Endovascular Treatment of Cerebral Vasospasm Following S.A.H.
Cerebral vasospasm (CV) remains one of the most feared complication of subarachnoid hemorrhage associated with severe morbidity and mortality. After HHH therapy and intravenous nimodipine infusion, some patients still show evidence of neurological deficit
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Endovascular Treatment of Cerebral Vasospasm Following S.A.H.
x. Barreau, M. Pastore, M. Piotin, C. SpeUe, and J. Moret Introduction Cerebral vasospasm (CV) remains one of the most feared complication of subarachnoid hemorrhage associated with severe morbidity and mortality. After HHH therapy and intravenous nimodipine infusion, some patients still show evidence of neurological deficit due to CV. Many studies have demonstrated the benefits of papaverin infusion but this drug appeared to have a transient and moderate efficiency on the patient outcome and may be reserved for diffuse CV. Percutaneous angioplasty associated with vasodilating drugs has been shown to offer greater chance of longlasting re-opening of the narrowed vessels. This articles reviews different techniques for endovascular management of CV and several studies relating to efficacies of PTA and or papaverine/nimodipine intraarterial infusion. Keywords: Cerebral vasospasm; intracranial angioplasty.
Epidemiology Cerebral vasospasm (CV) is defined as a significant narrowing of the cerebral arteries occurring after subarachnoid hemorrhage (SAH). The frequency of this feared complication of SAH has been widely studied. Angiographic vasospasm occurs in approximately 70% of aneurysmal SAH [4]. The incidence of CV is influenced by the time between the SAH and the angiographic study, and is more frequent between the sixth and eighth day after SAH. Clinical manifestations are encountered in 30 to 50% of CV [8, 9, 27], demonstrating that the non-symptomatic CV is more frequent than the symptomatic one. The international cooperative study on the timing of aneurysm surgery [27] stated that 13,5% of the patients die or are disabled secondary to vasospasm.
Mechanisms of CV
General Considerations The initial trigger for CV is blood effusion into the subarachnoid space. Following SAH, the vascular response is divided into two phases. The first phase consists of an acute vasoconstriction occurring I to 3 days after hemorrhage. This phase is responsible for high mortality related to intracranial pressure elevation [13], cerebral blood flow [1] and cerebral perfusion diminution [24). The second phase is a delayed phase responsible for severe neurological deficits and is believed to be more refractory to treatment than the first phase.
Biomolecular Mechanisms of Cerebral Vasospasm In a recent paper Dietrich [3] reported the fundamental mechanism of CV. In his review CV is demonstrated to be related to different cellular responses specially directed at endothelial and vascular smooth muscle cells regulation. Briefly, oxyhemoglobin and bilirubin initiate the vascular response. These substances are released in the subarachnoid space after clot lysis and disturb the equilibrium between vasoconstrictor and vasodilator systems. Endothelium-dependent relaxation is impaired by nitric oxyde (NO) scavenging and oxygen radical release. As hemoglobin can bind NO, this reaction may result in a decrease of guanylate cyclase activity triggering vasoconstriction. Moreover, the prod
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