Cerebral vasospasm. Part I. In cerebral vascular malformations

This review enumerates the many proposed mechanisms of vasospasm, including cellular elements, agents derived from the blood and injured cerebral tissues, alteration of calcium: magnesium ratios, free radical reactions, hypothalamic injury, clogging of the subarachnoid space, obstructions of the vasa vasorum and necrosis of the media with subintimal proliferation and intraluminal acidosis. At present, no single agent has been demonstrated as the only source of vasospasm, and whether the disorder is spasm or a chronic arteriopathy remains the subject of argument. The factors influencing the frequency, timing, severity and distribution of angiographically documented vasospasm are discussed, including data from our own population-based study over a 3 year period showing an incidence of vasospasm of 73%. Special emphasis is given to the observation that differences in patient populations play a major role in the incidence and severity of reported vasospasm: those from non-selective populations show a higher incidence of vasospasm and a greater severity of the syndromes attributed to spasm. Hypotheses are offered to account for the low frequency of vasospasm in hemorrhages from arteriovenous malformations and mycotic aneurysms. Clinical syndromes of vasospasm are reviewed, with special emphasis on our own material. The mode of onset and subsequent course of syndromes include those of sudden onset consistent with embolism, and those of gradual onset suggesting a low flow state. Their relationship to the severity of the subarachnoid hemorrhage and the vasospasm is presented. The paucity of syndromes of isolated deep infarcts of the lacunar type is noted. An account is given of the many failed therapies and the future hopes for early surgery. Innovations in medical therapy, including the use of some platelet inhibitors available only in some countries, and rationales for the use of aspirin and even heparin is discussed.