Cerebral Vasospasm After Subarachnoid Hemorrhage

Updated: Sep 12, 2022
  • Author: William W Ashley, Jr, MD, PhD, MBA; Chief Editor: Brian H Kopell, MD  more...
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Practice Essentials

Cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH) is a well-described phenomenon that is defined as narrowing of the large and medium-sized intracranial arteries [1] ; most often, it affects the anterior circulation supplied by the internal carotid arteries. Cerebral vasospasm leading to delayed cerebral ischemia (DCI) continues to be a major complication and source of morbidity in cases of aSAH. [2]

As a consequence of the significant neurologic morbidity or mortality stemming from posthemorrhagic vasospasm, a great deal of interest and research has been focused on understanding its physiologic mechanism and developing effective preventive and therapeutic measures. However, the etiology of cerebral vasospasm remains poorly understood.

Management involves both prevention and active treatment. [3] No single therapeutic algorithm has shown to be uniformly effective in preventing vasospasm and its subsequent neurologic sequelae, though a number of therapeutic strategies have found to have varying degrees of utility.

The hemodynamic augmentation strategy known as triple-H therapy, which includes hypertension, hemodilution, and hypervolemia, has been an important component of treatment. Increases in mean arterial pressure (MAP) alone have been shown to be beneficial and have been achieved with various medications. Calcium-channel antagonists have been widely investigated for prevention of vasospasm in aSAH; nimodipine is currently recommended as first-line medical treatment for preventing post-aSAH cerebral vasospasm. 

More invasive means of treating vasospasm depend on the utilization of cerebral angiography and include intra-arterial vasodilator administration and balloon angioplasty. Guidelines have recommended these modalities as reasonable for treatment of symptomatic patients who are not responding to hypertensive therapy.



There are many postulated theories as to the etiology of cerebral vasospasm after aSAH, but the mechanisms ultimately responsible for vasospasm are still incompletely understood. There is evidence that the normal physiologic mechanisms and signaling molecules that regulate cerebral arterial diameter are altered. [4] The alteration of these regulatory processes results in excess cerebral arterial vasoconstriction. Molecules of interest in this regard include nitric oxide and endothelin.

Nitric oxide, a vasodilator produced by endothelial cells, helps maintain cerebral arterial dilation. There is some evidence that the breakdown products of red blood cells may be harmful to endothelial cells, and this harmful effect may compromise the ability of these cells to produce vasodilatory molecules such as nitric oxide. [1]  Endothelin, a vasoconstrictor, [5]  has been found to be elevated in cerebrospinal fluid (CSF) after aSAH and may play a role in cerebral vasospasm and DCI. [1, 6]

Research efforts are ongoing with the aim of further elucidating the mechanisms of vasospasm in the hope of developing better treatments.



Cerebral vasospasm has been estimated to occur in 12-30% of the approximately 30,000 North American patients who experience aSAH each year. [7, 8] It has been estimated that close to 50% of patients suffering from aSAH die before reaching medical care. Of those patients who are able to reach neurosurgical centers and have their aneurysm treated, an estimated 14% either die or sustain significant morbidity as a result of cerebral vasospasm. [8]

There are certain patient characteristics that may increase the likelihood of vasospasm occurring in a patient with aSAH. Some of the strongest predictors of vasospasm relate to the severity of the aSAH as graded according to several well-accepted classification systems. Both the Fisher Scale and the Hunt-Hess grading system have been shown to correlate with the incidence of vasospasm.

On the Fisher Scale, the thickness of the aSAH clot and the presence of intraventricular hemorrhage (IVH) are strong predictors of vasospasm. [9, 10] These are the primary determinants of the Modified Fisher Scale, with a higher Fisher score being directly correlated with the risk of vasospasm. [10]

The Hunt-Hess grade, which is determined primarily by clinical symptoms, is also strongly predictive of vasospasm. Hunt-Hess grade III-IV subarachnoid hemorrhages are associated with a much higher risk of subsequent severe vasospasm and DCI, but some postulate that this is only a proxy for the volume of subarachnoid blood present. [11] Other risk factors that have been associated with vasospasm are hypertension and cigarette smoking. [11]



The prognosis for patients suffering from cerebral vasospasm and DCI after aSAH is most closely related to the severity of the initial hemorrhage and the immediate clinical condition of the patient. These factors are closely linked to the risk of severe vasospasm.

One caveat to consider is that the degree of vasospasm, as assessed by angiography, is not always fully aligned with the clinical deterioration of the patient. There is evidence that some patients may develop severe vasospasm on angiography that is clinically silent, whereas other patients suffer devastating DCI and infarction but do not have the same degree of vasospasm on angiography. In general, patients suffering from vasospasm are at risk for ischemia causing cerebral infarction and thus permanent neurologic deficits.