained in bed would quickly sedate so that the patient
could be moved to the treatment room and succinylcholine safely administered.
By the 1980s “modified ECT” had become the universal standard, but not
universal practice. In some countries, as in India, the expense of the additional
chemicals and the belief in the need for an anesthesiologist led either to the
inhibition of treatments or continued use of “unmodified” treatments. 15

Are Subconvulsive Treatments Effective?

Were the benefits of electroshock and insulin coma inherent in the changes
in physiology associated with seizures and coma or responses in the patient’s panic
and fear? What was the role of electricity and the seizure? To address these
questions, we induced sleep using amobarbital, muscle weakness by
succinylcholine, and controlled the dosage of electricity at levels that did not induce
a grand mal seizure. These methods reliably elicited “subconvulsive” non-seizure
“sham treatments.”
Of 24 patients in whom seizures were induced, 17 responded clinically and
were discharged from the hospital; of 27 patients treated with subconvulsive sham
currents, only 4 responded. Nineteen of the non-responders went on to convulsive
treatments and 16 became responders. The EEG recordings of the subconvulsive
treatments failed to show characteristic slowing. We confirmed that subconvulsive
treatments were clinically ineffective and supported our belief that the therapeutic
benefit was inherent in the seizure and not in the passage of electricity alone. 16
These findings ran parallel to those of a well-designed study conducted by George
Ulett in St. Louis that also confirmed the seizure as essential to the treatment’s
benefit.

The results of our study were published in my 1979 textbook Convulsive
Therapy. That year the British psychologist Timothy Crow challenged the profession
to prove the need for the seizure. His challenge elicited multiple UK government
supported studies presented in an all-UK conference in September 1979 in
Leicester, and in a published appraisal edited by Robert L. Palmer. No study
supported efficacy of non-convulsive treatments, reconfirming the critical role of
the induced seizure. 17

15

�Are Chemical-induced Seizures as Effective as Electrical?

In 1959 flurothyl (Indoklon), a new seizure-inducing chemical agent was
proposed as a replacement for electrical induction. Hexaflurodiethyl ether, a
volatile congener of the inhalant anesthetic diethylether, is both anesthetic and
seizure-inducing. After a few inhalations the subject loses consciousness; additional
breaths elicit a full grand mal seizure, usually within a few minutes.
Four research teams – Joyce and Iver Small at University of Indiana, Albert
Kurland at the Maryland Psychiatric Center, Björn Laurell in Sweden, and I and my
associates at Hillside Hospital compared the effects of flurothyl and electrically
induced seizures. Seizures were readily induced, with similar motor, seizure and
interseizure EEG patterns. Both were clinically effective. Flurothyl seizures were of
longer duration. Laurell reported lesser retrograde amnesia with flurothyl. In our
study, 15 patients received unmodified flurothyl seizures and 12 unmodified ECT.
The clinical benefits, behavior patterns, fracture rates, and degrees of EEG slowing
were the same.

For lack of an identifiable advantage over electricity, the induction of
seizures by flurothyl fell by the wayside. The drug’s high cost and persisting ethereal
aroma in the treatment room were deterrents. The smell was unpleasant, objected
to by both patients and staff members. Further, the ease with which a seizure was
induced frightened the professional staff as the treatment room soon was suffused
with an ethereal aroma. Installing an in-wall exhaust air conditioner reduced the
smell and mitigated the fears, but could not eliminate them. No advantage for
flurothyl seizures was seen and we abandoned the method.18
Decades later, the pre-occupation with memory loss led to widespread
reduction in treatment efficacy because many practitioners shifted to unilateral
electrode placement, ultra-brief currents, and minimal dosing. Increasing reports of
treatment failures sent me to re-assess the experience with flurothyl as a potential
non-electricity seizure induction method. In the first quarter of the 21st Century,
when repeated hospital site procedures for renal dialysis and chemotherapies and
radiation for cancers are widely accepted, anesthesia sessions using flurothyl could
well achieve the therapeutic advantages of induced seizures without the fright
associated with electricity and the words “electric shock.” The review showed that
flurothyl-induced seizures were clinically effective, that the effects on cognition and
memory were less, encouraging a reassessment of flurothyl seizures. 19 Alas, I failed
to entice any clinician to undertake such reassessment.

16

�Is Isoflurane anesthesia therapy a replacement for ECT?
In the 1980s, Gerhard Langer and his colleague Greta Koinig in Vienna
induced repeated sessions of isoflurane anesthesia in depressed patients believing
such anesthesia sessions could replace ECT-induced seizures. Isoflurane is an
inhalant anesthetic that quickly induces stupor, inhibition of EEG rhythms, and a
flat-line EEG. Their report that six sessions on alternate days relieved severe
depressive illness and was an effective replacement for ECT prompted my visit to
the clinic in Vienna in 1983. I observed the feasibility of inducing isoelectric (“flatline”) EEG periods with the anesthetic and decided to replicate this experience.

With the collaboration of Stony Brook anesthesiologists, isoflurane
anesthesia sessions were undertaken in six patients who had been readmitted with
recurrences of severe depression after earlier courses of ECT. In 21 of 26 anesthesia
sessions, an isoelectric “flat-line” EEG lasting between 5 and 12 minutes was
recorded. We did not observe reductions in depression rating scale scores, nor
persistent changes on memory tests, nor characteristic changes in the inter-session
EEG. After these failures, the patients were treated with conventional ECT with
clinical recovery in five of the six. Isoflurane EEG suppression was deemed not an
effective alternative for the seizures of ECT. 20 Periodically, this technology prompts
interest and is re-evaluated. The studies have been poorly controlled and the
reports convey authors’ enthusiasm without evidence of persisting behavioral or
physiologic effects.
Role of Acetylcholine: Anticholinergic Drugs and EEG and Behavior
In the 1950s little was known of the physiology of the slow rhythms in EEG
after induced seizures other than that their presence was necessary for clinical
benefit. As the significance of EEG slow-wave activity was recognized, the chemistry
of seizures was studied. George Ulett and LaVerne Johnson in St. Louis reported that
anticholinergic atropine and atropine-like drugs blocked both post-seizure EEG
slowing and the anticipated behavioral recovery after ECT. Herman Denber
reported that injections of the chemical diethazine, another anticholinergic agent,
reduced EEG slow wave activity after ECT. We replicated the finding for diethazine
and also found that the antiparkinson agent procyclidine and various experimental
anticholinergic drugs known as the JB-series also reduced post-ECT slow wave
activity.
When anti-cholinergic drugs were introduced late in the course of ECT, when
mood and thought disorders were relieved, the EEG reversal was accompanied by
behavioral worsening – patients no longer expressed denial language and
increasingly complained of the recurrence of their symptoms. A day later, when
EEG slow-wave activity had again returned, symptom relief was again expressed.
We concluded that EEG slowing is a consequence of increased brain cholinergic
17

�activity. Puzzling over the brain effects of repeated seizures led me to consider a
cholinergic hypothesis for the recovery with ECT.

Free acetylcholine and acetylcholinesterases were elevated in the
cerebrospinal fluid (CSF) of epileptic patients. CSF acetylcholine levels increased
during ECT. In cats subjected to graduated head trauma, the amount of free
acetylcholine and cholinesterases in the CSF increased with the severity of the
trauma.

I imagined that induced seizures, like cerebral trauma and epileptic seizures,
altered cerebral permeability, increased free acetylcholine and cholinesterase levels
in the brain, slowed EEG frequencies and increased amplitudes and rhythmic bursts.
I pictured these biochemical changes as the basis for the behavioral effects we were
seeing with ECT. 21
Study interest in acetylcholine waned as interest in brain neurotransmitters
shifted to epinephrine, and then to dopamine and serotonin, as pharmacologists,
excited by their ability to measure these neurotransmitters in animal brains tracked
the effects of each of the new psychoactive moieties, that were then enthusiastically
welcomed by clinicians and the public. At this juncture, half a century later, I find
little interest in acetylcholine in clinical psychiatry or epilepsy.

Neuropsychological Tests and EEG Slowing

Immediately after a seizure, the patient awakens in confusion, poorly
oriented as to location, date, or month, and often unable to recall the names of the
attendant personnel. Commonly, the recovery is complete within an hour. The
duration and severity of a patient’s errors vary with the number and frequency of
seizures, the sedative and electricity doses, but most important is patient age -elderly patients are confused longer. With recovery to mental health, orientation
normalizes and patients return to home, school and work. We tested the responses
on the Face-Hand Test and found normal responses in the weeks after the last
treatment.

With increasing numbers of treatments, denial test scores and the changes
with amobarbital paralleled scores on EEG measures, as earlier research had
suggested. Persistence in denial was more often scored in older patients, in the less
well-educated, and in immigrants with English as their second language. Scores on
the Rorschach test were loosely correlated with the treatment outcomes but the
specificity and predictability of the Rorschach criteria was low. Social attitude was
tested by the 10-item California F-Scale, a measure of prejudice and
authoritarianism that became of considerable interest in the wake of the NaziFascist eras. The patients with high authoritarianism scores were more likely to
show benefits from ECT. 22
18

�Book Two: After an ECT Research Hiatus, Renewed studies
During a four-year sojourn at the Missouri Institute of Psychiatry an ECT
facility was not open to me -- psychopharmacology and quantitative EEG were the
focus of our studies. Soon after I returned to New York in 1966 to direct studies of
opioid abuse at Metropolitan Hospital, I received a letter from Richard Abrams, an
Army medical officer scheduled to join the college medical residency program the
following July, asking if I would meet him at a December conference of the ARNMD
in New York City. He had compared the clinical benefits and changes on memory of
ECT using non-dominant unilateral or bilateral electrode placements at a military
hospital. He had administered seizures three times or five times weekly for 20
treatments in 10 subjects and reported no difference in efficacy nor in cognitive
effects between treatments of the two electrode placements. He wanted to continue
such studies and asked for my support and collaboration. I was still interested in
understanding the mechanism of electroshock and agreed to support his studies.

New York Medical College’s Department of Psychiatry lacked an ECT
treatment unit at any of its clinical sites. The department chairman, Alfred
Freedman, referred me to Lothar Kalinowsky, a member of the teaching faculty, who
was treating his ECT patients at Gracie Square Hospital (GSH), a private hospital
facility on East 76th Street in Manhattan. Kalinowsky was an early student of ECT,
having witnessed its first applications in Rome in 1938 when he was studying with
Ugo Cerletti and Luigi Bini, the developers of electroconvulsive therapy. He had
published a leading textbook on the somatic therapies in 1946. He agreed to be a
consultant to our work, arranged for GSH Medical Board approval of the study and
for the collaboration by the clinicians who treated their patients in the hospital.
Abrams and I asked: What is the optimal placement of electrodes in inducing
seizures? We randomized patients to seizures induced either with non-dominant
unilateral or with bitemporal electrode placements, measuring clinical, cognitive,
and EEG changes at weekly intervals. And, could the treatment course be shortened
by applying multiple treatments in one sitting? Recognizing that most patients
recovered from a melancholic depression after 6 to 10 seizures, Paul Blachly, an
Oregon physician, had reported that multiple seizures in one session were as
effective as the same number of seizures spaced over many days.

The Differences Electrode Placement Makes, Again 23

We tested 76 patients with a mean age of 63.4 years, 43 treated with bilateral
and 33 with unilateral placements. By diagnosis, 60 patients were endogenous
depressed and 16 reactive (neurotic) depressed. At the time, unilateral placement
was considered less efficient in generating seizures and indeed some patients in the
sample required additional seizures during their treatment course.
19

�We found bilateral ECT to be clinically more effective than unilateral ECT,
with better and earlier outcomes regardless of age, number of treatments, or
coincident medications. The memory tests during the treatment course changed
less in the unilateral treated patients than the bilateral, varying with the task
selected. On auditory tasks, the patients receiving bilateral treatments showed
greater decrements than those receiving unilateral treatments; on a visual task,
however, performance was unimpaired by either treatment. 24

EEG frequency slowing was greater after bilateral placement than after
unilateral. An asymmetry was also observed in EEG slowing, accentuated on the
right side with right unilateral electrode placement, and on the left side in
bitemporal-treated patients. Although we did not understand the significance of
either the degree of slowing nor the sidedness, these findings confirmed that the
degree of EEG slowing was related to clinical outcome. The lesser EEG changes and
asymmetry of unilateral ECT were signs of lesser physiologic changes--and lesser
benefit compared to bilateral ECT. 25

Can Multiple ECT Treatments Per Session (MMECT) Shorten the
Treatment Course?

In 38 patients we applied either 4 or 6 seizures within a single anesthesia
session. Different placements – bitemporal, non-dominant unilateral, or anterior
frontal -- were tested. Only one patient achieved clinical remission after one session
through bilateral electrodes, though we thought the benefits were accelerated in
several others. The degree of EEG slowing was not enhanced, however, and the
asymmetries were the same as we found in our single treatments. Post-ictal sleep
among the MMECT patients was prolonged with greater disorientation and clouding
of consciousness especially among the older patients. Neither we nor the
experienced clinicians whose patients we treated were convinced that multiple
treatments in a single session were an effective modification.
We confirmed Richard Abrams’ experience that unilateral electrode
placement could elicit effective relief with lesser effects on cognition, but at a price
of lesser efficacy. Seizures induced through unilateral electrode placement, even
with the maximal energies of alternating higher energy currents, were less effective
than those developed through bilateral placements. The physicians at GSH,
experienced practitioners with extensive clinical practices, were not surprised by
our results. Many, including Renato Almansi, David Impastato, Lothar Kalinowsky,
and William Karliner, were emigres from Europe who previously had each tested
different electrode placements, electric currents, and dosing schedules and had
concluded, based on their clinical experience, that unilateral placements were
inefficient, requiring more seizures for relief and entailing higher early relapse
rates.
20

�ECT in Systemic Medical Illnesses.
In 1972 I accepted an appointment at the Stony Brook Medical School to
teach psychopharmacology and develop an ECT Service at University Hospital. As
the responsible clinician in the choice of treatments in an academic general hospital
I explored ECT in patients with systemic medical disorders and psychiatric
symptoms. We successfully treated mentally retarded adolescents, pregnant
women, patients with brain tumors, brain aneurysms, cardiac pacemakers,
malignant catatonia, anemia, Parkinsonism, delirium, and pseudodementia.

ECT in Adolescents. ECT for children and adolescents was broadly
interdicted by child psychiatrists as a matter of faith. They believed that ECT
permanently damaged the developing brain. They did not ask for ECT consultations
nor would they consider prescribing psychoactive drugs until the 1990s. Gabrielle
Carlson, the Stony Brook Director of Child Psychiatry, would not allow her residents,
many of whom had been trained in ECT while on the adult service, to consider ECT
in any of their patients. The adult service, however, admitted adolescent patients
over age 13. We successfully relieved adolescent patients in delirious mania,
suicidal depression, malignant catatonia, and psychosis induced by LSD and
cannabis. Young patients tolerated the treatments easily and the relief of psychosis
was rapid with almost all returning home and to school.

Mentally retarded patients are not protected from disorders in mood or
psychosis by their condition, but when they suffer such illnesses, ECT is interdicted
by beliefs that inducing seizures would further damage their brains. As our
experience with adolescents became known, MR patients were referred for
treatment and we described positive outcomes with remarkable improvements in
their quality of life. A 14-yr-old mentally retarded boy with persistent self-injurious
behavior (SIB), unresponsive to social and medication treatments was referred for
treatment. He was admitted wearing helmet, glove, and camisole restraints to keep
him from injuring his head, monitored by full-time aides for continuing protection.
With parental consent a trial of ECT was begun. Within two weeks the restraints
were no longer needed and he was allowed the freedom of the hospital unit. Over
the next half year, continuation ECT sustained him in his community residence
without the recurrence of his self-injurious repetitive behaviors. Decades later, Dirk
Dhossche, a graduate of the Stony Brook University residency training programs
and a participant in the catatonia studies, and Lee Wachtel, Director of the
Neurobehavioral Unit of the Kennedy Krieger Institute of Johns Hopkins University,
would identify SIB as a form of catatonia in autism, relieved by ECT. 26
ECT in Pregnancy. Many clinicians feared ECT during pregnancy,
anticipating damage to the fetus by the electric currents and by the mother’s
seizure, inducing miscarriage. But as fetal malformations were increasingly
21

�associated with psychoactive drug use during the first two trimesters of pregnancy,
ECT was increasingly ventured. We simultaneously monitored the maternal and the
fetal heart rates during each treatment. As the seizure in the mother unfolded, we
could hear the rapid increase in her heart rate from 70 bpm to the 110s while that of
the fetus ran at its own steady rapid rate of 110 to 130 bpm. The fetal heart rate did
not increase during the seizure, showing only a small transient increase during the
post-seizure recovery. After more than a dozen such monitored seizures, we no
longer requested fetal monitoring and routinely accepted pregnant psychotic
patients for ECT. We learned how to treat patients in each pregnancy trimester and
optimally position a large pregnancy for proper oxygenation and anesthesia. The
benefits of ECT were not limited by pregnancy and is now an accepted treatment.
Pseudodementia. Confused elderly patients with poor memory, poor
orientation, and poor self-care are considered demented and commonly labeled to
be suffering Alzheimer’s disease. In some patients, however, the behavior is not the
result of a structural brain defect but the consequence of a melancholic depressive
illness labelled "pseudodementia." Both the mood disorder and the dementia signs
disappear with effective antidepressant treatments. All patients admitted to my
psychiatric ward suffering “dementia” were carefully evaluated and many treated
for melancholia.

This lesson was brought home to me by a 58-yr-old depressed, often mute,
staring, and posturing woman who had been diagnosed as suffering from
Alzheimer’s disease at two prior hospital centers. For eight years she had been
continuously cared for in her home by her husband and daughters. When Helen was
admitted to University Hospital with acute pneumonia, she was confused,
disoriented, and depressed. A trial of antidepressant medications offered
temporary relief but a full course of ECT resolved her dementia. She returned home
to care for herself and her family. She relapsed, however, and monthly continuation
ECT sustained her for years. Each relapse was marked by mutism, staring and
repetitive picking at pictures and wall signs. When these symptoms were
recognized as signs of catatonia, treatment with lorazepam extended the periods of
her relief and only occasionally was ECT required. She lived for another decade,
caring for her home and family, and taking part in community affairs. 27

As we could not distinguish pseudodementia from a structural dementia by
our examinations, we offered medications, especially the older tricyclic
antidepressants, finding good relief in about a quarter of the trials. An 85-year-old
man with a 2-year progression of dementia requiring continuous nursing care was
admitted for evaluation. Among the test findings he exhibited a positive
dexamethasone suppression test consistent with melancholic depression. ECT was
offered and accepted. Within three weeks he became oriented and able to care for
himself. Continuation treatment with imipramine sustained his benefit and on one
clinic visit he appeared well-dressed, accompanied by a well-dressed mature
woman, declaring that they were to be married that week.
22

�Sadly, in the ensuing years since I left active service the prejudice against ECT
is so strong that my recommendation among consultations for senile dementia were
frequently rejected. The risks of ECT and of tricyclic antidepressants are small
compared to the potential gain to a more normal mature independent life.
Delirium. Many psychiatric consultations in a general hospital are to
evaluate delirium, the common confusional and disoriented syndrome associated
with systemic diseases, trauma, anesthesia, and surgery. After successfully relieving
patients in delirious mania with ECT, we successfully treated deliria in post-surgical
patients, those with abnormal systemic hormonal and fluid balances, and in alcohol
withdrawal. We often found signs of catatonia in delirious patients, justifying the
recommendations for ECT or high doses of benzodiazepines.
Systemic medical risks. Many authors ascribe undue risks for ECT in
patients with systemic illnesses. Brain lesions, tumors, and vascular abnormalities
are considered “absolute contraindications” for ECT on the fear that the seizure
would increase cerebrospinal fluid (CSF) pressures leading to cerebellar herniation
and death. But the CSF pressures do not rise during our modified treatments. We
reported safe treatment in a patient with a growing meningioma and in another
patient with a large arteriovenous malformation. 28 Treatment of mentally ill
patients in atrial fibrillation found conversion to normal sinus rhythm to occur and
led us to recommend ECT with anticoagulation treatment as safe. 29

Optimizing Treatments.

Anesthetics. After the hiatus from the ECT studies at Hillside Hospital in the
1950s, we again evaluated ways to optimize our treatments. The sedation and
amnesia associated with the anesthetics etomidate, propofol, and ketamine, which
were similar to that of methohexital, sometimes proved valuable. We again found a
special use for ketamine in delirious patients – an intramuscular injection sedated a
very disturbed patient within a few minutes, allowing us to move the patient from
the ward room to the treatment room, and successful treatments followed without
need for additional anesthesia. The induced seizures were more robust and their
durations longer with ketamine.
Neither etomidate nor propofol offered better amnesia than methohexital.
Propofol raised seizure thresholds and shortened the duration of seizures. In
elderly patients its use elicited seizures of poor quality. The rise in threshold
associated with propofol is useful, however, in treating adolescents since their
seizures are often prolonged even at minimal electrical dosing.

Seizure durations. We studied the varying durations of monitored seizures
by EEG, heart rate, and motor movements. In such recordings EEG durations were
generally greater than 40 seconds, and arbitrarily considered “prolonged” when
23

�greater than 180 seconds. We often used intravenous diazepam to end seizures that
ran over 150 seconds. Measured durations of EEG were longer than that of the
motor seizure and both were commonly longer than the duration of the heart rate
increase. We augmented seizure duration by injections of theophylline and caffeine.
Although both agents lengthened seizure durations, such use had no observable
benefit in treatment outcome and we discarded their use.
How best to select energy to induce an optimal seizure? Concern for the
cognitive side effects led to popular use of ever lower energies, just sufficient to
elicit a motor seizure, often measured as 10 to 30 seconds. Were these seizures
“adequate” for clinical benefit? We evaluated our recordings and identified a
pattern of a slow build-up of amplitudes, onset of slow wave bursts mixed with
spike activity, sudden ending in an electrically silent period. Seizures less than 40
seconds did not show these characteristics. For a number of years, clinicians were
confused about seizure duration and efficacy. Some considered a series of short
seizures, with added durations greater than 25 seconds “adequate” but such short
seizures were clearly ineffective. Adequate seizures are best defined when greater
than 40 seconds in duration with the full elicited EEG pattern.

ECT in schizophrenia.

The role of ECT in treating schizophrenia is confusing. Early I used the
guidelines for diagnosis that labeled patients who were persistently psychotic, with
language and speech abnormalities, episodic excitement and aggressive behavior as
meeting the Kraepelinian criteria for schizophrenia that were adopted in the official
American Psychiatric Association DSM classifications. We had no test to identify or
verify such diagnoses so the treated patients were highly varied in their syndromes.
The report of the 1978 APA Task Force on ECT offered little guidance, citing
promising reports from clinicians with wide experience and the failure of organized
clinical trials. I was invited to write several reviews on the role of ECT in
schizophrenia, each time offering ambivalent opinions in the report. 30 No
consensus could be reached because the diagnosis of schizophrenia was itself
ambiguous, not distinguishing among long-term, chronic hospitalized patients and
short-term acutely ill in ambulatory settings.

The types of schizophrenia identified as paranoid, disorganized, undefined,
and residual (each best viewed as variations of “hebephrenia”) were unresponsive
to ECT. The single form of schizophrenia that was responsive was the catatonic. But
as described later, this form was erroneously identified as schizophrenia, and is best
appreciated as a uniquely identifiable, verifiable and treatable disorder.
The presence of mood disorder in conjunction with schizophrenia confuses
the matter. A melancholic psychotic illness is difficult to distinguish from
schizophrenia and the insecurity is commonly arbitrated with the label of “schizoaffective” illness. Except for neurosyphilis, some hormone and vitamin deficiencies,
24

�catatonia and melancholia, all other psychiatric diagnoses are “in the eye of the
beholder” and are not test verifiable. By contrast, the diagnoses of systemic medical
illnesses have come to depend more and more on verification tests. The “medical
model of diagnosis” is rejected in psychiatry – indeed the DSM classifications,
including the DSM-5 of 2013 specify that no tests are known and none are
applicable and that the diagnoses are best made by the association of symptoms
recorded in interviews, illness course, and family associations. In studies of
catatonia and melancholia, my associates and I, however, have argued that the
search for verification tests is essential to the development of a psychiatric
science. 31

Clozapine and ECT. A patient’s slow responses to chlorpromazine or
fluphenazine is often augmented by concurrent ECT. When clozapine was first
tested for the relief of psychosis, it was associated with an acute blood dyscrasia and
withdrawn from the formulary. At the behest of clinicians who believed they saw
unique beneficial properties in its use, however, prescription of clozapine was
reinstated, but limited to patients who had failed at least two prior medication trials
and whose serum clozapine levels could be tested weekly. We did not see a
particular clinical benefit for clozapine alone in our patients. When we augmented
clozapine treatment with ECT, the augmentation was occasionally useful.
Such combined treatments was encouraged , however, by the EEG of
clozapine. With clinical doses the EEG pattern becomes filled with bursts of slow
waves, and the risk of overt seizures at high dosages. Such physiologic effects
justified a clinical trial. We treated psychotic patients with clozapine and then,
when the results were poor, augmented the treatment with ECT. We thought the
synergy of the two treatments might be clinically useful and considered a proper
clinical trial.

The faculty at Hillside Hospital had supported clozapine use in therapyresistant psychotic patients. Many patients, however, were poor clozapine
responders and they constituted a large population in their clinic. After I resumed
an affiliation with Hillside Hospital in 1997 for the CORE studies I raised the
question of augmenting clozapine with ECT. I obtained financial support from
NIMH for a random-assignment study of ECT in clozapine-treatment failures. Half
the patients who had not responded to at least eight weeks of serum-level
monitored clozapine treatment continued with ECT augmentation and half
continued clozapine alone. A 40% reduction in PANSS positive symptom scores
without change in negative symptoms was recorded in about half the patients.
What was missing in this study was treatment by ECT alone after withdrawal of
clozapine. Intensive statistical manipulation of the ratings found minimal statistical
advantages. 32

25

�Brain concentrations of fluphenazine. Was the increase in response of
patients whose neuroleptic treatment was augmented by ECT seizures due to
elevated brain concentrations of the neuroleptic agent? Studies by Tom Bolwig of
Copenhagen had reported an increase in permeability of the blood-brain barrier
after induced seizures in rats and in humans. We measured the brain
concentrations of fluphenazine in rats treated with electroconvulsive shock but
were unable to record a difference. 33

The CORE Study of ECT in Depressed Inpatients.
In 1992 the psychologist Harold Sackeim of Columbia University applied for
NIMH support for a multi-site study of continuation medications – placebo,
nortriptyline, and the combination nortriptyline and lithium -- after ECT (using
unilateral electrode placements) among unipolar major depressed patients. The
NIMH consultants reviewing the application asked why he did not consider
continuation ECT instead of placebo, since high relapse rates with no continuation
medication were well documented. He demurred insisting on the placebo treatment
arm. The reviewers, however, were unwilling to support such a study of
continuation medications alone. The chairman Jonathan O. Cole argued for support,
however, agreed to by the members provided a parallel study could be developed
comparing continuation ECT with continuation medication of combined lithium and
nortriptyline.
With Cole’s encouragement I enticed Charles Kellner (Medical University,
Charleston SC), Teresa Rummans (Mayo Clinic, Rochester MN) and John Rush
(University of Texas, Dallas TX) to collaborate in a multisite collaborative study with
the criteria for selection of patients, outcome evaluations, and combined
medications identical to the Columbia University Consortium study. The single
distinction was the CORE use of bilateral electrode placements at a minimum of 1.5
times the measured seizure threshold while the Columbia group used unilateral
electrode placements with dosing set at 1.5 to 2.5 times the measured seizure
threshold in their treatments.
Patients meeting the clinical criteria for unipolar depressed patients were to
be identified by an interview with a trained social worker using questions from a
standard behavior rating scale. Initially, patients labeled bipolar depressed were
excluded from the study, although many were treated with the same protocol after
rejection from the study. The outcomes of the two subtypes did not differ, so we
designed a second study treating both unipolar and bipolar depressed patients
randomly assigned to bitemporal, bifrontal, and right unilateral placements. Both
CORE studies were funded in 1997 by NIMH. 34
In Columbia’s CUC study the six-month relapse rates were much as
anticipated: 80% for placebo, 62% for nortriptyline alone, and 36% for the
26

�combined lithium and nortriptyline. In the CORE study, the relapse rate for lithiumnortriptyline was 39%. With Continuation-ECT 32% relapsed, 22% dropped out of
the study, and 46% continued in 6-month remission. We were disappointed with
these ECT results and realized that the C-ECT treatment schedule had been
arbitrarily set, less effective than what clinicians reported as necessary in
ambulatory treatment schedules.
When patients relapsed and we were able to induce seizures on clinical
criteria alone, almost all patients sustained their remission with ECT as needed, like
the treatment of diabetes or heart failure. To sustain an ECT benefit we needed to
be flexible and introduce treatments when symptoms recurred. This lesson had
been learned by practitioners in the early decades of ECT practice; and summarized
in the review by the 1996 ACT ECT Task Force. (We foolishly erred in the CORE
study based on our desire to be comparable to the CUC study.) 35

Much was learned, however. Seizures induced with unilateral electrode
placements (RUL) are inherently inefficient. The lesser immediate (and transient)
memory-loss effects associated with a unilateral electrode are a poor justification
for outcome inefficiencies and the increase in the number of seizures and anesthesia
sessions. The benefits of bifrontal ECT are slightly inferior to bitemporal ECT but
can be justified by their ease of application.
ECT is as effective in patients with bipolar depression as in unipolar. The
common belief that ECT is less effective in bipolar depressed patients is false, a
consequence I believe of the pharmaceutical industry’s marketing drive to establish
a place for inefficient “mood stabilizers” and anticonvulsants separate from the
prescription of lithium and antidepressants in psychiatric disorders, and the
unwillingness of research leaders to recognize ECT as effective and safe.
ECT rapidly reduces suicide preoccupations in melancholic and delusional
depressive illnesses. In the more severely ill, those with high ratings on suicide
assessment (item 3) in the HAMD24 rating scale, the suicidal self assessments were
reduced 60% with six treatments within two weeks, justifying ECT as the primary
treatment in patients who require special protections for suicide risk.

Delusions in depressed patients identify a population of ECT-responsive
patients. In the 1970s, Alexander Glassman and his colleagues at Columbia
University reported that delusional depression did not respond to blood-level,
monitored imipramine treatment. They did respond to ECT, however. While the
overall ECT remission rate for the major depressed in the CORE study was 84%, the
rate among the psychotic depressed patients was much higher, at 95%. The
common policy of first treating psychotic depressed patients with medications,
especially the use of less effective serotonin targeted antidepressants, with or
without atypical antipsychotic drugs, cannot be justified. Like the use of RUL
treatments, the insistence that psychotic depressed patients be subjected to one or
two medication trials before ECT is questionable in its efficacy and its ethics.
27

�The Persisting Stigma: Memory Loss and ECT
The argument that memory loss is a critical risk in all induced seizure
treatments persists, however, encouraged by the constant singing of a “memory
loss” mantra by psychologists and by some in the laity. At this writing, more than
half a century after the initial studies, the use of unilateral electrode placement
persists despite compelling evidence of its lesser efficacy in the studies sponsored in
the UK in the 1960s and the more extensive NIMH-supported studies by the
Columbia University Consortium (CUC) and the 4-hospital Consortium for ECT
(CORE) that clearly showed that seizures induced through unilateral electrodes
were clinically less effective, lowered recovery rates by 40% and increased the
mean number of treatment sessions from 7 to 10.5. 36 Physicians are applying
unilateral electrode placements knowingly offering patients lesser effective
treatments that increase risks of treatment failure and higher relapse rates.

What is the impact of ECT on memory? Patients who come to this treatment
are severely ill, often with long periods of poor self-care, poor sleep, weight loss, and
preoccupation with the self, the body’s discomforts, and little attention to work or
family. They are then advised that they will need anesthesia, and electricity will
course through their heads. They are warned, verified by the consent that they (and
often members of their family) are asked to read and sign that explicitly states that
they may lose memory, become confused and disoriented. They are then given a
chemical intravenously that puts them to sleep, electrodes are pasted on the head,
and a grand mal seizure is induced.
Every seizure disrupts the brain’s physiology and chemistry. Awakening is
slow, with confusion and disorientation persisting for some minutes in all subjects,
much longer in the elderly and brain compromised. Most patients since the 1960s
have first been treated with brain toxins – every “psychoactive” pill, whether
antidepressant, anxiolytic, or neuroleptic or whether the alcohols, marijuanas,
opioids or sedatives that are publicly attractive -- induces persistent changes in the
brain’s electrophysiology that is measurable by the EEG. Responses to questions in
the first hours after a treatment are slow, deliberate, and confused. And, it is
fashionable nowadays, and surely by the psychologists and nurses who test for
memory effects, to fire questions, one after another before treatment and again as
soon as the patient’s eyes are open.
Where are you?
What is my name? What is your name?
Where do you live?
How much is 23 times 11?
What is today’s date?

28

�And on, and on.

When tests are repeated after many hours, the answers are slow but now
correct. But after a series of treatments the errors may persist for days, especially in
the elderly and in the chronically ill who have been the most brain-altered by an
extensive potpourri of medicines.
When specific neuropsychological tests are presented before treatment and
again a week, a month, and 6 months after the last treatment, the recovery of
cognitive functions is progressive so that in time the recovered patient functions as
well, often better than during the illness. In batteries of more than 20 tests,
psychologists have generally found that the normal functions have returned with
only personal memories still offering errors. Of course, psychologists have
prominently carried the “memory loss, memory loss” mantra against ECT by
attention to these singular test data, not relating their test measures to the clinical
changes and benefits in the patients.

I have repeated psychological testing in all my ECT studies, at Hillside
(twice), New York Medical College, and Stony Brook. I am often surprised by the
quick return of functions with recovery after the illness. In the elderly I am not
surprised by the patients who, in the hours after a treatment, speak poorly,
recognize a relative hesitantly, and soil themselves. For the many who recover,
these deficits disappear, and they return to pre-illness activities. Patients and family
members are satisfied; so much so, that they insist on ECT when the illness recurs.

Slow recovery is common in the repair of any illness. Think of the pains and
discomforts in the long rehabilitations after a fracture, after major surgery, after
acute trauma. The recovery after electroshock is the same slow and repair quality of
major surgery. Shouting “memory loss, memory loss” is the same as shouting
“painful walking, painful walking” after hip surgery.

What is to be made of the anti-ECT positions of psychologists, psychiatrists
and psychotherapists? The slander that infected ECT from the immediate post
World War II period persists and frightens practitioners so that they do not realize
that by offering inadequate treatments they are encouraging ongoing negative
attitudes. The enthusiasm of the ECT practitioners for non-seizure treatments and
the scalp tickling of the “brain stimulation” movements (encouraged by payments by
sponsoring industrial companies) thrives on the falsehood that these treatments “do
not affect memory."
My personal experience lead me to conclude that memory effects are
transient and no more limiting than the pains and blood loss after surgery. The most
realistic and best documented reviews of the cognitive data are to be found in
Richard Abrams’ textbook. 37

29

�Book Three: Electroshock in the Public Eye
Creation of Induced Seizures as Therapy
Was the mark of Cain that prejudices the use of inducing seizures to relieve
emotional illnesses deserved? The carnage of the First World War released
inhuman attitudes and tolerance, even enthusiasm, for attacks on human bodies in
the name of treating the severe psychiatric ill. Prolonged sleep for days on end was
accompanied by pneumonia and death; comas and seizures induced by insulin led to
prolonged coma and death; lobotomy, especially the ice-pick variety, was associated
with seizures, hemiplegia, and death. Skills in neurosurgery encouraged open brain
surgery and electrode placement and stimulation by deep brain stimulation, leaving
many with permanent brain lesions. Although electroshock had none of these risks,
it was lumped together since the practitioners of one were called upon for all.
The first inductions of seizures by chemicals did not go well. Ladislas
Meduna, at a state hospital in Budapest, induced seizures by injecting the irritant
camphor-in-oil into patient muscles. Few injections resulted in a seizure, all were
painful and irritated the tissues. He next tested the intravenous chemical
pentylenetetrazol (Metrazol), which, although more efficient, failed often enough
that patients became extremely anxious, frightened, and refused further treatment
after experiencing panic induced by a partial seizure. Despite panic and pain, the
occasional fracture, the immediate confusion, the relief occasioned by many of the
first patients encouraged its continued use. In his review of his experience, Meduna
reported half his patients improved sufficiently to leave the hospital. 38

In May 1938 two Roman physicians, Luigi Bini and Ugo Cerletti, devised a
more assured and less frightening method using electricity that quickly replaced
chemical inductions and has since become the principal method of inducing seizures
worldwide. Although the inductions were still frightening to both patients and
clinicians, they aroused little public concern. They were better accepted within
medical practice, and less feared than insulin-induced comas, prolonged sleep, or
leucotomy.

The names “electroshock” and “shock therapy” added to public concerns but
did not stop the practice. That the treatment relieved the suicidal depressed, the
hopelessly psychotic, and the uncontrollable manic encouraged widespread use in
the world’s sanitaria and physicians’ offices. This success occurred at the time when
the leaders of psychiatry were enthusiastically following the flag of psychoanalysis,
promising cures for the psychiatric ill after months and years of “talk therapy”
catering to the walking wounded. Psychiatric leaders committed themselves to the
psychology of the mind, separate from the functions of the body and the brain.
Every report of relief of an emotional disorder by fits and the repeated highlight of
another Freudian therapy had failed or required a new therapist stimulated
defensive attacks by psychiatry’s leaders that electroshock did not help the patient
30

�“understand or resolve his conflicts.” The benefits of inducing seizures were
considered transient and, furthermore, damaging to the brain and antithetic to
psychoanalysis since seizures extinguished personal memories.
ECT Immediately Rejected By the Profession

Immediately after the end of World War II, American psychiatric leaders
formed a select political society, the Group for the Advancement of Psychiatry, that
issued its first broadside on “Shock Therapy” on September 15, 1947. The handbill
complained that electroshock’s widespread use in office practices offered only
temporary relief. The benefit was considered inferior to the psychoanalytic
understanding of life’s experiences and the resolution of conflicts that were the
basis for a patient’s distress. I had studied psychodynamic theory at New York’s
William Alanson White Institute and had undertaken a personal analysis for five
years. I saw no challenge to a “biological explanation” of a patient’s history and
symptoms and the reality that “somatic” treatments relieved my patients. No matter
how I presented my experiences of rapid relief induced by repeated seizures, I was
met by disbelief. In the 1970s romanticizing Freud became fashionable for
Hollywood and Broadway, accompanied by images of Frankenstein’s monster, the
electrified man, as the frightening alternative.
Public reports of an excessive use of ECT in children in Massachusetts in
1970 sharpened the attacks. State legislators frantically proposed laws to prohibit
ECT. Milton Greenblatt, the director of the state’s mental health program, argued
that legislative restrictions would interfere with accepted medical practice and
negotiated the tabling of the proposed legislative bills until the actual experiences
could be studied. He commissioned a survey of ECT in Massachusetts to be
conducted by Fred H. Frankel, Professor of Psychiatry at Boston’s Beth Israel
Hospital and an expert in hypnosis treatments.

The 1973 review of practices in Massachusetts did find hospitals where ECT
use was excessive, seizure inductions haphazard, and medical care facilities
inadequate. Greenblatt issued medical guidelines to standardize ECT practice. His
report and the regulations satisfied both legislature leaders and the practitioners,
markedly improving clinical practice, becoming a national model for treatment
facilities. The resolution encouraged a broader acceptance of the treatment and a
reference source for establishing treatment facilities.
First American Psychiatric Association ECT Task Force (1975)

Early in my career in psychiatry, at annual meetings of the American
Psychiatric Association (APA) I joined the Section on Brain Function &amp; Behavior
where ongoing arguments on how to optimize ECT were active. Discussions on ECT
were also featured as clinicians assembled annually at the Electroshock Research
Association, Society of Biological Psychiatry, and similar associations dedicated to
lobotomy, insulin coma, and carbon dioxide therapy. When Milton Greenblatt
31

�deflected the drive of the Massachusetts legislature in 1970 to interdict the use of
ECT, he organized the survey of ECT and also asked me to edit a special number of
his journal Seminars in Psychiatry on the scientific status of ECT. 39

Legislative restrictions against the use of ECT and lobotomy with specific
interdiction in persons under age 18 surfaced again in 1972, this time in California.
In response, psychiatrists led by Dr. Gary Aden applied for court relief from
legislative interference in accepted medical practice. The court agreed that the
legislative restrictions of medical practice were unacceptable. The legislature
responded by using the state’s power to monitor health and safety to limit the
number and frequency of treatments, restrict guidelines for consent, require
extensive reporting of treatments, and prohibit its use in persons under the age of
18. The regulations forced many patients in need of treatment to go out of state as
California physicians abandoned the treatment. These regulations are still in effect
in 2021 and severely limit ECT use, especially in adolescents. The same restrictions
were adopted in Texas in 1993 and in other states to a lesser degree.

Requests for professional support by California psychiatrists led the
American Psychiatric Association to establish a Task Force on ECT in 1975, and
appointed Fred Frankel of Boston as its chairman. I was an appointed member. The
report published in May 1978 described whom to treat, how to assure safe
procedures and effective treatments, and discussed concerns about cognition and
memory and how to minimize these effects.
A query about ECT practices had been sent to 20% of the Association’s
membership. Responses were received from 75% of those canvassed. Was ECT an
appropriate treatment for any of 11 different psychiatric diagnoses? The responses
showed widespread confusion as to whom to treat. ECT was considered useful for
patients with major depression (86%), less so for manic excitement (42%), and
marginally for schizophrenia (25%). About 22% of the responding practitioners
had used or recommended ECT in the prior 6 months. Featured in this confusion
was the inadequacy of the official psychiatric classification schemes, their use
providing poor descriptions and inadequate diagnoses and not assuring optimized
treatment plans.

The Task Force members were experienced in clinical care and most
procedural questions were readily resolved. A thorny issue was endorsement of
treatments using unilateral electrode placement. At a committee vote, I and another
clinician member could not recommend the use of unilateral placement, arguing
that its inefficacy necessarily led to increased numbers of seizures with attendant
anesthesia risks, lengthened hospital stays, higher costs, and potential for increased
morbidity. The reported lesser effect on cognition was transient, not justifying the
inefficacy of the treatments and prolongation of illness.

32

�When the Task Force report was submitted to the APA Board of Trustees for
publication under its imprimatur, the policy leaders insisted nevertheless that the
unilateral form of treatment be endorsed (along with the bilateral), to support the
practices and beliefs of some members.
How best to assure consent? Patients referred for ECT are severely ill,
depressed, psychotic, delirious, and suicidal, often mute and negativistic, raising
questions as to their competency to understand the risks and benefits of proposed
treatments and to consent freely. Can a patient so ill as to be referred for seizure
therapy properly evaluate the risks of memory losses described by psychologists
and in the public press? Medical practice treats patients by voluntary consent, the
patient appearing at the physician’s office and choosing whether to follow the
physician’s prescriptions. Can the same rules apply for electroshock?

The Task Force members recommended a lengthy printed description of the
procedure with detailed risks to be read by and to each patient, to be signed
voluntarily, and properly witnessed. The form would name the treating personnel,
and specify the maximum number of treatments under the consent.

I was conflicted in this discussion. My father was a general medical
practitioner; I had seen his interactions with patients and their families, and how
they respected him and readily accepted his recommendations, including his
insistence for an independent second opinion in complex diagnoses. I experienced
the same deference when I took over his practice during his holidays and again
when I opened a community office in Great Neck for consultations in neurology and
psychiatry. In the Task Force discussions, I was one of two physicians who, at first,
did not see the need for a written “contract”, but agreed before submission to the
APA.
ECT was viewed as a surgical procedure (since it uses anesthesia) with a
potential for harm that must be specifically consented to by the patient. Patient
autonomy would be respected by describing the anticipated benefits and risks
before treatment and treating only those who voluntarily agreed. Further
protection was to be achieved by a family member also reading the descriptions,
discussing the procedures and risks, and witnessing the patient’s signature.

Exceptions to voluntary consent were recommended for those with mental
deficiency or dementia. These were considered to be the family and community
responsibility. State-mandated procedures for judicial authorization for treatment
on an incompetent patient’s behalf were supported by the task force.

The recommendation of a signed, voluntary consent for treatment was the
main benefit of the Task Force Report. The text was considered an “official” action
of a national association and served as a guide for the opening of new ECT treatment
centers throughout the nation in the post-1978 years. I was often invited to visit
33

�and organize new treatment units based on the Task Force Report. The
recommended procedures were sufficiently conservative to be widely adopted.

The Task Force report was distributed at the May 1978 APA annual meeting
in Miami with each task force member presenting an aspect of the report to a large
audience. I was the spokesperson for the technical recommendations. The report
was generally accepted and praised. The concept of a written consent was argued
but accepted. The note accepting treatments through unilateral placements,
however, met strong protests from practitioners, notably New York’s Lothar
Kalinowsky. Much of his criticism was directed at me as the spokesperson. The
practitioners, themselves extremely well experienced with bilateral and unilateral
electrode placements, argued that treatments through unilateral electrode
placements were so inefficient as to put patients at risk of prolonged illness and
suicide, poor outcomes, longer courses of treatments, and higher relapse rates.
Out-Patient ECT: Association for Convulsive Therapy Commission
Post-World War II, ECT patients had been increasingly treated as outpatients
in doctor’s offices, both for their treatment courses and continuation treatments.
But as ECT in the 1980s demanded collaboration of a qualified anesthesiologist,
ECT became a hospital-based procedure. The prescription of a fixed number of
treatments, usually 6 to 10, became commonplace. Such courses had been sufficient
with the high energy, bilateral placement seizure inductions favored by the early
office practitioners and those treating patients at Gracie Square Hospital. When
patients showed signs of relapse, ambulatory continuation treatments were readily
undertaken. During the 1970s, with repeated public and professional attacks on
ECT, physicians often negotiated a fixed number of treatments for a course. The idea
that the length and frequency of an ECT course could be prescribed in advance, even
agreed to in the patient-signed consent, was widely accepted as recommended by
the ECT Task Force of the American Psychiatric Association in its 1978 report. The
treatment image became one of a specifically effective treatment, much like a
prescribed antibiotic for an infection. But ECT treatment for depression or mania or
even catatonia is more like that of insulin for diabetes: an acute fixed schedule is
prescribed and is immediately effective but open-ended continuation dosing is
necessary for sustained relief.
When ECT was re-introduced in the 1980s, many clinicians thought that
psychoactive medications would sustain ECT relief. After a course of ECT patients
were prescribed psychoactive medications, often in unique combinations of
polypharmacy, and while success was common, relapse became an increasing
burden.

In 1987, Thomas Aronson and colleagues from the Stony Brook out-patient
treatment facility reported greater than 50% relapse rates within 6 months for my
ECT-treated delusional depressed patients regardless of continued medications. I
34

�was chagrined and saw the need for continuation ECT. Our ECT Service treated
patients three days a week, so we set aside one day (and later two) for out-patient
treatments. We no longer asked patients to consent to a fixed number of treatments
but asked their consent for continued observation and treatment “as needed”
beginning as in-patients and continuing in our ECT out-patient clinic for six or more
months.

How best to prescribe and manage continuation treatments was widely
discussed in the journal Convulsive Therapy and at meetings of the Association for
Convulsive Therapy (ACT). That Association established a Task Force that surveyed
usage, evaluated risks, and recommended guidelines, publishing their conclusions in
1996. I chaired the group and published a report that became a guide for
continuation treatments. 40

The Stigma Persists: The Public Joins the Attack

The popularity of psychotherapy and psychotropic drugs in the 1960s led to
a sharp decline in ECT use. But as medication treatments increasingly failed and
families asked what else could be done, ECT use resurfaced. The shadow of
lobotomy and patient and psychologists' complaints of memory loss encouraged
persistent attacks against ECT, and as these became more strident, my public
support for the procedure brought me much public criticism. Burton Roueche’s
exaggerated description of a government economist’s memory loss in the 1974 New
Yorker article “All About Eve” brought Marilyn Rice to public attention. She
instituted a malpractice suit against the psychiatrist who administered the
treatments complaining that she had not been warned that her memory would be
affected and that she would be unable to work. 41 She went on to develop and lead
the public action group Committee for Truth in Psychiatry that launched further
attacks on ECT. She frequently appeared at public forums to challenge ECT use,
proclaiming her persisting loss of memories. (The Court supported the physician
defendant.)
After Marilyn Rice died in 1992 the Committee for Truth in Psychiatry was
led by Linda Andre, who made the same claims after her treatment course following
a suicide attempt by drug overdose. She was a vivacious, well-spoken, and
attractively dressed woman who attended public meetings and paid particular
attention to meetings in which I presented my work. She challenged speakers and
attended the 1992 international ECT meeting in Graz, Austria to voice her
opposition to the treatment. The international audience was surprised by her
personal attacks. She attended my public lectures and protested my presentations
at annual Continuing Medical Education psychiatry training sessions in various
cities. On one occasion, when the floor was opened to questions, she attacked me as
dishonest and paid to lie about the effects of ECT. She walked up to the podium
offering me a tray containing a pig’s head surrounded by dollar bills.
35

�Church of Scientology and Malpractice Legal Suits
In the 1960s, the national political and social movement of Scientology led by
the futurist Ron Hubbard opportunistically attacked psychiatry with special
attention to the prescription of psychotropic drugs in children and adolescents and
the brain effects of ECT and lobotomy. The members and their children
demonstrated with shouts and anti-ECT posters in the halls and at entrances to
American Psychiatric Association meetings and other sessions at which ECT was
discussed. On occasions when its members arranged for complaints to be aired on
TV talk shows, I was asked to defend the treatment but refused to take part. The
hosts delighted in challenging professionals on their incomes and on the damage
that had been done to the patients who complained bitterly about memory losses.
Yet, many patients spoke well, encouraged by the host whose mission was to
support the “poor” patient and to castigate physicians for damaging patient’s brains.
The Church of Scientology also encouraged and financed malpractice suits
against practitioners, asserting that patients had lost memories of long periods of
their lives, particularly the most personal family memories. I appeared as a witness
for the defense on numerous occasions with Peter Breggin, John Friedberg, and
Harold Sackeim as expert witnesses for the plaintiffs.

The cases were weak and my defense of the practitioners was successful in
every instance except that of Peggy Salters in South Carolina in 2005. She had been
given ECT as an outpatient with 13 treatments in 19 days. The physician deemed the
patient suicidal, but failed to offer her hospital protection. She complained that her
memory was so damaged that she could no longer work. While I did not believe that
the patient had suffered compensible damage, the physicians had not followed
standard practice in protecting the suicidal patient nor in justifying almost daily
treatments. I deem the judgment for the patient correct.
Media Attacks: BBC-PBS Madness with Jonathan Miller.
In 1990 I received a call from a London TV production company asking if I
would help with the presentation of convulsive therapy in a planned 5-hour
BBC/PBS documentary on the history of treatments of the mentally ill to be titled
Museums of Madness. The producer, Jonathan Miller, had impressive qualifications
as a Cambridge University graduate in neurology and the son of a psychiatrist. He
had acted in the original cast of the successful Broadway play Beyond the Fringe
(1960-64), directed performances in theatre and opera, and written and directed a
popular 13-hour BBC production The Body in Question (1979). While playing on
Broadway he attended Saturday morning Grand Rounds in Neurology at the
Neurological Institute with H. Houston Merritt.
36

�I met with Miller and Grace Kitto of Brook Productions and agreed to their
filming of my patients and the treatment procedures at University Hospital. I
arranged that they return again three weeks after the first filming to record the
patient’s progress and that I see the frames of my patients before they were aired.

For filming on May 17, 1990 I selected patients with different diagnoses who
were early in their course of treatment. SK, an 18-year old delusional psychotic man
who had been in repeated treatments for more than two years; EF, a 60-year old
psychotic depressed woman who was posturing, repetitive in speech, and unable to
care for herself; ET, a melancholic depressed woman with a history of mania and
excitement; and JF, an elderly man who had been depressed, lost much weight, and
careless in his self-care. Appropriate consent for filming was obtained for each
patient. The filming of interviews and treatments went smoothly.
The team returned three weeks later for follow-up filming. Patient SK was
better oriented, EF answered questions without repetitive speech or acts, ET smiled
and was friendly and better oriented, while JF assured us that while he could not
recall why he was being treated, he felt well and was ready to go home. Asked about
memory, he thought that his memory was as good as it ever was. The treatments
were not painful at all, he said, and surely less uncomfortable than seeing the
dentist.
On October 15, 1990 on my way back from meetings in Berlin, I visited the
Brook Production Studios in London to review the print. The presentation of the
patients and the treatment were very well done and I was pleased. My concept of
neuroendocrine dysfunction as the basis for the disorders that are relieved by
seizures was well presented.

Many months later, when the series was aired in the U.S., Miller’s voice-over
set a very different tone:
‘The administration of an electric shock through the skull is a comparatively
crude assault on the brain.
‘. . . as machines were invented to whirl, swirl, shock, rock, and douche the
patient back to sanity, the sick brain was treated to a series of traumatic assaults
presumably in the hope that its distorted parts would be jolted into place.
‘. . . the treatments resulted in violent convulsions with serious bruising . . .
fractures of limbs and spine . . . and other atrocious consequences.
‘. . . despite its understandably sinister reputation, ECT, Metrazole and
insulin have much more in common with the whirling chairs and rotating cradles
which they superseded, in that they were addressed to the brain as if it were a
single undifferentiated organ.”

37

�Miller’s failure to find a positive thread in the histories presented by the
patients left many viewers with a bad taste, and the series was not presented again.
In a recent biography of Miller, the author Kate Bassett makes much of Miller’s
conflicts with his father, a leading forensic psychiatrist, as the basis for his negative
attitude to medicine. Whether this relationship contributed to his views of
psychiatry or not, he was among many creative writers who saw psychotherapy and
psychoanalysis favorably, indulged by themselves, friends and family members,
seeing electroshock treatments as hazardous, ineffective, and not acceptable in their
social class.
An Active Defense: A Beautiful Mind: The Nobelist John Nash and Insulin Coma.

A call from the biographer Sylvia Nasar in 2001 asking whether I had
experience with insulin coma therapy made me aware of the life history of John
Nash, the 1994 Nobelist in Economics. A brilliant mathematician, Nash had
successfully completed his doctorate at Princeton University, publishing a thesis on
game theory that was reputed to revolutionize economics. While teaching at MIT in
May 1959 he became delusional, overactive, impulsive, and fearful, meeting criteria
for delirious mania. He was treated in Boston’s McLean Hospital by psychotherapy
and chlorpromazine. Aware that his statements led to his incarceration he hid his
beliefs and was discharged to the community. He left his teaching position and
returned to Princeton.

The paranoid psychosis persisted and he fled to Europe and sought to give up
his American citizenship. Returning to Princeton in 1971 floridly delusional, he was
admitted to Trenton State Hospital. His Princeton colleagues implored the Medical
Director that Nash was a potential Nobelist and warranted the most effective
treatment. Insulin coma treatment, although discarded elsewhere, was still in use.
It was the most heavily staffed service, and in response to his colleagues’ pleas, Nash
was assigned for treatment in that unit. He responded by relief of his overt
delusions but the director suggested the follow-up treatment be ECT. Nash’s wife
and colleagues refused that “brain-damaging treatment” and he was continued on
medication with chlorpromazine. Nash did not recover and did not return to
productive work; he remained cared for by his wife and attended lectures at
Princeton.
Nasar’s biography A Beautiful Mind was to be the basis of a Hollywood film
and she wanted advice on the actual experience of the treatments that Nash had
been given. I described my experience at Hillside Hospital, noted that seizures
occurred in more than 10% of the coma sessions. The film highlighted the seizure,
and I was pleased by the portrayal of the illness and the treatment in the film.

I reviewed my experience with insulin coma and concluded again that the
central therapeutic events were the incidental seizures, not the coma or an effect of
insulin, or any other aspect of the treatment. Like injections with camphor and
38

�Metrazol, insulin coma was best viewed as an inefficient form of induced seizure
therapy. As the originator of ICT, Manfred Sakel insisted that the comas selectively
destroyed sick brain cells leaving only healthy cells. He argued that the seizures
were incidental, irrelevant side-effects. But experienced clinicians welcomed the
seizures and often added ECT during coma sessions for the poorly responsive. I
realized that the efficacy of insulin coma therapy lay in the occasional grand mal
seizure, that ICT is best seen as an imperfect form of induced seizure therapy. 42

39

�Book Four: The Enigma: How Do Seizures Alter Behavior?
Seizures are Inherent Reflexes
Grand mal seizures are patterned reflexes seen in our species, indeed in all
mammals. Seizures that occur spontaneously constitute the debilitating disease of
epilepsy. Ladislas Meduna’s 1934 discovery that inducing seizures in the
psychiatric ill relieved both abnormal thoughts and the peculiar and repetitive
motor behaviors of schizophrenia was a remarkable and still unheralded discovery
in the history of medicine. By 1938 electric currents had been shown to
immediately induce a seizure with minimal pain and less risk than Meduna’s
chemical methods, and the electrical induction of seizures -- electroshock -- quickly
became a widely accepted treatment of the psychiatric ill.

The induction of a bilateral grand mal brain seizure is the central therapeutic
event. A patterned EEG of a minimum duration of 30-40 seconds is the principal
marker of an adequate treatment. An increase in hypothalamic-pituitary hormones
in the blood and cerebrospinal fluid is another marker. No characteristic of the
induction stimulus itself, whether chemical or electrical, is essential for clinical
benefits. Attempts to treat patients by subconvulsive electric or magnetic currents
or by non-seizure inducing anesthesia (isoflurane) dosing have been unsuccessful in
eliciting behavioral benefits.
Although many patients report immediate changes in mood, motor activity,
and thought, repeated seizures over many days or weeks are typically necessary for
lasting clinical benefits. Attempts to sustain the clinical benefits by psychotropic
drugs are occasionally successful, but for persistent benefits repeated seizures are
best.
How do seizures alter behaviors? We do not know. My thinking on this
question has evolved over the years. Early in my career and with the hubris of the
novice I combined physiological and psychological features in “a unified theory of
the action of physiodynamic theories.” That construct was re-labeled the
neurophysiologic-adaptive view a few years later. I argued that the changes in
behavior, toward greater denial of illness, was facilitated by altered brain
physiology. 43

My studies with anticholinergic compounds showed me that drugs that
inhibit brain acetylcholine reversed the mood benefits of ECT. The elevated levels of
brain acetylcholine associated with recovery in mood and thought seemed sufficient
to justify what in 1962 I described as a cholinergic theory. I argued that seizures
increased the brain levels of acetylcholine and cholinesterases, and that these
changes altered neuroendocrine functions, mainly of the hypothalamic-pituitaryadrenal and hypothalamic-pituitary-thyroid axes. This hypothesis was consistent
40

�with the ongoing enthusiasm for changes in the brain transmitters that were
thought the basis for the changes in behavior associated with psychotropic drugs.

As chemist’s skills improved and concentrations of endocrine hormones in
the blood could be measured, my interest focused on vegetative signs in psychiatric
illnesses. Attention to the TSH hormone response to TRH and abnormal thyroid
physiology was quickly followed by interest in adrenal hormones and the
dexamethasone suppression test in depressive illness. Not only were thyroid and
cortisol abnormalities markers in the psychiatric ill, the abnormalities normalized
with effective treatments. I sought to confirm these reports in our patients treated
with ECT at the Northport Veterans Administration hospital in Eastern Long Island.
When Jan-Otto Ottosson also saw merit in a neuroendocrine image of ECT, we
formulated a neuroendocrine theory that we published in 1980.44 After forty years,
I believe this theory remains the most viable explanation for the efficacy of induced
seizures in patients ill with melancholia. While this theory may not be applicable to
the benefits in other psychiatric illnesses, it is a pointer that warrants greater study.
The Theories

The behavior changes induced in the psychiatric ill by the bizarre technology
of repeatedly inducing grand mal seizures is puzzling and has encouraged a plethora
of theories, some based on brain and body physiology and chemistry, and some on
magical thinking. My ruminations and their origins have evolved with my
experience.
Neurophysiologic-adaptive theory. At Bellevue Hospital in the 1940s my
teachers were much interested in anosognosia, the failure of awareness or the active
denial of a deficit in motor functions (as in post-stroke) or denial of sensory loss (as
in denial of blindness), as I described in Chapter 1. Special attention was paid to
how humans perceived multiple stimulations as when two pinpricks or finger
strokes were simultaneously applied to different body parts.

Even in patients with brain functions compromised by trauma, age, infection
or tumor, a single sensory stimulus may be readily perceived but the perception of
two simultaneous stimuli varies with the subject’s alertness and vigilance. The
errors are evidence of compromised brain functions, of the syndrome loosely
described as the “organic mental syndrome.” After head injury, stroke, brain tumor,
aging, infection or repeated seizures, only one stimulus is reported (extinction), or
the second stimulus is perceived at another body site (displacement), or pointed into
space before them (exosomesthesia). Under the influence of injected amobarbital,
perception errors and the expression of denial language increase. These reports
became the basis for the Face-Hand Test.
During the course of electroshock, errors increased with numbers of
treatments. The greater the degree of EEG change, the greater the perceptual
errors. Among the scientists at Bellevue, Edwin Weinstein, Louis Linn, and Robert
41

�Kahn proposed “denial” as the mechanism for the relief afforded depressed patients
by electroshock. They catalogued a “language of denial” making it possible to score
the number of denial terms in an interview transcript. When amobarbital was
injected at a fixed concentration and a specified rate, the number of expressed
denial terms increased, especially in brain compromised patients.

I studied the expression of denial during ECT by weekly amobarbital and EEG
tests and recording patient responses. As EEG slow wave activity increased with
more seizures, so did expressions of denial in those patients who showed the
greatest relief of depressed mood., I adopted this explanation of the changes in
behavior during ECT as an increase in denial. Depressed patients commonly
complained of insomnia, anorexia, fatigue, weakness, and loss of interest in daily
activities. After treatment, the complaints are relieved and when asked what is
wrong, they deny their earlier complaints. Since the connection between denial and
improvement had been proposed by my teachers, and as EEG and sedation tests
verified their proposition, I adopted denial as an explanation. 45 I did not seek
greater understanding of physiology until years later.
Such an explanation was applicable in the patients with melancholic and
psychotic depression, but was not relevant for the response of those in delirious
states, catatonia, mania, or psychosis. These states are marked by disorientation
and confusion, mutism and negatism, hyperactivity and disorders in thought that
needed broader explanations than the simplistic denial of symptoms. Their
responses required another explanation.

Cholinergic theory. My interest in the effects of psychoactive drugs on the
EEG led me to study the effect of drugs on the ECT process. A colleague, Herman
Denber, interested me in studying the behavioral effects of diethazine, an
experimental anticholinergic drug that blocked acetylcholine stimulation. The
chemical was a new moiety created in industry with the hope that it might have
clinically favorable psychoactive properties. He was unable to identify a clinical
benefit, reporting that patients became more disorganized and irritable. I tested
diethazine to our improving ECT patients, those with signs of denial and recovery
from a depressive state and with high degrees of EEG slowing. The slow waves were
blocked and the records became filled with low voltage fast rhythms. Patients
became irritable, anxious, agitated and again depressed, a reversion to their pretreatment states. We inferred that the relief of depressed mood with ECT was
related to increased levels of acetylcholine in the brain.
George Ulett and his colleagues at Washington University had administered
atropine, a potent anticholinergic drug, during the ECT treatment course and
reported that it blocked EEG slow waves and elicited pre-treatment behaviors in the
patients. Similar reversal of mood was also reported after injections of the
experimental anticholinergic JB-329 (Ditran) and its congeners, supporting the
connection between brain cholinergic levels and mood.
42

�Much interest was shown in acetylcholine in neuroscience research in the
1950s. Free acetylcholine and acetylcholinesterases were elevated in the
cerebrospinal fluid (CSF) of epileptic patients. CSF acetylcholine levels increased
during ECT. In cats subjected to graduated head trauma, the amount of free
acetylcholine and cholinesterases in the CSF increased with the severity of the
trauma. Again, hubris allowed me to picture the physiologic consequences of
induced seizures as similar to those of head trauma. 46

I imagined that induced seizures, like cerebral trauma and epileptic seizures,
altered cerebral permeability increasing free acetylcholine and cholinesterase levels
in the brain, slow EEG frequencies and increase amplitudes and rhythmic bursts. I
pictured these biochemical changes as the basis for the behavioral effects we were
seeing with ECT.
My focus on acetylcholine as the critical agent in treatment followed the
happenstance finding that anticholinergic agents reversed the seizure-induced EEG
and behavioral changes. But study interest in acetylcholine waned as interest in
brain neurotransmitters shifted to epinephrine, and then to dopamine and
serotonin, as pharmacologists, excited by their ability to measure these
neurotransmitters in animal brains tracked the effects of each of the new
psychoactive moieties, that were then enthusiastically welcomed by clinicians and
the public. At this juncture, half a century later, I find little interest in acetylcholine
in clinical psychiatry or epilepsy.

The Neuroendocrine Hypothesis. When I was asked in 1977 to supervise an
acute treatment unit and its ECT facility at the Veterans Administration hospital in
Northport, much academic interest was being shown in brain peptide hormones in
the psychiatric ill, particularly those of the thyroid, adrenal, and pituitary glands.
The Nobel Prize for Medicine that year was awarded for the demonstration of
peptide hormones in the brain and for the radioimmune assay that measured their
presence.

Hormone changes in our patients became measurable by thyroid and adrenal
function tests. These glands are instrumental in maintaining the daily wakefulness
cycle, the response to fear and stress, and monitoring sleep and other bodily
functions. The TRH stimulation test, the release of TSH to an intravenous bolus of
TRH, was blunted in a quarter of the severely depressed patients. After a course of
ECT, we did not find the changes in TRH levels that we had hoped would help us
decide whether the treatment course was successful.

Cortisol derived from the adrenal gland was a useful marker. Serum cortisol
levels were unusually elevated in institutionalized depressed patients, an
observation in the 1970s that led an Australian psychiatric team under Brian Davies
and Bernard Carroll to study cortisol functions in their patients. They developed the
dexamethasone suppression test (DST) as a measure of adrenal function. Their
reports are filled with extensive observations of hormone functions and psychiatric
43

�illness but the note that particularly stimulated my interest was their experience
with ECT in melancholia.

In five melancholic patients the cortisol measures were deemed abnormal
(elevated and not suppressed by the steroid dexamethasone) before treatment.
After ECT the clinical features of melancholia remitted and the cortisol measures
normalized. Then two of the patients relapsed, again exhibiting signs of melancholia
with abnormal cortisol functions. Second courses of ECT resolved the clinical
illness, again normalizing the cortisol measures. Carroll described an additional
seven patients in whom treatments had not resolved the depressive illness nor
normalized the DST. The test, it seemed, was a marker of illness severity and of
treatment response.

At the Northport hospital a research fellow Yiannis Papakostas confirmed the
relationship between severity of depression, abnormal DST, and the response to
ECT that Carroll had described. The test was difficult to perform and the end-point
criteria needed more careful study, but the changes in the neuroendocrine tests
with improvement in melancholia led to more detailed studies of the response to
ECT.
Seizures, both in epileptic fits and in those induced in ECT, released the
pituitary adrenocorticotrophic hormones (ACTH) and prolactin into the CSF and
blood. By 1978 attention was directed to the association of the contributions to
behavior of the products of the hypothalamus, pituitary and adrenal glands, (HPA
axis) in melancholic depression and the response to ECT. At the 1978 New Orleans
NIMH Conference on ECT, I described my experience with the DST, supporting
Bernard Carroll’s experience. At the same conference Jan-Otto Ottosson
independently supported the same endocrine findings. Melancholic psychotic
patients have abnormalities in functions of the HPA endocrines, and these return to
normal after recovery.
I described a “neuroendocrine” hypothesis for ECT in Convulsive Therapy:
Theory and Practice and cited what was known of the process:

“A theory of convulsive therapy must account for the significance of the
seizure but disregard the mode of induction, the direct actions of currents, and
the distinctions caused by various electrode placements. It must consider the
difference in response among patients with diverse psychopathologies and the
time, measured in days, needed for a favorable outcome. Biochemical
explanations must relate to changes in the brain rather than in the blood, urine
or other tissues. Psychological, personality, and linguistic considerations may
affect the behavioral response and should be considered, but these are probably
not central to the antidepressant efficacy of induced convulsions.”

And I described the hypothesis thus:
44

�“Hypothalamic dysfunction is a core process in endogenous depressive
psychosis. Convulsive therapy alters hypothalamic activity both by direct
stimulation of hypothalamic cells and by increasing the functional
neurotransmitter activity in the brain, thereby releasing substances, probably
peptide hormones, that alter the vegetative functions of the body and the
endocrine glands. Specific substances are released that modify mood and the
behaviors associated with mood disturbances. The biochemical events that
precede and accompany the seizure are the trigger for increased neurohumoral
activity. In ECT, the direct stimulation of electric currents augment but are not
necessary for the effects on hypothalamic functions.”
The mechanism was envisioned for patients with psychotic depression in
whom the efficacy of ECT was well grounded, inducing remission in more than 90%
of the cases. In the same chapter I discussed the evidence for ECT’s effect on mania,
catatonia, and schizophrenia. While the treatments were successful in mania and
catatonia, we lacked studies of endocrine changes to support a connection similar to
that with melancholia. In schizophrenia the efficacy of ECT was insecure, being
successful in acute illnesses and in catatonia, but ineffective in the more common
chronic ill with the hebephrenic forms of the illness.

In the 1980s I attempted a study of peptides in the cerebrospinal fluid during
ECT. Of nine patients with psychotic depression referred for ECT with mean scores
on the Hamilton Depression Rating Scale greater than 25, eight were nonsuppressors on the DST. I collected their lumbar CSF before ECT and then after
treatments number 6, 10, 12 and 14. The samples were collected within one day
after a treatment, and in five patients additional treatments were deemed necessary.
The frozen samples were shipped to Charles Nemeroff and Garth Bissette at Duke
University and to Huda Akil at the University of Michigan for analyses for the
peptides of the corticotrophin-releasing factor, somatostatin, and beta-endorphin.
The samples showed significant falls in levels of corticotrophin releasing factor and
ß-endorphin but a non-significant rise in somatostatin. 47
The findings were not encouraging to the neuroendocrine hypothesis. While
the hypothesis could be erroneous, our actual procedures did not meet the more
optimal criteria that would be used today. We made arbitrary choices in our
treatment mode. We used unilateral electrode placement with EEG monitoring of
seizure duration, selected sampling in mid-course of treatment, with varying
resolution of the illness and the DST, and were only able to test for a limited number
of peptides. The study demonstrated the complexity of studies of the ECT
mechanism. While I was interested in proceeding further, I lacked facilities for
chemistry. Instead, I was in a position to pay more attention to the clinical questions
of the ECT process that became the CORE studies undertaken between 1993 and
2005.

45

�Conferring in the Search for the Mechanism
Believing that it must be possible to understand the relief of certain
psychiatric illnesses by inducing seizures, I have participated and encouraged
discussions of possible mechanisms throughout my working life. Surely the
extensive experience that inducing seizures improves the behaviors and the lives of
many severe mentally ill must be a challenge in present day biology. What follows is
a chronological account of moments in this endeavor.

1972. The first encouragement came in convincing a committee at the NIMH
to support a symposium on ECT mechanism. The committee asked two leading
neurobiologists, Seymour Kety and James McGaugh, to join me in organizing a 1972
meeting in San Juan, Puerto Rico, titled Psychobiology of Convulsive Therapy.
Attention was focused at the meeting on the neurophysiology of seizures, the role of
changes in cognition, and the neurochemistry of catecholamines. 48
The panelists dedemed persistent changes in EEG recordings essential to the
behavior changes in the therapy. In the absence of persistent EEG changes, only
weak and transient behavior effects occurred.
Changes in memory were not essential to the behavior benefits. The
complaints of loss of recent memories were side-effects of the electricity, the
anesthetics, and the seizure. The changes were not central to the effects of seizures
on mood and thought.

Much interest was shown in newly discovered brain neurotransmitters that
“explained” the effects of psychoactive drugs on brain functions and behavior.
Changes in the neurotransmitters were considered an explanation of the behavioral
effects of repeated induced seizures as well. Seymour Kety cautioned, however,
that

“. . . there is no dearth of demonstrable biochemical changes which are
associated with electroconvulsive shock. Indeed, the difficulty lies not in
demonstrating such changes, but in differentiating between those which are
more fundamental and those that are clearly secondary, and also in attempting
to discern which of the changes may be related to the important antidepressive
or amnestic effects and which are quite irrelevant to these.”

In the 49 years since that meeting, the ECT literature has been filled with
correlations of brain and systemic increases of many biochemical and behavior
measures. But no study has offered a consistent association between
neurotransmitter functions and changes in mood and thought, either for induced
seizures or for any of the many psychoactive pills.

46

�1978. Continuing interest in ECT encouraged NIMH leaders to organize a
larger conference in February 1978 in New Orleans on “Efficacy and Impact” with a
larger panel of clinicians and scientists. In the six years since the San Juan
Conference interests had broadened to the safety of regressive ECT (intensive daily
treatments that were applied in chronic psychotic patients), the efficacy of different
electrode placements, changes in electric currents from alternating to brief pulse
currents, the clinical usefulness in patients with mania and schizophrenia, and the
relation to endocrine measures. At this conference I became aware that Jan-Otto
Ottosson had also been stimulated to examine the changes in neuroendocrine
measures, and we joined in publishing the neuroendocrine hypothesis for the
mechanism of induced seizures in Psychiatry Research in 1980. I was so impressed
with the relation of neuroendocrine changes to behavior that in writing my 1979
textbook Convulsive Therapy: Theory and Practice, I credited the neuroendocrine
explanation for ECT as the most viable.
1985. The hostility and controversies about ECT encouraged the NIMH to
hold a public Consensus Conference in October 1985. Although the panelists
included experienced practitioners, greater attention was paid to the critical
opinions and biases of lay and professional critics. The discussions were raucous
and were accompanied by shouting and hostility. The published reviews added
little to either the clinical or the mechanism interests, reflecting the continuing
rejection of and prejudice against the treatment in the public and the professions.

1986. Motivated by the circus of the Consensus Conference, Sidney Malitz
and Harold Sackeim organized a conference at the New York Academy of Sciences
in 1986. The presentations covered the broad issues of clinical efficacy varying with
diagnosis, results of biochemical, neurophysiologic, neuroendocrinologic, and
psychologic changes during the course of treatments, and mechanisms of action.
Jan-Otto Ottosson detailed the essential characteristics of an effective seizure and
treatment course; Bernard Lerer and Baruch Shapira looked at the impact of
seizures on neurotransmitters; and Robert Post and his NIH colleagues discussed
the anticonvulsant effects of seizures. They saw the anticonvulsant effects in mania
in the therapeutic stream, endorsing anticonvulsant medicines to treat manic
behaviors. Harold Sackeim and colleagues reported a rise in seizure thresholds
during the course of ECT treatments, arguing that the benefits of induced seizures
were in the anticonvulsant effects. Pierre Flor-Henry focused attention on the
theoretic lateralized changes in the non-dominant hemisphere as the basis for the
behavior change with seizures. These proposed mechanisms were no more exciting
than the presentations a decade earlier in the San Juan conference, and they
stimulated little further study.
1989. Still hoping that invited discussions might encourage study, and as
Editor of the journal Convulsive Therapy, I asked Harold Sackeim to invite authors
with an interest in the mechanism to write reviews for a special number of volume
5. An impediment to formulating a single hypothesis is the efficacy of induced
seizures across the broad spectrum of psychiatric disorders. Surely, no single
47

�mechanism can explain the diverse effects in melancholia, mania, catatonia,
delirium, and Parkinsonism. The same hurdles were described by Pesach
Lichtenberg and Bernard Lerer and by Sukdeb Mukherjee in discussing the relief of
mania. In a reprise of the debates on the merits of unilateral electrode placements,
Richard Abrams challenged the reported advantage for treatments induced in the
right hemisphere rather than the left, raising the importance of the details in any
induced seizure study seeking to understand mechanism. Charles Nemeroff and I, in
the midst of our collaborative studies of peptides in CSF, asked whether we
anticipated higher or lower levels of peptides as the basis for melancholic
depression and relief by ECT. We favored the image of lower levels of peptides
active in maintaining normal mood and suggested that the seizures might release an
active peptide that we named antidepressin. Our optimism in picturing an additional
peptide was generated by the increasing number of substances that were being
publicly characterized as altering mood, alertness, and cognition in the psychiatric
ill. But, nothing has come of it, another nagging consequence of my not having
developed skills in biochemistry.

1992. In editing a second edition of his textbook Abrams repeated the
diversity argument that the efficacy of induced seizures over many illnesses made
theorizing not particularly useful until a better understanding of psychiatric illness
emerged. He saw our understanding as similar to that of the peoples in the 18th
Century picturing burning as a process involving the imaginary substance
phlogiston. He concluded that we await the intervention of a modern Anton
Lavoisier, the French scientist who discovered oxygen, 20% of the air we breathe
and the basis for burning substances by their combination.

1998. The continuing challenge of mechanism led Charles Kellner, the
succeeding editor of Convulsive Therapy, to ask Bernard Lerer to invite opinions on
what was learned about the neurobiology of seizures. Lerer again complained of the
difficulty of seeking a single mechanism for a procedure with such a broad effect
among many disorders. Reviews by John Mann and Ron Duman were no more
useful. Nor was an explanation based on the anticonvulsant actions of seizures.
Studies of the brain neurotrophic factor, neuropeptides, TRH and related peptides,
and neuropeptide Y each fell to the criticism by Kety that the broad effects of
seizures on many brain chemicals made it unlikely that changes in any single
measure would be relevant to the mechanism. At best, any single measure would be
a marker of the breadth of the changes induced in brain biology.
2014. The present editor of the Journal of ECT, Vaughn McCall organized
another review of mechanisms. He asked Pascal Sienaert to organize the reports
that were published in June 2014. Each survey considered the main measurable
consequences of seizures – changes in the EEG and psychological tests,
neurotransmitters, neuroendocrines, and immune and cardiovascular systems. I
chose to remind readers that the central event was the seizure and not in any aspect
of electricity, by noting the equivalent efficacy and consequences of flurothyl
induced seizures to those induced electrically.
48

�Roger Haskett of the University of Pittsburgh discussed the neuroendocrine
hypothesis. Haskett had studied cortisol in melancholia and ECT in collaboration
with Bernard Carroll when both were at the University of Michigan in the 1980s.

In retrospect, the discovery of the changes in human behavior by repeated
inductions of seizures is a remarkable page in the history of medicine. As I read the
invited articles on mechanism submitted to JECT in 2014, I do not see a better
explanation than that of the impact of seizures on the hypothalamic-pituitaryadrenal and hypothalamic-pituitary-thyroid systems.

49

�Book Five: The Road to Catatonia
During my days in medical school and residency training I assume I observed
catatonic patients. Indeed I recall walking through hospital wards, dressed in the
short white coat of the student, with two 500 mg vials of Amytal sodium in one
pocket, a metal autoclave box containing a sterile syringe and needles, a tourniquet
and bottled water in the other, to sedate the excited and the manic and to relax and
obtain the cooperation of the negativistic and the mute. But during the decades of
clinical practice as a research physician in New York and St. Louis hospitals, I cannot
recall recognizing catatonia as a distinct syndrome. In my research positions, I had
little front-line responsibility to examine and treat the acutely ill.
It was during my visit to the Bakirköy Hospital in Istanbul in 1965 that I saw
nude women, standing in rigid Christ-like postures in hospital windows and rows of
posturing men as we went through the wards. Catatonia is a systemic disorder of
acute onset with mutism, posturing, rigidity, and stupor, and at other times as
intense excitement and delirium. Patients remained ill for months and years filling
long-stay hospital wards. Now, we have the technical means and the skill to
recognize and treat these patients successfully and rapidly. Turan Itil, my research
colleague at the MIP in St Louis, and I were visiting the Istanbul Bakirköy hospital to
supervise a study of a new neuroleptic, butaperazine. Our arrival was welcomed by
a patient band, colorfully dressed in 19th Century Turkish pantaloons and
multicolored shirts, beating drums and cymbals, and playing the baglama string
instruments -- an image of a mental hospital before the psychopharmacology era.
My enduring interest in catatonia was aroused in 1980, when I became
responsible for supervising the care of acutely ill patients and teaching students on
the in-patient unit at University Hospital at Stony Brook. My experience with a fully
restrained delirious woman and the resolution of her illness excited my interest..

The Teaching Case

On a morning in the Fall of 1987 I was teaching an expert class in ECT when a
patient from the medical service was referred for evaluation. A class of five
graduate physicians saw a restless, delirious and febrile 25-year-old woman in fourlimb restraints, nasogastric and urinary catheters and intravenous fluids running.
When alert, she was negativistic, posturing, rhythmically thrashing, alternating
mute and screaming. She was suffering the systemic disease of lupus
erythematosus, an acute autoimmune disease, being treated with intravenous
methylprednisone for the lupus and sedated with haloperidol and lorazepam. An
EEG had shown seizure-like activity and phenytoin was prescribed to block
spontaneous seizures. She was in an acute manic and catatonic delirium.

50

�Was she a candidate for ECT? The physicians, influenced by the severity of
her systemic illness, the restraints, parenteral feeding, and manifest weight loss,
thought not, that the treatment was likely to do her more harm. They demurred
even after I described the rapid relief with ECT in three patients with the same
psychiatric complications of lupus that had earlier been reported by Samuel Guze at
Washington University. Contrary to the class opinion, the severity of her excited
illness supported treatment with ECT since the treatment was remarkably safe even
in the most systemically ill patients.

