What is cerebral vasospasm?

From the Guidelines

Vasospasm is a sudden, temporary narrowing of a blood vessel due to contraction of the smooth muscle in its walls, which can occur in various blood vessels throughout the body, including cerebral arteries following subarachnoid hemorrhage. This condition can lead to restricted blood flow, potentially causing tissue ischemia and damage if prolonged. Common triggers include cold exposure, stress, certain medications, smoking, and underlying vascular conditions. The management of cerebral vasospasm is crucial to prevent delayed cerebral ischemia (DCI) and improve outcomes in patients with aneurysmal subarachnoid hemorrhage (aSAH) 1. Some key recommendations for the management of cerebral vasospasm include:

• Oral nimodipine to reduce poor outcome related to aneurysmal SAH (Class I, Level of Evidence A) 1
• Maintenance of euvolemia and normal circulating blood volume to prevent DCI (Class IIa, Level of Evidence B) 1
• Consideration of volume expansion, induction of hypertension, and hemodilution (triple-H therapy) for symptomatic cerebral vasospasm (Class IIa, Level of Evidence B) 1
• Cerebral angioplasty and/or selective intra-arterial vasodilator therapy as alternative or adjunctive treatments (Class IIb, Level of Evidence B) 1
• The use of intra-arterial vasodilators, such as nimodipine, with careful monitoring of systemic hypotension and intracranial pressure (ICP) 1. The most recent guideline from the American Heart Association/American Stroke Association (2023) recommends a range of endovascular options for treating vasospasm, including vasorelaxation/spasmolysis with intra-arterial vasodilators, and emphasizes the importance of careful patient selection and monitoring 1. Overall, the management of cerebral vasospasm requires a multidisciplinary approach, careful patient selection, and individualized treatment strategies to optimize outcomes and minimize complications.

From the FDA Drug Label

In animal experiments, nimodipine had a greater effect on cerebral arteries than on arteries elsewhere in the body perhaps because it is highly lipophilic, allowing it to cross the blood-brain barrier; concentrations of nimodipine as high as 12. 5 ng/mL have been detected in the cerebrospinal fluid of nimodipine-treated subarachnoid hemorrhage (SAH) patients. The precise mechanism of action of nimodipine in humans is unknown Although the clinical studies described below demonstrate a favorable effect of nimodipine on the severity of neurological deficits caused by cerebral vasospasm following SAH, there is no arteriographic evidence that the drug either prevents or relieves the spasm of these arteries Nimodipine has been shown, in 4 randomized, double-blind, placebo-controlled trials, to reduce the severity of neurological deficits resulting from vasospasm in patients who have had a recent subarachnoid hemorrhage (SAH).

Vasospasm is not explicitly defined in the provided text, but it is mentioned as a condition that occurs after a subarachnoid hemorrhage (SAH) and causes neurological deficits.

• It is implied to be a spasm of cerebral arteries that can lead to delayed ischemic deficits and permanent deficits.
• The text does not provide a direct definition of vasospasm, but it describes its effects and the impact of nimodipine on these effects 2.

From the Research

Definition of Vasospasm

• Vasospasm is a potentially devastating complication after aneurysmal subarachnoid hemorrhage 3
• It is characterized by prolonged smooth muscle contraction, leading to hypoperfusion and cytotoxic responses that induce cerebral ischemia 4

Pathogenesis of Vasospasm

• The pathogenesis of vasospasm is initiated by prolonged smooth muscle contraction 4
• It is thought to be caused by a combination of factors, including the release of vasoactive substances and the activation of various cellular pathways 5

Diagnosis and Treatment of Vasospasm

• Computed tomography perfusion and transcranial Doppler are useful tools for diagnosing and monitoring vasospasm 5
• Treatment options include hypertension, hyperdynamic therapy, endovascular approaches with balloon angioplasty, and intra-arterial infusion of calcium channel blockers such as nimodipine, nicardipine, and milrinone 3, 6, 5
• Combination therapy through various routes may be the most useful approach to reduce the complications of vasospasm 5

Current Research and Therapies

• Current research is focused on improving morbidity and mortality in patients with cerebral vasospasm 4
• Various pharmacological and nonpharmacological treatments are being targeted at different pathways involved in the pathogenesis of vasospasm 5
• Endothelin receptor antagonists, statins, cilostazol, and eicosapentaenoic acid are some of the drugs being studied for their potential benefits in treating cerebral vasospasm 4