http://exhibits.library.stonybrook.edu/mfp/files/original/f7c87e4b8450f1ed2913d4dcd19d8101.pdf 28b2641c12bb8afccfb2c988034e1cc8 PDF Text Text Reprinted from the ISRAEL STRAUSS COMMEMORATIVE VOLUME Journal of the Hillside Hospital Volume V, Numbers 3 - 4 October, 1956 �DENIAL OF BLINDNESS FOLLOWING CEREBRAL ANGIOGRAPHY MAX FINK, M.D.1 In the ﬁfty-eight years since the original report of Anton (1), there has been controversy in the literature as to whether denial of blindness is the result of a speciﬁc focal cerebral lesion or of a generalized disturbance of brain function without speciﬁc localizing signiﬁcance.2 In reviewing the cases of denial of blindness, the majority of reports describe the patients as “confabulating,” “disoriented,” or “showing a Korsakoff psychosis.” Such descriptions lend support to the concept that denial occurs in a milieu of altered cerebral function. Studies of denial of hemiplegia, usually described under the term “anosognosia,” bring out identical arguments as to the signiﬁcance of the phenomenon for localized dysfunction. Indeed, in many reports of denial of blindness, note is made of simultaneous denial of hemiplegia or of other defects. The literature of denial of illness, as well as clinical and experimental evidence to support their concepts, has been recently summarized by Weinstein and Kahn (23). They conclude that various forms of denial are a unitary phenomenon without cerebral localizing value, and that denial is an adaptation to a defect in the milieu of diffusely altered cerebral function. In this regard, most of the defects denied are of rapid onset, are not limited to one defect, are accompanied by confabulation, amnesia, changes in mood and absence of anxiety. The degree of altered cerebral function which provides the milieu for such adaptation is usually severe. Thus, their reports, as well as those of other authors cited (see footnote 2), Director, Research Service, Hillside Hospital, Glen Oaks, N. Y. 2The reviews of Critchley (6) and Weinstein and Kahn (23) present the two aspects of this problem. For speciﬁc reports ascribing the phenomena to focal cerebral disease see Barkman (2), Gerstmann (10), von Hagen and Ives (21, 22), Ives and Nielsen (l2), and Paul (16). Reports ascribing the phenomena to diffuse cerebral disturbances include Lunn (13), Redlich and Bonvicini (l7), Redlich and Dorsey (18), and Sandifer (19). 238 1 �DENIAL OF BLINDNESS 239 describe the phenomena of explicit denial of blindness and of hemiplegia as occurring in patients with brain tumors, subarachnoid hemorrhages and vascular disease. The following case history is presented as exemplifying various aspects of the syndrome of denial. The data support the thesis that the phenomenon is an adaptive response to a defect under the conditions of altered cerebral function, rather than the result of focal cerebral pathology. A patient, under observation for enlargement of the sella turcica presumably the result of pituitary adenomatous growth, was subjected to cerebral Iodopyracet (Diodrast) angiography. Before the procedure he was alert and oriented, but immediately following the second series of injections of Iodopyracet, he developed left hemiplegia, which gradually resolved. In the ensuing hours, blindness developed and was denied by the patient. The syndrome persisted for 48 hours, and then resolved. When the patient was seen in a follow-up visit eight months later there was an amnesia for the period of denial. Case Report:3 E. S., a 58-year-old right-handed male, was admitted for diagnostic study to the Monteﬁore Hospital with a sixmonths history of headaches and blurring of vision. Four months previously he had an episode of ptosis of the right lid associated with dilatation of the right pupil, which had persisted for a few weeks. Headaches became increasingly severe, and X—ray examination of the skull prior to admission demonstrated an enlarged sella turc1ca. He related his own history; appeared neither acutely nor chroni— cally ill; was alert, well oriented, and cooperative, with good memory and calculating ability. He was jovial, made friends readily, and was well liked. He denied previous severe illnesses, or persistent somatic complaints. He was fastidious about his personal belongings and was reluctant to intrude. The general examination was normal except for palpable