Evolution of diaschisis in a focal stroke model.
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 [18F]fluorodeoxyglucose small-animal positron emission tomography. Cerebral blood flow was measured with [14C]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.[1]References
- Evolution of diaschisis in a focal stroke model. Carmichael, S.T., Tatsukawa, K., Katsman, D., Tsuyuguchi, N., Kornblum, H.I. Stroke (2004) [Pubmed]
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