The findings suggest that the incidence of vasospasm is low in association with TSAH and that the cause is different compared with ASAH. There is no evidence that the presence of TSAH in cases of diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome.

The sealing effect of fibrin sealant on cerebrospinal fluid leakage was significantly greater with the rubbing method than with the spray method. The strong sealing effect obtained with the rubbing method is thought to result from firm linkage between the ePTFE surgical membrane and the fibrin sealant and also from fibrin being formed even in needle holes and spaces in the sutured site.

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IntroductionCerebral vasospasms after subarachnoid hemorrhage (SAH) have been studied from various aspects, which is a poor outcome resulting from SAH with a ruptured cerebral aneurysm. For example, it has been reported that symptomatic patients had higher cerebrospinal fluid (CSF) levels of interleukin-6 and interleukin-8 than asymptomatic patients [1,2], and nitrites/nitrate increased in the CSF in SAH patients [3,4].Previous studies showed that C-type natriuretic peptide (CNP) is the primary active natriuretic peptide in the ANP = atrial natriuretic peptide; BNP = brain natriuretic peptide; CNP = C-type natriuretic peptide; CSF = cerebrospinal fluid; NO = nitric oxide; SAH = subarachnoid hemorrhage.Available online http://ccforum.com/content/5/1/037 Abstract Background: Cerebral vasospasm is a poor resulting outcome of a ruptured cerebral aneurysm; to clarify the mechanism of vasospasm it is important to improve this outcome. C-type natriuretic peptide (CNP) is present in the brain as a cerebral vasodilator; it is also an endothelium-derived relaxing factor produced via cGMP. We speculated that CNP might be an inhibitor of cerebral vasospasm after subarachnoid hemorrhage (SAH).

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