enlargement of the right lobe of the thyroid gland. Neurological examination was normal except for the cranial nerve examination. His pupils were dilated, the right larger than the left. The reaction to light was sluggish on the right, and the pupils reacted well to near vision. The fundi showed well-outlined papillae with clear margins, deﬁnite temporal pallor, and normal vascularization. Visual acuity was 15/20 on the right, and 15/40 on the left. Visual ﬁelds to 1/2000 white test object demonstrated a relative bitemporal hemianopsia without macular sparing. The lumbar puncture and routine blood and urine studies were normal. Skull X-ray revealed enlargement of the sella turcica; atrophy of the anterior and posterior clinoids; and calciﬁcations along 3 Patient studied through the courtesy of Dr. Nathan Savitsky at the Monte- ﬁore Hospital. �240 MAX FINK the lateral border of the sella. Pneumoencephalography demonstrated encroachment of the cisterna chiasmatis and pontis by a mass originating from the sella. An electroencephalogram showed a slight degree of electrical abnormality on the left side, mainly inferior and posterior. Alpha frequencies and amplitude were symmetric. For further clariﬁcation of the pathologic process, carotid angiography was recommended. Under local anesthesia, the right common carotid artery was exposed, and forty cc. of 35% Iodopyracet (Diodrast) was administered. Since the serial angiograms thus made were unsatisfactory, another injection of 15 cc. Iodopyracet was made. Immediately following this injection, the patient developed a complete left hemiparesis, including the face. He was restless, confused and irritable. He appeared drowsy; failed to obey commands and was irrelevant in speech. Vasodilators were administered, and the hemiparesis showed some improvement. That evening he was restless, directing his gaze most often to the right. When spoken to from his left side, he would turn his head to the right or backward, before ﬁnally localizing the voice correctly. He answered questions relevantly. Visual acuity was reduced to light perception, and pupillary reactions were present, though sluggish. He was unable to localize the position of a light nor identify ﬁngers or objects; yet he denied his inability to see, confabulating seemingly appropriate responses. He was oriented for place but only approximately for time and date. Despite a large neck bandage, he denied the recent cutdown. A lumbar puncture was performed. The initial pressure was 140 mm. CSF, ﬁnal pressure of 60mm. after the removal of 8 cc. of clear, colorless ﬂuid which had no cells and a protein content of 43 mg%. Twelve hours later, now oriented in space and time on gross questioning, he was still unable correctly to localize light or perceive objects. There was a residual left hemiparesis. He denied both his weakness and his blindness. When walking about the room he stumbled over objects and bumped into the wall and the bed. He correctly identiﬁed the various examiners by their voices, and named a coin, key, pencil and comb by touch. There was no sensory loss on single stimulation; gait was hesitant; and the reﬂexes were increased on the left with bilateral Babinski responses and absent abdominal reﬂexes. Thirty-six hours later the hemiparesis had cleared except for a residual left Babinski response. He perceived light and localized it well in‘space, but image formation for reading or ﬁne identiﬁcation was impaired. Despite the partial nature of his vision, he still failed to recognize his impairment, confabulating many responses. An electroencephalogram at this time showed a change from the original record. There was bilateral asymmetry with high per cent time delta activity and a slowed, poorly organized alpha rhythm, mostly on the right. Forty-six hours later his vision had returned so that he was able �DENIAL OF BLINDNESS 241 to read. He was oriented, alert, affable and friendly. He maintained that he had been able to read and to see throughout the previous two days. He had an amnesia for the surgery, the hemiparesis and the blindness. During the ensuing weeks, visual acuity returned to normal; with visual ﬁelds manifesting minimal bitemporal hemianopic defect. An electroencephalogram one week later showed posterior voltages to be less depressed; per cent time delta activity had decreased; and