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• W1987601332 abstract "HomeStrokeVol. 37, No. 2Advances in Subarachnoid Hemorrhage Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBAdvances in Subarachnoid Hemorrhage Valery L. Feigin, MD, PhD and Max Findlay, MD, PhD, FRCSC Valery L. FeiginValery L. Feigin From the Clinical Trials Research Unit (V.L.F.), Department of Medicine and School of Population Health, University of Auckland, New Zealand; and the Division of Neurosurgery (M.F.), Department of Surgery, University of Alberta, Edmonton, Alberta, Canada. Search for more papers by this author and Max FindlayMax Findlay From the Clinical Trials Research Unit (V.L.F.), Department of Medicine and School of Population Health, University of Auckland, New Zealand; and the Division of Neurosurgery (M.F.), Department of Surgery, University of Alberta, Edmonton, Alberta, Canada. Search for more papers by this author Originally published12 Jan 2006https://doi.org/10.1161/01.STR.0000200558.38774.d5Stroke. 2006;37:305–308Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 12, 2006: Previous Version 1 Although subarachnoid hemorrhage (SAH) comprises only 1% to 7% of all strokes,1 the loss of productive life years in the general population from SAH is comparable to that of cerebral infarction2 because of the relatively young age of onset and poor outcome in SAH.1,3,4 However, unlike other stroke subtypes, the incidence of SAH exhibits little geographical variation and did not significantly change over the last decades.1 In the most recent overview of 14 longitudinal and 23 case-control studies of risk factors for SAH published in English from 1966 through March 2005,5 it was concluded that smoking, hypertension, and excessive alcohol are the most important risk factors for SAH. Exposure to these risk factors individually and/or in combination promotes formation, growth, and rupture of intracranial aneurysm(s),6–8 a major cause of SAH. The consistency of the data across studies involving different designs and populations suggests that cigarette smoking and elevated blood pressure are causally related to SAH.9 There is also evidence that genetic factors play an important role in the pathogenesis of SAH.10 Accumulating evidence suggest a temporal (seasonal and diurnal) pattern in the occurrence of SAH,11,12 but reasons for these temporal patterns remain unclear. However, there is still lack of good quality population-based epidemiological studies on incidence, trends, and outcomes of SAH in different populations (especially from developing countries).Diagnosis and InvestigationMisdiagnosis of SAH occurred in 12% of 482 SAH patients admitted to a large American tertiary care hospital and was associated with a smaller hemorrhage and normal mental status on first assessment as well as poorer 1-year outcome resulting from neurological complications before correct diagnosis (primarily rebleeding).13 All patients with suspected SAH, including those with mild symptoms after an otherwise typical thunderclap onset, should have an emergency computed tomography (CT) scan without contrast interpreted by an expert. Hyperdense blood located near common aneurysm locations in the basal cisterns is usually diagnostic, but parenchymal clot in the temporal or basal frontal lobes and intraventricular hemorrhage are also suggestive of an underlying aneurysm.14 If CT scanning is considered normal (uncommon in the first 24 hours after aneurysm rupture), lumbar puncture for cerebrospinal fluid analysis must be performed. It is often necessary to distinguish a true SAH from a traumatic spinal tap,15 and although no single method is fail-safe, the presence of visible xanthochromia after centrifugation of bloody cerebrospinal fluid strongly suggests SAH.Since its introduction to the clinical management of SAH in the 1990’s16 the use of CT angiography for rapid aneurysm detection and treatment planning has become increasingly practical and popular, particularly since the introduction of rapid multislice CT scanners.17–22 Three-dimensional anatomical information provided by CT angiography or computer reconstruction of catheter angiography23 is useful when planning and performing aneurysm repair. The utility of magnetic resonance studies in the setting of acute SAH has