INT'L. J. PSYCHIATRY IN MEDICINE,VOI. 22(3) 269-274.1992
NEUROSARCOIDOSISPRESENTING AS SCHIZOPIIRENIFORMDISORDER
MOHAMED SABAAWI, M.D. JOSE GUTIERREZ-NUNU, M.D.
M. RICHARD FRAGALA, M.D. Malcolm Grow Medical Center Andrews Air Force Base, Washington, D.C. Uniformed Services University School of Medicine
ABSTRACT
A patient whose clinical presentation met criteria for schizophreniform disorder was ultimately found to have neurosarcoidosis, and the psychiatric symptoms responded to steroid treatment. The ongoing search for organic etiology was prompted by the presence of cognitive decline, perseveration and rare bizarre automatisms. This is virtually the first reported association between schizophreniform disorder and sarcoidosis. We reviewed the literature on neurologic involvement and psychiatric manifestations in sarcoidosis as well as the concurrence between organicity and schizophrenic psychosis. The importance of attending to all elements of the mental status examination in a patient with complex atypical findings is underscored. ( h t l J. Psychiatry in Medicine 22:269-274, 1992)
Key Words: sarcoidosis, neurosarcoidosis, schizophreniform disorder, organic mental dsorder, SIADH, stereotypic behaviors
Neurosarcoidosis is a systemic granulomatous disease of unknown etiology. Neurologic involvement has been recognized in less than 10 percent of cases, but rarely reported without other systemic manifestations. Common neurologic findings include cranial neuropathy (especially the seventh nerve), basal meningitis, peripheral neuropathy, space occupying masses, hypothalamic and pituitary lesions [l-31. Psychiatric symptoms have been reported in several patients with 269 Q 1992,Baywood Publishing Co.,Inc.
doi: 10.2190/4AHB-AH4N-URK2-T22J http://baywood.com
270 / SABAAWI, GUTIERREZ-NUNEZ AND FRAGALA
known neurosarcoidosis. These included organic mental disorders with disturbances of orientation, sensorium, memory and judgment [4,5], retarded depression [ 5 , 6 ] , and a case of narcolepsy [7]. Isolated psychiatric syndromes, however, are extremely rare. There are only two reported cases in the German literature of psychotic presentation in sarcoidosis; one patient initially diagnosed with Wernicke-Korsakoff psychosis [8] and the other presented with persecutory delusions [9]. Although the development of psychosis resembling schizophrenia have been described in a wide range of cerebral disorders [lo-181, this has been virtually unreported before in sarcoidosis. CASE REPORT
The patient was a thirty-two year old right-handed Black female, a single parent, who had a good work history and no previous psychiatric symptomatology or history of substance abuse. She had two years of business college with average grades. She was in good health until several weeks prior to hospitalization when she gradually developed symptoms of paranoia, loose associations, decreased recent memory, poor concentration and fatigue. She also complained of intermittent nausea and vomiting, and mild bifrontal headaches. Medical and neurological evaluations failed to show an etiology (general and neurological examinations, toxicology screen, chest x-ray, barium meal, serum electrolytes, liver, kidney and thyroid profiles, serum B12 and folate, VDRL and FTA, HIV testing, head CT and EEG studies were all normal. CBC revealed leukopenia and mild anemia thought to be secondary to iron deficiency). When admitted to Psychiatry, she voiced persecutory delusions towards her mother, reported thought insertion and broadcasting, and appeared to be attending to inner stimuli. Her affect was flat with occasional inappropriate laughter. She seemed perplexed, had difficulty concentrating, displayed moderate recent memory deficits, but was alert and welloriented. She met DSM-111-R criteria for Schizophreniform Disorder. Psychometric testing (Wechsler Adult Intelligence Scale-Revised, Cognitive Mental Status, Trail Making-A & B, Denman Memory Scale, and Boston Naming Test) revealed full scale IQ of 65, moderately impaired recent verbal memory, and modest visuospatial deficits. In the ensuing weeks, she displayed occasional perseveration without relation to psychic content, “Good morning, morning, morning doctor!” and rare bizarre stereotyped mannerisms, e.g., making sounds like a baby sucking on a bottle while rubbing both preauricular areas with her fingers. A trial of low dose Stelazine (5 mg p.0. bid.) was attempted with some improvement in psychotic symptoms, but no changes in cognitive deficits. After serial negative EEG and CT head scans, a finding in hyponatremia (123 mEq/L) was noted two months later. This led to a diagnosis of Syndrome of Inappropriate Antidiuretic Hormone (SIADH) secretion thought to be secondary to possible encephalitis. Ophthalmologic examination now showed “pseudopapilledema” (eye grounds were normal on admission). Lumbar puncture was
NEUROSARCOIDOSIS / 271
