title: Contribution of alcohol abuse to cerebellar volume deficits in men with schizophrenia.
abstract: BACKGROUND
  It is controversial whether cerebellar tissue volume deficits occur in schizophrenia and, if so, what regions and tissue types are affected. Complicating such investigations is the high incidence of alcoholism comorbidity in patients with schizophrenia that itself can contribute to cerebellar abnormalities.
  
  
  METHODS
  We studied 61 healthy men (control subjects), 25 men with alcoholism, 27 men with schizophrenia, and 19 men comorbid for schizophrenia and alcoholism with the use of magnetic resonance imaging. Cerebellar structures were outlined manually, tissue classification was determined statistically, and regional volumes were corrected for normal variation in head size and age.
  
  
  RESULTS
  Patients with schizophrenia alone had enlarged fourth ventricles (1.5 SD relative to controls) but showed no cerebellar tissue volume deficits. The alcoholic group had gray and white matter vermian deficits (-0.5 SD), most prominent in anterior superior lobules, and gray matter hemisphere deficits (-0.8 SD), but not fourth ventricle enlargement. The comorbid group had cerebellar hemisphere (-1.3 SD) and vermian gray matter volume deficits (-0.7 SD) and fourth ventricular enlargement (1.6 SD); these abnormalities were greater than in either single-diagnosis group, despite significantly lower levels of alcohol consumption compared with the alcoholic group. Gray matter volume in the anterior superior vermis correlated with lifetime alcohol consumption in the schizophrenic and comorbid groups when combined.
  
  
  CONCLUSIONS
  Cerebellar tissue volume deficits were detected in schizophrenia only when accompanied by alcoholism. By contrast, fourth ventricular enlargement occurred in schizophrenia even without alcoholism, although it was exacerbated by alcoholism. These findings support a model of cerebellar supersensitivity to alcohol-related tissue volume deficits in schizophrenia.
authors.affiliation: Department of Psychiatry and Behavioral Sciences (5717), Stanford University School of Medicine, 401 Quarry Rd, Stanford, CA 94305-5717, USA. edie@stanford.edu
authors.forename: E V
authors.initials: EV
authors.lastname: Sullivan
authors.forename: A
authors.initials: A
authors.lastname: Deshmukh
authors.forename: J E
authors.initials: JE
authors.lastname: Desmond
authors.forename: D H
authors.initials: DH
authors.lastname: Mathalon
authors.forename: M J
authors.initials: MJ
authors.lastname: Rosenbloom
authors.forename: K O
authors.initials: KO
authors.lastname: Lim
authors.forename: A
authors.initials: A
authors.lastname: Pfefferbaum
mesh_terms: D000328:Adult; D000367:Age Factors; D017668:Age of Onset; D000428:Alcohol Drinking / Q000453:epidemiology; D000437:Alcoholism / Q000175:diagnosis* / Q000453:epidemiology; D010054:Brief Psychiatric Rating Scale / Q000706:statistics & numerical data; D002531:Cerebellum / Q000033:anatomy & histology*; D002552:Cerebral Ventricles / Q000033:anatomy & histology*; D015897:Comorbidity; D006801:Humans; D015994:Incidence; D008279:Magnetic Resonance Imaging / Q000706:statistics & numerical data*; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D012559:Schizophrenia / Q000175:diagnosis* / Q000453:epidemiology; D012720:Severity of Illness Index