there was desynchronization of the record on delta the of accentuation focal abnormality There was opening. eye in the right frontal leads. Three weeks later the electroencephalo— inwith abnormalities of the resolution increased showed gram creased and bilaterally equal per cent time alpha; decreased per cent time delta and resolution of the electrical asymmetry of the hemispheres. On examination eight months after this episode and after a course of radiation therapy for pituitary adenoma, this patient was alert, oriented and cooperative; with only occasional complaints of headache. The neurological examination was completely negative with normal visual acuity and a slight (10°) bitemporal hemianopic defect with 1/1000 white test objects. He denied any experience of blindness or weakness but did recall the neck dissection that preceded the angiography. When told of the experience, he jokingly denied the weakness and the blindness by saying that I was mistaking him for another patient. Discussion: Two aspects of this case report warrant ampliﬁcation: the signiﬁcance of the denial phenomenon and the cause of complications following cerebral angiography. The various aspects of denial of illness described by Weinstein and Kahn are well exempliﬁed here. The acute onset of hemiplegia and blindness was followed by a period of restlessness, disorientation, and altered consciousness. Within a few hours, these gross symptoms were replaced by a calm, disinterested, smiling attitude in which the multiple defects of left-sided weakness and blindness were denied. He confabulated, was disoriented for time and date, and later was amnestic for this period. An electroencephalogram demonstrated bilateral diffuse slow wave activity of high voltage. Furthermore, despite the visual loss, the phenomenon of spatial inattention4 was observed. This complex of symptoms and signs is generally noted in diffuse cerebral disorders. While much effort has gone into localizing these defects, it is difficult to conceive a single focal lesion affecting the visual tracts bilaterally, the right hemisphere in an Various terms have been applied to the unawareness of one half of the body and the body space, such as imperception for one half of body (Schilder, 20), hemi-depersonalization (Ehrenwald, 7) and autosomatagnosia (Gerstmann, 10). See also Critchley (6, pp. 237-241), and Brain (4). 4 �242 MAX FINK area productive of hemiplegia and the frontal areas assumed to be productive of apathy, denial, and loss of anxiety. While the possibility of a focal lesion as the basis for this syndrome cannot be ruled out, it is more tenable to conclude that diffuse cerebral dys~ function was present. This conclusion is supported by the electroencephalogram, and also by experimental evidence noted below, demonstrating the effect of intra-arterial Iodopyracet as inducing severe vasospasm followed by generalized cerebral edema and increased permeability of the blood-brain barrier. The signiﬁcance of the phenomenon of denial is to be seen in its defensive nature. While undergoing a test procedure, the patient suddenly suffers a catastrophic disability. His initial response of severe anxiety, manifested by restlessness, startle reaction, and irritability, is soon replaced by explicit denial. This primitive, “psychotic” defense is normally present only in childhood. But under the special conditions of cerebral dysfunction, with disturbances in spatial and temporal orientation and perception, denial of reality becomes tenable. It is maintained so long as the disability and the milieu of cerebral dysfunction persist. In this patient, as soon as visual perception was sufficient for reading, confabulation and explicit denial were no longer actively maintained for ongoing events. In the special situation of interviews with the staff during the period of visual and motor loss, the patient manifested no concern and confabulated responses readily. When visual acuity returned and his hemiparesis cleared, he maintained the same is imthis it In attitude. unconcerned regard affable, friendly, of denial in factor the explicit characterological to note portant illness. To the extent that the information is now available, this patient manifested a considerable number of the features described by Weinstein and Kahn (24). Special note should be made of the