*7.8.2 Vasospasm and delayed cerebral ischemia*

Cerebral vasospasm is an essential source of morbidity and mortality in subarachnoid hemorrhage patients. Vasospasm is one of the most common acute complications. It can happen within 3–15 days with a peak incidence at 7 days after aneurysmal SAH. Symptomatic vasospasm occurs in 20–40% of subarachnoid hemorrhage cases and is considered as the least understood component in their care. The symptom severity depends upon the artery affected and the degree of collateral circulation. Strokes from vasospasm account for nearly 50% of the early deaths in patients who survive the initial subarachnoid hemorrhage treatment. It is characterized by a pathological; diffuse, affecting all layers of the involved arterial wall; and long-lasting narrowing of the lumen of the vessel of large-capacity cerebral arteries

**229**

*7.8.4 Diagnosis*

*7.8.4.1 Transcranial Doppler*

spasm. It can be performed at the bedside.

readily followed to identify those at higher risk [17].

*Calcium Channel Blockers*

*DOI: http://dx.doi.org/10.5772/intechopen.90778*

Risk factors for vasospasm include:

1.The severity of bleeding

4.Age less than 50 years

6.Glasgow Coma Scale score < 14

5.Hyperglycemia

*7.8.3 Mechanism*

at the base of the brain either close or distal to the bleeding site. And it is associated

3.The location and extent of blood on CT scan and radiologic grading scales

While the underlying mechanisms causing vasospasm are not fully understood, a proliferative inflammatory arteriopathy is the pathological feature of cerebral vasospasm. The intima shows disruption of the internal elastic lamina, and the media is thickened and fibrotic, with an increased smooth muscle cell proliferation. The adventitia is infiltrated with inflammatory cells, and the neuronal endings are impaired [14]. A significant predictor of vasospasm after SAH is the volume of blood present around the cerebral arteries of the circle of Willis which can be measured by transcranial Doppler (TCD), although it has been clearly demonstrated that prolonged exposure of cerebral arteries to perivascular blood is essential for the development of vasospasm. It is not possible to identify a single causative molecule as the culprit of vasospasm. However, vasospasm is believed to be produced by spasmogenic substances generated during the lysis of subarachnoid blood such as oxyhemoglobin (a product of auto-oxidation of hemoglobin), nitric oxide, and endothelin-1.

Those agents may be contributors to the pathological event of vasospasm.

and can stimulate endothelial cells to produce endothelin-1.

Oxyhemoglobin may directly or indirectly trigger arterial vasoconstriction. Oxyhemoglobin can also exert a scavenging effect on nitric oxide. It has been demonstrated that nitric oxide (a potent vasodilator) depleted during vasospasm

Endothelin-1 is the most potent and long-lasting vasoconstrictor effect, which is also associated with morphological changes, mimicking the delayed cerebral vasospasm. It has been shown that endothelin-1 levels are increased, not only in the cerebrospinal fluid during SAH and severe neuronal injury due to vasospasm or bleeding event. Moreover, endothelin levels change in neurological symptoms, but they do not predict vasospasm as assessed by transcranial Doppler. These observations suggest that endothelin-1 acts as a marker of cerebral ischemic injury [15, 16].

It is a noninvasive tool and is useful for the detection and evaluation of vaso-

It used as a screening tool in high-grade World Federation of Neurological Surgeons (WFNS) scale patients in whom a neurological examination cannot be

with reduced perfusion of the territories distal to the affected vessel.

2.The proximity to the significant intracerebral blood vessels

#### *Calcium Channel Blockers DOI: http://dx.doi.org/10.5772/intechopen.90778*

at the base of the brain either close or distal to the bleeding site. And it is associated with reduced perfusion of the territories distal to the affected vessel.

Risk factors for vasospasm include:

