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Neurology Research International
Volume 2013 (2013), Article ID 506584, 12 pages
Review Article

Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia

1Department of Neurological Surgery, University of Texas Health Sciences Center at San Antonio, San Antonio, TX 78229, USA
2Department of Neurological Surgery, Vanderbilt University School of Medicine, Nashville, TN 37212, USA

Received 7 November 2012; Revised 26 June 2013; Accepted 26 June 2013

Academic Editor: Mamede de Carvalho

Copyright © 2013 Kevin R. Carr et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cerebral vasospasm (CVS) is a potentially lethal complication of aneurysmal subarachnoid hemorrhage (aSAH). Recently, the symptomatic presentation of CVS has been termed delayed cerebral ischemia (DCI), occurring as early as 3-4 days after the sentinel bleed. For the past 5-6 decades, scientific research has promulgated the theory that cerebral vasospasm plays a primary role in the pathology of DCI and subsequently delayed ischemic neurological decline (DIND). Approximately 70% of patients develop CVS after aSAH with 50% long-term morbidity rates. The exact etiology of CVS is unknown; however, a well-described theory involves an antecedent inflammatory cascade with alterations of intracellular calcium dynamics and nitric oxide fluxes, though the intricacies of this inflammatory theory are currently unknown. Consequently, there have been few advances in the clinical treatment of this patient cohort, and morbidity remains high. Identification of intermediaries in the inflammatory cascade can provide insight into newer clinical interventions in the prevention and management of cerebral vasospasm and will hopefully prevent neurological decline. In this review, we discuss current theories implicating the inflammatory cascade in the development of CVS and potential treatment targets.