الفهرس 
Anatomy of the Cerebral VasculatureOnly 14 pages are availabe for public view
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Abstract
C
erebral vasospasm is the most significant cause of mortality and morbidity in the patients surviving SAH long enough to reach medical care, even exceeding direct effect of aneurysmal rupture as well as rebreeding. It ranges in severity from mild reversible dysfunction to severe permanent deficits secondary to ischemic infarction, extensive enough to be fatal in 7 % of SAHs. Also the earlier onset of the vasospasm is associated with greater deficit.
Radiological cerebral vasospasm is identified in 30-70% of arteriogram performed around the 7th day following SAH, whereas DIND (delayed ischemic neurological deficit associated with radiographic cerebral vasospasm (CVS) occurs only 20-30% of patient with SAH.
The onset of cerebral vasospasm never occurs before the 3rd day post SAH with a maximum frequency of onset during days 6-8 post SAH (however, rarely can occur as late as day 17). Typical at risk period is quoted as days 3-14. ؤclinical CVS is almost always resolved by day 12 post-SAH, once radiographic CVS is demonstrated, it usually resolves slowly over 3-4 weeks. The onset is usually insidious, but in 10 % of the patients it has an abrupt and severe deterioration.
Findings suggestive of cerebral vasospasm usually develop gradually and may progress or fluctuate, and they usually vary according to the affected vessel territory.
The pathogenesis of cerebral vasospasm has remained poorly understood despite all recent advances in immuno-histochemistry and molecular biology. It is believed that the important role to the pathogenesis of vasospasm has the depletion of nitric oxide (NO), which is a potent vasodilator. Posthemorrhagic NO depletion has been demonstrated to cause cerebral vasoconstriction.
Endothelin-1 (ET-1) is a potent vasoconstrictor, which is produced in ischemia and is bound to specific receptors on smooth muscle cells causing vasoconstriction and endothelial proliferation.
The diagnosis of vasospasm after SAH is often made using a combination of patient history, physical examination, CT scanning to determine the extent of rupture, catheter angiography and TCD ultrasonography, along with other imaging modalities such as CT angiography, MR imaging, MR angiography. Despite multimodality analysis of vasospasm, the ability to predict delayed ischemic neurological deficit (DIND) is still limited.
In a recent study, investigators demonstrated that when both TCD ultrasonography and catheter angiography revealed vasospasm, the positive predictive value for the occurrence of cerebral infarction was 67%. Conversely, when both studies indicated an absence of vasospasm, the negative predictive value of this combination was 72%.
A number of medical, endovascular, and surgical therapies are currently in use or being investigated in an attempt to reverse cerebral vasospasm, but only a few have proven to be significantly useful. Although much has been elucidated regarding its pathophysiology, the treatment of cerebral vasospasm remains a dilemma.
Early recognition of vasospasm and the potential risk of DIND are essential because the rapid implementation of standard therapies such as triple-H (hypertension, hypervolemia, and hemodilution) therapy, intraarterial vasodilator application, and balloon angioplasty serves to counteract vasospasm and prevent the occurrence of DIND. However, the prompt use of these therapies depends on the ability to predict impending vasospasm or to diagnose it at its early stages.
The concept that coiling, as a less invasive form of treatment, can protect against vasospasm, has not a justified level of evidence. As a matter of fact, vasospasm does not only develop on the arterial territories from aneurysmatic compromised arteries, but also on neighboring and even on far away located areas.