Dr. Jain is a consultant in neurology and has no relevant financial relationships to disclose.)
The term "cerebral vasospasm" means "narrowing" or a contracted state of the cerebral arteries in vivo. Vasospasm following subarachnoid hemorrhage is an important cause of cerebral ischemia and is the most frequent serious complication in survivors of subarachnoid hemorrhage. This article discusses the pathomechanism of vasospasm and rationale of various approaches to management. Impairment of nitric oxide production and vasodilator function is an important mechanism associated with the pathogenesis of cerebral vasospasm. This explains the effectiveness of nitric oxide donors such as nitroglycerin as vasodilators. In the overall management of the patient with cerebral vasospasm, attention should be paid to the associated disturbances in the brain.
• Cerebral vasospasm or narrowing of cerebral blood vessels usually occurs following subarachnoid hemorrhage.
• It is an important cause of mortality and morbidity in patients with ruptured intracranial aneurysms.
• Several methods of treatment are based on various concepts of the pathomechanism of vasospasm and include both medical and interventional procedures.
Historical note and terminology
The term "cerebral vasospasm" means "narrowing" or a contracted state of the cerebral arteries in vivo as seen on angiograms or observed during surgical exposure of the cerebral blood vessels. A review of the literature on cerebral vasospasm after aneurysmal subarachnoid hemorrhage has shown that angiographic vasospasm occurs in 67.3% of cases when angiography is timed for the highest likelihood. Delayed ischemic deficit or symptomatic vasospasm occurs in 32.6% of cases (Dorsch 1995).
More than 2400 years ago, Hippocrates described neurologic deterioration and delayed death following apoplexy, which was likely due to vasospasm associated with ruptured intracranial aneurysm (Clarke 1963). Vasospasm was first described in the mid-19th century by Gull, and vasospasm theory was used to explain transient ischemic attacks (Peabody 1896). Identification of vasospasm in relation to ruptured intracranial aneurysm was not made until after the introduction of cerebral angiography. Vasospasm was first described as an angiographic finding in patients with intracranial aneurysms in 1951 (Ecker and Riemenschneider 1951). In 1956, the first observation of vasospasm during surgery for intracranial aneurysms was published (Logue 1956). Then, in 1958, vasospasm was demonstrated to be induced by surgical manipulation and counteracted by local application of papaverine (Pool et al 1958). These authors hypothesized that the effect of rupture of an aneurysm would be like that of trauma of manipulation. Relation of the spasm to the blood in the subarachnoid space was suspected in the late 1950s, but it was not until 1965 that vasospasm was produced experimentally in animals by application of blood to the intracranial arteries (Echlin 1965). Suspicion that "something in the blood" was responsible for vasospasm led to the treatment of washing out the blood from the subarachnoid space (Shigeno et al 1982). The first pharmacological approach to the prevention of vasospasm was the use of drugs (such as reserpine) that lower the levels of active monoamines (such as norepinephrine) in the circulating blood and the brain (Zervas et al 1980). By this time, more than 80 compounds had been tried as treatment for vasospasm, but none were found to be the solution. In 1982, hypervolemia and induced arterial hypertension as treatment for vasospasm were introduced (Kassell et al 1982). Therapeutic strategies for the management of vasospasm-induced subarachnoid hemorrhage were classified into 4 categories: (1) prevention of vasospasm, (2) reversal of vasospasm, (3) improvement of cerebral perfusion, and (4) neuroprotection (Fandino et al 2007).
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