performed showing increased intracranial pressure (opening pressure of 200 mm water), elevated protein (228 mg/dL), decreased glucose (31 mg/dL), pleocytosis and elevated IGG (49 mg/dL). Gram stain and routine cultures, fungal cultures, India ink, AFB smear and cultures, HIV testing and cytology were all negative. Repeat head CI'now showed bifrontal areas of decreased density deep in the white matter. MRI revealed extensive enhancement of the basal meninges extending over the cortex, interhemisphericfissure, and cerebellar hemispheric surfaces. A high signal was also noted bilaterally deep in the frontal lobes consistent with the low density lesions seen on the CT scan. Neurologic findings now evolved to reveal mild pareses of cranial nerves VI bilaterally and left cranial nerve 111, mild ataxia, and sensory deficits consistent with peripheral neuropathy. Extensive connective tissue workup was negative except for elevated serum globulins (4.5 g/dL) and ESR (46 mmh). Several urine, serum, and CSF cultures, and serologic tests for multiple fungal agents (including cryptococcus, coccidioides, histoplasma, and sporothrix) were negative. Subsequently, the patient underwent a meningeal biopsy (from the inferior frontal and the middle temporal lobe) showing mild chronic meningitis with no granulomas, and cerebral angiogram (normal without evidence of vasculitis). Neuropathological consultation suspected a diagnosis of primary neurosarcoidosis (chest x-ray remained normal as were gallium body scan, serum ACE levels and pulmonary function tests). Salivary, parotid and lower lip biopsies were negative. However, twenty-four hour urine calcium clearance was elevated (375 mgm with repeat value of 424 mg per day), and brain stem as well as visual evoked potentials were abnormal. Finally, the presence of sarcoid granulomas was confirmed on conjunctival biopsy. After having received empirical trials of Tegretol for two weeks with levels up to 7.4 mcg/ml and Dilantin for four weeks with levels up to 17.5 mcg/ml, four drug anti-tuberculosistherapy, high dose PCN G for three weeks, and fluconazole treatment (all without benefit), the patient was finally treated for sarcoidosis with steroids (60 mg of Prednisone q.d.) with significant improvement in intellectual functioning (psychometric re-evaluation: full IQ of 83 with intact recent verbal memory and spatiovisual skills), resolution of psychotic symptoms and dramatic improvement in her physical complaints (CSF abnormalities and SIADH remained essentially unchanged, but CT scan and MRI findings improved significantly). DISCUSSION
This patient presented with psychotic, cognitive and physical symptoms without demonstrable organic lesion. Functional psychosis was diagnosed because psychiatric presentation predominated and initial extensive organic workup was negative. However, the presence of cognitive decline, perseveration and stereotyped mannerisms prompted relentless search for organic etiology until
272 / SABAAWI, GUTIERREZ-NUNEZ AND FRAGALA
a diagnosis of neurosarcoidosis was confirmed. None of these symptoms alone would contradict a schizophrenic process but the constellation pointed to organicity. This case was unique because psychosis preceded neurologic signs and resembled schizophreniform disorder. Neurologic findings were generally consistent with those reported elsewhere with radiographic evidence of basal leptomeningitis and multifocal white matter abnormalities [19-21]. However, the lack of seventh nerve palsy or abnormalities in CXR, Gallium scan and serum ACE levels was atypical [1-31. Additionally, the occurrence of mannerisms have not been described before in neurosarcoidosis and probably represented complex partial seizures. Further implications of automatisms are difficult to determine in this case because they occurred only on two occasions and did not recur either during or after anticonvulsant trials. Also, the patient’s overall course was one of steady decline and not episodic. This, as well as her positive response to steroids seemed to indicate that cognitive and psychotic symptoms were related to sarcoid lesions and not seizure activity. The concurrence of organicity and schizophreniform psychosis has both theoretical and clinical significance. It has been suggested that lesion site is a critical factor [22-241 but a recent study of 65 patients showed no such association [25]. The multiplicity of lesion sites in our patient makes this relationship more problematic, although the presence of discrete frontal lesions is consistent with positron tomography and regional blood flow findings of possible frontal dysfunction in schizophrenia [26-271. Of course, the possibility of a superimposed functional psychosis cannot be eliminated albeit unlikely due to good premorbid functioning, negative family history and good response to steroids. Clinically, this case illustrates the significance of pursuing an aggressive and persistent search for an organic etiology when clinical intuition conflicts with negative organic workup.
