Background and Purpose-Cortical spreading depression (CSD) has been much studied experimentally but never demonstrated unequivocally in human neocortex by direct electrophysiological recording. A similar phenomenon, peri-infarct depolarization, occurs in experimental models of stroke and causes the infarct to enlarge. Our current understanding of the mechanisms of deterioration in the days after major traumatic or ischemic brain injury in humans has not yielded any effective, novel drug treatment. This study sought clear evidence for the occurrence and propagation of CSD in the injured human brain. Methods-In 14 patients undergoing neurosurgery after head injury or intracranial hemorrhage, we placed electrocorticographic (ECoG) electrodes near foci of damaged cortical tissue. Results-Transient episodes of depressed ECoG activity that propagated across the cortex at rates in the range of 0.6 to 5.0 mm/min were observed in 5 patients; this rate of propagation is characteristic of CSD. We also observed, in 8 of the 14 patients, transient depressions of ECoG amplitude that appeared essentially simultaneous in all recording channels, without clear evidence of spread. Conclusions-These results indicate that CSD or similar events occur in the injured human brain and are more frequent than previously suggested. On the basis of these observations, we suggest that the related phenomenon, peri-infarct depolarization, is indeed likely to occur in boundary zones in the ischemic human cerebral cortex.
The pathophysiology of peri-lesion boundary zones in acute brain injury is highly dynamic, and it is now clear that spreading-depression-like events occur frequently in areas of cerebral cortex adjacent to contusions in the injured human brain. An automated method to assay microdialysate from peri-lesion cerebral cortex in 11 patients with intracranial haematomas requiring surgery was used. Perfusate (2 lL/min) flowed directly into a flow-injection system for assay of glucose and lactate at intervals typically of 30 secs each. Four channels of electrocorticogram (ECoG) were recorded from a subdural strip adjacent to the catheter. Several patterns of change in metabolites were identified in different time domains. Overall, the number of transient lactate events was significantly correlated with the number of glucose events (r 2 ¼ 0.48, P ¼ 0.027, n ¼ 10). Progressive reduction in dialysate glucose was very closely correlated with the aggregate number of ECoG events (r 2 ¼ 0.76, P ¼ 0.0004, n ¼ 11). It is proposed that the recently documented adverse impact of low dialysate glucose on clinical outcome may be because of recurrent, spontaneous spreadingdepression-like events in the perilesion cortex.
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