Vasospasm in the cerebral arteries occurs in approximately 30% of patients with SAH and frequently occurs 7 to 10 days after hemorrhage with spontaneous resolution by day 21 [6]. Vasospasm is associated with delayed cerebral ischemia defined by delayed development of neurologic deficits after SAH not related to aneurysm treatment or other neurologic complications, such as hydrocephalus, cerebral edema, or metabolic derangements [26]. Morbidity and mortality in SAH increases between 10% and 20% after onset of clinical symptoms of delayed cerebral ischemia [27], and the symptoms are frequently nonreversible [28,29]. Imaging findings of vasospasm and guidance of treatment does not appear to improve clinical outcome after the onset of clinical symptoms [28]. Despite the association of moderate to severe vasospasm and poor clinical outcome [30], only 50% patients with large-vessel vasospasm develop clinical ischemic neurologic symptoms [6], and delayed ischemia can occur in the absence of imaging findings of vasospasm [26]. However, given the clinical implications of delayed cerebral ischemia, early screening and detection of vasospasm remains recommended [6]. Arteriography Cervicocerebral Conventional catheter-directed cerebrovascular arteriography is the reference standard for characterization of intracranial vasospasm. However, only approximately 50% of radiographic large-vessel vasospasm develops delayed cerebral ischemia, and given the invasive nature and potential rare neurologic complications, other less invasive screening methods are often performed before catheter angiogram [28]. In a large, international multicenter randomized trial, the presence of angiographic vasospasm was strongly associated (odds ratio of 9.3) with the development of cerebral infarction. In the same study, a small number of patients (3%) developed infarction without evidence of vasospasm on angiogram [31].
Cerebrovascular Diseases Aneurysm Vascular Malformation and Subarachnoid Hemorrhage PCAs. Vasospasm in the cerebral arteries occurs in approximately 30% of patients with SAH and frequently occurs 7 to 10 days after hemorrhage with spontaneous resolution by day 21 [6]. Vasospasm is associated with delayed cerebral ischemia defined by delayed development of neurologic deficits after SAH not related to aneurysm treatment or other neurologic complications, such as hydrocephalus, cerebral edema, or metabolic derangements [26]. Morbidity and mortality in SAH increases between 10% and 20% after onset of clinical symptoms of delayed cerebral ischemia [27], and the symptoms are frequently nonreversible [28,29]. Imaging findings of vasospasm and guidance of treatment does not appear to improve clinical outcome after the onset of clinical symptoms [28]. Despite the association of moderate to severe vasospasm and poor clinical outcome [30], only 50% patients with large-vessel vasospasm develop clinical ischemic neurologic symptoms [6], and delayed ischemia can occur in the absence of imaging findings of vasospasm [26]. However, given the clinical implications of delayed cerebral ischemia, early screening and detection of vasospasm remains recommended [6]. Arteriography Cervicocerebral Conventional catheter-directed cerebrovascular arteriography is the reference standard for characterization of intracranial vasospasm. However, only approximately 50% of radiographic large-vessel vasospasm develops delayed cerebral ischemia, and given the invasive nature and potential rare neurologic complications, other less invasive screening methods are often performed before catheter angiogram [28]. In a large, international multicenter randomized trial, the presence of angiographic vasospasm was strongly associated (odds ratio of 9.3) with the development of cerebral infarction. In the same study, a small number of patients (3%) developed infarction without evidence of vasospasm on angiogram [31].