Table of Contents Author Guidelines Submit a Manuscript
Neurology Research International
Volume 2013 (2013), Article ID 415813, 7 pages
Review Article

Cerebral Vasospasm in Traumatic Brain Injury

Department of Neurosurgery, University of Southern California, 1200 North State Street, Suite 3300, Los Angeles, CA 90033, USA

Received 29 October 2012; Accepted 4 June 2013

Academic Editor: Linda M. Liau

Copyright © 2013 Daniel R. Kramer 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.


Vasospasm following traumatic brain injury (TBI) may dramatically affect the neurological and functional recovery of a vulnerable patient population. While the reported incidence of traumatic vasospasm ranges from 19%–68%, the true incidence remains unknown due to variability in protocols for its detection. Only 3.9%–16.6% of patients exhibit clinical deficits. Compared to vasospasm resulting from aneurysmal SAH (aSAH), the onset occurs earlier and the duration is shorter. Overall, the clinical course tends to be milder, although extreme cases may occur. Traumatic vasospasm can occur in the absence of subarachnoid hemorrhage. Surveillance transcranial Doppler ultrasonography (TCD) has been utilized to monitor for radiographic vasospasm following TBI. However, effective treatment modalities remain limited. Hypertension and hypervolemia, the mainstays of treatment of vasospasm associated with aSAH, must be used judiciously in TBI patients, and calcium-channel blockers have offered mixed clinical results. Currently, the paucity of large prospective cohort studies and level-one data limits the ability to form evidence-based recommendations regarding the diagnosis and management of vasospasm associated with TBI.