Correspondence
BIOL PSYCHIATRY 1991;29:730--734
733
lones-Gotman M, Zatorre RJ (1988): Olfactory identification deficits in patients with focal cerebral excision. Neuropsychologia 26(3):387-400. Kopala !., Clark C, Hurwitz T (1989): Sex differences in olfactory function. Am J Psychiatry 146:1320-1322. Potter H, Butters N (1980): An assessment of olfactory
deficits in patients with damage to prefrontal cortex. Neuropsychologia ! 8:62 !-628. Wysocki C.J, Beauchamp G K (1984): Ab~ly to smell androstenone is genetically determined. Proc Natl Acad Sci 81:489--4902.
Cerebellar Atrophy and Catatonia
or more cerebellar vermian snlcl enlarged, (c) cerebellopontine cistern enlarged, (d) superior cerebellar cistern enlarged, and (e) 4th ven~cle enlarged. fine difference in the number of subjects with cerebellar atrophy was evaluated using the ×2 statistic with Yate's correction. For cells with n < 5, Fisher's exact test was used. CT scans were all performed on a Picker-600 CT Scanner with a resolution powe," in the lmm range or beaer, dependent upon tissue type and density. Scans were done with and without contrast. There were siEnificanfly more catatonic subjects (29%) with at least one of the criteria of Allen et al (1979) for cerebellar atrophy compared with schizophrenic (8%), affective (5%), and nonpsychiatric controls (0%) (p < 0.05 in each category). There were no significant differences between the other groups. The findings of this study indicate that catatonJa may be associated with cerebellar atrophy. None of the subjects in this sample had more than two criteria for cerebellar atrophy, suggesting that if this atrophy is actually associated with catatonia, it is probably a mild degree of atrophy. In this study I have tried to limit the problems of vague nosology by using a small group of s-Jbjects with similar, obvious, and highly specific symptoms. L,a this study catatonia was considered a nonspecific s y n ~ m e and not a diagnostic entity. Cerebellar atrophy was considered a concurrent sign that may identify a risk factor for stuporous catatonia; therefore, no causal association can be implied. Further research using larger groups of subjects and more refined imaging techniques is encouraged.
To the Editor: Catatonia is a syndrome often :haracterized by stupor and motor rigidity. It is as,.ociated with major psychoses and can occur under a variety of conditions. The pathophysiology of this condition is currently unknown. Until now, no gross structural changes in the brains of catatonics have been reported Previous work has suggested an association between cerebellar atrophy and psychotic conditions presenting with predominantly negative or autistic features (Weinberger et al 1979; Murakami et al 1989; Courchesne et al 1988; Heath et al 1979). In a recent pilot study of ours standardized criteria for identification of cerebel!ar atrophy were applied to the computed tomography (CT) scans of subjects with and without catatonia and the results were statistically compared. Seventeen subjects admitted with the syndrome of catatonia were compared with 30 patients with chronic noncatatonic schizophrenia, 20 patients with psychotic affective disorder, and 15 nonpsychia~c controls. All subjects were selected from consecutive admissions to a university hospital. Criteria for inclusion as a catatonic subject were tourism, motor rigidity, irrational behavior, and the absence of frank neurological or metabolic disease. These symptoms for catatonia were selected because they could be objectively observed and thus easily measured. All controls were matched for age and gender. Psychiatric controls were matched for exposu~ to medication and electroconvulsive therapy. The scans were randomized and then assessed using the criteta of Allen et al (1979). The assessment was done blind to psychiatric condition. The criteria ~re based on enlargement of the CSF spaces for the identification of cerebellar atrophy on CT scans. These criteria are (a) cerebellar hemisphere sulci larger than 1 mm, (b) two
James Alien Wilcox
Texas Tech University Department of Psychiatry 4800 Alberta Ave El Paso, TX 79005
734
BIOL PSYCHIATRY 1991;29:730-734
References Allen JH Martin JT McLain LW (1979): Computed tomography in ¢~'ebeU~atrophic processes. Rad/o/ogy 130:.379382. Courchesne E, Yeung-Courchesne R, Press GA, Hesselink JR, Jernigan TL (1988): Hypuplasiaofcerebellar vennal lobules VI and VII in autism. N Engl J Med 318:!3491354. Heath RG, Franklin DE Shraberg D (1979): Gross ,~thology
Correspondence
of the cerebellum in patients diagnosed and ereated as ~ disord~. JNerv MemDis 167:585592. Murakami JW Courchesne E Press GA, Yeung-Comchesne R Hesselink JR (1989): Reduced cerebellar hemisphere si~ and itss relation~ip to vemml hypoplasia in autism. Arch Neuro146:689-694. Weinberger D~ Torrey EF Wyatt PJ (1979): Cerebellar atrophy in chronic schizophrenia. Lancet i:718-719. Letter.