With consent of her family and her physicians, a course of ECT was begun on
hospital day 28. Within 10 days and 7 treatments the delirium was relieved,
restraints were lifted and cooperation improved. But family and physician fears and
prejudices against continuing ECT forced me to stop her treatment, a decision that I
strongly objected. She regressed rapidly, again required restraints, and her family
now pleaded for further treatment. A second ECT series from days 68 to 90
resolved her catatonic illness. By day 100 she was discharged with medical relief of
lupus and without signs of catatonia or delirium, to remain well and report the care
of her family at one-year examination.
The severity and life-threatening nature of her illness, the rapid resolution
with ECT, and my realization of her behaviors as “catatonia” intrigued me. Gregory
Fricchione, then chief of Stony Brook’s Consultation and Liaison Service and very
experienced with catatonia, having developed lorazepam treatment while studying
at Boston’s Massachusetts General Hospital, had referred her for ECT after failed
treatment with high doses of lorazepam. For the next few years we studied
catatonia together. I became fascinated with the remarkable change from a
delirious and moribund woman to a recovering mother with relief of a syndrome
that I had hardly studied. I became interested in the story – how catatonia was
discovered and described in Germany in 1874, how another German psychiatrist
incorporated catatonia in his concept of schizophrenia that prevented much
progress in its study.
Catatonia as a Type of Schizophrenia

In 1874 Karl Kahlbaum, the director of a private sanitarium in Görlitz,
Germany, clustered peculiar motor behaviors of some of his patients into a single
syndrome of “Die Katatonie.” In a rich text of 26 clinical vignettes, he clustered
mutism, immobility, negativism, posturing, staring, grimacing, stereotypy,
mannerisms, and several other motor signs as a single syndrome. The underlying
illnesses that brought the patients for hospital care varied, with 12 patients severely
depressed, nine suffering from seizure disorders, three with neurosyphilis, and two
with tuberculosis. In a poignant final chapter of his book, Kahlbaum sadly notes that
he could offer no useful treatment except to hope for spontaneous remission, which
actually did occur in some cases. Death was all too common. 49
51

�By 1899 Emil Kraepelin, the German psychopathologist, teacher, and author
of numerous textbooks, having recognized the same signs, published dramatic
photographs of posturing and grimacing patients. He observed his chronic mentally
ill patients for many years and characterized two principal syndromes. The patients
with delusions, language difficulties, and hallucinations that began during
adolescence and progressed to dementia were suffering from dementia praecox.
Those with depressed moods alternating with mania suffered from manic-depressive
illness. Catatonia was seen in both groups. In later editions of his textbooks,
Kraepelin described catatonia as a marker of dementia praecox.
This association of catatonia with dementia praecox was accepted by the
Swiss psychiatrist Eugen Bleuler who renamed the illness as schizophrenia. His
approach was based on the beliefs of psychoanalysis, seeing catatonic symptoms as
accessory manifestations of Freudian complexes, thereby marginalizing their
importance in the diagnosis of schizophrenia for generations of psychiatrists,
sidestepping the analysis of psychiatric nosology and obscuring efforts to
conceptualize catatonia.

When official classifications of psychiatric disorders by the American
Psychiatric Association emerged in the 1950s, schizophrenia, catatonic type was the
singular recognition for catatonia. This characterization dominated the psychiatric
classifications during all of the 20th Century. It was this association that I was
taught.
But Catatonia Is Not Schizophrenia

Awareness that catatonia was not limited to patients with schizophrenia
came slowly. By 1973, after examining the records of 2500 hospitalized patients
with extended follow-up at the University of Iowa, James Morrison reported that
10% met criteria for catatonia at their index admissions. Re-examination of the
records of those patients at a later date found 40% had, at some point, recovered
completely after treatment with sedative hypnotics or ECT. Morrison argued that
these recovered patients could not be examples of schizophrenia, a disorder for
which treatments, at best, reduced the severity of symptoms but did not relieve the
illness.

A year later Richard Abrams and Michael Alan Taylor, two students from my
classes at New York Medical College, identified 55 patients with one or more
catatonia signs admitted to two wards at New York City’s Metropolitan Hospital
over a 14-month observation period. Only four patients among these satisfied the
research diagnostic criteria for schizophrenia, while more than two-thirds met the
criteria for affective disorders, usually mania. They reported the salutary effects of
treatments and a factor analysis of the data identified two factors, one associated
with mania and good outcome with treatment.
52

�That same year, Alan Gelenberg in Boston described eight patients who
became toxic and febrile with severe Parkinsonian motor signs after receiving high
potency neuroleptic drugs. He cited the cases as instances of “the catatonic
syndrome.”

In 1980, Stanley Caroff in Philadelphia, after describing 60 reported cases of
neurotoxic responses to neuroleptic drugs, labeled an acute onset lethal catatonia
syndrome with fever, autonomic instability, altered consciousness, stupor, and the
rigidity and posturing signs of catatonia as the “neuroleptic malignant syndrome”
(NMS), a label that was widely adopted. He ascribed the syndrome to excessive
dopamine blockade and prescribed dopamine agonists such as bromocriptine. In
time we learned that these treatments were ineffective, and they were replaced by
lorazepam and ECT, the effective catatonia treatments today.
In Contrast to Schizophrenia, Catatonia is Treatable.

In 1930 William Bleckwenn, an American physician in Wisconsin, reported
that catatonia could be relieved by injections of 2.0 or more grams of amobarbital
(Amytal). Mute, staring, stuporous and posturing patients responded to injections
by speaking, answering questions, and self-feeding. These changes were reported
and also shown in a black-and-white film that was instrumental in launching the
practice I was taught.

A second effective treatment of catatonia, inducing grand mal seizures, came
de novo into the world on January 2, 1934 when Ladislas Meduna, a Hungarian
neuropsychiatrist, injected camphor-in-oil into the buttocks of chronic psychiatric ill
at the Lipótmezó sanitarium in Budapest. By happenstance, the majority of his
patients exhibited the negativism, mutism, and motor abnormalities -- now
considered signs of catatonia -- that were then considered signs of schizophrenia.
His method of induction was inefficient, however, eliciting a seizure in only one
third of the subjects. Behaviors changed little but the few that did improve
sufficiently impressed him to continue.
Later that year he used a better method of intravenous injections of
pentylenetetrazol (Metrazol), which elicited fuller and more reliable seizures. The
changes in behavior were so remarkable that he reported his cases in 1935 and
again a year later at a meeting in Switzerland that canvassed experiences in new
treatments of psychosis from 22 countries, setting the stage for worldwide interest
in seizures as therapy. Three years later he published his experience with 110
patients, reporting relief in more than half, especially among those acutely ill with
catatonia.

A year after that, the Italian physicians Ugo Cerletti and Luigi Bini
demonstrated the same relief-inducing seizures using electricity rather than
chemical injections. These treatments were remarkably successful in relieving
53

�catatonia, so much so, that once clinicians caught on, it was possible for a
neurologist in 1981 to ask decades later, “Where have all the catatonics gone?”
Is NMS a Form of Catatonia?

Recognition of the neuroleptic malignant syndrome came slowly into
professional awareness. The occasional sudden death of a psychotic patient treated
with chlorpromazine or other potent neuroleptic drugs raised little intellectual
interest until the Caroff report appeared. After reading his description we at Stony
Brook recognized three patients treated with neuroleptics who met his criteria for
NMS. Repetitive motor movements, mutism, posturing, and negativism marked
each story. We discontinued neuroleptic medications and, following Caroff’s guide,
prescribed bromocriptine. One patient responded slowly, but two did not. ECT
brought quick relief. Although my curiosity about catatonia was not aroused until
we treated the woman in delirious mania described earlier, we did find other cases
of NMS. 50

At the height of the summer of 1976, a 23-year old agitated and aggressive
psychotic man under my care at the Central Islip Psychiatric Center was refusing
food and fluids and required restraint and sedation. Intramuscular haloperidol was
administered. The ward was incredibly hot, he became dehydrated, febrile, suffered
a seizure, became stuporous, and died within 12 hours. Neither physical nor
psychological post-mortem reviews suggested a compelling reason. In retrospect,
his acute death was an unrecognized example of NMS, the toxic syndrome
associated with haloperidol that was waiting to be discovered.

Another example of NMS was the death of Libby Zion, an 18-year-old college
student being treated for depressed mood with phenelzine. In the summer of 1984
she was admitted to New York Hospital febrile, agitated, and disoriented with
abnormal motor movements. Meperidine was administered, her agitation worsened
and parenteral haloperidol was added. Now in stupor, her temperature quickly rose
to 107oF and she died. Her family sued the hospital for malpractice and in 1993 I
was asked to review the records as an expert witness in the hospital’s defense. The
many initial diagnoses did not consider NMS, but by the time of the legal case her
experience was recognized as an example of neuroleptic-induced malignant
catatonia.

As NMS became increasingly recognized, various treatments were tested. By
1983 Gregory Fricchione described four cases in which high doses of lorazepam and
withdrawal of the neuroleptic relieved the syndrome. Case reports of lethal
catatonia secondary to neuroleptic use followed quickly, each affirming the
connection and citing relief with cessation of neuroleptic use and treatment with
benzodiazepines and ECT. The significant connection between malignant catatonia
and prior experience of catatonia was made by Denise White of South Africa who
described five patients in whom the catatonia signs preceded the administration of a
neuroleptic. In a second report a year later catatonia was presented as a precursor
54

�to the malignant state, raising the question as to whether the neuroleptic malignant
syndrome, malignant catatonia, and the non-malignant forms of catatonia were
manifestations of the same psychopathology.

The acceptance of NMS as a form of catatonia was slow, inhibited by the
different treatments offered. Stanley Caroff and his colleagues believed that NMS
resulted from the neuroleptic inhibition of dopamine activity and focused treatment
with dopamine agonists bromocriptine and amantadine. Because the fever, muscle
rigidity, and weakness simulated malignant hyperthermia, they augmented
treatment with the muscle relaxant dantrolene. Despite poor responses and
continuing deaths, many authors applied this prescription. An international debate
ensued, carried on for more than two decades, whether NMS was best considered an
abnormality of dopamine metabolism and treated with dopamine agonists or
malignant catatonia and treated with benzodiazepines and ECT. The debate argued
at meetings of psychiatric societies and in the literature with Stanley Caroff, Gregory
Fricchione, Steven Mann, Patricia Rosebush, Theresa Rummans, Michael Taylor,
Gabor Ungvari, Denise White, and myself as the protagonists. The debates
strengthened my interest in catatonia, as I viewed NMS as a form of malignant
catatonia.

Essential to the different views was the failure to recognize the signs of
catatonia. For many observers the essence of NMS was the fever, autonomic
instability, and muscle rigidity, encouraging belief in an overlap with malignant
hyperthermia. Interest in catatonia was minimal, blocked by the prevailing belief
that catatonia was schizophrenia, despite the reality that few NMS patients met the
criteria for the thought disorder, impaired speech, delusions, and hallucinations that
characterized schizophrenia. Further, treatments of NMS-classified patients with
barbiturates and benzodiazepines were considered to risk tolerance development
and dependence, beliefs that were substantiated by the FDA’s restricted prescribing
rules. Dosing was limited to a few milligrams of lorazepam, inadequate for the relief
of catatonia. Few hospitals had ECT treatment units so clinicians could not
prescribe this treatment--but all could prescribe dopamine agonists and dantrolene.

Then, in 1990, Michael Taylor presented a detailed argument distinguishing
catatonia from schizophrenia in a historical and clinical review of its 100-year
history. He described both retarded and excited forms of catatonia and detailed
effective treatments with barbiturates, benzodiazepines, and ECT. He connected the
motor signs to the pathophysiology of the frontal lobes, presenting catatonia as an
entity of many causes and many forms, thus challenging its consideration solely as a
form of schizophrenia. 51
Simultaneously, the neurologist Daniel Rogers from the Burden Neurological
Hospital in Bristol, England presented a similar challenge. Of the100 chronic
schizophrenic ill he had examined, many exhibited catatonia and Parkinsonism.
Their presentations, though, were similar to those that had occurred during the
1918 encephalitis epidemic, indicating that catatonia was not confined to
55

�schizophrenia. He described a systematic examination and a rating scale to identify
catatonia, defining catatonia within neurology practice. 52
Both Taylor and Rogers questioned the Kraepelinian dictum that catatonia
was a form of schizophrenia. Their doubts were consistent with my own that
catatonia was not a marker of schizophrenia. That led me to argue for an
independent status for catatonia in the illness classifications.
The Drive to Official Definition.

Was catatonia a singular identifiable disorder with common characteristics
and homogeneous pathophysiology, or a galaxy of psychiatric aberrations with
different pathologies? The 1980 DSM-III identified catatonia by the presence of at
least one of the five signs of stupor, negativism, rigidity, excitement, or posturing. My
Stony Brook colleagues culled the more detailed descriptions of catatonia signs by
Kahlbaum, Kraepelin, Taylor, Rogers, Rosebush, and Lohr and Wisniewski to
develop a 23-item list of identifiable signs scored on a 3-point scale and described a
systematic examination that could be used to derive a diagnosis.

Using that rating scale in 1994-95 we examined every patient admitted to
our ward for catatonia signs. In potential catatonia cases, prescribed neuroleptics
were quickly withdrawn, the effect of a single dose of intravenous lorazepam or
diazepam was tested, and the patients treated with high doses of diazepam or
lorazepam or with ECT. We next surveyed all patients admitted to the Psychiatric
Service and the Psychiatric Emergency Room of University Hospital during a 6month period using our rating scale. Of 215 patients examined, 9% had two or more
signs of catatonia.
In the next year, of 470 patients examined we admitted 28 patients with four
or more signs of catatonia to the in-patient service of University Hospital. Of these,
15 were affectively ill, 4 psychotic, 3 with NMS, and 6 with various systemic medical
illnesses.
A review of the University Hospital records for the 5-year period beginning
in 1985 with discharge diagnoses of schizophrenia, catatonic type (DSM 295.2)
identified 43 charts. Of these, seven patients were also charted or discharged as
affective disorder, five as organic affective disorder, and seven as schizophrenia.
Eleven had been treated with ECT, with full relief in eight, confirming again the
remarkable efficacy of seizures to relieve catatonia.
The Sedative Verification Test

Could the relief of catatonia’s signs with intravenous lorazepam confirm the
diagnosis? Since William Bleckwenn had rapidly resolved catatonia with injections
of amobarbital, intravenous amobarbital had been widely used to gain speech for
the mute, encourage feeding and toiletting in the negativistic, quiet the aggressive,
56

�and arouse the stuporous. In 1983 Gregory Fricchione recommended that
amobarbital be replaced by lorazepam and that the reduction of catatonia signs be
considered a verifying test for catatonia. As verification of catatonia in patients with
2 or more catatonia signs for 24 hours or longer, we adopted the criterion of a 50%
reduction in the catatonia rating scale score, if it occurred within 10 minutes of the
intravenous administrations of 1 to 2 mg lorazepam. The prescription of 3 mg/day
of lorazepam, increased rapidly by 3 mg increments to 30 mg/day became our
treatment protocol. Of 28 patients identified with catatonia signs, 23 recovered
with lorazepam dosing alone, 5 did not. Of the four who consented to ECT, three
recovered with 2 to 3 treatments, while one required 11 treatments. This
experience was published in 1996 and the protocol became our standard diagnostic
and treatment procedure; within a few years these methods were widely adopted
and central to the recommendations of the textbook of catatonia that Taylor and I
published in 2003. 53
The Many Faces of Catatonia.

Beginning with our recognition of NMS, Michael Taylor and I soon accepted
other syndromes such as delirious mania, toxic serotonin syndrome, pervasive
refusal syndrome, NDMAR encephalitis, Self-Injurious Behaviors in adolescents, and
several other labeled syndromes that exhibited multiple signs of catatonia that were
relieved by known treatments. We thought that the syndromes must have a
common pathophysiology since the signs were overlapping and the same
treatments were effective.

Delirious mania. Catatonia is recognized in a sedated form of stupor,
mutism, posturing, and negativism. It also is recognized in an excited, manic state.
Catatonia is more often recognized among manic patients than among those with
depressive moods or psychosis. Among the patients admitted to our psychiatric
facility so excited and overactive as to require physical restraint, we increasingly
recognized the signs of catatonia. Some vacillated between aggressive screaming
and posturing mutely, with peculiar repetitive movements. Others were febrile,
hypertensive and tachycardic. Some were delirious, all were confused and poorly
oriented. Many had been treated with haloperidol or other high potency
neuroleptics precipitating the malignant febrile form of illness. Some had seized
and anticonvulsants had been prescribed.

Many patients required four-limb restraints or were maintained in a padded
isolation room. We withheld neuroleptics, prescribed high doses of parenteral
benzodiazepines, and were often able to minimize the excitement. But the severity
of the fever often forced more immediate treatment with ECT. Daily ECT found
relief of excitement, delirium, and fever had occurred by the third day in almost
every case.

57

�Taking patients who are suffering a malignant systemic illness and subjecting
them to the risks of anesthesia and induced seizures is counter-intuitive. But the
fatality rate of febrile catatonia and the life-saving quality of daily ECT was
demonstrated in 1952 by Otto Arnold and H. Stepan. They had treated 18 patients
in their first clinic in 1947/48 with delayed treatments and 16 in their second
1949/50 with prompt treatments. Of the 18, 15 died and 3 survived; of the 16, 13
survived and 3 died, The lesson of daily or multiple seizures was learned, and I
applied their experience on numerous occasions .

The Stony Brook hospital unit consists of rooms around a circular core. From
the entrance to the ward it is possible to see the doors to 3 to 5 rooms. I often came
to the ward by 7 am, seeing a chair outside a room, with an aide watching the
patient inside. These were the patients under 1:1 observation and care, often the
most delirious and excited, or late adolescents with self-injurious behaviors. A 29year-old HIV infected man had become severely depressed, suicidal, and delirious,
refusing his HIV medications. In the ER, he was injected with haloperidol, became
agitated and febrile. On the ward he was in 4-limb restraints, 1:1 observation, and
parenteral fluids. After increased dosing with lorazepam with little response, we
induced his first seizure. That afternoon he was out of restraints, only to relapse
slowly. His temperature elevated and treatments were repeated on each of the next
two days, with complete relief, cooperation and full self-care.
A 20-year-old college student was admitted in delirious excitement. After 4
daily ECT sessions he was discharged to continue out-patient ECT for a total of 10
treatments. He completed his college courses. A 25-year-old musician in delirious
mania was relieved by 5 daily ECT sessions, fully recovered by a full course of 12
treatments. Four years later, he was re-admitted after returning from an overseas
working trip during which he had become exhausted. Again, daily ECT relieved the
syndrome and he remained well.
In a review of the hospital records I found 9 additional patients with
delirium, mania, and signs of catatonia who had responded well to ECT. These
experiences encouraged additional treatment of non-manic delirious patients and
led me to recommend that ECT was an effective treatment for delirium, regardless
of cause.

An interesting misconception developed in the 1980s as the label “bipolar
disorder” was popularized as a diagnosis after its delineation in DSM-IV. Depressed
patients with a single manic episode in their history were labeled as suffering from
bipolar disorder, neglecting possible catatonic features. The treatments for bipolar
disorder span the breadth of the pharmacy, applying atypical antipsychotics, mood
stabilizers, lithium, anticonvulsants, anxiolytics, sedatives, and antidepressants in
complex combinations with notoriously poor outcomes. As excited patients are
forcefully restrained, treated with haloperidol and other potent neuroleptics, they
rapidly develop seizures, fever, become mute, refuse fluids and food, become
dehydrated and die, sometimes with fever and inanition or by improper tube
58

�feeding. Recognizing catatonia in severely manic and delirious patients and offering
catatonia treatments is an unheralded aspect of the understanding of mania.
But delirious mania is still not recognized in the revised nomenclature of
DSM-5 published in 2013. In his critique What Psychiatry Left Out of DSM-5, the
historian Edward Shorter identifies delirious mania as just one of many illnesses
that are not recognized. 54 Michael Taylor makes the same observation in his
personal history as researcher and clinician titled Hippocrates Cried. 55

Toxic serotonin syndrome. A 59-year-old married woman was admitted to
University Hospital with a long history of treatment for mood disorder. Her most
recent prescription had been the sedative trazodone at bedtime. She developed
urinary incontinence and the serotonergic agent nortriptyline was prescribed.
Within five hours after a single 25 mg dose, she became fearful, tremulous, sweating,
tachycardic, hypertensive, incontinent of urine with explosive diarrhea. Four days
later, she exhibited seizure-like movements of her extremities and lost
consciousness. At the psychiatric emergency room she was mute, rigid, tremulous,
tachycardic, sweating, and hypertensive. The examination was consistent with NMS
and lorazepam [1mg q6h] was prescribed, relieving the motor and vegetative signs
within two days. She remained depressed and retarded, however, and responded
well to ECT with lorazepam as continuation treatment. She had not been exposed
to neuroleptic agents as her husband, a high school biology teacher insisted,
showing his daily record of her symptoms and all administered medications. Toxic
serotonin syndrome (TSS) is an acute change in mental status with systemic signs
following the addition or increase in dose of a known serotonergic agent to an
established psychoactive medication regimen. No effective treatment is known
other than withdrawal of the precipitating medications and supportive care. The
overlap in signs of toxic serotonin syndrome with NMS, and the successful response
to catatonia treatments, argues that toxic serotonin syndrome is best considered
and treated as a form of malignant catatonia.
Pervasive refusal syndrome. A syndrome described in the UK in 1991 meets
our criteria for catatonia and represents another face of the syndrome. Four British
girls between the ages of 9 and 14 suffered “a profound and pervasive refusal to eat,
drink, walk, talk or care of themselves in any way over a period of several months.”
They required nasogastric tube feeding and spent such prolonged periods in bed
that they “occasionally requiring manipulations of the joints under general
anesthetic to prevent contractures.” After extended hospital care and family and
individual psychotherapies they eventually recovered.
A report of an 8-year old girl who stopped eating and drinking after a viral
infection and who was hospitalized for more than a year before being returned to
her family in partial remission was brought to my attention by Donald Klein; did she
meet our criteria for catatonia, he wondered. We agreed and asked the report’s
authors whether not testing and treating for catatonia was unethical. The authors
59

�offered a complex rejoinder without explaining the failure to apply proper tests.

A decade later I was consulted by the Irish child psychiatrist Fiona
McNicholas about an 11-year old prepubertal girl who developed symptoms of
asthma, abdominal pain, and insomnia. She refused to attend school or to eat or
drink, became withdrawn and mute, and required nasogastric feeding and hospital
care. After many months, a video of her behavior was sent to me. Mutism,
negativism, and posturing confirmed catatonia. Lorazepam testing and treatment
was recommended. The parents refused medication treatments but participated in
family therapy. At first the girl took part but in time she refused. After 18 months of
hospital care, as the date for her scheduled return home was imminent, she began to
speak, eat and care for herself. Over the next six years she completed her schooling
and went on to University.
These cases are labeled “pervasive refusal syndrome.” Less than 30
additional cases are cited in the literature, with a 3:1 ratio of girls to boys. Each
reported case required prolonged hospital care. Similar cases are labeled “elective”
or “selective mutism.” The patients meet criteria for catatonia but it remains
difficult for many physicians to consider catatonia except in the shadow of
schizophrenia. The tragedy in each case is the availability of effective treatments
and the clinicians’ refusal to offer a proper diagnosis and effective care.

Recent descriptions of a “Resignation Syndrome” among Syrian refugees in
Sweden and a “Nodding Syndrome” among children in the wars in Uganda find
behaviors of withdrawal, mutism, loss of self-care, failure to feed that clearly mimic
catatonia mutisms. Both these syndromes should be considered forms of catatonia.
Such recognition would offer effective relief and bring these syndromes under the
catatonia umbrella.

Anti-N-Methyl-D-Aspartate Receptor Encephalitis. A 2008 case report in
the New England Journal of Medicine describes a 26-year-old woman admitted for
headache, behavioral changes, abnormal movements, and mutism of seven weeks’
duration. After extensive laboratory examinations a serum anti-NMDAR
encephalitis test was reported positive, supporting the presence of an autoimmune
disease. Throughout her illness she had been somnolent, mute, and negativistic,
with repetitive movements of her arms and mouth, but these were not recognized
nor treated as catatonia. An ovarian teratoma was found, surgically removed under
anesthesia, and the encephalitis syndrome resolved within a day. Was the removal
of the tumor or was the anesthesia the therapeutic agent? The rapidity of the
resolution and her course favor the probability that catatonia was relieved by the
anesthesia.

Another report described a 16-year-old boy with protracted stupor,
psychomotor retardation, mutism, posturing, stereotypical movement, refusal to eat
and drink, and episodic agitation. A positive blood test supported an anti-NMDAR
diagnosis. The presence of catatonia was not recognized and no consideration given
60

�to its treatments. Instead, haloperidol and other antipsychotic agents were
prescribed worsening the symptoms. After seven months of nursing care the illness
abated. The experience was trumpeted as a clinical lesson in the American Journal
of Psychiatry despite the failure to recognize catatonia or to consider its treatment.
The signs of catatonia were commonly described in a 2008 report of 100
cases of encephalitis with positive NMDAR serum tests, but neither catatonia nor its
treatments were discussed. Case reports now dot the literature with most patients
being female and with resolution after resection of ovarian teratomas when found.
But the syndrome is also reported in males.

Limbic encephalitis is an acute autoimmune neurological disorder first
described in the 1960s as a ‘paraneoplastic condition’ – self-poisoning systemic
changes induced by tumors. More than 80 different autoimmune disorders are
described in the medical literature. The pathophysiology is poorly understood and
the treatments are empiric and of limited efficacy.

The diagnosis of anti-NMDAR encephalitis depends on a positive serum or
cerebrospinal fluid antibody test. The recommended treatments are tumor resection
when found and non-specific immunotherapy (corticosteroids, intravenous
immunoglobulin or plasma exchange) or immunotherapy medications
(cyclophosphamide or rituximab). These treatments have not been demonstrated
to be effective and are associated with prolonged illness. My appreciation is that
these patients have a systemic illness of acute onset, with a positive chemical test,
with a high incidence of tumor, and frequently expressed as catatonia. These
characteristics assure the syndrome's definition within the medical model.
Treatments for catatonia, when applied, have successfully relieved the illness.
A heightened enthusiasm for this diagnosis is reflected in an editorial in the
British Journal of Psychiatry in April 2012 calling for laboratory tests for antiNMDAR encephalitis in “all individuals with a first presentation of psychosis, or
people with psychosis and features of autonomic disturbance, movement disorder,
disorientation, seizures, hyponatraemia or rapid deterioration . . . with the
possibility of antibody-mediated encephalitis in mind.” The recommendation
continues: “This assessment should include, as a minimum, a neurological and
cognitive examination and early serum testing for antibodies against the NMDA
receptor and voltage-gated potassium channel. All patients testing positive for
these serum antibodies should be referred to neurological centres with expertise in
managing these cases.”

The enthusiasm for this diagnosis is also illustrated by the rapidly increasing
case-report literature. The initial references to anti-NMDAR encephalitis cited in
Medline are in 2007. By July 2014, the number had increased to 230 citations. and
by February 2021 increased to 1588 with 83 with catatonia, and 19 with the
catatonia treated with ECT.
61

�As with patients with pervasive refusal syndrome, recognizing catatonia in
anti-NMDAR encephalitis offers effective treatment. It is reasonable to consider
catatonia in the differential diagnosis and offer its tests and effective treatments but
this is still too seldom done.

Self-injurious behaviors in mental retardation and autism. Patients
identified in the past as suffering from mental retardation are now often discussed
as examples of autism or autism spectrum disorders. Many exhibit persistent
repetitive movements, often screaming and hitting themselves. Such self-injurious
behaviors cause much damage. Restraints, antipsychotic medications, and
deconditioning procedures are poorly effective. Courses of ECT, however, markedly
reduce the repetitive behaviors and many young patients have been returned to
home and community. They do require continuation ECT, however. A benefit of the
success of these treatments has encouraged broader acceptance of ECT among child
and adolescent psychiatrists.

Other repetitive behaviors in children and adolescents are recognized as
obsessive compulsive disorder (OCD) and Gilles de la Tourette syndrome (GTS).
These are commonplace among adolescents labeled as suffering autism or autism
spectrum disorders. A 2014 report describes an 18-year-old man with a 8-year
history of progressively severe GTS that responded rapidly to ECT. The scientific
literature is speckled with incidental relief of GTS and OCD with ECT that
encourages a more inclusive application of catatonia criteria to these syndromes
with the application of catatonia treatments.
The DSM Classification Debates: Where Should Catatonia be Classified?

The initial classification of psychiatric disorders published by the American
Psychiatric Association in 1952 was revised in 1968 and again in 1980. In each
version catatonia was singularly recognized as schizophrenia, catatonic type (295.2),
making catatonia signs markers of this broad class of psychosis and neglecting
evidence of catatonia among other disorders. The catatonia-is-schizophrenia
equation led physicians to prescribe neuroleptic drugs whenever catatonia signs
were recognized. Such treatments were not only unhelpful, but they often
precipitated a malignant neurotoxic state, worsening the illness, and causing death.
Only when the clinician distinguished the signs of catatonia were the patients
appropriately treated with barbiturates, benzodiazepines, and ECT. Taylor and I
argued that it was necessary to divorce Kraepelin’s marriage of catatonia to
schizophrenia and to recognize catatonia as a distinct, independent syndrome
warranting a home of its own.56
The 1994 revision (DSM-IV) retained the five types of schizophrenia and
added the independent class of “catatonia secondary to a general medical condition”
(293.89). I was pleased that an independent syndrome was recognized and hoped
that such a designation would increase its recognition and encourage the
62

�prescription of effective treatments. Indeed, over the next two decades, recognition
of catatonia increased and reports of malignant catatonia declined.

Another DSM revision was planned in 2008 with catatonia assigned for
consideration in the Psychosis Work Group. By this time an extensive literature
supporting catatonia as an independent entity had developed and a consortium of
catatonia scholars that I led asked that the catatonia type of schizophrenia (295.2)
be deleted and that catatonia be designated by a single code as a distinct, definable,
and treatable syndrome. The publication of DSM-5 in May 2013 deleted the class of
schizophrenia, catatonic type (295.2); continued the class of catatonia secondary to
a systemic medical condition (293.89); offered a class of “unspecified catatonia”
(781.89); and included a “catatonia specifier,” coded as xxx.x5, for ten principal
disorders including depression, bipolar disorder, and schizophrenia types. (A
specifier is a label added to a primary diagnosis to indicate a subtype of the primary
diagnosis. It avoids a decision about which aspect of the behavior, the psychosis or
the catatonia, is the verifiable diagnosis.)

The divorce of catatonia from schizophrenia has led many psychiatrists to an
earlier prescription of effective treatments, lowering rates of chronic illness and
death. Many variants of catatonia with unique effective treatments are now
recognized. Once considered rare, catatonia is now reported in about 10% of the
populations admitted to psychiatric hospital units, assuring earlier recognition and
more effective treatments.

During these recent DSM deliberations the initial debates occurred between
classical scholars represented by Gabor Ungvari and the catatonia scholars
beginning with the work of Michael Taylor and Richard Abrams in 1970s. Ungvari
supported the Kraepelin image of catatonia as the abnormal motor signs found
among patients with chronic psychosis. He had treated hospitalized long-term
Chinese ill in Hong Kong with lorazepam and saw little benefit, but he had not tested
the benefits of ECT. Modern scholars, however, are recognizing catatonia in acute
treatment hospitals, finding many cases that meet the Kahlbaum criteria for
catatonia. When Kraepelin identified catatonia in his chronically ill patients, he
assumed that he was describing the same syndrome. The experience of the DSM-I to
DSM-III classifiers was with similar chronic hospitalized ill since their office
practices of psychotherapy did not accept catatonic patients – those with mutism,
negativism, and posturing, for example. By the time of DSM-IV’s publication in
1994, however, some scholars had identified the catatonia described by Kahlbaum.
Their experiences led to the addition of the special class of “catatonia secondary to a
medical condition.”
The connection of the catatonia scholars to the Psychosis Work Group was
through Stephan Heckers, the chairman of Psychiatry at Vanderbilt University. That
he accepted our picture of catatonia as an independent treatable syndrome is seen
in his retrospective review published at the beginning of 2015. After examining 339
hospital charts, two or more signs of catatonia were recorded in 300 patients with
63

�232 validated by positive relief with lorazepam treatment or ECT. The mean
lorazepam dose was 6 mg/day with 84% responding. ECT was applied in 20% with
42 of 45 (93%) responding.
Publication of a Catatonia Textbook and an ACTA Supplement

Taylor and I decided to summarize our experience with catatonia and
published Catatonia: A Clinician’s Guide to Diagnosis and Treatment, a 256-page text
in 2003. At the same time we presented our experience in a review in the American
Journal of Psychiatry.
We are clinicians, not laboratory scientists. We identify illnesses, use
verifying tests, and explore effective treatments. We recognize that inducing
seizures is a most remarkable and unique discovery in medicine, one that has been
unfairly stigmatized by the professions of psychiatry, neurology, and psychology, as
well as by the public. The science is poorly taught in medical schools and
psychiatric residencies, many of which have no facility for its use, thereby denying
relief to many of the mentally ill who they serve.

Since that publication we have explored catatonia further. A decade later it
seemed timely to bring our knowledge up-to-date and I published a review as a
supplement to the Acta Psychiatrica Scandinavica. It is a biography of the syndrome,
how it was developed, its early exploration, the incorporation in schizophrenia, and
its rediscovery as a definable distinct entity. The essay reviews the arguments
about its classification, and the new forms that are recognized.
It also discusses an interesting association with animal tonic immobility, a
defense described in prey animals. Many catatonia signs – stupor, mutism,
posturing, repetitive behaviors – are characterisic of animals when they find a
predator in their neighborhood, and I suggest that catatonia is a relic of human
biologic history. Subsequently, I have argued that catatonia is an atavism, a relic of
the past when Homo sapiens was both predator and prey, with the defenses of flight,
fight, and dissimulation that are retained today.
How is catatonia best recognized and what is its place in the medical world?
We soon came to see it as a behavior syndrome, severe and occasionally fatal but
treatable, so much so that its resolution left no residual marks. Edward Shorter and
I discussed these many aspects of the syndrome and in the fall of 2016 resolved to
write its history. We organized our thoughts and decided that we could best assess
the syndrome as an atavism, a relic of the primitive stages of animal development
when fears encouraged defenses of freeze, flight, or fight. We formulated these
thoughts in an essay asking "Does persisting fear sustain catatonia?" in the Acta
Psychiatrica Scandinavica in 2017. 57
A proposal for a volume by Shorter and myself was accepted by the Oxford
University Press, and in July 2, 2018 the first copies of A Madness of Fear: A History
64

�of Catatonia with the deep blue cover image of Caravaggio's Medusa were published.
The text describes the 150 year story of a systemic medical syndrome, the
successful application of the Hunterian model of the identification of a systemic
illness. It joins neurosyphilis and melancholia as among the few behavior disorders
that is identifiable, verifiable and successfully treatable.

65

�Book Six: Melancholia and the Medical Model of Diagnosis
After publishing our text on Catatonia in 2003, MickeyTaylor and our wives
Ellen and Martha met for a celebratory lunch in Chicago.
"Well, what is next?"

We agreed that Melancholia was a discussable syndrome -- multiple forms
were widely recognized, each responsive to the tricyclic imipramine and to ECT,
and a verification test in the dexamethasone suppression test had been described.
Melancholia syndrome met our criteria for a medical diagnostic syndrome, parallel
to our image of the catatonia syndrome, and we both had successfully treated
melancholic patients. 58

Like catatonia, melancholia is not recognized as a clinical entity in any of the
American Psychiatric Association Diagnostic and Statitical Manuals, although it is
widely described in the clinical literature. Melancholia is accepted as a descriptor or
modifier for DSM diagnoses, not as a distinct identifiable entity, not accorded a
specific code. As a consequence its study is not well defined, not recognized in the
citation indices, and is poorly studied; it is buried in the Major Depressive Disorder
and Bipolar Disorder categories. The parallel with the catatonia story is uncanny. 59

During my Hillside Hospital experience, the treatment of severely depressed
patients, suicidal, anorexic, insomniac, mute and stuporous, with ECT was
remarkably effective. Often, inducing seizures daily resulted in complete relief in 24 days, with suicide risk, appetite, insomnia and withdrawal fully relieved. In our
RCT study of chlorpromazine and imipramine, we identified a population of
psychotic depressed patients that responded to both agents. 60

In my days in Missouri, we often identified melancholic patients but their
diagnosis and treatment was of no particular interest. In our studies of ECT at Gracie
Square, the clinicians recommended psychotic depressed, postpartum and partum
depressed for treatment without our particular attention to their identification.

The Dexamethasone Suppression Test: By the 1960s, chemists had
reported serum cortisol measures to be elevated in melancholic patients. By 1972,
the Australians Davies, Carroll and Mobray reported that a straighforward test, the
Dexamethasone Suppression Test (DST) was a marker of severe psychotic
depressive illness. Diurnal serum cortisol levels were elevated, and administration
of the steroid dexamethasone failed to suppress the elevated levels. One report by
Bernhard Carroll intrigued me. Five severely ill melancholic patients with abnormal
DST responded clinically to courses of ECT; their DST normalized. Two relapsed,
again with abnormal DST tests; re-treatment with ECT resulted in clinical
improvement, again with normalization of the DST. 61 Was the DST a marker of
melancholia and predictor of the response to ECT?
66

�I had been asked to supervise a psychiatric unit at the Long Island Northport
VA in 1972. I organized clinical trials of a potential psdychotropic drug flutroline,
which we found clinically ineffective. In 1968, the Fellow supervising treatments
Yiannis Papakostas, accepted the tasks of developing the chemical tests for cortisol
and TSH testing patients before and during the course of ECT.62 Of 20 unipolar
melancholic patients, 16 exhibited abnormal DST. Of the 14 treated with ECT, all
test normalized with recovery. These findings stimulated interest in cortisol as a
test of a specific form of depressive illness.

Over the next few years, numerous reports associating the DST and
depressive disorders, some finding a close association with severe depression and
psychosis, others finding poor relations. The APA TAsk Force on Laboratory tests
concluded that the test was not useful in identifying major depressive illness. 63 As I
and Bernard Carroll noted, a laboratory test with high specificity for melancholic
depression was applied to a broad class of "major depressive illness" that included
neurotic and characterological depressions, those unhappy with their social status
and lives. The patients with positive DST tests were the severely ill, often suicidal,
unresponsive to psychological therapies, but responsive to the more effective
antidepressant tricyclic medications and ECT. Never the less, the DST was rejected
as a test of a specific form of depressive illness; each variation of the DSM (-III, IV, 5) discarded all laboratory tests for the diagnosis of any of its hundreds of described
conditions.
Earlier I described my development of the CORE collaborative studies of
depressed patients treated with bitemporal ECT with continuation treatments
either lithium and nortriptyline or ECT. The study was an excellent opportunity to
test the DST and severe depressive illness, but the NIMH committee and managers
reviewing the study budget, rejected funding for the DST, justified by the APA Task
Force report. Never the less, we examined the rating scales of our depressed
patients for evidence of the loss of pleasure in all, or almost all, activities or lack of
reactivity to usually pleasant stimuli at baseline. Of 489 patients in the CORE study,
311 (63.6%) met criteria for melancholic features. The overall remission rate was
68.1%, with higher rates (78.7%) for those who did not meet the melancholia
specifier criteria and 62.1% of (or more) of six cited vegetative signs of
melancholia. The specifier is added on the basis those with melancholia specifier
(42). We concluded that the approximation of "melancholia" in our patients was a
poor substitute for the DST.64
After our meeting in Chicago, a flurry of letters, interim reports, literature
searches, led to our publication in the Spring 2006 by Cambridge University Press
of our melancholia textbook. 65 We described the century-old experience, defined
the syndrome by psychopathology and laboratory tests, treatments by medication
and ECT, and argued for its recognition as a distinct entity in psychiatric
classifications. The book was well presented but was priced very high, the
advertising minimal, and the distribution disappointing.
67

�Increasing interest in melancholia led to an international conference in
Copenhagen of authors who had studied melancholia, also in 2006.66 By the
conference end, melancholia was defined as an identifiable mental illness, the DST
was agreed as a defining test, and ECT as a definitive treatment. The argument for a
unique identity among behavior illnesses was again made. Discussions with
members of the DSM-5 panel for depressive illnesses were strongly made, but again
ignored in DSM-5 in 2013.
Disappointed with our failure to convince clinicians about the unique
qualities of melancholia, both Taylor, in his book Hippocrates Cried 67, and I, joining
with Edward Shorter, described the story in Endocrine Psychiatr that we published
in 2010.68

At this editing in March 2021, melancholia iremains buried among the
diverse illnesses coded as major depression and bipolar depression. Like catatonia,
the illness needs efforts to identify its biology, to bring it out of its burial, much as
was successfully done for catatonia.

68

�Book Seven: Studies in Electroencephalography (EEG)
EEG Introduced to Hillside Hospital 1953
Electrical rhythms from the intact human scalp were first described in 1929
by Hans Berger, a German psychiatrist. Within two years, in his third report, he
described the changes associated with morphine, scopolamine, and other
psychoactive drugs. Spontaneous seizures and the rhythms of the inter-seizure EEG
in epilepsy were next described. Would EEG recordings distinguish effective from
ineffective treatments in the induced seizures of ECT? Could the EEG identify a
successful course of treatment? Were the seizures induced by pentylenetetrazol the
same as those induced by electricity or by insulin?
While I had seen electroencephalograms of patients as a medical student and
a resident at Bellevue Hospital, I had no technical experience with the procedure.
Reports of recordings during epileptic seizures induced by Metrazol, the chemical
used by Meduna to induce seizures in schizophrenic patients, had dotted the
literature since 1938 followed by similar descriptions for insulin coma and for ECT.
During each procedure EEG frequencies slowed, amplitudes increased, and sharp,
spike-like waves appeared. Missed and partial seizures induced little or no change
in the EEG. Greater slowing of frequencies and increases in the duration and
amplitudes of slow waves and spike activity marked more intense seizures. The
altered rhythms persisted for weeks and, in a few patients, for months after the
treatment course ended.

I sought training in recording and interpreting the EEG. As my residency at
Hillside was to be completed in December 1952, I applied for a fellowship at the
Mount Sinai Hospital in New York City beginning January 1953. (By this time, too,
after five and half years of postgraduate medical training I opened a private-practice
community office in neurology and psychiatry, which I did in the summer of 1953 in
Great Neck, Long Island. )
With Hans Strauss and Mortimer Ostow I learned how to apply scalp
electrodes, maintain the EEG recorders, and interpret the records. The Medical
Director Joseph S.A. Miller, established an EEG Service with a Grass
electroencephalograph purchased with a $5,000 grant from the Dazian Foundation
obtained by Dr. Israel Strauss, the Founder of the Hospital. By the end of 1953 I had
appointed and trained an EEG technician and developed a protocol for the study of
the changes in EEG associated with ECT. An application to NIMH funded a five-year
study under Grant MH-927 "Altered Brain Function Following Electroshock" in the
summer of 1954.
Hans Berger had recorded rhythmic frequencies of 4 to 16 Hz. The more
common 8-12 Hz waves were labeled alpha waves, the faster (&gt;13 Hz) as beta, and
the slower labeled as theta (4.0-7.5 Hz) and delta (&lt;4.0 Hz) waves.
69

�At first the changes were measured from baseline crossing to baseline
crossing by a ruler to estimate mean frequencies. The peak amplitudes were
measured for each wave using calipers. In our first study of the changes after
induced seizures, the technician Hannah Mosquera and I measured the height and
width of each wave in 10-second epochs for 60 to 120 seconds in artifact-free
samples for each weekly recording. We scored the records as low, medium and high
degree changes. As the recordings were done weekly, we had six to eight records
for each subject. Progressive slowing of frequencies and increased amplitudes
marked treatment courses. In later records, bursts of slow waves with sharp spike
activity were seen. The best clinical recoveries occurred in patients with high
degrees of slowing and amplitude increases and we concluded that the EEG changes
were necessary for the recovery of the patients.

EEG recording became the center of my research interest, studying changes
during the hospital course of patients treated with ECT and ICT. We were unable to
record the actual seizure as our instruments were "blocked" by the electrical
stimulus. But we could examine the interseizure record. Treatments were given on
Mondays, Wednesdays, and Fridays with EEG recordings done on a regular schedule
for each patient on Tuesdays or Thursdays. These records showed varying degrees
of progressive slowing with increasing numbers of treatments.
The grand mal seizure was the central feature for changes in behavior and
the beneficial behavior effects. With increasing numbers of seizures the EEG
rhythms slowed and the amplitudes increased. The patients whose inter-treatment
rhythms changed very little did not recover from their illness. Those with greater
degrees of slowing had the better clinical evaluations. The development of slow
rhythms and higher amplitudes were markers associated with recovery.

Necessary, but not sufficient. Some patients with these rhythms did not show
beneficial behavior changes. At the time, we were treating a wide range of illnesses.
Many would meet criteria for major depression, bipolar disorder, and schizophrenia
in modern classifications. The schizophrenic patients, except those with the
catatonic form of the illness, showed the least benefit with treatment. The
specificity of seizure effects depended on psychopathology. Diagnosis became a
critical process by which patients with high likelihood of benefit could be selected
for treatment.
For the next four decades I reported on the EEG effects of ECT and ICT; then
the changes accompanying many new psychoactive drugs introduced after 1954. I
developed methods to quantify EEG changes using digital computer methods;
classified psychoactive drugs by their EEG characteristics; and developed and
defended the contentious concept of the "Association of EEG and behavior with
psychoactive drugs in man." 69

70

�EEG in Psychopharmacology
By 1954, the first clinical tests of chlorpromazine found it to be very effective
in reducing aggression, excitement, and paranoid thoughts. The EEG profile of
chlorpromazine differed from amobarbital and ECT. Imipramine (Tofranil, IMI), our
next new agent, was also distinguishable from chlorpromazine. Were these
differences related to their differing behavior effects? And how were the changes
related to behavior changes?
While the changes in EEG during ECT were easily seen and readily measured
by ruler and calipers, the changes accompanying the chemical agents were more
subtle, the changes much smaller. We looked for a more sensitive quantitative
measuring instrument and EEG quantification became an interest.

The Grey Walter Frequency Analyzer. During World War II the English
physiologist Grey Walter at the Burden Neurological Institute developed an
electronic frequency analyzer to measure the degree of EEG slowing to assess the
severity of head trauma. A single channel record, electronically filtered to minimize
movement artefacts, was sent through a bank of 24 electronic filters, each tuned to
respond to individual energies from 3 Hz to 33 Hz. The premise of its military
medical use was that increases in slow-waves were signs of brain dysfunction
following trauma.
In 1957, George Ulett at Washington University described his use of a Grey
Walter device to measure the effects of atropine and scopolamine on the postseizure EEG. He quantified the changes in brain electrical energy as mm pen
deflections within each frequency band and reported that both anticholinergic
chemicals reduced the percentage time and the magnitude of high amplitude EEG
slow waves induced by seizures.

I visited Ulett in St Louis and was impressed that the device did measure the
drug-induced EEG changes. I received funding from NIMH and Ulett built a device
for my studies at Hillside. We obtained the instrument in the autumn of 1959 and
used it in various studies, most prominently in the CPZ-IMI-PLO random assignment
study. While CPZ enhanced the amplitudes and slowed the frequencies, imipramine
increased the percent time of fast frequencies, distinguishing the brain effects of
each agent.
EEG Analysis by Digital Computer. In 1960, at the dedication of the Brain
Research Institute at UCLA, scientists from the Massachusetts Institute of
Technology presented the analysis of a short EEG segment using digital computer
programs. Ten seconds of analog electrical activity were digitized and then
measured by two statistical programs labeled power spectral density and period
analysis.
71

�The Walter analyzer was inherently unstable and sensitive to room
temperature. It required daily calibration. I was impressed that digital computer
analyses would be within the future for the analysis of psychoactive drug effects.
Central to my move to St. Louis was my request for funding to explore digital
computer analysis methods for medication studies. In early 1963 I approached the
computer center at Washington University to establish a laboratory for EEG analysis
at the Missouri Institute of Psychiatry. Donald M. Shapiro, a doctoral candidate in
digital computer processing, agreed to develop the computer programs. In the
autumn of 1964 an IBM 1710 digital computer system with a central processor
based on the IBM 1620 was installed at the MIP.

Over the next few years Shapiro developed signal processing programs to
record EEG on digital tape, filter electrical noise, digitize the analog measurements,
file the numeric values in the computer memory, and keypunch the data on Hollerith
cards for statistical analysis. After examining different analysis programs, we
concluded that the baseline cross and power spectral analysis gave us the best
measures of medication effects. Some years later, we compared the relative merits
of these analysis methods, concluding that the methods offered useful analogous
measurements.

IBM-1800 Analysis System: In 1966 I moved to New York Medical College to
study opioids and their antagonists, hashish, and marijuana, and to renew my
studies of ECT. Donald Shapiro joined me, and in 1967, with NIMH funding we
leased an IBM-1800 computer system that he programmed to quantify taperecorded EEG records. The programs for both power spectral density (Fourier) and
period baseline cross analyses were developed and applied. This system was
complex and while more stable than the Grey Walter frequency analyzer, also
required constant maintenance. Yet, we were enabled to quantify the EEG changes,
identify drug-related patterns, predict their clinical uses, suggest effective dosage
ranges, and relate the EEG changes to behavior. We also measured the time course
of single dose effects and related them to drug and metabolite plasma levels.
Following the introduction of chlorpromazine, then its congeners, and then
different agents related to imipramine, came a flood of putative psychoactive drugs
from industry laboratories. Psychopharmacologists were busy testing their effects
on physiology and behavior in animal species. How to find new chemical entities
with defined behavioral effects in man became researchable and fundable
questions. Testing drugs in mice and rats identified animal toxicity. Phase-1 human
toxicity trials in volunteers guided clinical use and safety. But what measures could
be markers for antipsychotic, antidepressant, or anxiolytic potential? While a broad
science of animal pharmacology catalogued the physiologic and behavioral effects of
known psychoactive agents, did such studies predict the effects of new agents in
man and in patients with different behaviors?
72

�Pharmacologists developed simple motor tests in animals responding to
known chemicals, and then brought to human trial those agents that matched the
pre-clinical response profiles of known drugs. Scientists at each pharmaceutical
company tested their chemicals in rabbits, mice, rats, cats, guinea pigs, and
occasionally in monkeys and chimpanzees. But their predictions did poorly when
tested in the clinic. Although proposed agents matched known active agents in the
pre-clinical animal trials, many failed in the clinic. Human trials became necessary
to identify the association between the tests in animals and in man. Clinicians in the
NIMH supported ECDEU program studied different physiology measures as markers
for the effects in patients.
In the Hillside CPZ-IMI-PLO trial, we had distinguished the EEG, physiologic,
psychologic and behavioral effects of the active agents, seeing each as profiles of the
classes of antipsychotic and antidepressant agents. We tested amobarbital and
amphetamine, then the new compounds megimide and fenfluramine. The novel
anticholinergic diethazine very rapidly desynchronized the slow waves developed
during ECT. Study of this compound and other experimental anticholinegic drugs
led to our hypothesis of a cholinergic basis for the clinical effects of induced
seizures.

Soon, the flood of psychoactive agents that were being prescribed in diverse
patterns to our hospitalized psychiatric patients elicited complex baseline EEG
patterns. The effects of each agent persisted for days and weeks, absorbed in body
tissues and slowly leached out and metabolized in time. Each exposure altered the
brain patterns in complex, difficult to define, ways. We could no longer find “a clean
head” in which to measure a new agent’s EEG effect. We sought to test agents in
prisoners, and came into conflict with changing concepts of ethics in human
research. Prisoners were not “free agents” and, although we were careful to assure
that their participation had only a monetary award and no change in their civil
penalty, we were discouraged from such use. In New York we studied new drugs in
healthy male volunteers, paying for their hourly participation, and found such trials
useful to identify the central effects of new entities.

The digital computer system offered quantitative measures of frequency and
amplitude changes with each agent. We developed EEG criteria for antipsychotic,
antidepressant, stimulant, and sedative drugs using the effects of chlorpromazine,
imipramine, amobarbital, and amphetamine as guides. We also identified patterns
for hallucinogens (LSD, mescaline), deliriants (atropine, scopolamine, diethazine),
opioids (heroin, methadone, levomethadyl), their antagonists (naloxone,
cyclazocine), marijuana, hashish and Δ-9-tetrahydrocannabinol, and a miscellany of
agents with reported behavioral effects including phenytoin, aspirin,
diphenhydramine, and novel peptides.
Numerous world laboratories studied the EEG effects of psychoactive agents
and with the leadership of the German scientists an International Pharmaco-EEG
Society (IPEG) was formed and met every two years. The behavioral and
73

�physiologic effects were defined in patient and volunteer trials. Many consulted
with industry pharmacologists and offered identifications of clinical activity that
was inconsistent with the predictions of drug effects in animal studies. While the
human studies were more reliable and predictive of the clinical activity of the
compounds, these were expensive, time consuming, and difficult to fund and carry
out. The association of EEG and human behavior was discussed at the 1966 meeting
of the CINP, in a symposium on "Anticholinergic Drugs and Brain Functions in
Animals and Man." The dissociation between predictions of behavior effects in
animals and man was not resolved. 70
As new entities were created in industry laboratories increased emphasis on
the absence of side effects resulted in compounds sent to the clinic with decreasing
efficacy. These were identified as selective serotonin and norepinephrine reuptake
inhibitors and the atypical antipsychotics. At clinical dosing and in volunteer trials,
the impact on EEG were hardly measurable. We were unable to identify patterns
the we had established for different behavioraltering agents. Our methodology was
criticized as failed, and discarded. But over the past three decades, the benefits of
these new agents were increasingly not distinguishable from placebo comparators.
Not understanding the role of brain change measurable by EEG in man has resulted
in a worldwide flood of ineffective medications.
Psychopharmacology Lessons Learned by Pharmaco-EEG
Over the three decades of activity, we profiled agents that were clinically
active and some marketed, measured the relative potency and dosage ranges of
sedative and stimulant drugs to guide clinical use, examined the psychoactive
properties of agents in the search for a new useful chemical core, and agents that
showed little promise that were abandoned. In some instances the EEG profile was
instrumental in predicting effective clinical uses and dosage ranges and targeting
marketing applications.

Doxepin (Sinequan). Based on its chemistry and its effects in animal tests
Pfizer pharmacologists recommended this tetracyclic compound for clinical trials as
an anxiolytic. After a year in clinical trials with a lack of an observable benefit in
anxious patients, investigators met at the company’s offices in Groton, CT to review
the experience. A pall hung over the discussions until three investigators, Turan Itil,
Herman Denber and I offered understanding from our EEG studies. We had failed to
find the patterns of anxiolytic drugs, but did see changes similar to those of the
antidepressant imipramine. We recommended doxepin be tested in depressed
patients. Guided by our findings, doxepin was was quickly reported effective in
depressed patients. It was successfully marketed as an antidepressant.
Mianserin (Tolvon, GB-94) was developed by the Dutch company Organon
and recommended for a use in treating migraine. The research director, Theodor
(Jack) Vossenaar, sent the compound for EEG assessment to Turan Itil in St. Louis
74

�who reported its EEG profile to be most similar to that of amitriptyline. Because the
pharmacologists considered the finding inconsistent with their experience as a
serotonin and histamine antagonist, Vossenaar asked me to replicate the EEG study.
I quickly confirmed Itil’s finding and the subsequent clinical testing and marketing
in Europe and Asia as an antidepressant was medically and economically successful.
I became invested in the EEG-mianserin story and presented the findings in many
venues.

Mirtazapine, 6-azamianserin. chemically related to mianserin, is a racemic
mixture. In preclinical chemical and animal studies, the dextro-enantiomer was
reported to be active and the laevo-enantiomer inactive. We examined the EEG
profiles of both enantiomers and found no difference between them in the
magnitude of the EEG changes with a pattern most similar to that of mianserin.
Clinical trials for each enantiomer found both to be clinically effective although
neither differed from placebo at the tested doses. The racemic mixture was
successfully marketed as the antidepressant Remeron in the1990’s.

Flutroline. Pharmacologic studies in dogs reported that a single 1-mg dose of
flutroline inhibited the vomiting induced by apomorphine for as long as one week.
Extrapolated to man, pharmacologists enthused that flutroline would be an ideal
antipsychotic, requiring a single oral dose each week, pictured as the “Saturday
night pill.” In our clinical trials in actively psychotic patients we failed to elicit an
antipsychotic effect, even at multiple and higher dosing schedules than initially
recommended. EEG measures in our volunteers also failed to show a measurable
change. The preclinical prediction of small doses being effective for days or weeks
was untenable and studies of the drug ended.
Aspirin, Anticonvulsants, Antihistamines. We looked at commonly
marketed agents with reputed behavioral effects seeking potential alternative
clinical uses in their EEG profiles. Acetylsalicylic acid (Aspirin) was reported to be
soporific at its common dosing of two tablets each at .0325 Gm. We tested single
doses of 0.65, 1.95 and 3.6 Gm in healthy adult men. The two higher doses elicited
quantitative EEG, symptom effects, and cognitive functions characteristic of
soporifics. Doses of 0.65 Gm were similar in direction and pattern but failed tests of
significance.

We sought to measure the basis for reports of changes in mood with the
anticonvulsant phenytoin, finding the EEG patterns to mimic those of antidepressant
drugs. The dosages for clinical benefit were high, so high as to risk toxicity.

In an enthusiasm for peptides following the identification of euphoriant
effects of beta-endorphin, we examined the effects of the peptides ACTH4-10 and desTyr-gamma-endorphin. We could not elicit systematic EEG changes at the dosages
and the parenteral routes that we were advised to use based on pre-clinical trials.
75

�The sedative effects of antihistaminic agents were well documented.
Diphenhydramine and terfenadine elicited soporific, not antidepressant or
anxiolytic patterns, and were not tested further.

Opioids and Cannabis. The same principles of EEG study of new agents
were applied to opioids and their antagonists, and hashish, marijuana and THC-∆-9.
We defined the EEG and behavior profiles of the compounds and measured the
speed with which the antagonists blocked the effects of heroin and levomethadyl. In
studies of marijuana and hashish the behavior and EEG effects were consistent with
THC-∆-9 content.
The Association/Dissociation EEG and Behavior Controversy.

Industry searches for new agents with potential for human benefit are
commonly based on similarities in chemical structure and observations in animal
trials. Early in our EEG studies, beginning with chlorpromazine and imipramine, our
descriptions of the effects in patients and normal volunteers differed from the
reports of EEG studies in animals. At meetings of EEG and biological psychiatry
societies, both Turan Itil and I were often criticized for reporting effects on
behaviors and EEG that differed from those reported in the animal trials that had
preceded our human studies. Changes in the resting alert EEG in patients and
healthy volunteers had elicited drug specific changes in frequency and amplitudes
that we related to their clinical effects.
During the course of ECT, EEG frequencies slowed and amplitudes increased.
During the ECT course some agents increased and others inhibited slowing, some
increased fast frequencies, and some altered amplitudes. The post-ECT EEG became
a sensitive index of brain function that varied in response to the chemistry of the
tested medication. These studies had been done at Hillside Hospital in the 1950s.

Diethazine had been a new agent with well-defined anticholinergic
properties that we administered to our patients during an ECT course. In postseizure recordings with slowed EEG frequencies and increased amplitudes,
intravenous diethazine sharply and quickly reduced amplitudes and increased the
mean frequencies. The patients became agitated, depressed, and reported their preECT symptoms. We inferred that seizures liberated free acetylcholine in brain and
CSF and increased concentration of brain cholinesterases. These observations led
me to suggest a cholinergic explanation of the ECT mechanism.
Replications of the same effect with Ditran and experimental anticholinergic
drugs of the JB series assured us of this pharmacology. When we measured the EEG
effects of imipramine in our patients, in volunteers and in ECT patients, we found
the same changes as we had seen with the anticholinergic agents. We inferred that
imipramine blocked free brain acetylcholine, a finding that was inconsistent with its
inferred pharmacology.
76

�At a Montreal conference in 1969, my suggestion of imipramine’s
anticholinergic activity was criticized since such effects had not been observed in
animals. The pharmacologists insisted that imipramine lacked such effects. In time
the anticholinergic effects of imipramine were increasingly recognized. The
anticholinergic properties were even flouted as riskful by marketeers seeking to
replace imipramine with newer agents.

The next year, at the World Congress of Psychiatry also in Montreal, nine
investigators from Europe and the United States, described their experiences with
new psychoactive agents on the EEG and behavior. EEG changes characterized the
qualities of psychoactive drugs – the defined changes predicted the behavior effects,
and their absence identified clinically ineffective agents or ineffective dosing.
Itil, I, and an increasing number of electroencephalographers studied druginduced changes in human volunteers. As we described drug-related patterns that
were clinically confirmed, greater interest in human screening of new clinical
entities developed world-wide. The study program that began at Hillside Hospital,
flourished at my laboratories in St Louis and New York.

Many industrial pharmacologic laboratories established animal testing
centers using implanted electrodes in diverse animal species. When
pharmacologists assayed the EEG effects of putative and established agents in rats,
mice, rabbits, cats and dogs, results differed from parallel findings in human studies.
The principal argument was made by Abraham Wikler who tested morphine,
atropine, n-allylnormorphine and mescaline in dogs in slings. The animal EEG
recordings showed sleep patterns; yet, their legs and eyes were moving rapidly. He
concluded that there was a dissociation between the induced behaviors and the EEG
effects. His inference was supported by pharmacologists studying other animal
species. At an international conference of the CINP in Washington DC in 1968, the
issue of pharmacologic “association” or “dissociation” was debated and resolved by
acknowledgement that the systemic and brain pharmacology of animals are not
identical to that of man. Indeed, an agent showing similar effects in an animal
species and in man is a happenstance that cannot be predicted in advance.
Preclinical studies in mice, rats, cats and dogs studies do not reliably predict drug
effects in humans.
We had our own experience with the differences between the behavioral
effects of drugs in animals and in man in St. Louis in the mid-1960s. Sam Gershon
had trained in Australia and studied lithium in the treatment of mania. On the
advice of Jonathan O. Cole, I invited him to join the MIP staff as pharmacologist. He
brought an interest in the actions of acetylcholine, studying the anticholinergic drug
Ditran and the cholinomimetic agent tetrahydroaminoacridine (THA). He
developed animal testing facilities and appointed a team of collaborating
pharmacologists and technicians.
77

�His animal of interest was the beagle dog. One occasion, when Gershon was
away from the Institute, the administrator asked me to approve the purchase of six
setter dogs as replacements for unavailable beagles from the animal breeder. The
price for the setters would be the same. Not knowing of any difference between the
species, thinking “a dog is a dog,” I approved the purchase.
A few weeks later, Gershon complained that his anticholinergic drug
experiments with setters failed to elicit the behaviors that were readily elicited in
beagles. That the pharmacologic sensitivities varied among dog types as well as
among animal species supported my argument that human trials were essential to
understanding psychoactive drug effects.
The Pharmaco-EEG Paradigm

Whether the EEG and behavior of psychoactive drugs are “associated” and
predictable in man as we maintained or were “dissociated” as pharmacologists
asserted, clarified the pharmaco-EEG paradigm in clinical studies. Today’s search
for new psychoactive agents is rooted in the happenstance that chlorpromazine was
a powerful sedative agent especially in paranoid, aggressive, hostile, and manic
patients. Similarly, the antidepressant relief accorded by imipramine encouraged its
trials in melancholic psychotic patients. These experiences invigorated a massive
industrial investment, mainly in animal studies, with lesser expenditures in the
clinics.
Much energy is being spent to find the effects of the agents on the brain’s
neurohumoral and neuroendocrine chemistry. Psychoactive substances alter
behavior to the extent that they change brain chemistry. The pharmaco-EEG
paradigm offers quantitative measures of these chemical changes that relate to their
behavior effects. We are able to predict the behaviors of psychosis, depression, or
anxiety, elicit a delirium or reduce a manic episode, from the EEG changes. Failure
to alter the EEG means that the agent has little effect on behavior, that it is
behaviorally inert, and best marketed as a placebo.
Human studies are expensive and the science of pharmaco-EEG failed its
promise and is no longer supported either in research laboratories or in individual
patient care in clinics. Sadly, the same questions are now being asked in human
studies using the present-day fashionable brain imaging methods with emphasis on
concepts of connectivity and the size of brain nuclei. It is difficult to see such
measures that are momentary images and not continuous as having more promise
than that of pharmaco-EEG, which readily permits continuing assessments over
time. Sadly, pharmaco-EEG in managing individual patients and in predicting the
effects of chemical agents and physical treatments is a discarded science. 71

78

�Book Eight: A Medical Experimentalist is Created
Medical School Experiences 1942-1945
My letter of admission to New York University College of Medicine arrived on
December 6, 1941, the day before the Japanese attack on Pearl Harbor and the entry
of the nation into war. That Sunday I was accompanying my father on a house call,
listening to radio news, when the attack was announced. My parents had actively
encouraged the emigration of friends and classmates from Vienna, acting as surety
for their transitions to America. They had avidly followed the news of the war in
Europe and were particularly agitated by the Nazi murders of Jews.

I began a three-year intensive medical school training program at New York
City’s Bellevue Hospital in June 1942. We were sent to Fort Dix in New Jersey for a
week’s military orientation and returned to classes as soldiers dressed as Privates
First Class in the U.S. Army. The war had called many experienced faculty members
to military duty offering students unusual opportunities for hands-on medical
experiences and responsibility for medical and surgical procedures far beyond our
knowledge and experience.

I vaguely remember the anatomy and chemistry lessons of the first year. The
cadaver was an elderly, skinny woman. My teammates were Felix Wroblewski, who
later did medical research at the Rockefeller Institute and Luther Cloud, an officer in
an insurance firm. Neuroanatomy was taught by Wendell Krieg, who asked each
student to make paper mache crossection models of the human brain. These models
were supplemented by brain slices preserved in formaldehyde in crocks that
allowed us to map the brain’s nuclei.

Neurosyphilis and Cerebrospinal Fluid: Clinical teaching began in the
second year and in an assignment to the syphilis clinics I was taught by Bernhard
Dattner, a 1938 émigré from Vienna. He had studied under Julius Wagner-Jauregg,
the 1927 Nobel Prize winner in Medicine for his report that malaria-induced fevers
relieved one third of patients of active neurosyphilis. While at Vienna's Allgemeines
Krankenhaus, the number of white cells and levels of protein in the cerebrospinal
fluid (CSF) were highest in the actively ill, making CSF examination indices of the
severity of the illness and guides to treatment.

Withdrawal of cerebrospinal fluid by lumbar punctures between Lumbar- 3
and Lumbar-4 vertebrae are often followed by headache. To reduce this incidence
Dattner obtained the CSF from the 4th ventricle by an occipital puncture to the
cisterna magna. For the next month I monitored the progress of the patients by CSF
measures obtained by ventricular taps. I assumed that it was a customary
procedure, despite the risk of penetrating ("pithing") the brain stem. The procedure
is now considered too riskful to be considered even by experienced neurologists.
79

�Neurosyphilis is a late development in the life course of syphilitic disease,
appearing years after the original infection. The symptoms develop slowly, making
difficult an accurate diagnosis with its devastating consequences in personal life and
the risks of the toxic treatments of mercury and arsenic. A principal sign of the
disease is pupillary irregularity and failure to narrow with a light stimulus (the
Argyll-Robertson pupil). When mental and neurologic symptoms appear, this sign is
present in less than 60% of known ill. Dattner argued that white cell counts and the
concentration of protein in the CSF offered better and more reliable criteria of the
severity and activity of the disease. The presence of cells, elevated protein and
positive colloidal gold reaction tests were the guide to fever treatments. The CSF
changes normalized in the patients who responded to the fever therapies.
While syphilitic patients were treated with arsenical preparations, the more
actively ill were also subjected to malarial or “sweat box” fevers. Patients remained
seated for hours in a box heated by lightbulbs with only their heads exposed. The
treatments were severely debilitating and assuring hydration and monitoring body
temperatures was one of my responsibilities. Follow-up studies did show
improvements in serological and CSF tests and some relief in psychiatric symptoms.
I was astonished by what patients were willing to suffer on the promise of cure.

During my schooling in 1943, Bellevue Hospital’s R-S buildings were filled
with more than 200 patients with syphilitic disorders. Six years later in 1949 when
I returned as a resident in neurology, 2/3 the beds no longer served these disorders,
the remarkable impact of penicillin therapy.
In later years, when I applied novel treatments for psychiatric ill, I sought
similar test guides to treatment outcomes – as in the Face-Hand Test, the
amobarbital denial test, and the high levels of slow wave and spike activity in the
interseizure EEG as measures of progress in ECT. Later I was fascinated by the
dexamethasone suppression tests in melancholia and the lorazepam response test
in catatonia.

Personally Experiencing Psychoactive Drug Effects. Student training in
pharmacology included individual experiences with medications administered to
and by fellow students – morphine, scopolamine, atropine, vasodilators, nitrous
oxide, amobarbital, and amphetamine are those that I recall. Doses were
pharmacologically active and our observations were recorded. Blood samples were
taken and nasogastric tubes passed. The hilarity induced by nitrous oxide inhalation
and the pleasant feelings associated with barbiturates made some of us look
forward to these classes. For others, the unpleasant experiences with scopolamine
and morphine drove them from the laboratory. 72

Osteomyelitis. Among children, infections of fractured bones required
intensive care. Débridement (surgically removing dead and infected tissues) was
followed by repeated flushing with warm saline and dressings to keep the wounds
clean to encourage healing. Plaster casts restrained the movement of limbs. In my
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�junior year during the rotation in pediatric surgery I debrided children’s wounds.
An ongoing research study applied live maggots to the open wound to clear the pus
and dead tissues. I cleansed bone fragments and tissue debris, washed wounds with
sterile saline solutions, created a plaster protective shell to immobilize the limb, and
applied live maggots for days at a time. Maggots digested pus and wound debris,
allowing surgical repair of the skin and bone. This usage disappeared with the
introduction of antibiotics but references now appear from time to time citing
maggot therapy in resistant infections.
Barbiturates. During a rotation on the active psychiatric service at Bellevue
Psychiatric Hospital in my senior year I was taught to use amobarbital (Amytal
Sodium) to control agitated and aggressive behaviors. It also relieved catatonic
refusal of food, mutism, and posturing. I do not recall the use in stuporous catatonic
patients, a use that became a central interest four decades later.

InterneshipTraining 1945-6

My first Random Controlled Trial; Penicillin in Empyema
My medical internship continued the same ‘hands-on’ experiences. During a
rotation on the pulmonary medicine service, patients with pleural cavity infections
(empyema) filled the beds. Every other day I introduced a large 18-guage trocar
between the ribs into the pleural space, removed pus, and washed out the pleural
space with warm saline. An ongoing experiment washed the pleural space with
either sulfadiazine or an experimental substance “x” with patients randomly
assigned by the odd or even final number of their chart record. Supplies of “x” were
locked in a safe in the hospital director’s office. Withdrawn samples were carefully
recorded according to the patient's chart number. Within a few weeks the
superiority of substance “x” became apparent, even to a neophyte physician – thick
pleural fluid thinned rapidly from yellow putrescent pus to pink serous to clear
fluid; fever curves flattened, pain and apathy disappeared, and appetite and activity
improved, all within 10 days of administration.

A young febrile Hispanic woman with empyema was admitted with her
nursing infant. The random medication assignment was for sulfadiazine Assuring
myself of the ethics of the switch for a nursing mother, I administered “compound
x” and did so daily. When the empyema rapidly cleared, the Attending physician Dr.
Eli Rubin was puzzled. Checking the records he noted the switch and in anger,
marched me to the Medical Director’s office and ordered my suspension from the
internship. I had broken two rules, direct orders of an Attending physician and the
research protocol. Cooler heads prevailed a few days later and I was re-instated but
the lesson of adherence to research assignment was learned. (Compound “x” was
penicillin.)
81

�Work schedules were exhausting, with 48 hours on call frequent, with
learning from an Attending physicians who supervised each patient’s care was
payment for the exhausting hours. The neurologist Nathan Savitsky visited his
patients at 7:30 each morning, inviting any interne to join. He was a dynamic and
knowledgeable teacher, citing the literature much as Google or Wikipedia provide
today. I joined him often and soon I was called to attend the autopsies of patients
we had examined together. The logic of the symptoms and course of illness and the
demonstrated neuropathology was impressive.

Residency Training: 1948-1952

New Science of Percutaneous Carotid Angiography
As the new hire at Montefiore Hospital’s residency in July 1948, I was first
assigned to the neurosurgery rotation. As a student assistant during brain surgery
with Dr. Leo Davidoff, the hours standing as a masked assistant in one place without
voice or movement were enervating, and I escaped to the clinic as quickly as I could.
The technology of percutaneous carotid angiography had just been perfected and
the neurosurgical residents taught me how to insert the needle into the carotid
artery by touch, rapidly inject radio-opaque dye, and call for three x-ray images at 2second intervals. I became skilled in identifying the signs of meningioma,
glioblastoma, subdural hematoma, arterial aneurysm, and arterial blockage.
In pneumoencephalography air is injected into the cerebrospinal canal and
ventricles through a needle puncture between lumbar vertebrae 4 and 5. The air
fills the ventricles outlining the spaces showing any abnormal images. I became
skilled in obtaining cerebrospinal fluid and used the technique in later studies. The
films showed tumors, bleedings, and encephalopathies, directing neurosurgical
intervention when appropriate. 73

Montefiore Hospital was a museum of chronic neurological disorders under
study for decades. The film library included examples of classic syndromes of
abnormal motor movements and seizures that I viewed to properly label peculiar
repetitive movements. I have no recollection of experience with psychiatric
patients.

In July 1949 I continued training at Bellevue Hospital, first as resident in
neurology and then in psychiatry. Percutaneous carotid angiography had not been
introduced to the hospital so I brought this new technique to the Neurology Service.
After obtaining permission from Prof E. D. Friedman to develop such tests, a fellow
resident Joseph Stein and I built a film holder for multiple images and collaborated
with radiologists to organize a service. The first films of a subdural hematoma
showed the blood vessels, displaced by a dark mass, clearly outlining the lesion and
its effects, encouraging surgical relief. Over the next year, we did 102 procedures,
82

�reporting a high diagnostic success rate and a 5% morbidity rate. Studies of the CSF
showed no persistent abnormalities as a result of these tests.
After one such procedure, a young man lay in bed, alert, relaxed, staring into
space. Asked what he was seeing and pointing to objects in the room, he pleasantly
confabulated responses of imaginary objects. He had developed an acute syndrome
of visual neglect and denial of blindness known as the Anton Syndrome. After a few
days of nursing care his condition resolved. My teachers interpreted the
phenomenon as an interaction between the physical changes induced by the
injection and the psychological “defense mechanism of denial” based on
psychoanalytic philosophy. It was a lesson in applied psychodynamic philosophy to
psychopathology.

Other clinical experiences were as intriguing. The popular folk singer Lead
Belly -- Huddie Ledbetter -- was admitted with advanced amyotrophic lateral
sclerosis. No effective treatment was known but my teachers thought the disease
resulted from neurotoxicity caused by the passage of toxins through the bloodbrain-barrier to progressively destroy neurons. Animal studies had shown that the
transmission of proteins through the barrier could be inhibited by infusions of large
molecule dyes such a trypan red. Lacking any effective treatment, daily infusions of
1% trypan red in saline were administered. Lead Belly was a very black man and
after a week of perfusions, his sclera, palms, and soles of his feet became brilliant
red. He died in December 1949.
Double Simultaneous Stimulation: The Face-Hand Test

Two teachers, Morris B. Bender and Edwin A. Weinstein encouraged my
interest in clinical research during my neurology residency at Bellevue Hospital.
While in the Naval medical service Bender, a clinician trained with the neurologists
Israel Wechsler and Israel Strauss at Mt Sinai Hospital, became interested in the
phenomenon of visual extinction on double simultaneous stimulation in a sailor with
a parieto-occipital shrapnel wound. The interaction of simultaneous administered
stimuli delineated sensory lesions better than single stimulation. Following
professorial tradition he called me and my colleague Martin A. Green to his office,
handing each a stack of 3x5 inch blank white cards, telling us to survey the
responses of patients to simultaneous tactile stimulations of the face and hands –
first in our patients on the Neurology wards, and then on the Psychiatry wards.
When we had a hundred such records he asked that we find 100 normal children,
then he sent us to Letchworth Village in Thiells, Rockland County to examine an
equal number of mental retardates.

Applying pin pricks or finger touches simultaneously to both cheeks or hands
were correctly perceived by normal adults. But in patients with diverse brain
dysfunction and diminished vigilance, as after head trauma, structural brain damage
with bleeding, tumor, or stroke, one stimulus was reported and the other was not,
even though the sensation of each single stimulus was readily perceived (extinction).
83

�At times the patients mislocated one of the stimuli on their body (displacement) and
occasionally insisting that the stimulus was applied to space in front of them
(exosomesthesia). These phenomena were not explicable by classical neuroanatomy.
The phenomena had been conspicuous in soldiers with severe head injuries and we
reported the same phenomena in patients with abnormal brain syndromes,
publishing reports on the Face-Hand Test (FHT) as a measure of gross brain
dysfunction, the organic mental syndrome.
Similar test abnormalities were demonstrated in normal children under the
age of 6, and in patients with mental retardation with low mental age scores on
Stanford Binet tests. The positive FHT was a rapid estimate of mental age,
normalizing at age 6. Impaired brain functions in the elderly were demonstrated in
those with impaired orientation and memory.

Intravenous injections of amobarbital increased omissions and
displacements. Sensory errors increased during the course of electroshock therapy
(when slow waves in the EEG became prominent after 3 to 9 seizures) when brain
functions were altered.

In later experiments carefully measured sensory stimuli demonstrated
extinction as sensitive to the stimulus strength as well as the state of vigilance. For a
time the FHT was widely recommended as a “soft neurological sign” of brain
abnormality but seems no longer to be so used.

84

�Book Nine: Personal Biography
I was born in Vienna on January 16, 1923, the same year that my father Julius
Fink graduated from the University of Vienna Medical School. He had special
training in the new science of radiology and took an externship in medicine and
radiology at the Bergen County Hospital in New Jersey.

My mother Broniaslawa Lowenthal (Bronia, Bronka) had been a medical
student at the University of Vienna. She was much courted and married Julius on
March 12, 1922, in her third year of training. I was born within a year. My mother
cared for me in Vienna while my father worked in New Jersey. My mother and I
sailed from Bremen on the SS George Washington on October 17, 1924 arriving in
New York on October 24, shepherded under the watchful eye of her younger brother
Adolf Lowenthal, who had been sent by the family from New York.
A Greek scholar Lazaros Triarhou published a report on the faculty and
students at the Wagner-Jauregg clinic in Vienna when W-J received the Nobel Prize
in 1927. A class picture shows the faculty and cites 6 women graduates who went
on to careers in neurology and psychiatry. He portrays two graduates, Alexandra
Adler and Edith Klemperer, who were consultants during my residency days at
Bellevue and my work at Hillside. Thinking of their education, I realized that they
were students in Vienna in early 1920s, likely classmates of my mother Bronia, who
left her education because of pregnancy. She tried to return to medicine in 1950,
was not accepted, and graduated the Columbia University School of Social Work in
1953.
In the picture, Josef Gerstmann, Bernhard Dattner, and Paul Schilder appear,
scholars who taught at Bellevue New York University during my schooling. Dattner
was particularly instrumental in developing my interest in tests and diagnosis.

In our family setting, I always “knew” that I would become a physician.
Admission to medical school in the U.S. was limited by the publicly acknowledged
quotas for Jews, and to successfully gain admission one needed to be “in the top of
the class.” My elementary and high school classes were at PS 77 and James Monroe
High School in the Bronx, a few streets from my father’s office at 1201 Elder Avenue.
My high school teachers, sympathetic to my goal and recognizing the problems in
college and medical school admission, encouraged me to be a leader of the Arista
Club, to publish articles in the German-language magazine Plaudermäulchen, and to
be the Manager of the football team, gaining my athletic “M” at graduation.
I graduated from high school in January 1939 at age 16 and enrolled at the
New York University College campus at University Heights of the Bronx for its
Feb/Sep program. In 1942, at age 19, I began medical school at NYU School of
Medicine. The demands of WW II collapsed our training period to 3 years, and I
graduated on June 12, 1945 at age 22, the youngest member of my class.
85

�My medical experience began in my father’s office, developing x-ray films,
clinical tests of blood and urine, and answering the telephone when he was out of
his office. He was a general medical practitioner in a free-standing office equipped
for clinical laboratory tests of blood and urine, x-ray, fluoroscopy, and
electrocardiography. He trudged to house-calls at all hours of day or night, in all
weathers. He was a model for my brother and me, both selecting medical careers.
My schooling emphasized an experimental, “hands-on” approach beginning
in college where teachers answered questions by suggesting experiments. When I
entered my junior college class, I volunteered for the project to count the numbers
of mitoses in the neural ependymal layer of the 48-72 hour developing chick, to
answer the question how the diurnal light-dark cycle impacted the growth rate.
Other students had measured the mitoses in the 24 to 48 hour and 72 to 96 hour
cycles. (As I recall, the light cycle did not affect the rates of mitoses.)

During medical schooling I lived at home in the Bronx, about an hour’s
subway trip. Although school began at 0900, the Army rules insisted that we be
present for roll call each morning at 0730. Such was not easy during the winter and
I soon was reprimanded for lateness and ordered to guard duty as punishment.
Students had some holiday time and on June 6, 1944 – D-Day - I and fellow
classmates were camping on Big Burnt Island in Lake George to hear the shouts and
waving paddles announcing the invasion as classmates canoed back from Lake
George Village.

