 |
 |

Atrophy of the Corpus Callosum, Cortical Hypometabolism, and Cognitive Impairment in Corticobasal Degeneration
Hiroshi Yamauchi, MD, PhD;
Hidenao Fukuyama, MD, PhD;
Yasuhiro Nagahama, MD, PhD;
Yukinori Katsumi, MD;
Yun Dong, MD;
Takuya Hayashi, MD;
Junji Konishi, MD, PhD;
Jun Kimura, MD
Arch Neurol. 1998;55:609-614.
Objective To investigate whether atrophy of the corpus callosum is associated with cognitive impairment and cerebral cortical hypometabolism in corticobasal degeneration.
Design Prospective clinicoradiological correlation with magnetic resonance imaging and positron emission tomography.
Setting A university hospital.
Patients Eight right-handed patients with clinically diagnosed corticobasal degeneration (mean±SD age, 64±8 years).
Main Outcome Measures Midsagittal corpus callosum areaskull area ratio (on T1-weighted magnetic resonance images), the sum of the scaled scores of the 6 subtests on the Wechsler Adult Intelligence ScaleRevised (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 areaskull 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 ScaleRevised.
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.
From the Departments of Neurology (Drs Yamauchi, Nagahama, Katsumi, Hayashi, and Kimura), Brain Pathophysiology (Drs Fukuyama and Dong), and Radiology and Nuclear Medicine (Dr Konishi), Faculty of Medicine, Kyoto University, Kyoto, Japan; and the Research Institute, Shiga Medical Center for Adult Diseases, Moriyama, Japan (Dr Yamauchi).
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
Correlation Between Antemortem Magnetic Resonance Imaging Findings and Pathologically Confirmed Corticobasal Degeneration
Josephs et al.
Arch Neurol 2004;61:1881-1884.
ABSTRACT
| FULL TEXT
Functional Imaging as a Window to Dementia: Corticobasal Degeneration
Seritan et al.
J. Neuropsychiatry Clin. Neurosi. 2004;16:393-399.
FULL TEXT
Long-term changes of hemodynamics and metabolism after carotid artery occlusion
Yamauchi et al.
Neurology 2000;54:2095-2102.
ABSTRACT
| FULL TEXT
Corticobasal ganglionic degeneration and/or frontotemporal dementia? A report of two overlap cases and review of literature
Mathuranath et al.
J. Neurol. Neurosurg. Psychiatry 2000;68:304-312.
ABSTRACT
| FULL TEXT
Language disturbances in corticobasal degeneration
Frattali et al.
Neurology 2000;54:990-992.
ABSTRACT
| FULL TEXT
|