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Cerebral vasospasm following aneurysm rupture

A protocol for therapy and prophylaxis

Alan S. Fleischer and George T. Tindall

R ecent studies have demonstrated that the presence of clinically significant cerebral vasospasm is an important determinant of outcome after rupture of intracranial aneurysms. 4 The two types of cerebral vasospasm are: 1) angiographic vasospasm, which has no clinical correlate and the importance of which is presently unknown; and 2) angiographic cerebral vasospasm, which correlates well with clinical findings due to focal or diffuse cerebral ischemia. Several forms of therapy have been advocated for the latter type of vasospasm, two of the most promising

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R. Loch Macdonald, Daniel J. Curry, Yasuo Aihara, Zhen-Du Zhang, Babak S. Jahromi, and Reza Yassari

I nterest has developed in the use of Mg ++ for treatment of ischemic stroke and SAH. Magnesium is worthy of investigation in cases of SAH because it has proved to be neuroprotective in experimental models of cerebral ischemia and excitotoxicity and is a vasodilator. 22 Pilot studies have been conducted in patients with SAH, but definitive answers will be difficult to obtain without conducting large, randomized trials. 7, 32 We reasoned that the effect of Mg ++ on angiographic vasospasm, however, could be definitively addressed in the nonhuman primate

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Tetsuji Inagawa, Mitsuo Yamamoto, and Kazuko Kamiya

I n describing the clinical manifestations surrounding subarachnoid hemorrhage (SAH), Fisher, et al. , 3, 4 reported that correlations between the site of major subarachnoid blood clots and the location of severe vasospasm as well as between the particular artery affected by vasospasm and the delayed clinical syndrome were almost exactly the same. These articles are very impressive, considering that there is a consistent anatomical relationship between the cisterns and the corresponding major blood vessels. On the other hand, early operation with evacuation

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Bryce Weir, Michael Grace, John Hansen, and Charles Rothberg

C ontroversy continues to swirl around the concept of vasospasm following subarachnoid hemorrhage (SAH) and its clinical significance. The difficulty in reconciling apparent disparities in the data from various authors partly stems from the fact that there is no objective measure of vasospasm. Earlier workers in the field made relatively subjective judgments as to the “presence” or “absence” of this phenomenon. Du Boulay 7 found some evidence of spasm in about two–thirds of cases following SAH, and he believed that when spasm was present it was always

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Taku Shigeno, Tatsuo Mima, Masashi Yanagisawa, Akira Saito, Katsutoshi Goto, Kazumasa Yamashita, Toshiharu Takenochi, Naosuke Matsuura, Yasuhide Yamasaki, Koji Yamada, Tomoh Masaki, and Kimitomo Takakura

D elayed cerebral vasospasm after subarachnoid hemorrhage (SAH) is a complex pathological process characterized by a strong and persistent contraction of arterial smooth muscle accompanied by an abnormal proliferation and necrosis of the cellular constituents of the arterial wall. 1, 6, 11 Although the mechanism of this disorder is still unknown, it has been considered that multiple endogenous vasoactive substances are involved. Polypeptide factors with vasoconstricting and/or mitogenic activities, such as endothelin 12, 19, 21 and platelet-derived growth

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Isamu Saito, Yasuichi Ueda, and Keiji Sano

71 patients between the seventh and 14th day after rupture, and in 36 patients after the 15th day postrupture. The chief causes for consciousness disturbance are listed in Table 1 , and it can be seen that in the treatment of intracranial aneurysms, vasospasm following SAH is one of the crucial factors affecting the prognosis of a patient. 3, 6, 11, 36, 56 Moreover, it is generally accepted that vasospasm is often associated with diminished cerebral blood flow 27, 30, 32, 44, 54 and neurological deterioration suggesting cerebral ischemia or infarction, 18, 22

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Kiarash Shahlaie, Krista Keachie, Irene M. Hutchins, Nancy Rudisill, Lori K. Madden, Karen A. Smith, Karen A. Ko, Richard E. Latchaw, and J. Paul Muizelaar

P osttraumatic vasospasm (PTV) is a significant source of secondary insult in patients with severe TBI, and independently predicts permanent neurological deficit and poor outcome. 9 , 26–28 , 32 , 33 , 43 , 59 , 64 , 69 Its reported incidence varies between 18.6% and 50% in the anterior circulation 7 , 9 , 19 , 20 , 34 , 35 , 46 , 48 , 59 , 64 , 67 , 71 and 19% and 37% in the posterior circulation. 41 , 55 , 64 Posttraumatic vasospasm typically develops 12 hours to 5 days after injury and persists for 12 hours to 30 days. 2 , 9 , 34 , 35 , 41 , 46 , 56

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Isamu Saito, Taku Shigeno, Koichi Aritake, Takeo Tanishima, and Keiji Sano

I t is now generally accepted that vasospasm following subarachnoid hemorrhage (SAH) caused by ruptured cerebral aneurysms has a crucial influence on the prognosis of patients. 2, 3, 5, 20 However, some reports have shown that vasospasm is not always associated with neurological symptoms or cerebral infarction, and that neurological symptoms due to vasospasm are elicited only when intracranial pressure (ICP) increased 10 or when other factors affecting cerebral blood flow coexisted with vasospasm. 6, 11, 18, 21 In a previous paper, 17 we documented some

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Kunihiko Osaka

T he pathogenesis of arterial spasm is not well understood in spite of intensive investigative efforts. In 1965, Echlin 21 demonstrated that topical application of fresh blood to the cerebral arteries induced vasospasm in the monkey. This finding was confirmed by many investigators and extravasated blood is now accepted as the cause of vasospasm. 20, 27, 37, 41, 45 Possible vasoconstrictor substances released from the platelets include serotonin, 2, 4–6, 8, 44, 53 prostaglandin, 31, 42, 43, 52 and unidentified polypeptides. 27, 28 Curiously, erythrocytes

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Luiz Carlos de Araujo, Rosario A. Zappulla, Wen C. Yang, and Sidney A. Hollin

C erebral vasospasm following craniotomy for intracranial aneurysm remains a significant neurosurgical problem. Postoperative neurological deficits associated with spasm are thought to be caused by cerebral ischemia. Diminished oxygenation of brain tissue is believed to result from decreased cerebral blood flow (CBF) secondary to arterial constriction and increased vascular resistance. Induced hypertension for treatment of cerebral vasospasm was originally carried out by Farhat and Schneider. 5 In recent years it has been used with encouraging results. 10