Vasospasm, synonymous with angiographic vasospasm, is defined as a delayed focal or diffuse, radiologically detectable narrowing of cerebral arteries and is present in 40-70% of patients following aneurysmal SAH. It has a relatively consistent course, typically appearing at 3-4 days following the hemorrhage, with a peak incidence and severity at 7-10 days. There is a gradual resolution, with normal vessel diameter at 3-4 weeks.
DID or symptomatic vasospasm is the development of a new neurological deficit that is not explained by any post-operative hematoma, hydrocephalus, seizure activity or metabolic disturbance. It occurs in 20-30% of patients following SAH, although, more recently, its incidence has been quoted to be as low as 10% and is clinically at its worst 3-14 days following the hemorrhage.
The mechanism by which vasospasm is effected is poorly understood. A multi-factorial origin is most probable, with the liberation of spasmogenic metabolites during clot lysis in the basal cisterns and the impairment of cerebral vasodilatation related to endothelial dysfUnction and structural changes in the arterial wall.
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