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a Department of
Neurology, Faculty of Medicine, Kyoto University, Kyoto, Japan, b Department
of Brain Pathophysiology, c Department of Radiology and Nuclear Medicine, d Department
of Neurology, Shiga Medical Center for Adults, Moriyama, Shiga, Japan, e Research Institute
Correspondence to: Dr Hiroshi Yamauchi, Research Institute, Shiga Medical Center, 5-4-30 Moriyama, Moriyama-city, Shiga 524-8524, Japan email yamauchi{at}shigamed.moriyama.shiga.jp
Received 15 March 1999 and in revised form 23 August 1999;
Accepted 3 September
1999
OBJECTIVES
It remains
controversial whether selective neuronal ischaemic change develops in
patients with occlusion of the large cerebral arteries. Previous
studies have shown atrophy of the corpus callosum with reduced cortical
oxygen metabolism in large cerebral arterial occlusive diseases, which
might be indirect evidence of loss of the neurons in cortical layer 3. Recent studies of patients with ischaemic cerebrovascular diseases have
demonstrated reduced central benzodiazepine receptor (BZR) binding in
the normal appearing cortical areas, which might be more direct
evidence of changes of the neurons. Although pathophysiology of the
decreased BZR is unclear, a decrease in the cortical BZR binding with
neuronal loss would cause atrophy of the corpus callosum. The purpose
of this study was to determine whether atrophy of the corpus callosum is associated with a decrease in cortical BZR binding in large cerebral
arterial occlusive diseases.
METHODSSeven patients
with occlusive diseases of the middle cerebral or internal carotid
artery and only minor subcortical infarctions were studied. Single
photon emission tomographic images of 123I labelled
iomazenil (IMZ) obtained 180 minutes after injection were analysed for
BZR binding. The midsagittal corpus callosum area/skull area ratio (on
T1 weighted magnetic resonance images) was compared with the cerebral
IMZ uptake/cerebellar IMZ uptake ratio.
RESULTSCompared with
23 age and sex matched control subjects, the patients had significantly
decreased callosal area/skull area ratio. The degree of corpus callosum
atrophy was significantly and strongly (
=0.99, p<0.02) correlated
with that of the decreases in the mean cerebral cortical IMZ uptake ratio.
CONCLUSIONCorpus
callosum atrophy may occur in association with a decrease in cortical
BZR binding in large cerebral arterial occlusive diseases. Corpus
callosum atrophy with decreased cortical BZR binding might reflect
cortical neuronal damage in large cerebral arterial occlusive diseases.
This article has been cited by other articles:
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  H. Yamauchi, T. Kudoh, Y. Kishibe, J. Iwasaki, and S. Kagawa Selective Neuronal Damage and Borderzone Infarction in Carotid Artery Occlusive Disease: A 11C-Flumazenil PET Study J. Nucl. Med., December 1, 2005; 46(12): 1973 - 1979. [Abstract] [Full Text] [PDF]
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 A. Shiraishi, Y. Hasegawa, S. Okada, K. Kimura, T. Sawada, H. Mizusawa, and K. Minematsu Highly Diffusion-Sensitized Tensor Imaging of Unilateral Cerebral Arterial Occlusive Disease AJNR Am. J. Neuroradiol., June 1, 2005; 26(6): 1498 - 1504. [Abstract] [Full Text] [PDF]
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