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      Safety and technical efficacy of over-the-wire balloons for the treatment of subarachnoid hemorrhage–induced cerebral vasospasm

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          Abstract

          Object

          Over the past decade, low-pressure, flow-directed balloons have been replaced by over-the-wire balloons in the treatment of vasospasm induced by subarachnoid hemorrhage (SAH). The authors assess the procedural safety and technical efficacy of these newer devices.

          Methods

          Seventy-five patients who underwent 85 balloon angioplasty procedures for the treatment of SAH-induced vasospasm were identified from a prospective quality-assurance database. Medical records and angiographic reports were reviewed for evidence of procedural complications and technical efficacy.

          No vessel rupture or perforation occurred, but thromboembolic complications were noted in four (4.7%) of the 85 procedures. Balloon angioplasty was frequently attempted and successfully accomplished in the distal internal carotid (100%), proximal middle cerebral (94%), vertebral (73%), and basilar (88%) arteries. Severe narrowing was present in 89 proximal anterior cerebral arteries. Angioplasty was attempted in 41 of these vessels and was successful in only 14 (34%). In 19 of the 27 unsuccessful attempts, the balloon could not be advanced over the wire due to severe vasospasm or unfavorable vessel angle. Follow-up angiography in a subset of patients demonstrated that severe recurrent vasospasm occurred in 15 (13%) of 116 vessels studied after angioplasty.

          Conclusions

          Over-the-wire balloons involve a low risk for vessel rupture. The anterior cerebral artery remains difficult to access and successfully treat with current devices. Further improvements in balloon design, such as smaller inflated diameters and better tracking, are necessary. Finally, thromboembolic complications remain an important concern, and severe vasospasm may recur after balloon angioplasty.

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          Most cited references20

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          Autoregulatory vasodilation of parenchymal vessels is impaired during cerebral vasospasm.

          Impaired CBF autoregulation during vasospasm after aneurysmal subarachnoid hemorrhage (SAH) could reflect impaired capacity of distal vessels to dilate in response to reduced local perfusion pressure or simply indicate that the perfusion pressure distal to large arteries in spasm is so low that vessels are already maximally dilated. Autoregulatory vasodilation can be detected in vivo as an increase in the parenchymal cerebral blood volume (CBV). Regional CBV, CBF, and oxygen extraction fraction in regions with and without angiographic vasospasm obtained from 29 positron emission tomography studies performed after intracranial aneurysm rupture were compared with data from 19 normal volunteers and five patients with carotid artery occlusion. Regional CBF was reduced compared to normal in regions from SAH patients with and without vasospasm as well as with ipsilateral carotid occlusion (P < .0001). Regional oxygen extraction fraction was higher during vasospasm and distal to carotid occlusion than both normal and SAH without vasospasm (P < .0001). Regional CBV was reduced compared to normal in regions with and without spasm, whereas it was increased ipsilateral to carotid occlusion (P < .0001). These findings of reduced parenchymal CBV during vasospasm under similar conditions of tissue hypoxia that produce increased CBV in patients with carotid occlusion provide evidence that parenchymal vessels distal to arteries with angiographic spasm after SAH do not show normal autoregulatory vasodilation.
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            Therapeutic approaches to vasospasm in subarachnoid hemorrhage.

            N W Dorsch (2002)
            Delayed vasospasm as a result of subarachnoid blood after rupture of a cerebral aneurysm is a major complication. It is seen in over half of patients and causes symptomatic ischemia in about one third. If left untreated, it leads to death or permanent deficits in over 20% of patients. The essential cause and the relative contribution of true muscle spasm and other changes in the vessel wall remain uncertain. The mainstays of treatment are careful maintenance of fluid balance, induced hypervolemia and hypertension, calcium antagonists, balloon or chemical angioplasty, and, in some centers, cisternal fibrinolytic drugs. Promising future lines of treatment include gene therapy, nitric oxide donors, magnesium, sustained release cisternal drugs, and several other drugs that are under experimental or clinical trial.
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              Intra-arterial papaverine infusions for the treatment of cerebral vasospasm induced by aneurysmal subarachnoid hemorrhage.

              Cerebral vasospasm secondary to aneurysmal subarachnoid hemorrhage that has become refractory to maximal medical management can be treated with selective intra-arterial papaverine infusions. Papaverine is a potent vasodilator of the proximal, intermediate, and distal cerebral arteries and can improve cerebral blood flow (CBF). When infused intra-arterially using endovascular microcatheter techniques, papaverine can effectively increase angiographic vessel diameter, decrease prolonged cerebral circulation time, and improve cerebral oxygenation. However, one of the major disadvantages of papaverine is its transient nature, which can result in recurrent and/or persistent angiographic and clinical vasospasm that may require multiple repeated infusions, despite a successful response to the initial treatment. Intra-arterial papaverine can be used alone or in combination with balloon angioplasty. This article reviews the mechanism of action, technique of administration, effects on CBF, clinical results, and complications of intra-arterial papaverine for the treatment of cerebral vasospasm.
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                Author and article information

                Journal
                Neurosurgical Focus
                FOC
                Journal of Neurosurgery Publishing Group (JNSPG)
                1092-0684
                September 2006
                September 2006
                : 21
                : 3
                : 1-7
                Article
                10.3171/foc.2006.21.3.14
                17029338
                9ee9a608-2fe6-4a0c-af8d-3aeaa7020ad0
                © 2006
                History

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