Stroke, Vol 20, 1516-1523, Copyright © 1989 by American Heart Association
H Iizuka, K Sakatani and W Young
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.
ARTICLES
Selective cortical neuronal damage after middle cerebral artery occlusion in rats
Department of Neurosurgery, New York University Medical Center, New York 10016.
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