Objective: To investigate whether atrophy of the corpus callosum is associated with cognitive impairment and widespread cerebral cortical hypometabolism in carotid artery occlusive disease.
Patients: Twelve patients with unilateral internal carotid artery occlusive disease (1 with severe stenosis and 11 with occlusion) and no cortical infarction in the chronic stage (mean +/- SD age, 64 +/- 5 years).
Main outcome measures: 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 oxygen (measured with position emission tomography by using the oxygen 15 steady-state technique).
Results: The degree of cognitive impairment varied but was strongly correlated with the severity of callosal atrophy (r = 0.92, P < .001). Patients with callosal atrophy and cognitive decline also showed decreased oxygen consumption in the bilateral cerebral cortices. Stepwise regression analysis revealed that the severity of white matter lesions, especially in the centrum semiovale, and that of cortical atrophy in the hemisphere with arterial disease were 2 important factors for callosal atrophy.
Conclusions: Callosal atrophy is associated with cognitive impairment and widespread cerebral cortical hypometabolism in carotid artery occlusive disease without cortical infarction. Callosal atrophy might reflect the severity of the disconnection between cortical regions, and this may be an important factor in the development of cognitive impairment with widespread cortical hypometabolism in carotid artery occlusive disease without large cortical lesions.