I came of age in America during the war years of the 1940s and 1950s, and
for seven decades I have been a treating clinician and researcher, caring for
neurologic and psychiatric ill. For many decades, the mentally ill had been
warehoused in large sanitaria far from city centers, at least until the seizure
therapies, electroshock and insulin coma, were introduced in the 1930s slowing the
growth of mental hospital populations from the peak in 1955 at 560,000 patient
beds to 170,000 in 2014 in the United States. The efficacy and the mystery of these
treatments, inducing grand mal seizures, became my lifelong challenge. The
treatment methods, however, were highly controversial in the public and within the
profession. For my interest I was often berated and have thought that a less hostile
life might have been preferred.
The 1950s and 1960s brought new psychoactive medicines that changed
brain chemistry and physiology, with resultant improvements in behavior,
encouraging a massive deinstitutionalization, pushing tens of thousands of the
severe psychiatric ill to leave U.S. hospitals and live at home, or on the streets, in
jails, in flophouses, or in and out of community hospitals. Identifying the benefits
and developing treatment protocols for these new medicines became a professional
challenge. As the effects of the new agents were measurable in the electrical
86

�readings of the scalp recorded electroencephalogram (EEG) patterns, and the
digital computer revolution offered means to quantify these effects, the new science
of pharmaco-EEG occupied 35 years of my research life.
My interest in the effects of psychoactive medications on the human brain
included active studies of the opioids and cannabis that were interdicted by
governments as addicting and life-threatening. In my later years I actively led an
effort to rescue the disorder of catatonia from its entombment within the poorly
understood concept of schizophrenia and show it as an independent, identifiable,
verifiable, and fully treatable syndrome. Bringing it out of its closet encouraged
worldwide recognition and improved diagnosis and effective care. Catatonia is
unique among the behavior disorders in having two effective treatments and a
useful verification test, which makes each recognition of the syndrome life-saving.

The arc of my professional career runs from a childhood in the Bronx,
medical school in New York City, a decade organizing Hillside Hospital’s research
facilities, a brief stint to establish a Psychiatric Research Institute in Missouri, back
to New York for a continuing academic career in different hospitals, then spending
35 years teaching psychiatry at the State University of Stony Brook. After meeting
requirements for professional certification in neurology, psychiatry, and
psychoanalysis, I spent my years as an experimentalist researcher and teacher.

Family Affairs.

I married Martha Pearl Gross, a graduate of Barnard College on September
11, 1949. We had met when I returned from a trip as the ship's surgeon on the
Grace Line's Santa Monica in March 1948. Martha was dockside awaiting her
parents who had been passengers on the cruise to Barranquilla and Cartagena. Her
father was ill with amyotrophic lateral sclerosis, and as the ship's surgeon I was
called for his care. After I called on her parents at their home in Great Neck, we
dated and married after her graduation in June. I continued my training at Bellevue
and in May 1951 our son Jonathan was born. We had an apartment at 404 East 54
Street in NYC. When I continued my training at Hillside, we moved to Martha's
parents' home in Great Neck, about 10 minutes from Hillside. Our son, Jonathan was
born on May 2, 1951, our daughter Rachel September 29, 1956, and our daughter
Linda June 3, 1958.. In early 1953 we bought a home in Russell Gardens at 11
Wensley Drive.
Dalliance with Psychoanalysis: School and Personal Analysis

My interest in psychoanalysis developed during my classes in Texas in 1946.
The enthusiasm for Freudian psychodynamic theory and practice rapidly infected
American psychiatric teaching and practice. Beliefs that Freudian images
explained the behaviors of the psychiatric ill and also offered effective treatment,
personal understanding, and clinical relief flashed through clinical psychology,
psychiatry, and popular culture in the theatre, film, and education. As a military
87

�veteran, I was entitled to educational training supported by the GI Bill and like many
peers, I decided to attend an analytic training program. The New York
Psychoanalytic Institute and Columbia University programs required full-time
attendance and clinic care of psychiatric patients but the William Alanson White
Institute organized its classes during evenings and week-ends. I enrolled for their
psychoanalytic course for physicians not for any faith in their beliefs but to continue
my neurology training.
I began a personal analysis with a WAW graduate Dr. Joseph Miller, meeting
for one hour three times a week for the next five years. The WAW did not see merit
in the “Freudian couch” approach so the discussion was face-to-face. A
psychological assessment by Dr. Ralph Crowley directed the early discussions.
School classes were small with Clara Thompson, Ralph Crowley, Frieda FrommReichman, and Janet and David Rioch among my teachers. David Rioch offered
elective classes in neurophysiology and brain function that were held on Saturdays
in Washington, D.C. We read the writings of Sigmund Freud, Karen Horney, Erich
Fromm, and Harry Stack Sullivan, emphasizing the social aspects of interpersonal
interactions rather than the classical studies of the unconscious and psychological
defenses. I completed the school’s requirements for a Certificate for Physicians in
1953.

During my residency at Hillside, my supervisor was Sidney Tarachow, a
teaching psychoanalyst from the Columbia University School of Psychoanalysis. He
enquired whether the presence of one or two parents during childhood influenced
the expression of a psychoneurosis. Did the absence of one parent by death,
separation or divorce early in childhood encourage the expression of an obsessivecompulsive neurosis while the childhood presence of two parents was associated
with a hysterical neurosis? It was a testable question. I examined the hospital
records for those diagnosed with a psychoneurosis, abstracted the family history
and evaluated the patient's main symptoms. We identified patients with dominating
obsessive or hysterical symptoms and found 50 records with sufficient data for
study. We did not find a difference in family histories to support the hypothesis. 74

Another study also failed to support the psychodynamic suggestion that
homosexuality was a root of paranoia. I was assigned the care of a 26-year-old
Jewish married man with severe panic episodes. The faculty diagnosis varied
between a neurosis with homosexual panic and paranoid schizophrenia. Supporting
the diagnosis of schizophrenia were his fantasies of aggression and the paranoid
imagery on his Rorschach Test responses. I presented his story to an audience of
psychoanalytic teachers. The discussion was robust in interpretations but
inconclusive as to diagnosis and treatment options. The proceedings were
published. Re-reading this report after 60 years showed the many changes in our
diagnostic styles, the rejection of homosexuality as a disease, the present tolerance
of American society of homosexuality as a life-style, and the awareness that our
later experience with medications would offer patients effective treatment with
imipramine.
88

�Neither the teachings of Freudian scholars at Hillside Hospital nor the social
psychological principles of the Sullivanian scholars at the William Alanson White
Institute impressed me as useful therapies. Nor did I have the patience to indulge
hour after hour, month after month, listening to a patient’s anxieties, social
difficulties, moods and fantasies. In time, my interests shifted and by 1958 I decided
to close my private office and devote my life to a medical research career.
Military career and travels as ship’s surgeon
My active military service as medical officer began in April 1946. After two
weeks of field training I was assigned to a regimental field station in Camp
Campbell, Kentucky, managing morning sick-call and incidental accidents and
injuries. That winter I received orders to attend the Army School of Military
Neuropsychiatry at Fort Sam Houston in Texas for a 4-month intensive program in
neurological and psychiatric examinations, management of traumatic injuries and
combat stress reactions, psychodynamic principles, and lectures on ECT, insulin
coma, and lobotomy. Many instructors were imbued with the fervor of
psychoanalysis, promising cures for the most severe mental disorders. We were
enthralled and so enthused that many of us sought psychoanalytic training when we
returned to civilian life.
After completing basic military training I was assigned to Kentucky’s Fort
Knox Station Hospital as Chief of Psychiatry. Three wards of 30 patients each
included a range of severely ill psychotic patients, some undergoing insulin coma
and some ECT. The nurses and technicians were competent and experienced, more
so than I, and my responsibilities of supervision were light. The nearest medical
school was in Louisville, about an hour away. I attended weekly Grand Rounds in
Neurology with Ephraim Roseman and took a course in the Rorschach test
procedures with Arthur Benton.

The war against Japan ended with the atomic bomb in August 1945, saving
the lives of many thousands of American soldiers as well as of many Japanese. By
1946 President Truman, faced with the costs of a very large active military service,
ordered the summary discharge of thousands of soldiers on duty. As a member of
an Officer's Board to decide on the qualifications for soldiers desiring to remain in
the post-war career Army and as the panel psychiatrist I used interpretations of the
Rorschach Test in the recommendation for discharge or retention. My comments
had little influence on the Boards’ decisions, as only the longest serving and meritawarded soldiers were recommended for retention. At the end of November 1947
my service was suddenly ended after 20 months active duty.
I had enrolled for residency training in neuropsychiatry at the Montefiore
Hospital with H. Houston Merritt for July 1948. The tantalizing question became
whether to advance my medical training experience to January or to spend the six89

�month gift of freedom elsewhere. After the continuing years of schooling and
military service the glamour and challenge of a position as ship’s surgeon led me to
Grace Line’s Hudson River Pier 57. A position was open on the S.S. Santa Maria, a
C-2 freighter with 52 passengers, leaving five days later to the west coast of South
America, with stops at ports in Columbia, Peru, and Chile. The duties of the ship’s
surgeon were "sick call" sessions twice a day, writing health status reports of
passengers and crew on entry to ports, examination of food storage areas and
freezers for vermin, and accompanying port health inspectors as they surveyed the
ship in each port.

It was possible to visit port cities during one to two days of loading and
unloading cargo. I visited the local mental hospital in Lima where Honorio Delgado,
a leader in psychoanalysis, cared for the severe mentally ill. He encouraged patient
art. Although the hospital was more like a prison with stone palettes, iron rings in
the walls to attach restraints, patient drawings and paintings adorned the walls of
the wards. These paintings were fore-runners of the enthusiasms for “Outsider Art”
in the 1970s.

After two 5-week voyages to Valparaiso, I signed on the Santa Monica for a 3week cruise to Cartajena and Barranquilla on the north coast of Colombia. My final
trip was on the American Export Lines Marine Perch, a large C-4 passenger ship that
served as troop carrier during the war and as refugee ship after the war. We
traveled to Palermo (Sicily), Naples (Italy), and Valleta (Malta). The ship had a large
medical complement and the work was easy.
In Naples, I hired a taxi for a 28-hour trip to tour Rome visiting the Roman
ruins during the night. When we landed in Malta, I visited the port and soon I had a
following of young boys and girls, pointing to my white uniform and especially my
white shoes. When I enquired as the cause of the hilarity at a silver shop managed
by a Jewish owner he pointed to the almost universal black clothes of women and
men, honoring the dead. “I must be rich, very rich, to wear white shoes.”
Peregrinations
In 1962, I was invited to direct a new research institute, the Missouri
Institute of Psychiatry on the grounds of the St. Louis State Hospital, with an
academic affiliation as Research Professor at Washington University School of
Medicine. We found a home in the Lake Forest suburb, and our children were soon
registered in the community schools. When our youngest child, Linda was schooled
daily, Martha enrolled at Washington University for an M.A. in Education, which led
to her lifelong elementary school teaching career.

We adjusted to a new community even though warnings of religious
intolerance appeared early. When we were looking for a home, I asked George Ulett,
90

�the head of the State mental health services who invited me, where he lived. “In
Ladue,” continuing with the advice, “You would not be happy there.” I did not catch
the warning but we soon experienced the strong smells of anti-semitism and
nativism that pervaded the St. Louis communities, the state, and even the hospital
government during our stay. My appointment to the MIP was announced as
“Austrian Heads Institute.”

Two years later the Missouri State legislature failed to renew the biennium
funding for the Institute, and I and the other scientists fled. I found a position at the
New York Medical College to lead the opioid detoxification center at New York City’s
Metropolitan Hospital beginning in July 1966. Martha and I found a home in Great
Neck and enrolled our children in community schools. Martha began teaching
students at the elementary school in Port Washington and then in Great Neck
schools.
I set up my computer center to analyze EEG at the Psychiatry Department
offices on East 102nd Street, developed an ECT study at Gracie Square Hospital, and
obtained a Federal contract to study the systemic effects of hashish in users in
Athens, Greece. I had exceptional students in Richard Abrams, Michael Taylor, and
Robert Levine and was fortunate in the collaboration of Rhea Dornbush, Jan
Volavka, Jiri Roubicek, and Donald Shapiro.

In July 1969 Herman Denber, the director of psychiatric research at
Manhattan State Hospital, invited me to join him on a single-engine Cessna 172
flight that he piloted over the Hudson Valley and the New York harbor. It was a day
of brilliant sunshine and I decided to learn to pilot a small plane. A flying school was
still active at LaGuardia Airport and I began my flying lessons on July 4, 1969. I
soloed Nov 13, 1969. For the next few years I leased airplanes at Long Island’s
Republic and Westchester airports. I piloted Jonathan’s move to Colby College in
Maine and flew to professional meetings. A transcontinental trip in May 1970 from
Westchester Airport, through Tulsa, then the next day on the southern route to San
Diego and San Francisco with Herman Denber to attend the APA meetings.
Interested in leasing a summer home in the Adirondacks in May 1972 Martha and
our daughters flew to Lake Placid. My last flights as pilot were in June 1973.
In 1972 a new medical school was established 40 miles East of Great Neck at
Stony Brook, Long Island. Chairman of Psychiatry Stanley Yolles invited me to join
his faculty to lead research in psychopharmacology and ECT. I gladly accepted to
avoid the hassles of travel to New York City and the social and political hostilities of
the addiction community and the city leaders. For the first few years I taught
students and residents at the Central Islip Psychiatric Center and the Veteran’s
Hospital in Northport. With the opening of University Hospital in 1980 I organized
my teaching, EEG, and ECT studies at that facility.
Martha and I bought a home in Nissequogue on the Stony Brook harbor in
1980. By that time our children had each graduated with doctoral degrees in the
91

�sciences and had begun their academic careers. Jonathan’s degree from Stanford
University led to a post-doc in volcanology and an academic career at Arizona State
University in Tempe. Rachel graduated in marine biology from Cornell and Duke
Universities and then taught at Mt Holyoke College in Massachusetts. Linda
received her undergraduate degree from Amherst College, among the first women
after the college became co-ed, and her doctorate in entomology at University of
Florida in Gainesville. She began a teaching career at Sweet Briar College in Virginia.
Each married at our Nissequogue home and soon the family grew with four
grandchildren.
My research work was well supported by NIMH and private foundations and
I led a consortium to study continuation treatments after successful ECT in
depressed patients. (The CORE studies.) For various administrative reasons I was
unable to carry out my portion of the NIMH funded collaborative study at Stony
Brook and I moved the project to Hillside Hospital, a return for me after 35 years.
For the next decade I supervised this study, developed others, and continued
teaching.

In 2005, at the age of 82, I left the study group at Hillside and retired to my
home to pursue writing. Since 1999 I have wrtitten articles and books with Michael
Taylor, Jan-Otto Ottosson, Edward Shorter, and multiple colleagues on convulsive
therapy, catatonia, ethics, and melancholia. I also continued to lecture and attend
national and international meetings until 2019.

Martha died suddenly on March 31, 2016. I remained at my Long Island
home spending my time writing. By 2018, I established a second home in South
Hadley, Massachusetts with my daughter Rachel. In June 2019 I sold my Long Island
home and moved to Rachel's home in South Hadley, Massachusetts.

92

�Books Authored by Max Fink
Electroencephalography in Human Psychopharmacology. EEG Journal, Supplement
23,
1964. NY: Elsevier.
Convulsive Therapy: Theory and Practice. NY Raven Press, 1979.

ELECTROSHOCK: Restoring the Mind. Oxford U Press, New York, 157 pp., 1999.
Electroshock: Healing Mental Illness. NY: Oxford U Press. 2002.

Ehics in Electroconvulsive Therapy. NY: Routledge. 2004. (Ottosson J-O, Fink M.)
Catatonia: A Clinician's Guide to Diagnosis and Treatment. Cambridge UK:
Cambridge U Press, 2003 (Fink M, Taylor MA.)

Rediscovering Catatonia: The Biography of a Treatable Syndrome. Acta psychiatr
Scand. 127: Supplement 441;1-50, 2013.
The Madness of Fear: A History of Catatonia. NY: Oxford University Press, 2018.
(Shorter E, Fink M.)

Melancholia:The Diagnosis, Pathophysiology, and Treatment of Depressive Illness.
Cambridge UK: Cambridge University Press, 2006. (Taylor MA, Fink M,)
Endocrine Psychiatry: Solving the Riddle of Melancholia. NY: Oxford U Press.
(Shorter E, Fink M.), 2010.
Edited Books:

Fink M. (Ed.) Convulsive Therapy. Seminars in Psychiatry. Grune &amp; Stratton, 1972.

Fink M, Kety S, McGaugh J, Williams T. (Eds): Psychobiology of Convulsive Therapy.
Washington, DC, V.H. Winston and Sons 1974.

Bradley P, Fink M. (Eds): Anticholinergic Drugs and Brain Functions in Animals and
Man, P. Bradley and M. Fink (eds.), Progress in Brain Research, Vol. 28,
Elsevier, 1968.

Dornbush RL, Freedman AM, Fink M., Chronic Cannabis Use.. Annals N.Y.
Academy of Sciences, 282: 430 pp., 1976.

Stefanis C, Dornbush RL, Fink M. Hashish: A Study of Long-Term Use (eds.).
New York, Raven Press, 181 pp, 1977.

93

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8

Archives: When the historians Edward Shorter and David Healy visited my home
in 2006 to examine my files and books for their history of the shock
therapies, they were impressed by the extent of the files and asked what I
planned to do with them.1 They encouraged their being publicly archived.
The Stony Brook University Library archivist Kristen Nyitray examined and
agreed to archive the collection. These files are established as the Max Fink
Archives in the Special Collections at the Main Library of Stony Brook
University. I also deposited my library; these books are indexed in the
University files and in WorldCat.
Contact: Kristen J. Nyitray, Head, Special Collections and University
Archives, University Archivist, Associate Librarian, Stony Brook
University.
&lt; kristen.nyitray@stonybrook.edu&gt;
t: 631.632.7119 / f: 631.632.1829
Rachlin HL, Goldman GS, Gurvitz M, Lurie A, Rachlin L. Follow-up study of 317
patients discharged from Hillside Hospital in 1950. J Hillside Hosp 1956;
5:17-40.

Fink M Shaw R, Gross G, Coleman FS. Comparative study of chlorpromazine and
insulin coma in the therapy of psychosis. J. Amer. Med. Ass., 1958; 166: 18461850
Sylvia Nasar's biography A Beautiful Mind was filmed; I was the consultant to the
producers in the making of the film. Discussed in Book Three.

Fink M. A Beautiful Mind and insulin coma: social constraints on psychiatric
diagnosis and treatment. Harvard Review of Psychiatry 11: 284-290, 2003.

Fink M, Bolwig T. Electrotherapy of melancholia: The pioneering contributions of
Benjamin Franklin and Giovanni Aldini. J ECT 2009; 25:15-18.

Beginning January 1953 with Hans Strauss and Mortimer Ostow I learned how to
apply scalp electrodes, maintain the EEG recorders, and interpret the
records. The Medical Director Joseph S. A. Miller, purchased a Grass
electroencephalograph with a $5,000 grant from the Dazian Foundation
obtained by Dr. Israel Strauss, the Founder of the Hospital.

In the 10 years of its existence, Ira Belmont, Martin A. Green, John C. Kramer, Max
Pollack, Eric Karp, Donald F. Klein, Abraham Kaplan, Arthur Willner, Karl
Andermann, Joseph Jaffe, Hyman Korin, George Krauthamer, Nathaniel Siegel,
Henry J. Lefkowits, Harold Esecover, and Barre Alan, collaborated in the
studies. Arnold G. Blumberg of the Medical Department was an active
collaborator..
94

�9

By 1977 in USA, Paul Blachly created an ECT stimulating device using brief pulse
stimuli that recorded the EEG of the seizure. His device, labeled MECTA, has
been widely adopted. The technology became world standard.

10
11

12

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14
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18

Fink M, Kahn RL, Green M. Experimental studies of the electroshock process. Dis.
Nerv. Syst., 19: 113-118, 1958.

In the last two decades, ECT has been denigrated as a "neurostimulation." Since
neurostimulation devices are applied in neurotic depressed and character
disordered subjects, increased outpatient usage has changed the character of
modern treatment to encompass low energy, short seizure, RUL placement
treatments that fail to influence severely ill, but act mainly as placebo
psychotherapiess similar to the weakened SSRI, SNRI antidepressants and
atypical neuroleptics that dominate outpatient care since the 1990s.
Fink M, Taylor MA, Shorter E, Vaidya NA. The failure of the schizophrenia concept
and the argument for its replacement by hebephrenia: applying the medical
model for disease recognition. Acta Psychiatr Scand 2010; 122: 173-183.
The question is the basis for the neuroendocrine hypothesis of ECT, that the
seizure pattern is based on systematic changes sensed by pathology in the
organism that can be redressed, much as a sneeze or a cough clears physical
passages.
Bennett, A.E. The introduction of curare into clinical medicine.Present and
potential usefulness. Am Sci 46; 34:434-431.

While on a lecture tour in 5 cities in India in 1991, the first question at each site
was my attitude to the use of unmodified ECT, inducing seizures without
sedation and motor relaxation. When I expressed my experience, recalling
the benefits of my first experiences at Hillside in 1952, I opined "unmodified
ECT is better than no ECT." The audience applauded. The argument persisted
for many years as the cost of the agents and the fee of the anesthesiologist
surpassed the reimbursements for the ECT procedure.
When the anti-psychiatry cries of psychologists became strident again in 2020s,
with claims that ECT had not been properly tested in an RCT with sham ECT.
The sham-ECT study data was republished in 2001 in JECT.
Palmer RL. Electroconvulsive Therapy: An Appraisal. NY: Oxford U Press, 1981

Fink M, Kahn RL, Karp E, Pollack MA, Green MA, Alan B, Lefkowitz HJ. Inhalantinduced convulsions. Arch. Gen. Psychiat., 4: 259-266,1961.
95

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25

26
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29

Cooper K, Fink M. The chemical induction of seizures in psychiatric therapy:
Were flurothyl (Indoklon) and pentylenetetrazol (Metrazol) abandoned
prematurely? J Clinical Psychopharmacology. 2014; 34(5):602-7.

Fink M, Greenberg LB, Gage J, Vikun S. Isoflurane anesthesia therapy: A
replacement for ECT in depressive disorders? Convulsive Ther 1987; 3: 269277.
Fink M. Cholinergic aspects of convulsive therapy. J. Nerv. Ment. Dis., 1966; 142:
475-484.

The results are widely published by Robert Kahn, Max Pollack, and Ira Belmont.
The results are summarized in Convulsive Therapy: Theory and Practice, NY:
Raven Press, 1979.

We received four-year funding from NIMH for the project. After we introduced
the study to the GSH practitioners, many agreed to cooperate and to let us
treat their patients according to our protocols. They endorsed their patients’
cooperation for EEG and psychological tests. Aside from Richard Abrams and
myself, our study collaborators were Jan Volavka, Jiri Roubicek, Rhea
Dornbush, and Stanley Feldstein from the Biological Psychiatry Research
division of the New York Medical College.
This is my second study reporting the greater efficacy of seizures induced by
bilateral electrode placements. The CORE study replicated again.

Fink M, Abrams R, Volavka J, Roubicek J, Dornbush R. Lateralized EEG changes
after unilateral and bilateral electroconvulsive therapy. Dis. Nerv. Syst., 31
(11) Suppl.: 28-33, 1970.

Wachtel LE, Dhossche DM. Self-injury in autism as an alternative sign of catatonia:
implications for convulsive therapy. Med Hypotheses 2010; 75(1):111-4.
Bright-Long L, Fink M. Reversible dementia and affective disorder: The Rip van
Winkle Syndrome. Convulsive Ther 1993; 9: 209-16.
Greenberg LB, Mofson R, Fink M. Prospective electroconvulsive therapy in
delusional depressed patient with a frontal meningioma. Br J Psychiatry
1988; 153: 105-107.
Petrides G, Fink M. Atrial fibrillation, anticoagulation, and electroconvulsive
therapy. Convulsive Ther. 1996; 12: 91-98

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31

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33

34
35
36

Fink M. Is EST a useful therapy of schizophrenia? In J.P. Brady and H.K.H. Brodie
(eds.): Controversy in Psychiatry. Philadelphia, W.B. Saunders Co., 183-193,
1978.
Fink M. EST and other somatic therapies of schizophrenia. In L. Bellak (ed.):
Disorders of the Schizophrenic Syndrome. Basic Books, New York, 353-363,
1979.
Fink M., Sackeim HA. Convulsive therapy for schizophrenia? Schizophrenia Bull.
1996; 221: 27-39
Fink M, Taylor M.A. The medical evidence-based model to identify psychiatric
syndromes: Return to a classical paradigm. Acta Psychiatr Scand 2008; 87:
81-84 .

I did not believe that ECT augmentation of clozapine in clozapine non-responders
was effective. When George Petrides, with the encouragement of John Kane
to publish a "positive" report, I withdrew my association. Augmentation by
ECT of fluphenazine and chlorpromazine treatment in psychosis are better
documented.
Greenberg LB, Zervas I, Suckow RF, Cooper T, Jandorf L, Fink M. Rat brain
concentration of fluphenazine during a course of electroconvulsive shock.
Convulsive Ther 1990; 6: 273-9.
I moved the study site to Hillside Hospital with George Petrides as Principal
Investigator.

Fink M. What was learned: Studies by the Consortium for Research in ECT (CORE)
1997-2011. Acta Psychiatrica Scand. 129: 417-426, 2014.
Fink M, Taylor MA. Electroconvulsive therapy: Evidence and challenges. JAMA
2007; 298: 330-332 .
R. Electroconvulsive Therapy. Edition IV. NY: Oxford University Press,
2002.

37Abrams
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39
40

Meduna L: Die Konvulsionstherapie der Schizophrenie. Halle Germany, Karl
Marhold, 1937.

Fink M. (Ed.): Convulsive Therapy (ed.). Seminars in Psychiatry 4: 1. Grune &amp;
Stratton, Inc., New York, 70 pp.

Fink M, Abrams R, Bailine S, Jaffe R. Ambulatory electroconvulsive therapy. Ta
force report of the association for convulsive therapy. Convulsive Ther. 1996;
12: 42-55.
97

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44
45
46
47

Fink M. Complaints of loss of personal memory after electroconvulsive therapy:
Evidence of a somatoform disorder. Psychosomatics 2007; 48:290=293.
Fink M. A Beautiful Mind and insulin coma: social constraints on psychiatric
diagnosis and treatment. Harvard Review of Psychiatry 2003; 11: 284-290.
Fink M. A unified theory of the action of physiodynamic therapies. J. Hillside
Hosp.,1957; 6: 197-206.

Fink M, Ottosson J-O. A theory of convulsive therapy in endogenous depression:
Significance of hypothalamic functions. Psychiatry Research 2: 49-61, 1980.

Fink M. The mode of action of convulsive therapy: the neurophysiologic-adaptive
view. J. Neuropsychiat., 3: 231-233.1962.
Fink M. Cholinergic aspects of convulsive therapy. J. Nerv. Ment. Dis., 1966; 142:
475-484.

Nemeroff C, Bissette G, Akil H, Fink M. Neuropeptide concentrations in the cerebrospinal
fluid of depressed patients treated with electroconvulsive therapy. Corticotrophinreleasing factor, beta endorphin and somatostatin. Br J Psychiatry 1991; 158: 59-63.

48
49
50
51
52
53

Fink M, Kety S, McGaugh J, Williams T. (Eds): Psychobiology of Convulsive
Therapy. Washington, DC, V.H. Winston and Sons

Kahlbaum KL. Die Katatonie oder das Spannungsirresein: eine klinische Form
psychischer Krankheit. Berlin: Verlag August Hirshwald, 1874.

Greenberg LB, Gujavarty K. The neuroleptic malignant syndrome: Review and
report of three cases. Comprehens Psychiatry 1985; 26:63–70.

Taylor MA. Catatonia: A review of a behavioral neurologic syndrome.
Neuropsychiatry, Neuropsychology Behavioral Neurology. 1990; 3(1):48-72.
Rogers D. Motor disorder in psychiatry. Chichester UK: John Wiley &amp; Sons, 1992.
Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia: I: rating scale and
standardized examination. Acta psychiatr. Scand 1996; 93 (2): 129-36.

Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia: II. Treatment with
lorazepam and electroconvulsive therapy . Acta Psychiatr. Scand 1996; 93 (
2):137-43.
54

Shorter E. What Psychiatry Left Out of DSM-5. NY: Taylor &amp; Francis, 2015.
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Taylor MA. Hippocrates Cried: The Decline of American Psychiatry. NY: Oxford U
Press, 2013.

Taylor M, Fink M. Fink Catatonia in psychiatric classification: A home of its own.
Am J Psychiatry 2003; 160: 1233-1241.
Fink M, Shorter E. Does persisting fear sustain catatonia? Acta Psychiatr Scand
2017; Nov; 136(5):441-444.

Our experience together had been at New York Medical College during his
residency training and when he and his colleague Richard Abrams joined the
Stony Brook University faculty.

Clinicians versed in ECT see the rapid response of catatonia and melancholia, in
their varied forms, to repeated induced seizures. The DSM commissioners, all
five teams from 1952 to 2013, lacked members with experience in ECT.
Many were known opinion leaders and paid consultants to industry, with
ambulatory office practices and little experience with the severely ill, so had
no experience with the many forms of catatonia and melancholia. Further, in
the decades from 1980 to 2013, they were paid well as industry consultants
to support the new agents, the SSRI, SNRI, and atypical neuroleptics, and
reject the tricyclic antidepressants (imipramine, amitriptyline) and the
typical neuroleptics (chlorpromazine, fluphenazine) as toxic.
Fink M, Klein DF, Kramer J. Clinical efficacy of Chlorpromazine-Procyclidine
combination, Imipramine and placebo in depressive disorders.
Psychopharmacolgia (Berl.), 7: 27- 36.

Davies BJ, Carroll BJ, Mowbray RM: Depressive Illness: Some Research Studies.
Springfield, IL: C. C Thomas, 1972.

Papakostas Y, Fink M, Lee J, Irwin P, Johnson L. Neuroendocrine measures in
psychiatric patients: Course and Outcome with ECT. Psychiatry Res 1981;4:
55-64.
Glassman A. APA Task Force on Laboratory Tests in Psychiatry: The
Dexamethasone Suppression Test in Psychiatry. Am J Psychiatry
1987;144:1253-1262

Fink M, Rush J, Knapp R, et al. DSM melancholic features are unreliable predictors
of ECT response: A CORE Publication. JECT 2007; 23(3): 139-146.
Taylor MA, Fink M. Melancholia: The Diagnosis, Pathophysiology, and Treatment of
Depressive Illness. NY: Cambridge University Press, 2006.
99

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Bolwig T, Shorter E. Melancholia: Beyond DSM, Beyond Neurotransmitters. Acta
Psychiatrica Scandinavica Supplement 433; 115:1-183, 2007.
Participants included, in addition to the Editors, Gordon Parker, Michael
Taylor, William Coryell, Athanasios Koukopoulos, Donald Klein, Bernard
Carroll, Jules Angst, Walter Brown, Max Fink.
Taylor M. Hippocrates Cried. The Decline of American Psychiatry. NY: Oxford
University Press, 2013.

Shorter E, Fink M. Endocrine Psychiatry: Solving the Riddle of Melancholia. NY:
Oxford University Press, 2010.

Bradley P, Fink M. (Eds): Anticholinergic Drugs and Brain Functions in Animals and
Man. Progress in Brain Research, Vol. 28, Elsevier, 1968.
Fink M. EEG classification of psychoactive compounds in man: review and theory
of behavioral associations. Psychopharmacology: A Review of Progress, 19571967: D. Efron, J. Cole, J. Levine and J.B. Wittenborn (eds.): U.S. Govt. Printing
Office, Washington, DC, pp. 497-507.

Fink M. Remembering: the forgotten neuroscience of pharmaco-EEG. Acta
Psychiatr Scand 2010; 121: 161-73.

In my schooling, self-administration of trial medication was accepted as part of
my educational experience. By 1980s, a change had occurred among
students. When teaching psychopharmacology I offered self-exposures to
various psychoactive medications,many of which I had experienced. The
students refused, and I was admonished by the Dean that such teaching was
not acceptable.
As the death of President Kennedy was announced over the hospital radio, I was
in the r-ray suite, inserting a needle in a patient's spinal canal for a PEG.

Dr. Tarachow presented these findings at a meeting of the American
Psychoanalytic Association in New York in 1953. I was denied admission to
the meeting as I had not graduated from an accredited psychoanalytic
institute.

100

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                    <text>May 17, 2017

A Boy from the Bronx: A Recollection
Max Fink, M.D.

Arline Alda’s “Just Kids from the Bronx” enticed me to recollect the first 20 years of my
life.1 The personal stories of her friends and those of her husband Alan Alda of childhoods spent
in Bronx apartment houses and public schools described the rich lives of European immigrants
first to the city and their spread to the outer borough of the Bronx with their farms and parks and
unimproved acres. Her 19-year old brother Adolph came from New York to shepherd us across
the Atlantic on the SS George Washington. We joined my mother’s families the Gottliebs and the
Lowenthals in a cluster of apartment houses on Fifth Avenue just north of Central Park. The
park, bicycle paths, lake and boat pond were our playgrounds.
After my father received the New York State license to practice medicine, my parents
travelled along the newly developed Pelham Bay Park elevated train line, along the southeast
corridor of the Bronx, stopping at one exit after another, walking the streets near each station,
seeking an apartment suitable for a doctor’s office. A five story apartment building at 1201
Elder Avenue just 50 yards from the elevated train station offered a six room ground floor
apartment. The corner store was a pharmacy and soda fountain and a luncheonette with
newspapers and magazines on the other side. 2 The dual track train stood on steel columns along
Westchester Avenue, over trolley car tracks that offered a busy and noisy transportation hub.
Multi-story brick houses with honey locust trees filled the avenue.

PS 77 elementary

school3 was two streets to the North and East on 172 Street and Ward Avenue, with the James
Monroe High School just one street to the North. My parents joined the reformed synagogue on

�Elder Avenue and 172 Street.4 This enclave became a vibrant Jewish community that sustained
my father’s practice. Other practitioners settled in the neighboring streets and the need for
hospital facilities led community physicians to establish the two-story Hunts Point Hospital and
then a few years later a much larger Bronx Hospital, both offering facilities for practitioners to
treat their patients.5
My mother’s brother Max Lowenthal established his office and home on Washington
Avenue, a few streets from the Bronx Hospital. His home was on a large lot offering a
playground for our family visits. His oldest son Charles was a Scoutmaster and both my brother
and I were active Boy Scouts.
In time my parents rented an apartment (#3) in the same building as our home. Melvin
and Ruth Muroff, lifelong friends lived in Apartment #2. (Apartment #4 was the office of our
dentist Dr. Heyman.)
In 1928, my father’s mother Dvora Grunwerg migrated and was established in Apartment
#5. She occupied the first two rooms leaving the large living room with windows facing the
elevated railroad as a play area for my brother Sidney and myself. We adapted to the screeching
brakes of train halts and noises of the doors and motors every few minutes, day and night. The
living room was our playground, with Lionel electric trains on the floor, chemical experiments,
chess and marble games on tables. My grandmother adhered to orthodox Jewish practices and
tolerated our noises and arguments.
My father’s office windows faced the street. Although Elder Avenue was lightly
travelled, my friends and I were admonished to keep the noise levels low. My father parked his
car in front of the building entrance, a notice that he was in his office. His open “office hours”

�were 12 to 1 and 6 to 8 each day. My brother and I were expected to join him for dinner each
day at 5:30.
The office telephone was monitored at all times so early in my life I learned to answer the
ring with ”Dr. Fink’s office” and record the messages. When my father went to a movie house
or a play or opera in the city, he sought an aisle seat after notifying the usher that he was
available for calls.
I had a mutt dog called Pal. He developed seizures, often vomited, and more often
whimpered and cried for long periods. My father had various medications in his office and I
soon learned that the pink capsule (secobarbital, Seconal) would quiet Pal nicely. One night,
when my parents were at a movie house, Pal was very upset. I fed him two capsules and went
back to reading and listening to radio music. Not hearing from Pal, I found him under the dining
room table, unconscious and not responding. Panicked, I called my father and blurted that he
should come home quickly for an emergency. After a hurried drive through the broad streets of
Southern Boulevard, over the trolley tracks, he rushed in and when I showed him the “dead” dog,
he listened and examined and opined that the dog would soon recover. My chagrin was an early
lesson in the need for examination before ringing a panic button.
During the financial depression of the 1930s a barter system was in place. I was often
sent to the grocer, butcher and fish shops, pharmacy and laundry, bringing home packages after
my mother had called. I rarely needed cash money except to use the train or trolley systems.
By 1936 the developing Spanish Civil War and the anti-Jewish restrictions in Germany
became daily family concerns as my parents sought to bring Jewish relatives and school
classmates to America. To obtain a visa the immigrants needed evidence that they would not

�become wards of the government. My parents established bank accounts in the names of each of
the relatives with a joint owner, often using me as the citizen.6
PS 77 and the James Monroe High School were well regulated. Boys wore white shirts
and dark shorts or knickerbocker pants (knickers) clustered just below the knee; girls wore white
midi-blouses and dark skirts. While the halls were noisy between classes, hall “monitors”
maintained order. Being a “monitor” was an “honor” and despite my small size, I was an active
hall monitor.
Desks bound to the floor filled classrooms. I was short and usually sat up front and did
not realize until I took eye tests for a driver’s license at age 16 that I was near-sighted. My first
pair of glasses were a revelation.
I surely was a “nerd” and in the practice of the time I skipped grades four times,
graduating from elementary school at age 12. I qualified for the prestigious Manhattan high
schools, but my parents refused permission saying that the James Monroe High School was just
four streets away and required no travel.
The school had four program “tracks” and I was soon established as college bound on
the academic track. I studied German to meet the language requirement and became an editor of
the monthly Plaudermäulchen (“chatterbox”) and wrote each issue’s crossword puzzle.
I was favored by Ms. Sweet, teacher of English literature and head of the Arista, the honorary
academic society. Tall and lean, always well dressed, she was an enthusiastic reader of murder
mysteries, sharing them with students. When she learned that I wanted to go to medical school,
she sent me to the coach of the football team, Mr. Wiedman who offered me a position as a
“team manager.” I kept records of the games, team equipment, medical supplies, and monitored
travel arrangements for off-site games. At the end of the game season I arranged a team dinner,

�once at a New York City retaurant on Times Square. At the school graduation I was awarded an
athletic letter M, a note in my college application that may have supported my college
admission as a “well rounded student.”
I graduated high school in January 1939 at age 16 and enrolled in New York University’s
College at its Bronx campus for its Feb-Sep program.7 I lived at home and used the trolley line
to come to school. By the second year I established myself as a library assistant in the Gould
Memorial Library and a research fellow in the biology programs under Carl Sandstrom and
Horace W. Stunkard.8 I soon found niches in the Library and Biology Buildings in which I could
leave a cot and some clothes and I often remained on campus for days on end.
As an editor of the Heights Daily News, the college’s 4 to 8 page newspaper, I spent a night each
week at the printshop in Fort Lee, New Jersey, editing page proofs and setting type for headlines.
I wrote stories of campus events and visiting lectures.
The aroma of print ink settled in my clothes and led me to work from time to time in the
art book multi-color print shop of Martin Jahoda. Martin was émigré relative of my father’s
medical school classmate Julius Halpern who fled Vienna with his wife Frieda and daughter Eva
on March 12, 1938 (the day that Hitler was welcomed into Vienna). The family lived nearby on
Elder Avenue as he studied for the New York State medical licensing examinations. I coached
him in English and as a gift he gave me a Leica camera that was compact and easily fit my
trouser’s pocket. I used it throughout my medical school career.
My parents moved their home to Pelham Manor at 528 Manor Ridge Road before WW II.
I did not live at that home. My parents had supported the Elder Avenue Synagogue and they led
the organization of the Pelham Jewish Center in their village. It took many years of effort to
overcome the community’s restrictive covenants against Jews and blacks, the prevailing Nimby

�attitude of Westchester County communities at the time. The Center and Synagogue opened on
the Esplanade in 1953.
My brother Sidney was born in 1927. He followed the same trajectory in the same public
schools that I attended. He graduated Columbia College in 1948 and Columbia’s College of
Physicians and Surgeons for his medical degree in 1952. His residency training in medicine at
Montefiore Hospital was followed by years of research as a Damon Runyon Fellow. He
specialized in gastroenterology and by 1959 he left the Bronx for a career in community
practice.9
I recall our Victrola, a large mahogany box that played 10- and 12-inch vinyl records.
My parents and then I collected records, mostly symphonic and operatic. My parents had been
well versed in opera during their education in Vienna. Radio music dominated our living room
as we avidly followed the news, hours of symphonic and operatic music, and the stories of
Manchu the Magician, the Lone Ranger and Jack Armstrong, the All-American Boy and other
“soap operas” for boys.
What else do I recall of my experience in the Bronx? During childhood, cars and trucks
were few, much if not most traffic was horse-drawn wagons, leaving manure on the streets.
White-clothed Sanitation sweepers kept the streets clean; but we were accustomed to playing ball
in littered streets.
The Bronx River flowed three streets west of Elder Avenue. “The mud flats” of its
banks, the Morrisania Farms with milk cows and chickens just to the north. The Bronx
Zoological and Botanical Parks a quarter mile north, well within walking distances, were our
playgrounds. We played stickball, practiced skills with marbles (immies, steelies, aggies), tossed
and collected Goudey Indian and World War I Air Ace Cards, and built carts using 4-wheel

�roller skates. On week-end afternoons we took the train to New York City to visit the Museum
of Natural History with its dioramas and Saturday afternoon films like Nanook of the North and
the conquest of the North and South Poles by Admiral Peary and Roald Amundsen. I learned to
swim at the Castle Hill pools and ride horses at Pelham Bay Park.
Speaking of Indian cards, in 1990 my daughter Linda was teaching at Middlebury College. She
and Martha went on a shopping trip leaving me to wander US Route 7 alone. A bookshop
showcase contained Goudey Indian Cards of 1936 vintage. Nostalgia led me to buy three for $5.
For the next decade I bought, bartered, and exchanged cards at ephemera shows until I had a full
set of 216 cards in good to excellent condition. These have been a prize collection in my library
and are now at the Oregon Museum of Science and Industry in Portland.
I received my letter of admission to New York University Medical School on December
6, 1941 the day before the Japanese attack on Pearl Harbor. That summer I began my studies at
Bellevue Hospital and was inducted into the Army Specialized Training Program (ASTP) for my
medical school years. Because Bellevue faculty made up one of the Hospitals sent overseas, we
were taught by a very junior faculty. I participated in many research protocols and was
encouraged to undertake procedures as obtaining blood and spinal fluid, set fractures, deliver
babies, and do minor surgery.
On graduation in June 1945 I started an internship at Morrisania City Hospital in the
Bronx. In April 1946 I went on active military duty, was trained in neuropsychiatry at the army
School of Military Neuropsychiatry in San Antonio and served 20 months stateside. At age 24, I
was suddenly discharged in November 1947 with the end of the war and troop demobilization.
Having been in school continuously since childhood I elected to spend the next six months as a
ship’s Surgeon on the Grace and American Export Lines. On a Grace Line cruise to South

�America I met Bertie and Harry Gross of Great Neck, and met their daughter Martha when we
returned at the end of the cruise to Pier 57 in NYC. We began our courtship and Martha and I
married in September 11, 1949 after her graduation from Barnard College in June.10
Throughout medical school days I lived at Elder Avenue, often taking the subway to the school.
My internship at Morrisania City Hospital from July 1945 to June 1946 and my residencies at
Montefiore and Bellevue Hospitals kept me within the borough. On January 2, 1952 I joined the
staff of Hillside Hospital on the eastern edge of Queens. I had already established a base at
Martha’s parents home in Great Neck in 1949 and thereafter my connection to the Bronx was
limited to visits to my father’s Elder Avenue office until his death in 1965 at age 67.
My mother Bronia was my father’s assistant when he opened his office. After my brother and I
spent our days in school my mother took part in community services, especially during the war
years. She organized a storefront child care center on Elder Avenue, nurtured it to become an
affiliate of the Federation of Jewish Philanthropies. She developed centers at Clason Point and
then at Bronx River Housing. During the war years she was chairwoman of the local rationing
board. She was a well known community leader.
Bronia’s medical education was interrupted by my birth during her fourth year at the
University of Vienna. After the war, when Sidney and I were well along in our schooling she
sought to enroll in a New York City medical school to continue her medical education, but was
refused admission. With her experience as a community leader, she turned to training in social
work, graduating from the Columbia University School of Social Work in 1956. Thereafter she
worked at the Lenox Hill Hospital until retired by age at 65 (1967); then at the Brandywine
Nursing Home where she worked for an additional 12 years,

�My uncle Max Lowenthal had three children. His daughter Irma was very close to my
mother and after her children were grown, she too was active in Bronx projects. She married a
physician Henry Fleck. She was born in Poland in 1919, emigrated in 1921, and died in 2004 at
age 84. Her obituary describes her extensive efforts in enhancing Bronx culture.11
Our families were educated and nurtured in the Bronx. It was a happy environment with
little to anticipate the riots and burnings and the white flight of the 1970s.12 During the years of
the economic depression, a barter economy and volunteer community efforts encouraged child
care and welfare for the poor. It was a nurturing community.

1

Alda, Arline. Just Kids from the Bronx. New York: Henry Holt &amp; Co., 2015.

2

The luncheonette was managed by the Muroffs who were lived next door neighbors. Their son Melvin, 2 years
older than I, became a lifelong close friend. A graduate of the Menninger Foundation Institute in Topeka, he later
practiced clinical psychology in Scarsdale, New York. He and his wife Blanche were loyal friends and supporters
of my research as members of the Board of the International Association for Psychiatric Research.
3

4

Now redesignated Public Schools 195 and 196, at the junction of Ward Avenue and 172 Street.
My brother and I obtained our Jewish education and celebrated our Bar Mitzvahs at this center.

5

By 2015 neither hospital, nor the Morrisania City Hospital were still to be found.

6

My parents became citizens in 1928, and I was designated as a citizen at the same time.

7

For students who completed high school admission in February an intensive summer program allowed students to
join the sophomore class in September.
8

My research problem was to study the impact of light and darkness on the mitosis diurnal cycle in the ependymal
layer of the 48 to 72 hour chick. Others had studied th 24 to 48 and 72 to 96 hour cycles. We found no changes in
mitosis rates.
9

After a period of research at Montefiore Sidney began a clinical practice in Paterson, New Jersey with a group
headed by Irving Selikoff, an eminent researcher in pulmonary diseases,. He moved to an academi position in
Chicago, then at the Veterans Hospital in Providence. He married Eleonor Engelman, a student at Barnard College.
They had 3 children Michael (now in Chicago working for more than 25 years as an analyst at United Air Lines);
Deena on the faculty in Mathematics and Computer Science at New York University’s Courant Institute; and Bert, a
publicist for Rogers &amp; Hammerstein Music studios. While in Providence Ellie died; Sidney joined the US Air Force
as medical officer, where he met and married nurse Nesta Hignett, moved to the Veterans Hospital in Hampton
VA. After her death he retired to Hampton community.

�10

Martha died suddenly on March 31, 2016. Her ashes are under a Japanese Cherry tree on our lawn in
Nissequogue. We had been happily married for 67 years. We have 3 children born between 1951 and 1958.
Jonathan is Professor and VP for Research at Portland State University; Rachel is Professor of Biology at Mount
Holyoke College, and Linda is Professor of Ecology at Sweet Briar College.
Jon married Nina DeLange in Phoenix and they have a daughter Laurel and a son Andrew. Laurel
graduated Arizona State University and obtained the Master’s degree at the University in Brisbane, Australia.
Andrew is completing his sophomore year at University of British Columbia in Vancouver, Canada.
Rachel married Tom Dennis, a Professor of Astronomy/Physics and has Rose Dennis who graduated Mt
Holyoke College on May 15, 2016 and Hieu Dennis who is completing his 2 nd year at Union College.
Linda married the Monarch Butterfly scientist Lincoln Brower who taught her during her career at Amherst
College. They do not have children.
11

http://www.nytimes.com/2004/02/26/nyregion/irma-fleck-84-who-battled-decay-in-the-bronx-is-dead.html?_r=0;
http://timesmachine.nytimes.com/timesmachine/1971/01/12/83198899.html?pageNumber=26;
http://www.nytimes.com/1986/09/17/opinion/l-a-way-for-hay-fever-victims-to-fight-back-763486.html;
http://www.nytimes.com/1989/06/07/opinion/l-violence-of-old-men-vs-the-idealism-of-youth-what-tocquevillesaid-279689.html
12

Mahler J. Ladies and Gentlemen, the Bronx Is Burning: 1977, Baseball, Politics, and the Battle for the Soul of a
City. NY: Farrar, Straus, Giroux,2006.

Appendix 2: The Forgotten Merits of Diagnostic Tests

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,ﬁ,

.

1

Confinia Neurologica

9/

NEURQPHYSWLUEY [ABQRMURY
HILLSIDE HOSPITAL
GLEN OAKS' N' Y-

Borderland of Neurology -— Grenzgebiete der Neurologie
Les conﬁns de la Neurologie
Edidit: E. A. SPIEGEL

Basel

S. KARG ER
Separatum Vol. 12, Fasc. 4 (1952)

:

3

.

New York
Printed in Switzerland

From the Department of Neurology and Psychiatry, New York University College
of Medicine and the Neurological Service of the Third Division, Bellevue Hospital,
New York City

A Clinical Evaluation of Carotid Angiography
by MAX FINK and JOSEPH M. STEIN

._.I
I

‘

f

.3
I

Since carotid angiography has become a routine procedure in
the management of intracranial conditions, an evaluation of its use
is necessary. Both the indications and hazards of the procedure
must be considered in recommending it for diagnostic purposes. It
seemed valuable, therefore, to review the angiograms done on the
neurological service of a general hospital. During the past 20
months, 117 percutaneous diodrast angiograms were completed by
members of the resident house staff. The majority were done di-

rectly by the authors.
A variety of neurological conditions including suspected brain
tumors, vascular anomalies, subdural hematomas, vascular diseases and diffuse degenerative diseases were selected by the attending staff as suitable candidates for angiography. In each case, a
percutaneous carotid angiogram was performed according to the
usual descriptions (1). Either local inﬁltration by novocaine or
general anesthesia by pentothal or surital was used. A CournandGrino needle was inserted into the carotid artery at the level of
the thyroid cartilage. In most instances the common carotid artery
was cannulated; in a few instances the internal carotid alone.
Ten to twelve cc. of 35 % diodrast solution were used in each
injection. A simple manual multiple cassette holder was used. This
permitted three consecutive lateral ﬁlms and a single anteroposterior (A—P) view.
In each case the A—P and lateral ﬁlms were immediately
developed, and, if indicated, the injection was repeated. If no
pathology was noted on these ﬁlms, the procedure was repeated
on the other side whenever advisable. Bilateral procedures were
carried out in 26 subjects.

�182

Max Fink and Joseph

M.

Stein

Results
Diagnoses of various conditions were made prior to angiography.
Of these, “brain tumor suspects” made up the largest group;
suspected vascular anomalies and subdural hematoma were the
next largest groups (see Table I). The interpretation of the ﬁlms
was based on descriptions by Moniz (2 a), Lima (2b), and Green
and Arana (l b) .
Brain Tumor Suspects
Of 55 patients in whom intracranial masses were suspected,
angiographic diagnoses of brain tumor were made in thirty. Of
these, 25 were conﬁrmed by subsequent surgery or air studies. Conﬁrmation was not obtained in three patients because further studies
were contraindicated by patient’s age or family’s refusal to give
permission. In two cases the angiograms were interpreted incorrectly and these cases are described.
Case I: D.H. a 48 year old woman was admitted to Bellevue Psychiatric Hospital because of headaches and progressive confusion. The examination revealed
early papilledema, left central facial palsy, skull tenderness on the right and memory
deﬁcits. An electroencephalogram showed a right cerebral focus.
Bilateral carotid angiography under general anesthesia revealed deﬁnite elevation (displacement) of the parietal branches of the right middle cerebral artery.
Subsequent to this procedure the spinal ﬂuid syndrome was noted to be positive
for active syphilis. Anti-luetic treatment was instituted and the patient improved

rapidly.
Five weeks later, the right carotid angiogram was repeated.
These ﬁlms showed the parietal vessels to have a normal conﬁguration.
Case II: 0. 0., a 64 year old male was admitted because of recent onset of
grand mal seizures and left-sided weakness. Examination revealed a mild left
hemiparesis, most marked in the lower extremity. There was a positive Babinski
response and increased reﬂexes. The cerebrospinal ﬂuid syndrome was normal.
A right carotid angiogram under local anesthesia was performed and demonstrated good ﬁlling of the anterior and middle cerebral arteries. There was straightening and depression of the pericallosal artery on the lateral views; and increased
vascularity near the termination of the anterior cerebral artery on the A—P ﬁlm.
These changes were interpreted as evidence of a parasagittal tumor mass displacing
blood vessels.
A pneumoencephalogram was done and this did not demonstrate the mass. The
patient improved without treatment and was discharged. He was readmitted a few
weeks later with evidence of an acute brain stem syndrome. In View of the course
of the illness and multiplicity of lesions, it was believed that the patient’s symptoms
were due to degenerative changes, and not a neoplasm. No further studies were
undertaken.

In this group of suspected brain tumors

22 angiograms did

not
show any pathology. Eleven of these were conﬁrmed by air studies
or autopsy. In two patients, however, satisfactory angiograms
failed to demonstrate lesions later demonstrated by other studies.

�A Clinical Evaluation of Carotid Angiography

183

III:

F. M., a 57 year old man was admitted to the hospital because of
left hemiparesis, bladder and bowel incontinence, and grand mal seizures of 4 weeks
duration. On examination, there were severe personality changes, and a spastic left
hemiparesis with pathological reﬂexes. Cerebrospinal ﬂuid syndrome was normal.
A right carotid angiogram under pentothal anesthesia was done. Two sets of
lateral ﬁlms and one A—P view were taken. The ﬁlms showed no evidence of cerebral tumor.
One week later a ventriculogram demonstrated a large right fronto-temporal
mass. The presence of a malignant glioma was conﬁrmed by surgery.
Case IV: J. S., a 49 year old man developed left sided seizures and aphasia
during hospital treatment for furunculosis. On neurological examination there was
evidence of a lesion in the right hemisphere. On skull x-ray the pineal shadow was
shifted to the left.
An arteriogram on the right side under general anesthesia was done and no
pathology demonstrated. A pneumoencephalogram, however, revealed a deformity
of the right frontal born.
The patient expired one month after angiography and at postmortem, multiple
cerebral abscesses were demonstrated bilaterally.
Case

Other erroneous angiographic diagnoses were made in patients
who proved to have vascular thromboses. In two patients with
signs of a brain tumor, the angiograms revealed an avascular area
in the parieto-temporal region with displacement of middle cerebral
vessels. Surgical exploration revealed edematous necrotic brain
tissue, without evidence of tumor. Each case came to autopsy, and
TABLE

I

ANGIO GRAPHIC DIAGNOSES
Group

No. of

Patients

Intracranial Mass
Vascular Anomaly
and Aneurysms
Suhdural Hematoma
Occlusive Vascular Disease
Other (f)

55

_

Pos.

30

Pos.
Neg.
Not
Diagnosis Diagnosis Incorrect
Neg. Diagnostic (3) Conﬁrmed Conﬁrmed Diagnosis

22

3

25

1

2

21
17

9
9 (d)

ll

11

7

13

2

4
10

8

—
—

l

ll

4

(b)

1

(c)

9
6 (e)

7

—

1

——

5

——

——

Notes:
(a) Technically unsatisfactory ﬁlms.
(b) Two cases conﬁrmed by surgery but 7 other patients'with anomalies demonstrated on arteriograms were not subjected to further studies.
(c) The 11 patients with negative arteriograms were not subjected to further study.
((1) Includes seven diagnoses of subdural hematoma, one of intracerebral hematoma
and one of brain tumor.
(e) F ailurc of the anterior or middle cerebral, or internal carotid artery to ﬁll on
at least two consecutive injections, while the remainder of the circulation
ﬁlled well.

(f) Includes three “follow-up” angiograms, seven patients with diﬁuse degenerative disease and three patients with lesions of the skull.

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Max Fink and Joseph

M.

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in both, thrombosis of a branch of the middle cerebral artery was
found. The angiograms could not be differentiated from those seen
in cases of tumors in the same region.
Vascular Anomalies: Twenty-one patients suspected of intracranial vascular anomalies or aneurysms were subjected to angiography. The angiograms were bilateral in only three of these, and
unilateral in the other nine. One set of ﬁlms were not satisfactory
and were not repeated.
Seventeen of these patients had manifested spontaneous subarachnoid hemorrhages. In nine cases an anomaly was clearly
outlined on the arteriogram. Five of these were aneurysms at the
base, and four, vascular malformations of the hemisphere. No anomaly was demonstrated in eleven cases.
Conﬁrmation of ﬁndings by other methods of study was most
difﬁcult to obtain in this group. In the nine cases where the anomaly was demonstrated, further conﬁrmation was achieved in two
cases. In one, an angiomatous malformation was amputated at
operation. In the other, an aneurysm of the anterior communicating artery was dissected at post mortem. Air encephalograms were
normal in two patients, despite the angiographic evidence of a large
angioma of the cerebrum. The speciﬁcity of angiography in the
diagnosis of vascular malformations is demonstrated by such cases.
Of the eleven patients with negative angiographic ﬁndings,
two were subjected to air studies. These ﬁlms were normal. The
other nine patients were discharged without further study.
Subdural Hematoma: The diagnosis of subdural hematoma was
made angiographically in seven of seventeen patients suspected of
traumatic intracranial hematomas. The characteristic separation
of the vascular patterns from the internal table of the skull as seen
on the A—P projection was the basis for these diagnoses. In each
of these cases the diagnosis was conﬁrmed by trephination.
Furthermore, in the eight patients in whom a diagnostic vascular
pattern was not seen, diagnosis of no blood in the subdural space
was made. These diagnoses were all conﬁrmed by pneumoencephalography.
In two patients angiography demonstrated an intracerebral
mass, rather than a subdural process. In one case, this diagnosis
made it possible for the surgeon to approach the lesion by a well
localized and deﬁnitive procedure. The diagnosis was conﬁrmed in
the second at autopsy.
Vascular Disease: Angiographic studies were done in 11 patients
in whom occlusive vascular disease was believed to be the basis

�A Clinical Evaluation of Carotid Angiography

185

for their neurological ﬁndings. Failure of a portion of the vascular
distribution to ﬁll on two consecutive injections was observed in
seven of these cases, and normal vascular patterns were seen in
the other four. In the ﬁrst group incomplete ﬁlling of the middle
cerebral artery was seen in four cases; of the anterior cerebral
artery in one case; and of the internal carotid artery in two cases.
The vessels which appeared involved on the ﬁlms were in each
instance the same vessels as indicated by the patient’s clinical
syndrome.
In four of these patients pneumoencephalography demonstrated
areas of atrophy in the involved region of the brain. In one case,
post mortem studies conﬁrmed the angiographic ﬁndings. No conﬁrmation was obtained in the other six cases.
Miscellaneous Group: Of the 13 angiograms in the group, seven
were done in patients with diffuse cerebral disease of a degenerative
type. These ﬁlms were not characteristic but in each case air
studies demonstrated an enlarged ventricular system without
shift or deformity. In three patients with lesions of the skull angiography failed to demonstrate any cerebral involvement. Pneumoencephalograms were done in only two of these patients and
were normal.
Complications: In an evaluation of the indications for a diagnostic procedure the incidence and severity of complications must be
considered. In this series of 117 angiographic studies, 36 patients
suffered a total of 43 complications. There were ﬁve cases with
severe and permanent complications. In all other instances the
complications were mild and transient. Of the transient complications, 22 hematomas of the neck were recorded. This was recorded
only when the hematoma was large. In one case, in a child, the
hematoma was large enough to cause tracheal shift and respiratory
difﬁculties. It was necessary to intubate the patient and maintain
the airway during the evening of the procedure. Transient hemiparesis or transient increase in an existing hemiparesis was seen
in 7 cases, and a grand mal seizure was observed in 2 patients. In
each instance the phenomena disappeared within 48 hours. In 4
cases urticaria, chills and vomiting followed angiography, and
seemed to represent an allergic response to the diodrast. In one
patient, in whom a vascular anomaly was demonstrated, fresh
blood was manifest in the spinal ﬂuid the morning after the procedure.
Of the severe complications, death occurred within 24 hours of
angiography in two patients (cases V, VI). In three other patients

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Max Fink and Joseph M. Stein

severe complications were directly related to angiography. In a
young child an osteomyelitis of the transverse process of the ﬁfth
cervical vertebra resulted after a difﬁcult cannulization (case VII).
A permanent mixed aphasia (case VIII) and an intensiﬁcation of
a pre-existing hemiparesis (case IX) were also observed.
Case V: G. B. male, 62. Craniotomy, three months before arteriography, had
demonstrated a right middle fossa spongioblastoma polare which was spreading
along the sphenoid ridge and had crossed the midline. The patient completed a
course of x-ray therapy and was alert and ambulant. A vertebral angiogram was

suggested to evaluate the intracranial mass. The patient was sedated with demerol,
scopolomine and luminal. Three injections of 11 cc. each of 35% diodrast, were
made. The record states that: “while attempt was made to enter right common
carotid, patient became cyanotic, respirations shallow, and pulsations of the artery,
which were strong, became weak.” The patient expired within 20 hours after
developing hematemesis, melena, and two grand mal seizures. No autopsy was
obtained.
Case VI: R. W., a 40 year old male, was admitted because of sudden onset of
headache and stiff neck. The spinal ﬂuid was grossly bloody and the diagnosis of a
spontaneous subarachnoid hemorrhage made. Patient developed pneumonia and
ran a septic course. This responded to antibiotic therapy and patient seemed well
one month after admission when he developed a second episode of subarachnoid
bleeding. One week later, while patient was comatose, a right carotid angiogram
was done. The ﬁlms were not diagnostic and patient expired within 18 hours of
the procedure.
An aneurysm of the anterior communicating artery with hemorrhage extending
into the lateral ventricles was seen at post mortem.
Case VII: N. B., a 5 year old girl, was admitted because of petit mal seizures
for two months. Examination demonstrated left homonymous hemianopsia and an
electroencephalographic focus of abnormal activity on the right parieto-occipital
region.
A right percutaneous carotid angiogram was done under general anesthesia,
with difﬁculty, and a normal vascular pattern demonstrated. Patient had a large
hematoma of the neck with tracheal shift, necessitating intubation that night.
Patient recovered rapidly, but complained of pains in the neck and kept the head
ﬁxed with chin turned to the left. Repeated x-ray examinations eventually disclosed an area of rariﬁcation in the transverse process of the ﬁfth cervical vertebra.
This responded to immobilization and chemotherapy. When seen six months later,
the child had recovered completely.
Case VIII: M. C., a 30 year old male, was admitted to the neurological service
because of left sided headaches of a few years duration and three episodes of loss
of consciousness during the previous six months. On examination there was diminution in perception of tactile stimuli in the right hand. This defect was exaggerated
by double simultaneous stimulation. Electroencephalography demonstrated a
persistent focus in the left parietal region. The pneumoencephalogram was normal.
A left percutaneous carotid angiogram was done. Four injections of diodrast
were made. After the last injection a complete hemiplegia, hemisensory syndrome
and hemianopsia was observed on the right. The patient was totally aphasic but
responsive. During the ensuing weeks the weakness and sensory changes cleared,
so that when seen one year after the episode, only minimal sensory changes in the

�A Clinical Evaluation of Carotid Angiography

187

right upper extremity were observable. The aphasia, however, after some initial
resolution, persisted. The patient expressed himself with difﬁculty and made
many errors, could not carry out complicated commands, and made errors in
imitating mouth and hand movements.
The angiographic ﬁlms were interpreted as within normal limits except that
the vessels of the middle cerebral group were few in number and widely separated.
Case IX: E. B., a 64 year old man, was admitted because of headache and
“nervousness” of some months duration; and repeated episodes of loss of consciousness without convulsive movements for one month. On examination there
were mental changes, hyperreﬂexia and a positive Babinski on the left, but no

manifest weakness or sensory changes.
A right percutaneous angiogram was done with local anesthesia using four
injections of diodrast. Immediately after the last injection the patient lapsed into
a torpid state, his eye movements became dissociated, and the left upper and lower
extremities were ﬂaccid. During the ensuing days, the torper diminished until the
patient could respond verbally to command, but the hemiplegia became spastic. It
persisted until the patient was transferred to another hospital one month later.
The angiograms were interpreted as normal. A pneumoencephalogram revealed
bilaterally dilated ventricles Without shift or distortion.

A number of factors such as sensitivity to the contrast medium

the amount of drug and rapidity of injection (3b), and existing hypertension (3 c), have been suggested as causes for complications. In the present series, these factors are not outstanding in
the patients who developed complications when these are compared to the uncomplicated cases.
Either conjunctival or intradermal diodrast sensitivity tests
were carried out in every subject. In one case, the onset of wheezing, sweating, and palpitation after the intradermal test caused us
to cancel the studies. In all other subjects, including the patients
with complications, the sensitivity tests were negative. This was
notably true in the four patients who developed “allergic-like”
reactions of urticaria, chills, and vomiting, following the angiography, but who failed to react to the test dose.
There is no apparent relation in the data between complications
(excluding hematoma of the neck) and the number of injections of
diodrast (see Table 2).
(3 a),

TABLE II
No. of Injections
No. of patients with complications
No. of patients without complications
*

1
1

3

more than
2
0
9

3
6

4

5

6

6

2

1

6
0

27

22

13

8

3

Total"
16
85

Excluding 16 uncomplicated cases in whom total dosage was not recorded.

Similar analyses of the factors of anesthesia and the number of
carotid punctures at one session (unilateral or bilateral angio-

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Max Fink and Joseph

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graphy), reveal no signiﬁcant correlation between these factors,
taken singly, and the incidence of complications.
Arterial hypertension was not a contraindication in the selection
of patients for angiography. Ten hypertensives (all with diastolic
pressures of 100 mm. Hg. or more, and systolic pressures of more
than 160 mm. Hg.) were subjected to angiography, and in none of
these were there any complications. Of the patients with severe or
transient complications (other than hematoma of the neck) none
had hypertension.
Discussion
Recent reviews have emphasized the diagnostic reliability of
carotid angiography in vascular anomalies (4), suspected brain
tumors (lb, 5), traumatic cerebral states (6), and occlusive vascular
diseases (7). Our observations conﬁrm the recommendations of the
authors in the ﬁrst three groups.
Prior to angiography’, the diagnosis of vascular anomaly could
not be conﬁrmed except by surgical exposure or autopsy. Since air
studies are not reliable in demonstrating vascular anomalies or
is
choice
of
in establishing
the
procedure
angiography
aneurysms,
such diagnoses. In 43 % of the patients in this series in whom such
a lesion was suspected, the anomaly 'was satisfactorily demonstrated by angiography. In an unpublished series of similar cases
studied by one of us (Fink) at Monteﬁore Hospital, ﬁve aneurysms
were demonstrated in 14: suspects.
Similar results are recorded by other authors (4), and numerous
recommendations have been made to increase these results. Routine vertebral injection, combined with bilateral carotid punctures,
will demonstrate anomalies in the posterior portion of the Circle of
Willis (14). Oblique A—P views at 45 degrees have been recommended to demonstrate small aneurysms of the carotid (4 (1). With
these modiﬁcations in the procedure, it is to be expected that the
incidence of positive identiﬁcation of anomalies will increase.
The role of angiography in the management of spontaneous
subarachnoid hemorrhage is not clear. Recent reviews emphasize
the importance of demonstrating the lesion where surgical intervention is indicated (4b, e). The effect of angiography during the
acute phase of bleeding has not been clariﬁed. Many authors have
recommended angiography only after the bleeding has ceased.
Others, such as Wechsler and Cross (7 b), suggest early use of angiography during active bleeding. This principle of waiting until
bleeding ceased was adhered to in the cases in this series, and no
statement of the effect of angiography on bleeding can be made.

�A Clinical Evaluation of Carotid Angiography

I89

Angiography is the diagnostic procedure of choice when a supratentorial brain tumor is suspected. It is recommended for lesions
located in the anterior two-thirds of the cerebrum. Occipital lobe,
posterior fossa and some midbrain tumors are not consistently
demonstrable by this technique. Angiography is recommended in
subjects with papilledema, since this procedure, unlike air studies,
does not make immediate surgical intervention necessary (5, 7).
Furthermore, numerous reports emphasize the differences in the
patterns made by gliomas, meningiomas, intracerebral hematomas
and vascular tumors (1, 2, 3c, 5). Such clues are helpful to the
surgeon in planning the operative procedure. In a few of our cases,
multiple foci of a metastatic tumor were demonstrable on the ﬁlms,
clarifying the management of the case. Such discriminations are
usually not possible by other diagnostic techniques.
The diagnostic reliability of angiography in cases of brain tumor
is high. In this series, 25 of 29 conﬁrmed brain tumors were outlined
by angiography. In a series of 96 brain tumor suspects, 39 of 42
veriﬁed neoplasms were demonstrated (5 a). In the series from
Monteﬁore Hospital angiography revealed the neoplasm in 45 of
52 conﬁrmed cases. Similar satisfactory correlations are seen in
the negative angiograms of these three series. This diagnostic
reliability of 88 % compares favorably with encephalography. The
value of air studies in brain tumor diagnoses has been frequently
reported. In one such study by Grant (8), ventriculography demonstrated the lesion in 130 of 150 cases—an incidence of 87%; while
pneumoencephalography in 69 cases, revealed the tumor in 81%.
Further indications for angiography are in cases of traumatic
intracranial hemorrhage. Numerous reviews emphasize the displacement of the anterior cerebral artery and separation of the
ﬁne vessels from the calvarium on the A——P ﬁlm as diagnostic of
subdural hematoma (6). Furthermore, angiography differentiates
intracerebral and subdural lesions, altering the surgical approach
(6 a). This was clearly demonstrated in two of our patients in whom
subdural hematoma was suspected, but in whom the angiogram
demonstrated an intracerebral mass.
In cases of cerebral vascular accident angiography appears less
helpful. Failure of a vessel to ﬁll may be due to a variety of reasons
including slowing of the circulation, vascular spasm, and anomalies
of the system. These factors have been emphasized (7b). Angiography, however, is not contraindicated in vascular disease. It provides a useful means in differentiating a thrombosis from an intracerebral clot, or from a tumor, in cases where the diagnosis is unclear.

�190

Max Fink and Joseph M. Stein

While the indications for angiography are many, they cannot
be evaluated without a discussion of the risks involved. The complications of the procedure are of three types: (a) transient local
phenomena; (b) transient cerebral vascular phenomena; (e) permanent severe deﬁcits. In the ﬁrst group of transient phenomena
are burning pains in the head during injection, hematoma of
the neck, and allergic reactions. Hematoma of the neck is a potentially dangerous complication (see our Case VII) but in a recent
review no sequellae were observed (9). Allergic reactions are infrequent and usually mild. It was noted in this series that the routine intracutaneous or conjunctival testing for sensitivity was not
found satisfactory in predicting these complications.
Transient hemiparesis, aphasia, seizures and elevated blood
this
In
(10).
have
been
following
angiography
reported
pressure
series these complications were observed in nine cases—an incidence
of 8%. A similar incidence was observed in the Monteﬁore Hospital
series. That these phenomena are probably due to temporary
vascular insufﬁciency (spasm?) is evidenced by the clinical pattern
of neurological ﬁndings and their duration. Of seven patients with
hemiparesis, the deﬁcits had disappeared within three hours in
three patients, while in three others it was gone in 24 hours. In one
of the subjects angiography was repeated in the other side six days
later, without complication. In the seventh patient, arteriography
had demonstrated an aneurysm of the internal carotid artery on
the left and the common carotid artery was ligated on that side.
One month later, angiography was repeated on the right side and
following the ﬁrst injection of diodrast, the patient developed a right
hemiplegia. This disappeared during the ensuing 72 hours.
Vascular syndromes of the anterior and middle cerebral arteries
have been observed. In one patient a lower limb monoplegia
developed after two injections of diodrast. A third injection on the
same side was done within 15 minutes of the appearance of the
defect. The arterial views obtained showed good ﬁlling of all
branches. The monoplegia disappeared within 12 hours. These
complications were not observed in patients with hypertension.
Deterioration of a patient’s condition or death following angiography has been reported in a number of instances. Bull (5d)
summarizes the mortality rate of the procedure as 3 per 1000,
which he states compares favorably to ventriculography. More
recently, Dunsmore, Scoville and Whitcomb (10b) report three
fatalities in 147 cases, and Olsson (11) reports three cases of “deterioration of patient’s condition” in a series of 360 angiograms.

�A Clinical Evaluation of Carotid Angiography

.

191

There were two fatalities in our present series, and one patient had
a severe aggravation of a pre-existing hemiparesis. Each of these
patients, like those of Dunsmore, Scoville and Whitcomb and
Olsson, were severely ill before the procedure.
In contrast to this are the large series of Curtis (5b), Wickbom
(1 c), Torkﬂdsen (Sc), Lindgren (la), and Green and Arana (1b)
wherein no deaths were related to the procedure. It is possible that
with widespread use of angiography, subjects with more advanced
cerebral lesions are selected for these studies and the risks thereby
increased.
A number of reports by Olsson and associates (3b, 11, 12)
emphasize the summation of the toxic effects of large doses of
diodrast given over a short period of time. They indicated the
nature of the toxicity as an increased permeability of the blood
vessels and a change in hemodynamics. Furthermore, the relation
between concentration of diodrast and toxicity was demonstrated
by Cross (13) when he introduced diodrast for angiography. His
observation that seizures follow the use of 50% and 70% diodrast
has been conﬁrmed by numerous investigators.
Despite the use of 35% diodrast and low total dosages of diodrast, in this series, complications ensued. There was no signiﬁcant relation between dosage and complications. Other factors
must be operative and some hint has been given in the observation
on circulation time (41') and the effect of other injurious agents
summating with diodrast (3).
Conclusion

Angiography is preeminent in the management of cases of intracranial disease suspected of vascular anomalies, supratentorial
tumors, and traumatic hematomas. It is a satisfactory non-surgical
method of demonstrating a vascular anomaly, malformation or
aneurysm. In the diagnosis of supratentorial masses it will outline
90% satisfactorily. In addition to establishing the presence of a
tumor, arteriography is superior to other diagnostic technics in
yielding evidence as to the type of mass and its locus. In cases with
papﬂledema, surgery is not made immediately mandatory by the
procedure. It is not a satisfactory method in demonstrating obscure
and diffuse lesions of the ventricular system, or tumors of the
posterior fossa or occipital lobe.
In cases of traumatic intracranial lesions, angiography is a
satisfactory method in outlining subdural hematomas, and differentiating such lesions from intracerebral hematoma or tumor.

�192

Angiography is

Max Fink and Joseph M. Stein

thromboses
cerebrovascular
in
not clearly helpful

and hemorrhages.
would
and
not
transient,
the
for
most
part,
Complications are,
are
The
complications
in
cases.
most
the
limit
procedure
seem to
bilatnumber
or
anesthesia,
not directly related to hypertension,
factors
a
Other
play
diodrast.
of
erality of injections, or amount
is necessary.
further
and
role
study
more important
Summary
reviewed
were
carotid
angiograms
A series of 117 percutaneous
in
involved
angiography.
risks
and
for
indications
the
to evaluate
studied
including supraconditions
were
intracranial
of
A variety
and
hematoma
traumatic
anomalies,
vascular
tentorial tumors,
of
intraevidence
with
disease.
patients
Fifty-ﬁve
cerebrovascular
cranial tumors were subjected to angiography, and a positive
in
conﬁrmed
were
These
diagnoses
diagnosis was made in thirty.
ﬁlms
misinterpreted.
the
were
subjects
In
two
only
of
the
cases.
83%
in
in
conﬁrmed
50%;
were
the
diagnoses
Of the negative ﬁlms,
demonlater
lesion
show
fail
a
to
did
the angiograms
only two cases
intracranial
with
suspected
21
Of
patients
strable by air studies.
of
In
two
outlined
angiography.
by
vascular anomalies, nine were
air
manifest
on
not
revealed
anomaly
an
these, the angiograms
traumatic
of
suspected
of
seventeen patients
studies. In a group
in
made
seven
was
diagnosis
positive
intracranial hematoma, a
in
cases,
eight
ﬁndings
the
well
negative
as
as
These
diagnoses
cases.
all
conwere
in
two
demonstrated
cases,
intracerebral
tumors
and
lesions
cerebrovascular
of
In
studies.
cases
ﬁrmed by subsequent
complications
Transient
value.
of
diagnostic
not
angiography was
consisted
and
of
the
one-third
patients,
in
of angiography were seen
In
urticaria.
and
seizures,
of hematoma of the neck, hemiparesis,
These
and
severe
permanent.
ﬁve patients (4 %) complications were
discussed.
factors
the
and
described
cases are
cerebral
of
angiorisks
limited
the
conclude
that
authors
The
of
the
in
usefulness
management
its
from
detract
do
not
graphy
intracranial vascular malformations, suspected supratentorial
tumors and traumatic lesions.
Zusammenfassung
117 durch perkutane Injektion in die Arteria carotis gewonnene
und
Indikationen
der
Gesichtspunkte
Angiogramme werden vom
Gefﬁﬁanomalien,
Tumoren,
Gefahren besprochen. Supratentoriale
der
GehirngefﬁBe
und
Erkrankungen
Haematome
traumatische

�A Clinical Evaluation of Carotid Angiography

193

werden besprochen. 55 Patienten mit Zeichen von intrakraniellen
Tumoren wurden mit Angiographie studiert; in 30 wurde eine
positive Diagnose gestellt. In 83% der Falle wurde die Diagnose
bestatigt. In 2 Fallen wurden die Filme falsch gedeutet. In 50%
der negativen Filme wurden die Diagnosen bestatigt. Nur in
2 Fallen vermochte das Angiogramm nicht eine durch Luftfiillung
demonstrierbare Lasion zu zeigen. In einer Gruppe von 21 Patienten mit vermuteten intrakraniellen GefaBanomalien wurde in
9 Fallen die GefaBstﬁrung demonstriert. In 2 dieser Falle zeigte
Angiographie die Anomalie, wahrend Luftfiillung ein negatives
Resultat ergab. In einer Gruppe von 17 Patienten mit Verdacht
auf traumatisches intrakranielles Haematom wurde eine positive
Diagnose in 7 Fallen gestellt. Diese Diagnosen, wie auch die negativen Befunde in 8 Fallen, und intracerebrale Tumoren, die in
2 Fallen demonstriert wurden, konnten durch weitere Studien bestatigt werden. In Fallen von Gehirnlasionen, die durch GeféiBprozesse bedingt waren, hatte Angiographie keinen diagnostischen
Wert. In 1/3 der Falle kam es zu voriibergehenden Komplikationen
(Haematoma des Halses, Halbseitenlahmung, Kréimpfe, Urticaria).
Bei 5 Patienten (4%) waren die Komplikationen schwer und
dauernd. Diese Falle und ihre Besonderheiten werden besprochen.
Die Autoren gelangen zu der SchluBfolgerung, daB die begrenzten
Risiken der cerebralen Angiographie von der Anwendung dieses
wertvollen Verfahrens in F ﬁllen von GefaBanomalien, supratentoriellen Tumoren und traumatischen Lasionen nicht abhalten sollen.
Résumé
Les auteurs passent en revue une série de 117 angiographies
carotidiennes percutanées, dans le but d’évaluer les indications et
les risques qu’elles comportent. La série d’aﬁ'ections intracraniennes étudiée comprend des tumeurs supratentoriales, des anomalies
vasculaires, des hématomes traumatiques et des affections vasculaires du cerveau. Cinquante-cinq patients présentant une symptomatologie de tumeur intracranienne furent soumis a l’angiographie et un diagnostic positif put étre fait dans trente cas. Ces
diagnostics se conﬁrmérent dans 83% des cas. Chez deux patients
seulement, les radiographies furent mal interprétées. Parmi les
angiographies négatives, 1e diagnostic clinique fut conﬁrmé dans
50% des cas; dans deux cas seulement les angiogrammes ne montrérent pas de lésion qui, plus tard, put étre mise en évidence par
injections d’air. Parmi 21 patients suspects d’anomalie vasculaire

�194

Max Fink and Joseph

M.