received some interest but remains limited, especially in unstable patients.24Medical TreatmentMedical treatment of patients with aneurysmal SAH is directed toward the prevention and management of neurological (eg, aneurysm rebleeding, hydrocephalus, cerebral vasospasm and ischemia and seizures) and systemic complications (eg, hyponatremia, cardiac arrhythmia and myocardial damage and neurogenic pulmonary edema).25,26A recent randomized trial showed that immediate administration of antifibrinolytic agent tranexamic acid (1 g IV, followed by 1 g every 6 hours until aneurysm repair carried out as soon as possible) reduced the rate of often devastating early aneurysm rebleeding from 11% to 2.4%.27 Short-term antifibrinolytic treatment may protect from acute aneurysm rebleeding, but long-term antifibrinolytic treatment in patients in whom late aneurysm repair is planned does not improve overall outcome because the reduction in the rate of rebleeding before delayed surgery is offset by an increase in poor outcome secondary to cerebral ischemia.28 Pain management, sedation, and control of hypertension are also important in the prevention of aneurysm rebleeding, particularly in distressed, agitated patients seen soon after aneurysm rupture. In conscious patients without evidence of raised intracranial pressure, active hypertension treatment is indicated. Although the best antihypertensive agent and blood pressure in this situation is unsettled (although undoubtedly related to individual patient’s baseline blood pressures), intravenous labetolol and a target mean arterial pressure of <130 mm Hg are reasonable.25Strict avoidance of hypovolemia, hypotension, and hyponatremia are important in preventing delayed cerebral ischemia (DCI) in patients with SAH.25 Hyperthermia and hyperglycemia are associated with DCI and should also be prevented using paracetamol, cooling blankets, and insulin when indicated.29,30 Routine use of the calcium blocking agent nimodipine (60 mg orally every 4 hours) provides a modest but significant improvement in outcome.31 There is no evidence that corticosteroids are of benefit.32 Antiplatelet agents in the prevention of DCI warrant further investigation.33 Neuroprotective strategies being investigated in SAH have recently been reviewed.34 Noteworthy new treatments under investigation include intravenous magnesium sulfate, which was associated with a trend toward improved outcome in 2 phase II randomized trials,35,36 and the statin agents pravastatin and simvastatin, which in separate phase II randomized trials reduced angiographic vasospasm and DCI when given for 14 days after aneurysmal SAH.37,38 Endothelin A is a powerful vasoconstrictive autocoid implicated in the pathogenesis of vasospasm. Clazosentan is an endothelin receptor antagonist, which has been shown to reduce vasospasm in a phase II study,39 and it is currently under investigation in a phase III trial.Although a great deal of anecdotal evidence has led to the routine use hypervolemia and induced hypertension to reverse symptomatic DCI in patients with delayed-onset vasospasm after SAH, there is little information on the efficacy of either blood volume expansion alone or in combination with hypertension and hemodilution (“triple-H therapy”) to either prevent or reverse cerebral ischemia.40,41 Endovascular vasospasm reversal, particularly with balloon angioplasty, has emerged as an important intervention for treating medically refractory DCI before irreversible infarction, although again it has not been validated in a randomized trial.34,42Aneurysm AblationPatients with ruptured aneurysms should be immediately transferred to an institution with a comprehensive neurosurgical service, and there is evidence linking high-volume hospitals staffed by experienced clinicians to better patient outcomes.43–45 Despite a lack of scientific proof that it is a superior strategy, aneurysm ablation timed as early as possible to maximally prevent aneurysm rebleeding is a uniform policy in most centers.46,47A multicenter randomized trial involving 1001 good-grade SAH patients found that mild intraoperative hypothermia (target temperature 33°C using surface cooling techniques) provided no benefit in terms of neurological outcome and was associated with a higher incidence of