Association between acute sympathetic response, early onset vasospasm, and delayed vasospasm following spontaneous subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) is accompanied by a marked acute sympathetic response, and evidence exists for sympathetic participation in the development of cerebral vasospasm (VS). The purpose of this observational investigation was to assess the association between acute central catecholaminergic activity, early VS and delayed VS following SAH. SAH grade 3–5 patients who received ventriculostomy, and in whom bilateral temporal transcranial insonation was performed, were enrolled. Cerebrospinal fluid (CSF) was sampled (<48hours) and assayed for catecholamines, which were correlated to measures of early and delayed sonographic anterior circulation VS. Clinical independent predictors of early VS included age (odds ratio .946 [95% confidence interval .902–.991]), CT scan score (4.27 [1.30–14.0]) and neurogenic cardiomyopathy (6.5 [1.24–34.1]). Age (.925 [.859–.996]) and CT scan score (8.30 [1.33–5.17]) also independently predicted delayed VS. Any early VS independently predicted conventionally defined delayed VS (10.9 [2.64–45.0]), and severe delayed VS was independently predicted by any early VS (9.87 [2.45–39.7]) and by conventionally defined early VS (12.3 [2.80–54.1]). The norepinephrine:3,4-dihydroxyphenylglycol ratio (NE/DHPG) independently predicted severe delayed VS (3.38 [1.01–11.35]), for which DHPG was a negative predictor (.356 [.151–.839]). Epinephrine was a negative predictor of any early VS (.574 [.357–.921]), any delayed VS (.372 [.158–.875]), and delayed conventional VS (.402 [.200–.807]). Early and delayed VS appear to be related processes that are generally unrelated to the acute central sympathetic response following SAH. The one exception may be severe delayed VS which may be associated with noradrenergic activation.