Stein

intracram'enne, 9 purent étre révélés par l’angiographie. Dans deux
cas, les angiogrammes révélérent une anomalie que les ventriculogrammes n’avaient pas rendu manifeste. Dans un groupe de 17
patients suspects d’hématome traumatique intracranien, un diagnostic positif fut conﬁrmé dans 7 cas. Ces diagnostics, de meme que
les résultats négatifs de 8 autres cas, et les tumeurs intracérébrales
démontrées dans 2 cas, furent tous c0nﬁrmés par des études ultérieures. Dans les cas de lésions cérébrales d’origine vasculaire,
l’angiographie est restée sans valeur diagnostique. Des compli—
cations passagéres de l’angiographie furent observées dans un tiers
des cas et consistérent en hématomes de la région du cou, hémipareses, crampes, et urticaire. Chez 5 malades (4%), des complications durables et plus graves apparurent. Ces cas sont étudiés
en détail et les facteurs on cause discutés.
Les auteurs concluent que les risques limités de l’angiographie
cérébrale ne sauraient faire renoncer a une méthode aussi utile
pour le diagnostic des malformations vasculaires intracraniennes,
des tumeurs supratentoriales et des lésions traumatiques.
REFERENCE S
1. a) Lindgren,

E.: Br. J. Radiol. 20, 326, 1947. — b) Green, J. B., and Arana, R.:

Am. J. Roent. and Rad. Ther. 59, 617, 1948. — c) Wickbom, 1.: Acta Radio]. Suppl.
72, 1, 1948. — 2. a) Moniz, E.: “L’Angiographie Cérébrale”, Masson &amp; Cie, Paris,
1934. — b) Lima A.: “Cerebral Angiography”. Oxford Univ. Press, London, 1950. 3. a) Olsson, 0.: Acta Radiol. 35, 65, 1951.
b) Broman, T., Forssman, B., and
Olsson, 0.: Acta Radiol. 34, 135, 1950. — c) Torkildsen, A.: Acta Psych. and Neur.
Suppl. 55, 1, 1949. — 4. a) Lowman, R. M., and Duﬁ, S. D.: Amer. J. Roent. and
Rad. Ther. 53, 341, 1945. — h) Poppen, J. L.: Radio]. 53, 347, 1949. — c) Wickbom, I.: Acta Radiol. 34, 387, 1950. — d) Lo'fstedt, S.: Acta Radiol. 34, 339, 1950.
e) Wechsler, I. 5., Gross, S. W., and Cohen, I.: J. Neur. Neurosurg. and Psych. 14,
25, 1951. — f) Raney, R., Raney, A. A., and Sanchez-Perez, J. M.: J. Neurosurg. 6,
222, 1949. — 5. a) Culbreth, G. E, Walker, A. E., and Curry, R. W.: J. Neurosurg.
7, 127, 1950. — b) Curtis, J. B.: Brit. J. Surg. 38, 295, 1951. — 0) List, C. F.: Radio].
55, 327, 1950. ~ d) Bull, J. W. D.: Postgrad. Med. Jour. 26, 157, 1950. — e) Fabritius, H. F., Frovig, A. G., and Kristiansen, K.: Arch. Neurol. and Psychiat. 61,
352, 1949. — 6. a) Wickbom, I.: Acta Radiol. 32, 249, 1949. — b) Kristiansen, K.:
Surgery 24, 755, 1948. — c) Webster, J. E., Dawson, R., and Gurdjian, E. S.:
J. Neurosurg. 8, 368, 1951. ~ d) Raney, R. B., and Haney, A. A.: Calif. Med. 73,
342, 1950. — 7. a) Govons, S. R., and Grant, F. C.: Arch. Neurol. and Psychiat.
55, 600, 1946. — b) Wechsler, I. S., and Gross, S. W.: J. A. M. A. 136, 517, 1948. —
c) Lusignan, F. W., and Gross, G. 0.: Calif. Med. 73, 240, 1950. — d) Alorris, A. A.,
and Fulcher 0. H.: Surg. Clin. North Amer. 30, 1783, 1950. — 8. Grant, F. C.: Arch.
Neurol. and Psychiat. 27, 1310, 1932. — 9. Berdal, P., and Emblem, L.: Acta
Psych. and Neurol. 26, 1, 1951. — 10. a) Chusid, J. G., Robinson, F., and MargulesLavergne, M. P.: J. Neurosurg. 6, 466, 1949. b) Dunsmore, B., Scoville, W. B.,
——

-—

——

�A Clinical Evaluation of Carotid Angiography

195

and Whitcomb, B.: J. Neurosurg. 8, 110, 1951. — 11. Olsson, 0.: J. Neural. Neurosurg. and Psychiat. 12, 312, 1949. — 12. Broman, T., and Olsson, 0.: Acta Radiol.
30, 326, 1948. — 13. Cross, S. W.: Arch. Neurol. and Psychiat. 46, 704, 1941. —
14. Sugar, 0., Holden, L. B., and Powell, C. B.: Amer. J. Roent. and Rad. Ther.
61, 166, 1949.

�[ha

/

A

M777, APP/f5; (#4)/7.rz.

omen tummu W mm “KW
W

II: link,

3.».

ma
asap}:

:1.

Stein, IL».

.7"*'*‘ , 9W
.m
§
"v.1
"t; ,
‘
waiver-1w canon of Indiana and the lam-01931.11 8min
if the aura mun-u. hollow Rental, lav mark 633:.
-

.V

T?!“

1*

'

=

'

�line. antacid

aaczozruphw

tn mum of 1:1th

an: bocgnn a ruuttun proaoﬁuro'xn
cautions. In ovulation at 18..

no in nun-um. lath 15h. inﬂation and mm at cm proa«dun mt be amid-M in humans it for «lacunae
aux-pom. It «and valuable, thereto”, to an.” tn «non-m
am on tho Wei-clan um.“ or u acuml human . Min;
m put to math, :17 panama“: Mount animu- nn can»
put“ him-n or the minim hm amt. m mama were
«at directly by tho “than .
5 variety of “urological amnion: including
11min Mon, moan: alt-mun, ”Maul hunts-nu, vascular
dunno: Ion “law by tho
dam“ and arm.
“twang um: u with» «Midﬁe- ror WWW. In «ch
mu, 9020qu met“ mien-u was performed «cording to
the W1 «Manama (1) .' mum.- 10011 infiltration by normal”
A
01f 3mm manhunt. by mutant}, or «mm m and.
Gem-Grin» mu. m inﬁrm into the mend artery at tho
101010: 1'.» thyroid M11130. In no“ mum» the «non

«3th

WM"

0..

carotid artery

13th “an.

.‘

m mm;

in a

In butane“ tho into!!!)

M 1:0 mm: u. ref 35! “can“

inﬂation.

A

solution were and in «on
«1:91. mm). “18133110 auntie Miner m and.
that amounts." luau). 11m tad a um. mun.

m: 130th
yuurior

(5-21 view.

m

In «on me the Au! and lateral £11m
mantel:
«#010904. lad, 1: indium. the injection In mutant. 1: no

It: noted on than mm,
the other 11¢. than» manna.

pathology

the

vacuum at

Bilateral

mum on

panam- urn

�2.

«aid but in 36 gnaw».
..

mm amtlm‘ mu nu prior mum.
Wu
at the», ”bum W mu“ am
1m.“ my.
:0

of

"

up the

muted moun- manna lad «mu but... an an mt

“m “wanna” or the film's!"
(«0 m1:
m:
mod tn «mimic» t7 In“ (a). amt»),- md ﬁrm I Am:

1m.»

1-).

(1b).

‘
‘

'

m amount). mm «spotted,at
ammo nun-u «WWMMthMy.
than. nu «ma «haunt sum or as: .m».
continuum m not attained in turn ”that: boom mm
than m quM B: gaunt“ m or “all”: W
M cm ”mm“. In
on» the mom I»! 1&amp;th
described.
than»
of 55 pun-nu in

were

by

25

-

two

tumour m

m» m

an A; 3.3». a #8 na- a:s.“ W m «Ilium to 1011mm
humane mam been“ mm m manna" amt-n.
m ail-inﬂux mallard «1-11 mum-u, 10ft mm rum
pa”. mm Wu 0:: the ”at and nun «11:18:.

m

An

rim 3mm}. “on
Ilium-n1 mm magma under new“ mamas
mound donut. olmtim (”apnea-ant} or the mum Who.
of tho right
W). Mm. museum in this

ﬂaunt/annulus”:

the

a.

.-.

w.
uphill mm Indra” m not“ to

be

We
posits." for “’61"

until” . Annama- mm: m taunted
'

11pm“

with.

nw inks later,

the right

and

the

mum:

mum mum as meat“.

�“

&gt;

luv

In

want-um“
m
ﬁr

NHI

II

,

mkamm
WWW

(Minimum: mutant—imam m»
H CW u
(CHI-um m
‘

.

.‘

WWW‘rude-buﬂm

�3.

it... (11:: Innuud

tho par1ota1 vantols ta have n nomlll

cen—

figuration.

6.3. II: 0.0., a

yin: 91¢.la10 an: Idlitted buotule at
roeunt onset at grina.unl aniline. .nﬂ lortantdcd untknoia,
lxnuhntion rO'Dnlid a I114 10th bullpIrCItl, taut unwind in the
6%

lénbr caﬁrunity. lhnru in: a punitive llbiulki response and
incr¢:sod rutlaxtn.Moorutvuop1n31 fluid OIRQrUID III nounu1.
A right curatld
nn¢1o¢run undar local unauthonia III pur~
rarlnd and dIInnIttltod 390d 21111n¢ at tin Interior and l1ddlo
oorobrn1 uttering. that. Ill straightening and dcprognian at tho

pertain“). mar:
am- the

an...

on

up

mm; um;

and

manned yum-mt:

“mum. at cm manor mm: at»; on the 1.1- an.

changes wort intorprutod
Ian- 41-piuozn; blood vetucln.

ll

avtdlnoo at a pnruaagsitnl tumor
‘

pnnunninaophnlocrul,ula done and thin did not dclnnntruec
thy IIII. It. patiant anarovud withaut troutncnt and lit dinohnrsod.
In It: rtlanattod a to! lick! 1:10: with avid-not or an aunt. talin
Ital syndronn. In '10! a: tin ¢uuruo a! uni 111ncll and.nultxplxoity of 1051.33, at in: bolicvod that the pntiaut'n uyggtanl
A

1

'

taro

duo

to doccatrntiio ahnaccs, and net a unoplaun. lo turthgr

Itudiou var. andnrtaknn.
In this group or lunpcatod brain tumors 22 ausiogruln 414 not
than any pathnlo;7. ilovcn at that. 10:. canrialnd by I1! studio:
or tntapsy. In tun pationts, houovcr, untilrtotery angiogra-s

failed to dalunltrutc lesions lttcr

other Itudicl.
mum to m

danmmstrntod by

an. m; n... .1 57:»:- em m m
hospitdl koala-c of lift Inilplroutu, bladaor and
and

mud no.1

gum: or

1;

inks

aux-«zen.

6::

bcuul incontinence,

man. than

�#.

never. poroonnlity ohoncoo, and o opootlo loft honiporoo1o with
pathological roam: . embrupinll nun snare-o was nor»). .

were

right oorottd onciogron.undor pontothnl onoothnoin on: dono.
outs of lotorll £11.. and on. to? via! Into taken. in: films
A

two

thouod no ovidonoo or lorehrol tumor.
can rock Into: a vantrtoulogrln dolonotrotod a large right
con“
trontooto-porol IISI. Ibo protons. of a malignant slioln

ill

tin-0d by ournory.

:

Goo. IV; 3.3.é°:bzzkzoor old man developed

loft stood toizuroo

Iphlliu during/$rottlont for turunonlooil. on anurolucicll
ennuinltion chore woo ovidonoo at n lotion in tho risho honiophoro.
en Ikull x—ro: tho piuill outdo! In: shirtod to tho 102%.
An ortorioaru on on right nu
scum). mom-1a m

and

done ond no pathology dononotratod.

ma

A

pnounoonoophnlosrln, houovor,

revollod a dofornity of the right frontal horn.
in: patient uzpirod on: lonth otter oust-graph: and ot pout.

norm, mum} emu-u 0”qu mm anon-mm autumn.
9th.: erroneous onaiocrlphio d1oanoIOI our. and. in patient.
who provod #0 have vooonlor throubosoo. In tlo potionto with Iisnl
the oncxosru-o rovoolod on oraoaulnr are: in tho
poricto-tonporol vision with dioplooonont o: Iiaolo oorohrll voooolo.
Surgical exploration rovoolod odouotono necrotic brain tilooo,
without ovidonoo of tolor. loch oooe oono to antopoy and in both
or

I brain only».

man:- or . branch or. on. man «mm mm m rm. o:m

angiogruno onulo not be dittoronttotod from thou. noon in on...
tnnoro 1n the Inn: raglan.
Vaoogggg.tnoup11oog ﬂuonty~ono patient: Iuopootod or intro»
'

ornniol vaooulor Inouolioo or Quintin-o not. oubjootod to lnslo~
stools. 1h» Insaosrunl wort billtdrtl in only throo or thooo. and

���7.

mt N contact“.

um“.
m nu

In this aorta of 117 WWMB
36 ”tum- “from a to“: at is «unusual.
and peanut «mutation. In an mm
can with
the «mutation
and
at in
Of the a»: mo
«Quantum. 22

m

«W

mm
m an mum.
man:
mm.
mm
MmmuMuHthmm-uw. ammo. in
am. mutumnmwummmmm'
manta: mun It as mm to tntubtn m yum:
mmmmmmmmmumpmmm;
mun mom mm: man a «um
mummuwmu.
mnmmnmmomm
a nun“. :3 Wk mm. m
within
.

an

ou-

pm mm

#8

W. talcum-Wont... cummmuurmmwowhy. all no.“ to rcpt-aunt an mung mpm h m atom-Mt.
Inmautmh

umummmmmmmrua
Hummutumnmauammmm
W.a: m mm causation. loath um um Mr.
in in ”man (mu 7. n). In tum ash-r

W

or

1“

mm.
Inamcuul‘uumum otmmvmupmuat th:mn mm mm mm m s difficult W31“ (mo
m). W: m spa-nu (em um m mmmuu-n
a: Mum mm“ («m I!) m an. «W.
mum: sum emanation we «may “um 80
an

A

m
mm.
panamamumnmmmmmmmmmuu
a

Wow. than. 11mm Mm
m twink“ I mm mm. tau ”Omnimtm

ma. all... 63.

elm

was... an muons

am and Mt.

A

completed a

13W and as
most“ to «3.1qu

war» a: may

mm mam

was

���10.

at 1a.; or

np1nud¢c

on.

mth.

aunne1ausntgt u1thout convulu1vo unvunnne: for

«nan-11:11:,»

and a pou1t1vt lub1nlk1 on

than mm mm
tbs 10:1.ths

no

I

sensory «Itasca

am», Winn

lua1tcut weaknass a:

‘

1 31331 percutancona In31u3zun was inns u1th 10011 tainthna1n
nn1n3 {our 1njoot1ons of diodralt. &gt;xllad1a$oly Ittcr tho last
1nJ¢¢t1an thy pat1ont lapsed 1319 a 102911 3:11., M1: cyuruovanantt
3101.0 d1llo¢18ttd, and tan loft layer and In!!! tatul1t1o§ I09.

N

mum
nonpanﬂ

anon.

am

the

tmu Mum mm m

Vtrhully to «allnnd. but tum han1pl¢31t booinpit10at 00114
tplnt1c. It porn1ltad ant11 tn. put1on1 its trunnruraod to ancillt
anap1¥I1 can nanth 11102.

tn31usrnll I110 tatcrprttod an annual. A pnaulalnoaphnlo~
3run.rovualtd b1latcrnlxy 61.301 vuntr1c10u u1thout nh1tt er
1%.

.d1lvort1an.1 walker
(31) the

at stator: that’s:

Ions111v1ty tn the eonsrust Indtwn,

amt a; m me many at 1111009103 (33),

and

mum

tar «aupl1ant1onl
In in. prusuat 19:10., till. {natori It. nut ant-taun1n3 1n tn.
pat1enta uh. 107110301 «unpliont1aa- when tunic tr. 01.31301 10 tin
hwptrtonn1un (38), havu bola a133Ot$ed as OIIIOI

_

unoonpl1enta1’onacs.

l1thsr eonsaapt1v11 at 1ntaadnrlal aiadrnst gonn1t1v1ty tent:
turn cnrr1od out 13,0?!93 luhaoot. In out cute, in: cane: at
«humus, means, an: myzuum mu- the
m: am»
an to ouncol tan I9I11II.

3111th mm
1B1:

In

111

1mm:
1n51ud1n3 an.

athgr turnouts,

amuuum, m Im1t1uty to». m mun.

Ill notably

true

1n

tbs {tar pat1outs

who dtvu1opod “n11.331c~

rsaot1ons of urtiolr1t, oh111n,“ van1t1n3, tolleu1a3 tho
In31osraphy. but who £11101 to rule: to tbs tent 4916.
Shaw. 1: an apparent rolae1an 1n tho ant: bntanon «anp11out1ons
11km”

�13..

(luntudias hunttuun If

In.

it. acct)

and

tin

ms

it 13:00t10an

1 2 3

mania: or 1n1¢otzunn

t 5 6 Iﬂﬂ"th‘ﬂ‘6

lo. .1 patiouta 11th cu-pzioctiaun'l e 6 6 I 1;
lo. at pt... without «uncanny 3 9 1m :38

'

it

Ebﬁazﬁ
'

o

16

'3

as

*Ixnluata; 16 Inna-plsnusad «Isa: 13.1huu tutu: data.» uua ngt

rocordnd.

o: m t’utoru or nae-than and m'
author I: carotid punstaraa at on. Ion-1:: (unilaturtl or bilaterll
Iagiacrlph!) rtvttl as significant entrolltton botluon thtao riotorl.

3mm mm»

t3. inolaunno at calvlaltxaau.
Arm-1n max-«mun m in a eonmuuan in m.
poxootxon or patzants tar Ingtosrlphy. ihn.hw)hrtoanzvoa (:11 with
diastnlia prisaurio at zoa-n. It. or'nnvi. and urtialto ar0§turtu at
more than lﬁaun. In.) It». subjueted to nasitgrOphy, and in nan. at
Shut. the. that. lay tonplioaticna. .0: thn paticnta with Icvorc up
titan singly.

and

--

‘tsnnszont oclplzsaﬁiaan («chit than hGIRQﬂlﬂ ot‘tho unak) aunt and
V

hrpdrﬂlnlzan.
unseat mortal: hart alphlatlid tan diagnottta rtlzuhalat:
it alrutid lasincruah: 1n vascular nan-alto: (k), auapoetod brutu
talnru (lb. 5), tram-I310 aurchmt1~utdbn (6). tan ooaluntvu vascular
axsaaaon (7). our ebucrvataons coatirn.thn rocounnadatzana at tho

ham 1:. um run m

m.in.

_

diagnnst- a: van¢u1nr nan-n17
could nut he ountlmuld Cincpt iv insulin} Impaiurt at luttpuy.
Itnte sir trudiyi are nut vuiiuilo 1n dlnanntrntins vautnlur annualaos
a!”IEIIrIIIITMInﬂtﬂcrlrhr“tﬁmiﬁlﬁpiiﬂtiuri"ttwin%00w%nwiiitblllhins

Iran? to ausiouruphw.

�13.

sign ailsnnsts.

Xn-haﬁ

at

th@“p&amp;t10nﬁs

in this surint-An shun.nnth

,

n luntan was unspoctea, tho yam-p1: was natzutaggarilr“dauauntmatad
um
«am:
or
miagrap‘hy; man ‘mnu‘blishad

w

am»

um“

lbnte£tta0lnbsp£bai, five anenrwnnn wore dn-waatritoa-an la anapoota.
ﬁtnilar ”caulk: are rooardea by tthar ﬁlth!!! {¥), can anagrams

mmemuona

have.

hem

nae ta inn-cue than

Wis.

Routine

mtehml injectim, scanned with bilateral 6:th panama. will
«laminate maladies 1n the posterior portion at the 611-010 at
‘ﬂillin (1!). Oblique A.P views tt #5 403:... have been ruoanuoadnd
to damonltratc until aneurysms er tn. aaratid (#d). with thtne
noditicatiana 1n~the prooed&amp;re, 1t 13 to—bq§gxpeoted that the
incidence at positive 1d¢ntﬂiut1m at
will
the rule of angiogrnphy 1n the management or apontansaua

am”

mm.

Iuharaahnoid hannrrhnes 13 not alear. Recent review: emphlstxo in.
1n»9rt&amp;a¢e of alnnnltrtting tha Xenian nhmrs turaiaal intervaattun
1! indiettnd (ﬁt. a.) !hc affect of Iaszonxlphw 03:13:
twat.

it.

53:10 a: blending his act beta a1nr::1¢d. lung nuthnra tutu roan-acalid
:a;1¢lxnphy only :ttor tho blending has 09:306. 0th.». such an

(m. mm «:1: m u mama-v man
m
nun mm. m. mun um... um um mu m
tn in
5::o0t
in

mum: and
adhorul

at

4

or

the cases

thin 3095's, and no ntutqnnnt of tho

Inciozraphw an binoding can be undo.
Aagiogrnyh: in tho diagnoctio panoodnro o: «halt. visa a

Quaratoatawiil human tumor :1 auspoetod. it 1: rcounnandnd tar Ionian:
lecaﬁol in :3. Iatortcr tlu~thsrds a: tht_¢¢rolvun. ana$p1tt1 1th..
posterior toast and nuns unabrszu innnru a». uni conntttnntly

Mutable by

this

Hath pip111@dama,

team”.

11mm“! in lawn”
WW
ant
unltki

ztntc than venucdnro,

lit ntuditc. anon

��1‘.
In snot: or cnrcbgll vuucniqr;acutdant,Inciﬂlllvi¥~tnrﬂﬁrl,1003

helpful. .rlilurv 0:,a rental to

£111 any Do

an:

t. u.vurtety t:

mamas 310m»:ntm1umut1m. .mmm min. in!
”mm at m sum. mm mum mm boon ”but!“ (75).
1;- aot ,imwmwludzu
Mimi!»
mum man. It
proud” \- mam. mu 1i: arm-gamut” o. twain tron m
tntrusarnhmtl 010%, or f!!! a tunes, in OIIOI Ihnre tho I1tsnonll-as
mucus

W.

unelcwr.

'

ﬂhile the indications tar angiography are many, that cannot be
evaluated uithuut ; aincuauian at thy risk: involved. ‘iha emm911a1~
,tiuau or the praceanre are a: turccthpoat.(n) trunnient latul
phcnunanlg (b) trannient cerebral vascular phenlnnnlg (o) pcmlanant

2mm «£1411».

,

xn the

vburaias Dﬂlnl 1n the

:1“:ng at trmniont mama m m

It‘d during

1nJooeton, hauttuul in.tho noak, and
ullorzie venetiann.. numatann.1n the acek in a potentially dangcraus
samplicntien (see aur.Caso VII) but in a ragent review no Inqucllas

varc,aha§rve¢=(9). »Allor¢10 notation: «we larreqaant and usually
llld. .1: in: nat¢¢ in thin action that ﬁns manila. intvaautlanouu
or csngunntivua talking tar sensitivity It: not fauna untitraotorw $n

prudiottus ﬁnale-clnpliotticnl.

lblnninat,hun1paanszs. aphlltl. :eiunros nna citritod blaod
pruuunre haw: hath reported fallouina unstogrtphv (16). In that
series than. qunmlieationn n!!! OttarVQdfin nine canal »~ an incidenae
of 35. {A similar tantdanao uni-nhucrvud In tho lbntcrluao Ibnpaell
30:103. lint.th030

Philll'n!.!rﬁ pribttly in: to tunporary vaaaulnr

innutriuionﬂr (I’lﬂlﬂ) 1: I71lnnn¢d by the cliniunl pattorn at
nourolngzctl findings and thair‘dnrutzun.. at asv¢u 3:310:90 with

�it. M101”

15.

m

an tin-00
unwanted 01ml: than.
0m:- it no so” in an laws. In m
panama, mu m
of the amsun autograph: m "mm in a. 0M um 01: an
um, 01MB «manna. In tho 0mm: mum, Woo-0m

banana-«10,

and

tm

mammmuumamummuamnmm
left me the
0min
1mm that
m

m»: later,
in»

first

0m

may m

0100.

an

mm m mind”that run
an tho

0100 and

mum

M01090! 0 right M4-

13:00:10! 0: 01941-0“. tho

MWMmth-Wﬂm.
Vacant OW
M
0mm mm.»

9103“.

of that mun-101-

hue

been observed.

02:0:

m 13300151”:

in: do» within

15

010010

plant 0 1000: am manna 007010904
0:? “can”.
third Quintin 0: m "I! 0140

In an.

A

mm 0: tin 09m“ 3: m «rent.

an.

m
mumnmnwsmnmgumma.
within
Wu.
omnuum m0 not
unwind:

61mm

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etudiee.
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eevere end peeeenent. Sheee oeeee ere deeerihed end the restore
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�</text>
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                <text>[Preprint] and publication. Confinia Neurologica. From the Department of Neurology and Psychiatry, New York University College of Medicine and the Neurological Service of the Third Division, Bellvue Hospital, New York City.</text>
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                    <text>ABSENCE OF A PARENT AS A
SPECIFIC FACTOR DETERMINING
CHOICE OF NEUROSIS

Preliminary Study
SIDNEY TARACHOW,

MD.1 and MAXIMILIAN FINK, MD.2
New York, N. 'Y.

Psychoanalytic experience has made important contributions to
the problem of the differential etiology of various neuroses, psychoses, and character disturbances. This has been accomplished
chieﬂy by the identiﬁcation of the decisive areas of conﬂict in the
patient. Among the factors involved are the nature of the instincts
in the conﬂict, the time of the decisive conﬂict, the intensity of the
frustrations or traumata, the availability of substitute gratiﬁcations, and the characteristics of the historical situation (Fenichel,
1).

It

is difﬁcult to evaluate the speciﬁcity of any one of these

factors in the choice of a particular neurosis. Recent investigations
tend to show that while a particular neurosis may apparently be
an expression of conﬂict at a certain level of development, nevertheless experiences at some earlier or previous level may produce
tendencies which provoke, potentiate or distort conﬂicts of a subsequent period of development.
With increasing psychoanalytic knowledge, the task of isolating
concrete factors inﬂuencing speciﬁc choice of neurosis becomes
ever more difﬁcult. It becomes even more difﬁcult if one attempts
to assess the intangible factor of ego strength of an individual in
his struggle to control and express his various instincts or his
attempts to fashion defenses or character traits. Nevertheless, it
1Attending Psychiatrist, Hillside Hospital, Glen Oaks, N.
2 Fellow in Psychiatry, Hillside Hospital, Glen Oaks, N. Y.
67

Y.

�68

TARACHOW—FINK

should be possible to ﬁnd a way of approaching mental operations
in a systematic way which would lead in the direction of solving
the problem of speciﬁcity of choice of neurosis.
In seeking a systematic way to solve this problem, it occurred
to us that perhaps certain elements in the external historical
situation might lend themselves more easily to the preliminary
steps of such a search. If a certain external historical situation were
isolated and studied, perhaps it could be correlated with certain
invariable psychic consequences. Freud (2) made such an observation when he noted that men who have weak or absent fathers
tend to develop homosexual trends.
The external historical factor we selected was the presence or
absence of both parents during the important developmental years
of the child. We decided to investigate the relation of this external
factor to the success or failure of the resolution of ambivalent
feelings, the ability to fuse the instincts of love and hate. For reasons to be noted we selected hysteria and obsessive-compulsive
neurosis as the clinical expressions of the success or failure of the
fusion.
We then set up the following hypothetical basis for this study
and made a tentative prediction of the data to be discovered. A
child brought up by both parents will solve the problem of resolu—
tion of ambivalent feelings more satisfactorily than a child who
has lost one parent for any signiﬁcant period of time. A child
facing only one parent does not have both his love and his hatred
equally and freely available to be directed to the parent. If he
loves the single parent the hate will tend to be repressed, and vice
versa. A child with both parents, on the other hand, has two
objects against whom both sides of the ambivalence can be directed in turn. He can hate one and love the other, or the opposite.
Two objects give the child much more liberty than one. This
freedom would not hinder resolution of ambivalence, but rather
facilitate it. He would have all his feelings relatively more available to him in comparison to the child with one parent. When the
time arrives for the necessary fusion of feelings for more mature
relationships the child who had had both parents is in a better
position. Both sides of the ambivalence having been available, the
fusion is more complete and normal. The other child, having
relatively only one side of the ambivalence available, never succeeds

�CHOICE OF NEUROSIS

69

in fusing his ambivalent feelings and remains with a burden of
one-sidedly more repressed and defused instinctual feeling.
According to our hypothesis the child who had two parents and
had succeeded in fusing his feelings would tend to develop hysteria, if he developed a neurosis. The other child would tend to
develop obsessive compulsive neurosis. This follows from the
familiar psychoanalytic formulations of defused ambivalence in
the compulsive neurosis and the fused genital level of feeling in
hysteria. This hypothesis was tested by consulting the case material from Hillside Hospital. We searched for clearly deﬁned
cases of each category and studied the incidence of absence, death
or loss of one parent for any reason whatever. Only clear-cut cases
were used. All mixed and intermediate syndromes were eliminated,
as were phobias and anxiety states.
Sixty-one records have so far been found suitable: of these,
twenty-seven were patients with conversion hysteria and thirty-four
with compulsive-obsessive neurosis. Separation from a
parent was deﬁned as the absence of a parent for periods exceeding one
year
before the child’s ﬁfteenth year of age. Note was made of the time
of the separation, the reason, the duration, and the
age of onset
of the neurotic symptoms.
Of the twenty-seven patients with conversion hysteria, three
(11%) were subjected to periods of separation. In each the separation
occurred between the ages of ﬁve and nine; in two by death and
in one by emigration. In the latter the period of separation was
of six years’ duration.
Of the thirty-four patients with obsessive-compulsive neurosis,
ﬁfteen (44%) suffered extended periods of separation. Nine occurred
between the ages of ﬁve and nine, four before the age of ﬁve, and
one each at thirteen and ﬁfteen. Separation was caused by death in
nine subjects, hospitalization in three, and emigration in three. In the
latter the separation lasted from one to three years, during the
child’s age of three to seven years. In four subjects there were
double separations. In one subject there was hospitalization of a
parent for a year, return home as an invalid for two years and
then death. In three other subjects there was death of one
parent
and illness of the other at another time in the child’s life. In all
instances the parental loss occurred before the clinical onset of
neurotic symptoms.

�70

TARACHOW—FINK

These data point in the same direction as the hypothesis suggested, namely, that loss of a parent tends to increase the difﬁculties
of solving the problem of ambivalence.3 So many other factors
enter into the situation that we would limit ourselves to the conclusion that these ﬁndings warrant further study of the suggested
correlation.
Other studies of parental deprivation have taken a somewhat
different direction. Oltman et al. (5) studied the difference in rate
of parental deprivation, comparing various psychoses with neuroses. They found that the incidence of loss of a parent did not
vary in schizophrenia and manic-depressive psychosis from their
control group, while psychoneuroses were higher. Their control
group was State Hospital personnel, with 32 per cent deprivation.
Psychoses showed 34 per cent and the neurotic subjects 49 per
cent. The psychoneurotic group was not diagnostically further
differentiated. Madow and Hardy (4), in a study of clinic population in the Army, found parental deprivation by death in 36 per
cent of the neurotics. They used as a control, life insurance statistical tables which indicated an 11 to 15 per cent incidence of
parent loss before the age of sixteen. A third study (3) of a student
health clinic population in a State University indicated that 31
loss
of
neurotic
the
cent
through
subjects
reported
parent
per
death, while only 131/2 per cent of the controls (normal students)
did. None of these workers were searching for the factors we are,
and there is no breakdown into the various neurotic categories.
These observations cannot be used comparatively with our speciﬁc
point in mind. In general the data from the literature indicate
that the incidence of parent loss is greater in neurotic subjects
than in psychotic and control groups, although the various control
groups show a lack of uniformity. Our own subjects taken as
a group (this excludes many mixed neuroses, phobics and anxiety
states) show an average incidence of parent loss of 30 per cent.
The incidence in the obsessional neurotic is higher than in the
cited controls, while in hysteria it coincides with the lower percentages of the controls.
Apart from the subtleties of the psychodynamic processes which
this study overlooks there are also gross difﬁculties in evaluating
3Chi square was calculated as 6.32 which is signiﬁcant at the .01-.02 level.
The chi square was corrected for continuity by Yates’ method.

�CHOICE OF NEUROSIS

71

the statistics. First of all, the sampling is small. This will be
remedied as the study continues. No other study differentiated
among the neuroses, and diagnostic criteria probably vary from
one institution to another.
This study can be reﬁned and develoPed in a number of directions. The dynamics with reference to the separation could be
explored. The presence or absence of parental surrogates should
be looked into. Other factors of separation such as deafness or
blindness or parent’s going out to work must all be considered.
SUMMARY

A hypothesis was formulated stating that unresolved ambivalence (instinct defusion) may be related to the absence of one
parent during the critical formative years. It was tentatively predicted that obsessive-compulsive neurosis (illustrative of instinct
defusion) would therefore show a high rate of parental deprivation and that hysteria (illustrative of instinct fusion) would show
a low rate. The actual data were: thirty-four cases of obsessive-compulsive neurosis showed 44 per cent of parental loss: twenty-seven
cases of hysteria showed 11 per cent parental loss. We consider this
at least a provocative difference. Even though many intrapsychic
factors enter into the problem of unresolved ambivalence, these
data warrant further study along these and related lines.
REFERENCES

(l) Fenichel, 0.: The Psychoanalytic Theory of Neurosis. New York: W. W.
Norton 8: Co., 1945.
:2(2) Freud, S.: Three Contributions to the Theory of Sex. In The Basic Writings of Sigmund Freud. New York: Modern Library, 1938.
(3) Ingham, H. V.: A Statistical Study of Family Relationships in
Psychoneurosis. Am. J. Psychiat., 106:91-98, 1949.
(4) Madow, L. and Hardy, S. E.: Incidence and Analysis of the Broken
Family
in the Background of Neurosis. Am. J. 0rthopsychiat., 17:521-528. 1947.
(5) Oltman, J. E., McGarry, J. J., and Friedman, 8.: Parental Deprivation and
the “Broken Home” in Dementia Praecox and Other Mental Disorders, Am. J. Psychiat., 1082685-694, 1952.

�Reprinted from
JOURNAL OF THE HILLSIDE HOSPITAL
Volume II, Number 2

April, 1953

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                    <text>9Q

J. Hillside Heapital,
1957

6: 197-206,

A UNIFIED THEORY OF THE ACTION OF

PHYSIODYNAMICTHERAPIES1
MAX FINK,

MD.2

The proper role of the physiodynamic therapies (convulsive,
insulin coma and lobotomy) in psychiatry remains poorly deﬁned.
In part, this results from the lack of an adequate formulation of
their mode of action. In the past six years increasing evidence for a
neuropllysiologic-adaptive view of electroconvulsive therapy has
been presented (41, 32, 38, I). This view ascribes the therapeutic
process in electroshock to a persistent alteration in cerebral function
which provides the milieu for a change in adaptation of the subject
to his environment. The type of adaptation evoked is dependent
upon the personality of the subject, the environmental situation,
and the duration of the induced alteration in cerebral function.
Concurrently, an awareness of a similar mode of action in insulin
coma (31) and lobotomy (40) has developed.
During the past four years we have studied the relation between
alteration in various indices of brain function and the behavioral
response of psychiatric patients to therapy. The neurophysiologicadaptive view of electroshock has been supported and ampliﬁed (11,
12, 13, 19, 21); evidence for a similar view of insulin coma has been
presented (22); and recently the concept has been extended to the
newer “tranquilizers" (9). These studies provide the basis for a
generalization concerning the efﬁcacy of these therapies. It is our
purpose in this report to examine the experimental evidence to
determine whether or not the mode of action of each of these thera—
1From the Department of Experimental Psychiatry, Hillside Hospital, Glen

Oaks, N. Y.

Read at the. 2nd International Congress of Psychiatry, Zurich, September

6, 1957.

Aided by Grant M-927 of the National Institute of Mental Health, National
Institutes of Health, U. S. Public Health Service; and the Board of Directors’
Research Fund of the Society of the Hillside Hospital.
2 Director, Department of Experimental Psychiatry, Hillside Hospital.
197

12-»

�198

MAX FINK

pies may result from their ability to induce sustained alteration in
cerebral function; and the corollary question, whether measurable
alteration in cerebral function is a necessary condition for the efﬁ—
cacy of these therapies, or a “complication" or "untoward effect."
The indices of brain function used in these studies have varied.
These include memory scales (2G), visual (20) and tactile (10) perceptual tasks, and changes in language patterns of orientation both
clinically (19) and after intravenous amobarbital (21). In electroencephalographic studies of this problem, changes in the delta index,
both in routine records (ll, 12) and after activation by intravenous
thiopentone (32, 33), and in the beta index (16) have been applied
Successfully. For this review, two indices will be stressed: changes in
the delta index of the unactivated EEG, and clinical neurologic
signs. These indices have been selected because of their successful
application in the analysis of the electroshock process, and because
data is available for each of the therapeutic modalities.
OBSERVATIONS

(a) Electroshock

4.1
"1M

The following notes summarize our experimental studies of the
role of 'changes in EEG delta activity in the response of subjects to
electroshock (11, 13). In these studies, electroencephalograms were
obtained before treatment, and at weekly intervals on a day after a
treatment in consecutive electroshock referrals. Grand mal treatments were administered three times a week, for twelve to twenty
treatments. The EEG records were quantitatively analyzed for the
amount of induced delta activity, and classiﬁed into categories of
“high,” “moderate” and “low” degrees of delta activity. At the end
of treatment, the patients were independently rated for their shortterm clinical response into the categories of “much improved,"
“moderately improved” and “unimproved."
In the initial series of patients, a signiﬁcant relationship between
the early induction of high degrees of delta activity, and clinical
ratings of “much improved” was observed. Eighty per cent of the
records in the much improved group were high degree delta by the
fourth to sixth treatment; and the percentage was sustained at 90
per cent in the third’ and fourth weeks. In contrast, none of the unimproved patients developed high degree delta records in the ﬁrst
three weeks, and only 20 per cent of the records in the fourth week
were so classiﬁed.
In a subsequent predictive study, the EEG records during the

a

wan-pow

�THEORY OF PHYSIODYNAMIC THERAPIES

199

second and third weeks of treatment were analyzed. Of the patients
who had high degree delta records on both occasions, 67 per cent
were rated as much improved, while of the patients without such
records, 70 per cent were in the unimproved and moderately improved categories.
Roth (82, 33), studying the EEG delta activity evoked by intravenous thiopentone after electroshock, has related both the stability
and the rate of remission of patients with endogenous depressions
to the peak value of the induced slow activity. He concluded that
patients not attaining a speciﬁed delta activity level "have not acquired an adequate physiological basis for recovery,” and recommended measurement of delta activity levels after thiopentone as a
guide to the clinical management of patients.
Further information is obtained from convulsive-subconvulsive
control studies. While convulsive electroshock induces degrees of
delta activity that vary from low to high, subconvulsive therapy
rarely alters EEG patterns or induces low degrees of delta activity
(13). In their comparative study of different convulsive and subconvulsive techniques, Ulett, Smith and Gleser (38) demonstrated a
signiﬁcantly greater recovery rate for the convulsive than the subconvulsive group.
In a similar study (13) recently completed here, twenty-seven
patients received a course of subconvulsive therapy. Electroencephalograms, taken at weekly intervals, demonstrated minimal
changes—none of the records were scored as middle or high delta
activity. Of the twenty-seven patients, no change in behavior was
noted in twenty-three, and of these, nineteen were referred for a
second course of treatment. Grand mal electroshock induced a high
degree of delta activity in fourteen. All patients in this group
showed signiﬁcant changes in behavior, while of the ﬁve who did
not show the delta response, only two showed a behavioral change.

Tranquilizing Drugs
When the newer drug therapies are studied from the viewpoint
of their electroencephalographic and clinical neurologic effects, a
meaningful classiﬁcation emerges. Furthermore, a relationship between the degree and type of induced change in cerebral function
and therapeutic efﬁcacy may be noted. The ability of these agents
to induce such signs of central nervous system dysfunction as motor
rigidity, depression, excitement and seizures are well known. Less
well documented, however, are the clearly deﬁnable electroencephalographic patterns. Based on observations made in chronic admin(b)

�MAX FIN K

200

istration of drugs in adult psychiatric patients, the EEG changes
may be classiﬁed according to predominant changes in the frequency
spectrum. There are three broad types:
Increased slow wave activity with hypersynchrony
(“bursts")—“delta shift"
II._ Desynchronization with voltage and frequency
irregularity and irregular theta activity—“desynchronization”
III. Increased high voltage fast activity—“beta shift.”
Of the group of drugs inducing a delta shift, the phenothiazine
derivatives chlorpromazine, promazine, and perphenazine are clear
examples. Each drug induces seizures in nonepileptics or exaggerates
seizures in epileptic patients (7, 8, 15, 29, 37). Each drug induces
clinical parkinsonian neurologic patterns when given in adequate
dosage. In our laboratories, we have induced parkinsonism in all
patients receiving chlorpromazine (l4) and have observed seizures
in 10 per cent of a group of psychotic patients without previous
ltistnl'y of seizures. Induced delta activity, including burst activity,
\ms nlm-ned in more than half the patients in this series.
Rrxrxpiue also ernkes delta activity when given in large doses
(3- \t liitth tlnugt‘ levels. it exaggerates seizures in epileptics and
"I'lihrs wzmtes in animals (35). .-\t the usual clinical dosages, howr.:-:, ”supine imluu's desynrhronization of frequencies with a
t; w-lrtxh‘ mitease in theta activity (28), without seizure induction
in: mm definite motor rigidities. In a series of patients treated here
("T'H. parkiuwuism was induced in all patients. EEG
Changes were
limited to desynchronization only, without delta burst activity.
The primary response of two other drugs, mepazine and benacty.
.
Ime. is the induction of EEG desynchronization. Mepazine, a phen()t‘ttLt/mt‘ derivative. induces desynchronization with small amounts;
it n\n\ \ \ l‘h'lt'h .‘n‘H\'n\ has nx‘u t\\\‘ll 'li‘it‘l‘ﬁk‘n. nor have
.-'
m: Immd reports either of seizures or parkinsonism in the clinical
literature. Benactyzine, a potent anticholinergic compound, induces
a blocking of alpha, ﬂattening of the record and occasional theta
activity (5, 17). Neither seizures nor parkinsonism have been described for this agent.
Meprobamate is the clearest example of the group of drugs inducing a beta shift in the EEG (3). This agent further differs from
the phenothiazines and reserpine in not producing parkinsonism
and not only are clinical seizures not induced, but deﬁnite antiepileptic activity has been described (30). Habituation is readily
1.

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w

�THEORY OF PHYSIODYNAMIC THERAPIES

f

201

achieved, and withdrawal phenomena of agitation and seizures have
been observed (42). In these actions, meprobamate is more like
barbiturates than like the other new tranquilizers.
If we determine the clinical efficacy of these agents, we note a
parallel between the induced EEG effects and their potency in
altering behavior. The drugs that most readily induce a delta shift
in EEG frequencies—the phenothiazine compounds—are those with
the greatest clinical efﬁcacy in the therapy of psychoses. The compounds with lesser activity in this direction are less efﬁcacious clinically.

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Insulin Coma Therapy
The effects of insulin coma therapy on the nervous system are
well documented. During each coma, EEG delta activity is induced,
which usually persists for minutes to a few hours after gavage. Not
infrequently, in approximately one third of patients receiving deep
coma therapy in this hospital, seizures, aphasia or prolonged coma
results. After such events, EEG changes of delta activity persist for
days, and in cases of prolonged coma, for weeks and months (43).
The relation between prolonged coma, altered brain function
and behavioral response has been discussed at length. Revitch (31)
reported eight cases of prolonged coma and concluded that improvement may be attributed to the induction of organic brain damage,
similar to lobotomy. Yaeger, Simon, Margolis and Burch (43), describing twelve cases of prolonged insulin coma, noted a correlation
between length of coma, degree of organic confusion, remission of
mental symptoms and degree of EEG abnormality. Shagass and
Rowsell (34), emphasizing EEG data, and Kwalwasser and Caplan
(27) presented individual cases to support the same conclusion.
We reported a similar relationship between prolonged coma and
behavioral response in a case study (22). A 34-year-old schizophrenic
patient with paranoid ideation developed a left hemiplegia during
insulin coma therapy. With the onset of neurologic signs of hemiparesis, hemianopsia, hemisensory syndrome and spatial inattention,
there was a marked change in speech and behavior. He became lucid,
loquacious and denied his illness. His former paranoid-withdrawal
type pattern was replaced by a friendly cooperative attitude. These
changes were accompanied by delta changes in the EEG, as well as
language changes after amobarbital indicative of altered brain
function. The neurologic symptoms resolved, but the behavioral
changes persisted so that he was discharged two months later as
“much improved."

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�202

MAX FINK

(d) Lobotomy
to study lobotomy
While we have not had the opportunity
of
of view of this summary, the reports
the
point
from
EEG
patients
a similar relationship.
numerous observers clearly documentin all subjects postoperatively
of
changes of delta activity are present
Walter et al. (40) in a study
(6) and persist for varying periods.
EEG
persistence of abnormal
150 patients, found an 80 per cent
be?
relation
noted
a
also
authors
activity after three years. These
of
postextent
and
and the degree
tween clinical improvement
operative slow wave activity.
“complication," being variPostoperative seizures are a frequent
(25).
in up to 20 per cent of subjects
ously reported as occurring
of brain
extent
the
between
Furthermore, there is a relationship
Circumscribed surgical
tissue cut and the therapeutic outcome.
improvement rate lower than
lesions, regardless of locus, have an
are frequently inadequate
unilateral lobectomy; and these latter
bilateral procedure (36).
and are “improved” upon by a

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DISCUSSION

are essayed from the
When the various physiodynamic therapies
mode
in brain function, a common
point of view of an alteration
which
therapies represent devices
of action becomes apparent. These
function, with resultant change
induce appreciable changes in brain
and lobotomy induce measurable
in behavior. Convulsive therapy
directly; insulin coma primarily
diffuse changes in brain function
the phenothiazine and reserpine
when complications ensue; and
when given in adequate dosage.
groups of tranquilizers
function affect behavior is
How persistent changes in cerebral“reversed" or “obliterated."
is not
not clear. Psychotic behavior
the central nervous system milieu,
in
Rather, with an alteration
of behavior including perception,
there is an alteration in all aspects
attitude. The speciﬁc adaptive
mood, affect, memory, judgment and
each subject and is dependent on numerous
response is variable for
Premorbid personality (18),
historical and environmental factors.
and the duration of
environmental situation and expectations (13),
have recently been discussed as
the alteration in brain function (12)
under these conditions.
determinants of the behavioral response evaluated by the psychiaThe induced changes in behavior are
the degree of “improvement."
trist, administrator or family as to based
the
upon such factors as
These ratings are value judgments,
tolerance
behavioral response, the environmental
type of induced
.

JUN-laws

�THEORY OF PHYSIODYNAMIC THERAPIES

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203

and the observer's expectations. In this context, the physiodynamic
therapies do not induce “improvement"——-rather they induce behavioral change which is secondarily evaluated as improvement.
The alteration of cerebral function is therefore not a “complication" or an "untoward effect" but the desired goal of these forms of
therapy. Of the many “organic" therapies introduced during the
past thirty years, none apparently has been a speciﬁc agent for the
therapy of psychoses (in the sense that penicillin is speciﬁc for neurosyphilis and nicotinic acid for pellagra dementia), but rather devices
with greater or lesser degrees of applicability and efﬁcacy in altering
behavior by altering the cerebral milieu.
In this context, the various physiodynamic therapies are not speciﬁc for a type of psychosis. The early enthusiasm that reserpine or
chlorpromazine was speciﬁc for schizophrenia, or hypotheses that
ascribe signiﬁcance to an antagonism between these drugs and “psychosis" or "schizophrenia" are not tenable. Similar enthusiasm
claiming a speciﬁcity of insulin coma for schizophrenia is also untenable, and support for this view is presented in a recent chlorpromazine-insulin coma control‘study (l4).
EEG analysis of these therapies permits a more explicit deﬁnition of the induced alteration in brain function. Changes in cerebral
function reﬂected by a shift in the spectrum of EEG frequencies
toward the slower range, with a concomitant increase in voltage and
a periodicity described as “bursts" or “hypersynchrony” provide the
change in milieu that is more effective in altering behavior. The
signiﬁcance of the delta shift has been clearly demonstrated in
electroshock therapy; and can be inferred from the available data
in lobotomy, insulin coma, and the tranquilizers.
That a delta shift has some speciﬁcity is seen in the analyses of
the drug effects. Those drugs that induce the delta shift—the phenothiazines and reserpine—have been consistently reported as effective
modiﬁers of psychotic behavior. Changes in brain function reﬂected
by EEG desynchronization only, or a shift in frequency spectrum to
the faster range, have a limited efﬁcacy in altering psychotic behavior.3 The signiﬁcance of a delta shift is further seen in the
limited efﬁcacy of subconvulsive electroshock when compared to
convulsive electroshock in the management of psychoses.
Another aspect of the alteration in brain function which may be
deﬁned is the change in seizure threshold. With the delta shift in
3 These observations suggest the application of EEG screening of new chemotherapeutic compounds for therapeutic efﬁcacy according to their ability to
induce delta burst activity with a minimum of side effects.

�MAX FINK

204

the EEG, an increase in clinical seizures would be anticipated. This
is indeed true. Seizures have been described following electroshock
(4, 24); they are prominent after lobotomy (40) and a common “complication” during and occasionally following insulin coma therapy
(23). With the tranquilizers, the parallel of clinical efficacy and
seizure induction is most striking. Phenothiazine compounds induce
seizures commonly; reserpine rarely; benactyzine not at all; and
meprobamate is a potent anticonvulsant! The lowering of seizure
threshold parallels the extent of the EEG delta shift induced by
these compounds. Similar analyses can be made for the potentiation
of sedative action and induction of parkinsonism—both potent indices of an alteration in cerebral function.
The neurologic basis for the delta shift and increase in seizure’
frequency is unclear. Whether this represents a persistent change in
function of some speciﬁc brain stem nuclear system, as the centrencephalic, thalamic or hypothalamic, is conjectural. From the wide
range of agents that can induce a delta shift, with or without hypersynchrony, it appears more likely that the EEG changes reflect an
alteration in the diffuse biochemical activity of the nervous system
rather than in a focal activity of speciﬁc cellular masses.
SUMMARY
1.

The neurophysiologic and clinical neurologic aspects of con-

vulsive therapy, “tranquilizers,” insulin coma and lobotomy, are
reviewed.
2. The efﬁcacy of each therapy in the treatment of psychoses is
related to the ability to induce a persistent change in cerebral function, of which a delta shift in the EEG spectrum and an increase in
incidence of seizures are two indices.
3. Alteration in cerebral function is an essential prerequisite of
behavioral change with each of these therapies. Such alteration is
neither a “complication,” nor an “untoward effect," but is the sine
qua non of the mode of action of these therapies.
4. No evidence has been educed in these studies that the physiodynamic therapies are speciﬁc agents for the relief of psychoses; nor
do they affect a speciﬁc segment of the nervous system; nor do they
induce speciﬁc behavioral'changes.
5. The therapeutic process of convulsive therapy, insulin coma,
lobotomy and tranquilizers may be ascribed to the induction of a

persistent alteration in cerebral function which provides the milieu
for a change in adaptation of the subject to his environment.

r.—-r,y.,.",,,,

�THEORY OF PHYSIODYNAMIC THERAPIES

205

REFERENCES
(1)

(2 V

i
l

l
:

Aird, R. B.: Strait, L. A.: Pace, J. “7.; Hernolf, M. K. 8: Bowditch, S. C.:
Neurophysiologic Effects of Electrically Induced Convulsions. A.M.A. Arch.
Neural. (9 Psychiat., 75:371-378, 1956.
Arellano, A. P. 8.- ]eri, R.: The Ellcct of Reserpine on the Scalp and Basal
Electrocncephalogram. EEG. Clin. Neurophysiol., 8:150 (abst.), 1956.
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(16)

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~

,,L...-.u..

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Coma. ]. New. 6'
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.

39W"

_

.

w

.

if

�A

Unified Theory of the Action of Physiodynamic Therapies

Max

Fink, M.D.

From

the Department of Experimental Psychiatry, Hillside Respital, Glen Oaks,

Read

at the

2nd

International Congress of Psychiatry, Zurich, September 6,

N.Y.

1957.

of the National Institute of Mental Health, National Institutes
of Health, U.S. Public acalth Service; and the Board of Directors' Research Fund of
the Society of the Hillside Bbspital.
Aided by

10-7-57

grant

M-927

�Iv:

unified

A

The

10/5/57

Theory of the Action of Physiodynamic Therapies

proper role of the physiodynamic therapies (electroshock, insulin

coma and lobotomy)

in psychiatry remains poorly defined. In part, this results

from the lack of an adequate formulation of

their

mode

of action. In the past

six years increasing evidence for a neurophysiologic-adaptive

view of

electro-

(hl, 32, 38, 1). This view ascribes the there“

shock therapy has been presented

peutic process in electroshock to a persistent alteration in cerebral function
which provides the milieu

environment.

The

for a

change

in adaptation of the subject to his

type of adaptation evoked is dependent upon the personality

of the subject, the environmental

situation,

and the duration of the induced

alteration in cerebral function. Concurrently,
of action in insulin coma (31) and lobotomy
During the past four years

we

(MO)

of psychiatric patients to therapy.

The

a

similar

view of

insulin

relation between

and the behavioral response

neurophysiologic-adaptive view of

electroshock has been supported and amplified (9, 10,

for

mode

has developed.

have studied the

alteration in various indices of brain function

similar

an awareness of a

coma has been

ll,

20, 21); evidence

presented (19); and recently the

concept has been extended to the newer "tranquillizers" (12).

These

studies

provide the basis for a generalization concerning the efficacy of these therapies.

It is

our purpose in

this report to

examine the experimental evidence

whether or not the mode of action of each of these therapies may

to determine

result

their ability to induce sustained alteration in cerebral function;

from

and the coroln

lary question, whether measurable alteration in cerebral function is a necessary

�-

-

2

condition for the efficacy of these therapies, or a "complication" or "untoward

effect."
The

include

indices of brain function used in these studies have varied.

memory

scales (26), visual (22)

and

tactile

changes in language patterns of orientation both

intravenous ambbarbital (20).
changes in the

clinically (21)

and

after

In electroencephalographic studies of this problem,

by intravenous thiopentone (32, 33), and

successfully. For this review,

have been

(13) perceptual tasks, and

delta index, both in routine records (9,

delta index of the unactivated

These

and

after activation

in the beta index (16) have been applied

two indices
EEG,

10) and

will

be

stressed: changes in the

clinical neurologic signs.

These indices

selected because of their successful application in the analysis of

the electroshock process, and because data is available for each of the therapeutic
modalities .

�OBSERVATIONS:

(a) Electroshock:
The

role of changes in

following notes summarize our experimental studies of the

EEG

delta activity in the response of subjects to electro-

In these studies, electroencephalograms were obtained before

shock (9, 11).

treatment, and at weekly intervals
electroshock referrals.
week,

for

after a treatment in consecutive

Grand mal treatments were administered

treatments.

12-20

on a day

The EEG

three times a

records were quantitatively analyzed for

the amount of induced delta activity, and classified into categories of "high",
"moderate" and "low" degrees of delta

patients

were independently

the categories of
In the

At the end of treatment, the

activity.

rated for their short term clinical response into

"much improved”, "moderately improved" and "unimproved".

initial series

of

patients, a significant relationship between

the early induction of high degrees of delta activity, and clinical ratings of
"much improved" was observed.

Eighty percent of the records in the

much improved

group were high degree delta by the h-6 treatment; and the percentage was sus-

tained at

90%

In contrast, none of the unimproved

in the third and fourth weeks.

patients developed high degree delta records in the
20%

third

weeks of treatment were analyzed.

delta records

on both occasions, 67% were

patients without such records,
categories.

70%

and only

classified.

of the records in the fourth week were so

In a subsequent predictive study, the
and

first three weeks,

EEG

Of

records during the second

the patients

rated as

who

had high degree

much improved,

while of the

were in the unimproved and moderately improved

�*“1

h

Both (32, 33) studying the

EEG

-

delta activity

thiopentone after electroshock has related both the

evoked by intravenous

stability and the rate of

remission of patients with endogenous depressions to the peak value of the induced slow

activity.

activity level,

He

......

"

concluded

that patients not attaining a specified delta

have not acquired an adequate physiological basis for

recovery," and recommended measurement of delta activity levels after thiopentone

clinical

as a guide to the

management of

patients.

Further information is obtained from convulsive-subconvulsive control

studies.

While convulsive electroshock induces degrees of

vary from low to high, subconvulsive therapy rarely alters
duces low degrees of delta

delta activity that
EEG

patterns or in-

activity (11). In their comparative study of different

convulsive and subconvulsive techniques, Ulett, Smith and Gleser (38)

demon-

strated a significantly greater recovery rate for the convulsive than the subconvulsive group.
In a similar study (11) recently completed here, twenty-seven patients

received a course of subconvulsive therapy.
weekly

Electroencephalograms, taken at

intervals, demonstrated minimal changes

as middle or high

delta activity.

Of

- none of the records were scored

the 27 patients, no change in behavior

was

noted in 23, and of these, 19 were referred for a second course of treatment.
Grand mal electroshock induced a high degree of

delta activity in fourteen.

All patients in this group showed significant changes in behavior, while of
the five

who

did not

show

the delta response, only two showed a behavioral change.

(b) Tranquillizing Drugs:
When

the newer drug therapies are studied from the viewpoint of

�-5their electroencephalographic

and

clinical neurologic effects, a meaningful

classification emerges. Furthermore, a relationship between the degree

and

type of induced change in cerebral function and therapeutic efficacy may be

noted.

The

ability of these agents to induce such signs of central nervous

system dysfunction as motor

rigidity, depression, excitement

and

seizures are

well known. Less well documented, however, are the clearly definable electro—
encephalographic patterns.

Based on observations made

of drugs in adult psychiatric patients, the

EEG

in chronic administration

changes may be

according to predominant changes in the frequency spectrum.

classified

There are three

broad types:

I.

Increased slow

wave

activity with hypersynchrony

("bursts") - "delta shift"

II.

Desynchronization with voltage and frequency irregularity
and

III.
Of

irregular theta activity - "desynchronization"

shift."

Increased high voltage fast activity - "beta
the group of drugs inducing a delta

derivatives chlorpromazine, promazine,
Each drug induces

shift, the phenothiazine

and perphenazine are

clear examples.

seizures in non-epileptics or exaggerates seizures in

epileptic patients (7, 8,
neurologic patterns

15, 29, 37).

when given

Each drug induces

in adequate dosage.

clinical parkinsonian

In our laboratories,

have induced parkinsonism

in all patients receiving chlorpromazine

have observed seizures in

10%

(1%)

and

of a group of psychotic patients without previous

history of seizures. Induced delta activity, including burst activity,
observed in more than

we

half the patients in this series.

was

�-5Reserpine also evokes delta
At high dosage

levels,

it

activity

when given

in large doses (2).

exaggerates seizures in epileptics and induces

seizures in animals (35). At the usual clinical dosages, however, reserpine
induces desynchronization of frequencies with a moderate increase in theta

activity (28), without seizure induction but with definite motor rigidities.
In a series of patients treated here (39), parkinsonism was induced in

patients.

EEG

all

changes were limited to desynchronization only, without delta

burst activity.
The primary

the induction of

EEG

response of two other drugs, mepazine and benactyzine, is
desynchronization. Mepazine, a phenothiazine derivative,

induces desynchronization with small amounts of theta

activity has not been described, nor
or parkinsonism in the

have we found

activity (7). Delta

reports either of seizures

clinical literature. Benactyzine, a potent anticholin-

ergic compound, induces a blocking of alpha, flattening of the record and
17). Neither seizures nor parkinsonism have

occasional theta activity (5,
been described for

this agent.

Meprobamate

beta shift in the
and

EEG

is the clearest

example of the group of drugs inducing a

(3). This agent further differs

reserpine in not producing parkinsonism

from the phenothiazines

and not only are

clinical seizures

not induced, hut definite anti-epileptic activity has been described (30).
Habituation is readily achieved, and withdrawal phenomena of agitation and
seizures have been observed (h2).

barbiturates than like the other

If we

determine the

In these actions, meprobamate
new

is

more

like

tranquillizers.

clinical efficacy of these agents,

we

note a parallel

�-7between the induced
drugs

EEG

effects

and

their potency in altering behavior.

that most readily induce a delta shift in

thiazine

compounds - are those with the

therapy of psychoses.

The compounds

EEG

frequencies - the

The

pheno—

greatest clinical efficacy in the

with lesser activity in this direction

are less efficacious clinically.
(c) Insulin

Coma

The

well documented.

Therapy:

effects of insulin

During each coma,

persists for minutes to a

few hours

EEG

coma

delta activity is induced,

after gavage.

imately one third of patients receiving deep

seizures, aphasia or prolonged

coma

therapy on the nervous system are

coma

which usually

infrequently, in

Not

approx—

therapy in this hospital,

results. After such events,

of delta activity persist for days, and in cases of prolonged

changes

EEG

coma,

for

weeks

and months (h3).

relation between prolonged

The

coma,

altered brain function

ioral response has been discussed at length. Revitch
of prolonged coma and concluded

tion of organic brain

damage,

that

(31) reported

improvement may be

insulin

eight cases

attributed to the

similar to lobotomy. Yaeger,

Burch (#3), describing twelve cases of prolonged

and behaVo

induc—

Simon, Margolis and

coma, noted a

correlation

between length of coma, degree of organic confusion, remission of mental symptoms
and degree of

EEG

abnormality. Shagass and Rowsell (3h), emphasizing

and Kwalwasser and Caplan (27) presented

EEG

individual cases to support the

data,
same

conclusion.
We

reported a similar relationship between prolonged

response in a case study (19).

A

3h

coma and

behavioral

year old schizophrenic patient with paranoid

�-8ideation developed a left hemiplegia during insulin

coma

therapy. With the onset

spatial

of neurologic signs of hemiparesis, hemianopsia, hemisensory syndrome and

inattention, there

was

a marked change in speech and behavior.

loquacious and denied his illness.
was

by

He

ludic,

became

His former paranoid—withdrawal type

pattern

replaced by a friendly cooperative attitude. These changes were accompanied

delta changes in the

as well as language changes

EEG,

dicative of altered brain function.

The

neurologic

after amobarbital

symptoms

in—

resolved, but the

behavioral changes persisted so that he was discharged two months later as

"much

improved."
(d) Lobotomy:
While we have not had the opportunity
from the point of view of
document a

this

summary,

similar relationship.

all subjects postoperatively
(#0) in a study of 150

after three years.

EEG

(6) and

to study

patients

lobotomy

the reports of numerous observers clearly

changes of delta

activity are present in

persist for varying periods. Walter et al.,

patients, found

an 80%

persistence of abnormal

These authors also noted a

EEG

relation between clinical

ment and the degree and extent of postoperative slow wave

activity
improve—

activity.

Postoperative seizures are a frequent "complication," being variously
reported as occurring up to

relationship

between the

20%

of subjects (25). Furthermore, there

extent of brain tissue cut

and the

is

therapeutic

Circumscribed surgical lesions, regardless of locus, have an improvement
lower than

unilateral lobectomy;

are "improved" upon by a

and these

a
outcome.

rate

latter are frequently inadequate

bilateral procedure (36).

and

�DISCUSSION:
When

view of an
These

the various physiodynamic therapies are assayed from the point of

alteration in brain function, a

therapies represent devices

of action becomes apparent.

common mode

which induce appreciable changes in

brain

function, with resultant change in behavior. Electroshock and lobotomy induce
measurable diffuse changes in brain function
when

directly; insulin

coma

primarily

complications ensue; and the phenothiazine and reserpine groups of

quillizers

when given

How

tran—

in adequate dosage.

persistent changes in cerebral function affect behavior is not

clear. Psychotic dehavior is not "reversed" or "obliterated". Rather, with
an

alteration in the central nervous system milieu, there is

all aspects of behavior including perception,
and

attitude.

is dependent

The

affect,

alteration in

memory, Judgment

specific adaptive response is variable for each subject

on numerous

historical

and environmental

sonality (18), environmental situation
of the

mood,

an

alteration in brain function

factors.

and expectations

(10) have

(ll),

and

Pre-morbid perand the duration

recently been discussed as

determinants of the behavioral response under these conditions.
The induced changes

in behavior are evaluated

by the

administrator or family as to the degree of "improvement."

psychiatrist,

These

ratings are

value judgments, based upon such factors as the type of induced behavioral

response, the environmental tolerance and the observer's expectations. In this
context, the physiodynamic therapies do not induce "improvement" - rather they
induce behavioral change which

is secondarily evaluated as

improvement.

alteration of cerebral function is therefore not a "complication" or

The

an "untoward

�-10..
effect" but the desired goal of these forms of therapy.
therapies introduced during the past thirty years,

Of

the

many

"organic"

none apparently, has been a

specific agent for the therapy of psychoses (in the sense that penicillin is
specific for neurosyphilis and nicotinic acid for pellagra dementia), but rather
devices with greater or lesser degrees of applicability and efficacy in altering
behavior by altering the cerebral milieu.
In

this context, the various physiodynamic therapies are not specific

for a type of psychosis.
was

The

early enthusiasm that reserpine or chlorpromazine

specific for schizophrenia, or hypotheses that ascribe significane to

an

antagonism between these drugs and "psychosis" or "schizophrenia" are not tenable.

Similar enthusiasm claiming a specificity of insulin

coma

for schizophrenia is

also untenable, and support for this view is presented in a recent chlorpromazine—

insulin

coma
EEG

control study (1h).
analysis of these therapies permits a

the induced alteration in brain function.
by a

shift in the spectrum of

EEG

Changes

more

explicit definition of

in cerebral function reflected

frequencies toward the slower range, with a

concomitant increase in voltage and a periodicity described as "bursts" or
"hypersynchrony" provide the change in milieu

behavior.

The

that is

more

effective in altering

significance of the delta shift has been clearly demonstrated in

electroshock therapy; and can be inferred from the available data in lobotomy,

insulin

coma, and the

That a delta
drug

effects.

reserpine

tranquillizers.
shift has

Those drugs

- have been

some

specificity is seen in the analyses of the

that induce the delta shift

- the phenothiazines and

consistently reported as effective modifiers of psychotic

�- 11 -

of psychotic behavior. Changes in brain function reflected by

EEG

desynchroniza-

tion only, or a shift in frequency spectrum to the faster range, have a limited
efficacy in altering psychotic behavior.

*

The

significance of a delta shift

is further seen in the limited efficacy of subconvulsive electroshock

when com-

pared to convulsive electroshock in the management of psychoses.
Another aspect of the

is the

change

alteration in brain function

in seizure threshold.

delta shift in the

With the

in clinical seizures would be anticipated.

which may be defined

This

been described following electroshock (h, 2h),

EEG,

an increase

is indeed true. Seizures have
are prominent after lobotomy

(ho) and a common ”complication" during and occasionally following

insulin

coma

therapy (23). With the tranquillizers, the parallel of clinical efficacy and
seizure induction is most striking.
commonly;

reserpine rarely; benactyzine not at all;

anticonvulsant!
EEG

Phenothiazine compounds induce seizures

The lowering of

delta shift induced

and meprobamate

is a potent

seizure threshold parallels the extent of the

by these compounds.

Similar analyses can be

made

for

the potentiation of sedative action and induction of parkinsonism - both potent
indices of an alteration in cerebral function.
The

quency
some

neurologic basis for the delta shift and increase in seizure

is unclear.

Whether

fre—

this represents a persistent change in function of

specific brain stem nuclear system, as the centrencephalic, thalamic or

hypothalamic, is conjectural.

From

the wide range of agents that can induce a

screening of new chemo—
therapeutic compounds for therapeutic efficacy according to their ability
to induce delta burst activity with a minimum of side effects.

* These

observations suggest the application of

EEG

�-

12

-

delta shift, with or without hypersynchrony,
EEG

changes

it

appears more likely that the

reflect an alteration in the diffuse biochemical activity of the

nervous system rather than in a focal

activity of specific cellular masses.

�- 13 SUMMARY:

1.
shock,

The

neurophysiologic and clinical neurologic aspects of electro-

"tranquillizers, insulin
H

2.

The

coma and lobotomy,

efficacy of each therapy in the treatment of psychoses is

related to the ability to induce a persistent
of which a delta shift in the
seizures are
3.

two

EEG

change in

cerebral function,

spectrum and an increase in incidence of

indices.

Alteration in cerebral function is

behavioral change with each of these therapies.
a "complication," nor an "untoward
mode of

are reviewed.

an

essential prerequisite of

Such

alteration is neither

effect," but is the sine 92a

action of these therapies.
h.

No

evidence has been educed in these studies

that the physiodynamic

therapies are specific agents for the relief of psychoses; nor
specific

non of the

segment of the nervous system; nor do they induce

do they

affect a

specific behavioral

changes.
5.
and

The

therapeutic process of electroshock, insulin

tranquillizers

may be

in cerebral function

coma, lobotomy

ascribed to the induction of a persistent alteration

which provides the milieu

the subject to his environment.

for a change in adaptation of

�L.A., Pace, J.W., Hernoff, M.K. and Bowditch, S.C.
(1956): Neurophysiologic Effects of Electrically Induced
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Aird, R.B.,

Strait,

Jeri, R. (1956): The Effect of Reserpine on the
and
Basal Electroencephalogram, EEG. Clin. Neurophysiol.
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Arellano, A.P. and
g:

150

(abet).

Berger, F.M. (1957): The Chemistry and Mode of Action of Tranquillizing Drugs, Ann. N.Y. Acad. Sci. é]: 685-699.

I.J.

Spontaneous Seizures and Related Electroencephalographic Findings Following Shock Therapy, J. Nerv.
Ment. Dis. 122: 581~588.

Blumenthal,

(1955):

Coady, A. and Jewesbury, E.C.O. (1956):

A

Clinical Trial of

Benactyzine Hydrochloride ("Suavital") as a Physical
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Cohn, R. (l9h5):
&amp;

EEG

Psychiat.

Study of Prefrontal Lobotomy, Arch. Neurol.

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351—357.

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Fabisch,

Effect of Chlorpromazine on the Electroencephalogram
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185—190.

10.

Fink,

M.

Fink,

M.

Quantitative Studies of Slow Wave
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§: 158 (abst).
and Kahn, R.L. (1956):

Delta Activity to
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Psychiat. (in press).

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Studies,

ll.

.

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Fink, M., Kahn, R.L. and Green, M.A.: Experimental Studies of the
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M.

(1957): Therapy of Schizophrenia: Role of Alteration of
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Psychiatry, Zurich.

�- 15 REFERENCES

13.

Fink, M., Green, M.A. and Bender, M.B. (1952). The Face-Hand Test as
a Diagnostic Sign of Organic Mental Syndrome, Neurology' 2:
h6—58.

14.

Fink, M., Shaw, R., Gross, G. and Coleman, F.S.: Comparative Study
of Chlorpromazine and Insulin Coma in the Therapy of
Psychosis, J. Amer. Med. Assoc. (in press).

15.

Hankoff, L.D., Kaye, E., Engelhardt, D.M. and Freedman, N. (1957):
Convulsions Complicating Ataractic Therapy, Their Incidence
and Theoretical Implications, N.Y. State J. Med. 51: 2967-2972.

l6.

Hoagland, H., Malamnd, w., Kaufman, 1.0. and Pincus, G. (l9h6):
Changes in Electroencephalogram and in Excretion of 17
Ketosteroids Accompanying Electro-shock Therapy of Agitated
—

Depression, Psychom.

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17.

Jacobson, E. (1955): Suavitil, et Nyt Stof Med Specifik Virkning
pa Centralnervesystemet, Ugeskrift for Laeger, 117: 1147—1151.

18.

Khhn, R.L. and

19.

Kahn, R.L., Graubert, D. and Fink,

20.

Kahn, R.L., Fink,

Fink, M.: Personality Factors in Behavioral Response
to Electroshock Therapy, Conf. Neurol. (in press).
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of Parts of the Body After Insulin
Hospital. '3: 13h-1h8.

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Delusional Reduplication
Therapy,

J. Hillside

and Weinstein, E.A. (1956): Relation of Amobarbital
Clinical Improvement in Electroshock, A.M.A. Arch. Neurol.
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Test to
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&amp;

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(1957): Changes in Languages During Electroshock
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Kahn, R.L. and Fink,

M.

(in press).

(1957): Perception of Embedded Figures After
Induced Altered Brain Function, Am. Psychol. 12: 361 (abst.).

22.

Kahn, R.L. and Fink,

23.

Kalinowsky, L.B. and Koch, P. (1952): Shock Treatment, Psychosurgery
and Other Somatic Treatments in Psychiatry, New York: Grune
&amp;

2h.

Karliner,

M.

Stratton.

W.

(1956):

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Epileptic States Following Electroshock Therapy,
HOSp.

2:

258—263.

�- 16 REFERENCES

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(1955):

M.

Prefrontal

Findings, in
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EEG

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&amp;

Ink—1&amp;8.

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and Kwalwasser, S. (1956): Relation of Changes
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Korin, H., Fink,

M.

Conf. Neurol.

16:

88-96.

27.

Kwalwasser, S. and Caplan, M. (1952): A Case of Prolonged Insulin
Coma: Treatment, J. Hillside Hosp. 1: Ins-155.

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Liberson,

W.

EEG

T. (1956):

Effect of "Tranquillizing"

Clin. Neurophysiol.

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29.

Liddell,

30.

Perlstein,

D.w. and

Retterstol,

M.A. (1956):

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Protracted

Damage and
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(1951): Changes in the EEG Under Barbiturate Anesthesia
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for the Theory of ECT Action, EEG Clin. Neurophysiol. g: 261-280.

32.

Roth,

33-

Roth, M., Kay, D.W.K., Shaw, J. and Green, J. (1957): Prognosis and
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3h.

Shagass, C. and Rowsell, P.W. (195k): Serial Electroencephalographic
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A.M.A. Arch. Neurol. &amp; Psychiat. 12: 705—711.

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Sigg, E.B. and Schneider, J.A. (1957): Mechanisms Involved in the
Interaction of Various Central Stimulants and Reserpine,
EEG. Clin. Neurophysiol.
2: h19-h26.

36.

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A.M.A. Arch. Neurol.

&amp;

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gg; ugh—503.

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2: #27-hh0.

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Stewart, L.F. (1957):

38.

Ulett, G.A., Smith,

K.

Convulsive and

Control Group,

6.0. (1956): Evaluation of
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and Glesser,
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112: 795-802.

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#0.

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The EEG Changes in Unilateral and Bilateral Frontal Lobotomy,
111: 590-59h.
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hi.

Symbolic
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Wikler, A.:

Personal Communication.

(1953):
Yaeger, C.L., Simon, A., ﬁargolis, L.H. and Burch, N.R.:
Electroencephalographic Studies in Posthypoglycemic Coma,
J. Nerv. &amp; Ment. Dis. 118: h35—hhl.

�A

Unified Theory of the Action of Physiodynamic Therapies

Max

Fink,

M.D.

From

the Department of Experimental Psychiatry, Hillside Hospital, Glen Oaks,

Read

at the

2nd

International Congress of Psychiatry, Zurich, September 6,

N.Y.

1957.

Institute of Mental Health, National Institutes
of Health, U.S. Public Health Service; and the Board of Directors' Research Fund of
the Society of the Hillside Hospital.

Aided by grant M-927 of the National

10-7-57

�Iv:
A

The

10/5/57

Unified Theory of the Action of Physiodynamic Therapies

proper role of the physiodynamic therapies (electroshock, insulin

coma and lobotomy)

in psychiatry remains poorly defined. In part, this results

from the lack of an adequate formulation of

their

of action. In the past

mode

six years increasing evidence for a neurophysiologic-adaptive
shock therapy has been presented (hl, 32, 38, 1).

view of

electro-

This view ascribes the thera-

peutic precess in electroshock to a persistent alteration in cerebral function
which provides the milieu

environment.

The type

for a

change

in adaptation of the subject to his

of adaptation evoked is dependent upon the personality

of the subject, the environmental situation, and the duration of the induced

alteration in cerebral function. Concurrently,
of action in insulin

mode

coma (31) and lobotomy (ho) has developed.

During the past four years

we

have studied the

alteration in various indices of brain function
of psychiatric patients to therapy.

The

view of

insulin

relation between

and the behavioral response

neurophysiologic-adaptive view of

electrhshock has been supported and amplified (9, 10,

for a similar

similar

an awareness of a

coma has been

ll,

20, 21); evidence

presented (19); and recently the

concept has been extended to the newer "tranquillizers" (12).

These studies

provide the basis for a generalization concerning the efficacy of these therapies.

It is

our purpose in

this report to

examine the exPerimental evidence

whether or not the mode of action of each of these therapies may

to determine

result

their ability to induce sustained alteration in cerebral function;

from

and the corol-

lary question, whether measurable alteration in cerebral function is a necessary

�-2condition for the efficacy of these therapies, or a "complication" or "untoward

effect."
The

include

indices of brain function used in these studies have varied. These

memory

scales (26), visual (22)

and

tactile

changes in language patterns of orientation both

(13) perceptual tasks, and

clinically (21)

changes in the delta index, both in routine records (9, 10) and
by intravenous thiopentone (32, 33), and

successfully. For this review,
have been selected because of

after

In electroencephalographic studies of this problem,

intravenous amobarbital (20).

delta index of the unactivated

and

in the beta index (16) have been applied

two indices
EEG,

and

after activation

will

be

stressed: changes in the

clinical neurologic signs.

These indices

their successful application in the analysis of

the electroshock process, and because data is available for each of the therapeutic
modalities .

�OBSERVATIONS:

(a) Electroshock:
The

role of changes in

ll).

shock (9,

following notes summarize our experimental studies of the

EEG

delta activity in the response of subjects to electro-

In these studies, electroencephalograms were obtained before

treatment, and at weekly intervals on a day after a treatment in consecutive
electroshock referrals.
week,

Grand mal treatments were administered

for 12-20 treatments.

The EEG

three times a

records were quantitatively analyzed for

the amount of induced delta activity, and classified into categories of "high",
"moderate" and "low" degrees of delta

patients

were independently

the categories of
In the

activity.

At the end of treatment, the

rated for their short term clinical reaponse into

"much improved", "moderately improved" and "unimproved”.

initial series

of patients, a significant relationship between

the early induction of high degrees of delta activity, and clinical ratings of
Eighty percent of the records in the

"much improved" was observed.

much improved

group were high degree delta by the h-6 treatment; and the percentage was sus-

tained at

90%

in the third and fourth weeks. In contrast, none of the unimproved

patients developed high degree delta records in the
20%

three weeks,

and only

of the records in the fourth week were so classified.
In a subsequent predictive study, the

and

first

third weeks of treatment

delta records

were analyzed.

on both occasions, 67% were

patients without such records,
categories.

70%

EEG

records during the second

0f the patients

rated as

who had

much improved,

high degree

while of the

were in the unimproved and moderately improved

�Roth (32, 33) studying the

EEG

h

.
delta activity

thiopentone after electroshock has related both the

evoked by intravenous

stability and the rate of

remission of patients with endogenous depressions to the peak value of the induced slow

activity.

activity level,

"

He

......

concluded

that patients not attaining a specified delta

have not acquired an adequate physiological basis for

recovery," and recommended measurement of delta activity levels after thiopentone
as a guide to the clinical management of patients.
Further information is obtained from convulsive-subconvulsive control

studies.

While convulsive electroshock induces degrees of

vary from low to high, subconvulsive therapy rarely alters
duces low degrees of delta

delta activity that
EEG

patterns or in-

activity (11). In their comparative study of different

convulsive and subconvulsive techniques, Ulett, Smith and Glaser (38)

demon-

strated a significantly greater recovery rate for the convulsive than the subconvulsive group.
In a similar study (11) recently completed here, twenty-seven patients

received a course of subconvulsive therapy.
weekly

Electroencephalograms, taken at

intervals, demonstrated minimal changes

~

none of the records were scored

as middle or high delta activity. 0f the 27 patients, no change in behavior

was

noted in 23, and of these, 19 were referred for a second course of treatment.
Grand mal electroshock induced a high degree of

delta activity in fourteen.

All patients in this group showed significant changes in behavior, while of
the five

who

did not

show

the delta response, only two showed a behavioral change.

(b) Tranguillizing Drugs:
When

the newer drug therapies are studied from the viewpoint of

�-5.
their electroencephalographic

and

clinical neurologic effects, a meaningful

classification emerges. Furthermore, a relationship between the degree

and

type of induced change in cerebral function and therapeutic efficacy may be

noted.

The

ability of these agents to induce such signs of central nervous

system dysfunction as motor

rigidity, depression, excitement

and

seizures are

well known. Less well documented, however, are the clearly definable electroencephalographic patterns.

Based on observations made

of drugs in adult psychiatric patients, the

EEG

in chronic administration

changes may be

according to predominant changes in the frequency spectrum.

classified

There are three

broad types:

I.

Increased slow

wave

activity with hypersynchrony

("bursts") - "delta shift"

II.

Desynchronization with voltage and frequency
and

III.

irregular theta activity

—

"desynchronization"

shift."

Increased high voltage fast activity - "beta

Of the group of drugs inducing a

derivatives chlorpromazine, promazine,
Each drug induces

irregularity

delta shift, the phenothiazine

and perphenazine are

clear examples.

seizures in non—epileptice or exaggerates seizures in

epileptic patients (7, 8, 15, 29, 37).
neurologic patterns

when given

have induced parkinsonism in
have observed seizures in

10%

Each drug induces

in adequate dosage.

clinical parkinsonian

In our laboratories,

all patients receiving chlorpromazine (1k)

and

of a group of psychotic patients without previous

history of seizures. Induced delta activity, including burst activity,
observed in more than

we

half the patients in this series.

was

�-

6 -

Reserpine also evokes delta activity
At high dosage

levels,

it exaggerates

when given

in large doses (2).

seizures in epileptics and induces

seizures in animals (35). At the usual clinical dosages, however, reserpine
induces desynchronization of frequencies with a moderate increase in theta

activity (28), without seizure induction but with definite motor rigidities.
In a series of patients treated here (39), parkinsonism was induced in

patients.