phenomenon of spatial inattention. The patient’s original visual complaint of blurred vision was accompanied by a minimal bitemporal hemianopia, apparent only on testing with 1/2000 white test objects. During the period of visual loss he was unable to locate a light and confabulated responses. One week later the bitemporal hemianopia was present to 3/2000 white test object, but in addition there was an irregular left homonymous upper temporal ﬁeld defect to 5/2000 white. Evidence of a left homonymous ﬁeld defect persisted in examinations for three weeks, after which only residual bitemporal defects were persistently reported. Left spatial inattention was prominent in the ﬁrst 48 hours of this syndrome only, at the time when visual im- �DENIAL OF BLINDNESS 243 pairment was maximal, and when hemiparesis was present. When the hemiparesis receded, visual function returned, and orientation was intact, then spatial inattention disappeared. Thus, spatial inattention was an aspect of the total disturbance in function, possibly motivated by the left-sided defects, and was probably not dependent on a speciﬁc visual ﬁeld defect. The syndrome of blindness and its denial following cerebral angiography is unique. Focal lesions producing transient hemiplegia, hemisensory defects, seizures, aphasia, and various cranial nerve syndromes have been described. In a series of 117 percutaneous carotid angiograms, Fink and Stein (9) noted an 8 per cent morbidity of such transient phenomena. Other series variously report such complications from 3 to 15 per cent of the cases.5 These ﬁgures do not include the few patients in whom the complications as hemiplegia, aphasia or exaggeration of their basic disease are permanent; or who succumb. In these studies of the complications of angiography, emphasis is placed on the relation of the concentration of the contrast medium, the rate and quantity of contrast substance injected and the time within which the injections are repeated. In experimental studies Olsson (14), Broman and Olsson (5) and Bloor et al. (3) demonstrated summation of toxic effects when the contrast substance was rapidly injected into animal arteries; and noted increased vascular permeability, cerebral edema and petechial hemorrhages not limited to the side of the injection. While it is possible that the complications of angiography are the result of thrombus formation at the needle site and focal embolization, it is more likely that diffuse toxic cerebral vascular changes are induced as seen experimentally. The diffuse character of the defects and the transient nature of the phenomena in this patient are readily understood in this context. Summary and Conclusions: In the course of carotid angiography in a patient with evidence of a pituitary adenoma, an acute transient episode of blindness and hemiplegia developed. Following a short period of restlessness and confusion, the patient became calm, denied his blindness and weakness, confabulated responses to questions, was disoriented, and manifested spatial inattention. The diffuse nature of the cerebral dysfunction underlying this syndrome is emphasized by noting the distribution of the presumed lesions, the bilateral, diffuse slowing of the electroencephalogram, 5For reviews of the complications of cerebral angiography, see Engeset Fink and Stein (9), Green and Arana (ll), (8), Perese et a1. (15) and Wickbom (25). �244 MAX FINK and the diffuse nature of the toxic sequellae of intra-carotid Iodopyracet (Diodrast). The defensive-adaptive signiﬁcance of the syndrome of denial of blindness and hemiplegia is discussed, with emphasis on the development of this attitude under the special conditions of altered frames of temporal and spatial reference provided by altered cerebral function. REFERENCES (1) Anton, G.: Uber Herderkrankungen des Gehirnes welche von Patienten selbst nicht wahrgenommen werden. Wien. Klin. Wchnschr., 11:227-229, 1898. (2) Barkman, A.: De l’anosognosie dans l’hemiplegie cerebrale. Acta Med. Scand., 62:235-254, 1925. (3) Bloor, B. M.: Wrenn, F. R.; Margolis, 6.: Experimental Evaluation of Certain Contrast Media Used for Cerebral Angiography. ]. Neurosurg., 8:585—594, 1951. Brain, W.: Perception and Imperception. ]. Ment. Sci, 1022221-232, 1956. Broman, T. and Olsson, 0.: Tolerance of Cerebral Blood Vessels to a Contrast Medium of the Diodrast Group. Acta Radiol., 30:326-342. 