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Schizophrenia-like illness following head injury
CASE REPORT
HENRY A. NASRALLAH, M.D. RICHARD C. FOWLER, M.D. LEWIS L. JUDD, M.D.
Schizophrenia-like illness following head injury There is a large literature on psychoses associated with head injuries. The most extensive review of the subject is that of Davison and Bagley,' in which they conclude that the incidence of schizophreniform psychosis in brain-injured subjects is significantly higher than in the general population, that genetic predisposition does not seem to playa role in such cases, and that there seems to be an association with temporal lobe lesions. They also noted that information about treatment and prognosis was lacking in the literature. Here, we report a case of a young man with a good premorbid history (as far as we could establish), and no first or second degree family history of psychiatric illness, who developed schizophrenic symptoms subsequent to head trauma, and whose clinical course over , the past six years strongly resembles chronic schizophrenia despite significant improvement in his posttraumatic cognitive deficits. C. . ntpOrt Six years prior to the current assessment a 22-year-old
Dr. Nasrallah is chiefofthe psychiatry service at the Veterans Administration Medical Center, Iowa City, and associate professor of psychiatry at the University of Iowa College of Medicine; Dr. Fowler is staff psychiatrist at the Veterans Administration Medical Center, San Diego, and assistant professor of psychiatry at the University of California San . Diego School of Medicine; and Dr. Judd is prOfessor and chairman of the department of psychiatry at the U.C.S.D. School of Medicine. Reprint requests to Dr. Nasrallah, VA Medical Center, Iowa City, IA 52240. APRIL 1981 • VOL 22 • NO 4
college student was struck by a car while riding his bicycle. He immediately lost consciousness and was hospitalized. Initial examination revealed a semicomatose man. responsive only to painful stimuli. There was evidence of trauma to the left side of his face and chest as well as a left hemotympanum. Neurologic examination was unremarkable except for bilateral Babinski reflex and an ankle jerk greater on the right than left. A subsequent examination, after the patient emerged from coma, revealed a left lateral rectus palsy (which persisted for several weeks) but no sensory deficits. and normal funduscopy and visual fields. Electroencephalography showed low-to-moderate-voltage asynchronous polymorphic activity over the right hemisphere. maximal in the paracentral regions. Skull x-ray film showed a left basilar skull fracture. An echoencephalogram was normal but a right carotid angiogram showed decreased arterial vasculature in the right frontal area with late filling of the right frontal vein, a finding consistent with right frontal-lobe contusion. A left carotid angiogram revealed early filling of the deep venous system consistent with contusion or ischemia of the left basal ganglia. Six days after the accident the patient had multiple focal seizures involving the left side of his face and one involving the right side. These were treated with anticonvulsants and there were no subsequent seizures. There was litlle change in his mental state until 16 days after the trauma, when he began responding to verbal stimuli. Subsequent improvement was rapid and the patient was alert and talking by the fourth week. Neuropsychological assessment at that time showed scores in the normal range on the Bender VisualMotor Gestalt and on the Graham Kendall Memory for Design. However, Wechsler Adult Intelligence Scale full scale 10 was 56 (verbal. 52; performance. 66). Although there was no documented evidence of psychosis during that 359
Case report
period, the patient's mother recalls that he did express concerns about voices on the radio accusing him of homosexuality within hours of emerging from coma. The subsequent course was uneventful until six months after the injury, when the patient received his first psychiatric examination. This visit to a mental health clinic was initiated by the patient at the suggestion of his surgeon, but his motives for seeking help were obscure. His mental status examination revealed no specific complaints; no evidence of delusions or hallucinations; neutral mood; and appropriate affect. His flow of thought was moderately tangential but otherwise coherent and logical. Cognitively, he