Grant: Fellowship: Bisby (Prize)

Subarachnoid hemorrhage (SAH) is a special type of stroke that typically results from a ruptured intracranial aneurysm, a weakening in the wall of a blood vessel. This type of life-threatening bleeding occurs in over 3000 Canadians per year, usually in working-age adults. If one is fortunate enough to survive the initial bleeding episode and the subsequent surgical treatment of the aneurysm, a patient may still develop secondary strokes 3 to 14 days after the initial bleed. These delayed strokes are the most significant cause of morbidity and mortality after SAH and may be potentially preventable. There is only one medication (an anti-hypertensive) that has shown to improve outcomes after SAH. The molecular pathway causing these delayed strokes is still not clear, and this is an active area of research. Our laboratory hypothesizes that the cause of these delayed strokes is a pro-inflammation molecule called tumor necrosis factor alpha (TNFa). Specifically, we hypothesize the breakdown of blood products (hemoglobin) after SAH increases TNFa in the walls of small blood vessels, which results in the delayed strokes. Successful blockage of this pathway with etanercept, may lead to positive results in these experiments, and will provide a new treatment target for clinical trials.