1948. (6) Critchley, M.: The Parietal Labes. London: E. Arnold 8: Co., 1953 (see Chap. VIII, pp. 225-255; IX, pp. 258-263). (7) Ehrenwald, H.: Verandertes Erleben des Korperbildes mit konsekutiver Wahnbildung bei linksseitiger Hemiplegie. Mtschr. Psychiat. (2» Neural, (4) (5) 75:89-97, 1930. (8) Engeset, A.: Cerebral Angiography with Perabrodil. Acta Radial, Suppl, 56, 1944. (9) Fink, M. and Stein, J. M.: A Clinical Evaluation of Carotid Angiography. Conﬁm'a Neural, 12:181-195, 1952. (10) Gerstmann, J.: Problem of Imperception of Disease and of Impaired Body Territories with Organic Lesions. Arch. Neural. (5' Psychiat, 48:890-913. 1942. J. R. and Arana, R.: Cerebral Angiography: A Clinical Evaluation Based on 107 Cases. Am. ]. Raentgenol., 59:617-650, 1948. Ives, E. R. and Nielsen, J. M.: Disturbances of Body Scheme. Bull. L. A. Neural. Soc., 22120-125, 1937. Lunn, V.: Uber mangelnde Wahrnehmung der eigenen Blindheit. Acta (11) Green, (12) (13) Psychiat. é} Neural, 16:191-242. 1941. (14) Olsson, 0.: Cerebral Angiography: Tolerance for Contrast Media of Diodrast Type. J. Neural, Neurosurg. é, Psychiat., 12:312-316, 1949. (15) Perese, D. M.: Kite, W. C.; Bedell, A. J.; Campbell, 12.: Complications Following Cerebral Angiography. A.M.A. Arch. Neurol. é} Psychiat., 712105-115, 1954. (16) Potzl, 0.: Uber Storungen der Selbstwahrnehmung bei linksseitiger Hemi- plegie. Ztschr. ges. Neural. (9 Psychiat., 93:117-168, 1924. (17) Redlich, E. and Bonvicini, G.: Uber das Fehlen der Wahrnehmung der eigenen Blindheit bei Hirnkrankheiten. Jahrb. f. Psychiat., 29:14.23, 1908. (18) Redlich, F. C. and Dorsey, J. F.: Denial of Blindness by Patients with Cerebral Disease. Arch. Neural. {‘7 Psychiat., 53:407-417, 1945. (19) Sandifer, P. H.: Anosognosia and Disorders of Body Scheme. Brain, 69:122137, 1946. (20) Schilder, P.: Localization of the Body Image. Assoc. Res. New. Dis., 13:466-484. 1932. {9'- Ment. �DENIAL OF BLINDNESS 245 (21) von Hagen, K. and Ives, E. R.: Anosognosia, Imperception of Hemiplegia. Bull. L. A. Neural. Soc., 2:95-103, 1937. (22) von Hagen, K. and Ives, E. R.: Two Autopsied Cases of Anosognosia. Bull. L. A. Neural. Soc., 4:41-44, 1939. (23) Weinstein, E. A. and Kahn, R. L.: Denial of Illness. Springﬁeld, 111.: Charles C. Thomas, 1955. (24) Weinstein, E. A. and Kahn, R. L.: Personality Factors in Denial of Illness. A.M.A. Arch. Neurol. (5» Psychiat., 69:355-367, 1953. (25) Wickbom, I.: Angiography of the Carotid Artery. Acta Radiol., Suppl., 72,1948. �" Mamma: . mm. W W W6 63mm WWW mm,ljh9.* 3 Iran tau _.; a» V 1 3, Baum Sam», mill-ids Hospital, 61m Oaks, law mm ”imam, Rinaldo Hospital. 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For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Published Works Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Denial of blindness following cerebral angiography. J Hillside Hosp. 1956:5:238-245. Type The nature or genre of the resource Text Identifier An unambiguous reference to the resource within a given context mfp-02-01-001-20-024 Date A point or period of time associated with an event in the lifecycle of the resource 1956 Creator An entity primarily responsible for making the resource <a title="Fink, Max, 1923-" href="http://id.loc.gov/authorities/names/n79039548" target="_blank">Fink, Max, 1923-</a> Subject The topic of the resource Published Works -- Articles and Reviews Relation A related resource The Max Fink Collection Description An account of the resource [Preprint] and reprint. Reprint from the ISRAEL STRAUSS COMMEMORATIVE VOLUME Journal of the Hillside Hospital Volume V, Numbers 3-4 October,1956 Rights Information about rights held in and over the resource <a title="IN COPYRIGHT - EDUCATIONAL USE PERMITTED" href="http://rightsstatements.org/vocab/InC-EDU/1.0/" target="_blank">IN COPYRIGHT - EDUCATIONAL USE PERMITTED</a> Source A related resource from which the described resource is derived Special Collections and University Archives, University Libraries. Stony Brook University Libraries (State University of New York). Language A language of the resource en-US Format The file format, physical medium, or dimensions of the resource application/pdf Publisher An entity responsible for making the resource available Contributor An entity responsible for making contributions to the resource Published