*7.8.4.3 MRI*

MRI can help to identify and diagnose cerebral ischemia at the early stage.

## *7.8.4.4 Cerebral angiography*

Cerebral angiography is the gold standard radiographic tool for the diagnosis of cerebral vasospasm. Angiography is used to identify patients with symptomatic vasospasm who might benefit from treatment.

In 30–70% of patients with SAH, angiographic vasospasm occurs, but it leads to clinically evident signs and symptoms in 20–30% of patients who experience delayed ischemic neurological deficits. About half of the symptomatic group of patients suffer severe permanent neurological dysfunction or death.

#### *7.8.5 Treatment*

The specific treatment of cerebral vasospasm helps improving cerebral blood flow to avoid delayed ischemic neurologic deficit by reducing ICP, optimizing the rate of cerebral oxygen demand, and enhancing cerebral blood flow with one of the following approaches: indirect pharmacological protection of brain tissue or direct mechanical dilation of the vasospastic vessel.

Nimodipine is the standard of care in aneurysmal SAH patients. Nimodipine 60 mg every 4 hours can be used for all patients with aneurysmal SAH once the diagnosis is made for 21 days. Nimodipine is to be given orally or by nasogastric tube because intravenous administration causes serious adverse events, including death. The mechanism of benefit of nimodipine in SAH is unknown. Oral nimodipine is the only Class I evidence regarding cerebral vasospasm used in the publication of the AHA subarachnoid hemorrhage guidelines [22]. Early aneurysm treatment, HHH-therapy (hypertension, hypervolemia, and hemodilution), cerebral angioplasty, and selective intra-arterial vasodilator therapy were recommended based on Class II evidence.

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*Calcium Channel Blockers*

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

angiographic abnormalities if they are used.

In summary, nimodipine was initially studied in SAH to prevent vasospasm. However, despite its vasodilatory effects on cerebral vessels, the evidence of nimodipine effects on the incidence of either angiographic or symptomatic vasospasm is not convincing [23]. Nevertheless, nimodipine has been demonstrated to

**7.9 Calcium channel blockers for reversible cerebral vasoconstriction syndrome**

Reversible cerebral vasoconstriction syndrome (RCVS) represents a group of conditions that show a reversible narrowing of the cerebral arteries with clinical manifestations that typically include thunderclap headache and less commonly neurologic deficits related to brain edema, seizure, or stroke. The clinical outcome is usually benign, although major strokes can result in severe disability and death in a minority. The pathophysiology of the abrupt-onset headache and the prolonged but reversible vasoconstriction is not known. Reversible angiographic narrowing

RCVS has been associated with a variety of conditions including pregnancy, migraine, use of vasoconstrictive drugs, neurosurgical procedures, hypercalcemia, unruptured saccular aneurysms, cervical artery dissection, and cerebral venous thrombosis. The diagnosis of RCVS is based upon the characteristic clinical, brain imaging, and angiographic features. Nimodipine and verapamil and brief courses of magnesium sulfate, serotonin antagonists, and dantrolene have been administered to relieve the vasoconstriction. Data from two prospective case series suggest that nimodipine does not affect the time course of cerebral vasoconstriction [25, 26]. However, nimodipine might relieve the number and intensity of headaches and has documented effects on the smaller vasculature not easily imaged by angiography. Calcium channel blockers can be discontinued after resolution of symptoms or

improve outcomes in SAH and is the agent of choice in these patients [23].

suggests an abnormality in the control of cerebrovascular tone [24].

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

*New Insight into Cerebrovascular Diseases - An Updated Comprehensive Review*

operator-patient dependent, and its value is debated.

(MCAvelocity/ICAvelocity) > 6 [18].

80 and 93%, respectively [21].

*7.8.4.4 Cerebral angiography*

vasospasm who might benefit from treatment.

mechanical dilation of the vasospastic vessel.

*7.8.4.2 CT scan*

*7.8.4.3 MRI*

*7.8.5 Treatment*

It is a highly specific noninvasive exam but has a low level of sensitivity, and it is

Noninvasive angiography with CT angiography (CTA) to confirm vasospasm for patients with elevated velocities on transcranial Doppler ultrasound. The plane CT scan is useful for ruling out other causes in the event of the occurrence of a deficit or worsening of the clinical state like rebleeding or ischemia. Several prospective cohorts showed a correlation between CTA and DSA in predicting vasospasm and that many unnecessary angiograms could be avoided by using CTA as a screening test [19, 20]. A recent meta-analysis found a sensitivity and specificity for CTA of

MRI can help to identify and diagnose cerebral ischemia at the early stage.

Cerebral angiography is the gold standard radiographic tool for the diagnosis of cerebral vasospasm. Angiography is used to identify patients with symptomatic

In 30–70% of patients with SAH, angiographic vasospasm occurs, but it leads to clinically evident signs and symptoms in 20–30% of patients who experience delayed ischemic neurological deficits. About half of the symptomatic group of

The specific treatment of cerebral vasospasm helps improving cerebral blood flow to avoid delayed ischemic neurologic deficit by reducing ICP, optimizing the rate of cerebral oxygen demand, and enhancing cerebral blood flow with one of the following approaches: indirect pharmacological protection of brain tissue or direct

Nimodipine is the standard of care in aneurysmal SAH patients. Nimodipine 60 mg every 4 hours can be used for all patients with aneurysmal SAH once the diagnosis is made for 21 days. Nimodipine is to be given orally or by nasogastric tube because intravenous administration causes serious adverse events, including death. The mechanism of benefit of nimodipine in SAH is unknown. Oral nimodipine is the only Class I evidence regarding cerebral vasospasm used in the publication of the AHA subarachnoid hemorrhage guidelines [22]. Early aneurysm treatment, HHH-therapy (hypertension, hypervolemia, and hemodilution), cerebral angioplasty, and selective intra-arterial vasodilator therapy were recommended based on

patients suffer severe permanent neurological dysfunction or death.

In 2004, the American Academy of Neurology conducted a systematic review of the literature and concluded that TCDs could be used reliably to screen for the presence of vasospasm in the only MCA. Their criteria for the diagnosis or exclusion of vasospasm include flow velocity > 200 or 120 cm/s, respectively, significant increase in the flow velocities from day to day (>50 cm/s), and a Lindegaard ratio

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Class II evidence.

In summary, nimodipine was initially studied in SAH to prevent vasospasm. However, despite its vasodilatory effects on cerebral vessels, the evidence of nimodipine effects on the incidence of either angiographic or symptomatic vasospasm is not convincing [23]. Nevertheless, nimodipine has been demonstrated to improve outcomes in SAH and is the agent of choice in these patients [23].
