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Yasuhiro Aida, Tomoya Kamide, Hiroshi Ishii, Yasuko Kitao, Naoyuki Uchiyama, Mitsutoshi Nakada and Osamu Hori

S ubarachnoid hemorrhage (SAH) is a cerebral vascular disease with a high fatality rate worldwide, and more than 50% of survivors suffer permanent disabilities. 12 , 36 One of the reasons behind the poor outcome after SAH is vasospasm (VS), especially symptomatic vasospasm (SVS), which occurs as a complication in the subacute periods of SAH. SVS produces a delayed neurological deficit in 19%–46% of SAH patients, which may further lead to the secondary cerebral infarction. 3 , 34 , 40 Many treatment strategies, such as the administration of nimodipine as a Ca 2

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Peter D. le Roux, David W. Newell, Joseph Eskridge, Marc R. Mayberg and H. Richard Winn

continue to deteriorate despite hypervolemic hypertensive therapy and the use of calcium channel blockers, 3, 9, 10, 21, 24, 25, 37 urgent aneurysm obliteration and immediate postoperative angioplasty might be a reasonable approach in patients who present with severe symptomatic vasospasm and an unsecured ruptured aneurysm. The present report describes the use of this technique in five patients with delayed ischemic deficits following SAH. Clinical Material and Methods Patient Population During a 4-year period (June, 1988, to June, 1992), five patients

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Todd M. Lasner, Robert J. Weil, Howard A. Riina, Joseph T. King Jr., Eric L. Zager, Eric C. Raps and Eugene S. Flamm

, several studies have evaluated other potential risk factors for the development of symptomatic vasospasm. Rabb and colleagues 21 identified that age less than 35 years, amount of SAH, and clinical grade were independent predictors of clinical vasospasm. Inagawa 10 confirmed that the amount of SAH and clinical grade were predictive of symptomatic and angiographic vasospasm but found that age (using 59 years as the cutoff point) was not predictive of vasospasm. There have been no studies that have evaluated other clinical factors frequently found in patients with

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Suresh N. Magge, H. Isaac Chen, Rohan Ramakrishna, Liyi Cen, Zhen Chen, J. Paul Elliott, H. Richard Winn and Peter D. Le Roux

, study data have suggested that a younger age is associated with a greater risk of vasospasm. 3 , 14 , 41 , 50 , 52 , 60 These differences result, in part, from how vasospasm is diagnosed (for example, angiography, TCD ultrasonography, or based on symptoms) and how “advanced age” or age categories are defined. In particular, the answer to the question of whether age is associated with symptomatic vasospasm remains mixed, with various studies suggesting that a younger age is associated with a lower 35 or higher 4 , 6 , 48 , 56 incidence of vasospasm or that no

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Takao Kamezaki, Kiyoyuki Yanaka, Sohji Nagase, Keishi Fujita, Noriyuki Kato and Tadao Nose

D elayed ischemic neurological deficit due to cerebral vasospasm is one of the most serious consequences of aneurysmal SAH. The incidence of angiographic vasospasm is in excess of 50%, with symptomatic vasospasm occurring in 30% of patients. 9 Because of this high rate of morbidity, rapid treatment of delayed cerebral vasospasm is needed before ischemic damage occurs, thus making the early detection of delayed cerebral vasospasm essential. Considerable research effort has been directed toward demonstrating both the mechanisms and potential predictors of

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Yutaka Hirashima, Hideo Hamada, Masanori Kurimoto, Hideki Origasa and Shunro Endo

.0) 0.471  no 2 (5.0) 6 (10.0) Noted variables included patient sex and age, Hunt and Hess grade, 14 Fisher grade, 8 location of ruptured aneurysm, and acute hydrocephalus in patient groups with and without SV. Symptomatic vasospasm following SAH was defined as significant transient or permanent neurological deterioration, such as hemiparesis or aphasia. We monitored vasospasm every day by performing transcranial Doppler ultrasonography studies in all patients and confirmed it on digital subtraction angiography when transcranial Doppler

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Alejandro A. Rabinstein, Mark A. Pichelmann, Jonathan A. Friedman, David G. Piepgras, Douglas A. Nichols, Jon I. McIver, L. Gerard Toussaint III, Robyn L. McClelland, Jimmy R. Fulgham, Fredric B. Meyer, John L. D. Atkinson and Eelco F. M. Wijdicks

. 17 Despite potential referral biases, a systematic assessment of the experience in a single institution can provide valuable information. We present a study of all patients treated at our institution for aneurysmal SAH over a period of 10 years to determine the influence of treatment modality (craniotomy and clip application compared with endovascular coil occlusion) on the rate of symptomatic vasospasm and long-term clinical outcome. Clinical Material and Methods We reviewed the clinical and radiological information of all patients admitted to the Mayo

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Adib A. Abla, David A. Wilson, Richard W. Williamson, Peter Nakaji, Cameron G. McDougall, Joseph M. Zabramski, Felipe C. Albuquerque and Robert F. Spetzler

findings in patients with symptomatic vasospasm (clinical deterioration from delayed cerebral ischemia). Vasospasm Determination The methods for determination of vasospasm used in this study have been published previously. 9 The presence of radiographic vasospasm and degree of vasospasm were determined by an independent neuroradiologist. Conventional angiography was obtained in all but 3 patients; 1 patient each underwent CT angiography, MR angiography, or CT perfusion as confirmatory tests for vasospasm in the absence of angiography. Symptomatic vasospasm, also

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Atsuhiro Nakagawa, Ching-Chan Su, Kiyotaka Sato and Reizo Shirane

). Circulating blood volume values on the 3rd and 7th days after operation were significantly higher than preoperative values (p < 0.01). There was no significant difference in sex, age, or preoperative Hunt and Hess grade when comparing Groups A and B. None of the Group A patients suffered from symptomatic vasospasm, whereas four patients in Group B did. Fig. 2. Bar graph showing postoperative changes in cBV in Group A patients. There was no significant change throughout the study period. Fig. 3. Bar graph showing postoperative changes in cBV in women

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Andrew D. Firlik, Anthony M. Kaufmann, Charles A. Jungreis and Howard Yonas

C erebral arterial vasospasm continues to be a major contributor to morbidity and mortality in patients who have suffered aneurysmal subarachnoid hemorrhage (SAH). 2, 8, 12, 15, 17 Transluminal angioplasty has been advocated as a treatment strategy when symptomatic vasospasm persists despite maximum medical management. 1, 5, 8, 11 Although these reports demonstrate neurological improvement after angioplasty, the effects of arterial dilation on cerebral blood flow (CBF) have yet to be fully characterized in this setting. This is the first study designed to