History

Cerebral vasospasm occurs in the setting of recent aneurysmal subarachnoid hemorrhage (aSAH). Vasospasm most often presents within 3-7 days after aSAH but can occur at any time within the 21-day window following the initial hemorrhage. Vasospasm often causes delayed cerebral ischemia, which can present clinically in a number ways, depending on the severity of the vasospasm and on which intracranial vessels are most affected.

The most common presentation is neurologic deterioration manifested as decreased level of consciousness or onset of new focal neurologic deficits. Patients may complain of weakness, sensory changes, new or increasing headache, visual deficit, or other neurologic symptoms. In obtunded patients (eg, those with high-grade subarachnoid hemorrhage), cerebral vasospasm may be clinically silent. Diagnosis of cerebral vasospasm in these patients requires vigilance and regular radiologic surveillance (see Workup).

Physical Examination

Physical examination may reveal a constellation of signs and symptoms of ongoing vasospasm, depending on the severity of the condition and on which intracranial vessels are most affected.

Nonlocalizing symptoms include the following:

Lethargy
Disorientation
Meningismus
New or increasing headache

Focal neurologic deficits are related to the particular vessel involved, as follows:

Anterior cerebral artery (ACA) distribution - Disinhibition, confusion; mutism; lethargy, delayed responsiveness, abulia; leg weakness; with involvement of the recurrent artery of Heubner (a large ACA perforator), contralateral faciobrachial weakness without cortical findings
Middle cerebral artery (MCA) distribution - Hemiparesis, faciobrachial weakness, monoparesis; aphasia, apractagnosia; neglect
Posterior cerebral artery (PCA) distribution - Visual disturbance, hemianopsia

A diagnostic algorithm for post-aSAH cerebral vasospasm is depicted in the image below.

Diagnosis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

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Complications

The complications of cerebral vasospasm may consist of further clinical deterioration and poor neurologic outcome. Vasospasm leads to cerebral ischemia, and in severe cases, acute ischemic stroke from cerebral infarction can occur. This progression leads to irreversible neurologic deficits.

Neurologic outcomes can vary widely, depending on the unique circumstances of each patient. Focal deficits are likely to persist if the large intracranial arteries (eg, the ACA, MCA, and PCA) are severely affected by vasospasm. It has been estimated that approximately 7% of patients suffering severe vasospasm following aSAH will have permanent neurologic deficits, and another 7% will die.^[8]

Differential Diagnoses

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Media Gallery

Diagnosis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage.
Initial presenting head CT scan showing subarachnoid hemorrhage and blood filling basal cisterns.
Initial cerebral angiogram from patient with subarachnoid hemorrhage.
Three-dimensional reconstruction of cerebral angiogram showing anterior communicating artery aneurysm.
Follow-up head CT scan showing subarachnoid blood.
Cerebral angiogram obtained on posthemorrhage day 5 in patient symptomatic from vasospasm. Angiogram shows severe narrowing of right anterior cerebral artery.

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Table 1. Recommendations for Endovascular Treatment of Cerebral Vasospasm

Table 1. Recommendations for Endovascular Treatment of Cerebral Vasospasm

Degree of Radiographic Vasospasm	Clinical Findings
	Asymptomatic	Symptomatic
Mild	No intervention	Vasodilation (rare)
Moderate	Vasodilation	Vasodilation ± balloon angioplasty
Severe	Vasodilation ± balloon angioplasty (rare)	Vasodilation + balloon angioplasty