Abstract
The mechanisms of vasospasm after subarachnoid hemorrhage (SAH) are still not fully known. Most likely, local factors mediated by blood extravasation from the ruptured aneurysm under arterial pressure into the subarachnoid space are involved [10]. However, evidence that vasospasm is manifested both in extra- and intracranial arteries after SAH indicates that other factors might be involved in the patophysi-ology of vasospasm [3]. It is certain that, in the majority of cases, the most intensive vasospasm occurs near the largest blood collection in the subarachnoid space. However, it may also develop in cerebral vessels in other parts of the subarachnoid space in which CT reveals no blood, and even in extracranial arteries. Thus, local as well as systemic mechanisms appear to exist. Such a mechanism could be the stimulation of the sympathetic nervous system (SNS) that occurs in conjunction with SAH. The hypothesis that the SNS could be involved in vasospasm is not new and has never been thoroughly refuted [1, 4, 5].
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