title: Atrophy of the corpus callosum, cortical hypometabolism, and cognitive impairment in corticobasal degeneration.
abstract: OBJECTIVE
  To investigate whether atrophy of the corpus callosum is associated with cognitive impairment and cerebral cortical hypometabolism in corticobasal degeneration.
  
  
  METHODS
  Prospective clinicoradiological correlation with magnetic resonance imaging and positron emission tomography.
  
  
  METHODS
  A university hospital.
  
  
  METHODS
  Eight right-handed patients with clinically diagnosed corticobasal degeneration (mean+/-SD age, 64+/-8 years).
  
  
  METHODS
  Midsagittal corpus callosum area-skull area ratio (on T1-weighted magnetic resonance images), the sum of the scaled scores of the 6 subtests on the Wechsler Adult Intelligence Scale-Revised (Digit Span, Arithmetic, Picture Arrangement, Object Assembly, Block Design, and Digit Symbol), and cerebral metabolic rate of glucose (measured with positron emission tomography by using fludeoxyglucose F 18 as a tracer).
  
  
  RESULTS
  Compared with 36 age-matched right-handed control subjects, the patients had significantly decreased callosal area-skull area ratio. The reduction in this ratio was greatest in the middle half of the corpus callosum. The atrophy of the corpus callosum was accompanied by a decreased mean cortical glucose metabolic rate with hemispheric asymmetry and a decrease in the sum of the scaled subtest scores of the Wechsler Adult Intelligence Scale-Revised.
  
  
  CONCLUSIONS
  Atrophy of the corpus callosum with middle predominance is present in corticobasal degeneration, and this atrophy is associated with cognitive impairment and cerebral cortical hypometabolism with hemispheric asymmetry. Atrophy of the corpus callosum might reflect the severity of the disconnection between cortical regions, and this may be an important factor in the development of cerebral cortical dysfunction in corticobasal degeneration.
authors.affiliation: Department of Neurology, Faculty of Medicine, Kyoto University, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Yamauchi
authors.forename: H
authors.initials: H
authors.lastname: Fukuyama
authors.forename: Y
authors.initials: Y
authors.lastname: Nagahama
authors.forename: Y
authors.initials: Y
authors.lastname: Katsumi
authors.forename: Y
authors.initials: Y
authors.lastname: Dong
authors.forename: T
authors.initials: T
authors.lastname: Hayashi
authors.forename: J
authors.initials: J
authors.lastname: Konishi
authors.forename: J
authors.initials: J
authors.lastname: Kimura
mesh_terms: D000368:Aged; D001284:Atrophy; D001480:Basal Ganglia Diseases / Q000378:metabolism / Q000473:pathology*; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology*; D003072:Cognition Disorders / Q000378:metabolism / Q000473:pathology*; D003337:Corpus Callosum / Q000473:pathology*; D005260:Female; D006801:Humans; D016014:Linear Models; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D019636:Neurodegenerative Diseases / Q000378:metabolism / Q000473:pathology*; D011446:Prospective Studies; D014055:Tomography, Emission-Computed