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Abstract: 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. [Copyright &y& Elsevier]

We studied the endothelial nitric oxide synthase (eNOS or NOS-3) gene as a potential modifier of the cerebral response to ischemia by investigating the association of two common polymorphisms with ischemic stroke volume. We genotyped an intronic variable number tandem repeat and a single nucleotide polymorphism, G894T, in 132 patients with nonlacunar ischemic strokes in whom clinical data and stroke lesion volume were recorded. Our results show that all genotypes are in Hardy-Weinberg equilibrium. After adjustment of covariates, neither of the NOS-3 polymorphisms showed significant differences comparing the genotypes and mean stroke volume (analysis of variance). Our results do not suggest a major gene effect of the NOS-3 gene as a modifier of the cerebral response to ischemia. [Copyright &y& Elsevier]

Replacement of the aortic arch for atheroma with cerebral embolization is in its infancy. The appropriateness of such intervention is controversial. Over a 10-month period, a 58-year-old woman suffered multiple debilitating cerebral vascular accidents manifested by motor, sensory, and memory deficits and documented by computed tomographic scanning and magnetic resonance imaging. Carotid and vertebral arteries were free of arteriosclerotic disease. Transesophageal echocardiography demonstrated two large atheromas with friable, pedunculated forms, one in the aortic arch and one in the very proximal descending thoracic aorta. Transcranial ultrasound revealed recurrent cerebral microembolic events. Cerebrovascular events continued, and the atheromas increased in size, despite treatment with Coumadin and aspirin. Under deep hypothermic arrest, the segment of the aortic arch harboring the atheroma was excised and replaced with a Dacron graft. Repeat transcranial ultrasound revealed cessation of embolic signals. All cerebrovascular events ceased. No further anticoagulation therapy was required. The patient has made substantial recovery from the preoperative deficits and continues to do well 1 year after aortic arch replacement. Resection of mobile aortic arch atheromas is likely to become increasingly important in the future as transesophageal echocardiography leads to their more common identification as a cause of cerebral ischemic events. [Copyright &y& Elsevier]

Abstract: Subarachnoid haemorrhage in pregnancy is often the result of aneurysmal rupture or severe hypertension. A young woman with postpartum eclampsia and ‘normal’ blood pressure developed sudden-onset head pain, and was found to have minor biconvexity subarachnoid hemorrhages. Serial angiograms of the cervicocranial vessels revealed no evidence of aneurysm or arteriovenous malformation. A follow-up angiogram revealed diffuse vessel narrowing, consistent with postpartum angiopathy. Treatment consisted only of nimodipine for the prevention of vasospasm. The patient made an excellent recovery, without residual neurological deficits. [Copyright &y& Elsevier]