Selective cortical neuronal damage after middle cerebral artery occlusion in rats.

Abstract

We studied histopathologic changes in cerebral cortex of 20 rats after middle cerebral artery occlusion by using the Fink-Heimer suppressive silver impregnation method and conventional stains. At 6 hours after occlusion, Fink-Heimer-stained sections revealed abundant coarsely granular, intensely argyrophilic neurons in the ischemic cortex. These distinctive argyrophilic neurons could be clearly differentiated from neurons that suffered postmortem changes; argyrophilic neurons were present in all layers of the lateral parietal cortex but in only the superficial cortical layers II and III in the parasagittal area of the frontoparietal cortex and the temporo-occipital area. At 24 hours after occlusion as the ischemic region progressed to pannecrosis, argyrophilic neurons were still evident in peri-infarct regions, with more prominent neuritic silver deposits but no changes in number or spatial distribution. Over 2-7 days, the argyrophilic neurons gradually disappeared while many fine silver-impregnated degenerating terminals appeared in the peri-infarct regions. At 3-6 weeks after occlusion, no more argyrophilic neurons were seen in the cortex although degenerating axons were still present in the deep white matter. Our results indicate selective neuronal damage in the superficial cortical layers and massive axonal degeneration in the cerebrum surrounding infarcts. The neuronal damage does not appear to progress beyond 6 hours after middle cerebral artery occlusion. The Fink-Heimer method has many advantages over existing conventional stains for documenting selective neuronal damage in focal cerebral ischemia. (Stroke 1989;20:1516-1523

Right hemisphere structures predict poststroke speech fluency

“…Given previous imaging studies showing that axonal loss and demyelination associated with Wallerian degeneration (WD) can be detected in DTI as decreased FA and increased RD in white matter distant from the injury, 37,38 we hypothesize that our CC findings are due to WD caused by the left hemisphere lesion. 39 Our finding that increased lesion/ ROI overlap ratio in the left hemisphere predicted lower FA values in the whole CC ROI and CC-SMA ROI lends additional support to this hypothesis.…”

Neural damage in the rat thalamus after cortical infarcts.

“…In our previous studies, selective neuronal death in the peri-infarct cortex and subcortical area was obvious in FinkHeimer sections as early as 6 hours after MCAO and reached a maximum within 24 hours. 7 Kataoka et al 12 have reported decreased succinate dehydrogenase activity in ipsilateral thalamic neurons 5 days after MCAO. Although reports of human autopsy cases are few, neuronal degeneration or cell loss with GFAP reactions has been observed in the ipsilateral thalamus after cortical lesions including stroke, injury, and surgical interventions.…”

Neurochemical analysis of focal ischemia in rats.

“…16 Whether increases in free radicals generated by xanthine oxidase contribute to tissue damage is unresolved. Most studies suggest that infarcts are complete by 4-6 hours, 17 yet uric acid increases persisted for 21 days and were maximal at 1 day. It is therefore possible that changes are merely secondary.…”