postoperative bacteremia.48 Intraoperative and postoperative angiography helps ensure correct anatomical repair of aneurysms.49,50 SAH is associated with obstructive hydrocephalus, and several cohort studies have suggested that microsurgical opening (“fenestration”) of the third ventricle into the basal subarachnoid cisterns reduces the need for ventriculoperitoneal shunting.51,52 Extended “decompressive” craniectomies help relieve intracranial hypertension in patients (generally poor grade) with large intracerebral hemorrhages or generalized brain swelling,53 but the quality of life experienced by survivors is frequently poor.54It has been several years since publication of the International Subarachnoid Aneurysm Trial (ISAT) results.55 That study randomized 2143 primarily good-grade patients with ruptured aneurysms (mostly small and located in the anterior circulation) between aneurysm clipping and endovascular coiling. At 1 year there was no difference in fatality rates between the 2 treatment groups, but for combined death and dependent rates there was an absolute risk reduction of 7.4% associated with coiling, which was significant.56 Endovascular treatment has been accepted by most to be the preferred treatment modality for basilar artery aneurysms, which are relatively uncommon and difficult to repair surgically,57 so the main impact of ISAT has been a steady increase in the use of endovascular coils in the management of anterior circulation aneurysms, depending on the availability of endovascular expertise at individual centers.58 Technical developments include introduction of the Neuroform stent to help treat wide-necked and complex cerebral aneurysms,59,60 and coils coated with polymeric materials to stimulate a more robust cellular reaction in the thrombosed aneurysm and theoretically reduce aneurysm reformation.61 Accumulating clinical experience confirms that early and midterm results after endovascular repair can be very good,62–65 although it does not appear to be cheaper or reduce resource utilization compared with surgery at the present time.66,67 The major limitation of endovascular coiling remains incomplete aneurysm obliteration (more common in large, complex and wide-necked aneurysms) associated with remnant growth or aneurysm recanalization, seen in up to one-third of treated aneurysms over just several years, and rebleeding.64,68 This risk mandates long-term follow-up angiography and in many patients retreatment with either more coiling or microsurgery along with the attendant risks of these interventions. The impact of coiling on the incidence and severity of vasospasm remains unclear,69 and shunt-dependent hydrocephalus was comparable between surgical and endovascular treatment groups in 1 study.70 Patients with large intracerebral hemorrhages whose aneurysms are coiled may require subsequent surgical clot evacuations.71 Longer term follow-up of patients with ruptured aneurysms treated with endovascular coils is required in order to establish what method of aneurysm repair is best suited for anterior circulation aneurysms.PrognosisDeath or dependence (poor outcome) occurs in almost 70% of patients with aneurysmal SAH and is attributed to DCI in approximately one third of the patients.72 DCI typically develops ≈3 days after the hemorrhage with the maximal risk between 4 to 14 days.73 Previous research has shown that advanced patient age (>60 years), a large amount of subarachnoid blood on CT scan,74 and a depressed level of consciousness on admission75 are important predictors for the development of DCI in patients with aneurysmal SAH. There is evidence that cardiac dysfunction and pulmonary edema are commonly observed during SAH.76 A modified version of the Massachusetts General Hospital Scale for predicting outcome after SAH has recently been validated.77 Rebleeding occurs in ≈7% of SAH patients and is associated with the clinical severity of SAH and aneurysm size.78There is lack of population-based data on long-term outcomes in SAH. In a recent Australasian study,4 incomplete recovery at 1 year after SAH was found in 46% of survivors, of which ongoing memory problems were recorded in 50%, mood abnormalities in 39%, and speech problems in 14%, whereas a substantial proportion of survivors had diminished level of health related quality of life. No predictors of complete recovery from SAH were determined in this study. In a large population-based Finnish stroke incidence study,79 low socio-economic status was shown to be associated with poorer outcomes in SAH.FootnotesCorrespondence to Valery Feigin, Clinical Trials Research Unit, University of Auckland, Private Bag 92019, Auckland, New Zealand. E-mail [email protected] References 1 Feigin VL, Lawes CM, Bennett DA, Anderson CS. Stroke epidemiology: a review of population-based studies of incidence, prevalence, and case-fatality in the late 20th century. Lancet Neurology. 