Evolution of diaschisis in a focal stroke model

被引:98
作者
Carmichael, ST
Tatsukawa, K
Katsman, D
Tsuyuguchi, N
Kornblum, HI
机构
[1] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pediat, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pharmacol, Los Angeles, CA 90095 USA
[4] Univ Calif Los Angeles, David Geffen Sch Med, Ctr Mol Med, Dept Energy, Los Angeles, CA 90095 USA
关键词
cerebral cortex; neuronal plasticity; somatosensory cortex; tomography; emission computed;
D O I
10.1161/01.STR.0000117235.11156.55
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background and Purpose-Stroke produces diaschisis in adjacent and connected regions. The sequential changes in diaschisis over time and the relationship of regions of diaschisis to functional cortical areas and regions of poststroke neuroplasticity have not been determined. Methods-Small cortical strokes were produced in the barrel cortex of rats. Relative glucose metabolism was determined in vivo over time with [F-18] fluorodeoxyglucose small-animal positron emission tomography. Cerebral blood flow was measured with [C-14] iodoantipyrine. Regions of hypometabolism and hypoperfusion were compared with histological damage in the same animals. Results-Small cortical strokes produce an initial network of hypometabolism in a broad region of cortex adjacent to the stroke and in the striatum and thalamus on day 1. Cerebral blood flow is diminished only immediately around the cortical infarct on day 1. A substantial area of cortex adjacent to the stroke remains hypometabolic on day 8. This persistent cortical hypometabolism occupies the somatosensory cortex, forelimb motor cortex, and second somatosensory area. Conclusions-Focal stroke produces ipsilateral diaschisis in connected cortical regions that is clearly distant from subtotal damage and may play a role in poststroke neuroplasticity.
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收藏
页码:758 / 763
页数:6
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