About this Journal Submit a Manuscript Table of Contents
Stroke Research and Treatment
Volume 2013 (2013), Article ID 819340, 10 pages
http://dx.doi.org/10.1155/2013/819340
Review Article

Subarachnoid Hemorrhage, Spreading Depolarizations and Impaired Neurovascular Coupling

1Department of Pharmacology, University of Vermont College of Medicine, Burlington, VT 05405-0068, USA
2Neurovascular Research Laboratory, Department of Radiology, Stroke Service and Neuroscience Intensive Care Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02115, USA
3Gonda Multidisciplinary Brain Research Center, Bar-Ilan University, Ramat-Gan 52990, Israel

Received 27 December 2012; Accepted 8 February 2013

Academic Editor: Ryszard M. Pluta

Copyright © 2013 Masayo Koide 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.

Abstract

Aneurysmal subarachnoid hemorrhage (SAH) has devastating consequences on brain function including profound effects on communication between neurons and the vasculature leading to cerebral ischemia. Physiologically, neurovascular coupling represents a focal increase in cerebral blood flow to meet increased metabolic demand of neurons within active regions of the brain. Neurovascular coupling is an ongoing process involving coordinated activity of the neurovascular unit—neurons, astrocytes, and parenchymal arterioles. Neuronal activity can also influence cerebral blood flow on a larger scale. Spreading depolarizations (SD) are self-propagating waves of neuronal depolarization and are observed during migraine, traumatic brain injury, and stroke. Typically, SD is associated with increased cerebral blood flow. Emerging evidence indicates that SAH causes inversion of neurovascular communication on both the local and global level. In contrast to other events causing SD, SAH-induced SD decreases rather than increases cerebral blood flow. Further, at the level of the neurovascular unit, SAH causes an inversion of neurovascular coupling from vasodilation to vasoconstriction. Global ischemia can also adversely affect the neurovascular response. Here, we summarize current knowledge regarding the impact of SAH and global ischemia on neurovascular communication. A mechanistic understanding of these events should provide novel strategies to treat these neurovascular disorders.