My basic science research focuses on understanding the cerebral microcirculation. This is largely in relation to the alteration of the microcirculation following an aneurysmal subarachnoid hemorrhage. Subarachnoid hemorrhage resulting from rupture of a brain aneurysm often demonstrates significant morbidity and mortality in spite of aneurysm obliteration to prevent re-hemorrhage. In humans, delayed vascular constriction can occur 5-7 days after SAH: proximal blood vessels lose reactivity and demonstrate narrowing unresponsive to smooth muscle relaxants, often leading to delayed cerebral ischemia. However, ischemic deficits can also arise from regions with minimal vasoconstriction on angiography or transcranial Doppler studies, and drugs preventing large vessel vasoconstriction may fail to improve clinical outcome. Microvascular dysfunction and acute brain injury from SAH are also important in the evolution of ischemia. Animal models of SAH can replicate features of human SAH, particularly partial vessel rupture and release of arterial blood, ischemic and cognitive changes but demonstrate a shorter time course of vasoconstriction (maximum at 2-3 days). Hippocampus has a less robust blood supply than neocortex, with resulting lower oxygen values in vivo, in addition to a predisposition to ischemia and cell loss. My laboratory has clearly demonstrated that both the pial and penetrating arterioles are affected and therefore may account for some of the morbidity despite successful treatment of the aneurysm.
My clinical research includes evaluating new and novel tools to treat a wide variety of problems such as brain aneurysms and skull base tumors.