BIOL PSYCHIATRY 1991;29:730--734
733
lones-Gotman M, Zatorre RJ (1988): Olfactory identification deficits in patients with focal cerebral excision. Neuropsychologia 26(3):387-400. Kopala !., Clark C, Hurwitz T (1989): Sex differences in olfactory function. Am J Psychiatry 146:1320-1322. Potter H, Butters N (1980): An assessment of olfactory
deficits in patients with damage to prefrontal cortex. Neuropsychologia ! 8:62 !-628. Wysocki C.J, Beauchamp G K (1984): Ab~ly to smell androstenone is genetically determined. Proc Natl Acad Sci 81:489--4902.
Cerebellar Atrophy and Catatonia
or more cerebellar vermian snlcl enlarged, (c) cerebellopontine cistern enlarged, (d) superior cerebellar cistern enlarged, and (e) 4th ven~cle enlarged. fine difference in the number of subjects with cerebellar atrophy was evaluated using the ×2 statistic with Yate's correction. For cells with n < 5, Fisher's exact test was used. CT scans were all performed on a Picker-600 CT Scanner with a resolution powe," in the lmm range or beaer, dependent upon tissue type and density. Scans were done with and without contrast. There were siEnificanfly more catatonic subjects (29%) with at least one of the criteria of Allen et al (1979) for cerebellar atrophy compared with schizophrenic (8%), affective (5%), and nonpsychiatric controls (0%) (p < 0.05 in each category). There were no significant differences between the other groups. The findings of this study indicate that catatonJa may be associated with cerebellar atrophy. None of the subjects in this sample had more than two criteria for cerebellar atrophy, suggesting that if this atrophy is actually associated with catatonia, it is probably a mild degree of atrophy. In this study I have tried to limit the problems of vague nosology by using a small group of s-Jbjects with similar, obvious, and highly specific symptoms. L,a this study catatonia was considered a nonspecific s y n ~ m e and not a diagnostic entity. Cerebellar atrophy was considered a concurrent sign that may identify a risk factor for stuporous catatonia; therefore, no causal association can be implied. Further research using larger groups of subjects and more refined imaging techniques is encouraged.
To the Editor: Catatonia is a syndrome often :haracterized by stupor and motor rigidity. It is as,.ociated with major psychoses and can occur under a variety of conditions. The pathophysiology of this condition is currently unknown. Until now, no gross structural changes in the brains of catatonics have been reported Previous work has suggested an association between cerebellar atrophy and psychotic conditions presenting with predominantly negative or autistic features (Weinberger et al 1979; Murakami et al 1989; Courchesne et al 1988; Heath et al 1979). In a recent pilot study of ours standardized criteria for identification of cerebel!ar atrophy were applied to the computed tomography (CT) scans of subjects with and without catatonia and the results were statistically compared. Seventeen subjects admitted with the syndrome of catatonia were compared with 30 patients with chronic noncatatonic schizophrenia, 20 patients with psychotic affective disorder, and 15 nonpsychia~c controls. All subjects were selected from consecutive admissions to a university hospital. Criteria for inclusion as a catatonic subject were tourism, motor rigidity, irrational behavior, and the absence of frank neurological or metabolic disease. These symptoms for catatonia were selected because they could be objectively observed and thus easily measured. All controls were matched for age and gender. Psychiatric controls were matched for exposu~ to medication and electroconvulsive therapy. The scans were randomized and then assessed using the criteta of Allen et al (1979). The assessment was done blind to psychiatric condition. The criteria ~re based on enlargement of the CSF spaces for the identification of cerebellar atrophy on CT scans. These criteria are (a) cerebellar hemisphere sulci larger than 1 mm, (b) two
James Alien Wilcox
Texas Tech University Department of Psychiatry 4800 Alberta Ave El Paso, TX 79005
734
BIOL PSYCHIATRY 1991;29:730-734
References Allen JH Martin JT McLain LW (1979): Computed tomography in ¢~'ebeU~atrophic processes. Rad/o/ogy 130:.379382. Courchesne E, Yeung-Courchesne R, Press GA, Hesselink JR, Jernigan TL (1988): Hypuplasiaofcerebellar vennal lobules VI and VII in autism. N Engl J Med 318:!3491354. Heath RG, Franklin DE Shraberg D (1979): Gross ,~thology
Correspondence
of the cerebellum in patients diagnosed and ereated as ~ disord~. JNerv MemDis 167:585592. Murakami JW Courchesne E Press GA, Yeung-Comchesne R Hesselink JR (1989): Reduced cerebellar hemisphere si~ and itss relation~ip to vemml hypoplasia in autism. Arch Neuro146:689-694. Weinberger D~ Torrey EF Wyatt PJ (1979): Cerebellar atrophy in chronic schizophrenia. Lancet i:718-719. Letter.