EEG

changes were limited to desynchronization only, without

all
delta

burst activity.
The primary

the induction of

EEG

response of two other drugs, mepazine and benactyzine,

is

desynchronization. Mepnzine, a phenothiazine derivative,

induces desynchronization with small amounts of theta

activity has not been described, nor
or parkinsonism in the

have we found

activity (7). Delta

reports either of seizures

clinical literature. Benactyzine, a potent anticholin—

ergic compound, induces a blocking of alpha, flattening of the record and
1?). Neither seizures nor parkinsonism have

occasional theta activity (5,
been described for

this agent.

Meprobamate

beta
and

shift in the

EEG

is the clearest

example of the group of drugs inducing a

(3). This agent further differs from the phenothiazines

reserpine in not producing parkinsonism

and not only are

clinical seizures

not induced, but definite anti—epileptic activity has been described (30).
Habituation

is readily achieved,

seizures have been observed (ha).

barbiturates than like the other

If

we

determine the

and withdrawal phenomena of

agitation

In these actions, meprobamate
new

is

and

more

like

tranquillizers.

clinical efficacy of these agents,

we

note a parallel

�- 7 between the induced
drugs

that

thiazine

most

EEG

effects

their potency in altering behavior.

and

readily induce a delta shift in

frequencies - the pheno-

the greatest clinical efficacy in the

compounds - are those with

therapy of psychoses.

EEG

The

The compounds

with lesser activity in this direction

are less efficacious clinically.
(c) Insulin

Coma

The

well documented.

Therapy:

effects of insulin

During each coma,

persists for minutes to a

EEG

coma

delta activity is induced,

after gavage.

few hours

imately one third of patients receiving deep

seizures, aphasia or prolonged

coma

therapy on the nervous system are

coma

which

usually

infrequently, in approx-

Not

therapy in this hospital,

results. After such events,

changes

EEG

of delta activity persist for days, and in cases of prolonged coma, for weeks
and months (h3).

relation between prolonged

The

coma,

altered brain function

ioral response has been discussed at length. Revitch
of prolonged

coma and concluded

tion of organic brain

damage,

that

(31) reported

improvement may be

insulin

eight cases

attributed to the induc-

similar to lobotomy. Yaeger,

Burch (h3), describing twelve cases of prolonged

and behav-

Simon, Margolis and

correlation

coma, noted a

between length of coma, degree of organic confusion, remission of mental symptoms
and degree of

EEG

abnormality. Shagass and Rowsell (3h), emphasizing

and Kwalwasser and Caplan (27) presented

EEG

individual cases to support the

data,
same

conclusion.
we

reported a similar relationship between prolonged

response in a case study (19).

A

3h

coma and

behavioral

year old schizophrenic patient with paranoid

�- 8 -

ideation developed a left hemiplegia during insulin

coma

therapy. With the onset

of neurologic signs of hemiparesis, hemianopsia, hemisensory syndrome and spatial

inattention, there

was

a marked change in speech and behavior.

loquacious and denied his illness.
was

by

became

He

ludic,

His former paranoidowithdrawal type pattern

replaced by a friendly cooperative attitude. These changes were accompanied

delta changes in the

as well as language changes

EEG,

dicative of altered brain function.

The

behavioral changes persisted so that he

neurologic
was

after amobarbital in-

symptoms

resolved, but the

discharged two months

later

as "much

improved."
(d) Lobotomy:
While we have not had the opportunity
from the point of view of
document a

this

summary,

similar relationship.

all subjects postoperatively
(to) in a study of

after three years.

150

EEG

to study lobotomy patients

the reports of numerous observers clearly

changes of

delta activity are present in

persist for varying periods. Walter et al.,
patients, found an 80% persistence of abnormal EEG activity
(6) and

These authors

ment and the degree and

also noted a relation between clinical improve-

extent of postoperative slow

wave

activity.

Postoperative seizures are a frequent "complication," being variously
reported as occurring up to

20%

of subjects (25). Furthermore, there is a

relationship between the extent of brain tissue cut

and the

therapeutic

Circumscribed surgical lesions, regardless of locus, have an improvement
lower than

unilateral lobectomy;

are "improved" upon by a

and these

outcome.

rate

latter are frequently inadequate

bilateral procedure (36).

and

�DISCUSSION:
When

view of an

the various physiodynamic therapies are essayed from the point of

alteration in brain function, a

therapies represent devices

These

of action becomes apparent.

common mode

brain

which induce appreciable changes in

function, with resultant change in behavior. Electroshock and lobotomy induce
measurable diffuse changes in brain function
when

when given

How

clear.

is

primarily
tran—

in adequate dosage.

persistent changes in cerebral function affect behavior is not

Psychotic dehavior is not "reversed" or "obliterated". Rather, with

alteration in the central nervous system milieu, there is

all aspects of behavior including perception,
and

coma

complications ensue; and the phenothiazine and reserpine groups of

quillizers

an

directly; insulin

attitude.

The

mood,

affect,

an

alteration in

memory, Judgment

specific adaptive response is variable for each subject

dependent on numerous

historical

and environmental

sonality (18), environmental situation

factors.

and

Pre-morbid per-

and expectations (11), and the duration

of the alteration in brain fUnction (10) have recently been discussed as
determinants of the behavioral response under these conditions.
The induced changes

in behavior are evaluated

by the

psychiatrist,

administrator or family as to the degree of "improvement." These ratings are
value judgments, based upon such factors as the type of induced behavioral

response, the environmental tolerance and the observer's expectations.

context, the physiodynamic therapies
induce behavioral change which

do not induce "improvement" -

is secondarily evaluated as

In this

rather they

improvement.

alteration of cerebral function is therefore not a "complication" or

The

an "untoward

�- lo -

effect" but the desired goal of these forms of therapy.
therapies introduced during the past thirty years,

Of

the

many

"organic"

none apparently, has been a

specific agent for the therapy of psychoses (in the sense that penicillin is
specific for neurosyphilis and nicotinic acid for pellagra dementia), but rather
devices with greater or lesser degrees of applicability and efficacy in altering
behavior by altering the cerebral milieu.

this context, the various physiodynamic therapies are not specific

In

for a type of psychosis.
was

The

early enthusiasm that reserpine or chlorpromazine

Specific for schizOphrenia, or hypotheses that ascribe significane to an

antagonism between these drugs and "psychosis" or "schizophrenia" are not tenable.

Similar enthusiasm claiming a specificity of insulin

also untenable,
insulin

coma
EEG

and support

control study

for this

view

coma

for schizophrenia is

is presented in a recent chlorpromazine-

(1’4).

analysis of these therapies permits a

more

explicit definition of

the induced alteration in brain function. Changes in cerebral function reflected
by a

shift in the spectrum of

EEG

frequencies toward the slower range, with a

concomitant increase in voltage and a periodicity described as "bursts" or
"hypersynchrony" provide the change in milieu

behavior.

The

that is

more

effective in altering

significance of the delta shift has been clearly demonstrated in

electroshock therapy; and can be inferred from the available data in lobotomy,

insulin

coma, and the

That a delta
drug

effects.

tranquillizers.
shift has

Those drugs

some

Specificity is seen in the analyses of the

that induce the delta shift - the phenothiazines

and

reserpine - have been consistently reported as effective modifiers of psychotic

�-11...
of psychotic behavior. Changes in brain function reflected by

tion only, or a shift in frequency

Spectrum

efficacy in altering psychotic behavior.

is further

to the faster range, have a limited

*

The

significance of a delta shift

seen in the limited efficacy of subconvulsive electroshock when

Another aspect of the

alteration in brain function

in seizure threshold.

change

With the

which may be defined

delta shift in the

in clinical seizures would be anticipated. This is indeed true.
been described following electroshock (h, 2%), are prominent

(to) and a

common

comp

‘

pared to convulsive electroshock in the management of psychoses.

is the

desynchroniza—

EEG

EEG,

an increase

Seizures have

after

lobotomy

"complication" during and occasionally following insulin

coma

therapy (23). With the tranquillizers, the parallel of clinical efficacy and
seizure induction is most striking.

reserpine rarely; benactyzine not at all;

commonly;

anticonvulsant!
EEG

Phenothiazine compounds induce seizures

The lowering

delta shift induced

and meprobamate

is a potent

of seizure threshold parallels the extent of the

by these compounds.

Similar analyses can be

made

for

the potentiation of sedative action and induction of parkinsonism - both potent

indices of

an

The

quency
some

alteration in cerebral function.
neurologic basis for the delta shift and increase in seizure fre-

is unclear.

Whether

this represents a persistent change in function of

specific brain stem nuclear system, as the centrencephalic, thalamic or

hypothalamic,

is conjectural.

From

the wide range of agents that can induce a

* These observations suggest the application of EEG screening of new chemo~
therapeutic compounds for therapeutic efficacy according to their ability

to induce delta burst activity with a

minimum

of side effects.

�- 13 SUMMARY:

1.
shock,

The

neurophysiologic and clinical neurologic aspects of electro-

"tranquillizers," insulin
2.

The

coma and lobotomy,

are reviewed.

efficacy of each therapy in the treatment of psychoses is

related to the ability to induce a persistent change in cerebral function,
of which a delta

shift in the

seizures are

indices.

3.

two

EEG

spectrum and an increase in incidence of

Alteration in cerebral function is

behavioral change with each of these therapies.
a "complication," nor an "untoward
mode

an

essential prerequisite of

Such

alteration is neither

effect," but is the gigs 333

299 of the

of action of these therapies.
M.

No

evidence has been educed in these studies

that the physiodynamic

therapies are Specific agents for the relief of psychoses; nor
specific

do they

affect a

segment of the nervous system; nor do they induce Specific behavioral

changes.
5.
and

The

therapeutic process of electroshock, insulin

tranquillizers

may be

in cerebral function

coma, lobotomy

ascribed to the induction of a persistent alteration

which provides the milieu

the subject to his environment.

for a

change in adaptation of

�-

1a -

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Strait, L.A.,
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13.

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1h.

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Depression, Psychom.

Med,

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19.

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20.

Kahn, R.L., Fink,

Personality Factors in Behavioral Response
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(1955):

of Parts of the Body.After Insulin
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Coma

Delusional Reduplication
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and Weinstein, E.A. (i956): Relation of Amobarbital
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&amp;

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Psychiat.

{1§:

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Kahn, R.L. and Fink,

M.

(1957):

(in press).

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Kahn, R.L. and Fink,

23.

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(1956):

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�-

16

-

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25.

Klotz,

26.

Korin, H., Fink,

M.

Prefrontal
lhh-lh8.

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EEG

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&amp;

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in

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Conf. Neural. 1Q:

88-96.

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Liberson,

W.

EEG

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Effect of "Tranquillizing"

Clin. Neurophysiol.

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and

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Drugs on EEG,

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�-

17

-

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Chlorpromaiine: Use to Activate Electro~
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Wachspress, M., Blumberg, A.G., Fink,

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Yaeger, C.L., Simon, A., Margolis, L.H. and Burch, N.R.: (1953):
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Glesser, 6.0. (1956): Evaluation of
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Personal Communication.

�-

12 _

delta shift, with or without hypersynchrony,
EEG

changes

it

appears more

likely that the

reflect an alteration in the diffuse biochemical activity of the

nervous system rather than in a focal

activity of specific cellular masses.

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�QFURTHER OBSERVATIONS MADE SINCE THE ARTICLE

"Electro-cncephalo-

graphic Evidence of Bersonality Changes by Ataraxic Drugs in
Mentally Disturbed Patients." WAS WRITTEN.
l) A number of mistakes due to faulty or non-standardized technique in the assessment of alpha
a) Duration of the recording:

It

was found

that

some

activity for the first

stability

patients

had

were made.

little

alpha
five to ten minutes of the
who

recording deve10ped a more stable alpha activity,

later

it is

on.

therefore suggested that samples of alpha activity should be taken at least ten minutes after the
beginning of the E.E.G. recording.
b) Period of the day:
Slight differences of habitual alpha activity were
observed in one and the same patient according to the
time of the day when the E.E.G. recording was taken.

applies also to the period of the last meal.
It is therefore suggested that the E.E.G. tracings

The same

should be taken at the same time of the day and at the
same intervals after the last mealhad been taken.
c) Waiting of the patient before the E.E.G. recording.

It

observed that if patients had to wait for long
periods in the waiting room before his E.E.G. recordwas

ings were taken the alpha activity was poorer than on
d) Noises.
The

effect of any noises, particularly of any talk,

during the E.E.G. recording changed thexalpha E.E.G.

pattern imedia-telyss
It seems therefore that the total absence of any noise
is necessary to produce a valid E.E.G. recording for
the assessment of alpha
0)

A

stability.

Special alpha run, allowing the simultaneous trac-'

ing of temporal and parietal occipital alpha was found
to be useful.

�2) The alpha

stabilizing effect of Largactil

and

Serpasil.

a) Single administration:

intravenous and intramuscular administration
of a single large dose of Largactil (100 mg.) or Serpasil (5 mg.) often had little or no effect on the
1.

The

alpha

stability.

ii.

The

period of

administration of the
3

days to

2

same

drugs, over a

weeks, did produce an alpha

stabilization.
b)

Age

groups:

effect of these two drugs, in sufficient
quantities, was observed in all children whose habitual alpha activity was poor.
ii. In adults there were some exceptions to the rule,
particularly elderly people suffering from depression.
0) Quantitl:
The effect of alpha stabilization, even after a long
period of administration, was sometimes only observed
when large quantities of the drugs were given.
It is therefore suggested that in case of a negative
E.E.G. effect the test should be repeated after in1.

The

creasing the dosage of the drug.
d) Temporal Alpha:

It is

observed that in sons cases the alpha stabilization occurred equally in the temporal and parietal
occipital regions. Most often however, the alpha

stabilization

was more marked

in the temporal regions,

infrequently the alpha stabilization occurred
in the temporal regions only.

and not

e)

An

experiment was conducted on 30 schizophrenic pmients,

10

patients received Serpasil 3 grs. daily, 10 patients
received a new drug to be tested and 10 patients received a placebo. E.E.G. tracings were taken before the
'administration of the drugs and on one occasion after
the course of drugs was started. Psychological tests
were made to assess the clinical improvement.

�It

that the patients who had received Serpasil
showed a statistically significant improvement of their
alpha-stability. The ten patients who had received the new
drug that was to be tested showed a significant diminution
was found

of alpha-stability in the temporal regions. The patients
who received the placebo showed a random distribution of improvement or deterioration of their temporal alpha rhythm.
The

correlation between

improvement of

alpha-stability int.-

the temporal region and clinical improvement was about +0.45
only, in all 30 cases, whether this was due to the effect of
drugs or not.
The Doctor who was

conducting the experiment, the

statistician

of the Mental Hygiene Department and our own observations in
our E.E.G. Department showed that many relevant factors during
the psychological testing (in which unfortunately "socialis-

ation“

was

not a part) suggesting improvement were not controle'

led.

f) It is

that alpha-stability
may be correlated with relaxation and alpha-blocking with tension, though this is certainly not the full story, probably
a reasonable hypothesis to assume

only an approximation. About 80% of true melancholics, who are
certainly not relaxed, have an exceptionally high alpha index.
Ostow's suggestion thatwalpha activity generally respons to a

preparation for constructive thinking and the disappearance of
the alpha activity when the constructive process was put into
action, probably, is nearer to the truth. The more correct
hypothesis would seem to be that relaxed patients generally
ruminate less than tense subjects.
3) Further references bearing on the subject of alpha stabilization:
a) "By hypnotic suggestion to relax, Ford and Yeager reported
the induction of "good" alpha patterns in several patients with
anxiety states, whose previous E.E.G.'s showed little or no
alpha-rhythm.' Relaxation suggestions were not followed by EE.G.
changes in subjects whose E.E.G.'s

rhythm."

naturally

showed "good"

�-

4 _

Ford, W.L. and Yeager, C.L. "changes in the electroencephalogram in subjects under hypnosis. "Dis.nerv.
systo 1948, 9, 190—192.

H

a) There are several references in the literature to
the fact that short courses of electro-shock-treatment
tend to increase the E.E.G. alpha activity.

4)

W:

quoting a reference of Ellingson a mistake occurred
in my article which should be corrected.

When

Should read

-

preposition by Saul and Davis that passive indiv—
iduals tend to have regular persistent alpha rhythms of
high index has been often cited in the literature and
“The

appears to have been accepted as fact. Sisson and E11ingson reviewed the evidence upon which that preposition
was based and found it unconvincing.”

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                    <text>50
ALTERATION OF BRAIN FUNCTION
IN THERAPY
MAX FINK

following summary of observations made at a 200-bed voluntary, nonproﬁt, open-ward psychiatric hospital during the past
three years is presented as the basis for discussion. The major
interest of our Research Service is an investigation of the mode of action
of various somatic therapies, especially electroshock and drugs. The
disciplines represented in the research unit are clinical and psycho«
dynamic psychiatry, neuropsychology, and experimental and clinical
psychology. The following data summarize various studies that have
previously been reported only in part:
(I) High-dose reserpine for relief of anxiety: double-blind placebo
study.
(2) Chlorpromazine-insulin coma study.
(3) Electroencephalographic effects of various drugs.
(4) Electroshock process: concurrent psychiatric, psychologic, and neurophysiologic observations.
HE

OBSERVATIONS

Reserpine
In a placebo-controlled, double-blind study of oral and intramuscular
reserpine, consecutive patients referred for drug therapy were rated for
degree of manifest anxiety.1 The patients with high degrees of anxiety
received randomized three-week periods iof reserpine therapy, divided
into the following daily dosage periods: 10 mg. of reserpine (5 mg. oral,
5 mg. intramuscular), 5 mg. of reserpine (oral or intramuscular), or
Reprinted from Psychopharmacology Frontiers. Proceedings of the Psychopharmacology
Symposium of the Second International Congress of Psychiatry held in Zurich, Sw1tzerland on September 2-4, 1957. Published and copyrighted 1959 by Little, Brown and
Company, Boston 6, Massachusetts, USA.

�326

PSYCHQPHARMACOLOGY FRONTIERS

placebo. Drugs were administered daily. None of the observing therapists
knew which sequence was being followed or the dosages administered.
Relief of anxiety symptoms related to drug dosage was seen in 20 per
cent of the group. In 80 per cent no relief was noted, and of these, onethird exhibited severe depressive reactions which eventually responded
to electroshock therapy. The high doses of reserpine administered resulted in signiﬁcant clinical manifestations in every patient. The be~
havioral changes induced were directly related to the degree of concomitant physiologic disturbance.
It was the conclusion of this study that high-dosage reserpine therapy
has limited usefulness in the relief of anxiety symptoms. The dangers of
induced depressions were clearly manifest, and the uncomfortable nature of the side effects of drug administration has resulted in a limited
application of this drug in this environment.

Chlorpromazine-insulin coma
During a ﬁfteen-month period, all patients referred by the supervising
psychiatrists at this hospital for insulin coma therapy were divided by
random sampling into an experimental group and a control group.2
The control group received classical insulin coma treatment, following
the basic technique of Sakel. All patients received ﬁfty comas, each of a
duration of one hour or longer, at the physiologic level of Babinski
reﬂex or absent lid reﬂex or deeper. The experimental group received
chlorpromazine therapy in rapidly increasing dosages until toxicity had
been induced. When toxic signs of rigidity, drooling, ﬁxed facies, seizures,
dermatitis, or marked weakness appeared, the dosage was gradually reduced until a maintenance level was obtained. Patients were sustained
on this regime for a period of three to four months. In both groups, behavioral observations were made by investigators none of whom was the
for
referred
treatment, resulting
were
Sixty
patients
therapist.
patient’s
in two groups of 30 each.
The maintenance dosage of chlorpromazine was 300 to 2000 mg.
daily. Initial dosages ranged from 1400 to 3600 mg. daily.
Chlorpromazine induced motor retardation in all subjects. Overactive,
destructive behavior rapidly disappeared, and the patients were more
tractable, less negativistic, and less violent. One-third of the patients were
more sociable and less seclusive, and were noted to care for themselves in
a more presentable fashion. In the instances where severe parkinsonism
supervened, however, the patients were less able to care for themselves,
became sloppy, and failed to dress.
Affective changes during chlorpromazine were varied. Four patients
became increasingly agitated, tense, and tremulous, and either refused
to continue on the drug regime or were induced to do so only with

�MODE

or

ACTION

327

difﬁculty. Such an affective .storm appeared early in the therapy and
persisted.
..
In 4 other cases, depressive symptoms were signiﬁcantly relieved, with
an increase in affective lability and responsivity. In 2 patients, depressive
ideation increased and was associated with complaints of insomnia. The
medication was continued, however, with eventual alleviation. In most
patients mood changes were small.
Ideation was altered during the period of chlorpromazine therapy in 12
of the patients. Eight patients had a loss or a signiﬁcant diminution of
psychotic ideation. In 5, the hallucinatory and referential experiences
were no longer reported even on inquiry, and in 3 others, delusional
ideation was less prominent. In 1 patient, however, paranoid ideation
became more prominent. This was associated with increasing anxiety and
panic during drug administration, with resultant discontinuation of the
drug regime.
The clinical effects of insulin coma therapy have been exhaustively
reported, and the ﬁndings in this series are comparable to those previously published.
With regard to the evaluation of improvement, all 60 patients of this
study have been discharged from the hospital. Table I lists patients according to the four-fold classiﬁcation in use in the hospital at the discharge conference.
TABLE

I

DISCHARGE RATINGS

Chlorpromazine Insulin Coma
Recovered
Much improved
Improved
Unimproved

2

4

0
5

l7

l5

7

10

Inherent in the design of this study were high doses of chlorpromazine,
pushed until symptoms of toxicity appeared. In this context, therefore,
all patients developed signiﬁcant drug effects. In all, rigidity of extremities appeared, frequently accompanied by a decrease in facial expression, drooling, and festination. Untoward complications are listed
in Table II.
Electroencephalograms were obtained in 20 of the chlorpromazine
patients. On adequate doses, concomitant with a change in clinical
behavior a moderate amount of low-voltage 4 to 7 cps delta and theta
activity was observed. This activity was exaggerated by hyperventilation.
In the 3 patients in whom seizures were induced, the delta activity was
not signiﬁcantly different from the remainder of the group. There was a

�328

PSYCHOPHARMACOLOGY FRONTIERS

suggestive relationship between the degree of the induced slow-wave
activity and the drug dosage.
TABLE

II

COMPLICATIONS

Chlorpromazine

Agitation and panic
Dermatitis, severe
Seizures

Refusal of further therapy
Hypotension
Secondary reaction, frequent
Prolonged coma (more than 6 hours)
Insulin resistance
Regression of behavior

4
3
3
2

Insulin Coma
3

5
2

2
—
—

Dab—409ml

2

It was the conclusion of this study that neither Chlorpromazine in
high doses nor insulin coma is a speciﬁc treatment for schizophrenia. It

was noted that these treatments were devices to temporarily alter behavior that had been socially unacceptable. Since Chlorpromazine was
safer, easier to administer, and more controllable in its effect and had
fewer side effects, it was recommended that it replace insulin coma.

Role of electroencephalographic changes in behavioral change
As noted in the following section, a direct relation between changes
in electroencephalographic delta and behavioral changes in electroshock had been observed in these laboratories. For this reason, a survey
of the role of various newer drug agents was undertaken to determine
the potential relationship between behavioral change and electroencephalographic effects.
Chlorpromazine and promazine are effective agents for the induction
of changes in motor patterns of behavior. Concomitant electroencephalographic effects are the induction of delta activity, a desynchronization of
the record, and a decrease in the amount of fast activity. Both drugs also
induce seizure activity spontaneously in patients who have not had
seizures prior to the administration of the drugs, and in whom pre-treatment electroencephalograms have not demonstrated dysrhythmic activity.
Reserpine, while inducing a deﬁnite parkinsonian syndrome, does not
generally induce seizures. At therapeutic levels, the changes in the
electroencephalogram are limited to an increase in fast activity. We have
not observed delta activity in any patient receiving reserpine.
In patients receiving meprobamate, also, delta activity has not been
observed. Records consistently demonstrate high-voltage beta activity,
similar to barbiturate. Clinically, meprobamate has some effect in

�MODE OF ACTION

329

reducing seizure activity. When dosages are suddenly reduced, we have
observed spontaneous seizures in 2 subjects. This observation is similar
to that noted in animals.3
Electroshock evalution studies
In the course of an extensive evaluation of the electroshock process,
a direct relationship has been observed between the degree of induced
delta activity and the degree of behavioral change.4 We observed that
serial records taken during the course of electroshock therapy and
measured for quantitative changes in delta activity could serve as a guide
to the therapeutic outcome. Of 11 patients who were clinically rated
much improved, 10 had high-degree delta records in the third and
fourth weeks of treatment, whereas of 7 unimproved patients only 1
had such a record. In a subsequent series,5 these observations were extended in a predictive study. It was suggested by these initial observations that the much improved patients were those in whom high-degree
delta activity had been induced early in the course of treatment and
sustained. Records taken during the second and third weeks of treatment were assessed. The results in 54 consecutive patients are noted in
Table 111. Of the patients who developed high-degree delta activity
during the second and third weeks of treatment, 67 per cent were
rated much improved, whereas only 30 per cent of the patients without
such activity were so rated.
TABLE

III

PATIENTS WITH HIGH DELTA ACTIVITY IN EEG DURING
SECOND AND THIRD WEEKS OF TREATMENT

EEG Delta
Both high (18)
One high (16)
None high (20)

Much Improved
12

(67%)
4 (25%)
6 (30%)

Clinical Rating
Unimproved
Moderately Improved
4 (22%)
8
7

(50%)
(35%)

'

2 (11%)

4 (25%)
7 (35%)

Delta activity in the electroencephalogram reﬂects the state of brain
function, and is a guide to alterations in that state. To verify the relationship between delta activity and behavioral change, concomitant amobarbital tests for altered brain function6 were done in this series of
patients. It was observed that the amobarbital test results were parallel
to the electroencephalographic effects.7 Of patients in the initial series
who had been rated as much improved, all had positive amobarbital
test reactions after the seventh to ninth weeks of treatment and sustained
this response. Of the unimproved patients, however, 15 per cent had

�PSYCHOPHARMACOLOGY FRONTIERS

330

positive amobarbital responses in the third week and 28 per cent in
the fourth week, but these responses were not sustained.
A comparison of both electroencephalographic observations and the
amobarbital test data, as related to the eventual clinical ratings, is seen
in Table IV.5
TABLE IV
’

EEG

AND AMOBARBITAL TEST RESULTS DURING
SECOND AND THIRD WEEKS OF TREATMENT

Much Improved Moderately Improved Unimproved

Both positive amobarbital
and high EEG delta activity
Either positive amobarbital
or high EEG delta activity
Neither positive amobarbital
nor high EEG delta activity

Totals

It

25

10

3

8

12

5

0

3

11

33

25

19

apparent that the cluster of positive amobarbital tests, high EEG
delta activity, and the much improved clinical ratings is a signiﬁcant
one; equally signiﬁcant is the cluster of negative amobarbital tests, low
to moderate EEG delta activity, and a clinical rating of “unimproved.”
In the clinical observations in the electroshock study varied behavioral responses were observed. These included the absence of noticeable symptoms with the return of pre-morbid behavior; hypomania,
euphoria, and denial; paranoid states with ideas of reference and delusional formation; confusional states with varying degrees of memory
disturbance; increased somatic complaints and preoccupations; states of
increased panic, excitement, and agitation; and varying degrees of withdrawal and seclusiveness. Similar psychopathologic reactions were observed in schizophrenic patients undergoing either chlorpromazine or
insulin coma treatments, or patients with severe manifest anxiety undergoing reserpine therapy.
In the electroshock group, the degree of behavioral change was directly
related to the degree of alteration in neurophysiologic indices. This
direct relationship between neurophysiologic change and behavior was
even more clearly manifested in a group of patients treated with subconvulsive therapy. In another control study, 27 subjects received subconvulsive therapy instead of grand mal therapy. The electroencephalo—
grams demonstrated either no delta activity or a minimal amount of such
activity during the course of treatment. In no patient were moderate
or high-degree delta activity records observed. In the amobarbital tests,
only 3 patients had positive reactions during treatment, and'in each
instance this. occurred only once. Of the 27 subjects no change in sympis

�MODE OF ACTION

331'

toms or behavior was noted in 23. Nineteen were later referred for a
second course of treatment. Of these, grand mal electroshock induced
changes in brain function reﬂected by high-degree delta activity and /or
repeated positive amobarbital tests in 14. All 14 showed signiﬁcant
changes in behavior, whereas of the 5 patients in whom physiologic
indices showed only minor changes, only 2 showed a deﬁnite behavioral change.
It is important to note that there was no direct relationship between
the physiologic changes and a speciﬁc type of behavioral change. There
was, however, a direct relationship between the degree of induced
physiologic change in brain function and the degree of behavioral
change. In a further attempt to determine the relationship between the
type of behavioral change and other variables, we have carried out
studies on the role of personality in the behavorial response.8 The initial
study of the role of personality was devoted to a study of the relation
between the characterologic disposition of patients to show denial
mechanisms and the clinical results. The relatives of 47 patients were
interviewed and denial personality scores were assessed, following a
structured interview. Denial scores range from 0 to 25, with a median of
11. The scores were then divided into two
groups: scores from 11 to 25
were classed as high denial and those from 0 to 10 as low denial.
Of patients with high denial personality scores, 58 per cent were in the
much improved group and only 1 patient was in the unimproved
group.
The ratings of improvement for the patients with low denial personality
scores were random, about one-third appearing in each rating category.
These studies support the present neurophysiologic adaptive hypothesis of the mode of action of electroshock therapy. This hypothesis
notes that alteration in brain function is the central effect of electroshock therapy and is a prerequisite to behavioral change. It also notes
that under the conditions of the induced change in brain function,
altered patterns of adaptation are expressed. The type of adaptation
varies, apparently dependent upon the personality organization.
CONCLUSIONS

Largely on the basis of these observations, as well as of reports of
numerous other observers, the following conclusions regarding the role
of physiodynamic therapies in schizophrenia are suggested:
(1) None of the present therapeutic regimes, including insulin coma
therapy, electroshock therapy, and the newer drug therapies including
chlorpromazine, reserpine, meprobamate, and promazine, are speciﬁc for
schizophrenic illnesses. No evidence has been educed that any of these
therapies have altered the basic schizophrenic process.

�332

PSYCHOPHARMACOLOGY FRONTIERS

(2) Behavorial change in electroshock has been shown to be depend-

ent on an alteration in brain function, as evidenced by serial changes in
delta activity in the electroencephalogram. Under these conditions, the
pattern of behavioral alteration varies markedly, depending on the degree
of induced cerebral dysfunction, the personality of the subject, and the
environmental situation.
(3) The newer drug therapies have effects on brain function in direct
proportion "to their ability to alter behavior as determined by clinical
observation. The parallel between electroencephalographic change and
behavioral change leads to the proposition that the mode of action
of newer drug therapies may be similar to that of electroshock therapy;
viz., by altering brain function in a nonspeciﬁc manner, behavioral
changes are induced.9 To the extent that the behavioral alteration is of
a kind that is rated as improved by the environment, the drugs are considered satisfactory therapeutic agents. In this regard, it is important to
note that improvement ratings are but a special case of behavioral
change, dependent on the type of adaptation elicited, the expectation of
the therapist, administrator, and family, and the tolerance of the milieu.

REFERENCES

l. Wachspress, M., Blumberg, A. G., Fink, M., and Miller, J. S. A. Evaluation
of high-dose reserpine therapy for relief of anxiety. 1. Hillside Hosp, 5: 67,
1956.

Fink, M., Shaw, R., Gross, G. C., and Coleman, F. S. Comparative study of
chlorpromazine and insulin coma in therapy of psychosis. ]. A. M. A. In press.
3. Wikler, A. Personal communication.
4. Fink, M., and Kahn, R. L. Relation of EEG delta activity to behavioral redr
Arch.
A.
A.
Neural.
M.
studies.
serial
electroshock:
in
quantitative
sponse
Psychiat., 78: 516, 1957.
5. Fink, M., Kahn, R. L., and Green, M. A. Experimental studies of the electroshock process. Dis. Nerv. System, 19: 113, 1958.
6. Weinstein, E. A., Kahn, R. L., Sugarman, L. A., and Linn, L. Diagnostic use
of amobarbital sodium (“Amytal Sodium”) in organic brain disease. Am. ].
Psychiat., 112: 889, 1953.
7. Kahn, R. L., Fink, M., and Weinstein, E. A. Relation of amobarbital test to
clinical improvement in electroshock. A. M. A. Arch. Neurol. 69' Psychiat., 76:
2.

23, 1956.

Kahn, R. L., and Fink, M. Personality factors in behavioral response to electroshock therapy. Conﬁnia neural. In press.
9. Fink, M. A uniﬁed theory of the action of physiodynamic therapies. J. Hillside
8.

Hosp, 6:

197, 1957.

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                    <text>Behavioral Patterns in Convulsive Therapy
MAX FINK. MD.
AND

ROBERT L. KAHN. Ph.D.
GLEN OAKS. L. |.. N. Y.

�Reprinted flow the Archives of General Psychiatry
July 1961, Vol 5, [71). 30— 36
Copyright 1961,]1y Agzeiican Zl/[edical Association

Individual differences in the behavioral
response to convulsive therapy are marked.
In psychiatric practice, patients with similar
psychopathologic syndromes, and of similar
sex and age, show a variety of clinical responses: Some improve and sustain such
change; some improve, only to relapse
quickly; and some fail to improve. These
differences have been related to the degree
and duration of induced neurophysiological
change?“6 premorbid patterns of personal—
ity,""11'15 sociopsychological characteristics,13'
15
and psychotherapeutic approaches.1 While
these studies have emphasized ratings of improvement, the derivative nature of this
evaluation and its dependence on staff attitudes, expectations, and family tolerance have
been stressed.2""5'8
The manifest behavioral patterns provide
the basis for the evaluations of clinical response. It is the purpose of this report to
describe behavioral patterns in patients
undergoing convulsive therapy and to relate
these to problems of the evaluation of improvement and to an understanding of the
convulsive therapy process.

Behavioral
Patterns in
Convulsive

Therapy

Of consecutive patients referred for electroshock therapy during 1956-1957, seventy-three patients were subjects of the analyses described here.
The patients were selected for treatment by the
resident therapist and the supervising psychiatrist
-——the investigators playing
no role in their selection. These observations were made during a

lllll|llllll|Illllllllllllllllllllllll|lllllllllllllllllllllllllllll|lllllllllllllllllllllllllllllllllllllllllllIlllllllllllllllllllllllll|lllllllllllilllllllllllllllllllllllllllllllllllllllllll

MAX FINK, MD.
AND

ROBERT L. KAHN, Ph.D.
GLEN OAKS, L.I., N.Y.

convulsive-subconvulsive electroshock study in
which subjects referred for therapy were randomly assigned to courses of subconvulsive or con—
vulsive treatments.
Electroshock was administered 3 times weekly
under thiopental sodium (Pentothal) premedica—
tion, using either a Reiter unidirectional or a
Medcraft alternating current instrument. Grand
mal or subconvulsive treatments were administered
by altering the strength of current. Neither

Submitted for publication Jan.6, 1961.
From the Department of Experimental Psy—
chiatry, Hillside Hospital.
Present Address: Division of Psychiatry, Monteﬁore Hospital, Bronx, N. Y. (Dr. Kahn).
Read in part, at the New York Divisional Meet—
ing, American Psychiatric Association, November,
1957.

Aided by Grant M- 927 of the National Institute
of Mental Health, National Institutes of Health,
U. S. Public Health Service
52

�CONVULSIVE THERAPY

31

ﬂecting the patient’s adaptation 2 to 4 weeks fol~
lowing the last treatment.

patient, therapist, nor evaluating physicians was
aware which course of therapy each patient received until after the evaluation period.
Changes in brain function were measured at
weekly intervals by tests of language patterns
both clinically and after amobarbital and by the
degree of slow-wave activity in electroencephalograms. The intercorrelation of these indices and
their relation to behavioral changes have been
reported previously?”
The manifest symptom patterns of the referred
patients were variable and included suicidal preoccupation, retardation, disturbances of mood and
affect, excitement, agitation, panic and tension,
delusions, ideas of reference, negativism, withdrawal, and somatic complaints. The clinical diagnoses were depressive psychoses of manic-depressive, involutional and reactive varieties, and schizophrenic psychoses of paranoid, mixed, catatonic,
and pseudoneurotic types.
Clinical behavior was assessed in weekly psychi—
atric interviews, structured perceptual task situa—
tions,“'15 and by conferences with the patient’s
therapist. In these observations, the evaluation of
improvement along the continuum of “recoveredunimproved” appeared inadequate and was supplemented by a rating of the degree of behavioral
change.
The degree of change in clinical and ward
behavior was rated on a 4-point scale of “marked,”
“moderate,” “minimal,” or “no change. H These
evaluations were not value judgments as to the
quality of the change, but rather quantitative es—
timates of differences in behavioral patterns under
similar conditions of observation. The assigned
rating was based on changes observed during the
treatment period and for 2 weeks post treatment.
Evaluations of improvement response were made
on the 4—point scale of “recovered,” “much im—
proved,” “improved,” and “unimproved or worse.”
These evaluations were value judgments, based
upon the behavior of the patient, the therapist’s
expectations, the tolerance by therapist and patient
of those aspects of behavior often called “side—
elfects of the treatment,” and the therapist’s judg—
ment as to the family’s attitudes to the patient’s
behavior. These evaluations were short—term, re-

Observations
A. Behavioral Change and Improvement.

A comparison of the behavioral ratings
and the improvement evaluations is presented in Table 1. That ratings of recovered
and much improved were associated with
high or moderate degrees of behavioral
change is an expected observation. Similarly,
that patients with minimal or no change in
behavior were evaluated as unimproved or
improved, is also expected. The signiﬁcant
relationship, however, lies in the patients
showing high and moderate degrees of behavioral change and still rated as showing a
poor clinical response. Of the 30 patients
observed with high degrees of behavioral
change, 17 were evaluated as recovered and
much improved, and 13 as improved or un—
improved.
B. Modes of Adaptation—Analyses of the
behavioral patterns of the subjects during
and following treatment permitted the description of various modes of adaptation.
For illustrative purposes we have described
4 behavioral patterns under the titles of
euphoric—hypomanic, somatization, paranoidvuithdrawal, and panic modes.
Euphoric-Hypomanic Mode: These subj ects appeared pleasant, affable, and friendly.
They dressed neatly, spoke quietly, and participated in ward activities with increased
interest. Occasionally they dressed gaudily
and smiled and giggled excessively. Pretreatment symptoms were not manifest, and
premorbid attitudes and behavior were again
prominent.

0f Evaluations of Behavioral Change and Clinical Improvement
(Convulsive and Subconvulsive Therapies)

TABLE l.——C0mparison

Improvement Rating
Ichavioral Change
High degree change
Moderate degree change
Minimal degree change
No change

F ink—K ahn

Recovered
(30)
(17)
(10)
(16)

Much
Improved
9
6
0
0

8
3

0
L?

53

Improved

Unimproved
and Worse

8
6

2

5

5

1

15

5

�32

-

In their psychotherapeutic interviews they
described their illness in a detached manner,
emphasizing “it” (illness) as having “dis—
appeared.” They denied having been ill and
facetiously suggested they were at the hos—
pital for a rest, or that the institution was
not a hospital, but a resort or a school.
Symptoms were described in the past tense,
and the quality of having been a different
person during the illness was reiterated.
Speech was marked by denial, displacement,
evasion, qualiﬁcation, and cliches.“ The
third person mode was frequently used, as
in such statements “the doctor
says I am
ill” or “my wife should have come here.”
Gross changes in memory were either not
apparent, or were described for the treat—
ment period only. The patients expected and
accepted these deﬁcits, and neither connection with treatment nor apprehension was
expressed.
They looked forward to home visits and
made realistic discharge plans. While conﬂicts with family members were described,
these were minimized and expressed mainly
in the past tense. Referential questions were
answered in a referential manner and with—
out an arousal of affect. For the more hypo—
manic subjects, questions about home
planning were responded to nonreferentially,
with marked use of inappropriate clichés.
When pressed with referential inquiries,
they quickly exhibited anxiety and discom—
fort, minimized their feelings, and changed
the focus of the session.
Such adaptations were sustained throughout the discharge planning period. The more
hypomanic features were rarely sustained
and within a few weeks were replaced by
a more stable euphoric or somatization type
of adaptation.
Somatization Mode: In these subjects, in—
cessant complaints about bodily symptoms
and loss of memory, demands for reassur—
ance and relief, and preoccupation with feel—
ings of unreality and confusion dominated
behavior. They remained unkempt and their
rooms were untidy. When such an adapta—
tion appeared early in therapy, further
treatment was refused.

ARCHIVES OF GENERAL PSYCHIATRY
Speech was principally in the present
tense and in the ﬁrst person, with few third
person references and a minimal use of
clichés, denial, or qualiﬁcations. In psycho—
therapy sessions, they were demanding and
hostile, reporting their problems in terms
similar to those used prior to therapy. They
complained that the treatment caused addi—
tional and more incapacitating difﬁculties.
To referential questions, answers were gen—
eraly correct, but associated with complaints
of memory impairment.
They described their family relations in
pretreatment terms, with an occasional “I
don’t remember” in response to experiential
inquiries. Discharge planning was difﬁcult,
since they insisted that their new symptoms
prevented any home adaptation.
On the ward, their hostile demands for
attention and relief of symptoms increased
with treatment. Participation in group ac—
tivities increased, however, for those sub—
jects who had previously been withdrawn
and seclusive.
Memory complaints were preeminent. Pa—
tients demanded reassurance that their
memory would return and repeatedly asked
if treatment would be harmful. They de—
scribed feelings of derealization and con—
fusion. Events, bodily feelings, and relations
to friends and relatives seemed strange,
fuzzy, unclear, and out of focus. While they
complained chieﬂy of memory impairment,
they also complained of back pain, headache,
tingling of ﬁngers and toes, nausea and
weakness, and ascribed these to the treatment.
At the end of treatment, the symptoms
for which hospitalization had occurred were
no longer present, and although complaints
were many, their relation to the treatment
and their transience was so universally ac—
cepted by both the staff and the patients,
that the results were evaluated as beneﬁcial.
This adaptive mode was sustained into the
postdischarge period.
Paranoid and Withdrawal Mode: Another
pattern was the appearance of paranoid
ideation, suspiciousness, hostility, ideas of
reference, and delusions. These patients
Vol. 5, July, 1961

�CONVULSIVE THERAPY

failed to care for themselves and remained
unkempt in their dress. Their rooms, in
which they remained much of the day, were
untidy. Speech was sparse and not spontane—
ous. When questioned about their illness,
they were hostile and demanded to know
why they were questioned. They refused
to answer inquiries or categorically denied
or agreed to all speciﬁc questions. Experi—
ential questions were answered referentially. When inquiry was insistent, they denied
illness and minimized the symptoms which
had resulted in their admission.
They refused or avoided sessions with
their therapist and insisted convulsive ther—
apy be ended because it was harming them.
When treatments were continued, they demanded release from the hospital, or pre—
cipitated discharge by elopement, suicide
attempts, or aggressive and destructive out—
bursts. They were unable to discuss their
relations with family or friends and focused
on demands for either release or relief from
somatic symptoms. Hostility was overt and
engendered a fearfulness in the staff. On the
ward, when coaxed out of seclusion, they
were loud, aggressive, and demanding. They
were suspicious of attempts at friendliness
and expressed thoughts that others wished
to harm them or talked about them.
While insisting on discharge, no realistic
discharge planning was achieved. Their View
of the environment was grossly distorted and
self—centered, preventing adequate care.
In testing, they were uncooperative, and
voiced angry suggestions of being experi—
mented upon or abused. Complaints of
memory impairment were infrequent and
occasionally denied even when clinically
manifest. On such occasions, they were en—
raged at the implied deﬁcit.
Panic Mode: These patients became increasingly anxious, agitated, restless, sleep—
less, and anorexic. In their dress, they were
neat and cared for themselves. Speech pat—
terns were unchanged and continued with
emphasis on ﬁrst person and present tense
modes. Symptoms were distressing and
prominently voiced. When asked about pre—
treatment symptoms, these were expressed
.

Fink—Kuhn

33

in the same terms as those used earlier,

with the complaint that treatment had made
everything worse.
Patients feared treatment and hid on
treatment days, or pleaded with the staff
to forego further applications. They threatened elopement and if this failed, submitted
administrative requests for discharge.
On the ward, they continued their pretreatment patterns of minimal participation.
On treatment days, they were withdrawn,
sullen, and negativistic, and cooperation was
poor. They demanded to see their therapists
and on such occasions insisted that treatment be discontinued. They were unable to
discuss family situations or their attitudes
to others, being preoccupied with their feelings of fear. In discussing their home, they
insisted on immediate discharge, while
stating they were severely frightened,
anxious, depressed, and unwell.
Ideation was unchanged with fearfulness
as the principal affect. Fears of damage
to the brain or mind was expressed, accompanied by the awareness that memory
impairment may be a Sign of such damage.
Complaints of memory impairment were
infrequent and when present, were ex—
pressed as a speciﬁc reason for discontinuation of treatment.
Patients were uncooperative and fearful
of testing and participated only if encour—
aged that such tests may be helpful in the
therapist’s decision about further treatment.
Occasionally, when treatment was discon~
tinued, a more stable adaptation of relief,
acquiescence, and denial appeared.
C. Adaptive Mode and Improvement
Ratings—Thus, for the various adaptive
behavioral patterns, a range of short—term
evaluations was observed. Those subjects
who developed and sustained the euphoric—
hypomanic modes were generally rated as
recovered or much improved. Patients with
somatization and panic modes were oc—
casionally rated as improved, although unimproved ratings were frequent. The
paranoid—withdrawal mode was evaluated as
unimproved or worse, as were patients exhibiting the panic modes. The relation be—

�34

ARCHIVES OF GENERAL PSYCHIATRY
TABLE 2.—Adapti7/e

Mode and Improvement
Improvement Rating

Modes

Euphoric-Hypomanic
Somatlzatlon
Paranoid-Withdrawal
Panic
No adaptive change‘
‘ Includes subconvulsive

(36)
(10)
7)
( 7)
(13)
(

Recovered

Much
Improved

11

14

0
0
0
0

l

10
5

0
0
0

2
2
l

Improved

Unimproved,
Worse
l
4

5

5
12

treated subjects Without second course of ECT.

tween adaptive modes and ratings
improvement is summarized in Table 2.

of

Studies relating physiological or psychological aspects of convulsive therapy to
clinical outcome have reported inconsistent
results}6 Thus, it has been reported that
depressed patients respond favorably to convulsive therapy while schizophrenic or neu—
rotic subjects do not; while other observers
indicate that neurotic depressive patients re—
spond badly, and that some schizophrenic
subjects do have favorable outcomes. Vari—
ous measures have been suggested as predic—
tors of improvement, only to fail on more
extensive testing. In such instances, the
differences in results and discrepancies in
convulsion can be related to the utilization
of a variety of global estimates of improve—
ment as the criterion of behavioral change,
without adequate speciﬁcation of the standards used in the evaluation.
Such standards differ widely, depending
on institutional populations and staff attitudinal factors. Varying attitudes toward
“side-effects,” the use of global rating scales,
and varying psychosocial attitudes affecting
goals of treatment have each served to make
results from different laboratories incom—
patible. Thus, in our evaluations of con—
vulsive therapy, the development of changes
in memory, recall, and orientation have been
considered as temporary manifestations of
therapy and disregarded in the clinical eval—
uations.3'19 Patients developing the euphoric
or hypomanic modes, despite concomitant
memory loss, have been rated as much im—
proved.
In a comparable study by Johnson et al.,10
the Lorr global ratings of behavioral change
were utilized. In this type of evaluation the
changes in memory and orientation are in—

Comment
These observations emphasize the variety
of behavioral adaptations that occur during
convulsive therapy and relate short—term
evaluations of improvement to the type of
behavioral change. Earlier observers of con—
vulsive therapy have described a range of
behavioral patterns, ascribing the changes
to ego adaptive responses, to the trauma
of the treatment, organic brain changes, or
psychologic signiﬁcance of the treatment.7'
9'21 These observations that
subjects with
similar psychopathologic syndromes receiv—
ing similar treatment may exhibit discordant
behavioral adaptations and be variously
rated as recovered or unimproved, are of
signiﬁcance for an understanding of the
convulsive therapy process.
In earlier studies, the conclusion was
reached that persistent alterations in brain
function were a necessary condition for

behavioral change in convulsive ther:«ipy.2""6
With changes in brain function, all aspects
of behavior undergo modiﬁcation. Percep—
tion, mood, affect, judgment, attitude, mem—
ory and recall are altered, and with these,
the subject’s adaptation in the environment.
Not all behavioral changes are viewed as
improvement, however. Improvement ap—
pears to be a special type of behavioral
response, being the subjective estimate by
an observer that the patient is “better.” It
is based, not only on the patient’s behavior,
but also on such nonspeciﬁc aspects as the
observer’s expectations, and tolerances, and
those of the family and environment.

56

Vol. 5,

lily,

1961

�CONVULSIVE THERAPY

cluded as negative scores in the improvement
scoring, so that a high number of subjects
were reported as “unimproved or worse.”
Besides population differences, this single
factor is sufﬁciently potent to alter the rela—
tionships between the 2 studies and justiﬁes
the discrepant observations.
The use of global estimates of behavioral
change in evaluating therapy has other signiﬁcant deﬁciencies. Psychiatric therapies
are rarely focused, or effective in modifying
a single symptom. The induced changes
affect a spectrum of behaviors, with varying
rates of change for different aspects. Global
estimates tend to lose differences in individual elements within the medial designations
necessary to deﬁne the whole response. In
such situations changes in behavior which
may be prominent, though not pervasive nor
enduring, may dominate the evaluation as to
overshadow other, potentially more signif—
icant changes. Thus, alterations in memory
and recall, or increased somatization or in—
creasing withdrawal may dominate unim—
proved evaluations; while explicit verbal
denial, clichés, and euphoria may lead to
recovered or much improved designations.
The use of improvement ratings may be
empirically justiﬁed as an early approxima—
tion in studies of a new therapeutic meas—
ure, but further analyses of the behavioral

‘

observations are required for understanding
and adequately applying the treatment. The
typologies described in this report are one
approach—one that has been helpful in our
understanding of the convulsive therapy
process and one that is now being tested in
studies of psychopharmacologic agents.
In addition to the differences in improve—
ment evaluations occasioned by attitudes to
“side—effects” and the use of global ratings,
there are differences due to the attitudes of
therapists toward various sociocultural pop—
ulations. The adaptation of explicit verbal
denial in a lower class patient in a community institution is welcomed by therapists
and family, but the same adaptation in an
upper class professional in a psychothera—
peutic hospital is considered poor or psy—
chotic. The display of rationalization.
Fin k—K01m

35

minimization and displacement, even when
accompanied by a return to premorbid work
levels, is considered marked improvement
in one setting, but is viewed as a lack of
improvement in another if goals of insight
had been set by the therapist. Interference
with memory and recall may be disregarded
by therapists for one sociocultural group,
but arouse empathic solicitude for patients
of another social class. Such factors affect
not only institutional attitudes, but within
an institution, therapists of different thera—
peutic orientations may have differing atti—
tudes towards evaluations and therapies. The
many recent sociocultural studies of thera—
pists, and their attitudes towards selection
of therapies, are indicative of these attitudinal differences.13'17-18'20'22
It is our impression, therefore, that im—
provement ratings are no longer useful devices in evaluating psychiatric therapies. For
the symptomatic therapies extant today,
which are seemingly not directed toward
the alteration of an etiologic factor, typologic
descriptions have a greater applicability and
empiric justiﬁcation. Typologies based on
concepts of diagnosis, target symptoms, or
on dynamic—structural formulations have
attempted to structure the pretreatment clusters in which therapies may be effective.
Treatment and post—treatment symptom improvement scales have been used with utility.
These are limited approximations, however,
and there is a need for a broader approach
to both the pretreatment and the treatment
behavior, and a phenotypic, adaptive be—
havioral typology, using multivariate tech—
niques of data analysis, seems worthy of
assessment.

Summary
An analysis of the variety of behavioral

adaptations of 73 voluntary psychiatric pa—
tients undergoing convulsive therapy resulted
in the description of 4 major patterns.
These are described as euphoric-hypomanic,
somatization, paranoid—withdrawal, and pan—
ic modes.
The relation of these modes to clinical
ratings of improvement is described. The

�36

ARCHIVES OF GENERAL PSYCHIATRY

derivative and generally nonoperational
nature of improvement ratings is empha—
sized. The difﬁculties in a communicative
deﬁnition of this variable is seen as a major
factor in the discrepant studies of indices
predictive of improvement in convulsive
therapy and in understanding the processes
of somatic therapies in psychiatry.

Therapy (With and W'ithout Atropine), Arch.
Gen. Psychiat. 2:324-336, 1960.
11. Kahn, R. L., and Fink, M.: Changes in
Language During Electroshock Therapy, in Psychopathology of Communication, edited by P.
Hoch and J. Zubin, New York, Grune &amp; Stratton,

Inc., 1958, pp. 126-139.
12. Kahn, R. L.; Fink, M., and Weinstein, E. A.:
Relation of Amobarbital Test to Clinical Improvement in Electroshock, A.M.A. Arch. Neurol. Psychiat. 76 :23-29, 1956.
13. Kahn, R. L.; Pollack, M., and Fink, M.:
Sociopsychologic Aspects of Psychiatric Treatment in A Voluntary Mental Hospital: Duration
of Hospitalization, Discharge Ratings, and Diagnosis, A.M.A. Arch. Gen. Psychiat. 1:565-574,

Max Fink, M.D., Department of Experimental
Psychiatry, Hillside Hospital, 75—59 263rd St.,
Glen Oaks, L.I., N.Y.

REFERENCES

H

Esecover, H.; Jaﬁe, J., and Kahn, R. L.:
Psychotherapeutic Techniques with Electroshock
Patients, J. Hillside Hosp. 7:17-25, 1958.
2. Fink, M.: A Uniﬁed Theory of the Action of
Physiodynamic Therapies, J. Hillside Hosp. 6:
1.

1959.
14.

Kahn, R. L.; Pollack, M., and Fink, M.:
F igure-Ground Discrimination After Induced
Altered Brain Function, A.M.A. Arch. Neurol.

2:547-551, 1960.
15. Kahn, R. L.; Pollack, M., and Fink, M.:
Social Attitude (California F Scale) and Convulsive Therapy, J. Nerv. Ment. Dis. 130:187—192,

197-206, 1957.

Fink, M., and Kahn, R. L.: Relation of EEG
Delta Activity to Behavioral Response in Electro—
shock: Quantitative Serial Studies, A.M.A. Arch.
Neurol. Psychiat. 78:516-525, 1957.
4. Fink, M.; Kahn, R. L., and Green, M.: Experimental Studies of the Electroshock Process,
Dis. Nerv. Syst. 19:113~118, 1958.
5. Fink, M.; Kahn, R. L., and Pollack, M.:
Psychological Factors Aﬂ'ecting Individual Differences in Behavioral Response to Convulsive
Therapy, J. Nerv. Ment. Dis. 128 :243-248, 1959.
6. Fink, M.; Kahn, R. L.; Karp, E.; Pollack,
M.; Green, M.; Alan, B., and Lef‘kowits, H. J.:
Signiﬁcance of Inhalant Induced Convulsions for
the Theory of the Convulsive Therapy Process,
Arch. Gen. Psychiat. 4:259-266, 1961.
7. Frosch, J., and Impastat, D.: The Effects of
Shock Treatment on the Ego, Psychoanal. Quart.
3.

1960.
16.

Kalinowsky, L., and Hoch, P.: Shock Treatments, Psychosurgery and other Somatic Treatments in Psychiatry, New York, Grune &amp; Stratton,

Inc., 1952.
17. Kaplan, A. 1., and Lefkowits, H. J.: Inﬂu—
ence of Staff Attitudes and Environmental Factors
on Treatment Selection, J. Hillside Hosp. 1961,
to be published.
18. Klerman, G. L.; Sharaf, M.; Holzman, M.,
and Levinson, D. J.: Sociopsychological Charac-

teristics of Resident Psychiatrists and their Use
of Drug Therapy, Amer. J. Psychiat. 117:111-117,
1960.

Korin, H.; Fink, M., and Kwalwasser, 5.:
Relation of Changes in Memory and Learning to
Improvement in Electroshock, Conﬁn. Neurol. 16:
19..

88-96, 1956.
20. McIver, J. and Redlich, F. C.:

17:226-239, 1948.
8. Frosch, J.;

Impastato, D.; Ottenheimer, L.,
and Wortis, S. B.: Some Reactions Seen After
Electric Shock Treatment, Amer. J. Psychiat. 102

Patterns of

Psychiatric Practice, Amer. J. Psychiat. 115:692-

311—315, 1945.

697, 1959.
21. Millet, J. A.

Glueck, B. C.: Psychopathologic Reactions
and Electric-Shock Therapy, New York J. Med.
42:1553-1557, 1942.
10. Johnson, L. C.; Ulett, G. A.; Johnson, M.;
Smith, K., and Sines, J. 0.: Electroconvulsive

Psychosom. Med. 6:226-237, 1944.
22. Pasamanick, B.; Dinitz, S., and Lefton, M.:
Psychiatric Orientation and Its Relation to Diag—
nosis and Treatment in a Mental Hospital, Amer.
J. Psychiat. 116:127-132, 1959.

:

P., and Morse, E.: On Certain
Psychological Aspects of Electroshock Therapy,

9.

58

Printed and Published in the United States of America

��Putt-ran at Bohgvioral chant. and Inprorcnnnt
1n canvullivo rhcrapy

In: Pink, x.n.

and nobcrt L. Kuhn, Ph.D.*

from the Dapartncnt or Expnrinontnl Psychiatry,

ulna oakn,

L.I., n.x.

Hillside noupitsl,

gratt K~927 of tho lattcnal Initituta a: nontal noulth,
lutional Institutua a: Hatlth, United Status Puhlie Hualth survzoo.
Reta in part, gt th.".!. 91'1319311 looting, American Payehintric
Aidod by

Association Northbor, 1951.
: Btvﬂiomit o: Psych-try. Mutation 30-91%“.
*Pruont
Bronx, 1.1.
VII: 1/61

“an"

�Individuol ﬂittoroncoo in tho bohoviorol roopouoo to
oonvoloivo thoropy oro oorkod. In poyohiotric proctico,
potionto with oanslor poyohopotholoxtc oyudroaoo, one or

oililor

varioty or olinieol rosponooo: oooo
toprovo old ouotoin ouch chongo; oooo 1-provo, only to rolopoo
quickly; ond oooo toil to taprovo. rhooo dittorooeoo hovo boon
rolotod to tho dogroo ond duration or indoood nourophyoiolociool
ehongo (3,6) prooorbtd pottorno or poroonoltty (5,11,15),
ooulopoyeholoctool chorootoriotioo (13,15) and porehothoropontto
opprooehoo (1). Vh11o thooo otudioo hovo onphooiood voting: 0:
taprovooont, tho dorivotivo unturo or thin ovoluotion ond 1t:
dopondonco on otort ottttudoo, oxpoctotiono ond tooily toloronco
oox ond ago, ohow o

has boon strooood

(2,h,5,8).

rho oonttoot bohoviorol pottorno provido tho boots tor tho
ovo$uot1ono of clinical rooponoo. It 1o tho purpooo o: thto

roport to doocriborbohovtorol pottorno 1n pottonto nndoraoinz
oonvolsivo thoropy, ond to roloto tho-o to problooo of tho
ovolootioo of taprovooont and to on ondorotondinx o2 tho coo-

vuloivo thoronyIProcooo.

�gethod:
or consecutive pe$$en$e reterred for electreehoek therepy
63:13; 1956—57. teveatybthree pettente were subjecte e: the
eaelyeee eeeeribed here. the patients were selected tor treeto
sent by the reeident therepiet end the aupervteiuc peyohietrteﬁ -

the inveetzceterp playing no role in their selection. These
convulsive—euhcenvulaSve
electroc
3
during
were
III.
obeervettene
eheok study a; whieh subject. referred tar enereyy were rendenly
unsigned to entrees e: cuboenvuletve er convulsive treetnente.
Electroeheek wee edginietered three tines weekly under
pentethel preunedieetiea, using either e letter unidirectional
er e xederett alternating entrent inattenent. arena eel or
enbeenvnleive treetnente were eduin1utered by titering the
etrongth of current. leither patient, therapist not eveluetinx
phyeiaiene tee evere which entree e1 therapy each pétient
received until titer the evaluation period.
weeiiy
intervals
cheese: in urea: tunetion were neeeered at
by test: of leagues. petterne both 011336.11: eta etter
eneberbitel, and by the degree e: 310: were activity in
electroencephelegrene. 2he interoerreletien e: theee indieee
3

�.3cooplointl. rho alinicol dioxnoooo woro doproootvo
of nonio—doproooivo, involutioaol ond rooetivo

and ooaotic
poyuhoooo

voriotioo; one oohioophrontc poyehoooo or poronoid, aixod,
oototonto and pooudonourotie typoo.
clinical bohovior woo oooooood in vookly poyuhiotric
intorviovo, otrootorod porooptuol took oituotiono (1h,15) and
with
contorouooo
tho potiont'o thoropiot. II thooo ohoorvo~
by
tiono, tho ovolootion of :Iprovouont along tho continual of
'rooovorod-untnprovod' oppooroa inoaoquoto, and woo topplonontod
by o roting of tho dogroo of bohoviorol ohongo.
rho dogroo of chonzo 1n olinieol tad word hohovior woo
totod on o four point ocolo or 'norkod', “nodoroto', 'nininol'
or'ho chango'. Thooo ovoluotiono woro not voluo Judznonto no
to tho quality of tho ohonxo, but rothor, quontitotivo ootinotoo
o: ditforouooo in hohoriorol pottorno undo: oinilor condition:

at otoorvotion. rho oooigood voting

woo hoood on ohongoo

oboorvod during tho trootnont poriod and

for too

vooko poot~

trootaont.
lvolootiono or ingrovonont roopoaoo woro undo on tho four
point ocolo or 'rocovorod', 'nuoh taprovod', ﬁtnprovod', and
“nailprovod or onroo'. rhooo ovolootaono ooro voluo Judgnouto,
hoood upon tho bohovior of tho patient, tho thoroptot'o oxpoctotiono, tho toloronoo by thoropiot and potiont of thooo oopoeto of
bohovior otton oollod *oido-orroeto of tho trootnont’, and tho
thoropiot'o Judgnont on to tho tonily'o ottitudoo to the potioat'o
hohovtor. fhooo ovolnotiono ooro abort-torn, rotlocting tho
potiont'o odoptotion two to tour wool“ following the lost troutnOHto

�gbaorvationo:
(a) Donatioral chango and Ingrovonont
coaparioon at tho bahavioral ratingo and tho
iaprovoaont ovaluationo 1o proooatod in tabla I. that ratings
at rocovorod and nuch iaptovod woro aaaociatod with high or
moderate dogrooa at bohavioral change it an oxpoctod obaorvation.
similarly, that patioato with ainiaal or no chango in behavior
taro avalaotod ao uni-proved or iaprovod, io aloe oxpootod. tho
aixaitioant rolatianahip, hovovor, lioa in tho patianta ohooing
high and oodorato dogrooo or bohavioral ohoazo and atill ratod
ao ohaoiaz a poor oliniaal roopoaao. at tho thirty patioato
obaorvad with high dogrooa or hohaviaral ohango, aovontoon voro
ovaluatod aa raeavorod and much iaprovod, and thirtoon ao
inprovod or aainprovod.

l

.. --.. .
ZLBLI

(b) undo:

at Adaptation

I

-“ﬂ--.

o: the bohavioral pattorna at tho oobaocto
daring and tailoring traataont poraittod tho description or
variauo today of adaptation. For illoatrativo purpoooa vo havo
doaoribod tour bohoriorol pattorna undo: tho titloa a:
oaghorie-hzgoaanio, oaaatiaation. garanoid-withdraoa; and
Analyooo

Rania nodoo.

Bughorio-lzzoaanie Roda: Thooo oubjocta appoarod
plaaaant, atrablo and friaudly. they are-sod neatly, opako
quiotly, and participated in word activitioo with ineroaaod

�Zlﬂﬁﬁ

I

atnpgrtann 0t Evaluationl Qt nohavttrnl change
and clinical Inpruvcnont
(c0uvu1317c and subconvnlutru 1h0r&amp;pico)

ﬁtting

XIErOVOIORt

locovorod
»

_

Itch

Inprdvod ﬁninpruvod and
Ingrovod
39:30

Bahaviorll Ghangc
nigh dogroo change (39)
ﬁ
lodorato
(17)

8

9

8

5

3

6

6

2

Juana

(‘10)

o

a

5

S

(16)

o

0

1

15

I.

change

'
'

I'

�.

~5-.

interest. 'oeeeeieeelly they dreeeed aeadily,

end exiled end

giggled excessively. Pre-treeteent eyepteee were net eenifeet
end preeerbid ettitudee end hehevier were egeie prenieeet.
In their peyohetherepeetie interviews they deecrihed their

illueee in e deteched leaner, eepheeieieg ”it“ (illneee)

ee

they denied having-been ill end
feeetieeely eeggeeted they were et the heepitel fer e reet; er
thet the inetitutiee wee net e heepitel, but e reeert er e
eeheel. Syeyteee were deeeribed in the pert teeee, end the
geelity of keying been e different pereen during the illeeee
hevins “dieeppeered’.

reitereted. Speeeh wee eerked by deeiel,.diepleeeeeet,
ereeiee, quelitieetiee end eliehee (11). the third pereen

wee

'

eede wee frequently need, ee in eeeh eteteeeete
the doctor
eeye 1 en 111' er *ey wife eheeld here eeee here.II
Greee ehenzee in neeery were either not eppereat, or were

deeeribed fer the treeteeet period only. the petieete expected end
eeeepted theee defieite, end neither eeeeectiee with treeteeet her
eppreheneien were expreeeed.
they looked forward te here wieite end eede reelietie
dieeherge pleee. While conflicts with feeily eenbere were
deeeribed, theee were eieieieed end expreeeed neiely in the peet
tenee. heferentiel qeeetieee were eeewered in e referential

nearer end without en ereeeel of effect. for the mere hypeeeeie
eebaeete, queetiene eheet here planning were reepended te nearefereetielly, with marked nee of inepprepriete eliehee. When
preeeed with referentiel inquiries, they quickly exhibited

�.5anxiety and dieeeatort, aiuiaieed their feelings and changed
the teeua.e£ the eeeeien.
Seek adaptatiene were euetained throughout the discharge
planning period. The mere hypeaaaie features were rarely
suetained, and within a for weeks were replaced by a mere
etable euphoric er aenatizatien types of adaptation.
,8enatizetien Hades In theee_enbdeete, incessant eeaplainte
about bodily eyaptene and lees e: eatery, deaands fer reaeeurenee
and relief; and preoccupation with feelings of nnreality and
eeeteeion doainated behavior. Ehey retained unkempt and their
When
each an adaptatien appeared early in
were
untidy.
reels
therapy, further treatment wee refused.
speech nae printiptlly in the present teaee and in the
first pereen, eith fee third peraen references and a ainiaai
use at clichea, denial er qualifications. In peyohetherapy
eeeeiene, they vere-deaandies and hostile, repertihg their
prehieae in terae eiailar to these need prier to therapy. !hey
eeaplained that the treatment eaaeed additieeel and mere incapacitating difficulties. re referential queatiens, answers were
generally correct, but associated with eenplainte of aeaery

inpairaent.
they deeeribed their taaily relations in yreotreatneet
terns, with en oecaaional '1 den't reaenber' in reepenee to
experiential inquiriee. Discharge planning eaa dittiealt, as
they insisted that their new eynptene prevented any home adaptation.

their heetile demands for attentien and relief
at eyupteas increased with treetaent. Participation in creep
activities inereaaed, however, tar these eabaeete who had
an the ward,

�-7.
previeaely been withdrawn and eeoleeive.
Heaory eeaplainte were pre-eaiuent. ratioate deaanded
reaaaaranee that their aeaery would return, and repeatedly
asked if treatment would he hararul. they deeoribod feelinge
of derealiaation and confusion. Erenta, bodily feelinge and
relatiena to friends and relativee eeeaed etrange, teeny,
unclear, and out of :oeue. While they oonplained ehietly e:
book
of
alao
ceaplained
pain, headache,
they
iarairnent,
aeaory
tingling o: tinsera and teee, aaaaea and roakaoee, and
aeorihed there to the troetaent.
which
end
symptom:
the
for
the
at
treatment,
heepitalit
iaatioa had occurred were no longer present, and although
and
to
the
treatment
were
relation
their
their
aany,
eoaploiate
transieaoe eae eo univoreally aeeepted by both the start and
the patients, that the rooalte rare evaluated or beneficial.
!hie adaptive node wee eeetained into the peat-dieoharge period.
Paranoid and Withdrawal lode: Another pattern tea the
appearance or paranoid ideation, euepicieuaneea, hostility,
ideae of reference and deleaiene. These patients failed to
care for theaaolvee, and roaained unkeapt in their dress. Their
reeaq.in which they reaained each or the day, were untidy.
Speech eaa eparee and not epontaneeaa. when questioned about
their illneae, they were hostile and demanded to know why they
were queetiened. they retaeed to anewer inquiriee er categorieally denied or agreed to all epecixio queetiene. Experiential
caeetiena were anewerod roterantially. When inquiry was
ioeietoat, they doeidd illneea and ainiaieed tho ayaptena which

�~8-

resulted 3: their ednieeien.
they retueed er eveided eeeeieee with their therepiet,
end ineieted eenvuledve therepy he ended beeeeee iteee herningy
then. When treeteente rere continued, they demanded releeee
free the_hoepite1, or precipiteted dieeherge by elepeneut,
euietde ettelpte er eczreeeive end deetreetdve outberete. They
were uneble to diecuee their reletiens with relily or triende,
and teeeeed either en deaende fer releeee or relief tree
resette eynptoee. Ieettlity wee overt, end engendered e
teertelneee 1n the etett. an the nerd, rhea eeexed out of see»
Ineien, they were lend, eggreeetve end deeend1ng. They were
eeepieieee e: etteepte at friendlteeee, end expreeeed theeghte
thet other: edehed to here the: or talked ebeﬁt then.
while ineieting en dteeherge, no reelietie dieeherge
pleating wee eehseved. their View er the envirtneent wee
creeely distorted end eelreeeutered, preventing'edeqnete care.
In testing, they were uneeeperetive, end rained angry
eeggeetiene a! being experirented ugen or ebueed. Complaints
at nenery impairment were intrequent, and occeeienelly denied
when
even
clinicelly meniteet. on such occasione, they were
eareged et the inplied deficit.
Peale Bede: Theee'pettﬂate beeene increeeingly enzione,
eglteted, reetleee, eleepleee end enorexie. In their dreee,
they were neet end eered ror themselves. Speech patterns
hed

were unehegged end eontinued with eepheeie on tiret pereon
and preeent tenee nodes. .synpteme were dietreee1ng end

prentuentiy voiced.

When

asked about preetreetment eynptore,

�.9.
theee were expreeaed in the aaae terae ae theee need earlier,
with the eaaplaint that treataent had aade everything weree.
Patienta reared treat-eat and hid an treataent daye, er
pleaded with the etatt to forage farther applications. they
threatened elepeaent and it thie tailed, enhaitted administrative
reqaeata fer discharge.
an the ward, they continued their preatreataent patterns

at

participatien. 0n treataent daye, they were withdrawn,
aalien and negativietie, and cooperation wae peer. they
deaanded te aee their therapiete and on each eceeeiene ineieted
that treataant be discontinued. they were unable to diecnee
{anily eitaatiene er their attitudee to ethere, being preo
eeeayied with their feeling: at tear. In dieeaeaieg their
minimal

heaa, they inaiated en iaaediate dieeharge, while atating they
were aewerely trightened, anxieaa, depreeeed and unwell.
’Ideatien was unchanged with tearfulneae ae the principal
.

affect. reare

te the brain er aied wae expreeeed,
aeeeapaaied by the awareaeee that aeaory iapairaeet may be a
sign at each damage. ceaplainta at aeaery inpairaent were in~
ex daaage

frequent and when present, were expressed ae a apeeitie reason
(or dieeeatinaatiea of treatment.
Patiente were uncooperative and fearful at testing, and

participated only

it

encouraged that such
decision about further

tests may be helpful
treataent. occasion.

in the therapist's
ally, when treatment wae diacentinued, a more stable adaptation
of relier, aeqaieeeenee and denial appeared.

�'

(3)

29:9"

tivo H96. and

rovunoat n;¢1 3
Thus, fo:_th¢ var1oua_gdaptivq bohnvitrnl ptttornl,
a runs; or ihort term evaluations were obsorvad. thus: subjects
aha devolaped and sustained the euphoric-hyponanie nodou were
generally ratoﬁ us rocaverod or nueh inpravod. Patients uith
ponatizatian gnd panic modes were ocgusiantlly rated as improved,
nithgugh uninprevod ratings were frequent. The paranoid-with.
ﬁgural node was evaluated as unimprGVad or worse, as were
model.
The relation batucon
the
panic
pn§;ontl czhibiting
adaptive node and ratings or improvonent are Ialnnrilod in
'

d‘

fable 1!.
1133!

II

-‘C- “CC-

�tivo.ﬂndc 3nd

Ada

rovonoat
Ingrovcnont Rating

Rtoovered

3.4..

anh

Improved Inprovcd ﬁninpravod,

Horn.

Euphoricvﬂyponanic

(36)

11

1h

10

1

Selatinttion
tiranotdniithdrauul

(10)

o

1

5

h

(

7)

0

o

2

5

Psntc

(

7)

o

o

2

5

ndaptivo ohtngoi (13)

0

0

1

12

I.

alnoludas snbcenvulsivo
trcntod unbaoctu without
cocond course 01 not,

�Bieeoeeien:
fheee ebeervatiene eaphaeiee the variety of behavioral
adaptatiene that-occur daring eonvaleive therapy, and relate

abort tern evaluatieee or iapreveaeot to the type of behavioral
change. larlier obeervere at oooveleive therapy have deeoribed
a range of behavioral patterns, aeoribing the ehaogee to age
adaptive reepenaee,to the traaaa of the treataent, organio brain
changes, or peyehologio oigoifioanoe of the treataeot (7,8,9,21).
These ebeervatione that subjects with eiailar peyohopethelegio
eyndreaee receiving aiailar treatment aay exhibit dieoordaot
behavioral adaptatiene, and be varioaely rated aa recovered or
aaiaproved, ie o! eigoirieanoe for an onderetahding e: the eonvnlaive therapy prooeee.
In earlier studies, the ooholoaioo val reached that
pereietené alteratioea in brain tanotioo were a neoeeeary eonditieo to; behavioral change in oonvaloive therapy (2,h,6). With
changes it brain tuaotioo, all aepeote of behavior undergo
modification. Perception, need, affect, Jadgaent, attitude,
aeaery and recall are altered, and with theee, the eabaeot'e
adaptation in the environment. let all behavioral ebaegee are
viewed aa iapreveaeot, however. Improvement appeare to be a
special type oi behavioral reepooee, being the eobjeotive
eetiaate by an obeorver that the patient ie 'hotter’. It ie
baled, not only on the patieot'e behavior, but also on each
oeo-apeoitie aepeeta aa the obeerver'a expeotatione, and
toleraooee, and these at the taaily and eovirenaent.
Studies relating physiological or peyehologioal aepeote

�-12or oonvnloivo therapy to

clinical

inreported that deproeeed

ontoone have reported

been
hae
Thne,
(16).
it
ooneietont roanlte
eohiaowhile
oonvnleivo
therapy
to
patients reopond favorably
oheorvore
other
while
do
not;
oabjoota
nonrotio
phrenio or
and
badly,
reepond
patiente
dopreeeive
neurotic
that
indioate
ontooaoe.
do
favorable
have
enhaeota
that ooae aohiaophronio
of
inprovoaa
predictora
been
enggeeted
have
Various noaanroe
each
inetanoea,
In
extensive
tootinx.
on
aoro
to
lent, only tail
can
eonolneion
in
and
diaoropanoioo
in
results
the dittorenooe
or
oetiaatoe
of
global
of
a variety
be related to the utilization
vithoot
behavioral
change,
of
the
criterion
ilproveaent an
evaluation.
the
need
in
etandarde
of
the
adequate epooitioation
Snoh etandarde differ videly, depending on institutional

atatt attitadinal taotore. Varying attitudeand
eoaloe
of
rating
global
the
nae
toaard 'aide-otteota',

popelatione and

o:
treataent
goale
afteoting
attitndee
varying peyohoeooial
have baoh eorved to lake reenlte tron different laboratorioe

oonvnloivo
therapy,
o:
ovalaationa
in
our
fhne,
inooapatiblo.
and
orientation
recall
in
ohangee
neaozy
o:
devolepaont
the
,
and
of
therapy
aanitoetatione
have been considered ae teaperary
dieregardod in the olinioal ovalaatione (3,19). Patients
oonoonitant
doepito
aodea,
hypeaanio
the
euphoric
or
developing
anon
been
on
ieproved.
have
rated
neaory loee,
In a ooaparable etndy by John-on gngg, (lo), the Lorr global
of
In
type
thie
utilized.“
were
change
rating! of behavioral
inolndod
and
orientation
are
in
ohanxee
the
neaory
evaluation

�-13-

negative oeoroa in the inprovenent nearing, no that a high
nnaher or enhaooto were reported an 'aninproved or nerao.‘
Booidoe population ditterenoee, thia einglo factor in
eattioiently potent to alter the relationehipe between the
two etadios, and Justitieo the diooropant eboervationa.
the nae or global eetinatea or behavioral change in
evaluating therapy hae other significant detieieneiee.
Psychiatric therapiea are rarely toenaed, or effective in
modifying a single eyaptea. the induced ohanxoo affect a
opeetrna oi hehaviera, with varying ratoa of change for ditterent aepoote. Global aetinateo tend to loae differenooe in
individual ole-onto within the nedial deoignatione neeoeaany to
define the whole reeponee. In oneh oitnationa ohangee in hehavier which nay he preninont, though not pervaaive nor enduring
nay doninate the evaluation an to overehadoe other, potentially
nore aignitioant ehanzee. than, alterationo in aenory and recall, or increaeed eonatination or inereaaing tithdrawal nay
daninato nninproved evaluations; while explicit verbal denial,
olieheo and euphoria nay lead to recovered or each iaproved
designations. the nae o: inprevenent ratings nay he enpirioelly
Jaatiried an an early approxiaation in studies of a new thorapeutio aoaonre, but inrthor analyoea o: the behavioral eboorva~
tiona are required for anderatanding and adequately applying the
treatnent. rho typologiea deooribod in this report are one
approaeh - one that hoe heon helptal in our nnderatanding or the
oonvaloive therapy prooeea, and one that in non being teatod in
etadiee o: payohepharaaeoloxie agento.
on

�ulhIn sddltlen to the differences in leprevesent evelestlens
eeessieeed by attitudes to 'elde-effeets' end the use ef glebel
due
to the ettitedes ef thereplsts
differences
there
ere
retinls,
tersrd rsrlees seeleesltsrsl peeeletiens. The edeptetien of
explicit verbsl denial in s lever clues pstient in e eennenlty
lestitntlee is welcomed by therspiste and really, but the seas
sdsptstleu in en upper elese professional in e peyehethsrspeetle
The
displsy ef
or
psychotic.
is
hospital
considered peer
when
and
even
nintnisstlen
displscenent,
retlensllsstien,
eeeenpenied by s return to preeerbid work levels, is eensidered
nsrked leprevenent in ens setting, but is viewed as e leek ef
inpreveneet is enether if ceels of insight hsd been set by the
thersplet. Interference with memory end reeell say he disregsrded
by therspists fer ene seeieeeltnrel group, but sreese espethle
eeliettede fer petlente ef endkher seeiel eless. Seek feetere
effect not enly institutienel,%tt1tedee, but riteln en 1nst1ts~
tion, therapists of different therepeutie erlestétlees sey here
evglestieae
nsny
thersples.
towards
sad
the
differing ettltedee
recent seeiecnlterel studies ef therspists, end their sttitedes
tevsrds eelsetion ef thersples, sre indiestive of these sttitndinsl
differences (13,17,18,2o.22).
It is our impression, therefore, thet inprevenent rstlngs
are no longer useful devices in evslusting psyrhietrie therepies.
For the eynptometie therapies extent today, which ere seemingly
net direeted tewerd the slteretien ef en etiologic fecter,
typelegte deecriptiens have s greeter spplleebility sud enpirie

�-15.

Justification. typologies haaad on concepts at diaxaaaia,
targat aynpaaaa or on dyaaaio-atractaral formulations harattaaptad to atructara tho pra-traataaat clusters in witch
thoraptaa nay be attaativa. fraatnant and paat—troatnant
ayaytan impravaaant acalaa have haan used with

utility.

Thaao

ara linitad approxinatiaaa, howavar, and thara 1a a naad far a
broader approach to bath tho pra-traataant and traatnant bahaviara, and a phanotypio, adaptiva bahaviaral typolacy, aaing
aaltivariata taohniqnaa at data analysis, aoana worthy a:
aaaaaaaant.

�w

in enelyeie_er the veriety e1 beheviorelvudeptetiene
or 73 velnntery peychietric petiente undergoing convulsive
therepy reeulted in the description er tear nejor patterne.
These are deecribed ee eupheric-hypenenic, eenetizetien,

paranoid-withdrawal end penie nedee.
the reletien er the-e nedee te clinical retinge e:
ieprevenelt ie deecribed. the derivative end generally
neu-eperetienel unture e: ieyrevenent retinge in enpheeieed.
the difficulties in e cennunieetive detinitien e: thie
veriehle ie eeen ee_e nejer teeter in the dieerepent etudiee
et indieee predictive e: inprevenelt in cenveleive therapy,
end in underetendinc the preeeeeee e: ee-etic therepiee in
peywhietry.