REFERENCES 1. 0.P. Sharma, A. M. Sharma, Sarcoidosisof the Nervous System, A Clinical Approach, Archives ofInternalMedicine, 151:1317-1321,1991. 2. B. J. Stem, A. Krumholz, C. Johns, P. Scott, and J. Nissim, Sarcoidosis and its Neurological Manifestations,ArchivesOfNeurology, 42:909-917,1985. 3. P. Delaney, Neurologic Manifestations in Sarcoidosis, Review of the Literature with a Report of 23 Cases, Annals of Infernal Medicine, 87336-345,1977. 4. W. B. Mathews, Sarcoidosis of the Nervous System, Journal of Neurology, Neurosurgery and Psychiafry, 28:23-29,1965. 5. 0. Hook,Sarcoidosis with Involvement of the Nervous System, Archives of Neurological Psychiatry, 71554-575,1954. 6. K. Gilmore, M. Rudden, and T. P. Kalman, Psychiatric Manifestations of Sarcoidosis, CanadianJournal of Psychiatry, 25329-331,1980.
NEUROSARCOIDOSIS / 273
7. I. Rubinstein, T. A. Gray, H. Moldofsky, and V. Hoffstein, Neurosarcoidosis Associated with Hypersomnolence Treated with Corticosteroids and Brain Irradiation, Chest, 94:205-206,1988. 8. W. Zerman, Die Meningoencephalitis Besnier-Boeck-Schaumann,Nervenarzt, 23:4352,1952. 9. R. Suchenwirth and V. Dold, Functional Psychosis in Sarcoidosis, Verhandlungen der Deutschen Gesellschafi f i r Innere Meduin 755'57-759,1969. 10. M. M. Vardy and S. R. Kay, LSD Psychosis of LSD-Induced Schizophrenia?Archives of General Psychiatry, 40877-883,1983. 11. A. Feinstein, M. Ron, and S. Wessedy, Disappearing Brain Lesions, Psychosis and Epilepsy, Journal of Neurology, Neurosurgery andpsychiatry, 53:244-246,1990. 12. F. K. Judd and G. D. Barrows, Encephalitis, Catatonia and Schizophreniform Illness, Australian Journal of Psychiatry, 12394-396,1983. 13. M. L.Malton, J. S. Rinkoff, B. S. Doft, and J. S. Kennerdell, Cryptococcal Endophthalmitis and Meningitis Associated with Acute Psychosis and Exudative Retinal Detachment, American Journal of Ophthalmology, 104:438-439,1987. 14. K.Felgenhauer, Psychiatric Disorders in the Encephalitic Form of Multiple Sclerosis, Journal ofNeurology, 23711-18,1990. 15. A. W. Beard, The Association of Hepato-Lenticular Degeneration with Schizophrenia, Acta Psychiatric Neurol Scandinavica, 34:411-428,1959. 16. E. Kraft, A. Schillinger, N. Finby, and M. Halperin, Routine Skull Radiography in a Neuropsychiatric Hospital, American Journal of Psychiatry, 121:lOll-1012, 1%5. 17. W. Lewin, T. F. Marshall, and A. H. Roberts, Longterm Outcomes After Severe Head Injury, BritishMedical Journal, 62:1533-1538,1979. 18. E. Horwath, J. Kramer, F. Coumosf, M. Empfield, and G. Gewirtz, Clinical Presentations of AIDS and HIV Infection in State Psychiatric Facilities, Hospital and Community Psychiatry, 40502-506,1989. 19. N. E. Leeds, R. D. Zimmerman, C. M. Elkin, M. Nussbaum, and A. M. LeVan, Neurosarcoidosis of the Brain and Meninges, Seminars in Roentgenology, 20387-392, 1985. 20. B. E. Kendall and G. L. V. Tatler, Radiologic Findings in Neurosarcoidosis, British Journal ofRadiology, 51 :81-92,1978. 21. D. W. Williams, A. D. Elster, and K. I. Stephen, Neurosarcoidosis: GadoliniumEnhanced MR Imaging, Journal of Computer Assisted Tomography, 14:704-707, 1990. 22. K. Davison and C. R. Bagley, Schizophrenia-like Psychosis Associated with Organic Disorders of the CNS: A Review of the Literature, in Current Problems in Neuropsychiatry, R. N. Herrington (eds.), Ashford and Headly Bros. Ltd., pp. 113-184, 1969. 23. C. Symenods, Disease of Mind and Disorder of Brain, British Medical JournaI, 2:l-5, 1960. 24. R. Y.Moore,Brain Lesions and Amine Metabolism, International Review of Neurobiology, 13367-91,1970. 25. A. Feinstein and M. A. Ron, Psychosis Associated with Demonstrable Brain Disease, Psychological Medicine, 20793-803,1990.
