Cerebral Vasospasm after Subarachnoid Hemorrhage: Putative... : Neurosurgery (original) (raw)

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Cerebral Vasospasm after Subarachnoid Hemorrhage: Putative Role of Inflammation

Dumont, Aaron S. M.D.; Dumont, Randall J. M.Sc.; Chow, Michael M. M.D.; Lin, Chi-lung M.D.; Calisaneller, Tarkan M.D.; Ley, Klaus F. M.D.; Kassell, Neal F. M.D.; Lee, Kevin S. Ph.D.

Departments of Neurological Surgery and Neuroscience, University of Virginia School of Medicine, Charlottesville, Virginia

Department of Neurological Surgery, University of Virginia School of Medicine, Charlottesville, Virginia, and Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada

Department of Neurological Surgery, University of Virginia School of Medicine, Charlottesville, Virginia

Department of Neuroscience, University of Virginia, School of Medicine, Charlottesville, Virginia, and Department of Neurological Surgery, Kaohsiung Medical University, Kaohsiung, Taiwan

Departments of Neurological Surgery and Neuroscience, University of Virginia School of Medicine, Charlottesville, Virginia

Departments of Biomedical Engineering and Molecular Physiology and Biophysics, and Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville, Virginia

Department of Neurological Surgery, University of Virginia School of Medicine, Charlottesville, Virginia

Departments of Neuroscience and Neurological Surgery, University of Virginia School of Medicine, Charlottesville, Virginia

Reprint requests:

Aaron S. Dumont, M.D., Department of Neurological Surgery, University of Virginia Health Sciences Center, Box 212, Charlottesville, VA 22908. Email: [email protected]

Received, July 17, 2002.

Accepted, March 11, 2003.

Abstract

CEREBRAL VASOSPASM IS a common, formidable, and potentially devastating complication in patients who have sustained subarachnoid hemorrhage (SAH). Despite intensive research efforts, cerebral vasospasm remains incompletely understood from both the pathogenic and therapeutic perspectives. At present, no consistently efficacious and ubiquitously applied preventive and therapeutic measures are available in clinical practice. Recently, convincing data have implicated a role of inflammation in the development and maintenance of cerebral vasospasm. A burgeoning (although incomplete) body of evidence suggests that various constituents of the inflammatory response, including adhesion molecules, cytokines, leukocytes, immunoglobulins, and complement, may be critical in the pathogenesis of cerebral vasospasm. Recent studies attempting to dissect the cellular and molecular basis of the inflammatory response accompanying SAH and cerebral vasospasm have provided a promising groundwork for future studies. It is plausible that the inflammatory response may indeed represent a critical common pathway in the pathogenesis of cerebral vasospasm pursuant to SAH. Investigations into the nature of the inflammatory response accompanying SAH are needed to elucidate the precise role(s) of inflammatory events in SAH-induced pathologies.