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October 1993

Callosal Atrophy Parallels Decreased Cortical Oxygen Metabolism and Neuropsychological Impairment in Alzheimer's Disease

Author Affiliations

From the Departments of Neurology (Drs Yamauchi, Fukuyama, Harada, Nabatame, Ogawa, Ouchi, and Kimura) and Radiology and Nuclear Medicine (Dr Konishi), Faculty of Medicine, Kyoto (Japan) University. Dr Nabatame is now with the Department of Neurology, Shiga (Japan) Medical Center for Adult Diseases; Dr Harada is now with the Department of Neurology, Shizuoka (Japan) Prefectural General Hospital.

Arch Neurol. 1993;50(10):1070-1074. doi:10.1001/archneur.1993.00540100061017

• Objective.  —To evaluate the relationship of corpus callosum atrophy to cerebral cortical oxygen metabolism and cognitive function in patients with Alzheimer's disease.

Design.  —Prospective clinicoradiologic correlation with magnetic resonance imaging and positron emission tomography.

Setting.  —A university hospital.

Patients, Participants.  —Ten right-handed male patients with Alzheimer's disease, aged 46 to 70 years (mean±SD 57±6 years), and 14 age- and sex-matched right-handed control subjects.

Main Outcome Measures.  —The midsagittal corpus callosum areas (on T1-weighted magnetic resonance images), cerebral metabolic rate of oxygen (measured with positron emission tomography using the oxygen-15 steady-state technique), and the IQs of the Wechsler Adult Intelligence Scale.

Results.  —Compared with control subjects, the patients had significantly decreased callosal areas with a posterior predominance of the degree of atrophy. The area of anterior and posterior halves of the corpus callosum had a significant correlation with the value of oxygen metabolism in the frontal and parietotemporo-occipital association cortices, respectively. The total area of the corpus callosum was significantly related to the total and verbal IQs of the Wechsler Adult Intelligence Scale.

Conclusion.  —Atrophy of corpus callosum reflects the severity and pattern of cortical damage associated with hypometabolism and cognitive impairment in Alzheimer's disease.

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