274 / SABAAWI, GUTIERREZ-NUNEZ AND FRAGAIA
26. M. S. Buchsbaum, D. H. Ingvar, R. Kessler, R. N. Waters, J. Cappelletti, D. P Van Kammen, A. C. King, J. I. Johnson, R. G. Manning, R. W. Flynn, L. S. Mann, W. E. Bunney, Jr., and L. Sokoloff, Cerebral Glucography with Positron Tomography in Normals and in Patients with Schizophrenia, Archives of General Psychiatry, 39 251-259,1982. 27. K. F. Berman, B. P. Illowsky, and D. R. Weinberger, Physiological Dysfunction of Dorsolateral Prefrontal Cortex in Schizophrenia,Archives of General Psychiatry, 45: 616-622,1988.
Direct reprint requests to: M. Richard Fragala, M.D. Chief, Division of Mental Health Malcolm Grow USAF Medical Center Andrews Air Force Base Washington, D.C. 20331
NEUROSARCOIDOSISPRESENTING AS SCHIZOPIIRENIFORMDISORDER
MOHAMED SABAAWI, M.D. JOSE GUTIERREZ-NUNU, M.D.
M. RICHARD FRAGALA, M.D. Malcolm Grow Medical Center Andrews Air Force Base, Washington, D.C. Uniformed Services University School of Medicine
ABSTRACT
A patient whose clinical presentation met criteria for schizophreniform disorder was ultimately found to have neurosarcoidosis, and the psychiatric symptoms responded to steroid treatment. The ongoing search for organic etiology was prompted by the presence of cognitive decline, perseveration and rare bizarre automatisms. This is virtually the first reported association between schizophreniform disorder and sarcoidosis. We reviewed the literature on neurologic involvement and psychiatric manifestations in sarcoidosis as well as the concurrence between organicity and schizophrenic psychosis. The importance of attending to all elements of the mental status examination in a patient with complex atypical findings is underscored. ( h t l J. Psychiatry in Medicine 22:269-274, 1992)
Key Words: sarcoidosis, neurosarcoidosis, schizophreniform disorder, organic mental dsorder, SIADH, stereotypic behaviors
Neurosarcoidosis is a systemic granulomatous disease of unknown etiology. Neurologic involvement has been recognized in less than 10 percent of cases, but rarely reported without other systemic manifestations. Common neurologic findings include cranial neuropathy (especially the seventh nerve), basal meningitis, peripheral neuropathy, space occupying masses, hypothalamic and pituitary lesions [l-31. Psychiatric symptoms have been reported in several patients with 269 Q 1992,Baywood Publishing Co.,Inc.
