Atrophy of the corpus callosum, cognitive impairment, and cortical hypometabolism in progressive supranuclear palsy
Hiroshi Yamauchi MD, PhD
Departments of Neurology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Japan Foundation for Aging and Health, Tokyo, Japan
Search for more papers by this authorCorresponding Author
Dr Hidenao Fukuyama MD, PhD
Departments of Brain Pathophysiology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Department of Brain Pathophysiology, Kyoto University Hospital, 54 Shogoin Kawaharacho, Sakyo-ku, Kyoto 606, JapanSearch for more papers by this authorYasuhiro Nagahama MD
Departments of Neurology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Search for more papers by this authorYukinori Katsumi MD
Departments of Neurology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Search for more papers by this authorYun Dong MD
Departments of Brain Pathophysiology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Search for more papers by this authorJunji Konishi MD, PhD
Departments of Radiology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Search for more papers by this authorJun Kimura MD
Departments of Neurology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Search for more papers by this authorHiroshi Yamauchi MD, PhD
Departments of Neurology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Japan Foundation for Aging and Health, Tokyo, Japan
Search for more papers by this authorCorresponding Author
Dr Hidenao Fukuyama MD, PhD
Departments of Brain Pathophysiology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Department of Brain Pathophysiology, Kyoto University Hospital, 54 Shogoin Kawaharacho, Sakyo-ku, Kyoto 606, JapanSearch for more papers by this authorYasuhiro Nagahama MD
Departments of Neurology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Search for more papers by this authorYukinori Katsumi MD
Departments of Neurology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Search for more papers by this authorYun Dong MD
Departments of Brain Pathophysiology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Search for more papers by this authorJunji Konishi MD, PhD
Departments of Radiology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Search for more papers by this authorJun Kimura MD
Departments of Neurology and Nuclear Medicine, Faculty of Medicine, Kyoto University, Kyoto, Japan
Search for more papers by this authorAbstract
Recent studies disclosed neurofibrillary degeneration in layer 3 of the association cortex in patients with progressive supranuclear palsy. This lesion may be associated with corpus callosum atrophy and may impair the function of cortical regions indispensable for complex cognitive activity. To investigate whether corpus callosum atrophy is associated with cognitive impairment and cerebral cortical hypometabolism, we studied 10 patients with progressive supranuclear palsy using magnetic resonance imaging and positron emission tomography with fluorodeoxyglucose as a tracer. Compared with 23 age-matched control subjects, the patients had significantly decreased callosal area-skull area ratios, with anterior predominance of the degree of atrophy. The corpus callosum atrophy was accompanied by a decreased mean cortical glucose metabolic rate, predominantly in the frontal region of the cortex, and poor performance on the picture arrangement subtest of the Wechsler Adult Intelligence Scale and the verbal fluency task. We conclude that corpus callosum atrophy with anterior predominance is present in progressive supranuclear palsy, and that this atrophy is associated with cognitive impairment and cerebral cortical hypometabolism, especially in the frontal cortical region. Corpus callosum atrophy may reflect the pathological changes in the cerebral cortex, accentuated in the frontal region, that contribute to the development of frontal lobe dysfunction in this disease.
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