Vasogenic brain edema in focal 4-aminopyridine seizures: the role of neuronal hyperactivity.

The protein transport of the neocortical blood vessels during experimental focal seizures was investigated in adult Wistar rats. The seizure focus was produced by the local application of isosmotic and isohydric 4-aminopyridine solution, while the electrocorticogram was monitored. The protein transport of the vessels was assessed through the histochemical detection of intravenously injected horseradish peroxidase. Serial sections of the whole seizure focus were evaluated in the light microscope, and the areas of protein extravasation were measured planimetrically. Two groups of animals were treated with diphenylhydantoin for 8 days, and the electro-corticographic and seizure experiments were then performed. Three main features of the pathological protein transport were found: 1) the increase in protein permeability was not mediated by a hypertensive crisis during the seizure; 2) the pathologic changes in the neurons and glia always preceded the breakdown of the blood-brain barrier; 3) this breakdown is probably closely related to neuronal hyperactivity, since it was prevented by diphenylhydantoin.