doi: 10.2190/4AHB-AH4N-URK2-T22J http://baywood.com
270 / SABAAWI, GUTIERREZ-NUNEZ AND FRAGALA
known neurosarcoidosis. These included organic mental disorders with disturbances of orientation, sensorium, memory and judgment [4,5], retarded depression [ 5 , 6 ] , and a case of narcolepsy [7]. Isolated psychiatric syndromes, however, are extremely rare. There are only two reported cases in the German literature of psychotic presentation in sarcoidosis; one patient initially diagnosed with Wernicke-Korsakoff psychosis [8] and the other presented with persecutory delusions [9]. Although the development of psychosis resembling schizophrenia have been described in a wide range of cerebral disorders [lo-181, this has been virtually unreported before in sarcoidosis. CASE REPORT
The patient was a thirty-two year old right-handed Black female, a single parent, who had a good work history and no previous psychiatric symptomatology or history of substance abuse. She had two years of business college with average grades. She was in good health until several weeks prior to hospitalization when she gradually developed symptoms of paranoia, loose associations, decreased recent memory, poor concentration and fatigue. She also complained of intermittent nausea and vomiting, and mild bifrontal headaches. Medical and neurological evaluations failed to show an etiology (general and neurological examinations, toxicology screen, chest x-ray, barium meal, serum electrolytes, liver, kidney and thyroid profiles, serum B12 and folate, VDRL and FTA, HIV testing, head CT and EEG studies were all normal. CBC revealed leukopenia and mild anemia thought to be secondary to iron deficiency). When admitted to Psychiatry, she voiced persecutory delusions towards her mother, reported thought insertion and broadcasting, and appeared to be attending to inner stimuli. Her affect was flat with occasional inappropriate laughter. She seemed perplexed, had difficulty concentrating, displayed moderate recent memory deficits, but was alert and welloriented. She met DSM-111-R criteria for Schizophreniform Disorder. Psychometric testing (Wechsler Adult Intelligence Scale-Revised, Cognitive Mental Status, Trail Making-A & B, Denman Memory Scale, and Boston Naming Test) revealed full scale IQ of 65, moderately impaired recent verbal memory, and modest visuospatial deficits. In the ensuing weeks, she displayed occasional perseveration without relation to psychic content, “Good morning, morning, morning doctor!” and rare bizarre stereotyped mannerisms, e.g., making sounds like a baby sucking on a bottle while rubbing both preauricular areas with her fingers. A trial of low dose Stelazine (5 mg p.0. bid.) was attempted with some improvement in psychotic symptoms, but no changes in cognitive deficits. After serial negative EEG and CT head scans, a finding in hyponatremia (123 mEq/L) was noted two months later. This led to a diagnosis of Syndrome of Inappropriate Antidiuretic Hormone (SIADH) secretion thought to be secondary to possible encephalitis. Ophthalmologic examination now showed “pseudopapilledema” (eye grounds were normal on admission). Lumbar puncture was
NEUROSARCOIDOSIS / 271
performed showing increased intracranial pressure (opening pressure of 200 mm water), elevated protein (228 mg/dL), decreased glucose (31 mg/dL), pleocytosis and elevated IGG (49 mg/dL). Gram stain and routine cultures, fungal cultures, India ink, AFB smear and cultures, HIV testing and cytology were all negative. Repeat head CI'now showed bifrontal areas of decreased density deep in the white matter. MRI revealed extensive enhancement of the basal meninges extending over the cortex, interhemisphericfissure, and cerebellar hemispheric surfaces. A high signal was also noted bilaterally deep in the frontal lobes consistent with the low density lesions seen on the CT scan. Neurologic findings now evolved to reveal mild pareses of cranial nerves VI bilaterally and left cranial nerve 111, mild ataxia, and sensory deficits consistent with peripheral neuropathy. Extensive connective tissue workup was negative except for elevated serum globulins (4.5 g/dL) and ESR (46 mmh). Several urine, serum, and CSF cultures, and serologic tests for multiple fungal agents (including cryptococcus, coccidioides, histoplasma, and sporothrix) were negative. Subsequently, the patient underwent a meningeal biopsy (from the inferior frontal and the middle temporal lobe) showing mild chronic meningitis with no granulomas, and cerebral angiogram (normal