Cerebral Vasospasm After Subarachnoid Hemorrhage

doi:10.1016/S0025-6196(12)60441-8

Mayo Clinic Proceedings

Volume 59, Issue 7, July 1984, Pages 498-505

https://doi.org/10.1016/S0025-6196(12)60441-8 Get rights and content

Chronic cerebral vasospasm remains the most important cause of subsequent morbidity in patients who survive the first 48 to 72 hours after a subarachnoid hemorrhage. Prolonged arterial narrowing compromises cerebral hemodynamics and results in cerebral ischemia. Among patients in whom symptomatic chronic cerebral vasospasm develops, almost half die or have a serious residual neurologic deficit. Present evidence indicates that sustained vessel narrowing results from structural changes within the arterial wall rather than from active contraction of vascular smooth muscle. The mechanism (or mechanisms) responsible for these changes is unknown, but damage from prolonged active arterial contraction, depression of vessel wall respiration, and an inflammatory response have all been proposed as explanations. Despite more than 30 years of intensive study, an effective treatment program for chronic cerebral vasospasm remains elusive. Recent therapeutic trials, however, based on efforts to interrupt the mechanisms responsible for these structural changes hold some promise.

Section snippets

FREQUENCY OF OCCURRENCE AND RELATED AND UNRELATED CLINICAL FEATURES

Depending on the criteria used to define it, cerebral vasospasm has been reported to occur in 21 to 78% of all patients after a subarachnoid hemorrhage,1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13 although most studies estimate its frequency of occurrence to be between 40 and 60%. Most often, angiographic vasospasm occurs in cerebral arteries near the source of the subarachnoid hemorrhage and tends to occur in the segments of cerebral arteries that are intimately related to the densest collections

TEMPORAL PROFILE

Experimental cerebral vasospasm after subarachnoid hemorrhage seems to be a biphasic event.21, 22 In dogs, arterial narrowing begins immediately after subarachnoid hemorrhage and reaches maximal intensity by 30 minutes. Within 2 days, this early phase of vasospasm reverses spontaneously. Early spasm, however, has been difficult to substantiate in humans.23, 24 Although this difficulty may reflect the transient nature of acute vasospasm, the fact that human cerebral arteries contract less

HEMODYNAMIC CONSEQUENCES

Differences in hemodynamic properties facilitate classification of cerebral arteries into at least two types: proximal large conducting vessels on the surface of the brain and distal small penetrating arterioles. In normal subjects, cerebral arterial resistance and, consequently, cerebral blood flow are primarily regulated at the level of the penetrating arterioles rather than by the conducting arteries. With modification of resistance in this arteriolar bed, cerebral blood flow is maintained

VASCULAR PATHOLOGIC FEATURES

Transmission electron microscopic examination of vasospastic cerebral arteries after experimentally induced subarachnoid hemorrhage in dogs and monkeys shows structural differences between arteries in the early phase of vasospasm and those in the chronic phase. Arteries examined within 48 hours after experimentally induced subarachnoid hemorrhage have few pathologic changes. The internal elastic lamina may appear corrugated as a result of arterial contraction. Subtle changes in the

FUNCTIONAL ABNORMALITIES OF VASOSPASTIC ARTERIES

Despite the fact that numerous investigators have successfully prevented or treated experimental vasospasm with a wide variety of vasodilating drugs, clinically the final result has been disappointing.⁶¹ Lack of a reliable animal model of chronic vasospasm prompted many investigators to study acute in vitro or in vivo vasospasm; consequently, these observations were irrelevant to the human situation. Recently, a canine model of subarachnoid hemorrhage has been described which reliably

PATHOGENESIS

Although the mechanism responsible for these vascular changes remains unknown, circumstantial evidence is consistent with several possibilities.

TREATMENT

Treatment of symptomatic vasospasm today relies on efforts directed at enhancing cardiac output, inducing arterial hypertension, and expanding the intravascular volume in an attempt to increase cerebral perfusion and promote cerebral blood flow.84, 85, 86 The techniques used vary from clinic to clinic and have recently been reviewed by Heros and associates.⁸⁷ Major differences in treatment protocols focus on the ideal hematocrit needed to optimize oxygen delivery but not hinder cerebral blood

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