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Richard P. White, Shang-Po Huang, A. Ainsworth Hagen and James T. Robertson

T here is convincing evidence that phenoxybenzamine (PBZ) and related compounds will prevent the occurrence or reduce the duration of cerebral vasospasm produced experimentally. 2, 7, 8, 13, 22 Moreover, PBZ injected intracisternally 1 will reverse cerebral vasospasm induced by the injection of blood into the subarachnoid space. This drug will also significantly reduce cerebral edema induced in mice. 16 The experimental findings, therefore, clearly indicate that this agent will ameliorate edema, prevent cerebral vasospasm, or reverse an existing vasospasm

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Yukio Maeda, Eiichi Tani and Tsumoru Miyamoto

M any etiological factors are involved in the evolution of cerebral vasospasm. Among prostaglandins studied so far, prostaglandin (PG)F 2α , PGF 1α , PGE 2 , PGB 2 , and thromboxane (TX)B 2 contracted the cerebral artery in vivo, in vitro , or both. 2, 4, 8, 19, 21, 27, 28 Recent advances in prostaglandin research have disclosed new prostaglandins: PGI 2 and thromboxane A 2 (TXA 2 ). Prostacyclin (PGI 2 ) has the capability to inhibit the aggregation of blood platelets, and dilates arterial smooth muscle. 5, 8, 14, 17, 18, 26 Its actions are

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Emanuele La Torre, Carlo Patrono, Aldo Fortuna and Daniela Grossi-Belloni

D espite a great number of experimental studies on the production of long-lasting spasm and the elucidation of its pathogenesis, 2, 5, 7, 14–16 the therapy of cerebral vasospasm from bleeding aneurysms still represents a challenge for neurosurgeons. Indeed, although an antifibrinolytic agent, 6 adrenergic blocking agents, 4, 13 and inhibitors of normal metabolites of the smooth fibers of the arterial wall 12 have all reduced this spasm experimentally, no one of these drugs has been judged suitable for clinical application. Another line of research has

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David J. Boullin, Philip Tagari, George du Boulay, Victoria Aitken and J. Trevor Hughes

C erebral arterial spasm is a major complication in the treatment of subarachnoid hemorrhage (SAH) due to aneurysm rupture. 9 Prolonged arterial narrowing as demonstrated by angiography is usually maximal 5 to 10 days after release of blood into the subarachnoid space. 13 In cases of severe spasm, the resultant reduction in cerebral blood flow may lead to ischemia in the territories of the arteries affected, and concomitant neurological deficits. Despite much investigation, the etiology of cerebral vasospasm remains obscure, and a rational chemotherapy for

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Francisco Espinosa, Bryce Weir, Donald Boisvert, Thomas Overton and William Castor

in animals have increased our knowledge of the condition, but it is not certain to what extent we can extrapolate the findings directly to vasospasm in man. We designed our experiments to test the hypothesis that the size of the SAH is critical to the development of chronic vasospasm. In monkeys, a large SAH was created by the injection of autologous blood in the maximum volume compatible with chronic survival. The size of the SAH as seen on the initial CT scan was correlated with both the incidence and severity of cerebral vasospasm for up to 21 days

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Tao Hong, Yang Wang, Hai-tao Wang and Huan Wang

C erebral vasospasm after SAH is a major complication following the rupture of intracranial aneurysms. 24 Despite extensive clinical and experimental studies, the pathogenesis of cerebral vasospasm is still controversial and poorly understood. Numerous substances have been implicated in the causes of this phenomenon, but none of these investigations has determined the predominant pathophysiological mechanisms. The cause of vasospasm is presently considered to be multifactorial. Many therapeutic approaches have been suggested; however, no effective

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Walter J. Levy, Janet W. Bay, Bhupinder Sawhny and Thomas Tank

improve with the regimen. Diuresis induced by the treatment was a problem in all of them, but it was closely observed and responded well. The improvements shown by these patients were substantial; they progressed to a higher grade of neurological status, with a substantial increase in motor performance. A short description of the cases follows. TABLE 1 Clinical summary in five patients with cerebral vasospasm Case No. Age (yrs), Sex Aneurysm Location * Days Treated Neurological Grade † Residual Deficit At Start of Regimen

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Nobuyuki Ozaki and Sean Mullan

V ascular spasm associated with cerebral hemorrhage has a grave influence on the prognosis of patients with subarachnoid hemorrhage, 10, 32, 37 severe head trauma, 22, 33, 39 and cerebral embolectomy. 19 However, there is very limited information regarding the pathogenesis of the vascular spasm that follows in these cases. Extravasation of blood is one of the obvious factors in the causation of cerebral vasospasm. 12– 14, 17, 20, 30, 35 Substances that are released from the platelets, such as serotonin, 2– 5, 9, 17, 28, 35, 42 prostaglandin, 21, 27, 36

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Neal F. Kassell, Gregory Helm, Nathan Simmons, C. Douglas Phillips and Wayne S. Cail

A lthough significant advances have been made in the treatment of cerebral vasospasm, the arterial narrowing that commonly occurs after subarachnoid hemorrhage (SAH) is still a leading cause of morbidity and mortality in patients with ruptured aneurysms. 6 Hypertensive hypervolemic hemodilution therapy, 5 calcium channel blocking agents, 10 and early surgery with clot removal have all contributed to the decreased incidence and severity of vasospasm. 4 Balloon angioplasty has been used with dramatic success in certain patients with vasospasm in the larger

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Experimental cerebral vasospasm

Part 2: Effects of vasoactive drugs and sympathectomy on early and late spasm

Hajime Nagai, Satoshi Noda and Hideo Mabe

V asospasm in patients with subarachnoid hemorrhage (SAH) from a cerebral aneurysm is associated with a poor prognosis whether or not the patient is treated surgically. 2, 4, 32, 36 Although many attempts have been made to relieve or prevent cerebral vasospasm with various drugs, no decisive effects have been obtained. 7, 13, 14, 22 A previous paper reported observation of a biphasic, early and late course of spasm after rupture of the posterior communicating artery in dogs. 23, 24 We felt that late spasm results from factors different from those producing