without evidence of vasculitis). Neuropathological consultation suspected a diagnosis of primary neurosarcoidosis (chest x-ray remained normal as were gallium body scan, serum ACE levels and pulmonary function tests). Salivary, parotid and lower lip biopsies were negative. However, twenty-four hour urine calcium clearance was elevated (375 mgm with repeat value of 424 mg per day), and brain stem as well as visual evoked potentials were abnormal. Finally, the presence of sarcoid granulomas was confirmed on conjunctival biopsy. After having received empirical trials of Tegretol for two weeks with levels up to 7.4 mcg/ml and Dilantin for four weeks with levels up to 17.5 mcg/ml, four drug anti-tuberculosistherapy, high dose PCN G for three weeks, and fluconazole treatment (all without benefit), the patient was finally treated for sarcoidosis with steroids (60 mg of Prednisone q.d.) with significant improvement in intellectual functioning (psychometric re-evaluation: full IQ of 83 with intact recent verbal memory and spatiovisual skills), resolution of psychotic symptoms and dramatic improvement in her physical complaints (CSF abnormalities and SIADH remained essentially unchanged, but CT scan and MRI findings improved significantly). DISCUSSION
This patient presented with psychotic, cognitive and physical symptoms without demonstrable organic lesion. Functional psychosis was diagnosed because psychiatric presentation predominated and initial extensive organic workup was negative. However, the presence of cognitive decline, perseveration and stereotyped mannerisms prompted relentless search for organic etiology until
272 / SABAAWI, GUTIERREZ-NUNEZ AND FRAGALA
a diagnosis of neurosarcoidosis was confirmed. None of these symptoms alone would contradict a schizophrenic process but the constellation pointed to organicity. This case was unique because psychosis preceded neurologic signs and resembled schizophreniform disorder. Neurologic findings were generally consistent with those reported elsewhere with radiographic evidence of basal leptomeningitis and multifocal white matter abnormalities [19-21]. However, the lack of seventh nerve palsy or abnormalities in CXR, Gallium scan and serum ACE levels was atypical [1-31. Additionally, the occurrence of mannerisms have not been described before in neurosarcoidosis and probably represented complex partial seizures. Further implications of automatisms are difficult to determine in this case because they occurred only on two occasions and did not recur either during or after anticonvulsant trials. Also, the patient’s overall course was one of steady decline and not episodic. This, as well as her positive response to steroids seemed to indicate that cognitive and psychotic symptoms were related to sarcoid lesions and not seizure activity. The concurrence of organicity and schizophreniform psychosis has both theoretical and clinical significance. It has been suggested that lesion site is a critical factor [22-241 but a recent study of 65 patients showed no such association [25]. The multiplicity of lesion sites in our patient makes this relationship more problematic, although the presence of discrete frontal lesions is consistent with positron tomography and regional blood flow findings of possible frontal dysfunction in schizophrenia [26-271. Of course, the possibility of a superimposed functional psychosis cannot be eliminated albeit unlikely due to good premorbid functioning, negative family history and good response to steroids. Clinically, this case illustrates the significance of pursuing an aggressive and persistent search for an organic etiology when clinical intuition conflicts with negative organic workup.
REFERENCES 1. 0.P. Sharma, A. M. Sharma, Sarcoidosisof the Nervous System, A Clinical Approach, Archives ofInternalMedicine, 151:1317-1321,1991. 2. B. J. Stem, A. Krumholz, C. Johns, P. Scott, and J. Nissim, Sarcoidosis and its Neurological Manifestations,ArchivesOfNeurology, 42:909-917,1985. 3. P. Delaney, Neurologic Manifestations in Sarcoidosis, Review of the Literature with a Report of 23 Cases, Annals of Infernal Medicine, 87336-345,1977. 4. W. B. Mathews, Sarcoidosis of the Nervous System, Journal of Neurology, Neurosurgery and Psychiafry, 28:23-29,1965. 5. 0. Hook,Sarcoidosis with Involvement of the Nervous System, Archives of Neurological Psychiatry, 71554-575,1954. 6. K. Gilmore, M. Rudden, and T. P. Kalman, Psychiatric Manifestations of Sarcoidosis, CanadianJournal of Psychiatry, 25329-331,1980.