was fully oriented, with good recent and remote memory as well as good attention and concentration (he repeated eight digits forward and five digits backward). A Minnesota Multiphasic Personality Inventory was interpreted as consistent with depression or schizo-affective disorder. A full scale IQ was 108. Over the ensuing weeks he was seen regularly in the outpatient clinic and was described as rambling, easily frustrated, and preoccupied with his disability. He also complained of headaches and insomnia. He received an antidepressant trial of imipramine 100 mg daily for three weeks but it was apparently not effective and the patient stopped taking it. He was then begun on thioridazine 200 mg daily because of increasing anxiety, and this had a calming effect. Thirteen months after the accident, the patient expressed suicidal ideas and hopelessness about recovery. This prompted his first psychiatric hospitalization. He was treated for depression with amitriptyline 150 mg daily at bedtime and haloperidol 5 mg daily at bedtime. He also remained on phenytoin 300 mg daily at bedtime. Clinical response was rapid and the patient was discharged after a brief stay. However, there was an apparent change in his mental status over the next two months. He began expressing concern that others considered him a homosexual. He also reported he was the subject of an "experiment" at the Veterans Administration Hospital and that his biking accident was part of the "experiment." Affective symptoms were no longer prominent, though readmission was prompted by an overdose of unknown amounts of thioridazine, phenytoin, and amitriptyline (most of which the patient vomited after ingestion with no medical sequelae). The patient later said that the overdose was his attempt to end the "experiment," thus indicating that the suicidal gesture was probably a delusional act rather than a result of depression and suicidal intel}!. Over the next five years, the patient had seven more psychiatric admissions. Delusions of reference, influence, thought contrOl, and persecution wer& always prominent, and speech and thoughts were disorganized; but sensorium was always clear. Treatment with a neuroleptic (usually fluphenazine decanoate) was begun on each admission with considerable symptomatic improvement. However,
after discharge he invariably stopped the neuroleptic (though he would continue the phenytoin) and he would relapse again and show schizophrenic manifestations. The periods between hospitalization were marked by social instability. He frequently moved from board-and-care homes to his own apartment or the homes of relatives. Attempts to resume school or obtain employment were unsuccessful and he did not date, though he frequently expressed concern about this. On his most recent hospital admission, six years after the accident, psychotic symptoms were again prominent. He believed people on television were talking about him and that a particular woman was controlling his thoughts. His speech remained disorganized and an inappropriate smile was often present when he talked about his delusional beliefs. He remained distressed by his circumstances and continued to express suicidal ideas. Clinical assessment of his intellectual functioning revealed no deficits and neurologic examination was within normal limits. A full scale IQ was 112 (verbal 113, performance 11 0) and the HalsteadReitan impairment index was 10 per cent. An EEG revealed a generalized grade II dysthythmia, and a computerized tomographic brain scan showed a left lateral ventricle that was slightly larger than the right.
Discussioa This case illustrates that psychopathologic changes with a clinical course indistinguishable from that of chronic undifferentiated schizophrenia can follow head injury. The patient appears to have been a previously healthy adult with no family or personal premorbid history that would indicate predisposition to schizophrenia, according to history from his mother and brother. Yet after his head injury, he developed first-rank Schneiderian symptoms as well as formal thought disorder (loose associations). The literature on psychosis associated with head injury describes mainly a schizophrenia-like psychosis but with nonspecific delusions and hallucinations, and rarely any formal thought disorder.2 The improvement in the patient's IQ six months after the head injury, followed by a relentless chronic downhill course with paranoid and hebephrenic features and only a partial response to neuroleptic drugs, all add to the similarity of this patient's posttraumatic illness to chronic undifferentiated schizophrenia. Up to 15% of schizophrenic patients present with a history of head injury preceding the onset of the first psychotic episode, and .07% to 9.8% (the range in eight studies involving 12,385 patients) of brain-injured patients eventually develop schizophrenia-like psychosis.· It is possible that head injury may serve as a "trigger" PSYCHOSOMATICS
