Cerebral perfusion imaging in vasospasm
Shivanand P. Lad, Raphael Guzman, Michael E. Kelly, Gordon Li, Michael Lim, Karl Lovbald, Gary K. Steinberg
2006
Neurosurgical Focus
ASOSPASM following cerebral aneurysm rupture is one of the most devastating sequelae and is also the most common cause of DIND. Vasospasm can be demonstrated using angiography in approximately 60 to 70% of patients with ruptured aneurysms. 29, 31, 38 Clinical vasospasm resulting in DIND occurs in 20 to 30% of patients within 3 to 14 days after aneurysmal SAH. Given that vasospasm is the most common cause of morbidity and mortality in patients who survive the initial bleeding episode, it is
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... ative not only to diagnose the condition but also to predict which patients are likely to become symptomatic. The pathophysiological mechanisms of vasospasm are complex and incompletely elucidated. The presence of oxyhemoglobin in the subarachnoid cisterns seems to be a key promoter of the phenomena that ultimately cause narrowing of the arterial lumen and impaired autoregulation. 24, 26, 31, 32, 36, 38, 39 The vascular changes are typically reversible: when severe, however, they may cause cerebral infarction and DIND. The amount of blood in the subarachnoid space on the initial brain CT scan, age youn-Neurosurg. Focus / Volume 21 / Vasospasm following cerebral aneurysm rupture is one of the most devastating sequelae and the most common cause of delayed ischemic neurological deficit (DIND). Because vasospasm also is the most common cause of morbidity and mortality in patients who survive the initial bleeding episode, it is imperative not only to diagnose the condition but also to predict which patients are likely to become symptomatic. The exact pathophysiology of vasospasm is complex and incompletely elucidated. Early recognition of vasospasm is essential because the timely use of several therapeutic interventions can counteract this disease and prevent the occurrence of DIND. However, the prompt implementation of these therapies depends on the ability to predict impending vasospasm or to diagnose it at its early stages. A number of techniques have been developed during the past several decades to evaluate cerebral perfusion, including positron emission tomography, xenon-enhanced computed tomography, single-photon emission computed tomography, perfusion-and diffusion-weighted magnetic resonance imaging, and perfusion computed tomography. In this article, the authors provide a general overview of the currently available perfusion imaging techniques and their applications in treating vasospasm after a patient has suffered a subarachnoid hemorrhage. The use of cerebral perfusion imaging techniques for the early detection of vasospasm is becoming more common and may provide opportunities for early therapeutic intervention to counteract vasospasm in its earliest stages and prevent the occurrence of DINDs. KEY WORDS • vasospasm • subarachnoid hemorrhage • perfusion imaging • cerebral blood flow • transcranial Doppler ultrasonography • neurosurgery 1 Abbreviations used in this paper: ACA = anterior cerebral artery; CBF = cerebral blood flow; CBV = cerebral blood volume; CT = computed tomography; DIND = delayed ischemic neurological deficit; MCA = middle cerebral artery; MR = magnetic resonance; PET = positron emission tomography; SAH = subarachnoid hemorrhage; SPECT = single-photon emission computed tomography; TCD = transcranial Doppler. V * CTA = CT angiography; DWI = diffusion-weighted MR imaging; FDA = Food and Drug Administration; MRA = MR angiography; MTT = mean transit time; PCT = perfusion CT; PWI = perfusion-weighted MR imaging.
doi:10.3171/foc.2006.21.3.7
pmid:17029346
fatcat:rexvecytwbbbrdbw3glzvxixce