�-17-

W'

1. Ieeeever, 1., latte, J. and Iain, R.L.: Peyehetherepeetie
rechaiqaee with lieetreeheek Patiente. J. lilieide

.3332..1; 17~2§, 1958.
link, 1.: i ﬁaified theory of the ietiea e: Phyeiedyuanie
rherapiee. J. lilleide legg. é; 197-206, 1957.
BIG
and
of
Delta Activity te
telatien
1.5.:
lake,
link, I.
lehavierel leepenee in lleetreeheek: Quantitative serial
Stadiee. A.!.i. ireh. laurel. &amp; Pezdhiat. 19: 516-525,
1257.

n.: prerinental Studiee or
«a. lleetreeheek Preeeee. Die. lerv. slat. 11: 113-119,
and
3.1.
Pellaek, a.a Payehelegieal rector.
take,
3.,
tier,

rant,§a.. lane, 1.1.

and Green,

1958.

Affecting Individual Differences in Behavioral Reapenee
to canvaleive Therapy. J.l,!.B. 13g. 2k3-2h8, 1959.
6. Fiat, u., Kenn, 3.5., tarp, 3., Pollack, 1., Green, H.,
Alan, B. and Lei‘kewite, LL: Significance of Inhalant
Induced neural-ion: tor the Theory er the convulsive
Therapy Preeeee. L.H.i. Arch. Gen. Pezehiat. (in press).
Preach, J. and Iepaetate, 9.: the Effects of shock Treataent
on the 3:0. Pezgheenal. Quart. l1: 226-239, 19h8.
Ireeeh, 6., Inpaeteto, 9., attenheiner, L. and Wartie, 8.3.:
Some Reactions Seen After Electric Sheet Treatment.
Amer. J. Pezghiat. 1021 311-315, 19h5.

�.13-

3.0.: reyehepethelegie Reactiene end Bleetrie-Sheek
Therapy.‘ 1.1: State J. led. g3. 1553-1557. 19h2.
10. Jehneen, L.c., Ulett, G.L., Jehneen, H., Snith, I. end
Sines, 3.6.: Electreoeavuleive therapy (with end
9. alueek,

Hithaut Atropine). Arch. Gen. Pazghie . g; 32h-336, 1966.
11. Kenn, 1.1. end Pink, l.c change: in Language Bering
Elactroahock therapy. re ehe‘ethelo er colnunioetien,
Ed. Roch, P. and Zubin,

3., Stuns e Stratten 126-139,

1958.

12.

R.L., link, x. end Weinetetn, B.A.i Reletien of
tnoberbitel rest to Clinical Inprevenent in Electroehock.
Arch. neural. e rezehiet. lg: 23-29,'1956.
13. Kuhn, R.L., Pollack, H. end flag, 3.: Seeiepeyeheloxie
Aspect; a: Peyehiatric Ireetnent in A Velentery Mental
Hospital: Duretien or Hoepitelixetiea, Discharge
hating: end Biegaeeie. 1.x.1. Arch. Gen. Pezehiet. ;}
Kehn,

565-57h, 1959.

1k. Iehn, R.L., rolleck, H. end rink, H.a Figure-around Discriminetien After Induced Altered Brein Functien.
A.H.L. Arch. lea-oi. g: 5&amp;7-551, 1966.
15. Kuhn, R.L., Pollack, I. end tint, H.c Sociel Attitude

(alliternie

W

? Scale) end Convulaive Therepy.
gig: 187~192, 1960.

J.I.H.D.

16. lelileweky, L. and Heck, 2.: Shack trout-eats, Peychoeurgery
end eﬁher Betetie Ireetnente 1n Peyehintry. Grtne end
___________._________________________.____

strn‘t.n. 3.1. ,

1952e

�lethed:
9t eeneecetire petiente referred fer eleetreeheek therepy
during 1956-57, eeveety-three petiente were eebjeete of the
ehelyeee deeerihed here. the pettente were selected fer treetnent by the reetdeut therepiet end the eupervieies peyehietriet the inveettsetere pleying he rele in their eeleetten. theee
eheervetieee were nede during e eeeveletve-eeheeevuletve eleetreeheek etedy in which euhaeete referred for therepy were rendeely
eeeirned to eeereee e1 eeheenveletre er eenreletve treeteente.
Bleetreeheek eee edeiaietered three tinee weekly under
pentethel pre-nedteetien, eeing either e letter unidireetienel
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                    <text>�Reprinted from Psychopathology of Communication
Grime &amp; Strstton. Inc., 1958
Printed in. (1.5.4.

9
CHANGES IN LANGUAGE DURING
ELECTROSHOCK THERAPY
By ROBERT L. KAHN, PH.D.,

I

AND

MAX FINK, M.D.*

Weinstein and his associates have described patterns
of symbolic adaptation in patients with cerebral dysfunction.l The
main emphasis in their work has been placed on altered language patterns. Their observations have shown the similarity and relationship
between various kinds of behavior which were previously regarded as
disparate phenomena. Instead of being isolated defects due to focal
brain lesions, these phenomena can be understood as uniﬁed aspects of
an altered pattern of adaptation under the conditions of a diffuse disturbance in brain function. Some of the factors which determine the particular type of adaptation shown include the premorbid personality and the
nature of the environmental stresses.
This emphasis on language has been shown to be a useful method of
study. For example, the presence of certain characteristic changes in
language under the influence of amobarbital sodium, such as disorienta—
tion for time and place, denial of illness, and reduplication, has been
standardized as a diagnostic test of brain disease in neurological patients?! 3
This technique has application in the study of other conditions of
altered brain function, as in the somatic therapies. The electroshock
population is of interest for two reasons. It is possible in these patients,
as it is not in those with neurological diseases, to manipulate experimentally the stimulus causing changes in brain function. Secondly, the mode
of action and the psychological changes associated with electroshock
treatment remain poorly understood. In a previous study we have shown
that a favorable clinical response to electroshock treatment is related to
early and persistent manifestations of language changes with amobarbiN RECENT YEARS

*

Department of Experimental Psychiatry, Hillside Hospital, Glen Oaks, New
York. Prepared with assistance from the National Institute of Mental Health, Public Health Service and the Dazian Foundation for Medical Research.

126

�CHANGES IN LANGUAGE DURING ELECTROSHOCK THERAPY

127

tal sodium characteristic of altered brain function} This ﬁnding was
considered to support the hypothesis advanced by Weinstein and
Kahnl’ 5 that the mechanism of therapeutic action of electrically induced convulsions lay in the creation of a condition of altered brain
function in which the patient might express his problems in a new
symbolic fashion, particularly in the form of denial.
The present investigation is a further attempt to test this hypothesis
by studying changes in language that occur with treatment. The following questions speciﬁcally were studied:
1. Are there characteristic identiﬁable changes in language which develop in the course of electroshock treatment?
2. Are these changes related to the clinical response?
3. Are these changes related to the degree of alteration of brain function?
4. Does the administration of amobarbital sodium prior to treatment
produce any changes in language which have prognostic value for the
eventual clinical response to treatment, the development of altered brain
function, and the development of language changes during treatment?
METHOD

Population: Sixty-ﬁve consecutive referrals for electroshock treatment
at the Hillside Hospital were studied. The Reiter electrostimulator was
used on 49 patients, while 16 were treated with the Medcraft. There were
20 men in the series and 45 women and ages ranged from 21 to 68.
Each patient was tested prior to treatment and retested during the
second week of treatment after having received 4-6 convulsions, and during the third week after having received 7-9 convulsions. On each of
these occasions the patient was ﬁrst tested clinically and then after
amobarbital sodium had been administered at the rate of .05 grams per
minute until nystagmus, slurred speech, drowsiness, and errors in counting backward were noted.2
The test consisted of a standardized series of questions concerning
orientation and awareness of illness. This study is based, however, on
the response to only three of the questions used: (1) What is your main
trouble? (2) Why did you come to this place? (3) If you could have
one wish, what would you wish for? All responses were recorded verbatim. Observations were also made on such nonverbal aspects as smiling, laughing, gestures, and other bodily movements.

�128

PSYCHOPATHOLOGY

or

COMMUNICATION

RESULTS

Patterns of Language Change Noted Clinically During Treatment
In evaluating the changes in language, the original responses to the
three questions given clinically prior to treatment were used as the baseline. The evaluation of what constituted a change was based on explicit
objective changes in grammar rather than on subjective or interpretative
changes as to affect, mood, feeling, pitch, voice quality, etc. In this
manner the following types of language change were noted clinically
during the course of treatment: (1) alteration in the syntactical use of
person, (2) evasion, (3) verbal denial, (4) qualiﬁcation, (5) change in
tense, (6) displacement, (7) stereotyped expressions and cliches, and
(8) smiling and laughing.
Alteration in the syntactical use of person. Instead of using the ﬁrst
person singular as in the pretreatment period, 28 patients used the second or third person and, occasionally, the ﬁrst person plural. To the
question concerning main trouble such responses were given as, “It’s
what they call a depression,” “They told me I was emotionally and
mentally sick,” “We’re having a lot of trouble with my mother-in-law,”
“My cousin brought me; she said I was nervous,” “What’s your main
trouble, or don’t you know?” and “My Mrs. is sick and I would appreciate it if they would let her in here as soon as possible.” The reason for
coming to the hospital was variously given as, “My wife brought me,”
“My father told me to come here,” or “My doctor said this was a good
hospital.” The wish was given as “Perfect health for my family,” “My
children, my husband, and all my good friends should be healthy and
happy,” and “There should be peace in the world.”
Evasion. Evasion in answering the question about their illness was
shown by 27 patients. This commonly took the form of answering this
question with another, as, “What do you mean by my main trouble?,”
“What do you expect me to say?,” “Well, what it it?,” and “What did I
say last time?” Other language patterns considered evasive included
such responses as, “I don’t know how to tell you,” “I don’t get what you
mean,” “Let me think,” “It’s hard to say,” and “I just don’t know how
to express it.’ One patient asked the examiner to give her a hint.
Verbal denial. Explicit verbal denial of illness was shown by 23 patients. They either said they had no main trouble, were well or else, after
giving evasive ‘I don’t know” responses, denied their illness and symptoms when speciﬁcally questioned about them.

�CHANGES IN LANGUAGE DURING ELECTROSHOCK THERAPY

129

Qualiﬁcation. Qualiﬁcation of a response in the direction of less commitment was shown by 19 patients. This language pattern was characterized by the use of such words as “guess,” “kind of,” “sort of,” “think,”
“apparently,” “probably,” “possibly,” “might be,” “seem,” “assumed,”
9,
and “perhaps. Thus such responses were given as, “I guess I have
been jittery,” “I seem to be very much depressed,” “Probably that I’m
nervous,” “I suffer from anxieties, apparently,” “Possibly worry about
the future,” “I have sort of gotten frightened,” “Mentally upset, I assume,” and “I think I’m a little insecure.”
Change in tense. In 18 patients there was a change in tense in describing their illness. In most cases the patient used the past tense: “I was
depressed when I came here” or “I had been nervous.” In other cases
the patient answered the question about his main trouble by putting it
in the future tense as a wish.
Displacement. In 20 cases there was a displacement of the complaint
to something other than originally given prior to treatment. This was
invariably less serious than the original complaint. Sometimes the displacement was in the form of a somatic complaint, as saying the main
trouble was “diarrhea,” “headaches,” “pain in the feet,” “I slammed the
ﬁnger in the door,” and “I’ve got an itch.” In other cases the displacement was to some concrete aspect of the hospital situation, as “My main
trouble is getting these treatments,” or “I’m upset because I was transferred to another ward.”
Stereotyped expressions and cliches. The use of stereotyped expressions and cliches was shown by 11 patients. They gave such responses
as “It seems to me under the proper circumstances I’d be all right,” “ [My
trouble is] monetary problems with people that are honorary and sincere,” “That’s the root of the whole thing,” “The only thing certain is
death and taxes,” “Learn my lesson and be a good boy,” “To be a person
of pep and reliability,” and “I just want to stop being a lazy lout.” One
woman responded to a question of her one wish with, “I think I should
consult my husband before I make a wish because he’s a lawyer and the
father of my children.”
Smiling and laughing. In 20 cases the patient was noted to smile or
laugh either immediately preceding or following his response to the
question concerning his illness.
Language Changes Shown with Amobarbital Sodium During Treatment
The language patterns after amobarbital sodium during the second

�130

PSYCHOPATHOLOGY OF COMMUNICATION

and third weeks of treatment were similar to those noted clinically. With
the drug, however, the changes appeared earlier in the course of treatment. A given language pattern might be noted in the second week of
treatment with the drug, but would not occur clinically until the third
week. In addition, the reactions to the drug took more extreme forms,
which are described as (l) cryptic responses, and (2) withdrawal reactions.
Cryptic responses. These were shown by 23 patients. Responses were
classed as cryptic when they had no obvious relevance to the test question or when their meaning was obscure, representing a very personalized expression. Thus one patient, when asked his main trouble, said,
“Nightmare of the afternoon of the evening of the nightmare.” Others
do
the
know
the
didn’t
“I
such
problems—couldn’t
as
responses
gave
problems,” “Getting my husband to write down what he does,” or “What
could I say—you don’t get the crossword.”
Withdrawal reactions. Some pattern of withdrawal was noted in 33
patients. This behavior was characterized by incomplete sentences, incoherent mumbling, neologisms, perseveration, the use of a foreign
language by bilingual patients, and delay or failure to respond to the
questions. These patients would characteristically lie with their eyes
open, would smile or turn their heads when the examiner spoke, and
would speak clearly and promptly and in English when asked questions
not pertaining to their illness.
Other Changes in Language
Other changes in language were noted both clinically and with amobarbital sodium in response to the other questions of the test battery but
not as a part of this study. There was frequent misnaming of the examiner or reference to him as “Mister.” With the drug those patients
who had a “positive reaction,” i.e., one characteristic of altered brain
function, showed the characteristic patterns of disorientation for place
and time and confabulation described in previous communications. (2)
Relation of Language Changes to Clinical Response
The evaluation of clinical response to treatment was made independently of this study. The patients were rated by the supervising psychiatrist in charge of the treatments, by the patient’s own therapist and supervising psychiatrist, and by the medical director. On the basis of these
ratings the patients were classiﬁed into three groups: 28 patients were

�CHANGES IN LANGUAGE DURING ELECTROSHOCK THERAPY

13].

considered much improved, no longer showing the symptoms which had
brought them into the hospital; 22 patients were rated as moderately
improved, showing some symptomatic relief but still showing disturbing
features; and 15 were regarded as unimproved, having shown only
equivocal or transient changes at best. The ratings were short term
evaluations, being made within two months after completion of treatment.
For quantitative purposes the language changes shown during both
the second and third weeks of treatment have been grouped together as
though the patients had been tested only once. If a particular pattern
was shown during both periods, the item was scored only once. Altogether, 89 per cent of the patients showed at least one of these patterns of
language change clinically during treatment. Such changes were found
in all of the much improved patients but in only 73 per cent of the unimproved group. It was apparent that there was a relation between the
degree of clinical improvement and the number of changes in language
patterns. When the data are analyzed for the patients who showed three
or more language pattern changes, there is a signiﬁcant difference between the groups (table 1). While 68 per cent of the much improved
patients showed three or more language changes, only 20 per cent of
the unimproved patients showed this degree of language change. Using
Chi-square, the over-all difference is signiﬁcant at better than the 1 per
cent level of conﬁdence.
TABLE

1.—Relation of Language Changes Shown Clinically to Response to

Treatment

Three or more
*
patterns

Fewer than three

Change

No.

Much improved
Moderately
improved
Unimproved

28

19

22

7

32

15

68

15

3

20

12

80

65

29

45 per cent

36

55 per cent

Total

*X’

=

11.26; P

&lt;

68 per cent

patterns
9

*

32 per cent

.01

When each language pattern is analyzed individually (as shown in
fig. 1) it becomes apparent that not all patterns discriminated equally

�132

PSYCHOPATHOLOGY OF COMMUNICATION

between the groups. In all but one case, a greater percentage of the
much improved group was most likely to show denial, use of the second
or third person, evasion, and displacement of complaint. The only lanmuch
the
between
found
diﬁerence
which
little
was
on
pattern
guage
improved and unimproved patients was the incidence of smiling and

laughing.
Analysis of the changes shown by the diﬁerent groups under amytal is
shown for the cryptic and withdrawal reactions only in ﬁgure 1. While
the crytic responses did not vary much with the different groups, the
showing of a withdrawal reaction differentiated the three groups signiﬁcantlyﬁ‘ occurring in 71 per cent of the much improved, 45 per cent of
the moderately improved, and only 20 per cent of the unimproved patients.
Relation of Language Changes to Electroencephalographic Response
In a previous communication a method of quantitatively evaluating
electroencephalographic records was described.6 Criteoria were established for rating records as showing relatively high, middle or low degree of slowing according to ﬁve criteria: average per cent time delta
waves (waves of six or fewer cycles per second), the highest per cent time
delta waves at any one lead, the lowest frequency in the record, the
highest amplitude of delta waves, and the longest duration of a burst
of delta waves. In the present study, an electroencephalogram was obtained prior to treatment and in the second and third weeks of treatment.
Each record was evaluated according to the dichotomy of showing a
relatively high degree of delta activity or not, using these criteria.
In table 2 the relationship is shown between electroencephalographic
slowing and changes in language. Those patients with the highest
degree of cerebral dysfunction, having high degree delta in both the
second and third weeks of treatment, show a greater number of language
changes both clinically and with amobarbital sodium. Using the withdrawal reaction as an index of the drug effect, however, the difference
just fails to be statistically signiﬁcant.

Pretreatment Language Patterns
The language patterns described in this study were considered as
changes only when they occurred after the original pretreatment clinical
test which was used as a baseline. Seven patients, however, showed some
"

X2

=

10.72, signiﬁcant at better than the 1 per cent level of conﬁdence.

�133

CHANGES IN LANGUAGE DURING ELECTROSHOCK THERAPY
TABLE

2.—Relation of Language Change to High Degree Delta on the Electroencephalogram During the Second and Third Weeks of Treatment

Withdrawal reactions
with amobarhital
sodium T

Change

No.

Three or more
changes clinically

Both weeks
high
Delta
Activity
One week
high
Delta
Activity
No high
Delta
Activity

25

16

16

8

50

9

56

24

6

25

8

33

= 7.62; P &lt;
TX” = 4.87; P &lt;
* X2

*

64 per cent

15

60 per cent

.05
.10

M

form of these language patterns in the initial clinical test. The manifestation of these same patterns by these patients at any other time was
accordingly not scored as a change.
When given amobarhital sodium prior to treatment, however, 30 patients (or 46 per cent of the total) showed some language change comparable to that noted during treatment. Table 3 shows the relation between
such changes at this time and the eventual clinical
response. These
changes were found in 68 per cent of the much improved patients, in 36
per cent of the moderately improved, and in 20 per cent of the unimproved groups.
TABLE 3.—-—Relation

of Pretreatment Language Changes with Amobarbital Sodium
to Eventual Clinical Response

Change

No.

Much improved
Moderately
improved
Unimproved

28

19

22

8

36

15

3

20

“ X2

=

10.30; P

&lt;

.01

Change with amobarhital sodium
68 per cent

*

�134

PSYCHOPATHOLOGY OF COMMUNICATION

In table 4 it is demonstrated that the pretreatment change with the
drug was also prognostic of the eventual physiological response to treatment as measured by the degree of electroencephalographic slowing.
The over-all distribution just falls short of statistical signiﬁcance, although when those who showed high delta activity in both periods are
compared with all the other cases as a group, the difference is signiﬁcant
at the 5 per cent level of conﬁdence.
of Pretreatment Changes with Amobarbital Sodium to High
Degree EEG Delta Activity During the Second and Third Weeks of Treatment

TABLE 4.———Relation

Both weeks
high Delta Activity
One week
high Delta Activity
No high
Delta Activity
"‘X2

= 5.27;

Change with amobarbital sodium

No.

Change

P

&lt;

*

64 per cent

25

16

16

6

38

24

8

33

.10

Finally, the initial response to amobarhital sodium was also prognostic
of the degree of language change shown clinically and to the manifestation of withdrawal reactions with the drug during treatment (table 5).
Between Pretreatment Language Response to Amobarbital
Sodium and Clinical Changes and Withdrawal During Treatment

TABLE 5.——Relati0n

No.

Pretreatment

Three or more
clinical lan*
guage patterns

barbital sodium

= 4.26; P &lt;
'l'X2 = 6.88; P &lt;
"‘X2

.05
.01

tions to amobarbital sodium '1‘

30

18

60 per cent

21

70 per cent

35

11

31

12

34

response to amobarhital sodium
N0 pretreatment
response to amo-

Withdrawal reac-

�CHANGES IN LANGUAGE DURING ELECTROSHOCK THERAPY

135

DISCUSSION

The relationship of the language changes to the development of altered
brain function and to the clinical response is consistent with our original
hypothesis concerning the mode of action of electroshock treatment. In
6
studies4’
we have shown that the clinical outcome is related
previous
to the presence and degree of alteration in cerebral function. Using the
“amytal test”2 and the EEG as indices, it has been found that those
patients with the earliest and most persistent manifestations of cerebral
dysfunction were most likely to have a favorable response. Such physiological changes create the milieu which facilitates behavioral change.
The present study, analyzing language patterns, clariﬁes the nature of
the behavioral changes that occur with treatment.
The language shown originally (prior to treatment) may be summarized in the statement, “I have this particular illness.” The subject of
this sentence answers the question “who,” the predicate refers to “what,”
and the verb describes the relationship, including the temporal and intensity aspects. During treatment the subject of the sentence may be modiﬁed by changes in the use of person, so that the sentence might read,
“You [or he, she, or they] have this particular illness.” Changes in the
predicate are shown by such patterns as displacement or evasion. In displacement the sentence might read, “I have some other kind of illness,”
while, with evasion, it would be, “I have something, but I don’t know
what.” Changes in the verb are shown by denial, qualiﬁcation, or alteration of tense. In denial the statement would be, “I don’t have this particular illness;” a qualiﬁed sentence would read, “I might have this particular illnessg” while with alteration of tense the sentence would be, “I had
this particular illness.”
Some language patterns modify the sentence as a whole. If the patient
smiles, or if he introduces his statement by saying, “The doctors tell me
that . . . ,” any part or all of the sentence may be modiﬁed. In other
reactions, particularly those noted under amytal, the patient avoids giving any meaningful statement at all. In the withdrawal reaction he says
nothing or omits part of the sentence. In the use of cliches or cryptic
expressions no speciﬁc referential meaning can be drawn from the language.
It is evident from this analysis that the language changes are not
random or bizarre, but form a patterned reorganization of communica-

�136

PSYCHOPATHOLOGY OF COMMUNICATION

tion characterized by an alteration in the patient’s attitudes to his problems and his illness. The patient either says he is not now and never has
been ill, displaces his illness temporally, spatially, or personally, is less
committed to his awareness of his illness by the use of qualiﬁcations, or
avoids the whole problem by evasion and noncommunication.
These patterns are comparable to those noted previously by Weinstein
and Kahn:l in patients with cerebral disorders, and referred to by these
authors as the “language of denial.” Similar language changes have also
been described following other somatic therapies. Frank“ 8 reports that
lobotomized patients avoid talking about the operation, and he states
that “the facility and glibness with which they say ‘well I had an operation for my nerves, I guess’ contain the quality of unconscious denial.”
Legault,9 working intensively with post-lobotomy patients, found persistent attitudes of denial. One patient, when asked why she came to see
the doctor, said it was her relatives’ idea. Many gave qualiﬁed responses,
saying they “supposed” they had had an operation. Others doubted that
the operation was on the brain, or used an evasive, stereotyped expression
as “some nerve in there,” or displaced the procedure as in, “Oh, yes, I
went to the hospital and got two black eyes.” When asked about the symtoms that led up to the operation, patients gave such response as, “It
seems to have gone.” In studying patients who showed clinical improvement following prolonged coma reactions in insulin coma therapy, we
have noted similar changes in language. In a case report10 we noted the
appearance of reduplicative phenomena, evasion, verbal denial, displacement, increased use of stereotyped expressions and cliches, cryptic responses, and much smiling and laughing, at a time when clinical improvement was most marked.
Since these language changes occur most frequently in patients who
are clinically evaluated as improved, may not the language patterns
themselves be the critical cues that give a favorable clinical impression?
There is traditionally much difﬁculty in rating patients after treatment.
Such evaluations are highly variable because of the lack of suitable
objective criteria. While there are other objective cues which can be used,
such as the amount of sedation required or the quantity of food eaten,
the appearance of these language patterns may constitute an operational
basis for clinical evaluation in the psychiatric interview.
Not all patients, however, who showed at least three of the language
changes were regarded as much improved, and not all of the much im-

�CHANGES IN LANGUAGE DURING ELECTROSHOCK THERAPY

137

proved patients showed this degree of change. There may be other
aspects of language and communication not covered by this study which
are signiﬁcant. Another explanation is that the use of these language
patterns may vary in time or in different situations. On the basis of our
previous observations of the “Amytal test” and the electroencephalogram
in electroshock patients, we should predict that unimproved patients
would show these language changes only transiently, while improved
patients would show them persistently. Future work should also be
directed toward comparison of language patterns shown when the patient
is speaking to a physician with those used when he is with his family or
friends. The degree to which members of the patient’s family are made
more comfortable by the changed language, and even their inclination to
use similar language, may explain the variability in the duration of
11 and
Both
Kahnl'
Weinstein
and
improvement following treatment.
Legault9 have indicated a relationship between the patterns of communication of the patient and those of his family.
Finally, our results demonstrate the prognostic usefulness of amobarbital sodium administered prior to treatment. The prognostic value of
the drug in the somatic therapies has been noted previously by Hoch12
and others,““14 who felt that patients who became more normal in
speech, ideation, and behavior under the inﬂuence of barbiturates were
most likely to improve with treatment. In the present study the manifestation of a change in language with the drug was related not only to
the development of altered brain function and to the clinical outcome,
but to the eventual manifestation of these language patterns clinically.
On this basis, an operational deﬁnition of the goal of electroshock therapy might be described as enduring clinical manifestation of those language patterns which occur initially only with amobarbital sodium.
SUMMARY AND CONCLUSIONS

consecutive patients referred for electroshock treatment
were studied prior to and during the second and third weeks of treatment.
Each patient was tested at these times both clinically and with amobarbital sodium with a standard series of questions concerning attitude toward
illness.
2. The results showed that characteristic changes in language occurred
both clinically and with amobarbital sodium during treatment. These
changes were signiﬁcantly related to the clinical response to treatment
1. Sixty-ﬁve

�138

PSYCHOPATHOLOGY OF COMMUNICATION

M

and to the degree of alteration of brain function as measured by the
electroencephalogram.
3. The presence of these language patterns with amobarbital sodium
prior to treatment was related to the eventual clinical response, the development of altered brain function, and the development of language
changes clinically during treatment.
70

a

6050

40
'lo

30

FIG. 1.

CLINICAL

WITH

AMOBARBITAL

r-——|

I

uucu Imovso-

Ei Ionmovw
Cl ‘ummovso

Relation of each language pattern to response to treatment.

4. It is felt that these language changes constitute an operational basis

for the evaluation of the clinical response.
5. The results support the hypothesis that the therapeutic mechanism
of electroshock treatment is the development of different patterns of
symbolic adaptation to the patient’s problems and illness under the conditions of altered brain function.
REFERENCES
1. WEINSTEIN, E. A., AND KAHN, R.

2.

L.: Denial of Illness: Symbolic and Physiological Aspects. Springﬁeld, III., Charles C. Thomas, 1955.
SUGARMAN, L. A., AND LINN, L.: Diagnostic use of amobarhital
sodium (“Amytal Sodium”) in organic brain disease. Am. J. Psychiat.

—, —,

112: 889-894, 1953.
3. —-~,
, AND MALITZ, 5.: Serial administration of the “Amytal test” for
brain disease: its diagnostic and prognostic value. Arch. Neurol. &amp; Psychiat.
71 : 217-226, 1954.

�CHANGES IN LANGUAGE DURING ELECTROSHOCK THERAPY

139

Relation between altered
brain function and denial in electroshock therapy. Arch. Neurol. &amp; Psychiat.

KAHN, R. L., FINK, M., AND WEINSTEIN, E. A.:

76: 23-29, 1956.
WEINSTEIN, E. A., LINN, L.,

AND

KAHN, R. L.: Psychosis during electroshock

therapy: its relation to the theory of shock therapy. Am. J. Psychiat. 109:

22-26, 1952.
FINK, M., AND KAHN, R. L.: Quantitative studies of slow wave activity following electroshock, Electroencephalog. Clin. Neurophysiol. 8: 158, 1956.
FRANK, J .: Clinical survey and results of 200 cases of prefrontal leucotomy.
J. Ment. Sci. 92: 497-508, 1946.

—:

Some aspects of lobotomy (prefrontal leucotomy) under psychoanalytic
scrutiny. Psychiatry 13: 35-42, 1950.
LEGAULT, 0.: Denial as a complex process in post lobotomy. Psychiatry 17:

153-161, 1954.
10. KAHN, R. L., GRAUBERT, D.,

ll.

FINK, M.: Delusional reduplication of parts
of the body after insulin coma therapy. J. Hillside Hosp. 4: 134-137, 1955.
WEINSTEIN, E. A., AND KAHN, R. L.: Personality factors in denial of illness.
AND

Arch. Neurol. &amp; Psychiat. 69: 355-367, 1953.
12. HOCH, P. H.: The present status of narcodiagnosis and therapy. J. Nerv. Ment.
Dis. 103: 248-259, 1946.
13. HARRIS, M. M., Honwn‘z, W. A., AND MILCH, E. A.: Regarding Sodium
Amytal as a prognostic aid in insulin and metrozol shock therapy of mental
patients (dementia praecox). Am. J. Psychiat. 96: 327, 1939.
14. GOTTLIEB, J. 5., AND HOPE, J. M.: Prognostic value of intravenous administration of Sodium Amytal in cases of schizophrenia. Arch. Neurol. &amp;
Psychiat. 46: 86-100, 1941.

��r
i

,

‘

4‘

__

W

g

1"

'

3

m' 13 1956

‘

L

g

0

cm

In

meme: mama wrmsnocx mm!
Robert L.

mm, mm. (1)

m m; 3.9.

(2)

x
a

3

E

m the Roman Service, Rama 303mm,

f

610::

om, In

Ion-k

Research Assistant (Psychology).

(1)

(2) Inmmumrtufﬂmumrdn

:

um,upon,bymtmavrmmhmmmmeumwmmum

l

hum). Instant-a

We quiz
.

.____.,_T
f

3

32

I

m

M“

7

,

,

,

‘

of Heath, Public Health Service, and tin

mm mum :m'

W/we‘bé
,

.

I

��.————n.~—

um w-w—w,

m

,

c121:

ll‘ynbolié

rum“, gamma: in we tan a: mu.
m pal-amt imadglﬁm 1- 5 mm»: «mm t0 tut this Methods by

studying changes in

1mm:

um. ocetu' wﬁh transom.

speculum,

in: quantum war. ”mad:
1) he then numb-nun 1631153113131. chug“ in language
in the
a: 93.00th tmmu
2) An thug changes routed tn the clinical
rum?

cm
3)

1;)

tho

Imm-

which develop
‘

mmwmmmadummrmumz
1:.an
m
&lt;3th

no»

mum-mum at amour-him swim prior to

mm mane

pm

«no any chaugu Salaam
mu tax-tho mutual 611M681
“spams t0 tmtmnt, tho Moment 6:! ahead brain mum, and the m1»-

mt of language We! during treatment?

�www.—

mm
Pbpﬂatim

8mm.” «causative mun-.1- for 0103th mama

3W.

n: tho 3:11.146. Hoopim were
ha

ma Rutter mootmtimlator

was used an

puma, m: 16 mm trhud with m Index-art. mm was 20 m m that

nﬂaoanthm,andthoagaamngoﬁfm21t068o

1361th mudprbrto What, and nuuuddurxng tbs soc.
nadmok o: tmhent arm-hum medMM amen... and man; the third
Each

Mattel-havingmiv'ud'l-‘P

convulsions.

am was first team clinically,

m

and

muchatthcnoemiona tbsp“-

that after

Win]. ”dim had bun mun-

mm, slurred speech, dram

intend at the at. of .05
Per mm mm
sine” and awn 1n counting hackurd was We! (2).

m tut consist-d of

a.

“1m and ”mane” at 111m".

a»

standardised

an» of Question concerning orient»

nu stumr in band, hammer,

on

thg

mm”

to

was a.) ﬂaw in your Iain troublo? 2) Why am you
com to this 131100? 3)Ifmcon1dhnve mum, whutwoﬂdmwinhfar? 111
responses was mom 19mm. Mmum am: also
on such mam}.
only three or

.

aspects as

questions

mum,

laughing, gestural: and cum- bodily

m

mu.

�._.

m-

WW.Mmmmmm.m

W

—...—

,

"Hwy—n

warm

munmmgtmmsmmmemom nmaeatothathm
questions

gm clinically prior to treatment. were and at tho Malina.

uﬁmofwhat

mﬁWaWmewut
a:
chug-l,

1)

as to affect, mod,

um mm: m. mum Amen a: mg.

mum m.

nag. change wars noud

oval-

objoeuva changaain

gm author than mm” or inﬁerprouuw
In
mung, pitch, vein.

The

clinical): during the

saw at {amen-at:

alumna in ma tynucuml m a: pox-on, 2) 0mm. 3) «M

ma. h) Mama, 5) ohms. mu, 6) amt, 7) stereotyped
11:

oxpzésum and cliches, and a)
1. Album

ﬁrst pom singular is

wing and 12mm.

,

in tho pmtmttmt

Warmingtha

patient. used the second
or third pom and occasionally the ﬁrst. person plural. to me question anoaming min trouble such reopen.” ward given us ”It's what they call a depress-

10a.”-

17823.64, 28

Whaytoldmlmmﬁomuyandmmliuck,‘ We'mhavingalatef

trouble with

w mﬂme-lm,“ my cousinbrnght

no; she said

I was

mus,“

mam troublo, er mm mm,“ and my lira. it sick and I tram
tppmciato it
bar in how u soon a pas-ibis.”
thq mum
team
for coming to the heapiul m anomaly given a W wife hm: no," "W
"What‘s

11‘

tamortaldm to

m hora! oriwdeow mid mama mumm.‘

will: an: grim as “Part-rat
'

The

3.0%

mu: for w M13,"

W alumna.-

my

Tho

husband and

anwgoodfm uhauldbelnnlﬂvandhappy' mﬁmmaummmm
m Md.“

�“”1

‘

~5i
I

LAW

Men Wiring
m.
m
M
2.

w

1::

21

patients. rm-

with a question, as

”What. do.

mm; m
Wm momma

the queetioh about their
tea: the tom of

you new by

m main trouble?,' “that

do you

«poet

mo; won, what 1:: m,“ and "What «he 1 may last than?“ Gum-1W
patterns considered and" included such responses as ”I don't know how
to tell
you,“ ”I don’t get what you mean," "Let ale think,“
um hard to any,“ ad “I
no

to

m

Just don‘t
hint.

how

to expanse

11:."

One

patient asked the «minor to give her a

W. mutwmmammummwzspu
an,”
Wm
W.

1mm. they either

math-y

had no

um

«am or an

axing evasive “I don't mow” reapeneeo, denied
specifically questioned about. him.
'

eomltmont
the use

their illness and

a... arm-

mention a: a meme in the dimtion a: 1»-

m ohm by 19 patients.

a: were. as

”31103:,"

ably, " "possibly,“ ”man. be,“
were given no

'1 gun: I have

”pmbably that I'm

This lulguago pattern was characterised
by

”kind of,

“an,“

been

'

,

“sort at " ”think " “apparentlyﬂ "prob-

“assumed," and “perhape." That such

Jittery,” “I seen to

he very

ream

mammaed,“

mom,” “I suffer from emotion, apparently,“ ”Poenbly early
about the fume," ”I have sort or! gotten
momma,“
upset, I
and ”I think I'a a little inseam..."

W.

”W

‘

Inlapntiente therewaeaohangein

um,”

mum»

in; their 1111:)“. In most cane the patient used the past tense, as "I wan
depressed when I one here” or 'I had been
mm.” In other canoe the patient answered
the question about his main trmzble by
'

131%(2mg. In 20 cases

mung it in the future
there no a diamamnt

tense as 3 Huh.

of the

Wt

‘

W

to something other than originally given prior to
treatment. This was mummy
lest Bonan- than the original comm. Sometimes the
dilplacamnt was in the
tom of a emetic complaint, as laying the main trouble
was ”diarrhea," “headaches,“

�WWWWMI—Fr‘

.6.

'

”pm in the tests," “I slams the rings;- in the door,“

stair case: the displacemnt
as

‘33: main

form»!

m to some mores. aspect or the:

itch.” In
hospital situation,

trauma in getting those treatments," or “I'm upset because I

to another
7.}

and "I‘vs got. an

was

trans-

wand.”

Suﬁsm mania and 011mg.

Tho

use of stereotyped sxpmssim

andsliohumaambyupltisntl. Thsygan-uehnnponauunltmtam
undo:- the proper circumstance: Igd be

alright,"

with pupils than. are honorary and sinners,“
“The only
'1‘0 be

thing

«mm is

“(my

tmblo in)

monetary

"Tut’- the root of the

(bath and taxes,“ "Loam

my

pmblou

whole thing,“

lesson and be a

good boy,”

person a! pep Ind

nhtbility,” and “I just want to stop being a hly lent.“
Muhammlpmbdto‘aqusstimothsrmwishuth, 'Imnkllhmaoonsultw
a.

W.

husband borers

8.
laugh

I make a wish

became ho'a a

lawn: and the {nth-r or

InﬁOcaauthopatimtmmtodtoamoor

01m manuly wounding or following his

coming

xv childish."

suspense to the question can-

nu 111m".
to.

language

”zoom um:- ambarbitsl mom during to. mono and tom:

units of treatment. were 11min:- to those noted clmenlly. with the drug, haunt,
the changes 5mm earlier in the sour» or treatment. A given Imguags
pattern
might be noted in the second was]: at insistent with tho drug, but. would not occur

annually until the third

mt.

In Audition, the motions to the drug took more
extreme forms, which are ascribed
cryptic responses and withdrawal remnants.

1.

W.

u

patients. 3031mm” wars class-sdas cmtiswhmthsyhndmobﬁm relevance to the testqueetion ormthsir
31118

was shown by 23

m obscure, 1'31)an a very momma-d «pr-union. Thu: ms patient,
MWMsMntmnble, ma'mghmoftmuumomofmmmgattm
naming

night-am.” Others gave such msponsoa an

to. problem," ”gutting no husband to
you duo‘s get. the

naturism."

'1 MN. know the pmblsm -

cm‘t do

ma dm mo he does,“ or ﬁrm oouu I uy ..

�M_W~«W.“hm... ,Wﬁr—yyw'V‘amn"WW—wzmw. wm-u.www‘wex"w\’murvxl'ww’byum—lam. 7, am....-.. We.
.:

.

~

.

,

V

.

...

7

or

Wham-x“...

.3».

&gt;

my-

a.

~u..r-_..L-r.-‘~w

ﬂaw. ,‘m,r__ wry",

“Tee

‘11ng reaction. 8m pattern or withdrawal was noted in 33 patients.

2.

m: behavior we: ohenoteriled by ineomlete
egim, pomemtdon, the use
or failure to

eve-pond

of e

totem Manage

by

bilingual patients, and delay

to the questions. meet; patiente would cheruoterietioelly lie

m1.

with their eyes open, would

or turn their heed

clearly end promptly and in

would speak

eentencee, incoherent mumbling, mela-

when

the

miner epoke,

and

Well when asked motions not pertaining

to their illness.

comm

sodium

My

endwith ambarbitel
oom- changes in hnguege were newborn
in neponee to the other qua-time of the tut battery but not part of thie
more use frequent dimming of the manner, or uteri-mg to hm :- .‘Eﬂater.’

with the drug these Intimate

who had

e “punitive reaction,“

my

one

characteristic

characteristic patterns of acclimation for
place and time and contebuhtion deeorlbed in preview! communion! (2) .
of altered

man Motion,

showed the

the evaluation of clinioel

memo

to treatment we

mede

independently of

thie may. The Intimate were mted by the supervising peyohietnet in charge of
the teammate, the patient‘ﬂ om therapist end eupenieing peydxiatﬂat, anaby
the
director. 0:: the beeie of these ratings the petiente were unsealed

“eel

into three gmpa:

W

turned,

28

pmenu um widened much

which brought then

aiming

em

into the hoepitel;

eynptometio

22

improved, no longer showing the

petiente were rated as moderately

relief, but still

ehowing

dimming restore"

15 were ragweed ee mmproved, having elbow: on]: equivocal or

trmeient

and

We at

beet. me rating: were abort term evaluations, being ude within two loathe after
coupletim of

them.

�PERCENTAGE SHOWING EACH LANGUAGE PATTERN
ACCORDING TO RESPONSE TO TREATMENT

70
60

CLINICAL

I—————————-‘

WITH

AMOBARBITAL

l———_I

I

MUCH IMPROVED

El

UNIMPROVED

I400. IMPROVED

�*8.
For quantitative purposes the language change: diam during both the

mead

third week: of tmtaent have been grouped together“ as though the patient: had
been tested only once. If e particular pattern we chm during both periods, the
the: me scored only wee. ntegether, 895 of the petiente enabled at least one at
and

then patterns of

We manually

dining treatment. Such changes were

fomdinullthemch mpmvoepauembntinonly7motuuunmpmdm.

It as

nmt. and the amber
[the

patients

a:

chengee

who showed

mungmgo patterns.

three or

more leaguege

language change.

em

a.“ is

analysed

for

Wed petm
enlyZOSottbeunimpmedpaﬂenu

ienteehmdthmotmnlmgugechangee,
this degree of

When

We-

petum changes, there is a signiﬁ-

I).

‘gieent differ-wee between the groups (Table
shaved

clinieel

apparent that. there me e relation between the degru of

681 of the much

Bung cm! the menu dietdbuﬁdnie lim-

mMatbetmtnmth-uwaercmnm.
Relatian

of.

W

m 1mm (28)
WW MW (22)

W

(15)

1‘0“!- (65)

Chang"

W

Shawn

3.

Wally to Ream“ to Treatment.

lie.

lo.

5

1

19

685

9

32:

7

)2!

15

681

3

201

12

895

29
'

W

36

551

:2 - 11.25
1!

&lt;m

Hheneachlengmge pettemiemelyeedmdivimm,um1nﬂ¢m1,

itbecaneeeppemtthetnotenpe‘btem

wcmmequmymmw.

Inﬁlbntoaeem,emmmtmeftmmmmdpeumuwmmn

’

�Y

«my

v m. n.“ .-‘

nmxw

“gamma. — yawn
,

v

mama-gm

m

w“... n-

,.—., »1—0”

—W -.~.-

-

V

,

,

n «Fur

run...“ .-

-

. 17,1,»

-

.

,

men-1mm, mottheeecmdormmpeum, Wanda-Newt
o!

ambush;

The

aﬂy

1111311130

petum

on While}:

little airtime

was found between

mmmmmmmdmmamemdmmmum.

.Anuymatmmemwmwrmmmup-meumm
termerypueandwithdmel mam anlyinrigun 1. mmaypuc reepeneee did

mtnrymeh

with the

afferent groups, the

withdml,

moving of e

mum differentiated the three gmupe eigﬁfimm: occurring in 711 of the mach
Whﬂdthemdenﬂhhpmndmdmmzﬁottbmnpmdpauwu.
x.

:

mu.“

Mum of
In a

e to

.,

vs;

mea
new

M
of qumtitaﬁvm Mam electro-

Mama
pm
ducribed (6).
emeMgraphic
'

a

resend:

records an

m

inning relatively high,

middle

,a;

criteria
62‘

~

were established

low degree

for rating

of abnonnliia according

to five agitating avenge percent. time delta. wee (waves at :11 cycles per mood
or lees), the highest percent time delta. mm at my one low. the lowest tremmney

lathe moord,thehigheetamplitudeofdelteme,
burst. of delta

me.

mummumote

In the present study, an electroencephelogm wee obtained
priortotmmntandm the ”Windmirdmk a: treatment. Each ”comm

«alum mending to the dichom at showing
eliw er m, using the-e axe-Lurk.
In Table

ality
V

and changes

the relation-hip

2

in

animation, Wag
show a

1mm.

am

reletively h1g1 demo at ebnon'e-

mm mm abetroonaeplulognphtc linem.

Tho: patients with the

in
Why
of

high

mate; mm:

18

I.

greatest degree at cerebral

both the «can!

I2 a 10.72,

thinner:- at

mmt,

hmge change- both clinicallyxand with Waite]. and“...
the mama.
mum at! mime-u: at the drug effect.
'

m,

was the
3m. ran- to be statistically signiﬁcant.
I»

end.

Wimt

1%

better than the

'

11

level or

comm.

�ﬂ‘rﬁwwwme—wmm.
.

‘ermmmﬁmvﬁmimmw'

TABLE

Relation of Language Ghana.

’60

High

3

WW

(25)

OnMunimzé)

‘

lo 315: Ahnamauw (2h)

mm

withdrawal Motion!
with W191}. Seem:

i

lo.

1

15

as

a

50%

6

255

-

15

601

_

9

5“

‘

B

335

. Yoa
P &lt; 0°,

:2

12

Language

when they

._._.r,._r.

Eloctmmmalom Dunne

,

m1:

&lt;

‘

Both Weeks 31g:

2h:

,

of Treatment

clinical]:

lo.

may
“at

on the

or Kan

changes

m._.—r.m~.

2.

83m and Third ﬂecks

the

,

P

pat-Mm «termed in that: stuck wan

manned afar tho original

’ has?
.19

&lt;

midsmd a:

change:

mmmm clinical test which an

and u a. baseline. Bum patients, 11mm, .Ihmd can form of than 1mm
puttem in the initial 91.1mm test. me minimum or thus same pattern!

bythaeepnuenuatmomrtimmmonnnmnatuconduachmgo.
mm gum

Wits). actual prior to tmtmt, War, 30 patients", at

Wot‘ﬂwmu,mmdmhngmgammnbhmmntnommtmh
neat. In‘hbh3thonhumbomahmgamhchmguat mamumhm
m'mmmeumm mm». Manfmdméﬁﬁdmmw
pmdpmmnu, thwzyséiutlmnoammynwdwamozmmmd

W.

.

‘

,

par" .—
.V

�w :u—v-r—wwxv—mww:

Relatim of

W

W3

Pn-tmmt Language

Ghangon

autumnal Mun

with

mm

and

clinical Mona

cm. with Ambarbital mu
1

Ho.
Knob Impravod (28)

Hodomtely

MIMI:

W

68$

19

(28)

8

36%

3

W

30

It“

(15)

Tom (65)

l

:3 - 10.30

P&lt;
In Tab}.
was

I;

.01

it 1. “inﬁltrated that the pm-vtmtmnt change with the

also prognostic of tho eventual

drug

Widow anionic to tmtment as mound

ouctmcaphalogmmc abnomanw. Tho mun distribution 3m;
tall: chart at statistical lawman, although
than who
my: almonby

m.

magic.

01'

m

mlityinboﬂpeuoda an conpnrodwiﬂzall’ehsothor
crence is significant at th- 51 1m]. 91‘ canﬂdonoo.
Relation of

ma

mnuam, thaw:-

Pwtmmt Languag- Ghanges with manual. Sodium and High Basra

Em Abnomliw Drug the Second and Third Weeks of Tmman‘b

Both Wuks High
One week

mmty (25)

M Announnw (16)

Chung: With Amobarbital Sodium
Ho.
1

16

6&amp;1

6

.

38$

’

la

High Abnormality (2h)

8

335

- 5.27
P&lt;olO

1a

�many,

the

initial

degru a! Ianguagl clung. I‘hm cunicamand
"actions with the drug during twat-ant (km: S).
tho

m
hcpom to
5

.

human at Pro-tantalum

sodium.an pregnant?“ at
to tho Mutation otirithdmnl

response to ambarbital

Language

.

NW
mm mm:

5041mm

.

1':

011mm Chang“

and Withdrawal Remuom

3

Clinical
PatternLeague.
03' Hora

lo.

Pmtmmm Respom to

max-mm Sodium

(30)

In l’ru—treatment Response
to Mammal Soditm (35)

18

,

11

:2 aims

9‘00;

Withdrawal Reaction!
ﬁo Amour-Mu]. Sodium

1

30.

i

601

21

705

311

12

3M

- 6.38
P&lt;ll°1

x2
_

�'Iwwa‘v-rI—Ku,WM wc-v—

~33-

w".—

«my. qzwrr

*

Discussim
the relationship or the language changes to the development of sltsred brain
function and to the clinicsl reepcnee is cmistent with our original vaethesie cenceming the nude
have shown

ct action or electmehock treatment. In previous stmnee

that the clinical

outcome

is related to the

(hﬁé) we

presence and degree of

alter-

”mm

test" (2) and the we as indicse, it
has been fomd that those patients with the earliest and most persistent Mutations
were met likely to have a favorable response. Such physioof cerebral
aticn in cerebral function. Using the

mm

logical changes create the milieu which facilitates behavioral change.
present study, analysing language petteme, clezii’ies the nature a: the
beheviorel changes that occur with treatment.
the language chem criginelly, mic:- tc. treatment, my be amused in the
The

statement, "I have this particular illness.”

The

subject or this sentence answers

the questicn 'Who,’the predicate refers to What,‘ and the verb describes the relationship, including the femoral and intensity aspects. During treatment the sub-

dectoi’thesentencemybenoﬂtiedbycmngesinthemotpereon, eothntthe
sentence night read "You (or he, she or they) have this particular illness." Changes
in the predicate are shown by such. ﬁettem as displacement or evasion. In displncs-

nent the eentencc night tied “I have ecu other kind of illness," em... with evasion,
whet.” Change: in the verb are
it would be, "I have something, but I don't

m

qualification or alteration of tones. In denial the statement would
be, “I don‘t have this particular illnessg' a. qualified sentence would read, “I light
have this particular illneseg“ while with alteration or tense the sentence would be,
"I as this particular illness,”
ﬂown by deniel,

Sons language psttems- modify

the sentence as a whole.

"

If

the patient

mice,

or 1: n. introduces his etstewent by saying. "no doctors tell me theta...“ any, pert
or all of the sentence my be emailed. Other reactions, particularly those noted
under mytcl amid giving any meaningful
statemt at ell. In the withdrawal reaction

w”...

�W,

wwcww—mw '-—-—'- ..r.-_m..—w.,

”ﬁr .,,,,.:.._._‘,._.. r_.‘-“‘1KvW“ﬁW——r—W‘w‘wwﬂwmwwi'w

,_,.
WWW .Vw—ya-awwmwnmr

an...

Wpemsaysnoﬂﬁngormiupertottlnsen’om. Intheuseotoliohesot
cryptic expxessions no specific referential meshing can be dram free the language.
or

numemm-WumtwmoW-mmom
bot rose mourned

him,

mrzaniutim

a

of

omioeuon Motorised by

so

alteration in the petient's attitudes to his problems and his illness. The patient
either says he is not now and never has
ill, displaces his illness temporslly,
or parsmslly, in less committed to his
or his illness by the
use of quelifioeums, or avoids the whole problem by evasion and
These pettems en oonpereble to these noted previously by Weinstein end
Kahn (1) in patients with cerebral disorders, and who Memo to than as the
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changes have also been described following other

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sheet the operation, end he states that " the teoility and glibness with which they
say Well 1 had so operation for
nerves, I guess' contain the quality a! moon-:'

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persistent attitudes a: denial. the patient. when asked why she ems to see the doot-or, said it was her, relatives' idea. new game qulii'ied responses, saying they
owned the operation was on the brain, or
used an evasive, stereotyped «passion as "sou nerve in there,” or aispleoed the
procedure es in “oh, yes, I went to the hospital and got one black eyes.“ when asked
“suppose“ they had an operation. Others

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                    <text>CHANGES IN VERBAL TRANSACTIONS WITH
INDUCED ALTERED BRAIN FUNCTION

JOSEPH JAFFE, M.D., MAX FINK, MD.

Reprinted from Tm: JOURNAL or

AND

ROBERT L. KAHN, PHJ).

NERVOUS AND MENTAL DISEASE
130, No. 3, March 1960

Volume
Printed in U.S.A.

�Reprinted from THE

JOURNAL OF NERVOUS AND MENTAL DISEASE
Volume 130, No. 3, March 1960

Printed in U.S.A.

CHANGES IN VERBAL TRANSACTIONS WITH
INDUCED ALTERED BRAIN FUNCTION
JOSEPH JAFFE, M.D.,1 MAX FINK, MD.

Repeated interviews with patients under—
going convulsive therapy reveal progressive
changes in the interpersonal relationship,
which are referable to verbal and non-verbal transactions. While non-verbal aspects
of communication are difﬁcult to quantify,
techniques are available for the measure—
ment of verbal behavior. Using such lin—
guistic methods, we have observed systematic alterations in language patterns during
convulsive therapy, which were related to
independent evaluations of behavioral
change and to improvement. The description
of these language patterns has provided a
useful quantitative method for understand—
ing interpersonal changes which occur during therapy.
In a syntactic—content analysis of recorded interviews during convulsive therapy
(6), such changes as denial (negation),
qualiﬁcation (subjunctive and .adverbial
modiﬁers), displacement (person and tense),
and cryptic and clichéd remarks were
scored. An increased incidence of these
changes in the patients’ speech was related
both to the degree of induced altered brain
function and to the evaluation of therapeutic response.
It has been clinically observed that when
the language of the patient is affected by
neurologic dysfunction, modiﬁcation of the
interviewer’s speech patterns occur. In the
syntactic-content analyses, in which a structured interview was used, the examiner’s
participation was restricted to statements in
the questionnaire. This two-person inter—
1Department of Experimental Psychiatry, Hillside Hospital, Glen Oaks, Long Island, New York.
This study was aided by grants 56-151, Foundations’ Fund for Research in Psychiatry, and M-927
of the National Institute of Mental Health, U. S.
Public Health Service. The technical assistance of
Mrs. Jean Kolodny and Mrs. Ann Horowitz is
gratefully acknowledged.
235

AND

ROBERT L. KAHN, PHD.

view group (or dyad) therefore assumed
special characteristics. Interactive effects
were minimized. The constraint of the questionnaire interrupted the reciprocal modiﬁcation of the examiner’s speech. In such a
dyad, scoring of the patient’s responses
alone constituted an adequate description
of changes in the verbal transactions of the
two-person communication system.
Judgements as to mental status are usually arrived at in less structured conversa—
tions between doctor and patient. It was
suggested that measurable changes in language patterns would occur even in con~
ventional clinical interviews, and furthermore that such changes would be related to
those observed in structured interviews.
The methods of dyadic analysis were developed (3—5) to permit a quantitative
description of verbal transactions in unstructured interviews (diagnostic, psycho—
therapeutic). In this analysis, the speech of
doctor and patient is considered as one continuous behavior, and the measurements
are performed on consecutive units, irrespective of speaker. The verbal ﬂow of the
interview is thus considered as a single out—
put, irrespective of speaker. The justiﬁcation for this maneuver rests ultimately on
the correlation of dyadic speech patterns
with those obtained by other methods, and
is an aim of the present study.
These scoring measures of unstructured
interviews have been applied to weekly interviews with patients undergoing convul—
sive therapy. It is the purpose of this report
to 1) determine the pattern of change in
dyadic language measures with convulsive
therapy; 2) study the relation of these
measures to the degree of induced altered
cerebral function; and 3) relate the dyadic
scores to syntactic language measures ob-

�236

JAFFE, FINK AND KAHN

tained concurrently in structured inter-

repetitive the interaction. For these studies,
both the mean and standard deviation of
views.
the TTR distribution of each interview sam—
SUBJECTS AND METHOD
ple was obtained.
For the syntactic speech analyses the paTwenty-seven consecutive referrals for
convulsive therapy in a voluntary mental tient was seen by another examiner during
hospital were studied. On a random basis, the same intervals. This interview consisted
ten patients were assigned to a control group of a standardized questionnaire composed
and the remaining seventeen constituted the of speciﬁc items concerning the major comexperimental group. Both groups were com— plaint, reasons for coming to the hospital,
parable for age and education; the convul- and temporal and spatial orientation (9).
sive group had a mean age of 47 and 11.7 The verbatim responses were analyzed for
mean years of education, while the mean the presence of syntactic language changes
age of the subconvulsive group was 47.8, previously described as occurring with inwith a mean of 10.5 years of education. The duced cerebral dysfunction (6).
Prior to, and at weekly intervals during
investigators had no part in the treatment
process, and did not know which cases treatment, an electroencephalogram was reserved as controls until data collection was corded in each patient. These records were
measured for the per cent time of induced
completed.
The experimental (convulsive) group was slow wave activity (1).
In the dyadic TTR analyses, experimengiven grand mal electro-convulsive therapy
three times weekly, under pentothal pre- tal (convulsive) and control (subconvulmedication for a minimum of 12 treatments. sive) groups were compared. In relating
The control subjects were treated in identi— dyadic TTR changes to induced slow wave
cal fashion except that they received sub- activity and to syntactic language analyses,
convulsive electrostimulation while under the mode of treatment was disregarded, all
pentothal premedication.
patients being considered as a single group.
All patients were interviewed prior to
RESULTS
treatment, and in the week of the 12th
1. Dyadic TTR: A consistent change was
treatment. An unstructured clinical diagnostic interview technique was used centered observed in the TTR patterns of the experiabout the patient’s symptoms and life prob- mental group. Scores for consecutive 25
lems. The patient was encouraged to talk word units of interaction in 500 word samfreely, with occasional guiding interventions ples were plotted before and during the
by the interviewer. Long silences resulted treatment course (end of the fourth week).
in increased interviewer activity. All inter- Figure 1 shows a graph of the TTR patviews were tape—recorded.
terns for one patient. Next to each graph is
For the formal dyadic analyses (3, 5), the frequency distribution of the 20 consecu—
the ﬁrst 500 words of each interview were tive scores shown. The change in the distranscribed in temporal sequence without tribution for this case was a decrease in the
regard to the speaker. This sample of dyadic mean and an increase in the standard deviaspeech was divided into consecutive 25 word tion of the dyadic TTR. This pattern of
units. The type-token ratio (TTR) was cal- change was characteristic of the expericulated for each unit. The type—token ratio mental group.
is the number of different words (types)
Table 1 shows changes in the group mean
divided by the total number of words (to- T TR score during treatment. Although there
kens). Thus, the lower the TTR the more was a decrease in both groups, the change

�237

LANGUAGE CHANGES WITH BRAIN DYSFUNCTION

was signiﬁcant (p &lt; .01) only in the convulsive group and not in the control (sub—
convulsive) group.
Table 2 shows the changes in standard
deviation of the group TTR scores during
treatment. There was a signiﬁcant increase
in standard deviation (p &lt; .01) in the
convulsive group. In the control (subcon—
vulsivc) group the standard deviation was
decreased during treatment. The change,
however, did not reach statistical signiﬁ—
cance.
2. Relation of Dyadic TTR to EEG
changes: The changes in dyadic TTR scores
were related to changes in brain function
as reﬂected in measurements of the amount
of slow wave activity on the electroencephalogram. For this purpose, the per cent time
delta activity in the EEG record obtained
in the same week as the interview was used.
While almost all members of the experimental group developed prominent amounts
of EEG delta activity during treatment,
none of the control group demonstrated
such changes. Using the method of rank
order correlation, the change in standard,
deviation of the dyadic TTR correlated
+65 with the per cent time of delta activity

TABLE 1
Change in Mean TTR with Electroshock

Subconvulsive
Convulsive

.92

j
.xv-rp/w.

p.
l—

.76

.

/.

-

-

with Electroshoclc

Subconvulsive
Convulsive

,5
3

83
°

.5660

,0
.92

El

e4

...76
.68

.60

.

.68

D—URING
TREATMENT

/

f

.76

T”

text).

.92

Lo

55

5“
83
m

Ea

/\T

I

.56/6068

.76

TTR

FIG. 1.

.84

ﬂ—I

6

0

10
17

During Difference
treatment treatment

8.6

8.1

76

9.2

—0.5

+1.6*

*Signiﬁcant at 0.01 level, using Wilcoxon’s
method of paired replicates.
TABLE 3
Relation of Syntactic and Dyadic TTR
Language ZWeasnres

Dyadic Analysis:
Syntactic Analysis

N

Change in

Mean

Fewer
than
two changes
Two or more
changes

Change in

Standard

Dev1at10n

15

—0.8

—0.1

12

—3.0**

+1.4*

&lt; .01). The greater increase in variability in the language measure was thus associated With the greater degrees of altered
brain function. Changes in the mean T TR,
however, were not signiﬁcantly related to
the changes in brain function (r = +19).
3. Relation of Dyadic TTR to Syntactic
Language Changes: A comparison of dyadic
TTR scores with syntactic aspects of the
patient’s speech obtained in independent
structured interviews was made. The patients were divided into those who showed
two or more syntactic language changes,
and those who showed fewer than two such
changes, regardless of the type of treatment (Table 3). For the patients showing
(19

0

N

Group

Pre—

Signiﬁcant at 0.02 level.
** Signiﬁcant at 0.01 level.

0’)

.

—0.8
—2.4*

TABLE 2
Change in Standard Deviation of TTR

25 WORD UNITS)

E2

80.3
79.2

*

————“‘7
/'

17

81.1
81.6

Signiﬁcant at 0.02 level, using Wilcoxon’s
method of paired replicates.

PRE-TREATMENT

1.0

10

treaItirient tiggfﬁiltegnt Difference

*

DYADIC TTR PATTERN
(CONSECUTIVE

N

Group

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Plot of TTR patterns for one patient (see

�238

JAFFE, FINK AND KAHN

two or more syntactic changes, both dyadic
indices showed a signiﬁcant change during
treatment. There were no signiﬁcant altera—
tions in TTR indices for the group showing
fewer than two syntactic changes.
DISCUSSION

These observations indicate a signiﬁcant
difference in dyadic transactions in the experimental (convulsive) and control (subconvulsive) groups—a difference which is
referable to a consistent change in the subjects receiving convulsive therapy. The ﬁnd:
ings are consistent with those reported by
Weinstein and Kahn (9) in their studies of
patients with altered brain function. They
observed increased use of the second and
third person, non-aphasic misnaming, cli—
chés, stereotyped expressions, condensations
and neologisms. These language patterns
were termed the “language of denial” and
were regarded as symbolic adaptations.
Kahn and Fink (6) noted similar language
changes in patients with brain function al—
tered by convulsive therapy. The present
observations indicate that verbal transactions during altered brain function are not
only more stereotyped qualitatively, as in
the use of clichés, but are also more stereotyped quantitatively as in the increased
repetition of words. Thus, analyses of the
more formal aspects of speech parallel
analyses of content.
Alteration in brain function was also related to changes in the dyadic indices. The
low, but signiﬁcant correlation between the
dyadic scores and EEG delta activity suggests that the two-person communication
system as a whole may reﬂect neurophysio—
logical alteration in one of its participants.
The low correlation is consistent with previous observations that the dyadic TTR pattern is sensitive to factors other than al—
tered brain function (5).
Other studies of the dyadic TTR and syntactic language measures during drug administration (2) are consistent with the
present ﬁndings. Administration of agents

which produce EEG hypersynchrony similar to that of convulsive therapy was associated with changes in both language measures in the direction of increased stereotypy
and repetitiveness. Agents which produced
EEG desynchronization, however, were associated with decreased repetitiveness and
a decreased number of syntactic alterations.
These observations, though limited to acute
drug interviews, indicate that similar
changes in language patterns can be antici—
pated in subjects following the chronic administration of psychotropic compounds. We
anticipate that alteration in patterns of lan—
guage may provide cues for the evaluation
of behavioral change in drug therapies as
well as in convulsive therapy.
It is of signiﬁcance that changes in dyadic
speech are measurable when the neurophysiological status of only one of the participants is altered. This observation is consistent with concepts of verbal behavior as
a two-person phenomenon, inseparable from
its interpersonal context (7, 8, 10). The
method and ﬁndings also demonstrate that
neurophysiologic effects can be investigated
in unstructured interviews and that the results may be related directly to those obtained under more structured experimental
conditions. Thus, the measurement of formal aspects of language in clinical interviews may be viewed as another tool of
neurophysiologic investigation.
CONCLUSION

Formal language measures in unstruc—
tured clinical interviews were undertaken
in the course of a study of convulsive and
subconvulsive therapies in a hospitalized
psychiatric population.
Dyadic TTR (Type—Token-Ratio) measures showed a signiﬁcant decrease in the
mean and an increase in the standard deviation in the subjects receiving convulsive
therapy, but no differences in those receiv—
ing subconvulsive therapy. The degree of
change in dyadic indices was related both
to the degree of induced delta activity on

�LANGUAGE CHANGES WITH BRAIN DYSFUNCTION

the electroencephalogram, and to changes
in syntactic language patterns obtained in
independent structured interviews.
Theoretic implications for the understanding of language changes during altered
brain function were discussed.
1.

REFERENCES
FINK, M. AND KAHN, R. L. Relation of EEG
delta activity to behavioral response in electroshock. AMA. Arch. Neurol. &amp; Psychiat.,
78: 516—525, 1957.

J. AND KAI-IN, R. L. Drug induced changes in interview patterns: Linguistic and neurophysiologic indices. In The Dynamics of Psychiatric Drug Therapy, SarwerFoner, G., ed. C. C Thomas, Springﬁeld, Ill.

2. FINK, M., JAFFE,

3.

In press.
JAFFE, J. An objective study of communication
in psychiatric interviews. J. Hillside Hosp.,
6: 207—215,1957.

239

J. Dyadic analysis of two psychoanalytic
interviews. Presented in Symposium on Psycholinguistic Analysis of the Psychiatric Interview, Divisional Meeting of A.P.A., New
York City, November 28, 1959.
JAFFE, J. Language of the dyad. Psychiatry, 21:

4. JAFFE,

.

249—258, 1958.

.

.

KAHN, R. L.

AND

FINK, M. Changes in language

during electroshock. In Psychopathology of
Communication, Hoch, P. and Zubin, J ., eds.,
Grune &amp; Stratton, New York, 1958.
SAPIR, E. Language: An Introduction to the
Study of Speech. Harcourt-Brace, New York,
1949.

.SKINNER, B. F. Verbal Behavior. Appleton—
Century-Crofts, New York, 1957.
. WEINSTEIN, E. A. AND KAHN, R. L. Denial of
10.

Illness: Symbolic and Physiological Aspects.
C. C Thomas, Springﬁeld, Ill., 1955.
ZIPF, G. K. Human Behavior and the Principle
of Least Eﬁort. Addison-Wesley, Cambridge,
Mass, 1949.

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                    <text>Clinical and electroencephalographic
effects of Megimide in patients
Without cerebral disease
Martin A. Green, M.D., and Max Fink, M.D.
the introduction of Megimide (beta, beta methylethylglutarimide) as an antagonist for barbiturate intoxication in 1955, considerable interest has been stimulated in its
clinical applicability. Initial reports noted its
efﬁcacy in barbiturate poisoning,1—4 but subsequent studies failed to substantiate this applicationf)"8 In this laboratory, barbiturates
are frequently administered under the standardized conditions of the “amobarbital test.”9
It was thus possible to assess the efficacy of
Megimide in altering the behavioral response
of human subjects to physiologic equivalent
amounts of barbiturate.
In addition to its suggested antagonism to
barbiturate, Megimide induces both paroxys—
mal discharges in the electroencephalogram
and clinical grand mal seizures.10—14 The present report concerns our experience with both
the behavioral and electroencephalographic effects of Megimide.
FOLLOWIXG

AIATERIAL AND METHODS

Thirty-four hospitalized voluntary psychiatric patients with psychoneurosis, depression,
or schizophrenia, ranging in age from 27 to
64 years, were studied. Megimide in a concentration of 5 mg. per cc. was administered
intravenously at the rate of 0.5 mg. per kg.
per minute, until deﬁnite changes were observed in the electroencephalogram and often
beyond this point. The amount of Megimide
varied from 45 mg. to 250 mg.
In 15 subjects Megimide was administered
without prior amobarbital. In 19 patients it
was given following the administration of in—
travenous amobarbital which was injected at
0.5 mg. per kg. every 40 seconds, in amounts
necessary to induce nystagmus, slurred speech,
and marked drowsiness or sleep.

All experiments were undertaken in the elec-

troencephalographic laboratory. An electroencephalogram was made prior to the injections
and was run continuously during the administration of both drugs. The electrode placement consisted of frontal, motor—parietal, occipital, anterior temporal, posterior temporal,
vertex, and earlobe'. Both scalp—to-earlobe and
scalp-to-scalp combinations were used.
RESULTS

The electroencephalogram in all subjects
prior to the administration of the drugs was
“normal,” that is, symmetric and non-dysrhythmic.
Electroencephalographic Response
In the amount and rate of injection of
Megimide employed, electroencephalographic
changes occurred in every patient. The type
of response and the amount of drug necessary
to induce such a response were highly variable.
The electroencephalographic changes included
irregular low- and moderate-voltage slow ac—
tivity, bursts of slow activity (usually of high
voltage), single spike discharges, and spikewave forms (ﬁgure 1 A, B, and C). These ef—
fects were diffuse and symmetric, with greatest prominence in the temporal leads.
The sequence of these responses was inconstant. Irregular, low-voltage slow activity
was the most frequent initial change in the
record. In other instances, bursts of highvoltage slow activity or spike activity appeared
initially. As the injection continued, the amplitude and per cent time delta activity inFrom the department of experimental psychiatry, Hillside
Hospital, Glen Oaks, Long Island, New York.
Read at the meeting of the Eastern Association of Electroencephalographers, New York, December 1956.
Aided by Grant M 927, National Institute of Mental
Health, National Institutes of Health, US. Public Health
Service.

Reprinted from NEUROLOGY, Minneapolis, September 1958, Vol. 8, N0. 9
Copyright 1958, by Lancet Publications, Inc.

�EFFECTS OF MEGIMIDE
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creased. Bursts of high—voltage slow activity
were seen eventually in almost all patients.
Spike discharges, however, were less frequent,
even with relatively large doses of Megimide.
For example, the tracings in one subject after
receiving 220 mg. of Megimide and in another
after receiving 250 mg. showed irregular diffuse slow activity without spike activity.
Seizures
Because of the nature of the population and
the goals of our study, we specifically avoided
administering Megimide in rates and amounts
that would produce clinical grand mal seizures.
Despite these precautions, a grand mal seizure
was inadvertently induced in one patient. A
33 year old woman was given 200 mg. of
Megimide at the rate of 50 mg. per minute.
Up to 150 mg. there was only a decrease in
the voltage of the alpha activity. After 200
mg. there was a sudden long run of diffuse,
rhythmic 4 to 5% cycles per second high voltage activity, with intermixed spike activity
which was immediately followed by the seizure. The electroencephalogram during injection and prior to the seizure showed minimal
changes, and the seizure was not anticipated

35M: MEGIMIDE

(Sac/MIN.)

SE“

F IG. 1. Different types of electroencephalographic response to Megimide. A, delta activity, irregularly and
in bursts, B, single spike activity, C, spike-wave activity

Subjective Response
The subjective reaction to Megimide was
minimal, even when the induced changes in
the electroencephalogram were severe. A few
subjects complained of nausea, “dizziness,”
“shakiness,” or a peculiar sensation in the abdomen. It was possible, however, to continue
the injection without further increase in the
symptoms. Two subjects became apprehensive,
and in one of these the injection had to be
discontinued.
Myoclonic jerks occurred frequently. They
were usually mild and conﬁned to one extremity. Less frequently they were bilateral
and more severe. The relationship between
these movements and spike activity was inconstant. The myoclonic jerks usually preceded
the appearance of spike activity, althOugh the
reverse occurred occasionally. The simultaneous appearance of spike activity with myoclonic jerks was infrequent.
The effect of Megimide was short-lived.
There were no instances of seizures or other
abnormal responses later in the day following
its administration. However, since intravenous
amobarbital followed in all patients, this may
have prevented such occurrences.
The clinical and electroencephalographic responses to intravenous amobarbital following
Megimide appeared similar to those seen in
subjects in whom amobarbital is administered
without prior medication. The slow-wave or
spike activity induced by Megimide disappeared and the usual patterns associated with
barbiturates developed (ﬁgure 2). However,

�NE UROLOGY

684

the well-modulated high per cent time beta
activity usually noted after barbiturate administered was less prominent.
M egz’mide Following Amobarbital
One group of subjects received intravenous
amobarbital prior to Megimide until drowsiness, slurred speech, and nystagmus were induced. The electroencephalogram showed the
patterns commonly associated with barbiturates, that is, an increase in voltage and per
cent time fast activity and a decrease in
amount and voltage of alpha activity. The most
prominent clinical change was the awakening
of the subject. Within the few minutes necessary for the injection, the patient became more
responsive, slurred speech disappeared, and
drowsiness, both on subjective and objective
evaluation, was minimal or absent. Nystagmus became inconstant, unsustained, or disappeared completely. Gait, including heel-totoe walking, was steady. However, the awakening effect was not uniform for all aspects
of behavior altered by barbiturate. For ex—
ample, if the subject became euphoric and
more talkative with barbiturate, such behavior
may have persisted in a milder form, even
after the drowsiness of amobarbital was abolished by Megimide.
These clinical changes were accompanied by
alterations in the electroencephalogram (figure 3). Patterns of drowsy activity disappeared. Alpha activity increased both in
amount and voltage. Fast activity induced by
amobarbital usually persisted unchanged or
was reduced only sightly. In some instances
it increased in amount and voltage. The prior
administration of amobarbital did not prevent
the appearance of paroxysmal discharges.

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FIG. 2. Effect of amobarbital following administration

of Megimide

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Megimide is similar to pentalenetetrazol
(Metrazol) in that it induces delta activity,
spike and spike-wave activity in the electro—
encephalogram, and clinical grand mal seizures. Such changes occur in nonepileptic subjects without brain disease, and considerable
individual variability in the threshold for these
changes exists. These discharges are nonspecific and cannot be used as evidence of
the presence of a seizure disorder.
The possibility of using Megimide in activating the electroencephalogram has received
study.10—1‘-’ Several investigators have noted a
more gradual onset of the electroencephalographic and clinical changes with Megimide
than with Metrazol. For this reason, the opinion is expressed that Megimide may be more
facile in reproducing both clinical and electro—
encephalographic seizures in patients with
seizure disorders. It should be emphasized,
however, that in the one patient in the present
study in whom a grand mal seizure occurred,
the seizure began suddenly and was not anticipated either from the electroencephalogram
or previous clinical responses.
Megimide is effective in counteracting the
clinical effects of small doses of intravenous
amobarbital. This property has been previously
demonstrated in animals3 and is being utilized

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Bursts of high-voltage slow activity, spike activity, or spike-wave activity often appeared,
usually during or after awakening. Such activity was not a necessary accompaniment of
the awakening response, however, since other
subjects in whom clinical drowsiness disappeared did not show such discharges.

500 mg.AMOBARBlTAL
(50 mq./40 SEC.)

Effect of Megimide following administration
of amobarbital
FIG. 3.

SEC.

�EFFECTS OF MEGIMIDE
in anesthesiology to shorten the recovery period from barbiturate anesthesia postoperatively.15 It is questionable whether this action
is speciﬁc for barbiturates or whether it also
applies to states of altered consciousness due
to other agents as well.16
CONCLUSIONS

Thirty-four psychiatric patients without
cerebral disease were given Megimide (beta,
beta-methylethylglutarimide) before and after
the administration of intravenous amobarbital.
2. Megimide produces irregular delta activ~
ity, bursts of delta activity, and spike and
spike-wave activity in the electroencephalo1.

685

gram. Such effects are similar to those produced by pentalenetetrazol (Metrazol).
3. Considerable individual variability exists
in the amount of drug necessary to produce
these changes.
4. A grand mal seizure was inadvertently
induced in one patient. The electroencephalogram during the injection and prior to the seizure showed minimal changes and the seizure
was not anticipated.
5. Megimide counteracts the clinical and
some of the electroencephalographic effects of
small doses of intravenous amobarbital.
Megimide supplied through the courtesy of A.
las Ltd., Slough, Bucks, England.

&amp;

I. Nicho-

REFERENCES
A., SHAW, F. H., CASS, N. M., and
\Van, H. M.:M. A new treatment of barbiturate intoxication. Brit.
J. 1:1238, 1955.

1. SCHULMAN,

to .

3.

4.
5.
6.
1.

8.
9.

F. H.: Further experiences with Megimide—a
barbiturate antagonist. M. J. Australia 2:889, 1955.
SHAW, F. H., SIMON, S. E., CAss, N., and SCHULMAN,
.-\.: Barbiturate antagonism. Nature 174:402, 1954.
HARRIS, T. A. 13.: A barbiturate antagonist. Lancet
1:268, 1955.
L()U\V, A., and SONNE, L. M.: Megimide in the
treatment of barbituric acid poisoning. Lancet 2:961,
1956.
PEDERSEN, ].: Amusing effect of Megimide and Ami—
phenazole in allypropymal poisoning. Lancet 2:965,
1956.
PLUM, F., and SWANSON, A. G.: Barbiturate poisoning
treated by physiological methods. J.A.M.A. 163:827,
1957.
CERSHON, S., and SHAW, F. H.: Effects of Bemegridc
on barbiturate overdosage in humans. Brit. M. J. 2:
1509, 1957.
\VEINSTEIN, E. A., KAHN, R. L., SUGARMAN, L. A.,
and LINN, L.: The diagnostic use of amobarbital sodium (“Amytal sodium”) in brain disease. Am. J.
Psychiat. 109:889, 1953.
SHAW,

10. COURJON, 1., and BONNET, H.: Comparative effects of
Metrazol and Megimide in activation of epileptic pa-

tients. EEG

11.

12.

13.
14.

15.

Clin. Neurophysiol. 8:710, 1956.
DROSSOPOULO, G., GASTAUT, H., VERDEAUX, G. and J.,
and SCHULLER, E.: Comparison of EEG “activation”
by pentamethylenetetrazol (Metrazol) and Bemegride
(Megimide). EEG &amp; Clin. Neurophysiol. 8:710, 1956.
Room, E. A., RUTLEDGE, L. T., and CALHOUN, H. D.:
Megimide and Metrazol (A comparison of their convulsant action in man and in the cat). EEG &amp; Clin.
Neurophysiol. 10:208, 1958.
SOD‘TRBERG, U.: Eﬂect of Bemegride (Megimide) on
cerebral blood flow and electrical activity of brain.
Arch. Neurol. &amp; Psychiat. 792239, 1958.
PEACOCK, J. M.: An electroencephalographic examina—
tion of the effects of Megimide and Daptazole in bar—
biturate narcosis. EEG 8: Clin. Neurophysiol. 8:289,
1956.
VVYKE, B. D., and FRAYVVORTH, E.: Use of Bemegride
in terminating barbiturate anesthesia. Lancet 2:1025,
&amp;

1.957.
16. BOTTINGER, L. E., ENGSTEDT, L., and STRANDBERG,
0.: Is Bemegride a speciﬁc barbiturate antagonist?

Lancet 1:932, 1957.

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                <text>Green, Martin A.; &lt;a title="Fink, Max, 1923-" href="http://id.loc.gov/authorities/names/n79039548" target="_blank"&gt;Fink, Max, 1923-&lt;/a&gt;</text>
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                    <text>Reprinted from The Journal of the American Medical Association
April 12, 1958, Vol. 166
Copyright 1958, by American Medical Association

COMPARATIVE STUDY OF CI] LORPROMAZINE AND INSULIN
COMA IN THERAPY OF PSYCHOSIS
Max Fink, M.D., Robert Shaw, M.D., George E. Gross, M.D.
and

Frederick S. Coleman, M.D., Glen Oaks, N. Y.
With the advent of “newer” drugs for the treatment of psychiatric illnesses and the concomitant
awareness that the effectiveness of insulin coma
therapy was limited, a control drug therapy—insulin
coma study was undertaken. Preliminary trials with
various medicaments available in 1954 demonstrated
chlorpromazine to be potent and relatively safe.
Concurrent reports had noted its value in schizophrenic illnesses, and it was therefore selected as
the experimental agent.
The study was designed to assess the therapeutic
efﬁcacy and indications for intensive chlorproma:
zine therapy, compared to classic insulin coma
therapy, an in open-ward, voluntarily hospitalized
psychiatric population.
Subjects and Method
All patients referred for insulin coma therapy
during the period Sept. 1, 1955, to Dec. 31, 1956,
were observed. Supervising psychiatrists made the
recommendation for insulin coma therapy independent of the research group. Their criteria for
referral were those implicitly held by the hospital
administration and were not altered for this study,
Randomly selected patients were placed on chlorpromazine therapy instead of insulin coma therapy.
This selection was made by the psychiatrist in
charge of the insulin therapy unit without prior
notice of the referring therapist or the supervising
psychiatrist. Sixty patients were referred for insulin
coma therapy during the study period, and half
of these received chlorpromazine.
Insulin Coma.—The standard technique of Sakel
for insulin coma was used. All patients received 50
comas, each of a duration of at least one hour, at
the physiological level of Babinski reﬂex, absent
lid reflex, or deeper. Recovery was induced by
gavage and occasionally by intravenous administration of glucose. Treatments were given ﬁve times
weekly for a period of three to four months.
Chlorpromazine.—To establish an equivalent
group, chlorpromazine was given for at least three
months. Dosages were determined by the research
team and were rapidly increased until well-deﬁned
physiological effects were observed. These included
rigidity, drooling and ﬁxed facies, seizures, or severe dermatitis. In most instances this was achieved
below 1,400 mg. daily, although dosages were increased to 3,600 mg. in one patient. In each instance, the drug dosage was slowly reduced until
From the Department of Experimental Psychiatry, Hillside Hospital.