for the emergence of schizophrenia-like psychosis in
predisposed individuals only. Yet, in one study of patients with head injury, family history of schizophrenia was not found to be different between the group of patients who developed schizophrenia-like psychosis and those who did not.) Davison and Bagley; in their comprehensive review of the literature, also concluded that there is no evidence for genetic predisposition to schizophrenia in patients with psychosis following head injury. The progression of the patient from a state of depession to a schizo-affective, depressed clinical picture and finally a schizophrenia-like course also resembles the prepsychotic phase of some schizophrenic patients prior to their full-blown illness. The depression is 1bought to be a reaction to the awareness ofan incipient psydlosis, but it is also known that cerebral injury is accompanied by catecholamine changes and clinical depression," and it is interesting to speculate that depression associated with schizophrenia may be due to certain cerebral biochemical or physiologic changes similar to those associated with cerebral injury. The possible damage to the basal ganglia in this patient is also consistent with evidence implicating basal ganglia dysfunction in schizophrenia.s In addition, the enlarged left lateral ventricle six years after the brain injury in this patient bears resemblance to recent of cerebral atrophy,6 enlarged lateral ventrides,7 and abnormal asymmetries8 in the brains of schizophrenic patients. Finally, the above case raises again the issue of heterogeneity in schizophrenia9 and supports the possibility that a certain subgroup of schizophrenia may be
rePorts
APIW. 1911 • VOL 22 • NO ..
related to potentially preventable organic etiologies such as perinatal brain insUIt,1O slow viral infections" (with subclinical encephalitis?), or mechanical injury and neurologic disease,l2·13 Research into the neuropathologic and neurochemical changes of schizophrenia-like psychosis associated with organic brain damage could further elucidate the mechanisms of schizophrenic illness. 0
REFERENCES 1. Davison K. Bagley CR: SchiZophrenia·like psychoses associated with organic disorders 01 the central nervous system: A review oltha literature. Br J Psychiatry (suppl) 4: 113-184. 1969. 2. WardasZko H: SchiZophrenic and pseudo-schiZophrenic symptomatology alter cerebral trauma. Neurol Neurochir Psychiat Pol 18:101·106.
1966. 3. Schulz B: Zur Erbpathologie der SchiZophrenic. Z Neurol Psychiat
143: 175-293. 1932. 4. Robinson RG. Bloom FE: Pharmacological treatment lollowing experi. mental cerebral infarction: Implications lor understanding psychological symptoms 01 human stroke. Bioi Psychiatry 12:669-680. 1977. 5. Lidsky TI. Weinhold PM. Levine FM: Implications 01 basal ganglionic dyslunction lor schiZophrenia. Bioi Psychiatry 14:3-12. 1979. 6. Weinberger DR. Torrey EF. Neophylides AN. et al: Structural abnormali. ties in the cerebral cortex 01 chronic schiZophrenic patients. Arch Gen Psychiatry 341:935-939. 1979. 7. Weinberger DR. Torrey EF. Neophylides AN. et al: Lateral cerebral ventricular enlargement in chronic schiZophrenia. Arch Gen Psychiatry
341: 735-739. 1979. 8. Luchins D. Weinberger DR. Wyatt RJ: SchiZophrenia: Evidence of a subgroup with reversed cerebral assymetry. Arch Gen Psychiatry
341: 1309-1311. 1979. 9. Tsuang MT: Heterogeneity of schiZOphrenia. Bioi Psychiatry 10:465-473.
1975. 10. Fish B: Neurobiologic antecedents of schiZophrenia in children. Arch Gen Psychiatry 34:1297-1313.1977. 11. Torrey EF. Peterson MR: Slow and latent viruses in SChiZophrenia. Lancet 2:22-24. 1973. 12. Lishman WA: Organic psychiatry. The Psychological Consequences of Cerebral Disorder. Oxford. Blackwell Scientific Publications, 1978. 13. Flor-Henry P: SchiZophrenia-like reactions and affective psychosis associated with temporal lobe epilepsy: Etiological lactors. Am J Psychiatry 128:399-404. 1969.