2003; 2: 43–53.CrossrefMedlineGoogle Scholar2 Johnston SC, Selvin S, Gress DR. The burden, trends, and demographics of mortality from subarachnoid hemorrhage. Neurology. 1998; 50: 1413–1418.CrossrefMedlineGoogle Scholar3 Linn FH, Rinkel GJ, Algra A, van Gijn J. Incidence of subarachnoid hemorrhage: role of region, year, and rate of computed tomography: a meta-analysis. Stroke. 1996; 27: 625–629.CrossrefMedlineGoogle Scholar4 Hackett ML, Anderson CS. Health outcomes 1 year after subarachnoid hemorrhage: An international population-based study. The Australian Cooperative Research on Subarachnoid Hemorrhage Study Group. Neurology. 2000; 55: 658–662.CrossrefMedlineGoogle Scholar5 Feigin VL, Rinkel GJE, Lawes CMM, Algra A, Bennett DA, van Gijn J, Anderson CS. Risk Factors for Subarachnoid Hemorrhage: An Updated Systematic Review of Epidemiological Studies. Stroke. 2005; 36: 2773–2780.LinkGoogle Scholar6 Juvela S. Risk factors for multiple intracranial aneurysms. Stroke. 2000; 31: 392–397.CrossrefMedlineGoogle Scholar7 Juvela S, Poussa K, Porras M. Factors affecting formation and growth of intracranial aneurysms: a long-term follow-up study. Stroke. 2001; 32: 485–491.CrossrefMedlineGoogle Scholar8 Taylor CL, Yuan Z, Selman WR, Ratcheson RA, Rimm AA. Cerebral arterial aneurysm formation and rupture in 20,767 elderly patients: hypertension and other risk factors. J Neurosurg. 1995; 83: 812–819.CrossrefMedlineGoogle Scholar9 Feigin V, Parag V, Lawes CMM, Rodgers A, Suh I, Woodward M, Jamrozik K, Ueshima H; on behalf of the Asia Pacific Cohort Studies Collaboration. Smoking and Elevated Blood Pressure Are the Most Important Risk Factors for Subarachnoid Hemorrhage in the Asia-Pacific Region: An Overview of 26 Cohorts Involving 306 620 Participants. Stroke. 2005; 36: 1360–1365.LinkGoogle Scholar10 Ruigrok YM, Rinkel GJ, Wijmenga C. Genetics of intracranial aneurysms. [Review] [109 refs]. Lancet Neurology. 2005; 4: 179–189.CrossrefMedlineGoogle Scholar11 Feigin VL, Anderson CS, Rodgers A, Bennett DA. Subarachnoid haemorrhage occurrence exhibits a temporal pattern - evidence from meta-analysis. European Journal of Neurology. 2002; 9: 511–516.CrossrefMedlineGoogle Scholar12 Fischer T, Johnsen SP, Pedersen L, Gaist D, Sorensen HT, Rothman KJ. Seasonal variation in hospitalization and case fatality of subarachnoid hemorrhage: a nationwide danish study on 9367 patients. Neuroepidemiology. 2005; 24: 32–37.CrossrefMedlineGoogle Scholar13 Kowalski RG, Claassen J, Kreiter KT, Bates JE, Ostapkovich ND, Connolly ES, Mayer SA. Initial misdiagnosis and outcome after subarachnoid hemorrhage. JAMA. 2004; 291: 866–869.CrossrefMedlineGoogle Scholar14 Thai Q-A, Raza SM, Pradilla G, Tamargo RJ. Aneurysmal rupture without subarachnoid hemorrhage: case series and literature review. Neurosurgery. 2005; 57: 225–229.CrossrefMedlineGoogle Scholar15 Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Eng J Med. 2000; 342: 29–36.CrossrefMedlineGoogle Scholar16 Anderson GB, Steinke DE, Petruk KC, Ashforth R, Findlay JM. Computed tomographic angiography versus digital subtraction angiography for the dianosis and early treatment of ruptured intracranial aneurysms. Neurosurgery. 1999; 45: 1315–1322.CrossrefMedlineGoogle Scholar17 Wintermark M, Uske A, Chalaron M, Regli L, Maeder P, Meuli R, Schnyder P, Binaghi S. Multislice computerized tomography angiography in the evaluation of intracranial aneurysms: a comparison with intraarterial digital subraction angiography. J Neurosurg. 2003; 98: 828–836.CrossrefMedlineGoogle Scholar18 van Gelder JM. Computed tomographic angiography for detecting cerebral aneurysms: implications of aneurysm size distribution for the sensitivity, specificity, and likelihood ratios. Neurosurgery. 