The effectiveness of chlorpromazine was
compared with that of insulin coma in 60 patients referred for insulin coma therapy. One-

half the group, selected on a random basis,
received chlorpromazine by mouth for at
least three months in doses adjusted so as to
fall just short of toxicity in the individual patient,- this dosage varied from 300 mg. to
2,000 mg. daily, with a median of 800 mg.
The insulin coma was induced by a standard
technique 50 times in each patient. Although
many minor differences were noted in comparing the effects of these two methods of
treatment, the ultimate results at the time of
discharge were essentially the same for the
two groups of patients. Neither treatment affected the basic schizophrenic process, but
chlorpromazine had the advantage of being
safer, easier to administer, and better suited
to long-term management.

a maintenance dose, just under that producing
toxicity, was obtained. This varied from 300 mg.
to 2,000 mg. daily with a median of 800 mg.
To determine the comparability of the subjects
in the random sampling procedures used in this
study, the groups were compared as to their psychi—
atric diagnoses and ages. Table 1 shows a comparison of the groups as to diagnoses and demonstrates
an equal distribution of subjects in each category.
In the analysis of the age distribution, the median
age for patients subjected to insulin coma was 24
years, with a range of 17 to 38; the median age
for patients receiving chlorpromazine was 28, with
a range of 19 to 42. Here, too, the distribution
shows no signiﬁcant difference.
For both treatment groups, behavioral observations were made by the research staff at weekly
intervals. After completion of the treatment period,
reports of the patients’ behavior were obtained
from the therapist and supervising psychiatrist. The
“improvement” rating was determined by the medical director at the patient’s discharge conference
and was based on the fourfold scale of recovered,
much improved, improved, and unimproved. Neither the authors nor the supervisor of the insulin
therapy unit participated in these evaluations.

�THERAPY OF PSYCHOSIS—FINK ET AL.

Vol. 166, No. 15

Observations
Clinical Observations—The following clinical effects were noted in patients who received chlorpromazine and in those subjected to insulin coma
therapy.
Chlorpromazine: Chlorpromazine induced motor
retardation in all subjects. Overactive, destructive
behavior rapidly disappeared, and patients became
more tractable, less negativistic, and less violent.
The nurses’ and therapists’ records noted patients
as “less easily excited and frightened,” “cooperating
TABLE l.—P.s-ychiatric

Psychoneuxosis .......................
Schizophrenia, paranoid
.....
Schizophrenia, catatonic ............
Schizophrenia, mixed .................
Schizophrenia, hebephrenic ..........
Manic-depressive psychosis ...........

Diagnoses

Insulin Coma

Chlorpromazine

1

2
10
7

10
7

8
3
1

6
2
3

better in ward activities,” and “less restless and less
panic-ridden.” One-third of the patients were more
sociable and less seclusive and were noted to care
for themselves in a more presentable fashion. In

instances where severe motor symptoms supervened, however, the patients were less able to care
for themselves; they became sloppy and failed to
dress themselves. Such periods were usually short
and could be signiﬁcantly modiﬁed either by a
reduction in drug dosage or by anti-Parkinsonism
drugs.
Affective changes during chlorpromazine treatment were varied. Four patients became increasingly agitated, tense, and tremulous and either
refused to continue on the drug regimen or were
induced to do so only with difﬁculty. Such an
affective “storm” appeared early in the treatment
and persisted. In four other patients, depressive
symptoms were relieved with an increase in affective lability and responsivity. Depressive ideation
increased, associated with complaints of insomnia
and anorexia in two patients. The medication was
continued, however, with an eventual alleviation.
In most patients, mood changes were small.
Ideation was dramatically altered during the period of chlorpromazine therapy in 12 patients. Eight
had a loss or a signiﬁcant diminution of their
psychotic ideation. In ﬁve, hallucinatory and referential experiences were no longer reported even on
inquiry, and, in three others, delusional ideas were
less prominent. In one patient, phobias were relieved and the patient could once again participate
in ward activities. In another, hypochondriasis was
sufﬁciently modiﬁed to permit a more meaningful
relationship between therapist and patient. In one
patient, paranoid ideation became more prominent.
This was associated with increasing anxiety and
panic during drug administration and resulted in
discontinuation of the drug regimen.

1847

Insulin Coma: The clinical observations in this
group were similar to those reported by others.‘
Alteration in behavior was prominent in all patients
once repeated comas were induced. Overactive,
hostile behavior rapidly diminished and was replaced by alternating periods of somnolence, irritability, and withdrawal. In most patients, nausea,
abdominal distress, belching, sweating, and lassi—
tude were common sequelae each afternoon and
assumed prominence in the recorded reports. These
symptoms often interfered with the patients’ ability
to care for themselves, and they became unkempt
in their dress.
Changes in ideation appeared slowly during the
course of therapy. In eight patients, paranoid and
delusional thoughts became less prominent, dis—
appearing in these on direct inquiry. Suicidal and
outWardly directed destructive thoughts were modiﬁed in three patients, only to recur in each at the
end of the treatment period.
Mood changes were small. Increasing agitation,
tension, and panic were reported in three patients,
leading in two to a refusal of further therapy. In
one depressed patient, relief of depressive symptoms was noted early in the treatment and was
sustained.
In the usual practice of the treatment unit, con—
current electroconvulsive therapy was instituted
when behavioral control by insulin coma alone was
limited. In six patients, such combined treatment
was instituted primarily because of a continuation
of overactive or delusional ideation. There was, in
four instances, a well deﬁned alteration in behavior,
but this was unsustained. None of these patients
was rated as improved on discharge.
Discharge Evaluation—All patients were dis—
charged from the hospital within four months of
the end of treatment. Table 2 lists the hospital discharge evaluations for patients treated with chlorpromazine and insulin coma.
Ratings in Patients Treated with
Chlorpromazine and Insulin Coma

TABLE 2.-—Discharge

Treatment

........................
........................

Recovered, no.
Much improved, no. ..................
Improved, no.
Iinimproved, no. .....................

Chlorpromazine

Insulin Comaﬁ

2

0

4
17

5
15

7

10

Included in the group of patients treated with
chlorpromazine who were rated as unimproved were
four who received inadequate course of therapy
(less than one month) because of complications of
the therapy. Of the 10 patients treated with insulin
coma who were rated as unimproved, four had inadequate courses of therapy, two because of complications (seizures and prolonged coma), one be—
cause she became more disturbed, and one because
of administrative transfer to another facility.

�‘

THERAPY OF PSYCHOSIS—FINK ET AL.

1848

It

apparent that there is no difference in the
clinical evaluation at the time of discharge between
the group receiving insulin coma and that receiving
chlorpromazine. To determine whether this sample
was biased because of its small number, we compared these discharge ratings with a similar group
treated in this hospital in 1950 and previously
reported.2 In table 3, the discharge ratings for both
is

TABLE 3.-—Discharge

Ratings Compared for 1950 and 1956

.............................
.......................
Improved, % ......... ....................
Unimproved, % ...........................
Recovered, %
Much improved, %

_

Present Group
(30 Subjects)

1950 Group
(48 Subjects)

0

14

17

19
42

50
33

‘25

years are compared. The percentage improvement
rates for each category are not signiﬁcantly different.
Toxicity and Complications—Patients receiving
chlorpromazine and those subjected to insulin coma
therapy were compared as to toxic reactions and
complications, with the following effects noted.
Chlorpromazine: Inherent in the design of this
study were high doses of chlorpromazine, pushed
to a level producing symptoms of toxicity. In this
context, all patients developed signiﬁcant drug
effects. Rigidity of extremities, accompanied by a
decrease in facial expression, drooling, and festination, was frequently observed. In three instances,
rigidity appeared as drug dosage was reduced.
Most patients became drowsy, retarded, and less
active in ward activities. In four patients increased
tension, agitation, restlessness, and excitement
supervened, leading to a discontinuation of the
drug regimen in two.
Seizures occurred spontaneously in three patients. Pretreatment electroencephalograms had
manifested no dysrhythmia, and no history of seizures had been elicited. In each, the drug medication was reduced, and seizures did not develop at
the lower dosages.
Dermatitis was a frequent complication. All patients developed a transient erythema to mild solar
radiation. Severe intractable skin reactions occurred
in three patients, with resultant discontinuation of
drug therapy in two. In the third, promazine hydrochloride therapy was substituted for chlorpromazine, with a relief of the dermatitis. The behavioral
effect of the promazine was indistinguishable in
this patient from that noted in patients receiving
chlorpromazine.
In this group, no patient developed clinical jaundice. This complication has been variously reported
as occurring in less than 0.5% of subjects treated.
In the preliminary studies at Hillside Hospital, 3
patients of a group of 20 developed transient clinical jaundice.

J.A.M.A., April 12, 1958

Electroencephalograms were obtained in 20 of
the patients who received chlorpromazine. With
increasing doses, the modulation of the record became more irregular in each. A moderate amount
of low-voltage 4-7 cps delta and theta activity was
induced, and this activity was exaggerated by
hyperventilation. There was a suggestive relationship between the degree of the induced slow-wave
activity and the drug dosage.
Insulin Coma: The complications of insulin coma
therapy in this series were not unusual. Insulin
resistance was noted only once and was eventually
overcome by the method of alternating dosages.
Prolonged reactions occurred in three patients. In
each, neurological examination and electroencepha—
lography demonstrated signs of persistent central
nervous system dysfunction for at least 10 days.
Aphasia, hemiparesis, and paresthesias were frequent in ﬁve patients and transient in eight others.
Seizures occurred in ﬁve patients and were recurrent in three. Frequent secondary reactions, nausea,
vomiting, abdominal distress, sweating, pallor, lassitude, and generalized weakness occurred in all
patients with varying frequencies.
The complications of both forms of treatment are
listed in table 4. Certain effects, such as dermatitis
and hypotension, secondary reactions, and prolonged coma are individual for each therapy, and
seizures, agitation, and refusal of therapy were
noted with both regimens. The frequencies of these
are not signiﬁcantly different.
Effects on Psychotherapeutic Relationship—Pa—
tients were referred for insulin coma therapy after
a period of verbal relationship therapy. Such referral implies a failure of interpersonal communication.
TABLE

4.-C0mplicati0ns of Treatment with Chlorpromazine
and Insulin Coma
Treatment

_______./\—————5

Agitation and panic ..................
Dermatitis, severe .....................

...............................
Refusal of further therapy ..........
Hypotension ..........................
Secondary reaction, frequent ........
Prolonged coma (&gt;6 hr.) ............
Insulin resistance .....................
Seizures

Chlorpronmzine

Insulin Coma

4

3

3

3
2

5
2

2

6
3
. . .

1

Chlorpromazine: During the period of effective
drug action, 15 of the patients treated with chlorpromazine were described by the therapist in
response to an inquiry as “more accessible,”
“speaking more freely,” and “more amenable to
psychotherapy.” The behavioral changes could be
classiﬁed in two groups: subjects in whom tension
and preoccupation with somatic symptoms became
much less, and those in whom hallucinatory or delusional preoccupations ended. Such changes in

�I

Vol. 166, No, 15

THERAPY OF PSYCHOSIS—FINK ET AL.

in—
described
as
an
we1e
frequuitly
'.*‘-1;welationship
stww‘arease in “contact In 13 subjects, psychotherapy
either was still‘not feasible” or had become less
feasible because of increasing uncontrolled tension,
anxiety, or preoccupation with the side-effects of
wthe drug regimen.

Insulin Coma: Similar observations were made
in the patients treated with insulin. Of the 30 patients, 7 were noted to be less tense and less anxious
during therapeutic sessions. The theiapists noted
that the patient “verbalized more freelv” and was
more aware of his environment.” Four patients
were speciﬁcally treated with a “modiﬁed anaclitic”
approach. In each instance, this relationship was
unsustained during treatment and the therapists
resorted to more conventional tactics. In the remaining patients (19), while supportive, educational, and environmental manipulating techniques
were applied, the therapists were no more successful than prior to insulin therapy. In 11 patients,
the physiological effects of the treatments (secondary reactions, sweating, nausea, vomiting, and
weight gain) were reported as interfering with
psychotherapeutic attempts.
Comment
Clinical Considerations—In these patients, nei—
ther chlorpromazine in high therapeutic doses nor
insulin coma speciﬁcally modiﬁed the psychotic
had
of
88%
these
Since
a diagpatients
process.
nosis of schizophrenic illnesses, we concluded that
neither treatment has a speciﬁcity in altering the
schizophrenic process. When given in adequate
dosage, however, both treatments are potent methods for the alteration of behavior. In the discharge
evaluations, the treatments are similar. In only
20% of the patients were induced behavioral patterns persistent, with the rating “much improved”
or “recovered.” For the others, the induced behavioral changes were transient or minimal.
Since these therapies fail to induce a recovery
from the psychotic process, consideration should
be given to their ameliorative, palliative, and supportive aspects. Symptomatic relief was frequent
but generally limited to the treatment period. Patients were made uncomfortable by both therapies,
however, and the complications and toxic effects
have already been noted.
In assessing the role of concomitant psychotherapy, there is little advantage in either therapy.
Both methods were said to enhance relationship
therapy, although the therapists’ evaluations favored chlorpromazine therapy. Excluding those
who deveIOped increased agitation, patients were
more comfortable, more alert, and physically better
able to discuss their feelings and experiences while
on chlorpromazine treatment. It is clear that“interpretive” psychotherapy is not enhanced, rather,

1849

supportive, educative, reorienting, and directive
types of therapy are. When there is a modiﬁcation
of agitated, hallucinatory, depressed, manic, or aggressive behavior, both the therapist and the patient
are more comfortable and better able to discuss the
reality aspects of the life situation.
Therefore, in this context, the ease of administration and the possibility of continued maintenance of chlorpromazine in an outpatient setting
assume decisive signiﬁcance. To maintain such
therapy after discharge and continue thereby the
relationship established in the hospital setting may
be an important element in sustaining the behavioral changes induced by hospitalization.
Other Studies.—While many reports of the treatment of psychosis by chlorpromazine have appeared, we are aware of only one similar comparative study. Boardman, Lomas, and Markowe,3 after
a review of the problem, reported a study of 100
patients randomly divided into two groups of 50
and treated with either insulin coma or chlorpromazine. The chlorpromazine dosage was lower than
that used in the present series (average 300 mg),
but the drug period (three months) was the same.
Their observations are directly comparable to this
study. They reported no difference either in discharge evaluations or in symptom assessments for
either treatment group.
The patients treated with chlorpromazine, however, remained in the hospital an average of 6.2
weeks less than the subjects treated with insulin.
This was a signiﬁcant difference between the
groups. They concluded, “There is inconclusive
evidence that chlorpromazine has advantages over
insulin in the treatment of schizophrenia [but]
insulin has disadvantages in the form of greater
danger and more unpleasantness for the patients
and greater strain on the nurses. Chlorpromazine
is the ﬁrst treatment of choice in schizophrenia, but
this conclusion is based on the immediate results
of treatment and has not yet been conﬁrmed by an
adequate follow-up study.”
Boardman and his co-workers emphasize the
problem of evaluating the therapeutic efficacy of
insulin coma. They note a number of reports that
raise doubts as to the efficacy of insulin coma
therapy in schizophrenia. Bourne,4 in an extensive
review of the merits of insulin therapy in schizophrenia, concluded, “There is no proof of any
speciﬁc therapeutic effect, and the long term prognosis is in no way influenced.”
The recent observations of insulin treatment of
5
schizophrenia by Ackner, Harris, and Oldham are
relevant. In a carefully controlled study, young
schizophrenic patients were randomly treated either
by insulin or by barbiturate coma in the same
ward and under similar conditions. Evaluations of
results were made by psychiatrists without knowl-

�1850

THERAPY OF PSYCHOSIS—FINK ET AL.

edge of which treatment the patients received. The
authors noted a similar outcome, whether the loss
of consciousness was induced by a barbitufate or
by insulin, and concluded that insulin was not a
speciﬁc therapeutic agent in the outcome.
In the follow-up studies done in this hospital,2
the therapeutic results of insulin coma therapy were
disappointing. Patients referred for insulin coma
had the longest period of hospitalization (6.5
months, as against 6.04 with'psychotherapy and
4.95 with electroshock), the poorest discharge‘ rating (33% recovered and much improved as against
63% with psychotherapy and 67% with electro—
shock), and, within four years, a 50% rehospitalization rate (compared to 33% with psychotherapy
and 29% with electroshock). While these observa—
tions reflect the idea that the more severely ill
patients are referred for insulin coma, they also
support the belief that insulin coma is not a specific
treatment for the patients referred.
From these reports we would conclude that,
despite considerable study and the passage of many
years, insulin coma therapy has not been shown to
induce persistent behavioral changes more frequently than other nonspecific, less dangerous, and
less expensive therapies. To the list of alternate
therapies of limited value in the management of
psychosis we may now add Chlorpromazine, not—
ing, however, its advantage of lesser risk and ease
of administration.
Dosage of Chlorpromazine.—F0r the purpose of
assuring an adequate level of Chlorpromazine dosage for evaluation, the amount of medicament
given was increased in all subjects to t0xic levels.
This level was too high for its behavioral effects,
as evidenced by the reduction in all responsive
cases to maintenance levels of 300 to 2,000 mg.
It is our impression that Chlorpromazine affects
the function of the central nervous system (as
evidenced by changes in modulation and per cent
time delta in the electroencephalogram and the
systemic phenomena of rigidity and lassitude)
and results in a nonspeciﬁc alteration in behavior.6A
Such behavioral change is varied and is dependent
on a variety of factors, of which the personality
organization and the expectancy of the milieu are
signiﬁcant. In this context, the induction of a state
of altered cerebral function is a necessary prerequisite to behavioral change. The only assurance
of achieving a therapeutic level, therefore, is the
appearance of toxicity and a lowering of dosage
from that level to a maintenance dose. The effects
of rigidity, drowsiness, and lassitude, therefore, are
necessary concomitants of the therapy and should
be induced in all patients in whom a therapeutic
effect is desired. In instances where an affective
“storm” supervenes, continuation of therapy at

].A.M.A., April 12, 1958

higher levels, with concomitant administration of
trihexyphenidyl hydrochloride (Artane) and benztropine (Cogentin) methanesulfonate should be
considered. Such an attitude in therapy is comparable to the application of digitalis in cardiology
and to the present concept of the mode of action of
electroshock therapy.6
Summary

In a.study of patients referred for insulin coma
therapy in an open-ward, voluntary psychiatric hospital, patients received randomly either insulin
coma therapy or intensive Chlorpromazine therapy.
Chlorpromazine was found to be as effective in
modifying psychotic behavior as insulin coma therapy. There was no difference in the improvement
rating on discharge, incidence of complications, or
effects on the psychotherapeutic relationship for
either therapy.
In comparison to insulin coma, Chlorpromazine
is safer, easier to administer, and lends itself to
long—term management. Patients receiving chlorpromazine therapy are more comfortable than those
receiving insulin coma. No evidence has been
educed that either therapy has altered the basic
schizophrenic process, nor is there any evidence
that there is greater specificity of either form of
therapy for schizophrenic illnesses.
75—59

263rd St. (Dr. Fink).

This study was supported by the Board of Directors"
search Fund of the Society of the Hillside Hospital.

Re—

The chlorpromazine used in this study was supplied as
Thorazine by Smith, Kline &amp; French Laboratories, Philadelphia.
The promazine hydrochloride used in this study was supplied as Sparine by Wyeth, lnc., Philadelphia.
References

and Hoch, P. H.: Shock Treatments,
Psychosurgery, and Other Somatic Treatments in Psychiatry,
ed. 2, New York, Grune and Stratton, lnc., 1952.
2. Rachlin, H. L., and others: Follow-up Study of 317
Patients Discharged from Hillside Hospital in 1950, J. Hillside Hosp. 5:17-40 (Jan) 1956.
3. Boardman, R. H.; Lomas, J.; and Markowe, M.: Insulin
and Chlorpromazine in Schizophrenia: Comparative Study
in Previously Untreated Cases, Lancet 2:487—494 (Sept. 8)
1. Kalinowsky, L. B.,

1956.
4. Bourne, H.: Insulin Myth, Lancet 2:964—968 (Nov. 7)

1953.

5. Ackner, B.; Harris, A.; and Oldham, A. J.: Insulin

Treatment of Schizophrenia: Controlled Study, Lancet 2:
607-611 (March 23) 1957.
6. Fink, M., and Kahn, R. L.: Relation of EEG Delta Activity to Behavioral Response in Electroshock: Quantitative
Serial Studies, A. M. A. Arch. Neurol. 81 Psychiat. 78:516—
525 (Nov.) 1957.
6A. Fink, M.: Uniﬁed Theory of Action of Physiodynamic
Therapies, J. Hillside Hosp. 6:197-206 (Oct.) 1957.

�Printed in U.

S. A.

�Cjéz,,4./rv./¢

COMPARATIVE STUDY OF CHIDRPROMAZINE AND INSULIN
COIvIA IN THE THERAPY 0}”? PSYCHOSIS *-

Max

ColemanAM.D.
Fink M.D., Robert Shaw M.D., George E. Gross M.D., and Frederick S.

* From the Department of Experimental Psychiatry, Hillside Hospital,
Glen Oaks, N.Y.

Supported by the Board of Directors' Research Fund of the Society of the

Hillside Hospital.

7-22-57: IV

�Comparative Study of Chlorpromazine and Insulin
Coma

in the Therapy of Peychosis

for the treatment of psychiatric
illnesses, and the concomitant awareness that the effectiveness of insulin
With the advent of "newer" drugs

limited, a control drug therapy-insulin coma study was undertaken. Preliminary trials with various medications available in l95h demonstrated chlorpromazine to be potent and relatively safe. Concurrent reports

coma

therapy

had noted

was

its value

in schizophrenic illnesses,

and

it was therefore

selected

as the experimental agent.

study was designed to assess the therapeutic efficacy and indications
for intensive chlorpromazine therapy compared to classical insulin coma
therapy in an openaward, voluntary hospitalized psychiatric population.
The

Subjects and Method
All patients referred for insulin

coma

therapy during the period

September 1, 1955 to December 31, 1956 were observed. Supervising psychiatrists
made

the recommendation for insulin

group. Their

criteria for referral

coma

therapy independent of the research

were those

implicitly held by the

beepital administration, and were not altered for this study. Randomly
selected patients were placed on chlorpromazine therapy instead of insulin

psychiatrist in charge of the insulin
therapy unit, without prior notice of the referring therapist or the super-

coma.

This selection was made by the

vising psychiatrist. Sixty patients were referred for insulin
during the study period, and half received chlorpromazine.

coma

therapy

�.2...

a) Insulin

Coma: The

patients received

standard technique of Sakel was used. All

50 comes, each

of a duration of

at least

one hour

at the

physiologic level of Babinski reflex, absent lid reflex, or deeper. Recovery
was induced by gavage and occasionally by intravenous glucose. Treatments
were given five times weekly,
b)

Chlorpromazine:

was given
team and

To

for a period of

B-h months.

establish an equivalent group, chlorpromaziner

for at least three months. Dosages were determined by the research
were rapidly increased until well defined physiologic effects were

observed. These included rigidity, drooling and fixed facies, seizures or
severe dermatitis. In most instances this was achieved below lhOO mgm daily

patient. In each instance,
slowly reduced until a maintenance dose, just under

although dosages were increased to 3600

the drug dosage

toxicity,

was

was obtained.

a median of 800

mgm

in

This varied from 300

one

mgm

to

2000

mgm

daily with

mgm.

To determine

the comparability of the subjects resulting from the

in this study, the groups were compared
as to their psychiatric diagnoses and ages. Table I compares both groups
as to diagnoses, and demonstrates an equal distribution of subjects in

random sampling procedures used

each category.

‘M%

c:

such-on

.m

&amp;

Chlorpromazine supplied as "Thorazine" through courtesy of Smith, Kline
3 French, Inc.

�.3TABLE

I

PSYCHIATRIC DIAGNOSES

Insulin
Psychoneuresis

Coma

Chlorpromazine

1

2

10

10

Schizophrenia, Catatonic

7

7

Schizophrenia, Mixed

8

6

Schizophrenia, Hebephrenic

3

2

HaniooDepressive Psychosis

l

3

Schizophrenia, Paranoid

In the analysis of the age distribution, the
patients

was

21;

for the insulin

with a range of 17 to 38 ; while the chlorpromazine patients

had a median age of 28 and a range of 19-122.
shows no

median age

Here, too, the

distribution

significant. difference.

For both treatment groups, behavioral observations were made by the

research staff

at

weekly

intervals . Following completion of the treatment

period, reports of the patients' behavior were obtained from the therapist
and supervising

psychiatrist.

Medical Director

The "improvement"

at the patient's Discharge

four~fold scale of recovered,

rating

was determ‘ned by the

Conference and was based on the

much improved, improved and unimproved.

None

of the authors, nor the supervisor of the insulin therapy unit, participated

in these evaluations.

�Observatigns

1. Clinical Observations

all subjects. Overactive, destructive behavior rapidly disappeared,
patients

in

ghlgrpromazine: Chlorpromazine induced motor retardation

a)

became more

tractable, less negativistic

and

less violent.

and
The

therapists' records note patients as "less easily excited and
frightened," "cooperates better in ward activities," and "less restless and
less panic ridden." One-third of the patients were more sociable and less

nurses'

and

seclusive,

and were noted

fashion. In instances
patients

were

to dress.
modified

to care for themselves in a

more presentable

where severe motor symptoms supervened, however, the

less able to care for themselves;

Such periods were

usually short,

became sloppy and

significantly

and could be

either by a reduction in drug dosage or by anti-Parkinson drugs.

Affective changes during chlorpromazine were varied.
became

failed

increasingly agitated, tense

continue

on

and tremulous and

patients

either refused to

the drug regimen or were induced only with difficulty.

affective "storm" appeared early in the treatment
other patients, depressive

affective lability

and

symptoms were

medication was

persisted. In four

relieved, with

an

increase in

patients. The
continued, however, with an eventual alleviation. In most

mood changes were

Ideation

and

Such an

reaponsivity. Depressive ideation increased, assoc-

iated with complaints of insomnia

patients,

Fbur

was

and anorexia,

in

two

small.

dramatically altered during the period of chlorpromazine

therapy in twelve patients. Eight had a loss or a significant diminution of

their psychotic ideation. In five, hallucinatory

and

referential experiences

�.5.
inquiry

were no longer reported even on

once

in three others, delusional

patient, phobias were relieved and the
again participate in ward activities. In another,

ideas were less prominent. In

patient could

and

One

hypochondriasis was sufficiently modified to permit a more meaningful

relatedness of therapist
became more prominent.

and

patient. In

one

patient, paranoid ideation

This was associated with increasing anxiety and

panic during drug administration, and resulted in discontinuation of the
drug regimen.
b)

Insulin

similar to those reported
prominent in

all patients

clinical observations in this group'were
others (1). Alteration in behavior was

The

Coma:

by

once repeated comes were induced.

hostile behavior rapidly diminished,
of somnolence,

irritability and

and was replaced by

Overactive,

alternating periods

withdrawal. In most patients, nausea,

distress, belching, sweating and lassitude were common sequellae
each afternoon, and assumed prominence in the recorded reports. These
abdominal

symptoms often

interfered with the patient's ability to care for themselves,

and ﬂiey became unkempt

in their dress.

in ideation appeared slowly during the course of therapy. In
eight patients, paranoid and delusional thoughts became less prominent,
disappearing in these on direct inquiry. Suicidal and outwardly directed
destructive thoughts were modified in three patients, only to recur in each
Changes

at the

end of the treatment

Mood

period.

changes were small. Increasing

agitation, tension and panic were

reported in three patients, leading in two to a refusal of further therapy.
In one depressed patient,

relief of depressive

symptoms were noted

early in

�-6the treatment, and was sustained.
In the usual practice of the treatment unit, concurrent electroconvulsive
therapy

was

instituted

when

behavioral control by insulin

limited. In six patients, such

combined treatment was

coma alone was

instituted primarily

because of a continuation of overactive or delusional ideation.

There was,

in four instances, a well defined alteration in behavior, but this
sustained.

None

was un-

of these patients was rated as improved on discharge.

2. Discharge Evaluation
All patients were discharged from the hospital within four months

of the

end of treatment.

Table

for both the chlorpromazine

and

II lists the hospital discharge evaluations
insulin

coma

TABLE

treated patients.

I};

DISCHARGE RATINGS

Chlorpromazine

Insulin

1. Recovered

2

O

2.

much Improved

h

5

3.

Improved

17

15

h.

Uhimproved

7

10

Coma

Included in the unimproved group of chlorpromazine patients are four
who

received inadequate course of therapy (less than one month) because of

complications of the therapy.

four

Of

the ten unimproved insulin

had inadequate courses of therapy

(seizures, prolonged

-

coma

patients,

two because of complications

coma), one because she became more

fourth by administrative transfer to another facility.

disturbed,

and the

�-7.

It is

apparent that there

is

no

difference in the clinical evaluation

at the time of discharge between the insulin coma
treated groups. To determine whether this sample

and the chlorpromazine

its

was biased because of

small number, we compared these discharge ratings with a similar group treated

in this hospital in

1950 and previously reported

(2). In Table

III,

the

discharge ratings for both years are compared.
TABLE

Present Group

1950 Group

(30 subjects)

(h8 subjects)

0

1h%

17%

19%

Improved

50%

h2%

Ikrhmproved

33%

25%

Recovered
Much

The

III

Improved

percent improvement rates for each category are not significantly different.
3. Toxicitx and Complications
a) ghlorpromazine: Inherent in the design of this study were high

doses of chlorpromazine, pushed to symptoms of

toxicity. In this context, all

patients developed significant drug effects. Rigidity of extremities,

accom—

in facial eXpression, drooling and festination was
frequently observed. In three instances, rigidity appeared as drug dosage
was reduced. Host patients became drowsy, retarded, and less active in ward
panied by a decrease

activities. In four patients increased tension, agitation, restlessness
and excitement supervened, leading

in two.

to a discontinuation of the drug regimen

�-8Seizures occurred spontaneously in three patients. Pre-treatment
electroencephalograms had manifested no dysrhythmia and no history of

elicited. In
seizures did not develop at the

seizures

each, the drug medication was reduced, and

had been

lower dosages.

Dermatitis was a frequent complication. All patients developed a

transient erythema ato mild solar radiation. Severe intractable skin reactions
occurred in three patients, with resultant discontinuation of drug therapy
in two. In dze third, promazine* therapy was substituted for chlorpromazine,
with a
was

relief of the dermatitis.

The

indistinguishable in this patient

behavioral effects of the promazine
from

that noted for the chlorpromazine

group.

In

this

group, no patient developed

clinical jaundice. This complication

has been variously reported as occurring in less than

%%

of subjects treated **.

Electroencephalograms were obtained in twenty of the chlorpromazine

patients. With increasing doses, the modulation of the record
irregular in each.
activity

A

became more

moderate amount of low voltage h-7 cps delta and theta

was induced, and

this activity was exaggerated by hyperventilation.

There was a suggestive relationship between the degree of the induced slow
wave

activity
b)

series

were

and

the drug dosage;

Insulin

Coma: The

complications of insulin

not unusual. Insulin resistance

eventually overcome

by

the

method of

coma

therapy in this

was noted only once, and was

alternating dosages. Prolonged reactions

* Supplied as "Sparine" through courtesy of Uyeth

&amp;

Co.

as In the preliminary studies at Hillside Hospital, three patients of a group
of twenty developed transient clinical jaundice.

�-9occurred in three patients. In each, neurologic examination and electroencephalography demonstrated signs of persistent central nervous system

dysfunction for

paresthesias

at least ten days. Transient aphasia, hemiparesis,

were frequent

transient in eight others.
were recurrent in three. Frequent

in five patients,

Seizures occurred in five patients, and

and

secondary reactions, nausea, vomiting, abdominal

lassitude

and

and generalized weakness occurred

distress, sweating, pallor,

in all patients in varying

frequencies.
The

complications of both forms of treatment are

listed in

Table IV.

Certain effects, as dermatitis and hypotension, secondary reactions and prolonged coma are individual for each therapy, and seizures, agitation and

refusal of therapy were noted in both regimens.

The

frequencies of these are

not significantly different.
TABLE IV
COMPLICATIONS

Chlorpromazine

Insulin

Agitation and Panic

h

3

Dermatitis, severe

3

-

Seizures

3

5

Refusal of further therapy

2

2

Hypotension

2

—

Secondary reaction, frequent

-

5

Prolonged

Coma ( +

Insulin Resistance

6 hours)

3

l

Coma

�.10.-

h. Effects

on the Psychotherapeutic Relationship

In.this setting, patients are referred for insulin coma therapy
after a period of verbal relationship therapy. Such referral implies a
failure of interpersonal communication.
During the period of effective drug action,

treated patients were described

by the

fifteen of the

chlorpromazine—

therapist in re6ponse to an inquiry

as "more accessible," "Spoke more freely" and were "more amenable to psychotherapy."

subjects in

The

behavioral changes could be classified into two groups:

whom

tension and preoccupation with somatic

symptoms became much

hallucinatory or delusional preoccupations ended.
Such changes in relationship'were frequently described as an increase in
"contact." In thirteen subjects, psychotherapy was either still "not feasible"

less,

and those

in

whom

less feasible because of increasing, uncontrolled tension,
anxiety or preoccupation with the side effects of the drug regimen.
Similar observations were made in the insulin treated patients. Of the
thirty patients, seven were noted to be less tense and less anxious during

or had

become

therapeutic sessions.
more

freely"

The

therapists noted that the patient "verbalized

and "was mere aware of

his environment." Four patients

were

specifically treated with a "modified anaclitic" approach. In each instance,
this relationship was unsustained during treatment and the therapists resorted
to

more conventional

ive, educational
therapists

tactics. In the

remaining patients (19), while support-

and environmental manipulating techniques were

were no more successful than

applied, the

prior to insulin therapy. In eleven

patients, the physiologic effects of the treatments (secondary reactions,
sweating, nausea, vomiting and'weight gain) were reported as interfering with
psychotherapeutic attempts.

�-11Discussion

1. Clinical Considerations
In these patients neither chlorpromazine in high therapeutic doses
nor insulin

specifically modified the psychotic process. Since 88% of
these patients were diagnosed as suffering from schizophrenic illnesses, we
concluded thatiieither treatment has a specificity in altering the schizocoma

phrenic process.

shen given in adequate dosage, however, both treatments are

potent methods for u1e alteration of behavior.
the treatments are similar.

ioral patterns persistent

In only

and

others, the induced behavioral
Since these therapies

20%

rated as

of the patients were induced behav-

much improved

or recovered. For the

transient or minimal.

Chang 5 were

fail to

In the discharge evaluations,

induce a recovery from the psychotic

process, then consideration should be given to their ameliorative, palliative
and supportive aSpects.

Symptomatic

to the treatment period.

Patients

relief

was

frequent, but generally limited

were made uncomfortable by both

therapies,

however, and the complications and toxic effects have already been noted.

In assessing the role of concomitant psychotherapy, there is
advantage of

either therapy.

Both methods were

said to

enhance

little

relationship

therapy although the therapists' evaluations favored chlorpromazine therapy.
Excluding those who developed increased

agitation, patients were more comfortable, more alert and physically better able to discuss their feelings and
experiences while on chlorpromazine, than on insulin coma. It is clear that
"interpretive" psychotherapy is not enhanced, but rather supportive, educative,

re-orienting and directive types of therapy.

When

there is a modification

of agitated, hallucinatory, depressed, manic or aggressive behavior, than
both the

therapist

and

the patient arernore comfortable

and able

to discuss

�-12the

reality aspects of the life situation.

Therefore, in this context, the ease of administration and the possibility of continued maintenance of chlorpromazine in an outpatient setting
assumes decisive

significance.

To

maintain such therapy

after discharge

continue thereby the relationship established in the hospital setting
an important element in sustaining the behavioral changes induced by

and

may be

hospital-

ization.
2. Other Studies
While many

appeared,

we

reports of the treatment of psychosis by chlorpromazine have

are aware of only one similar comparative study. Boardman,

Lomas and Harkowe

one hundred

(3), after a review of the problem, report their study of

patients randomly divided into

two groups of

SO

and

treated either

insulin coma or chlcrpromazine. The chlorpromazine dosage was lower than
that in this series (average 300 mgm) but the drug period (3 months) was the

by

Their observations are directly comparable to

same.
no

difference in the discharge evaluations, nor in

this study.

They reported

assessments for

symptom

either treatment group.
The chlorprcmazine

treated patients,

box-raver, remained

in the hoslaital

less than the insulin treated subjects. This was a
significant difference between the groups. They concluded that: "There is
inconclusive evidence that chlorpromazine has advantages over insulin in the
an average of 6.2 weeks

treatment of schizophrenia," but "that insulin has disadvantages in the form
of greater danger and more unpleasantness
on

the nurses. Chlorpromazine is the

phrenia, but this conClusion
and has

is

for the patients

first

and

greater strain

treatment of choice in schizo-

based on the immediate

results of treatment

not yet been confirmed by an adequate follow-up study."

�«n13-

his co-workers emphasize the problem of evaluating the

Boardman and

therapeutic efficacy of insulin

coma.

They note a number of

raise doubts as to the efficacy of insulin

coma

reports that

therapy in schizophrenia.

(h), in an extensive review of the merits of insulin therapy in

Boume

is no proof of any Specific therapeutic
the long term prognosis is in no way influenced."

schizophrenia concluded that "there

effect,
he

and

recent observations of insulin treatment of schizophrenia by

Harris and

Oldham ( S)

Aclmer,

are relevant. In a carefully controlled study, young

schizophrenic patients were randomly treated either by insulin or by barbit-

urate

coma

results

in the

same ward and under

were made by

patients received.

similar conditions. Phraluations of

psychiatrists without

The

knowledge of which medication the

authors noted a similar

outcome whether the

loss

of consciousness was induced by a barbiturate or by

insulin, and concluded
that insulin was not a specific therapeutic agent in the outcome.
In the fol] oar-up studies in this hospital (2), the therapeutic results

for insulin

coma

therapy were disappointing. In that report, patients

ferred for insulin

coma had

re—

the longest period of hospitalization (6.50 months

for electroshock), poorest discharge rating
(3325 recovered. and much improved, 1?. 63:5 for psychotherapy and 67% for electroshock), and within four years, a 5015 re-hospitalization rate (compared to 33%
for psychotheram and 29% for electroshock). while these observations reflect

1g

6.0).:

for psychotherapy and

14.95

the observation that the more severely
coma,

it also

ill

patients are referred. for insulin

supports the belief that insulin

coma

is not

a specific treatment

for the patients referred.
From

these reports

and the passage of many

we would conclude

years, insulin

that, deepite considerable study

coma

therapy has not been

shown

to

�.mpersistent behavioral changes more frequently than other non~specific,
less dangerous and less expensive therapies. To the list of alternate
induce

therapies of limited value in the
chlorpromazine, noting, however,

management of psychosis we may now add

its

advantage of

lesser risk

and ease of

adninis tration .
3. Dosage of Chlorpromazine

for

For the purpose of assuring an adequate level of chlorpromazine

evaluation, the medication
This level was too high

duction in

was

increased in

all subjects to toxic levels.

fox-its behavioral effects, as evidenced by the re-

all responsive cases to

maintenance levels of 300 to 2000

mgm.

our impression that chlorpromazine affects the function of the
central nervous system (as evidenced by changes in.modulation and percent
time delta in the electroencephalogram and systemic phenomena of rigidity

It is

results in a non-Specific alteration in behavior. Such
behavioral change is varied and is dependent upon a.variety of factors, of
which the personality organization and the expectancy of the milieu are sigand

lassitude)

and

nificant. In this context, the induction of a state of altered cerebral
function is a necessary prerequisite to behavioral change.

The

only assurance

of achieving a therapeutic level, therefore, is the appearance of toxicity,
and a lowering of dosage from that level to a maintenance dose. The effects
of rigidity, drowsiness and lassitude, therefore, are necessary concomitants
of the therapy and should be induced in all patients in whom a therapeutic

effect is desired. In instances uhere an affective "storm" supervenes, continuation of the drug at higher levels, with concomitant artane and cogentin,
should be considered. Such an attitude in therapy is comparable to the application of digitalis in cardiology, and to the present concept of the
action of electroshock therapy (6).

mode

of

�.15Conclusions

1.

In a study of patients referred for insulin

open ward, voluntary

insulin

coma

psychiatric hospital, patients

coma

therapy in an

randomly received

either

therapy or intensive chlorpromazine therapy.

2. Chlorpromazine was as effective in modifying psychotic behavior as

insulin

coma

therapy.

There was no

difference in the

improvement

rating

on

discharge, incidence of complications or effects on the psychoﬂaerapeutic

relationship for either therapy.
3. In comparison to insulin
administer, and lends

itself to

coma, dilorpromazine

long term management.

is safer, easier to
Patients receiving

chlorprcmazine therapy arernore comfortable than those receiving

insulin

coma.

that either therapy has altered the
basic schizophrenic process; nor is there any evidence that there is greater
specificity of either form of therapy for schizophrenic illnesses.
b.

No

evidence has been educed

�REFERENCES

l.

Kalinousky, L.B. and Hoch, P.H.: Shock Treatments, Psychosurgery, and.
other Somatic Treatments in Psychiatry, Grune and Stratton,
13.15. 3 1952.

Rachlin, H.L., Goldman, (3.5., Gurvitz, $1., Lurie, A. and Rachlin, L.:
Follow-up Study of 317 Patients Discharged from Hillside
Hospital in 1950, J. Hillside Hosp. §_: 174.0, 195 6.
3.

Insulin and Chlorpromazine
Comparative Study in Previously Untreated
Cases, Lancet, Sept. 8, 1956, pp. 1:87—1:91.

Boardman, R.H., Lamas,

J.

in Schizophrenia -

and liarkma‘e, M.:
A

Boume, H.: The Insulin Myth, Lancet, Nov. 7, 1953, pp. 961;~968.
Ackner, B. , Harris, A. and Oldham, A.J.: Insulin Treatment of
Schizophrenia - A Controller} Study, Lancet, March 23, 1957,
pp. 607-6110

Fink,

1-1.

and Kahn, R.L.: Relation of ETTG Delta
Response in Electroshock: Quantitative

Arch. Neurol. and Psychiat. (in

Activity to Behavioral
Serial Studies, AJ'LA.

press).

�January 31, 1957

Subject:

Drs.

From:
To:

- Insulin Control

Chlorpromazine
Max

Study:

Interim Report

Fink, Robert Shaw, George Gross and Fred Coleman

Dr. Joseph S. A. Miller, Dr. Simon Kwalwasser and the
Research Committee of Medical Board
Following

insulin
During

is

a summary of the observations

in the control chlorpromazine-

study, instituted September 1, 1955 and completed January 1, 1957.

coma

this period,

59

patients

were

referred for insulin

coma

Half

therapy.

of the group was placed, by random sampling, on chlorpromazine * therapy

in-

stead of insulin coma. Four patients received both insulin and chlorpromazine
therapy.

of the patients

of therapy of

less than

who

received chlorpromazine, seven received courses

one month.

patients, three had an

of the 29 insulin

inadequate course of therapy.

I.

During the period l95h—1955, preliminary

PROHLEH:

azime resulted in the awareness
and

safe. In view of the unusually poor

trials of

that the drug

showing of

was

the insulin

chlorpromp

both potent
coma

populat-

ion in the 1950 Fbllowaup Study (1), and the appearance of numerous articles

in the psychiatric literature

recommending chlorpromazine as a therapy

schizophrenia, a comparative study of chlorpromazine
taken.

The

a)

- insulin

for

coma was

under-

following questions were postulated:

What

b) What

is the clinical effect of adequate doses of chlorpromazine?
is its therapeutic efficacy'when compared to insulin coma

therapy?
0)

‘Ehat are the

indications (and contraindications) for the use of

chlorpromazine and/or insulin coma?

* Chlorpromazine supplied as "Thorazine" through the courtesy of Smith, Kline
and French

00., Philadelphia.

Rachlin, H,L., Goldman, G.S., Gurvitz, M., Lurie, A., and Rachlin, L.:
Follow—up Study of 317 Patients Discharged from Hillside Hospital in 1950,
J. Hillside HOSp., _5_: 17-ho, 1956.
(1)

�«2.

II.

All patients referred for insulin

SUBJECTS:

coma

therapy during the

period September 1, 1955 and December 31, 1956 were observed.
Supervising psychiatrists

made the recommendation

independent of the research group. Their
by the

hospital administration,

patients
made by

coma

therapy

criteria were those implicitly held

and were not

were placed on chlorpromazine

for insulin

altered for this study. Selected

therapy.

selection

The

was random and

the supervising psychiatrist of the physical therapy unit, without

prior notice of the referring therapist.

III.

a.) Insulin nga;

EETEQQ:

standard technic of Sakel was used.

The

All patients received 50 comes, each of a duration of one
hour or longer

at the physiologic level

flex or deeper. Recovery
ous glucose.

of Babinski reflex or absent

was induced by gavage and

lid re-

occasionally by intraven-

Treatments were given five times weekly, for a period of 3-h

months.

b.) Chlorpromazin

: To

establish a complementary therapeutic

group, chlorpromazine was given for

at least three

months.

Dosages were determined by the research team and were rapidly increased

clear-cut physiologic effects

ifest rigidity, drooling,
ere dermatitis.

were observed. These included

and fixed

clinically

mans

facies; or toxicity, as seizures or sev-

In each instance, the drug dosage was slowly reduced

a maintenance dose,

until

just under toxicity,

was obtained.

until

This was maintained

for the duration of the observation period.
Laboratory
blood counts,

tests

were

carried out at irregular intervals

liver function tests, glucose tolerance tests

and included

and electroenceph-

alogramS.

In both experimental groups, behavioral observations were

made at'weekLy

intervals. Following completion of the treatment period, reports of the ther-

�4-3-

apist and supervising psychiatrist were obtained. The rating of "improvement"
Conwas that established by the Medical Director at the patient's Discharge
ference.
IV:

RESULTS:

Chlorpromazine

A.

l.

until signs

creased rapidly

of

was achieved

in daily dosages

to 3600

in

mgm.

2000 mgm.

one

patient.

of chlorpromazine was in-

The dosage

QEEEEE.22.22EQEEEEEEEEEEF

rigidity appeared. In most instances this
below lhOO mgm. although dosages were increased
The maintenance dose

varied from

300 mgm.

to

daily.

2. Clinical effects of chlorpromazine:
motor retardation in

all subjects.

Chlorpromazine induced a

Overactive, destructive behavior rapidly

disappeared, and the patients were more tractable, less negativistic and less
violent. The nurses' and therapists' records relate that patients are "less

easily excited and frightened," "cooperates better in
"less restless

and

less panic-ridden."

ward

activities,"

and

One-third of the patients were more

sociable and less seclusive, and were noted to care for themselves in a more
presentable fashion. In the instances where severe parkinsonism supervened,
however, the patients were less able to care for themselves; became sloppy and

failed to dress.
by

Such periods were

short or could

be

significantly modified

anti-parkinson drugsn
Affective changes during chlorpromazine were varied.

In four instances,

the patients became increasingly agitated, tense, tremnlous and either refused
to continue on the drug regimen or were induced only with difficulty. Such an

persisted.
In four other instances, depressive symptoms were significantly relieved,
with an increase in affective lability and responsivity. In two patients, deaffective "storm" appeared early in the therapy

and

�.u.
pressive ideation increased and was associated with complaints of insomnia.
The medication was continued, however, with an eventual alleviation. In most

patients,

mood changes were

small.

Ideation was dramatically altered during the period of-chlorpromazine
therapy in twelve of the patients. Eight patients had a loss or a significant
diminution of psychotic ideation. In five, the hallucinatory and referential
xperiences were no longer reported even on inquiry; and in three others,
delusional ideation was less prominent. In one patient, phobias were relieved

to a degree that the patient could participate in ward activities. In another,
hypochondriasis was sufficiently modified to permit of a more meaningful

latedness of therapist

and

re—

patient.

In one patient, paranoid ideation became more prominent. This was

associated with increasing anxiety and panic during drug administration, with
resultant discontinuation of the drug regimen.
3. Effects en the psychotherapeutic relationship; Patients are
referred for insulin coma therapy after a period of verbal relationship therapy. Such referral implies a failure of interpersonal communication.
During the period of effectiwadrug

activity, ten of the patients

were

described by the therapist in reSponse to an enquiry as "more accessible,"
"spoke more freely" and were "more amenable to psychotherapy." The responses
could be classified into two groups: the subjects whose tension and pre—

occupation with somatic

symptoms became much

less and those in

whom

halluc-

inatory or delusional preoccupations ended. In each instance, the therapist
described the change in relationship as an increase in "contact". In twelve
subjects, psychotherapy was either still "not feasible" or "less so because
of increasing, uncontrolled tension."

�-5.
In no instance did the problem of drug addiction or drug dependence
play a role, nor was there an appreciation that drug therapy altered the

therapeutic relationship adversely.
h. §g§igg§
twenty four have

left the hospital.

thirty patients in this series,

or the

93 "improvement":

Table

I lists

the number of patients

evaluated by the Discharge Conference, according to the four-fold classification in use in the hospital. For comparison, the discharge ratings of the

insulin

coma

therapy patients, following the
TABLE

same

criteria,

have been included.

I

DISCHARGE RATINGS

Chlogpromazine

Insulin

l.

Recovered

1

O

2.

Much Improved

3

1

3.

Improved

15

10

h.

Unimproved

S

8

Coma

Included in the unimproved group of chlorpromazine patients are four
who

received inadequate courses of therapy (less than one month) because of

complications of the therapy.

or the eight unimproved insulin

coma

patients,

four had inadequate courses of therapy - two because of complications (seiz-

ures, prolonged coma), one because she was a severe
the fourth by administrative transfer to the V. A.
5. Toxicity g£_chlorpromazine:

management problem; and

Inherent in the design of

were the high doses of chlorpromazine, pushed

to

symptoms of

this study

toxicity. In

this context, all patients developed significant drug effects. In all, rigidity of extremities appeared; frequently accompanied by a decrease in facial
expression, drooling and festination. In a number of patients the pafkinsona.

�~6—

ian features appeared as the drug dosage was reduced.
symptoms were

became drowsy,

relieved

when

retarded,

the drug

and

was

discontinued.

less active in

ward

In.each patient the
Almost

all patients

activities. In four pat-

ients, increased tension, agitation, restlessness and excitement supervened,
to a degree that led to a discontinuation of the drug regimen.
Seizures occurred in three patients. Ineaach, the drug medication was
reduced, and seizures did not develop

at the

lower dosages.

Dermatitis was a frequent complication. Severe, intractable skin reaction occurred in three patients, with resultant discontinuation of drug
therapy in two. In the third, promazine * therapy was substituted for chloru
promazine, with a relief of the dermatitis. The behavioral effect of the
promazine was indistinguishable

in this patient from the chlorpromazine group.

All patients developed a skin photosensitivity so that

on exposure

to sun,

transient erythema developed.
Refusal of further medication because of drug effects occurred in two

patients. Both developed severe tension and agitation. In two other instances, agitation resulted in the therapist insisting upon a change in treatment regimen.

Table

II lists the complications of both treatments. Certain effects

are individual to the type of therapy, as dermatitis for chlorpromazine; and
prolonged coma, severe secondary reactions and nausea and vomiting in insulin
coma.

0there, as seizures, fainting spells,

and increased

are seen in both.
*-

Surplied as "Sparine" by the courtesy of Hyeth and Co.

states of agitation

�'77“

II

TABLE

COMPLICATIONS

Insulin

_Chlorpromazine

Coma

“

Agitation

h

and Panic

2

-

Dermatitis, severe

3

Seizures

3

3

Refusal of further therapy

2

2

Hypotension

2

-

Secondary reaction, frequent

-

5

-

3

~

1

Prolonged

Coma (+

6 hours)

Insulin Resistance

In this chlorpromazine series, no patients developed clinical jaundice.
This complication has been variously reported as occurring in

less than

%%

of

the subjects treated.* Liver function and blood element studies were done

in this group of patients.

Changes were small, and

at the recommendation of

the medical consultant, the studies were discontinued.
Electroencephalograms were obtained

patients.
and

On

in fifteen of the chlorpromazine

adequate doses, a moderate amount of low voltage

theta activity

was induced.

This

activity

h—7

cps.delta

was exaggerated by hypervent-

ilation.

There was a suggestive relationship between the degree of the induced

slow wave

activity

and the drug dosage.

6. Adjuvants tg_Chlorpromazine:

With the development of

rigidity,

festination, and drooling, patients received cogentin or artane medication.
Both drugs relieved the symptoms, and in a few instances, to a significant
* In the

initial studies at Hillside

twenty developed

Hospital, three patients of a group of

transient clinical jaundice.

�-8degree. Concomitant with the

relief of the rigidity a feeling of euphoria

and wellabeing was occasionally noted.

In one of the patients

who

developed

effect.
therapy, anti-

an affective "storm" the administration of artane had a salutary

In patients

who developed

seizures during insulin

coma

convulsant medication (dilantin, phenobarbital) has been routinely employed.
Such agents were
on lowered

not used with chlorpromazine as the seizures did not recur

dosages.

Insulin

B.

Coma

Theragz

clinical effects, complications, the treatment results of insulin
ccma therapy have been exhaustively reported. In this series, twenty-nine
patients began insulin coma therapy. Of these, nineteen have completed their
period of hOSpitalization and ten are either completing their treatment perThe

iod or are awaiting discharge.
The

over-all ratings of

"improvement" are

listed in Table I.

When comp

pared with the Hillside HOSpital Follow-up Study of 1955, the percent improve—
ment

in each category is not significantly different, although the trend is

less optimistically than the 1950 group.
In Table III the percentages are listed for each evaluation category of this
to rate the present series

somewhat

group compared to the 1950 populatidn.
TABLE

INSULIN

III

COMA THERAPY

Present Group

E

1. Recovered

0%

2.

Much

h%

19%

3.

Improved

52%

h2%

h.

Unimproved

hh%

25%

Such a

Improved

difference in trend,

if

sustained,

1h%

may

reflect a variety of

factors, including changes in criteria of "improvement;" prior administration

�.9...

tranquillizing agents exerting a selectivity on the population
admitted to the hOSpital; and changes in staff criteria for referral for in»
of the newer

Sulin

coma

therapy.

complication rate in this insulin group is comparable to published
studies. No unusual complications, and no deaths were observed.
The role of psychotherapy in patients undergoing insulin coma therapy
The

is complex. In this group, four patients were treated with a "modified anaclitic" approach and an effort at establishing a working psychotherapeutic
relationship was made. In the remaining patients, no unusual efforts at psychotherapy were made, with the consensus

that a supportive, educative, enviru

onmental-manipulative, reassuring type of therapy was achieved, to varying
degrees. Therapists reported (in 7 instances) that patients were less tense

less anxious during sessions while in coma therapy. In eight patients
the physiologic effects of the treatment (secondary reactions, sweating, nausea,
vomiting, weight gain) interfered with relationship therapy to a significant
and

degree.
C.

Therapeutic Results in Relation to Final Diagnosis
Table IV lists the final diagnostic categories for the patients in

each group.

All diagnoses were represented in each series with an equivalent

distribution.
TABLE

IV

EBYCHIATRIC DIAGNOSES

Insulin

Coma

Chlorpromazine

Psychoneurosis

l

2

Schizophrenia, Paranoid

0\

we

U1

O\

U1

\n

\»

to

+4

DD

Schizophrenia, Catatonic
Schizophrenia, Mixed
Schizophrenia, Hebephrenic
Manic Depressive Psychosis

�~10—

No

diagnostic group had a significantly better treatment response than

any

other with either form of therapy.

V.

DISCUSSION:

A.

Comparison of Chlorpromazine and

Insulin

Coma

Therapies:

Neither chlorpromazine in high therapeutic doses, nor insulin
are Specific treatments for schizophrenia.

The discharge evaluations

both treatments are not significantly different. There

is,

coma,

for

however, a def-

inite tendency for more patients in the chlorpromazine group to be rated in
the better classifications than in the insulin coma group. The trend assumes
significance

when

both the type of sampling and the qualitative aspects of

the treatments are taken into account.
the

The random sampling

is exemplified by

resultant matching of diagnoses.
Since these treatments have not resulted in a recovery from the psychotic

process, then their ameliorative, palliative and supportive aSpects must be
considered.

The

insulin

coma

patients are usually uncomfortable throughout

their treatment period. Nausea, vomiting, secondary reactions,
are

Prolonged coma

common.

loss of

is

a

and drowsiness

realistic threat; as well as the threat to

life.

The chlorprcmazine

patients also suffered considerable disagreeable side

effects. Parkinsonism, drowsiness,

and skin

reactions are significant,

must be considered as concomitant management problems.

and

Seizures and jaundice

are the most severe reactions, and to date, have not been permanent.

It is

possible to modify the significance of these side effects to a considerable
extent by anti-parkinson and anti-convulsant medication.
There

is no question, furthermore, as to the ease with which chlorprom-

azine can be administered, in contrast to insulin coma.
A

significant element in the use of these agents in the therapy of schiz-

�.11...

ophrenia is concomitant psychotherapy. Such relationship therapy
by both

It was

therapies.

apparent in the therapist's evaluations, however,

that the chlorpromazine regimen was
apy.

Patients, excluding those

comfortable,

alert

iences while

on

and

was enhanced

more conducive to concomitant verbal

who developed

ther-

increased agitation, were more

physically able to discuss their feelings and exper-

chlorpromazine, than insulin coma.

In another respect, the ease of administration of chlorpromazine

advantage. Patients

who respond

to drug therapy can

is of

be maintained on such

therapy for as long as needed, even on an outpatient basis, while the "course"
of insulin coma

is limited.

Are these treatments equivalent?

Can one be

substituted for the other?

While these questions cannot be answered by the data

the negative can be denied.
groups are not

The

in a positive assertidn,

results of these treatments in equivalent

different with regard to the discharge evaluation.

The changes

in behavior noted and the symptoms alleviated are not significantly different.
In this series, three patients had adequate courses of both regimens. Two
have been discharged"improved," and the third is still in the hospital. There
has been no

significant differences in their reSponse to either

form of therapy.

Comparison With Other Studies:

B.

While many studies of chlorpromazine in schizophrenia have appeared,
only one report of a controlled study

is available.

gt_al_ (2)
after an excellent review of the problem, report their results in one hundred

patients,
coma

randomly divided

into

two groups

of

SO

and

Boardman,

treated either

by

insulin

or chlorpromazine. Their chlorpromazine dosage was lower than in this

series (average

300 mgm) but the drug period ( 3 months ) was the same.

Their

observations are directly comparable to this series. They noted that the over(2)

et a1: Insulin and Chlorpremazine in Schizophrenia —
Study
of Previously Untreated Cases, Lancet g5 h87-h9l,
Comparative
(September) 1956.
Boardman, R.H.

A

�all clinical results were slightly more

favorable in the chlorpromazine group

than in the insulin group judging both by interview status and by a rating

scale of

difference was not of high statistical signif-

The

symptom change.

state, however, that the chlorpromazine patients remained in
the hospital an average of 6.2 weeks less; and that this difference was statistically significant. They concluded that: "There is inconclusive evidence

icance.

They did

that chlorpromazine has advantages over insulin in the treatment of schizophrenia," but "that insulin has disadvantages in the form of greater danger and
more unpleasantness for the patients and greater strain on the nurses.
Chlorpromazine is the first treatment of -choice in schizophrenia, but this
conclusion is based

on

the immediate results of treatment

and has not

yet been

confirmed by an adequate follow-up study."

In Boardman‘s review, due cognizance

therapeutic efficacy of insulin

come.

He

is

given to the problem of the

notes the number of'dissident re-

ports that raise doubts as to the role of insulin
In this regard,

for insulin

it is

therapy in schizophrenia.

important to note the results of the Hillside Follow-up

in which patients referred for

coma,

coma

such therapy had the

period of hOSpitalization, poorest discharge ratings, and a

ization rate (compared to

33%

for psychotherapy

and 29%

50%

longest

rehosPital-

for the electroshock

therapy groups).
Two

other control studies of chlorpromazine in psychoses are relevant

to this report.
"blind" study
ment

at

Feldman gjgggp (5)
Topeka

reporting the observations in a controlled,

State HOSpital noted a significant degree of improve-

for chlorpromazine. They&lt;eoncluded that "thorazine

was found

to be

useful in converting acutely disturbed psychotics into tractable, accessible
patients

who could

(S) Feldman, P.E.

then participate more actively in the hOSpital rehabili-

et al:

A

Controlled, Blind Study of Effects of Thorazine
Clinic, a9; 25-h7, 1956.

on Psychotic Behavior, Bull. Men.

�.13...

tatidn program." Tenenblatt

and Spagno

(6), describing the St. Elizabeth's

Hospital eXperience, in another control study, noted significant behavioral

effects in psychotic illnesses other than involutional psychoses.
Effect of Study

D.
An

on

Staff:

inherent factor in a control study of any therapeutic modality is

the effect that the knowledge of random selection of patients or the use of
placebos has on the therapist in his choice of therapy.

sulin

coma

referrals were to

be given

Knowledge

that in-

either chlorpromazine or insulin

coma

created a feeling of insecurity and impotence in the therapist. Their control
of the therapeutic situation was

in a decrease in the
drug

effects,

and

number of

felt

as severely constricted.

This resulted

referrals, an exaggeration of the physiologic

in the patients expressing doubts as to the therapeutic

efficacy of the drug despite significant changes in

ward behavior.

On

numer-

therapists called to enquire which therapy their patient,
referral for ICT had not yet been made, would get. Prior prejudice

ous occasions,
‘whose

suitability of either therapy resulted in the therapist's expressing disappointment at the modality used. In two instances, such preabout the

judices led to early discontinuation of chlorpromazine therapy,

when the

pat~

ient experienced eanLy signs of drug effects.
E. Dosage of Chlorpromazine:
For the purposes of assuring an adequate level of chlorpromazine for

evaluation, the medication was "pushed" in
level
in

was too high

all

all

subjects to toxicity. This

for its behavioral effects, as evidenced

responsive cases to maintenance levels of

by the reductidn

hOO-lOOO mgm.

The

effects

of parkinsonism, drowsiness and lassitude are prdbably necessary concomitants
(6)

Tenenblatt, 3.8. and Spagno, A.: A Controlled Study of Chlorpromazine
Therapy in Chronic Psychotic Patients, Quart. Rev. Peych. &amp; Neurol.,

�1":114-

of the therapy; and should be induced

effect is desired. In instances where

in all patients in
an

whom

a therapeutic

affective "storm" supervenes, con-

inuation of the drug at higher levels, with concomitant artane or cogentin,
should be considered.
VI.

CONCLUSIONS:

In a control study of patients referred for insulin

coma

therapy,

chlorprcmazine therapy was found to be as effective in modifying psychotic

behavior patterns as insulin
charge ratings to be

coma

therapy.

is

There

better for the chlorpromazine

a tendency for the

group than

dis-

for the insulin

coma group.

In comparison to insulin

coma

to administer, more controllable in

therapy, chlorpromazine is safer, easier

its effects,

and has fewer side

effects.

that either therapy has altered the basic
schizophrenic process; nor is there any evidence that there is greater specificity for either form of therapy for schizophrenic illnesses.
No

evidence has been educed

�February 3, 1958.

that at
a

bucuti

1..

t

:1

1251

:

or EEG Dona Maturity to Bohuioml
Quaint-Adv. 801-111 Studiu, “Hg, .
kaponn in metro-hock:
a:
Arch.
chhnt. 18; 516-525. 1957.

Fink,

H. and Kuhn,

my

a.L.s

3818321511

.

Mime

ﬂux-spin,
Units.“ Theory of the Action of
1957.
197-306.
g. Hillside 3032. 9:
ILL: Significance of Individual Variability in ma human to
moctmlhock, g. Bullio- Raga. Q: 229-21“), 1957.

link,

91.: A

3.

m,

h.

Join,

5.

Kuhn, 3.1.. and

$.

him, 8.1...

J.

«In An

abacus.” Study of Went-.1031

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_

PAGE

AAAS ........................................................ 5, 394, 396, Inside Back Cover

American Tobacco Company _____________________________________________________ Back Cover
Columbia University Press _____________________________________________________________________

6

Ford Instrument Company ______________________________________________________________________ 391

International Equipment Company _____________________________________________________ 398
Johnson Research Corporation..--__________--_.____-________________-_.-____; ______________ 5
Macmillan Company _________________________________________________________________________________

8

Measurements Corporation _____________________________________________________________________ 6
Microcard Foundation _____________________________________________________________________________ 392
Oxford University Press, Inc ________________________________________________________________ 391

Rinehart &amp; Company, Inc ________________________________________________________________________ 394
Ronald Press Company ___________________________________________________________________________ 2
Schwarz Laboratories, Inc ______________________________________________________________________

4

Ivan Sorvall, Inc ______________________________________________________________________________________ 7
Taconic Farms, Inc __________________________________________________________________________________ 394

University of California Press _______________________________________________________________ 393
University of Chicago Press ___________________________________________________________________ 3
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Gamept of Gamma]. Localisaﬁm to Hana Action Effects
1) Certain functionnascribod to

CNS

are "localiaable", as

motor power, motor aphasia; while others, an memory. Judgment,

Mm,

insight, m1-

culation, figure-ground, m nmlocaliuble. The first. greup am aortical
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have maimed

exam;

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is usually

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The

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offset, plus the localised defect.

�J.A.M.A., Dec. 13, 1958

PNEUMOTHORAX—MAURER ET AL.

2014

ination revealed adherence of the fundus and nodules
throughout the adnexa. A diagnosis of pelvic endometriosis
was made, and on Aug. 18, 1955, total hysterectomy with
bilateral salpingo-oophorectomy was performed. The patient’s postoperative recovery was again uneventful. In the
four and one-half years after the thoracotomy, the patient
has had no recurrent chest symptoms or pneumothorax.

Comment
Aberrant endometrial islands have been reported
in many locations, including the ovaries, uterine
ligaments, rectovaginal septum, sigmoid colon, urihernia
umbilicus,
bladder,
laparotomy
scars,
nary
sacs, appendix, vagina, vulva, cervix, lymph glands,
and small intestine, and in bizarre locations, such
as the upper and lower extremities, lungs, and
pleura.l Sampson’s2 original theory of transtubal
regurgitation of menstrual blood and endometrial
particles, published in his original paper in 1921,
could certainly explain the method of implantation
of endometrial growths on the pelvic and intraabdominal viscera, as well as on the inferior aspects
of either leaf of the diaphragm. The lymphatic and
hematogenous dissemination theory of Halban
would be necessary to explain distant endometrial
implants in the thigh, lung, and pleura.1a Distant
spread without passing through the pulmonary
capillaries could occur only by way of the vertebral
veins or “lung shunts” which have apparently been
demonstrated between the pulmonary arteries and
veins bypassing the lung capillaries.
In view of the concomitant ﬁnding of pelvic
endometriosis and the involvement of all layers of
the right leaf of the diaphragm, with perforation
and supradiaphragmatic seeding demonstrated by
thoracotomy, in the present case report, it would
seem logical to conclude that the endometrial
involvement of the diaphragm must of necessity
have occurred as the result of transtubal regurgitation and transperitoneal dissemination. Exact explanation of the method of development of the
pneumothorax on the right side is more difficult.
However, the clinical observation that all episodes
of pneumothorax occurred only during the time of
menstruation, and the inability to demonstrate any
source of lung leak or primary disorder in the lung
which could explain any possible leakage of air into

the pleural cavity, would suggest that the recurrent
pneumothoraces in the case reported here were the
result of erosion and perforation of the right diaphragmatic leaf by endometrial implant and the
fa]of
the
from
the
of
air
by
uterus
way
passage
lopian tubes into the peritoneal cavity and then by
way of the opening in the diaphragm into the
pleural cavity, with consequent pneumothorax. Although we are unable to ﬁnd any reports of spontaneous pneumoperitoneum occurring during the
menstrual cycle, the practical possibility of this is
suggested by the free anatomic communication between the cavity of the uterus with the peritoneal
space by way of the fallopian tubes. Practical application of this knowledge is regularly used in the
so-called Rubin test for patency of the tubes. During this procedure, carbon dioxide is passed into
the uterus and then by way of the tubes into the
peritoneal cavity. During the test, patients may
experience shoulder pain and present roentgenographic evidence of pneumoperitoneum.
Summary
Chronic recurring pneumothoraces resulting from
erosion of the diaphragm by endometrial implants
during periods of menstruation occurred in a young
woman. This was surgically corrected by excision
of the involved portion of the diaphragm. The un—
anticipated ﬁndings encountered at operation in this
patient present an additional indication for exploratory thoracotomy in all cases of unexplained, constantly recurring, spontaneous pneumothorax.
827 Union Central Bldg. (Dr. Maurer).

References
1.

(a) Novak, E., and Novak, E. R.: Textbook of Gyne-

cology, ed. 5, Baltimore, Williams &amp; Wilkins Co., 1956,
p. 546. (b) Nunn, L. L.: Endometrioma of Thigh, Northwest Med. 48:474—475 (July) 1949. (c) Hartz, P. H.: Occurrence of Decidua-Like Tissue in Lung: Report of Case,
Am. J. Clin. Path. 26:48-51 (Jan.) 1956. (d) Hobbs, J. E.,
and Bortnick, A. H.: Endometriosis of Lungs: Experimental
and Clinical Study, Am. J. Obst. &amp; Gynec. 4:832-843
(Nov.) 1940. (e) Nicholson, H.: Endometriosis of Pleura,
Thorax 6:75-81 (March) 1951.
2. Sampson, J. A.: Perforating Hemorrhagic (Chocolate)
Cysts of Ovary, Arch. Surg. 3:245—323 (Sept) 1921.

FUNCTION OF THE BRAIN.-—Any biological view of the function of the
brain leads us to an unavoidable conclusion: consciousness is not unique to man,
to the primates, or to the mammals: it goes back to the roots of vertebrate history and has been progressively elaborated in content, coloring and complexity roughly in proportion to the evolution of the neuromuscular system. It cannot even be
argued that consciousness is a unique vertebrate invention—the crab, the octopus, the
butterﬂy, the ant, all possess sensory devices imparting to them the awareness of their
world; all demonstrably engage in integrated time-binding, self-serving action, and it
must be presumed that all participate in some proportional measures in conscious
awareness of themselves and their environment—H. W. Smith, The Philosophic Limitations of Physiology, Perspectives in Physiology, Washington, D. 0, American

THE

Physiological Society, 1954.

�2013

Vol. 168, No. 15

TO
DUE
PNEUMOTHORAX
SPONTANEOUS
RECURRING
CHRONIC
ENDOMETRIOSIS OF THE DIAPHRAGM
Elmer R. Maurer, M.D., James A. Schaal, MD.
and

F. L. Mendez Jr., M.D., Cincinnati
Chronic recurring spontaneous pneumothorax is
results
which
disorder
usually
common
relatively
a
from rupture of subpleural blebs. Endometriosis of
the diaphragm, on the other hand, is an exceedingly
has
be
determined,
lesion
as
and,
nearly
can
as
rare
never been reported in association with, or as a
cause of, unilateral recurring pneumothorax.
The following case report is presented because
of the extreme rarity of the lesion involved and the
unusual association of pneumothorax with the menstrual cycle. It is the ﬁrst recorded instance of successful surgical treatment of chronic recurring pneumothorax by excision of a defect in the diaphragm
that has resulted from endometriosis.

communicated
This
diameter.
in
2
cm.
was an aperture

freely with the peritoneal cavity. The area of disease in the
diaphragm, along with the defect, was widely and completely excised. The consequent diaphragmatic opening was
0.
size
of
cotton,
sutures
mattress
with
interrupted
repaired
Examination of the specimen showed that the disease had
involved the complete thickness of the diaphragm. Final
inspection of the superior surface of the diaphragm revealed
which
1
in
diameter,
nodule,
cm.
purplish-red
a solitary
obviously represented a supradiaphragmatic endometrial
implant. This also was completely excised. Following reexpansion of the lung and the placement of an intrapleural
catheter for water seal drainage, the chest wall was closed
of
endometriosis
diagnosis
was
The
postoperative
in layers.
the right leaf of the diaphragm resulting in perforation and

Report of a Case
A 35-year-old woman was ﬁrst seen in consultation on
March 13, 1953, because of pain and dyspnea resulting

from a spontaneous pneumothorax on the right side. The
patient had had two previous spontaneous pneumothoraces
1952.
Nov.
14,
occurred
ﬁrst
on
the
having
the
right,
on
Findings on the general physical examination were negative
except for distant breath sounds over the upper right part
of the chest and hyperresonance of the percussion note due
revealed
chest
of
the
Roentgenograms
pneumothorax.
to a
a very minimal pneumothorax (15%) over the extreme apex
and the base of the right lung. No emphysematous blebs
were apparent in any portion of either lung. Because of the
small quantity of air in the chest and the absence of serious
thoratube
thoracentesis
or
of
air
the
by
removal
symptoms,
costomy was not thOught to be indicated. The patient was
discharged from the hospital for follow-up care by her attending physician. She was again seen in consultation on
March 20, 1954, approximately one year after the original
examination, because of 12 new episodes of recurrent pneumothorax on the right side. All pneumothoraces were associated with pain and mild dyspnea and had been veriﬁed
ﬁrst
the
chest.
For
of
the
examination
by roentgenographic
15
all
that
information
the
volunteered
the
patient
time,
episodes of spontaneous pneumothorax had come during
the period of menstruation. The important clinical signiﬁ—
time.
the
at
appreciated
not
observation
this
of
was
cance
Because of the chronicity of the lesion, open thoracotomy
with possible talc poudrage and excision of any blebs that
examinaroentgenographic
been
on
have
apparent
not
may
tion was recommended.
Right thoracotomy on March 31, 1954, revealed a persistent moderate pneumothorax on the right side. Careful
examination of all lobes of the right lung revealed no evidence of blebs. Testing of the lung with positive pressure,
while saline solution was dripped over the surface, disclosed
no points of air-leak. The lung parenchyma grossly presented a normal appearance and consistency. The most re—
markable ﬁnding involved the right diaphragm. Near the
point of emergence of the inferior vena cava and extending
radially and laterally in the central portion of the right leaf
of the diaphragm was a circumscribed, oval-shaped area of
attenuation which measured 4 by 3 cm. in diameter. Numersurface.
this
modulations
on
apparent
were
purplish-red
ous
In the central portion of the diseased area in the diaphragm

Photomicrograph of excised lesion, showing, endometrial
stroma and glands extending through ﬁbromuscular structure of diaphragm.
implant of endometrial nodules on the intrathoracic surface
of the diaphragm. Microscopic examination of the surgical
specimen showed extensive involvement of the ﬁbromuscular
stroma of the diaphragm by nests of endometrial stroma and
glands (see ﬁgure). The single nodule on the supradiaphragmatic surface was composed of endometrial tissue.
The postoperative course of the patient was entirely uneventful, and she was discharged from the hospital on her
ninth postoperative day, being afebrile and ambulant, and
with her right lung completely expanded.
Because of pain in the pelvis and dysmenorrhea, the patient was seen by a gynecologic consultant. Bimanual exam-

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                    <text>October 11, 1970
Dear Dick,
The 8-10 p.m. slot is fine. As for the additional
slot for “less formal interactions", I would hesitate to
commit myself—— after all, the daytime was meant for skiing, and
I suspect that the after 11 p.m. time will be the best for

daytime

interactions.

My

best regards.
Sincerely yours,
Max

Fink,

M.D.

�</text>
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                  <elementText elementTextId="105366">
                    <text>..

..

.,

&lt;

u

.4-

.

,
.

Fvw“

~nmw-m~W¢—v

~

w

“urn"

._.v.«

V.

..

Jammy

3,

1967

Assistant to the Director
Natimal Library of Medicine
8600 Rockville Pike
Bethesda, Maryland 2001“

Dear Sir:

Imuldbemtefulfwowiuofthepﬂotissues
wblished
BibLLagMphy 05 Mailed

of the
v-w

by NIH and

A-

Ream, recently
as described in a meant issue of Science.

V

~

y
&lt;-.

Thank you

for yum cooperatim.
Sincerely yams,

,rcpwwug—mwr

w
.7.

yup-4.»;

4
~

"

Max

W’

*"WWHWJ‘

W'II'W'WE'

“7-“?

—:

'rrma

'

Fink,

PM).

Professor of Paycmatry

Wzkp

�</text>
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.

"hm

:z'wrru,....-r.

December 22, 1969

4r

Dear A1,
-.

'WF’VM;'\

‘Y’Mi‘

com

v-vanhgrgwmmw

Don Klein of Hillside has asked if he could have
urine samples from our chronic marijuana subjects since

his chemist is trying to develop tests for
objection and Arthur sees no problem.
Any

THC.

reason not to cooperate?

.

Max

Fink, M.D.

I saw no

�</text>
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                    <text>June 13, 1971
Dear Andy,

I have reviewed your
arranged the following:

and

'

applications

and

have

Your appointment as Assistant Professor, effective
at an annual salary of $28,000 minimum (although

November 1, 1971

if my

letter

budgets are approved,

Your appointment

it will be

$30,000).

to the

an appropriate research
and the exact amount of
work
will
itself out in the

V.A.

at

staff position, the exact title is unclear,
salary

from them

next few

eeks.

is unclearn~ but that

By discussions with the V.A. authorities in washington, we
have a committment for a drug abuse treatment center for July, 1972;
and possibly for July, 1971. Alternatively, if I wish it, they will
entertain an application for a drug aabnse demonstration project
effective almost immediately. In either of these cases, the
research budget is likely to be very large, in the order of
$300,000 to 400,000, making your program the most heavily supported

one in the Division.

The petitions you have requested are signed and will be
processed through the medical college. Copies will be sent to you
as they are signed and approved.
The V.A. cannot make you a

full staff

memeber until
assured them that

you have a license to practice medicine. I
it was
your intention to take your examinations promptly and indicated that
you should be licensed by the end of 1972.
Keep

well,

and I look forward to your

joining

Sincerely yours,
Max

Fink,

M.D.

us

in

New

York.

�</text>
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                    <text>Septemebre 10, 1971

Dear Andy,

I spent 6-days in Europe,
exhausted, returned to find your
some maneuvers

for you.

two

in Washington, and

letters,

First, as to your questions.

and to the Department of Psychiatry,

somewhat

and immediately

tried

Your appointment to the V.A.

should,like all appointments at

the medical school, be independent of me or any other person—all appointments are for an indefinite term, and while tenure
is granted only after five years service, there are no discharges
of staff members except with an extensive warning.
to the visa, I called Washington and after

As

many

calls,

reached the best office. I indicated that your appointment to the
VA was in the national interest since you are coming to develop
a drug addiction treatment program focussed on the returning

Viet—Nam

file

a

veteran. Under these conditions,

special

will allow

"Temporary 'H"

petition"-~

it is

and

if

possible to
approved,

it

you to come to the states, and wait here for the
permanent number to be assigned. At that time, you will have
to visit the immigration offices (possibly in Washington) for
certain formalities. With this information, I am prepared to
file this petition on your behalf, and will do so as soon as it

is received.

The State Board problem is more thorny. Dr. Volavka has
struggled with the Board, and I would defer your questions to
him. As he is in Athens for a.few weeks, I will hold up this
inquiry until he returns, and ask hint to answer you.

I do not know about bathelo quarters at either location,
but will defer this inquiry also until some data is established
and then can ask

specifically.

In Washington this week, the principal question was the
ways to expedite the development of a narcotic antagonist
of long duration and to improve on the available drugs. Funds are
available, and should your enthusiasm not flag, I am confident
that we can build as strong a program as your energies will allow.

best

I am up to my eyeballs in work; and on top of it all, am
planning to return to Europe on September 21 for two or three
weeks. Our projects in Athens are doing very well; and the work
will be expanded to Jamaica this winter. I look forward to your
joingng the group-- I now have four fine co-workers in clinical
programs, and three experimentalists-- my best group ever.
Our

best to Betty.
As

ever,

�</text>
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                    <text>October 31, 1970
Dear Arnie,

Please pay the Hotel Hilton (attention Mr. Paul Steiner)
final charge for the 1970 meeting. Letter enclosed.

$137.42 as the

Please send a list of members, as of the latest date,
to Dr. Charles Shagass for the membership committee; to Jon Cole,
for the Nominating Committee; and to the AMA (address attached).

If you have an urge to invest some of the cash of the
Association, I can arrange to obtain Treasury Billaa for 91 or 182

dollar lots. It seems that you will have no
until late February, and if you wish to buy 91 day
bills, call me. There is no reason to touch the savings accounts;
and the securities are probably in as good a shape as one could
find. It is not prudent to invest in straight securities (the amount
being small) and other funds will do no better. I would suggest,
however, that additional funds be used to invest inn other securities,
and that dependence on one fund is unwise. In March, after the
returns for the meeting and membership are in, we can discuss the
possibility of selling some of the Lehman stbck (they pay their major
days

in

multi—thousand

major eXpenses

dividend in the spring) and investing in another fund.
Peace.

Sincerely yours,
Max

Fink,

M.D.

�</text>
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                    <text>March 12, 1970
Dear Bob,

It

last wrote. The
studies are still exciting papular interest, with many reprint
has bean sumo weeks since you

requests continuing to coma in. There are also kooky
some of which I have sent on to Mickey.

letters,

I am enclosing Carl Ffoiffer's lotto: to you-» he aunt
it to the Biological Psychiatry, but it is meant for both of you.
As he in an oxpotioncod investigator with an extensive exporieoco
in schizophrenia, I enjoyoé his report ané on sure you will also.
you

Surely, this work should be continued, and I hope that

will plan to continue as soon as this chore in over.