361
HENRY A. NASRALLAH, M.D. RICHARD C. FOWLER, M.D. LEWIS L. JUDD, M.D.
Schizophrenia-like illness following head injury There is a large literature on psychoses associated with head injuries. The most extensive review of the subject is that of Davison and Bagley,' in which they conclude that the incidence of schizophreniform psychosis in brain-injured subjects is significantly higher than in the general population, that genetic predisposition does not seem to playa role in such cases, and that there seems to be an association with temporal lobe lesions. They also noted that information about treatment and prognosis was lacking in the literature. Here, we report a case of a young man with a good premorbid history (as far as we could establish), and no first or second degree family history of psychiatric illness, who developed schizophrenic symptoms subsequent to head trauma, and whose clinical course over , the past six years strongly resembles chronic schizophrenia despite significant improvement in his posttraumatic cognitive deficits. C. . ntpOrt Six years prior to the current assessment a 22-year-old
Dr. Nasrallah is chiefofthe psychiatry service at the Veterans Administration Medical Center, Iowa City, and associate professor of psychiatry at the University of Iowa College of Medicine; Dr. Fowler is staff psychiatrist at the Veterans Administration Medical Center, San Diego, and assistant professor of psychiatry at the University of California San . Diego School of Medicine; and Dr. Judd is prOfessor and chairman of the department of psychiatry at the U.C.S.D. School of Medicine. Reprint requests to Dr. Nasrallah, VA Medical Center, Iowa City, IA 52240. APRIL 1981 • VOL 22 • NO 4
college student was struck by a car while riding his bicycle. He immediately lost consciousness and was hospitalized. Initial examination revealed a semicomatose man. responsive only to painful stimuli. There was evidence of trauma to the left side of his face and chest as well as a left hemotympanum. Neurologic examination was unremarkable except for bilateral Babinski reflex and an ankle jerk greater on the right than left. A subsequent examination, after the patient emerged from coma, revealed a left lateral rectus palsy (which persisted for several weeks) but no sensory deficits. and normal funduscopy and visual fields. Electroencephalography showed low-to-moderate-voltage asynchronous polymorphic activity over the right hemisphere. maximal in the paracentral regions. Skull x-ray film showed a left basilar skull fracture. An echoencephalogram was normal but a right carotid angiogram showed decreased arterial vasculature in the right frontal area with late filling of the right frontal vein, a finding consistent with right frontal-lobe contusion. A left carotid angiogram revealed early filling of the deep venous system consistent with contusion or ischemia of the left basal ganglia. Six days after the accident the patient had multiple focal seizures involving the left side of his face and one involving the right side. These were treated with anticonvulsants and there were no subsequent seizures. There was litlle change in his mental state until 16 days after the trauma, when he began responding to verbal stimuli. Subsequent improvement was rapid and the patient was alert and talking by the fourth week. Neuropsychological assessment at that time showed scores in the normal range on the Bender VisualMotor Gestalt and on the Graham Kendall Memory for Design. However, Wechsler Adult Intelligence Scale full scale 10 was 56 (verbal. 52; performance. 66). Although there was no documented evidence of psychosis during that 359
Case report
period, the patient's mother recalls that he did express concerns about voices on the radio accusing him of homosexuality within hours of emerging from coma. The subsequent course was uneventful until six months after the injury, when the patient received his first psychiatric examination. This visit to a mental health clinic was initiated by the patient at the suggestion of his surgeon, but his motives for seeking help were obscure. His mental status examination revealed no specific complaints; no evidence of delusions or hallucinations; neutral mood; and appropriate affect. His flow of thought was moderately tangential but otherwise coherent and logical. Cognitively, he was fully oriented, with good recent and remote memory as well as good