2003; 53: 597–606.CrossrefMedlineGoogle Scholar19 Hoh BL, Cheung AC, Rabinov JD, Pryor JC, Carter BS, Ogilvy CS. Results of a prospective protocol of computed tomographic angiography in place of catheter angiography as the only diagnostic and pretreatment planning study for cerebral aneurysms by a combined neurovascular team. Neurosurgery. 2004; 54: 1329–1342.CrossrefMedlineGoogle Scholar20 Kangasniemi M, Makela T, Koskinen S, Porras M, Poussa K, Hernesniemi J. Detection of intracranial aneurysms with two-dimensional and three dimensional multislice helical computed tomographic angiography. Neurosurgery. 2004; 54: 336–341.CrossrefMedlineGoogle Scholar21 Dammert S, Krings T, Moller-Hartmann W, Ueffing E, Hans FJ, Willmes K, Mull M, Thron A. Detection of intracranial aneurysms with multislice CT: comparison with conventional angiography. Neuroradiology. 2004; 46: 427–434.CrossrefMedlineGoogle Scholar22 Tipper G, U-King-Im JM, Prince SJ, Trivedi RA, Cross JJ, Higgins NJ, Farmer R, Wat J, Kirollos R, Kirkpatrick PJ, Antoun NM, Gillard JH. Detection and evaluation of intracranial aneurysms with 16-row multislice CT angiography. Clin Radiology. 2005; 60: 565–572.CrossrefMedlineGoogle Scholar23 Albuquerque FC, Spetzler RF, Zabramski JM, McDougall CG. Effects of three-dimensional angiography on the coiling of cerebral aneurysms. Neurosurgery. 2002; 51: 597–606.CrossrefMedlineGoogle Scholar24 Sato M, Nakano M, Sasanuma J, Asari J, Watanabe K. Preoperative cerebral aneurysm assessment by three-dimentional magnetic resonance angiography: feasibility of surgery without conventional catheter angiography. Neurosurgery. 2005; 56: 903–912.MedlineGoogle Scholar25 Wiebers DO, Feigin VL, Brown RD Jr. Handbook of Stroke. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006. In press.Google Scholar26 Wilson SR, Hirsch NP, Appleby I. Management of subarachnoid haemorrhage in a non-neurosurgical centre. [Review] [135 refs]. Anaesthesia. 2005; 60: 470–485.CrossrefMedlineGoogle Scholar27 Hillman J, Fridrikssojn S, Nilsson L, Yu A, Saveland H, Jakobsson K-E. Immediate administration of tranexamic acid and reduced incidence of early rebleeding after aneurysmal subarachnoid hemorrhage: a prospective randomized study. J Neurosurgery. 2002; 97: 771–778.CrossrefMedlineGoogle Scholar28 Roos YBWE, Rinkel GJE, Vermeulen M, Algra A, van Gijn J. Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage [Systematic Review]. Cochrane Database of Systematic Reviews. 2005. 4.Google Scholar29 Badjatia N, Topcuoglu MA, Buonanno FS, Smith EE, Nogueira RG, Rordorf GA, Carter BS, Ogilvy CS, Singhal AB. Relationship between hyperglycemia and symptomatic vasospasm after subarachnoid hemorrhage. [see comment]. Crit Care Med. 2005; 33: 1603–1609.CrossrefMedlineGoogle Scholar30 Juvela S, Siironen J, Kuhmonen J. Hyperglycemia, excess weight, and history of hypertension as risk factors for poor outcome and cerebral infarction after aneurysmal subarachnoid hemorrhage. [see comment]. J Neurosurg. 2005; 102: 998–1003.CrossrefMedlineGoogle Scholar31 Rinkel GJ, Feigin VL, Algra A, van den Bergh WM, Vermeulen M, van GJ. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database of Systematic Reviews. 2005:CD000277.Google Scholar32 Feigin VL, Anderson N, Rinkel GJE, Algra A, van Gijn J, Bennett DA. Corticosteroids for aneurysmal subarachnoid haemorrhage and primary intracerebral haemorrhage [Systematic Review]. Cochrane Database of Systematic Reviews. 2005. 4.Google Scholar33 Dorhout Mees SM, Rinkel GJE, Hop JW, Algra A, van Gijn J. Antiplatelet therapy in aneurysmal subarachnoid hemorrhage: a systematic review. Stroke. 2003; 34: 2285–2289.LinkGoogle Scholar34 Wu CT, Wong CS, Yeh CC, Borel CO. Treatment of cerebral vasospasm after subarachnoid hemorrhage–a review. [Review] [67 refs]. Acta Anaesthesiologica Taiwanica: Official Journal of the Taiwan Society of Anesthesiologists. 2004; 42: 215–222.MedlineGoogle Scholar35 Veyna RS, Seyfried D, Burke DG, Zimmerman C, Mlynarek M, Nichols V, Marrocco A, Thomas AJ, Mitsias PD, Malik GM. Magnesium sulfate therapy after aneurysmal subarachnoid hemorrhage. J Neurosurg. 2002; 96: 510–514.CrossrefMedlineGoogle Scholar36 van den Bergh WM; on behalf of the MASH Study Group. Magnesium sulfate in aneurysmal subarachnoid hemorrhage: a randomized controlled trial. Stroke. 