Matthew Edwardson, MD

Raya A, Zipfel GJ, Diringer MN, Dacey JR, RG, Derdeyn CP, Rich KM, et al. Pattern Not Volume of Bleeding Predicts Angiographic Vasospasm in Nonaneurysmal Subarachnoid Hemorrhage. Stroke. 2013


Vasospasm and delayed cerebral ischemia (DCI) are dreaded complications of subarachnoid hemorrhage (SAH). Why vasospasm occurs after SAH remains a mystery. The most accepted theory entails pro-spasmodic substances released in close proximity to cerebral vessels during subarachnoid clot lysis. It follows that a larger burden of subarachnoid blood should lead to increased rates of vasospasm and DCI; while this association has borne out in studies of aneurysmal SAH, it remains unproven in non-aneurysmal SAH.




Raya and colleagues retrospectively studied patients with atraumatic, angiographically proven non-aneurysmal SAH seen at Washington University in St. Louis and separated them into diffuse SAH (n=29) and perimesencephalic SAH (PM-SAH) (n=60). The authors found higher rates of vasospasm in the diffuse SAH group (OR 2.9, p = 0.08) and wondered whether increased clot burden might explain this. They used the Hijdra and IVH scores to estimate clot burden and found that the diffuse SAH group still had higher rates of vasospasm than the PM-SAH group even after correcting for Hijdra/IVH score (OR 2.2, p = 0.18). 

This study is intriguing because it implies that there are more factors at play than just volume of subarachnoid blood in determining risk for vasospasm and DCI. PM-SAH patients are well known to have lower risk for developing vasospasm / DCI. If this lower risk is not entirely attributable to lower subarachnoid clot burden, then what could it be? Location of blood in a less spasmogenic area is one possibility; perimesencephalic blood contacts fewer intracerebral vessels than blood engulfing the circle of Willis. Another possibility is the long-theorized venous rather than arterial source of subarachnoid blood in PM-SAH patients. If venous blood contains less pro-spasmodic substances than arterial blood it might explain the benign disease course in PM-SAH. This could lead to interesting avenues of research – trying to isolate substances found only in arterial blood and testing them for their spasmodic properties. Such research may one day help us unravel the mystery behind SAH-induced cerebral vasospasm.