attention and concentration (he repeated eight digits forward and five digits backward). A Minnesota Multiphasic Personality Inventory was interpreted as consistent with depression or schizo-affective disorder. A full scale IQ was 108. Over the ensuing weeks he was seen regularly in the outpatient clinic and was described as rambling, easily frustrated, and preoccupied with his disability. He also complained of headaches and insomnia. He received an antidepressant trial of imipramine 100 mg daily for three weeks but it was apparently not effective and the patient stopped taking it. He was then begun on thioridazine 200 mg daily because of increasing anxiety, and this had a calming effect. Thirteen months after the accident, the patient expressed suicidal ideas and hopelessness about recovery. This prompted his first psychiatric hospitalization. He was treated for depression with amitriptyline 150 mg daily at bedtime and haloperidol 5 mg daily at bedtime. He also remained on phenytoin 300 mg daily at bedtime. Clinical response was rapid and the patient was discharged after a brief stay. However, there was an apparent change in his mental status over the next two months. He began expressing concern that others considered him a homosexual. He also reported he was the subject of an "experiment" at the Veterans Administration Hospital and that his biking accident was part of the "experiment." Affective symptoms were no longer prominent, though readmission was prompted by an overdose of unknown amounts of thioridazine, phenytoin, and amitriptyline (most of which the patient vomited after ingestion with no medical sequelae). The patient later said that the overdose was his attempt to end the "experiment," thus indicating that the suicidal gesture was probably a delusional act rather than a result of depression and suicidal intel}!. Over the next five years, the patient had seven more psychiatric admissions. Delusions of reference, influence, thought contrOl, and persecution wer& always prominent, and speech and thoughts were disorganized; but sensorium was always clear. Treatment with a neuroleptic (usually fluphenazine decanoate) was begun on each admission with considerable symptomatic improvement. However,
after discharge he invariably stopped the neuroleptic (though he would continue the phenytoin) and he would relapse again and show schizophrenic manifestations. The periods between hospitalization were marked by social instability. He frequently moved from board-and-care homes to his own apartment or the homes of relatives. Attempts to resume school or obtain employment were unsuccessful and he did not date, though he frequently expressed concern about this. On his most recent hospital admission, six years after the accident, psychotic symptoms were again prominent. He believed people on television were talking about him and that a particular woman was controlling his thoughts. His speech remained disorganized and an inappropriate smile was often present when he talked about his delusional beliefs. He remained distressed by his circumstances and continued to express suicidal ideas. Clinical assessment of his intellectual functioning revealed no deficits and neurologic examination was within normal limits. A full scale IQ was 112 (verbal 113, performance 11 0) and the HalsteadReitan impairment index was 10 per cent. An EEG revealed a generalized grade II dysthythmia, and a computerized tomographic brain scan showed a left lateral ventricle that was slightly larger than the right.
Discussioa This case illustrates that psychopathologic changes with a clinical course indistinguishable from that of chronic undifferentiated schizophrenia can follow head injury. The patient appears to have been a previously healthy adult with no family or personal premorbid history that would indicate predisposition to schizophrenia, according to history from his mother and brother. Yet after his head injury, he developed first-rank Schneiderian symptoms as well as formal thought disorder (loose associations). The literature on psychosis associated with head injury describes mainly a schizophrenia-like psychosis but with nonspecific delusions and hallucinations, and rarely any formal thought disorder.2 The improvement in the patient's IQ six months after the head injury, followed by a relentless chronic downhill course with paranoid and hebephrenic features and only a partial response to neuroleptic drugs, all add to the similarity of this patient's posttraumatic illness to chronic undifferentiated schizophrenia. Up to 15% of schizophrenic patients present with a history of head injury preceding the onset of the first psychotic episode, and .07% to 9.8% (the range in eight studies involving 12,385 patients) of brain-injured patients eventually develop schizophrenia-like psychosis.· It is possible that head injury may serve as a "trigger" PSYCHOSOMATICS
