Déficit ischémique secondaire et hémorragie méningée, un nouveau paradigme

Despite improvements in the management of subarachnoid hemorrhage, delayed cerebral ischemia remains the main cause of poor prognosis among patients surviving the initial insult. The concept of cerebral infarction resulting from the vasospasm as the sole pathological process is now challenged. Our objective was to spread the knowledge behind the establishment of a new paradigm. A systematic review of the literature has been carried out by searching Medline and Ovid databases using subarachnoid hemorrhage, vasospasm, angiographic vasospasm, ultrasonic vasospasm, delayed cerebral ischemia, cerebral infarction, delayed neurologic ischemia, cerebral vasoconstriction as keywords; as well as expert recommendations and finally reference book chapters. Radiographic and/or ultrasonic vasospasm have been the focus of intense research for several decades. The beneficial effects of nimodipine on prognosis, regardless of any action on large vessel diameter, combined with the poor results of clazosentan on prognosis despite a reduction in the angiographic vasospasm have weakened a widely accepted theory. The actual hypothesis integrates several pathways in combination or not with angiographic vasospasm, and could lead, throughout a variety of scenario, to cerebral infarction and poor outcome. Arterial narrowing is neither necessary nor sufficient to induce delayed cerebral ischemia. Some pathways, suggested years ago, have recently risen in light of these new results, as important players in the pathogenesis of cerebral ischemia.