Gavin W. Britz, MB BCh, MPH
Director, Duke Cerebrovascular Center
Departments / Divisions- Surgery / Neurosurgery
- Radiology
Address
DUMC 3807
Durham, NC 27710
Appointment Telephone
919-668-0650
Office Telephone
919-668-0650
Fax Telephone
919-668-3392
- MB BCh, University of the Witwatersrand School of Clinical Medicine (South Africa), 1982-1987
- University of the Witwatersrand Faculty of Health Sciences (South Africa), 1988-1990
- Surgery, Johns Hopkins Hospital (Maryland), 1992-1993
- Neurosurgery, Atkinson Morley's Hospital, St. George's University School of Medicine, University of London (United Kingdom), 1998-1999
- Neurological Surgery, University of Washington, 1993-2002 (Chief Resident, 1999-2000)
- Cerebrovascular Surgery, University of Washington Medical Center, 2000
- Neuroradiology, University of Washington Medical Center, 2001-2002
- Interventional Neuroradiology, University of Washington Medical Center, 2002-2003
- MPH, Epidemiology, University of Washington, 2003
Clinical Interests
Treatment of cerebrovascular disorders (brain aneurysms, arteriovenous malformations, dural fistulas, arterial dissections, atherosclerotic diseases) and diseases affecting the skull base (meningiomas, chordomas, pituitary tumors, and craniopharyngiomas)
Research Interests
Stroke is the third leading cause of death in the United States and as many as 15% of all strokes are secondary to ruptured cerebral aneurysms. Outcome following rupture of a cerebral aneurysm remains poor and is associated with 30-day mortality rates between 45% and 80%, with half of all survivors sustaining irreversible brain damage. One of the significant causes of morbidity and mortality following subarachnoid hemorrhage (SAH) is cerebral ischemia. Cerebral ischemia is believed to result from vasospasm affecting the larger vessels in the brain. Consequently, previous research efforts have focused on mechanisms involved in cerebral vasospasm of these vessels in the brain. However, ischemic neurological deficits are observed with no evidence of vasospasm on angiography or TCD. Thus, there is a growing consensus that, in addition to large vessel vasospasm, disturbances of cerebral arterioles, not detectable by angiography, could be responsible for ischemia following SAH. His laboratory has recently demonstrated that these cerebral arterioles are affected and now is attempting to understand the underlying mechanism of their alteration of function. Understanding the mechanism could lead to new treatments that will improve the outcome of patients following an ruptured cerebral aneurysm.
This faculty member has no reported relationships with industry.
Representative Publications