for the emergence of schizophrenia-like psychosis in
predisposed individuals only. Yet, in one study of patients with head injury, family history of schizophrenia was not found to be different between the group of patients who developed schizophrenia-like psychosis and those who did not.) Davison and Bagley; in their comprehensive review of the literature, also concluded that there is no evidence for genetic predisposition to schizophrenia in patients with psychosis following head injury. The progression of the patient from a state of depession to a schizo-affective, depressed clinical picture and finally a schizophrenia-like course also resembles the prepsychotic phase of some schizophrenic patients prior to their full-blown illness. The depression is 1bought to be a reaction to the awareness ofan incipient psydlosis, but it is also known that cerebral injury is accompanied by catecholamine changes and clinical depression," and it is interesting to speculate that depression associated with schizophrenia may be due to certain cerebral biochemical or physiologic changes similar to those associated with cerebral injury. The possible damage to the basal ganglia in this patient is also consistent with evidence implicating basal ganglia dysfunction in schizophrenia.s In addition, the enlarged left lateral ventricle six years after the brain injury in this patient bears resemblance to recent of cerebral atrophy,6 enlarged lateral ventrides,7 and abnormal asymmetries8 in the brains of schizophrenic patients. Finally, the above case raises again the issue of heterogeneity in schizophrenia9 and supports the possibility that a certain subgroup of schizophrenia may be
rePorts
APIW. 1911 • VOL 22 • NO ..
related to potentially preventable organic etiologies such as perinatal brain insUIt,1O slow viral infections" (with subclinical encephalitis?), or mechanical injury and neurologic disease,l2·13 Research into the neuropathologic and neurochemical changes of schizophrenia-like psychosis associated with organic brain damage could further elucidate the mechanisms of schizophrenic illness. 0
REFERENCES 1. Davison K. Bagley CR: SchiZophrenia·like psychoses associated with organic disorders 01 the central nervous system: A review oltha literature. Br J Psychiatry (suppl) 4: 113-184. 1969. 2. WardasZko H: SchiZophrenic and pseudo-schiZophrenic symptomatology alter cerebral trauma. Neurol Neurochir Psychiat Pol 18:101·106.
1966. 3. Schulz B: Zur Erbpathologie der SchiZophrenic. Z Neurol Psychiat
143: 175-293. 1932. 4. Robinson RG. Bloom FE: Pharmacological treatment lollowing experi. mental cerebral infarction: Implications lor understanding psychological symptoms 01 human stroke. Bioi Psychiatry 12:669-680. 1977. 5. Lidsky TI. Weinhold PM. Levine FM: Implications 01 basal ganglionic dyslunction lor schiZophrenia. Bioi Psychiatry 14:3-12. 1979. 6. Weinberger DR. Torrey EF. Neophylides AN. et al: Structural abnormali. ties in the cerebral cortex 01 chronic schiZophrenic patients. Arch Gen Psychiatry 341:935-939. 1979. 7. Weinberger DR. Torrey EF. Neophylides AN. et al: Lateral cerebral ventricular enlargement in chronic schiZophrenia. Arch Gen Psychiatry
341: 735-739. 1979. 8. Luchins D. Weinberger DR. Wyatt RJ: SchiZophrenia: Evidence of a subgroup with reversed cerebral assymetry. Arch Gen Psychiatry
341: 1309-1311. 1979. 9. Tsuang MT: Heterogeneity of schiZOphrenia. Bioi Psychiatry 10:465-473.
1975. 10. Fish B: Neurobiologic antecedents of schiZophrenia in children. Arch Gen Psychiatry 34:1297-1313.1977. 11. Torrey EF. Peterson MR: Slow and latent viruses in SChiZophrenia. Lancet 2:22-24. 1973. 12. Lishman WA: Organic psychiatry. The Psychological Consequences of Cerebral Disorder. Oxford. Blackwell Scientific Publications, 1978. 13. Flor-Henry P: SchiZophrenia-like reactions and affective psychosis associated with temporal lobe epilepsy: Etiological lactors. Am J Psychiatry 128:399-404. 1969.
361