Journal
NEUROSURGERY CLINICS OF NORTH AMERICA
Volume 21, Issue 2, Pages 365-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.nec.2009.10.008
Keywords
Cerebral vasospasm; Subarachnoid hemorrhage; Inflammation; Leukocytes; Endothelial cells; Hemoglobin; Haptoglobin; Nitric oxide
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Morbidity and mortality of patients with aneurysmal subarachnoid hemorrhage (aSAH) is significantly related to the development of chronic cerebral vasospasm. Despite extensive clinical and experimental research, the pathophysiology of the events that result in delayed arterial spasm is not fully understood. A review of the published literature on cerebral vasospasm that included but was not limited to all PubMed citations from 1951 to the present was performed. The findings suggest that leukocyte-endothelial cell interactions play a significant role in the pathophysiology of cerebral vasospasm and explain the clinical variability and time course of the disease. Experimental therapeutic targeting of the inflammatory response when timed correctly can prevent vasospasm, and supplementation of endothelial relaxation by nitric oxide-related therapies and other approaches could result in reversal of the arterial narrowing and improved outcomes in patients with aSAH.
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