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                  <text>March 19, 1996
Greg Fricchione, MD.
Division of Psychiatry
Brigham &amp; Women’s Hospital
75 Francis Street
Boston MA 02115
Dear Greg,
What a terrible story about Anthony Bouckoms! I liked him very much;
last November I invited him to join me and Charlie Welch in an ECT symposium at the
Boston APA meeting. He did well, and he told us of the changes in progress at Hartford
Hospital. Pity, such an untimely personal and professional loss; more than doubly sad for
his wife and remaining children.
I have read the article on catatonia with interest. My suggestions -- I
cannot read any article without and editorial pen in hand -- are in the text and margins.
Overall, I think the essay presents the experience well. But, if we are to be of service, we
should be more deﬁnite about the conclusions which we wish to leave as the ‘messages’.

The ﬁrst message is to recognize catatonia, and that is done well. Andy and
George will probably wonder why you do not recommend the use of their handiwor -the catatonia rating scale. By the time you get this note, it will be published [it is in the
March number of the Acta]. Instead of tables 4-6, should you not adopt the rating scale
and test method? We will surely have no objection to such use. [There is one small point -both George and Andy saw the scale as their ‘special’ handiwork and in the text of the
article labeled the scale as the ‘Bush-Francis Catatonia Rating scale’ or BFCRS —- a
cumbersome title that will not sell well. I believe you can adopt the scale without the
mnemonic label, as I have done elsewhere]
Similarly, you may wish to amplify the paragraph discussing the Bush et al
experimental ﬁndings in incidence of cases and treatment results, much as you do for the
Ungvari and Rosebush data (pg 16).

�The discussion of the theory of the mechanisms in NMS, catatonia, and
malignant hyperthermia deserves a clearer message (pg 23). When NMS was discerned as
an entity in the late 1970s, it was seen as similar to malignant hyperthermia, leading to the
suggestion that dantrolene be tried. But no commonality between MH and NMS has been
demonstrated except the superﬁcial appearance of the syndromes. Further, the evidence
for the efﬁcacy of dantrolene alone in NMS is anecdotal at best. (I am not convinced that
it does anything material in CNS disorders.) It does no good to continue to recommend its
use in NMS.
In the theoretic argument (pg 24), you argue for a speciﬁc site for
pathophysiology. Perhaps you would include a statement that one should assess PET with
xxxx as the ligand or SPECT for lesions in yyyy and/or zzzz. Such speciﬁcity may bring
you more attention than the more general, non-speciﬁc loci recommended now. [I believe
Mickey Taylor did himself a disservice by hsi trepidation in not seeking to argue for more
speciﬁcity; as a result his work is usually seen as ‘something happens to the brain, more in
the front than the back, I think . . .]
Finally, the summary argumen -- which is usually the most read- should be
clearer about what you recommend as a course of treatment. The journal is ‘critical care
medicine’, read, I assume by clinicians. What I have learned since we treated our patient
on 16N together is that that all neuroleptics need to be discontinued promptly; that
supportive measures instituted; and that lorazepam needs to be ‘pushed’. My present
dosage range for lorazepam is up to 16mg/day. I see no need to ever consider
bromocn'ptine or dantrolene -- if lorazepam fails, ECT is the deﬁnitive treatment. If the
diagnosis of catatonia is secure, such Rx will surely optimize the best for the patient.

I have also pencilled in corrections for some of the citations.
On a more personal level, I do not need to be a co-author of another paper.
I am delighted to help in this effort -- and will gladly review a penultimate draﬁ -- and all I
warrant is a note of thanks in the acknowledgements.
Many thanks for the opportunity to read this review. My best regards.
Sincerely yours,

Max Fink, MD.
Professor of Psychiatry
and Neurology

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