title: Callosal atrophy with reduced cortical oxygen metabolism in carotid artery disease.
abstract: OBJECTIVE
  In cerebrovascular disease, brain atrophy may be a reflection of ischemic changes. Minor changes that are not detectable as infarction on computed tomography may result in atrophy with metabolic depression. We evaluated the relation between size of the corpus callosum and cerebral cortical oxygen metabolism in carotid artery disease.
  
  
  METHODS
  We used magnetic resonance imaging and positron emission tomography to evaluate 13 right-handed male patients with transient ischemic attacks or minor strokes and unilateral internal carotid artery occlusive disease, two with stenosis and 11 with occlusion. Computed tomography showed only minor subcortical abnormalities in the affected hemisphere. Midsagittal corpus callosum areas on T1-weighted magnetic resonance images, white matter lesions on T2-weighted images, and the cerebral metabolic rate of oxygen measured by the oxygen-15 steady-state technique were analyzed.
  
  
  RESULTS
  Compared with 13 age- and sex-matched control subjects showing the same degree of white matter areas of high intensity, the patients had significantly decreased callosal areas. The degree of corpus callosum atrophy was significantly correlated with the mean cortical oxygen metabolic rate. The same tendency was also found in five patients without infarcts on computed tomography. However, neither the callosal area nor the hemispheric metabolic rate was correlated with the extent of white matter lesions.
  
  
  CONCLUSIONS
  These findings indicate that atrophy of the corpus callosum occurs in association with a decrease in cortical oxygen metabolism. Corpus callosum atrophy may be a useful morphological index that reflects the cerebral cortical metabolic state in carotid artery occlusive disease.
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: H
authors.initials: H
authors.lastname: Nabatame
authors.forename: K
authors.initials: K
authors.lastname: Harada
authors.forename: J
authors.initials: J
authors.lastname: Kimura
mesh_terms: D000368:Aged; D001157:Arterial Occlusive Diseases / Q000150:complications / Q000378:metabolism; D001284:Atrophy / Q000378:metabolism; D002340:Carotid Artery Diseases / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000378:metabolism*; D003337:Corpus Callosum / Q000000981:diagnostic imaging / Q000473:pathology*; D006801:Humans; D002546:Ischemic Attack, Transient / Q000150:complications / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000378:metabolism*; D014057:Tomography, X-Ray Computed
chemical_list: D010100:Oxygen