NEUROSARCOIDOSIS / 273
7. I. Rubinstein, T. A. Gray, H. Moldofsky, and V. Hoffstein, Neurosarcoidosis Associated with Hypersomnolence Treated with Corticosteroids and Brain Irradiation, Chest, 94:205-206,1988. 8. W. Zerman, Die Meningoencephalitis Besnier-Boeck-Schaumann,Nervenarzt, 23:4352,1952. 9. R. Suchenwirth and V. Dold, Functional Psychosis in Sarcoidosis, Verhandlungen der Deutschen Gesellschafi f i r Innere Meduin 755'57-759,1969. 10. M. M. Vardy and S. R. Kay, LSD Psychosis of LSD-Induced Schizophrenia?Archives of General Psychiatry, 40877-883,1983. 11. A. Feinstein, M. Ron, and S. Wessedy, Disappearing Brain Lesions, Psychosis and Epilepsy, Journal of Neurology, Neurosurgery andpsychiatry, 53:244-246,1990. 12. F. K. Judd and G. D. Barrows, Encephalitis, Catatonia and Schizophreniform Illness, Australian Journal of Psychiatry, 12394-396,1983. 13. M. L.Malton, J. S. Rinkoff, B. S. Doft, and J. S. Kennerdell, Cryptococcal Endophthalmitis and Meningitis Associated with Acute Psychosis and Exudative Retinal Detachment, American Journal of Ophthalmology, 104:438-439,1987. 14. K.Felgenhauer, Psychiatric Disorders in the Encephalitic Form of Multiple Sclerosis, Journal ofNeurology, 23711-18,1990. 15. A. W. Beard, The Association of Hepato-Lenticular Degeneration with Schizophrenia, Acta Psychiatric Neurol Scandinavica, 34:411-428,1959. 16. E. Kraft, A. Schillinger, N. Finby, and M. Halperin, Routine Skull Radiography in a Neuropsychiatric Hospital, American Journal of Psychiatry, 121:lOll-1012, 1%5. 17. W. Lewin, T. F. Marshall, and A. H. Roberts, Longterm Outcomes After Severe Head Injury, BritishMedical Journal, 62:1533-1538,1979. 18. E. Horwath, J. Kramer, F. Coumosf, M. Empfield, and G. Gewirtz, Clinical Presentations of AIDS and HIV Infection in State Psychiatric Facilities, Hospital and Community Psychiatry, 40502-506,1989. 19. N. E. Leeds, R. D. Zimmerman, C. M. Elkin, M. Nussbaum, and A. M. LeVan, Neurosarcoidosis of the Brain and Meninges, Seminars in Roentgenology, 20387-392, 1985. 20. B. E. Kendall and G. L. V. Tatler, Radiologic Findings in Neurosarcoidosis, British Journal ofRadiology, 51 :81-92,1978. 21. D. W. Williams, A. D. Elster, and K. I. Stephen, Neurosarcoidosis: GadoliniumEnhanced MR Imaging, Journal of Computer Assisted Tomography, 14:704-707, 1990. 22. K. Davison and C. R. Bagley, Schizophrenia-like Psychosis Associated with Organic Disorders of the CNS: A Review of the Literature, in Current Problems in Neuropsychiatry, R. N. Herrington (eds.), Ashford and Headly Bros. Ltd., pp. 113-184, 1969. 23. C. Symenods, Disease of Mind and Disorder of Brain, British Medical JournaI, 2:l-5, 1960. 24. R. Y.Moore,Brain Lesions and Amine Metabolism, International Review of Neurobiology, 13367-91,1970. 25. A. Feinstein and M. A. Ron, Psychosis Associated with Demonstrable Brain Disease, Psychological Medicine, 20793-803,1990.
274 / SABAAWI, GUTIERREZ-NUNEZ AND FRAGAIA
26. M. S. Buchsbaum, D. H. Ingvar, R. Kessler, R. N. Waters, J. Cappelletti, D. P Van Kammen, A. C. King, J. I. Johnson, R. G. Manning, R. W. Flynn, L. S. Mann, W. E. Bunney, Jr., and L. Sokoloff, Cerebral Glucography with Positron Tomography in Normals and in Patients with Schizophrenia, Archives of General Psychiatry, 39 251-259,1982. 27. K. F. Berman, B. P. Illowsky, and D. R. Weinberger, Physiological Dysfunction of Dorsolateral Prefrontal Cortex in Schizophrenia,Archives of General Psychiatry, 45: 616-622,1988.
Direct reprint requests to: M. Richard Fragala, M.D. Chief, Division of Mental Health Malcolm Grow USAF Medical Center Andrews Air Force Base Washington, D.C. 20331
