Extravasated Protein as a Cause of Limbic Seizure-Induced Brain Damage: An Evaluation Using Kainic Acid

Abstract

Tonicoclonic seizure-induced alterations in cerebrovascular permeability (CVP) to protein (CVP-p) have been recognized for several years (see Klatzo, 1983). Although the mechanisms of this permeability change are not completely understood, free arachidonic acid (Bazan, 1970; Rodriguez de Turco et al., 1983; Siesjö et al., 1983) has been implicated (Chan et al., 1983). Several other characteristics of the change are known. The morphologic basis for increased CVP-p appears to be the pinocytotic vesicle, sometimes coalescing to form transendothelial channels which effectively shunt endothelial tight junctions (Westergaard, 1980). Alterations in CVP-p also depend partly on the increased arterial blood pressure accompanying seizures (Johansson and Nilsson, 1977). However, as Nitsch and Klatzo (1983) pointed out, the degree of hypertension attained during an attack would not be,in the absence of the seizure, of sufficient magnitude to provoke increases in CVP-p. Thus, seizure-induced disturbances in CVP-p probably involve an interaction between global systemic factors and more localized molecular phenomena occurring in the microenvironment of recruited neurons. Adding to the complexity of CVP alterations, there appears to be a pathoclisis whereby certain regions are more prone to alterations in CVP than are other recruited regions.