Inflammation in subarachnoid hemorrhage and delayed deterioration associated with vasospasm: a review

Abstract

Delayed deterioration associated with vasospasm (DDAV) after subarachnoid hemorrhage (SAH), (often called vasospasm) continues to be both a difficult entity to treat and a leading cause of morbidity in patients. Until recently, attention was focused on alleviating the vascular spasm. Recent evidence shows that vascular spasm may not account for all the morbidity of DDAV. There is renewed interest in looking for other potential targets for therapy. Inflammation has become a promising area of research for new treatments. This review explores the evidence that inflammation is a driver of DDAV by asking three questions: (1) If inflammation is important in the pathogenesis of the disease, what part or parts of the inflammatory response are involved? (2) When does inflammation occur in SAH? (3) In what compartment of the skull does the inflammation occur, the cerebrospinal fluid and meninges, the cerebral arteries, or the brain itself?

Figure 1

Depiction of possible instigators, actors and effectors of inflammation that could contribute to both vascular changes and poor outcomes in patients with delayed deterioration associated with vasospasm (DDAV) after aneurismal SAH.