Will you be able to come to San Pranoioco ? If so, the
Biological Psychiatry meetings are May 8~10 at the San Francisco
Hilton. I hope that you will be able to join us for dinnod sumo

evening.

.

.

Stanley has some of your work dooen- I asked in response
to Mickey a request, but it is unclear what has to be done next.
I suggested you or Mickey write directly to him. ané I am sure

he

will answer.

_

There is much that is going on here~- tho College is
increasing the paoo of its discussions of the move to Westcheoter;
our affiliation with Kirby Hospital (1/3 Manhattan 3toto) has
progressed to the joint appointmont of the new director (a former
student of mtno, Mort Woohoproao); and our contract for studies
in Athens has boon approved.
Stay out of miaohiof.

Sincerely yours,'

�</text>
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                    <text>November 29, 1970

Dear Bob,

It

and I am

has been some time since

we

have heard from Texas,

writing to bring you up~to~date with the programs here, and
to ask if your plans for 1971 are sufficiently clear to be discussed.
I have just written to Mickey, and have offered him a position in
the Division.

wuw

wmypwwr.

»

1";"0‘merélwmw‘

During the past month we have negotiated an agreement
with Albany that permits us to assume responsibility for Kirby
Hospital-- training and research- and the necessary clinical
programs. We plan to start with the MMHC units (5 &amp; 6): we will
name the unit directors, send residents from the MMHC pool, and
be responsible for teaching and treatment. The director will be
Kesselbrenner, who will be part of the NYMC faculty. We asked to
have the funds through the College but this was refused, and
we will appoint to their budgets. All appointments will be joint, and
for the two units the appointments will be to the Division of Biological
Psychiatry.

1,2,3 or

We

do

not

know whether we

will divide the

4

units into

number depending on the staff we can recruit
and the type of research programs we wish to start. ECT and penicillamine
4

sections, the

are already projected;
Would you

studies are in the planning stage.
like to join this Division this summer ?
new drug

If so, I will be pleased to

work out the details. (There are so many
other projects in the works, that the choice is a good one, now that

we

have some funds
Keep

again).

well,

and

write soon.
Sincerely yours,
Max

Fink, M.D.

�</text>
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                    <text>,.

ww- .

WWW-”1|.“r:-.--_-n;.T-.--

_~,_3

.

'

"WWW
&gt;

,

~

,

,

»

‘w-w “WWWIWWWIM gym—saw» .mw.~w-»wv-at”- 1,... .M V ,W "wt.

‘,__,_,

“f,

V”

.,

..

,.

.
.7—

,

June 28, 1970
&gt;‘nm’mvvmwv'qlmev-wun

Dear Dick,

-—m’n-w—Mn~w.mqr‘u

«4

r

With reference to the
for membership:

ACNP

request regarding nominations

I would like to nominate two of my associates, whose
work is well known to me, and who will be able to make significant
contributions to the College:

1.:“unwm

Jovan Simeon, M.D.- Assistant Professor at the
New York Medical College. He has been working with me since 1966,
and is now a project leader, working in adolescent and child psychopharmacology.
Ali Keskiner, M.D.— Associate Professor, University
of Missouri, St. Louis. I have known his work since he joined
the Missouri Institute of Psychiatry in 1965. He is an independent

investigator in schizophrenia, with particular interest in rehabilitation

-

..

wrwnr.

as

it

is enhanced by psychoactive drugs.

In addition, there are three young men at this College
independently and should be candidates in the
are
next few years:

who

now working

Richard Abrams, M.D.

Arthur Zaks,

M.D.

Richard Resnick, M.D.

Dr. Keskiner

have already seconded the nomination of
year; and will recommend Dr. Simeon next year, if

I believe that I

this

this is permissible.

Good luck

!

Sincerely yours,
Fink, M.D.
Professor of Psychiatry

Max

I

�</text>
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                    <text>usxonannux

March 24, 1972

Mrs. Ebert

T0:

—

EH34:

Dr. Max Fink

SUBJECT:

Painting

As

per our

memo

Maintonance

of March 15. requesting painting of room 42A

and Lab 42A; please add to

5;, to b. painted in the

this request,

same color (very

room 42 and Agboratogz

light blue).

Charge 39-270-0.

‘.

.
'l.\.u

.—

,-V.‘.\4

‘

MiaLh—h‘

‘

I
*Wkﬂgiﬁw

�</text>
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                    <text>w-

March 14, 1985
Dear Gerry,
Thank you for your note about answering public inquiries.

accordingly.

it

I

will act

Please accept this copy of Feynman's book, with my compliments. Ifound
that l have sent a few out to some friends.

so delightful,

also enclose a newsletter sent me by Arnold Mandell. For the past 20
years, Arnold Mandell has sought the Rosetta Stone to psychiatry in mathematical
models of brain function. i have always found him obscure and confused, and he has
always presented himself as a California guru. His messages have left me
unimpressed. But he has been named to every prestigious award, including a
MacArthur brilliant scholar, so I have had to temper my reactions with the
admonitionJhat my lack of appreciation is probably a fault of mine. After all, he
could not total all the awards committees, or could he? As a founding fellow of the
American College of Neuropsychopharmacology —- a self proclaimed select group
of neuroscientists -- i receive his broadsides periodically.
A

Perhaps these equations have meaning for you.
My

best regards.
Sincerely yours,

‘-

�</text>
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                    <text>January 25, l985
Dear Harold,
It was kind of you to ask about old psychiatric books.
following:

I

am looking for the

Meduna, Ladislaus von. Die Konvulsionstherapie der Schizophrenie. Carl Marhold
Verlagsbuchhandlung, Halle a. 5., 1937, 121 pp.

Wagner-Jauregg, Julius. Fieber- und Infektionstherapie. Ausgewahlte Beitrage
1887—1935. Verlag ﬂlr Medizin, Weidmann 6: Co., Wien, Leipzig, Bern. 1936,
299 pp.

Wagner-Jauregg, Julius. Lebenserinnerungen. Herausgegeben und erganzt von L.
Schbnbauer und M. Jantsch. Springer-Verlag, Wien, 1950, 187 pp.
Sakel, M. Neue Behandlungsmethode der Schizophrenic. Perles, \Vien, 1935.
These books are out-of-print and are among the bed-rock documents of the somatic

therapies era.

ECT is having a resurgence of interest. 1 am told that one article on ECT
appeared in a Boston newspaper science section on January 114 and another is
scheduled to appear either this week or next. There will also be an article in the
local papers, reflecting the recent meetings in New York.
All seems well here. We did miss you during the New Year's celebrations
Alice
and
at
Marty's. it was fun, and the weather was reasonable.
My best regards and my thanks for your kind

efforts.

�</text>
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                    <text>March 7, 1970

near Irene,
Thank you for the inquiry about a coufaronce on
phenothiazines. As you know, my primary interest is in the I have
neurophysiology of compounds, and not their chemistry, so
not had much of direct interest to contributa.to anrliar conferences.

be hald, preferably in
ﬁeverthelaaa, I think such a confarencu should where
much of the
England
1971 (late), in Europe, preferably in
work seems to be progressing rapidly.
An is generally experioncad in many confarenccs, a
amall mnetjng of £O—60 participants and an additional 30~50
observers 333mg to he the most useful.
The theme of the meeting shoulﬁ deciée on the participants,
and suraly the lander: of tha last nesting may ha the best to
assess the relevant interesting tapicn.
My

best regards.
Sincerely years,
Max

Fink, M.D.

Professor af Psychiatry

mf/

�</text>
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                    <text>March 7, 1970

ﬂoat Irena,

far the inquiry about a confatence on
phanathiazinas.
you knaw. my primary interest is in the
naurophysiology of compounds, and not their chemistry, so I have
not had munh of direct intereat to contributa.to warliar conferences.
Thank you
As

Heverthaless, I think such a eonferencc should be held, preferably in
1971 (late), in Europa. preferably in England whit: much of tha
work seams to be prngzeoaing rapidly.
As

is generally expariencad iuv

many

confurences. a

small wanting o£ aowse participants and an additional 30~50
observers anew; :0 he the moat nacful.

of the m&amp;ettng shauld decide on the participants,
9f the last wanting may ha the best to
lmadara
the
suraly
the
ralavant
internating topics.
assaaa

and

The them:

My

best regards.
Sincernly yours,
Max

Pink, M.D.

Professor of Psychiatry

mil

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                    <text>January 12, 1997
Dear Jack,
It was good to hear from you again; I also received a card from Sophie and
her family on holiday. All is well here. Martha has just returned from a short visit to our
two grandchildren in Phoenix. The are growing well and the reports were glowing. My
son, as a Department chairman, is in that phase of his life that he is dealing with ‘movers
and shakers’ -- deans, university presidents, and corporate executives. He likes the power.
At the same time, he is at a pinnacle of his research career, with much research money
and many students, and has to decide which effort -- the academic or the political -- to
follow. Martha reminds me that I was in the same phase when I was in Missouri as the
head of an institute. I am glad I chose the research.
On the topic of research, a few years ago I urged some leaders in ECT to
organize a study comparing the efﬁcacy of continuation ECT to that of continuation
medications [lithium and a tricyclic]. After three years of bargaining, the Government has
awarded grants to four hospitals in a collaborative effort. Unfortunately, the federal funds
are inadequate to do the study properly. In the past, universities were willing to support
the research effort, seeing such work as part of their academic responsibility. No longer.
The issue now is wholly -— how much money do you bring in as a clinician; how much
are we paying you; and if we cannot make a proﬁt, maybe it is time to go. So, I am in the
process of returning the money to NIMH.
The process has become ugly. The Dean has asked whether I am willing to
retire now. After all, he says, he can hire two psychiatrists for my salary. When I noted
that I have been accorded all sorts of honors as a teacher and as a leader in research, he
smiled and said that the school had paid me for such efforts in the past, but for me to ‘get
with it’ -- the times have changed. Martha and I have begun the necessary dialogue to
retire later this year, after I have completed my present assignments. These end in June
and after some months of terminal leave, I should be free.
My book ELECTROSHOCK is coming along nicely. I have written a
for
the laity. I have a good publisher [Oxford University Press]. All the main
description
chapters are written; I am busy with the end-notes and appendices. While it will not lead
many to this useful treatment, it will serve to answer some questions.

�As with my university, a similar immediate return seems to have affected
old
your
company. Earlier in the year, when mirtazepine [ORG 3770] was about to be
marketed, I reached the research director at Organon USA and suggested that we
undertake a clinical trial of mirtazepine in delusional depressed patients, with an eye to
deﬁning its efﬁcacy in hospitalized patients. I noted that the ﬁling data in the US. [which
he had sent me] was limited to out—patients. In return, he said that they were not at all
interested in testing mirtazepine in in—patients. [I do miss the days when it was possible to
talk directly to Organon’s leaders]
I replied that I ran a clinic of depressed patients and I offered to examine
mirtazepine in either our depressed patients after a course of ECT [was it as effective as a
tricyclic in continuation treatrnent?] or in those who were not so ill, and for whom we
could deﬁne the clinical efﬁcacy at the same time as its effects on adrenal functions.

Again, he wrote to say that they were not interested. Too bad. The competition for
attention in modern psychopharmacology is based wholly on hiring ‘names’ to give
‘talks’ about new drugs and to ‘testify’ as to their effects. Most of my peers are already
on the do g-leash for other compounds [of which there are about eight]. I fear that
mirtazepine will have no better fate than mianserin in this country.

Martha continues her supervision of student teachers; our daughter Rachel
in Massachusetts has adopted a lovely, bright, and intelligent Chinese girl whom we love.
And Linda has convinced her husband to take a position in Virginia -- they are building
their home on almost 200 acres of mountain-top nearby to her college.
I continue to give courses in ECT and lecture on my new-found interest,
the syndrome of catatonia. Martha and I are off to Melbourne in late February. That will
be our ﬁrst trip to Australia.
So, we move on from one phase to another. When I step down, it should
be possible to travel more freely. We will see. Meanwhile, Martha joins me in thanking
you for your kind note, and we wish you and your family continuing health in 1997.

�</text>
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                    <text>July 17, 1992

DearJana,
Thank you for the articles on bibliographic software. do wish that
could transfer from Scimate, but it works well enough. just took a course in
EMBASE and found, to my chagrin, that there are many more articles in ECT in
journals not indexed by MEDLINE than had thought. Unfortunately, EMBASE is
quite expensive, both in search time and in downloading citations. But had to
begin and downloaded citations for 1991-92 that did not have in MEDLINE.
I

I

I

I

I

i

am often asked why Convulsive Therapy is not indexed in MEDLlNE,
and can only answer that the MEDLINE review board makes its decisions in its
own way (like NlH Committees?). But Convulsive Therapy is indexed in many
other indices, and all can do is to urge readers to seek citation lists outside
I

I

MEDLINE.

incidentally, the last citation list contains a review of ECT in
Czechoslovakia. Their therapist are also male chauvinist pigs, shocking women
more often than men! But they seem to either have a different appreciation of
the efficacy of ECT in schizophrenia than we do [or their diagnostic criteria are
different]. assume the difference is probably the latter reason.
I

Let’s get together soon. My best to Vojta.
Max

�</text>
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                    <text>.Wr

w

v“'

-m"wrv-Awn—untn‘-’IAI—u4uw‘r'

November 18, 1977

»
.

-

'

Dear John,
“rthm1L"v&lt;~l".—"

nu

luv-w—

x

"

fur-n

"Pam

to viiit Jamaica is excellent. The only
with Michael Beaubrun, whom I visited in 1970 or
1971. While he agve the EEG part of his study to Korein and Karacen.
contact I had

we

Your idea

was

have remained friends, and I

from you. He

is the (or

which the reports

was) the
emerged.

trust that

he will respond to a letter
director or the Bellevue Hospital from

w

u
.

'u-

rww'mmz'nrwu1—‘clrIvmv'mwm.

you

will let

If you

me know

can see your way to return via

and we can reason the problem

New

York,

together.

I

hope

I'm busy these days wrestling with ECT again. I have
a number of questions which I think could be answered by yet another
study, and I am planning a VA collaborative study. Otherwise, the
programs here are purring along rather quietly.
my

best regards.

“mmywmwﬁtvmnn

Sincerely yours,
Max

Fink,

M.D.

�</text>
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                    <text>September 8, 1970
Dear Josh,

Enclosed is a proposed subcontract for the Athens
study. I have taken the model suggested by Mr. Graduall, and added
the modifications that I believe would cover our specific problems,
expenditures for personnel and volunteers in Greece. I have also
decided to append a full copy of the general provisions, some of
which apply Specifically and the others should provide some
evidence of NIH intent for anyone interested in reading them.
I would anoreciate your calling me at my office if the
changes are minor; and if major, I would appreciate yourrmaking
the appropraite amendments and I will send a messenger to pick

up

the corrected text.
Many

thanks.
Sincerely yours,

Max

Fink,

M.D.V

�</text>
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                    <text>September 12. 1966

ﬂie- Hurray
Active Translation Bureau. Inc.
1472 Broeawly
Entrance 147 W. 42nd 8t.. ﬁnite 306
new Ybrk. new York

Deer ﬂies Murray:
I would be grateful if you would translate
these doculente in e fedhion satisfactory to the
Department of Education in Albany.

Before translating the Yugoelevian document-

call

office and provide II with en
eetinnte o: the coat.
I would be grateful if you would complete this
6 you

ny

hetore October 5. as they will he needed on Octdber 7.
Thank you for your cooperation.
Sincerely youre.
Hex

rink.

H.D.

Proteeeor of Peydhiatry

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                    <text>'—

v“
w

m-rvr-w-v

January 14, 1921Dear

Peter,

you

Thank you

for your

two

letters.

I hope that you have overcome

illness-- it is a shame to miss the early classes, but I
will make these up.

your

know

that

The notes on the Clyde Mood scale were very helpful. I had
already compared the output to the placebo schles and was sure that
the CMS was helpful. Your suggestion of comparing the last five minutes
of EEG to the CMS is a very good one, and I will try to keep it in mind
as the data analyses proceed.

I have asked that you be reimbursed for your travel, and
due course.

.this should arrive in

Your notes about the start of the placebo paper are
good; but I am confused by the request for a return of the general
summary you left with me. The summary I read, I believe I returned.
I have made a folder on placebo/EEG/Irwin, and
is not there; nor is
does Bruce have it. Are you sure I did not return my
it at home; nor
copy to you ? If not, descibe it again, please. (I'm embarrassed,
because in the past I could always turn to kathy and she would
save me from an embarrassing memory 0.

it

Feb 1, and

We

Glasser has just appointed a research assistant to begin
I believe he will Spend much time on the problems as outlined.

shall see something

by mid-March.

Keep working and keep

well.

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                    <text>19 Mirth 1974

mm-

H

'1

mm-

pray:

sqmgeup

Charltn sangaau. 3.9.
-Prnnidnnt
Annriann Paychapathologtcal Anaactatian

Rantarn Panamylvanin Psychiattie Inatttuco

Pbiladulphtn, Paunlylvunia
.3.

Dog: Charlie:

ragarwwvz'yww.

Tb
w!

19129

Enclosed

ch: heat at

is

a eopy a! the nouinationl for APPA cumndttccs.
roanllncttoa. cvnryona nominated sccaptad.

my

1;»;

4
$2:

'tw-mx

m

I an 136.06 dnlijhtnd that Ed Saahcv will be eh. Chairman
of the next Frost-a Conﬂict... Enclosed is a lcttur for you and
Ed for your connldnration for thu progrun.
My

‘mﬂ‘ﬂ'm.

best rsgnrds.
Sinunraly yours,

huh-W5-

an,

m ﬂnk' HOD.

‘

mien

1"

"‘3‘"

£9215

rs,

u
2

MW».

-

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�</text>
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                    <text>February 28, 1966

Division 3, 1986 Praaaadims

Amriam Paycialagical Association
1206

Samumth Street,

Washingm, D.C. 20036

-

NM.

W:
Wadmdmftaapiaaafﬂanpart‘mScalpmd

mammsmwaamwmmm
AW
casting of tha
Stimlatim"
for yaw midaratim far the
Mariam Psychological Association.

malsomlosad.

1966

‘ma capias

of an abstract

‘mcfigmsdmatratMsmaftracbsat-vatmm
butamnatavailablatoday. Iwillsubdt

being

thanwithinﬁamxttandays.

Mywmrynwhfarymmidamtim.
Stately yours .
Max

m.

24.1).

Professor of Psychiatry

Hszp

�</text>
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                    <text>March 7, 1958

Division 3.

1966

Mandingo

American Psychologiool Association
1200 Sevontoonth ﬁtroet, N.w.
Washinatm, D. C. 20036
Gentleman :

copies of tho report
Way 1 3mm four draft
to $1113.11th
Roma Averaged Evoked Responseconsideration
Electrical Stimlatim" for your
(2&amp;1th1966
"Tho Scalp

for the

"‘161’5“

”WW/"'W'w‘

vv-~.,.nA,-..

or

.‘
“,2”.

No.61,”

mating of the Mariam Poydwlogiool Associatim.

Page 1 had one manqcialetod, and-I om

angina of a

mlmemt.

Monodalaoemfm

annotoforigimla

mddunoaotsofyeomoopion. Figumlintobeineortod

mmamornma.
Figures 2, 3,

mpegelt.
.vam‘wﬂvvqﬂ'ng

figures.

melanin; ofum

Thank you

.

mod n complemont

W13

1, 3. and

5

for yaw consideration.

.

Sincerely yours,
Max

mm
14?sz

Fink, H.D.

Professor of Payalﬁntry

�</text>
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                    <text>May

'
»

17, 1967

Officer

365th General Hospital

100 N. Forest Road
Buffalo, New York 1&amp;221

Dear Sir:

IamwritinginsupportofthemquestofDr.ArthurZaks

forassigunentintheNewYorkareadtminghissunmertmining

PW.

Dr.

Zakshasbeenanactiveparticipmtinthestudyof

cyclazocine which is a new agent in the treatment of narcotic
addicts. This study is a special research project of the
Department funded by the National Institute of Mental Health
and the New York State Narcotic Addiction Authority. He has
been centrally involved in evaluating the untoward effects Of
this canpomd. The studies are prOgressing actively and will
continue for the remainder of this year.

helpful if Dr. Zaks could continue his
observation of these patients. He has already deferred some
of his vacation time in order to continue the study program.

It

We

would be most

grateful if it were possible for him to
military time in the New York City area.

would be most

spend his

Sincerely yours ,

Fm,
m
Professor of Psychiatry
MOD.

Mszp
cc: Dr. Zaks

‘

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                    <text>4

J!

I‘m

(2

Dr. Harold Aaron

The Hedical

New

y ’y
r560 Q'
‘6,

.

only 11, 1969

Letter

York City

Dear Dr. Aaron,

interest.
clear.

I have read the summary, Methoqualone and REM, with
report seems direct and well written, and is very

The

As I am not in the habit
am unable to contribute

of regularly recording aleevaEG
records, I
to the content of the report, nor
to assess its fairness or accuracy.
for your interest, and for your offer of a trial
May I suggest that the address of record
is not the New York University College of Medicine, but the New York
Medical College:
Thank you

subscription to medical Letter.
Max

Fink, M.D.

Professor of Psychiatry

York Medical College
East 102 Street

New

5

New

York City 10029

Sincerely yours,
Max

mf/

Fink, M.D.

�</text>
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                    <text>731:038 (00h)

January 31. 1973
Abbott Lebels unlimited
78 Mill Road

Freeport,

L.I.,

New

York 11520

Deer Mrs. Verin,

request your printing 1,000 labels, following the
specifications of January 12:
We

.002 matte
Permanent
ﬂumbera

silver

~

Foil-

Dark red

in sequence beginning:

Text:

lettering

1000

International Associetion
for Psychiatric Research
P.0.

Box 269

Great Neck,

New

York

Proof requested.
Bid price: ‘126.36

(Tex exempt: HIS l38hhh)

Thank you.

Sincerely yours,
Mex

Fink,

M.D.

Executive Director

�</text>
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November 13 , 196M

Professor Sanshi Abe
of Hokkaido University
School of Medicine
Dean

Sappmo. Japan

Dear Professor Abe:
Dr. Kazuo Saito of the Departurmt of Public
Health at Hokkaido University Sdrool of Medicine has
applied for an appointment at this research and training center as a research fellow in neurophysiology.
He has suggested that we write to
you for additional

informatim.

_

We would be grateful for
any consents you
to nakemﬂrdjng Dr. Saito's experience, his
ability to relate to his co—workers, and any talents
that he may have exhibited muting his experience with
you. As you may guess, we are particularly interested
in his ability to relate to members of our staff, so
that his language ability is an inportant determinate.
Insofaras the program in reseamh at this
center are dedicated to evaluating the changes in
brain physiology associated with variws changes in the
matzent process of the severe mentally ill, much of
Dr. Saito's work will be in clinical and experimental
electroencephalography. Any cements that you may wish
to make regarding his ability in this type of work

may wish

would be appreciated.

‘

Thank you very much
"

for yew cooperatim.

Sincerely yours ,
Max

'

Fink,

Director

M.D.

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                    <text>Irv-w" _.... . urnv'vlwmnrﬁ‘v'vm rmt‘ arm—a

e n’

}

June 15, 1970
H. Abelson
Science
Editor,
1515 Massachusetts Ave.,
Washington, D.C. 00005

Dr.

Philip

N.W.

Dear Dr. Abelson:
”Death from Heroin,” in the June 12 issue
of Science, highlighted an important medical and sociological
problem. The conclugion that two methods of treatment, methadone
and emotional support, seemed promising, omitted what may be
another exciting and potentially significant advance in opiate
Your

editorial,

dependence hiatOry

- that of the use of Opiate antagonists.

Coincidentally, the same crisis in heroin deaths spurred
antagonist data.
early May to call a meeting to review the New
York Academy
The meeting was hastily convened June 4, at the
of Medicine, co-sponsored by the National Institute of mental
ﬂealth. We regret we did not know of your interest in this
issue, for we would have gladly invited an observer.

us in

.

have prepared a summary of the meeting for your considera—
tion for publication in Science. The list of participants includes
the American scientists actively involved in clinical trials, as
well as pharmacologiata and chemists with interests in opiate
attended
antagonists. Industrial and governmental representatives
with
an
and hopefully, returned to their laboratories and offices
appreciation of this approach to opiate dependence.
We

Publication of this meeting summary in Science may serve to
inform others, unable to attend, of this progress, and may stimulate
additional research endeavors.
Sincerely yours,
WWWT.M

Max Fink, M.D.
Professor of Psychiatry

1

.v-‘mw

Hszp
811C .
NW“.

,

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                    <text>March 9, 1965

L” Abm
animosity of Illinois
912 South Wood Straat
Dr.

mileage,

Illinois

Dear Loo:
Encloaad lo a lottar addroaaad to you at this office. I:
to an invitation from tho warship Conant“ for you to apply

for unbornhlp.

I

plauad to propoaa you for township. if you worn
lutaraacad. aubjact to one llnitatlon. Would you plan and no a
alogla page abut-ant of tho report which you am planning to ptoaont
to tho soolaty on Saturday morning. Hay l? I know that you an in
tho middla of moving. but 1: would ha roost helpful it I could how
an outline of your presentation ao that I can
with each
of tho othar participants.
would ha

mica“

'

Boot

Fink. 2M).
Professor of Payohiatry

Max

Minn
Enclosure

tagarda.

�</text>
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                    <text>April 3,

Dr. Leo

1965

;

AbOOd

Dimctor cf Research

thiwmity of Illinois
911 South Hood Smut
011mm),

Illinois

Who:

Imoncloaingadmfteopyofthomportbym.

Gamhmformsmimmmy l,

1955..

»

Sincerely yours,
Max

MF:jm

Encl.

Fink,

H.113.

meessw of Psychiatry

�</text>
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                    <text>April 19, 1965

Dr. Leo Abood
of Research

NW

miwmity of Illinois
911 Scum Wood

WW,

Strut

1mg

'

be:
Enclosedisadmrtofmmpovtbynr. Rimmmite

Dear

{3:st Biological Psychiauy Meeting. on Satmday,

May

1,

Sincerely,
Fink, M.D.
Professor of Psychiatry

Max

Khjm
ﬁnal.

�</text>
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                    <text>April 2",

1965

Dr. 130 Abood

mentor of

Ram
Illinois

Univumity of
911

MIllinoisStreet

Chicago.

Wood

Dear Dr. Abood:

Wedhachaftofmmpombyw.mumfor

the penal "Antidzolhwrgic Hallucinogem" for Saturday

May

1.

itavanotyetamngadforaplaee forlmcmonm
and

apmciateymmmetingm at the
ofthemmingmsiminﬂxemys‘dteatﬁmm
York Hilton Hotel, after the martian by Dr. 91003.
Saturday but wwld

Sincerely yours ,

PM, “0 D.
m
Professor of Paymim'y
Wzkp

�</text>
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                    <text>May

7, 1955

Dr. boAbood

center

for-81mm

mimityofkoamm
Rodnstor, NowYork
Durham

Iwanttotaksﬁdaoppmmitytoﬁmkyoumagajn
mmtatim. an Smmy, Professor Sdunitt
dcdieatcdaportimofhistalktomcalstudiessimﬂarto
for your my fin.

ymmdmdumfmtomwoﬂcatmm.

Ehclosedisalstterwhichlmmivedmer.manpsm.

Ilodcforwardtomceivingﬁwmctedﬂgmaandthe

ﬁxaloopyofywz‘pqaer.

Sincerely yours,
ﬂax Fink, H. D.

Professor of Psychiatry

�</text>
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                    <text>Hatch 9, 1965

Dr. Leo Ahead

Univutlity of Illinois
912 south Wood Street
Chicago.

Illinois

Deer Leo:

Incloaed ia a letter eddroeaad to you at thia office. It
ia an invitation from the warship Committee for you to apply
for Hilberahip.

I would be pleased to propose you for membership. if you were
interested. eubjoct to one liuitation. Would you please send no a

eiugle page abecraot of the report vhioh you are planning to preeent
to the Society on Saturday morning. May 1? I know the: you are in
the middle of moving. but it would he not: helpful if I could have
an outline of your preeentation so the: I can communicate with each
of the other participants.
neat regards,
Pink. H.D.
Professor of Psychiatry

HA:

HF:3I
Bnmloanro

�</text>
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                    <text>November 12 , 1985

lac Abocd
center for Brain Reseandm
(hivereity of Rochester
Fodmster, New York
Dr.

Deer MO:

in

for the forthcoming
Prom Omnittee
1966 has asked Dr.

The C.I.N.P.
Washington on March

meeting

“~81,
Philip Bradley
md myself to ammge e sywosium on the general topic of neuropharmacology. Wehavedecimdtoamgeesympositmmﬂw
subject of:
MWOLINERGIC

WW8

.

Anticholinergic hallucinogens have received cmsidereble study
and the data relates to the problems of central nervous systh
daclinergic mdmmism in the therapeutic effects of various
somatic treatments , and to the special problem of the dissocia—
tion of ms and behavior.
Recomizing your experience with these canpounds and yaw

interest in these pmblm we would like to invite you to
participate in this syupcsitm.
1. If you are able to accept this invitatim. would you
please send me a proposed title for your presentetim, and a
short paragraph describing the toms and type of data you wish
to present?
Upon

willoake

Dr. Bmdley and I
madman,
emmdedpmgmhalmcing the tin for

receipt of these

up

he C.I.N.P. Oomittee has
agreed that this symposium will have at least one session of
simltanews tmslaticn, so that reports may be presented in
the language of your choice.

presentations and discussions.

2. The C.I.N.P. has not stated a general publication policy
propose to publish these reports and discussions as a

and

we

his

cum expenses

separate volume.
from

3.

mtieipates that each participant will pay
in attending this testing. For those attending

The C.I.N.P.

hope.

a charter flight my be organised

by Dr.

milip

Bradley.

�I».

Abood

War 12, 1965

~2~

In the amt that travel fmds are nemaazy, please indicate.
the mount muestod to swplenmt your available fmds md we
will tumult these mqmsts to the Program and Emmtive
Camittees for their decision.
a. The Committee has asked that

are beingmda

by:

we

indicate arrangements

Miss Margaret K. Taylor

c/o C.I.N.P. Secretariat
3836—16131

Street,

Washingtm,

If

you am planning

to her dimctly?

Dr. Bmdlayandl
symposium.

NM.

D. C. 20010

to attend this muting.

would you
‘

write

lookforwardtohavingyoujoinminthis
Sincerely yours ,
Pink, M. D.
Professor of Psychiatry

Max

�</text>
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1965.
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I am enclosing a copy
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I mpmpoeingﬁmtyouwilltalkabwt "Bio-

chemical Cmmpts of Anticholimrgic Psydwtmﬁmtios".
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abstract.

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best regards.
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                    <text>January 13, 1965

Illinois
Street
Illinois

University of

912 South Wood

Chicago,

Burma

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OmittoooftheSociatyotBinlogicalPsyohktryhasmpmdthe
for mtatim at the 1965
panel. "Antishch
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mm,Apul130ﬂ1,mdmylstmd2nd. Imuldauggesttmtym

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affectingmmmivitymdbodytmm.
Imuldappmaiatemyatlnrmpﬂntawhidxmnypmvidaﬂmbasisfor

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.

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1965

Dr. Inc 3. Ahead
murmur of Research

thiwmity of Illinois
91] South Wood Strut
(111535800 Illinois
Dumbo:

I an writing to ball yau that the symposiun m Antidnliw-gie
Hallucinogen at the Socioty of Biological Paydxiatry has been
for
fatally
afternoon, My 1, at 2:30, at the New
Yuk Hilton Hotel.

m

Way

'

With the tin inwlwd, I an asking each of the participants
to meat their material in 15-40 mums, rims alluring
5 to lo
ﬂames of discussim for each pm.

rmmmstmnatamﬁsmsim,

Imamlosingabstmcts

ofﬂumpomofﬂuoﬁwrparticipmtsandasmaslhavethdr
pmuillwxdyauaopies.

Inwdcrtofm ﬁndismssims, Iwill take itupmnysclf-

toopenmediswssimofywrmport,butwouldliketoaskyou
teaponﬂmdiswaimofmu Gemhm‘s report. I menclminga
pmlimhmydruftofhispapermlhnmmmiwditfmnhimand

wouldliknywtomaditmdbepmpmdtoopmthedimaim.
HandymjoinmasmygmatforlmdmatﬂnﬂmYorkHﬂtm

Hotclltmmmﬂayl? 'Ihhwmldprwide-anopportmityforus
tombottormqmintadandmyp‘mvidcforamatimhﬂng
aftermm.

harm. Iwinmdymmdemuastothelmdwmma
Immtﬂutyourmvingiawmingalmgsmothly. Hybest

mm.

Simly yams,
Pink, H. b.
m
Wessex! of

mm

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                    <text>my 26,

1955

1):. L00 6. Ahead

00am for 8min March

Unimity a! Water
Water, New?“

Mimi

IhawooneatodanﬂnmpwtsofoursmosimianYm
wwwstﬂmittndthnmtom.mmistodny.
yourpaperimltodcﬂnlibertyofhavmgmylibmvimmmo
yamcitatiminﬁustyhofﬁuhodt. Aoopyofﬁntmiaod
listismlmod.
will, mythanks formparricimtim.

Whom

Shmmlyyum,
Fink, ”a D.
m
meesaar of Psydxiatxy

�</text>
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mm;.\

q-w.

W

‘..1—

”wax”,

-_..

October 26 , 1966
Dr. Leo G. Abood, Professor
The University of Rochester
River Canpus Station
Rochester, New York 114627

Dear Leo,

thanks for your letter of October 17. While I would
be pleased to recommend Bernie, I am in the difficult position
of his never having worked directly with me, so that I am
acquainted with his professional competence secondarily.
Many

As you know, Sam recon-ended

his initial

work

an independent

his appointment and supervised

in St. louis. After

role.

Sam

left,

Perhaps we can get together in Puerto Rico.

regards.

Bernie assuned
My

best

Sincerely yours ,
Fink, M.D.
Professor of Psychiatry

Max

mka

�</text>
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                    <text>November 10, 1972
Leo G. Abood, Ph.D.

University of Rocyhster
Rochester, New York 14627
Dear Leo,

In a recent discussion of the role of cholinergic agents
a report written by you in 1961 was brought to my attention:
Distribution of Piperidine in the Brain and its Possible Significance
in Behavior, NATURE 191: 201-202, 1961.
on

the

CNS,

Have you done any subsequent work

particularly in other spetiee

as to where I

may

Many

?

If so, I

find the reports.

thanks, and

my

with piperidine,

would appreciate some

direction

best wishes.
Sincerely yours,
:2

Max

4

f

1/

Fink, M.D.

Professor of Psychiatry

�</text>
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                    <text>July 10, 1955
Dr. Gerald Abraham

Moehav

Tel

ﬂaerut

Mood

Iarael

Dear Dr. Abraham:
my apologiea for not replying to your letter more
promptly; however, I have been away. The residency training
program in psychiatry at the Hiaaouri Institute of Psychiatry
ia a three-year. fully accredited program. Candidatea may come
to thia program tron overaeaa on an exchange student visa. It
is also possible to come to this eountry on a permanent immigrant
viaa and participate in this program.

Please accept

Enclosed

is

65 acadeeie

an outline of the.¢oureeo available during the 1964year. The staff of the Institute providea moat of

the didactic courses. and the program is affiliated with the
University of Missouri School of Medicine., The olinioal work is
undertaken both within the facilities of the Institute. end
thoae of the institutions of the Division of Mental Diseases, including the St. Louie State Hospital.

.

Stipenda are available for candidates on a three-year program
varying from $6. 900 to $8. 900 per atone. In addition, there ia
a tire-year career program in which candidates obtain their clini—
cal experience, aatiafaetory for the American Boards of Psychiatry
and Neurology, in inatitutiona of the Division of Mental Diseases,
as well as their academic training et the Inatitute.
While candidates are encouraged to begin their program in July, we
have. on occasion. admitted candidates in January. I! this oppor—
tunity intereata you, I would be pleased to receive a copy of your
curriculum vitae. and a small photograph. As I plan to be in
Israel from August 6 to 14, I would like to meet with you. I will
he in Tel Aviv most of that time. but expect to make side trips to
Haifa and Joruaalem. If you will indicate which site ie the beet
for you, I shall be glad to arrange to meet you at one of the

three cities.-

Sincerely yours,

MI/jb

Me: Pink.
-

Director-

M.

D.

�</text>
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                    <text>September 21. 1964
Dr. Gereld Ahrehen
heehev Ream
Tet-Head
-

7

legal

but

Dr. Abraham

After lame: yen in Israel,

eohhiem my tour throng: Europe and bed
en «alien:
return; I teem! your iile fairly complete
end 1: the 11m: meeting of the Resume; committee, your appointment was
considered. I In pie-ma he tell you the: your epplieetiee for 1 career
residency he: been ”peeved. eﬂ'eetive January 1. 1965. or July 1, 1965.
depending upon the dehe at your swivel.
Creation.

1'

(in my

in which mdidetee
we: miéemy is five your training program.
during the first, second end filth yen-e
in training 1: the Minoan
Institute of l’eyehiehry end the Sh; We ﬂute hospital. The third end
{earth yem m experienhe years end Maiden“ ere «abject he ueigemt
by the Dim»: e! the simian at henh11 Dieeeeee in inetitetioee of the
The

1,

ease

numb In semi-11, appointments
in Inetihutim in St. Louie. or terminate!“ a hmity en hour
quarter am from St. Louie.
Divider: within the

Shehe

ef

ere nude
and one-

initial stipend is $10,006 per 3711: with en mud incense of $1. 250.
Venetian, 11m tine. alignment. end other deteile ere eebjeet to the teleet the Divieien e! Hentel Dieeeeee.
The

mining program begins on the first of January or the
first of July only. I would be pleased to hen you join the shelf he em
11 yea wieh he «range it end during the initial few mthe of your appointmeet. I would like to hm you week within the inehihuhe proper in one of

While the reeideecy'
,

our eeeeereh presume.

I

look fewerd

to you joining

W!”

eta“.
Sincerely were .

rink,
Direhter

Hex

c oC.‘ﬁbre
‘

_

Inf/ls

11 SICttCn
Bro Rege
,

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11.13.

.

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                    <text>Jammy 5 ,

Dr. Gerald Abmlm

c/o S.S. Israel

1965

- Passenger

Haifa, Israel
Dear Dr. Abraham
We

lodcforwardtohavingywjoinus inSt. Innis.

memwillbenoproblemaboutyothagemimﬂnhospital
will
and

hold for your arrival. In addition we will
accept
provide mandarin-ls for your use on yam mival in St. Louis.
In the event that those are satisfactory, it is possible to use

the

Wims formextendodperiod.

discuss this with the Chaiman of the:
mu Ivan Sletten.

W

Youwillbe able to
Canni‘t‘tee,

.

I donotthinkyouhavetobeoonoemdaboutymmlate

start. I

am

sure that you will

with satisfaction .
.

mush the training program
~

Wl'xenymaniveinNmYomhwouldyouplease call
secretary, Mrs. Anita Watzig, collect at 3111 MIssim s-suus
so that she cm make me specific armaments regarding your
arrival in St. Iouis.

my

Sincerely yams,

m,
Director

HEX

mfzdk

cc: Dr. Gerald Abram
c/o S. 3. Israel
'

Zim Lines
New

York

City.

New

-

Passenger

York

MOD.

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                    <text>/j

4v

/

August 17, 1977

Dear Mark,

I have not had much experience with drugs that inhibit
libido outside the ones described in the third page of the report.
I, too, have had patients with schizophrenia treated with antipsychotic
drugs who complained that they were less interested in going home than
we thought they should be. A discussion showed that impotence was a

factor.
In

my

I have had more experience with sexual stimulating drugs.
work with opiates (also sexual downers and heroin was regularly

associated with impotence), I used the narcotic antagonists cyclazocine
We found that patients on cyclazocine showed increased
libido, aggressiveness to nurses, and even priapism. We were not sure
at first whether it was a direct result of cyclazocine or the blocihde
of the negative effects of heroin. In an experiment in depressed patients,
cyclazocine also stimulated libido, but here, also, we could not be sure
it was a direct resuly of cyclazocine or a result of the relief of
depression. When we tried the effects of nalozdne, the findings were
never clear. These data were reported by Alfred Freedman about 1972—73.
and naloxone.

studies of chronic hashish users in Athens, of #7 long-term
insisted that hashish use improved libido, performance,
and potency. We checked with the wives, and in social worker interviews,
2/3 favored intercourse with their husbands on hashish Again, we could
not be sure it was a direct effect of hashish or the absence of the
users,

In

my

more than 2/3

irritability these

men showed during withdrawal from hashish. The data
: Hashihh— Studies of Long—Term Use, edited
R. Dornbush and M. Fink, Raven Press, New York, 1977.

can be found in the volume

by C.

Stefanie,

I trust these

comments

are helpful.
Sincerely yours,
Max

Fink,

H.D.

�</text>
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«a:

j-ryup

..

"s-‘ww

--7

January 28, i9 88
‘

Mark Abramowicz, M.D.
The Medical Letter
New Rochelle, NY

Dear Dr. Abramowicz,
i am disappointed with present methods of psychoactive drug evaluation.
The debacles in assessment which are cited in the article on fluoxetine are
matched by the over-investment in the use of benzodiazepines as antidepressants.
The present methods of contract assessment in out-patients, with inadequate
monitoring of the case material or the 'blindness' of the assessors; the inflation of
rating scale data to suggest that individuals can be working with Hamilton
Depression Scores above 22; the very high fees paid assessor groups (up to
$2500/patient); the failure to consider the likelihood that practitioners do know
when the patients begin a new medication and therefore know when to inflate and
deflate scores; and the lack of placebo controls all serve to make modern
assessments of efficacy of antidepressant and anti-anxiety agents highly suspicious.

-

While I have not worked with this compound, 1 would still caution readers
more strongly -- " Until effective in-patient trials of fluoxetine against placebo

and active antidepressants are published in indeprendent review journals, the
responsible physician will use these compounds only in patients properly cautioned
that the results are tenuous and that the treatment must be seen as experimental."
Thank you for sending me the Medical Letter. The reports remain

invaluable.

mw’W'V-l"

Sincerely yours,

w

'

no

Max Fink, M.D.

Professor of Psychiatry
wmv-mmn-W'IWW'dW-IW

"I“lwu'ﬂ‘x-u'fwhz

'r-""WF'WIW

M1?!

"""mel

n

any-M

P.S. Much has changed in the treatment of severely depressed patients with
electroconculsive therapy. Perhaps it is time for the readers of the The Medical
Letter to read about the efficacy and safety of this treatment.
J

�</text>
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                    <text>October 26, 1966
Dr. Richard Abram
1014

Children

Shepherd Air Force Base, Texas 73611
Dear Dr. Abrams:
Dr. Madman has

sent

me

your

lettw of

October

11+.

Iwwldbepleasedtohaveywvisitdnmingyoxmnext

trip East. If you will call my secretary or write, I

would be pleased

to set

up

a definite appointment.

Sincerely yours ,
Fink, M.D.
Professor of Psychiatry

Max

MF:kp

�</text>
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                    <text>Novmnber 9 , 1966

Dr. Richard Abrams
10“ Childress

Sheppard AFB, Texas 76311

DearDr. Abrams:

aftermon of Friday, December 2, would be the best
for
I will be attending the meetings of the ARNMD at
Roosevelt and these may be of interest to you as
Hotel
the
The
afternoon session interests me least and I would
well.
be pleased to meet with you at 2:30pm at the registration desk.
Ifyouwill inquire formeat that time, Iwillbe inthe
The

me.

immediate neighborhood.

my

I

If there is

office

am.

any problem about finding me, please

369-7900 Ext. 2“? and my

The Hotel Roosevelt

is

secretary will

on Madison Avenue and “Sth

I look forward to meeting with

call

know where

Street.

you.

Sincerely yours ,

n
E

avg—my,”

Fink, M.D.
Professor of Psychiatry

Max
.4.——.,-n4.uwu‘

vI-r‘m

&lt;

mfkp'

'

�</text>
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                    <text>Decenber 19, 1966

I». Rickard

Abrams

1M Childrese

Sl'xepparﬁ AFB, Texas 76311

'

DearDr. Abram:

I havemad'yoxm letter of December 6 with great interest
andfindthepmpoeed studyereaeombleandim-tantcne. I

wouldliketodoevezythinglcmtoeeteblishit.

wt

The most critical determimtion at fimt. will be the
wave activity produced by milateml ECT. Surely, if
unilateral BCT produces a different warrant of slow wave activity
thanbilateralEC‘I‘andtheclinioelomditionsamthe same, then
the original hypotheses will have to be reviewed, as you suggest.

of slow

I do not think there is any diffimlty with regard to may of the
essential elemnta for the study accept a. biodmist. At the
presenttimellommmeinthemtropolitanNeWYor-kmewho
is interested in xmdertakirg the oinlinestmse or acetylcholine

measures

hitIthinkwecanlookforthat.

Ihevewrittmenotetotheduirmnofthemmntand

toDr.Hemld1&lt;aplanvdnieinc1m‘geofereeidencytr-aining
progran, requesting a review of your fwtlnaning two year residency
period so that adjuements may be made to provide an opportxmity
tomﬂmmﬂzie'sunycmmmtlywithyowtmining. Assam

asltuveanmr,lwillsemitmtoyou.

Year.

Mybestwiehes foreheppymlidayseasonandfortheblew
Sincerely yours,
Mex

Pink,

M.D.

Hofesaw of Psychiatry

HFﬂcp

�</text>
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                    <text>"1v

-

January 16 , 1967

1.,

.rcau—nrrm-

Dr. Richard Abrams
‘53)!

u»;

—_
-

—v

‘4

101+

Childress

Sheppard AFB, Texas 76311

-

rr-

DearDr. Abrams:

.w«.-.~':a,.«—~r.-

«SJEIFTV-‘K’JF"

.

"’x-&lt;'n'9

wjgvne—z-v

1-

was

-‘:-‘

47w“:

'

"

1'15!

1.

'5"-

.11;

A

mm

w

w

21

mix;

.Ef

Since writing you on January 9, I have read the article
at all. in the Arne/aim Jamal, 05 9191mm. This

by Martin

is a clearer exposition of the experiences

BCT

ment

With unilateral
interrelation of the nemery change data, improvescores and the allusion to EEG data are very clear.

and the

If these observations are confirmed, then the study you
suggested should be augnented by a detailed examination of
a variety of aspects of menbry function. Once a study is

to select patients and to treat them in two
different ways , it would be a most useful theoretical addition
to examine the possibility that the memory changes both in
quantitatife and qualitative aspects may be related to the
degree of altered brain function as measured by the techniques
umiertaken

you suggested.

Sincerely yours ,
Fink, M.D..
Professor of Psychiatry

Max

Mfzkp

�</text>
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                    <text>January 9, 1967
Dr. Richard Abrams
10” Childress

Sheppard AFB, Texas 78311

Dear Dr. Abrams:

I have discussed your request with Dr. Preednan and Dr. Kaplan
have reviewed the experiences you have already had in
relation to the study progran in the Department. I am pleased
and

z-a'

z.

:

ﬁﬂﬁww-vﬂ!

we

thattheChaimanhasbeenabletoaffirmthatastudypmgzun
should be

latter portion of your training.
months the initial assignments will

undertaken during the

«rum-1,2-

.
:9
_

Deming the

first

few

be made in those areas in which you lack specific experience
as narcotic addictiOn, the mental hygiene clinic and child
psychiatry. As soon as these are accomplished in a satisfactory
fashion, we believe that the study program you have outlined may
be undertaken.

critical part of the study is in the development of
EEG patterns with unilateral ECI‘.
I have read the
Zamora article and am mimpressed. I have requested the Martin
article but have not yet seen it. Surely, your om experience
becomes very critical and I wwld suggest that you outline the
observations which you yourself have made regarding the EEG
differences with unilateral and bilateral ECT. Especially, if
The

different

_

you have samples

of the records in subjects treated with unilateral
clinically and comparing these with other

ECI' showing improvement

subjects of approximately the

bilateral BCT.

same age

stoning improvement with

In reading your protocol of December 6 , the introduction
so is the hypothesis, Imam, of the
four alternate ezqalanations, the fourth is unclear.
The first

is straightforward and

three are quite good.

"‘5"?

,HCTAFWF-thwhm"!

'I'hemethodisrelevmtandImuldonlyaddthattheEEG

delta activity is to be recorded following

ECI' at a specific time,
hours. Your suggestion of the determinatims of
CSF acetylcloline and chinesterase is a good
one, but this may
be the most difficult part of the study to acoanplish.

probably

aways-1y,»

mm:

~1sz

_

,
‘

V

W

’2"?!

9
-.-

times»

Few:

was:

NWT):

2n

�-2-

Dr. Abram

~

January 9, 1967

_

At our last meetiru you suggested that you would like to
collect the literature relevant to this problem. The citations
which I have listed at the end of my. few reports are those that
appeared to me to be most relevant. Surely, by checking these
one can obtain the citations to many other articles which,
perhaps should be in your library. If you wish, I would suggest
thata the next opportunity for you to be inNew York that you
visit with me and we can go over my collection making such
notes as may be necessary to provide you with the basis for a
literature review. I have not carried out a systematic survey
of ECI‘ literature since 1959 and perhaps an alternate solution
would be to check through the major indices for literature and
ask for the articles which may have appeared in journals not

ordinarily available in the major

I

am

delighted that

this study program.
Good

we

New

York

libraries.

will have an opportunity to undertake

luck in your present programs.
Sincerely yours ,
Pink, M.D“v’
Professor of Psychiatry

Max

ME‘:kp

�</text>
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                    <text>February 21, 1967
Dr. Richard Abrams
10“ Childress

Sheppard AFB, Texas 76311

Dear Dr. Abram:

abstract should interest you. I have not
article, but think that it is important that

The enclosed

yet seen the
you do so.

Sincerely yours ,
Fink, M.D.
Professor of Psychiatry

Max

Mfzkp

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                    <text>February

9,

1967

Dr. Richard Abrams
10%

Childress

Sheppard AFB, Texas 76311
Dear Dr. Abrams:

I have read your letter and your report with interest. I
found the review of focal seizures quite good and you confirm
the need for a definitive EEG, behavioral and
study. The

my

data demonstrates clinical equivalents for unilateral
and bilateral BUT, the more important a definitive study becomes not only for the practical aspects but the theoretical as well.
For this reason, I regret very much that the EEG material
was not collected. However, you indicate that you may be able
to collect EEG records in the remaining subjects. If this is
so, for comparability it would be very helpful to have records
collected 2M to 30 hours after a seizure so that comparisons
can be made with my earlier studies.

more the

In reading the paper, which appears to be mislabeled, I am
impressed with the equivalents of the mennry tasks. However,
why were the clinical results not included? Surely, since these
patients were receiving treatment the records must show whether
symptom relief occurred, or whether there were changes in global
aspects of behavior, or whether there were some other secondary
effects, Perhaps you wish to wait until you have completed the

additional thirty subjects. But if you believe that this data
is sufficient for the menory results, it should be as sufficient
for the behavioral data. Incidentally, I think the title should
more properly be related to the detailed analysis of memory
changes than as a general statement of the daily administration
of unilateral BCI‘.
In your letter you indicate hat you have collected the
data at each five treatment intervals. It would be
helpful to exandne these as carefully as the results after

memory

twenty

treatxents because

give an idea as to whether
it will
two
differ.

the rate of change between the

groups may

'

�-2-

Dr. Abrams

he

February 9, 1967

Your question regarding Dr. Abood

is

either interested or has the

is

good, but

I

doubt

that

facilities to undertake these
clinical and our experimental

However, cnoe the
aspectsaredefinedIoancallsaneofthepeopleinNewYorklﬂce

deteminations.

Dr. Abood.

literature review sounds good and I will make available
to New York. As to the statistician who
my files
can perform the tests you require, if you will lay out the numbers
on sheets identifying the variables, I can try to get the work
The

done

in

when you come

New

York.

I have recently re-read the BOP studies of Dr. Paul Blachly
of the University of Oregon. He describes the administration of
multiple treatment in one day with EEG control and argues that
with proper ventilation the memory changes are minimal and the
clinical improvement enhanced. He has a single report which
appears in Compaehmiue PAchy, Volume 7, g: 100-107, April,
1966. As part of your reading I suggest you become acquainted
with this article. He too has theoretical suggestions which
warrant testing.
Keep up

the

good work.

Sincerely yours ,
Fink, M.D.
Professor of Psychiatry

Max

Mszp

,

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                    <text>April 3, 1957
Dr. Richard Abrams
101+

Childress

Shepherd AFB, Texas
Dear Dr. Abrams:
Enclosed are the

you requested.

original data and the calwlations which

The technique applied has beenthe Mann—Whitney
U Test, which is a mn~parametric test of significance in two
groups. The test is designed for such small populations as you
present. The test was applied for the differences between the

unilateral and bilateral populations before and after treatment
and for the differences resulting from treatmnt. The same was

done

for the

Beckomberga Rating Scale.

There are no differences in the two populations before
treatment, after treatment, or in the differences resulting
from treatment. But if one looks at the differences induced
by each treatment, there is significant effect for the change
in the Hamilton Depression Score with unilateral. ‘ECT and with
bilateral BCT, indicating that in your population the changes
induced by treatment were (as expected)

I

am

significant.
visiting Dr. Blachly on April 10 and will obtain a

first-hand impression of Tie methods and problems. This should
be useful when we begin our program
I will be at the APA meetings in Detroit and if you are
planning to come, we should arrange to get together. I will be
staying at the Hotel Pontchartrain.
‘

Sincerely yours ,
Fink, M.D.
Professor of Psychiatry

Max

MP:kp

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                    <text>May 15 ,

1967

Dr. Richard Abrams
10a Childmss

Shepherd APB. Texas

DearDr. Abrams:

sorry for the delay in answering your letter of
but
preparations for the APA occupied most of my
April
time. I have read your paper with interest and have taken
the liberty of marking it with the questions that occurred
to me as I read the text. I think it is sufficiently clear,
however, it should be submitted for publication.

I

am

1'4,

You are correct that the changes induced in unilateral
and bilateral ECI‘ were significant in their changes in the
Hamilton Rating Scale. The data for the Bedmberga Scale
were too scant to be useful.

I have had the opportunity to visit Dr. Blachly and
that his technique , which pennits three to six treatto be given in one morning, is probably a useful method
to be tried. He suggests that the differences between his
observations and those of others is related to the degree of
oxygenation. IhavealreadyspokentoDr. Kalinowskyand
perhaps we will be able to mdertake such a study, following
his line of investigation, if we can obtain the services of

found
ments

an experienced

anesthetist.

Such

‘

a study is of special

interest may since the its-patient services are undertaking
a special study of the rapid treatment of all admissions to
the service. They are particularly interested in any device
that may shorten the treatment period and such a mthod as

fits well

Dr. Blachly suggests

It would

be quite helpful

earlypartofJuly,

as

can plan the study more
My

with our present needs.

if you

could

Ithirﬂchillbe
definitively.

visit during the

inNewYorkmdm

best regards.
Sincerely yours ,

.,
3..

WIT/;:

Fink, M.D.
Professor of Psychiatry

his-.111W‘Wl

Max
.7-

r,
p"

W;—.qu..\h

rw‘rW-Wn

MF:)q&gt;

�</text>
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                    <text>February 19, 1971
Dr. Richard Abrams
York Medical College
York, New York

New
New

Dear Dick,

seminars in Psychiatry, a new quarterly publication edited

by Milton Greenblatt and Ernest Hertmann, has suggested that the
first issue of 1972 (February) be devoted to Recent Progress in
Convulsive Therapy. I an pleasedyyou have accepted the invitation
to contribute the report on "Clinical Results: ECT". The notes in
the outline are suggestions, and you are free to expand on the topic
as you wish.

is usually
typescript pages.

The volume

200~300

120«160 typeset pages, equivalent to
Your report should range from 25 to 30

double spaced pages (including
To meet the publishers
by the and of June?

citations).

deadline, can

'

you make a

draft available

It is a policy of the Seminars to re~issue reports of general
interest in hard cover. If we are successful (and I anticipate the
volume to have widespread interest), the volume should then be
cited both as a periodical and as a book, assuring a wide distribution.
I

hope you can

join us.
Sincerely yours,
Fink, M.D.
Professor of Psychiatry

Max

MF:kt

.

Mvw

5)."—

�</text>
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                    <text>,.w__~,_——m___—mw.____

Wmmm—W

w-wmmmmmm

r-vrrrw

November 8, l97l
TO:

Richard Abrams,
Rhea Dornbush

Jan Volevke

The various reporfs for +he ECT issue of lhe
Seminars in Paychiatry are in The hands of the publisher, and we
should receive galleys wlfhin 6 weeks. The issue is due to appear
in February.

publisher has indicafed Thai he will give each
of you a subscriplion, in grafifude for your cooperafion.
The

enclosing a copy of The idenfificaflon
sheaf, as submifled. if incorrecf, please advise.
l

am

l van? #0
express my personal thanks for your splendid
I
know the? l would nof have undertaken
and
enfhusiasm.
cooperation
I
no?
had
This efforl, if
fell lhaf you would do as well as you did.
i
The confribufion to ECT undersfandlng fhaf
make
hope fhe issue does

is so sorely needed.
My

Thanks.

�</text>
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                    <text>73828-628

April 19. 1973
Mr. &amp; Mr:. Henry retool,
7 What 8lst Stroot,

New

York

City,

E.Y.

Dear Hurt: and Hoary,
An I thumbod through my’nail the other day, 1nd
sonnnod o host of Journals and Junk. I saw the uncle-ed

covor, and without looking at tho credits
immodlotcly

I

it

do not

was can

of your friends;,

knew

think the roproduotlon does his

work

Justice. but I must admit that this kind of op—ort
in interesting. Perhaps «won more so is the fact that
I can recollect of no other modern pointing reproduced

on the cover of thin Journal for usny. many months.
They usually use a olaasiaol. representational type

art.

of

Martha must have told you that vo are Joining
you in Iuyporting a second house. w» have found a

cottage overlooking the voter in strong’s Nook (Betauket).
is tvolvo minutes from.my office at the Univorolty.
A: MLrthu says, it in possible to stood in the middle of
the living room with a dust cloth, turn 360°. ond have
completed the cleaning.

Th1:

I trust the family are wall.
my

boat regards.
Sincerely youro.

Mn: Fink. M.D.
Professor of Psychiatry

MP/id
Eno.

�</text>
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Amril 19th, 1973
Dr. Jchn R. ﬂushes,

Canaultina Editor,

EEG
aWTn-K‘Wﬂw&gt;'

qurnnl,

Book Ravicva,

Northwestern university,

303 3. Chicago Ava.,
Chictgo, Illinois 63611.

4_.‘rl'vl~'l

A;
w.

.
,rv

,r-w

v
—«

v'wp‘I-ﬂlnmsmr

=-—u:—.v.v,

W 30m.
I have received the voluna “International Review of
Reurubiology". and look tbrvurd to reviewing 1t fur the
EEG Jburnul. I have a tow chore: to do over the noxt few
vuckn, but should got to it during late Mhy, and helluva
I can must your July daadline.

Thai-v.11"

thy

err-"a

v-wo-

thank: for thinking of no.
my

4‘5'

den:

best regards,
Sincerely yours.

woman-UV»:

Fink. M.D.
Professor of Psychiatry
Mb:

“/""‘.‘.‘

gnmlr

.5
up.

warm}

A

«2—

v.:W’u-'&gt;¥"‘:--I..,-r~rr.~

,m

;
"mm-m,

v-vrwru

lwmmw

Mr/id

�</text>
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April 27. 1973
Mr. John R.

Coxsolino.

Harootio Investigator,

Suffolk County Health Dept.,
Eonpitol Affairs Division,
Route #113,

Rivorloizh Avo.,
Bimb.“ , Ho 1 a
Door Kr. Coozolino,

I rogrot that I nova had to cull you. The
enclosed letter from tho BHDD invottigntor indicates
that BHDD is unwilling to provide the necessary
registration until the State rogiutrotion hos been
completed.

Thank you

for your cooperation.
anooroly yours,

Pink, M.D.
Professor of Payohiztry
Mu:
Mir/1.1

Eno.

�</text>
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                    <text>_

..wr.wm'—__,ww

..

w.

”- \,w.,-.u—.M.r—. “mm—mam. w.,...,..,_..w,

November 18, 1985

Richard Abrams, M.D.
Department of Psychiatry

Chicago Medical School

3333 Green Bay Road

North Chicago, IL 60064
Dear Dick,

have received the enclosed invitation, at the suggestion of Arnold
Friedhoff. Before proceeding with the intent of cooperating, I need your advice as
to how such a presentation would impinge on our present agreement. It is my
impression that it is not a conflict.
I

My

best regards.
Sincerely yours,

Max Fink, M.D.

Professor of Psychiatry

.

�</text>
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                    <text>November 28, 1989
Prof. Oded Abramsky

Chief Scientist
Israel Ministry of Health
Jerusalem
Dear Prof. Abramsky,
I write this letter to encourage the application of Dr. Seth Kindler for
support as a research scientist at Ezrath Nashim and the Hebrew University. I
have known Dr. Kindler through his publications and his presentations at
international psychiatric meetings. I have known his mentor, Prof. Lerer for more
than a decade, and have been an enthusiastic supporter of their important

research in electroconvulsive therapy and the receptor mechanisms in depression.
Despite his youth, Dr. Kindler has an impressive record. He graduated
the Hebrew Medical School in 1982, and in seven years, completed his formal
psychiatric training, published important research findings, and developed
laboratory and clinical skills. He seeks to combine these in studies of the
neuroendocrine aspects of depressive disorders.
I am particularly impressed with the importance of these studies for

our understanding of the mechanism of action of ECT, a most useful treatment.
Prof. Lerer has already contributed much to this knowledge. In 1980, Prof.
Ottosson of Goteborg and I proposed a neuroendocrine theory of the mode of
action of ECT. Much work has been done in the United States, Greece, the UK,
and Israel on this theory. It remains Viable and I believe that Dr. Kindler’s
research into serotonergic mechanisms is important in our progress.
Few laboratories in the world are as well equipped and as interested in
research in the affective disorders as those at Ezrath Nashim which I visited a few
years ago. Under the leadership first of Prof. Belmaker and now Prof. Lerer, the
studies have made important contributions to our knowledge. Any encouragement
that can be given Prof. Lerer, as in the support of Dr. Kindler, should pay
handsome dividends in research and in the position of Israeli research in world
psychiatry.
I congratulate the Ministry of Health on having such a promising

opportunity to support important research.

Sincerely yours,
Max Fink, MD.

Professor of Psychiatry
Editor, CONVULSIVE THERAPY

�</text>
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                    <text>January 25, l97l
Dr. Wllllam Abruzzl, M.D.

Sfudenf Personnel Dlvlslon
Sfudenf Healfh Cenfer
Stale Unlverslly College
New Palfz, New York l256|
Dear Dr. Abruzzl:
As you know,

There Is no sallsfacfory +herapy of oplafe

dependence, and prevenflon and educaflon remaln lhe prlnclpal
roufes lo success. Methadone subsflfuflon ls useful and legal,

provldlng

a

pollllcally saflsfacfory solullon.

In +he research Iaboraforles, a process of decondlflonlng
wlfh +he ald of narcoflc anfagonlsfs, as naloxone and cyclazoclne,
ls under sfudy, buf The procedures are no? yef avallable for general

cllnlcal frlal.

I
suggesf you wrlfe Dr. Dole af Rockefeller
has
complefed a responsible revlew and recommends
Unlverslfy.
In
repealed doses (every 4 hours); and naloxoee (IV,
nalorphlne
I
when
If becomes avallable (Naloxone, Endo Labs,
mg/4 hours)
Garden
L.I., N.Y.).

For heroln
He

0.0.,

ley,

If you are pIannlng Io vlslf fhe clfy, you may wlsh To vlsl+
our unIf and speak To my assoclales who are +rea+lng our narcollc
addlcfs In a varlefy of ways.
Slncerely yours,
Max

FInk,

M.D.

Professor of Psychlafry
MF:k+

�</text>
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                    <text>.,

-1

r7'zVI'.'Vrr"‘-VmVm'r'r’wvvrwwwlwunv‘

-.

December 6, 1977

wv-vvm

’—.-V&lt;7nr'm

1:

r
..,

mum.

w

runway.

"Wllrwu-V‘H.

..‘,..

ray

:1
1-».

V

Wm.

Abruzzi, M.D.

Fox Farm, Loon Lake Road
Malone, New York
Dear Dr. Abruzzi,

c.v. exemplifies a rich experience. As to your questions,
is difficult to know how to answer the first. For decades, various
it
authors have suggested that cannabis is associated with psychosis. Two
theories have been stated—- that cannabis is a psychotogen, and that it
Your

'1iberates' psychotic tendencies that already exist. The issue is not
whether cannabis is a psychotogen, for that issue is spurious. Since there
is good evidence that cannabis inhalation alters brain function, it is clear
that with such alteration there must be changes in behavior and there
is no reason why such changes could not be manifest as psychotic symptoms.
After all, the definition of psychosis is in the eye of the beholder, not
in the symptoms themselves. , If you have some additional data, then why
not follow established custom and present the findings and the controls ?

it

became clear
At the New York Academy of Sciences meeting,
under
and
Costa
controlled
Rica,
the observers in Greece, Jamaica

that
conditions, could not confirm the development of psychosis in long-term
users. But reporteds from India (Chopra) and Egypt (Souief) did say that
psychosis was common. There is a need for someone from the U.S., with the
same support that the other fOreign studies obtained, to go to India and
Egypt and confirm

their observations. Perhaps,

a mission through your association at

studies

and would not do another.
Good

luck in your

summary

NYU.

I

you could undertake such
have done my bit in such

of the recent studies.
Sincerely yours,
Fink, M.D.
Professor of Psychiatry

Max

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Rad-mic Press Inc.
111 Fifth Avenue
New

York,

New

York 10003

mum:
Tm

qmitatiw

analysis of changes in

010mm signals

mmmmmmtmmmmummoragm
applications, 33033 to
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excellent reports have been written. me electronic: wands of
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by a popular mview
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pattern and

mum

Tim laboratories have Miopad various applicatiom of
digitnlmﬂwdsforﬂmpumoms. Warmvammimdmyw
qmstn for our program and have men aged to swim this
infomtim in a mammal mm]... We believe that “chum is
modforsmhamrmiaalcbcmnttobemadammmmlly
available and are sending it to you for yaw midwation for
publicatim. If this interests you, we would be pleased to
diam mlifimtiom and mdiﬁaatiom that may be meeasary
to provide a
man:

m wally applicabla Want.

you

for your miﬂemtim.

‘

Sixmly yours ,
Hm:

Fink, 3.0.

Professor of

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July 20,

1965

0mm]. Mounting Office

;

Retinal Imtitute of Mental Health

muted States Public Health Service
Bethesda, Marylmd

-

2001i;

Gentlmn:

RE:

m

MGR-01
ﬂ-l 8388—01

an herewith returning Treasury C136: No. 77,828,213“,
dated July 1“, 1985 made out to the Paymmtrlc Research
tandem, in the mum: of $12,000. This cheek represents
He

amhadvmminﬂuebovemmt,
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1965.
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                    <text>r... erw wwwn.

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July

’23, 1965

Centre; Accomting Office

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United States Public: Health Service
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RE:
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                    <text>July 1, 196‘

,

Laonard 3. Annex. Ph.D., M.D.
Madlcal Bepartaau:
Sande: Phaxuacautlcala
Haaovat. ﬂaw Jaraay
Baa: Dr. Achor:
On behalf of tha Psychiatric Raaaarch Foundation, I
«lab to :aka thla oppottunity to thank you and Sande:
Fharuacautlcala to: your favorable canaldaratlan of
out :aquaat for grant-1n-ald for our tasaarch and
training proazaha. The funds will ba uaad in tho
acudy prograna of EEG and human payehapharuacology,
unda: tha dlraetlon of Dr. Turan 1:11 and myself.

rha aupply of L89 recanely requested atrivad aafaly.
thanks again for you: kind canaldaratlon.

Many

Slncoraly youra.
Max

Fink. H.D.

Exacuclvu Director

MP/jh

ﬁne.

�</text>
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                    <text>July 23,

19M.
.

Leonard B. Aehot. Ph. 9.. M.D.
Medical Depsrtneet
Sande: Phszaseeetlcels
Hanover, New Jerney
Deer Dr. Asher:
During the pest week. we hsve ctystelleed our research pregrem
in.the enelysls of the EEG end behevlorel changes with thiorlde~
sine and chlerdlsespoxlde. When I celled Dr. Renae, he was kind
enough to send as samples of Kelleril (100 mg.) and corresponding

p18“b°l

e

These have been compared with the capsule: sent to us by Hoffman-

Lsknths, end theysere indistinguishable.
In ressseeslng our protocol, we hsve concluded the: a greater
degree of flexibility weuld be tntrbdueed into the progrsm 1f the
chlorideelne capsules were nude in 50 as. strength. Can this be
secoupllehed?

If so, we estimate that for the full study we will need 16,000
espsules of 50 as. strength, In eddltiau, we will need a total
at 16,000 cepsulss at placebe, end would request Sande: Phsrns~_
deutlcsls to supply us with belt thst amount. Would you consider,
therefore, this letter as e reqnsst fer supplies of thiarldezlns,
50 n3. espsules. 1n the smount quoted shove, and placebo?
We will need these supplies over s full year. and 1f the full
accent is not svellebls 1n the immediate futute, we would like to
reeeive s supply_eu££1¢1ent to begin the study within the next
few weeks.

Then! yen for your cooperation.

Sincerely yours,
Mu Fink.

,Dlrector

Ms De

HF/jb
‘P.3.

The espsulse of placebo were lebeled ﬁwOGISS, and the capsules
0! Hillsril.ss H-00267 (100 mu. thlorideziue hydrochloride).

‘

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                    <text>iarch 29, 1989
John M. Ackerman, M.D.
2417 Castillo

Street

Santa Barbara, California 93105
.v—

-

"

i am acquainted with publications describing electro—acupuncture ECT
(EACT) by Dr. Xue and his coworkers in Beijing, and another by Drs. He and
Zhuosan (in a separate report from Xian). Both reports appeared in CONVULSIVE
THERAPY in 1985. They suggested an equivalence in efficacy between EACT and
conventional ECT but greater safety for EACT. in the absence of a random

-._w;,.v~——..—.—-—

W.

V,

.,
&lt;

”w...”—

—w-mw—r—---

-.

"nu-v!"

Dear Dr. Ackerman,

'

assignnient study with independent assessments of outcome and cognition, we
remain in the dark as to the importance of these reports.

‘

The second report, "An investigation of Transient Absence of Brain Wave
During Convulsion of EACT and ECT" seems to be an abstract. The citation is not
given. From the abstract, it is not clear when in the course of the seizure, the
TAB W occurred. In 1966, Blachly and Gowing described the end-point of EEGmonitored seizures as 'precise' or 'imprecise‘. Recent studies of the end point find
that more than 2/3 of seizures end in a period of iso-electric activity, a flat EEG
which may be what is described by Dr. Xue as TABW. The period of isoelectric
activity in ECT varies but may be prolonged for more than a few minutes in
unusual cases. Usually the duration is under 30 seconds. We are now investigating
whether a precise end-point is a favorable prognostic sign (and am imprecise endpoint, an unfavorable one). If i am considering the same phenomenon (TABW =
isoelectric activity), then Dr. Xue's observation that 4.1% of cases with EACT had
TABW while 31.496 of ECT cases had TABW, would suggest that ECT was the more
favorable (effective) treatment. But such speculation needs to be examined with
Dr. Xue or another practitioner of EACT.

At one time, Dr. Xue correSponded with me and I invited him to visit Stony
Brook where l was prepared to let him demonstrate his technique in our unit. He
was unable to accept, so i do not have any direct experience with EACT.

ww.

'Wumv

‘vw'qm'wwwimmm

A

”m—

Like other modifications of ECT, the burden of proof of claims of efficacy

or safety lies with the protagonist. I do not know how many Cases would be required
to define a difference between EACT and ECT, or if there is a difference. i

suppose one could estimate the number of cases needed after observing EACT
practice in a few model cases. in assessing differences between unilateral and
bilateral electrode placements, for example, it required a few hundred cases to

demonstrate a difference.

�Dr. John Ackerman

EACT vs ECT

-

Page 2

If Dr. Johnson is enthusiastic to try EACT, an open clinical trial in
characteristic depressed (and delusional) cases would be of some interest. If he
could verify the claims that seizures were induced with remarkably low currents;
that needle electrodes were safe and effective; and that the number of treatments
needed were either equal or fewer than ECT, it might justify others trying EACT.
During Dr. Xue's visit, did he demonstrate EACT? if yes, I would be pleased
to talk to an American observer who may have participated in such a

demonstration.

'

"

Thank you for bringing Dr. Xue's arguments to my attention. if there is
more that needs discussion, you can call me most mornings at my office (5164M
2929).
Sincerely yours,

Max Fink, MAD.

�</text>
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                    <text>November 1n, 1979
Sigurd Aokermen, M.D.
Montefiore Hospital
Bronx, New York 10MB?
Dear Sig,

Enclosed are the two

reprints concerning our

studies of lactate in anxiety. The letter was a way to indicate that
we-had replicated the findings of Pitts and McClure. We did not go
further as the proposals, sent to NIMH, were not accepted. (Since
then, the reviewers have undertaken very similar studies.)
sample.

The EEG

report

summarizes our few records

in the
.

I hope these are of interest.
discussing your work.
My

It

was a

pleasure

regards.
Sincerely yours,

"ﬁfe-w
Fink, M.D.
Professor of Psychiatry
Mex

first

�</text>
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                    <text>-WV

.{1

,_

-v

....,...A.,,‘,

Mardh 22, 1971

Acts Psych. Scandinavica

Munksgaard

Frags Boulevard 47
2300 Copenhagen

3. ,

Denmark

Gentlemen:
We

like to purchase copies of:
Supplement 213, by Laurell on Flurothyl
Supplement 215, by D'Elia on Unilateral

would

Are

these available,

and

at

what cost?

Thank you.

Sincerely yours,
Fink, M.D.
Executive Director

Max

MF:kt

ECT.

�</text>
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                    <text>T
“WVNW

wmw.mwy“m

“m

v-

v—v-

March 22, 1971

Acta Paych. Scandinavica

Hunkagaard

Praga Boulavard 47
2300 Copanhaaau

8.,

Denmark

Gantleman:
Wa

would

lika to purchase copiea of:

Supplamant 213, by Laurell an Flurothyl
Supplamant 215. by D'Elia on Unilateral ECT.
Ara thaaa

availabla,

and

at what coat?

Thank you.

Sincerely youra,
Pink, M.D.
Executive Director

Max

MF:kt

�</text>
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                    <text>March 5, 1971
Miss Carolyn Adams
c/o 782 Hemlock Rd.
Union, New Jersey 07083
Dear Miss Adams:

the central effects of substances
clinical practice of neurology (neuropsychiatry).

we are investigating
we are not in the

While

of abuse,

letter is detailed about your search for help, but fails to mention,
help for what. Perhaps you should see your family physician or a member
of the staff at either the New Jersey School of Medicine in Newark (try
Dr. Louria) or at Rutgers Medical School, and allow them to recommend
the consultants you may require.

Your

If you wish to detail the history of the symptoms that trouble
you, I will ask one oﬁ our research staff to review the material and
perhaps we may make a more specific recommendation.
Sincerely yours,
Fink, M.D.
Professor of Psychiatry

Max

MF:kt

�</text>
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w~wmvnnv

“Hr-1""-

WWW—

1

March 5, 1971
Miss Carolyn Adams
c/o 782 Hemlock Rd.
Union, New Jersey 07083

Dear Miss Adams:

investigating the central effects of substances
are not in the clinical practice of neurology (neuropsychiatry).
Your letter is detailed about your search for help, but fails to mention,
help for what. Perhaps you should see your family physician or a member
of the staff at either the New Jersey School of Medicine in Newark (try
Dr. Louria) or at Rutgers Medical School, and allow them to recommend
the consultants you may require.
While we are

of abuse,

If

you, I
perhaps

we

you wish to
will ask one
we may make

detail the history of the symptoms that trouble
oi our research staff to review the material and
a more specific recommendation.

Sincerely yours,
Fink, 24.1).
Professor of Psychiatry

Max

MF:kt

�</text>
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.uwun-grp".

June 2, 1970
Dr. Henry Adams

university of Georgia
Athens, Georgia
Dear

D .

Adams,

my associates and I have read your recent report, ”Electroconvulsive Shock, Brain Acetyloholinesteraee Activity and Memory" with
considerable interest. we would like to become acquainted with any
subaequent studies from your laboratory.

are aware, Ulett and his co-workers were unable to
even with higher dosages of'atropine (oft
Johnoon et al., Arch gen Psychiat., 2:324—336, 1960). In reviewing their
experiences, and our own with various anticholinergic drugs, we became
concerned that studies (particularly in man) that dependeddbn the
anticholinergic effects in the central nervous system were often
unsuccessful because the peripheral effects of'atropine exceed the
central effects, especially at low dosages. While the same is less
true for scopolamine, this compound also has extensive peripheral effects.
we tested a variety of active anticholinergic drugs and reported that
benactyzine, Ditran and diethazine seemed to elicit a higher degree of
central activity in proportion to their peripheral effects.(cj2 EEG clin.
As you

replicate their findings,

Neurophysiol. ,

12.- 359—369,

1960) .

time ago, I reviewed the available data on central
and
anticholinergic
cholinergic activity and the convulsive therapy
and
am
I taking the liberty of’enclosing a reprint that may
process,
Some

be

of interest.

Again, our congratulations on a nice piece cf’work.

Sincerely yours,

m Fink,

M. D.

Professor of’Psychiatry
mf/

�</text>
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W. w

~

v.7 pr...- ——m
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an

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.,

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.7

,_ e

, ..

M.

.77.

September 15, 1977
John B. Adams, H.D.
College of Medicine

University of Florida

Gainesville, Florida

Re: Ali Kestiner, M.D.

Dear Dr. Adams,

It is a pleasure to write the following regarding

my

association

with Dr. Ali Keskiner. I first met him when he came to Missouri and joined
the staff of the Missouri Institute of Psychiatry, about 1963, at a
time when I was Director of the Institute. He accepted a position of

clinical responsibility in managing one of the Institute's 25 bed units,
and undertook clinical research in that population. In the course of

became interested in the aftercare of psychiatric patients
and he became the principal investigator in a long-term community treatment
project. At the time I left the Institute, in 1966, he was a leader of
a clinical team and a responsible researcher. I thought highly of his
work, and invited him to come with me to New York.

his work, he

His principal studies were in the clinical effects of new
in treating the mentally ill. At the time, our interest was
in the application of fluphenazine enanthste, and it was Dr. Keskiner's
contribution to demonstrate the efficacy of this compound for the
maintenance of the long term mentally ill in the community. He showed
the contribution that the drug could make when combined with social
casework and adequate aftercare management. His work was honored by
compounds

a number of awards.

effectively pleasant,
all my association, I fcund him friendly,
and firm. He
broad
His
knowledge
is
clinical
responsible.
relaxed,
relates well to staff and patients and his unit was often used as a
demonstration unit for visiting dignitaries. In his research protocols,
he was innovative and particularly sensitive to the personal needs of
the patients. He is a sensitive clinician and a well ‘brgenised teacher.
On a number of occasions he lectured to the residents and his lectures
In

and

were well received.

faculty,

I

and

am

pleased to

believe

he

recommend him for an appointment
do a commendable job.

will

to the teahhing

Sincerely yours,

.

Max Fink, M.D.
Professor of Psychiatry

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                    <text>rAngust 21, 1964

Paul L. Adams, M.D.

Assistant Protector of Psychiatry
Road. Child Psychiatry Division

Department of Psychiatry
College of Modicino

Univcrsity of Florida
Gaincsvillo. Florida
Dear Dr. Adams:

Dr. Habib Nathan has applied for a position in the clinical
roaocrch programs at this reaccrch and training center, and
has suggested that we may write to you for a recommendation.

at this institute are devoted to clinical psy~
chiatric research, primarily of a nouropharmacologicai and
nourophysiological variety. The grogrsms are designed also
The programs

as tho basis for tho training of residents in psychiatry.

would be grateful for any information you can give as regarding tho ability of Dr. Nathan to participate in clinical
psychiatric research programs; his parsonality as related to
his patients and codworkcrs; and his facility with the English
language.

we

Thank you very much

for your cooperation.
Sincerely yours.
Fiﬁk.
m
Director

mljb

M.

D.

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                    <text>....

v vw "nav'uwl: m'JKIL-‘r

-:"'n;'!.‘—K\

urn-n

u n. v-ww:""~ "'0’..’ll"~ ~r-wrmn~m

hwy-‘4

w.

at;

Wu.-

..~...--

._.

.

v

m

.7

,.

r,
v,‘,-.—
_.. “re—v7“
“'Kif’ . Kan—".7 '11 .w.
,

,

wVlrr‘ \m- w... Vg....N:
,

.

.

M

2 -.~

September 30, 1970
Addiction Research Foundation
344 Bloor Street West
Toronto 4, Canada

,..._.,

.

.Jymwuwu.

Wham.

rm

ﬁn-

Gentlemen:
I have received "An Interim Guide to the Cannabis (Marihuana)
Literature” by Oriana Josseau Kalant and I have read it with great
interest. I wish to commend the author for a clear and unbiased
review of a difficult subject. For those articles which I already
knew, I found the technical statements clear and usefhl.
Many

thanks for sending

me

a cepy.

Sincerely yours,

WT:

Fink, M.D.
Professor of Psychiatry

Max

Mszt

�</text>
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