Periinfarct and remote excitability changes after transient middle cerebral artery occlusion

Transient middle cerebral artery (MCA) occlusion results in substantially s maller cortical infarcts than permanent MCA occlusion if reperfusion is ini tiated within the first few hours. Only little information is available on the long-term functional outcome of the cortical regions "salvaged" by earl y reperfusion. To address this issue we examined basic electrophysiologic p arameters in vitro using standard extracellular recording techniques at 7 a nd 28 days after transient MCA occlusion (1- and 2-hour ischemia) in rats. Both neocortical areas ipsi- and contralateral to MCA occlusion were system atically mapped to delineate the extent of periinfarct and remote alteratio ns. In the periinfarct region we found a significant reduction of field pot ential amplitudes up to 3 mm when measuring from the infarct border at 7 da ys and up to 7 mm at 28 days. Paired-pulse inhibition, an indicator of GABA ergic transmission, was only moderately impaired in this region at 7 days a nd not significantly different from control at 28 days. Remote effects were observed both ipsi- and contralaterally. Ipsilaterally they were restricte d to a region close to the midline (presumably motor cortex) and were most likely attributable to the degeneration of corticostriatal connections. The extent of the contra lateral excitability changes was clearly related to t he size of the neocortical infarcts with large infarcts resulting in the wi despread reduction of field potential amplitudes and an impairment of paire d-pulse inhibition. The results show that there is a relatively large perii nfarct region with decreased overall excitability after transient MCA occlu sion which is Likely to have a profound effect on perilesional processes in volved in functional recovery. Remote excitability changes may contribute t o the functional deficit and are probably related to deafferentation.