Cerebral vasospasm following subarachnoid hemorrhage: time for a new world of thought

Abstract

Objective Delayed cerebral vasospasm has long been recognized as an important cause of poor outcome after an otherwise successful treatment of a ruptured intracranial aneurysm, but it remains a pathophysiological enigma despite intensive research for more than half a century. Method Summarized in this review are highlights of research from North America, Europe and Asia reflecting recent advances in the understanding of delayed ischemic deficit. Result It will focus on current accepted mechanisms and on new frontiers in vasospasm research. Conclusion A key issue is the recognition of events other than arterial narrowing such as early brain injury and cortical spreading depression and of their contribution to overall mortality and morbidity.

Cerebral Autoregulation after Subarachnoid Hemorrhage: Comparison of Three Methods

“…Furthermore, current understanding of the development of DCI suggests a multifactorial process with microemboli, microthrombosis, macrovascular spasm, and cortical spreading depolarization all playing a part. 39 These processes may not affect the entire cerebral vasculature equally, which may contribute to the observed differences between THRT, Sxa, and TOxa.…”

Genetic Elimination of eNOS Reduces Secondary Complications of Experimental Subarachnoid Hemorrhage

“…2,3 Antifibrinogen staining of cortical and hippocampal sections of saline-injected and SAH mice showed that mice with SAH had many fibrinogen-positive stained microvessels scattered throughout multiple layers of the cerebral cortex and hippocampus ( Figure 5B). In comparison, sections from eNOS KO mice showed fewer fibrinogen-stained microvessels in the brain ( Figure 5B).…”

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca 2+ -activated K + (BK) channels

“…Supporting this change in sentiment, clinical trials have found that the endothelin-1A receptor antagonist clazosentan significantly decreased the incidence of large-artery vasospasm but failed to improve outcome in SAH patients (8,9). Additional mechanisms that may contribute to SAH-induced DINDs include early brain injury, inflammation, cortical spreading depression, and focal cortical infarcts arising from perfusion deficiencies within the microcirculation (5,6,10,11). Perfusion deficiencies reflecting restricted blood flow through intracerebral (parenchymal) arterioles could result from microthrombi formation (12), vasoconstriction caused by extravascular blood or blood breakdown products (13,14), or impaired neurovascular coupling (15).…”

“…For decades, delayed blood-induced vasospasm of brain surface arteries was considered the major underlying cause of SAH-induced DINDs (4,5). Recently, this paradigm has been challenged, leading to a reevaluation of the causal relationship between angiographically defined vasospasm of surface conduit arteries and SAH-induced morbidity and mortality (5)(6)(7).…”

“…For decades, delayed blood-induced vasospasm of brain surface arteries was considered the major underlying cause of SAH-induced DINDs (4,5). Recently, this paradigm has been challenged, leading to a reevaluation of the causal relationship between angiographically defined vasospasm of surface conduit arteries and SAH-induced morbidity and mortality (5)(6)(7). Supporting this change in sentiment, clinical trials have found that the endothelin-1A receptor antagonist clazosentan significantly decreased the incidence of large-artery vasospasm but failed to improve outcome in SAH patients (8,9).…”