Department / Division:
Surgery / Neurosurgery

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
• Atkinson Morley's Hospital, St. George's University School of Medicine, University of London, Neurosurgery (United Kingdom) 1998-1999
• Resident, University of Washington, 1993-2002
• Chief Resident, University of Washington, 1999-2000

• Cerebrovascular Surgery, University of Washington, 2000
• Neuroradiology, University of Washington, 2001-2002
• Interventional Neuroradiology, University of Washington, 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.