During the last decade, accumulating experimental and clinical evidence has demonstrated that the presence of delayed vasospasm of the major cerebral vessels may just be a contributing factor but not necessarily the principal determinant of delayed cerebral ischemia and delayed ischemic neurologic deficit. Cerebral infarction can occur when vasospasm is not angiographically detected in the territorial artery, and poor outcome in aSAH seems to be directly dependent on infarction but independent of vasospasm . There is increasing evidence that other contributing factors may be involved in the development of delayed cerebral ischemia, and their characterization and treatment could improve the consistently poor clinical outcome in patients with aSAH. It has been pointed out that may be an early, short-lived phase occurring immediately after SAH and a subsequent phase that is prolonged or chronic. Both phases of vasospasm are considered to result from an abnormal constriction of the muscular layers of both microcirculatory vessels and proximal vessel and have been considered the main cause of cerebral ischemia after SAH. However, whether the 2 phases are independent or interactive with respect to the clinical course has not been settled.
|Numero di pagine||2|
|Stato di pubblicazione||Published - 2015|
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