[Is calcium a primum movens in the pathogenesis of cerebrovascular accidents?]

Concerning the physiological cascade associated with cerebral vascular accidents, numerous studies have been devoted to a search for a key element (outside the initial fall in blood perfusion) responsible for the noxious jumble that leads to tissue necrosis. As a fundamental element of cell physiology, calcium intervenes in a number of vital functions, but when present in excessive amounts it may engender disorders by accelerating reactions which it normally regulates. Thus, in cerebral tissue, and notably in acute ischaemia, calcium is held responsible for additional phenomena of coagulation, exacerbated neurotransmitter discharge or even cell poisoning by paralysis of mitochondrial respiration. Based on these data, attempts have been made to treat cerebral vascular accidents by the so-called calcium antagonists. Experimentally or clinically, the results obtained, although divergent, show that acting on calcium movements contributes to total or partial correction of the complex physiopathology of cerebral ischaemia. A new generation of calcium antagonists is needed to oppose the fundamental disorders engendered, notably those of mitochondrial function.