2005; 36: 1011–1015.LinkGoogle Scholar37 Tseng M-Y, Czosnyka M, Richards H, Pickard JD, Kirkpatrick PJ. Effects of acute treatment with pravastatin on cerebral vasospasm, autoregulation, and delayed ischemic deficits after aneurysmal subarachnoid hemorrhage: a phase II randomized placebo-controlled trial. Stroke. 2005; 36: 1627–1635.LinkGoogle Scholar38 Lynch JR, Wang H, McGirt MJ, Floyd J, Friedman AH, Coon AL, Blessing R, Alexander MJ, Graffagnino C, Warner DS, Laskowitz DT. Simvastatin reduces vasospasm after aneurysmal subarachnoid hemorrhage: results of a pilot randomized clinical trial. Stroke. 2005; 36: 2024–2026.LinkGoogle Scholar39 Vajkoczy P, Meyer B, Weidouer S, Raabe A, Thome C, Ringel F, Breu V, Schmiedik P. Clazosentan (AXV-034343), a selective endothelin A receptor antagonist, in the prevention of cerebral vasospasm following severe aneurysmal subarachnoid hemorrhage: results of a randomized, double-blind, placebo-controlled multicenter Phase IIa study. J Neurosurg. 2005; 103: 9–17.CrossrefMedlineGoogle Scholar40 Rinkel GJE, Feigin VL, Algra A, van Gijn J. Circulatory volume expansion therapy for aneurysmal subarachnoid haemorrhage [Systematic Review]. Cochrane Database of Systematic Reviews. 2005. 4.Google Scholar41 Egge A, Waterloo K, Sjoholm H, Solberg T, Ingebrigtsen T, Romner B. Systematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage. J Neurosurg. 2004; 100: 359–360.MedlineGoogle Scholar42 Schuknecht B. Endovascular treatment of cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Acta Neurochirurgica - Supplement. 2005; 94: 47–51, 2005.CrossrefMedlineGoogle Scholar43 Cross DT, Tirschwell DL, Clark MA, Tuden D, Derdeyn CP, Moran CJ, Dacey RG Jr. Mortality rates after subarachnoid hemorrhage: variations according to hospital case volume in 18 states. J Neurosurg. 2003; 99: 810–817.CrossrefMedlineGoogle Scholar44 Berman MF, Solomon RA, Mayer SA, Johnston SC, Yung PP. Impact of hospital-related factors on outcome after treatment of cerebral aneurysms. Stroke. 2003; 34: 2200–2207.LinkGoogle Scholar45 Cowan JA, Dimick JB, Wainess RM, Upchurch GR Jr, Thompson BG. Outcomes after cerebral aneurysm clip occlusion in the United States: the need for evidence-based hospital referral. J Neurosurg. 2003; 99: 947–952.CrossrefMedlineGoogle Scholar46 De Gans K, Nieuwkamp DJ, Rinkel GJE, Algra A. Timing of aneurysm surgery in subarachnoid hemorrhage: a systematic review of the literature. Neurosurgery. 2002; 50: 336–342.MedlineGoogle Scholar47 Laidlaw JD, Siu KH. Poor-grade aneurysmal subarachnoid hemorrhage: outcome after treatment with urgent surgery. Neurosurgery. 2003; 53: 1275–1282.CrossrefMedlineGoogle Scholar48 Todd MM, Hindman BJ, Clark WR, Torner JC; for the IHAST investigators. Mild Intraoperative hypothermia during surgery for intracranial aneurysm. N Eng J Med. 2005; 352: 135–145.CrossrefMedlineGoogle Scholar49 Chiang VL, Gailloud P, Murphy KJ, Rigamonti D, Tamargo RJ. Routine intraoperative angiography during aneurysm surgery. J Neurosurg. 2002; 96: 988–992.CrossrefMedlineGoogle Scholar50 Kivisaari RP, Porras M, Ohman J, Siironen J, Ishii K, Hernesniemi J. Routine cerebral angiography after surgery for saccular aneurysms: is it worth it? Neurosurgery. 2004; 55: 1015–1024.CrossrefMedlineGoogle Scholar51 Komotar RJ, Olivi A, Rigamonti D, Tamargo RJ. Microsurgical fenestration of the lamina terminalis reduces the incidence of shunt-dependent hydrocephalus after aneurysmal subarachnoid hemorrhage. Neurosurgery. 2002; 51: 1403–1413.CrossrefMedlineGoogle Scholar52 Andaluz N, Zuccarello M. Fenestration of the lamina terminalis as a valuable adjunct in aneurysm surgery. Neurosurgery. 2004; 55: 1050–1059.CrossrefMedlineGoogle Scholar53 Smith ER, Carter BS, Ogilvy CS. Proposed use of prophylactic decompressive craniectomy in poor-grade aneurysmal subarachnoid hemorrhage patients presenting with associated large sylvian hematomas. Neurosurgery. 2002; 51: 117–124.CrossrefMedlineGoogle Scholar54 D’Ambrosio AL, Sughrue ME, Yorgason JG, Mocco JD, Kreiter KT, Mayer SA, McKhann IIGM, Connolly ES Jr. Decompressive hemicraniectomy for poor-grade aneurysmal subarachnoid hemorrhage patients with associated intracerebral hemorrhage: clinical outcome and quality of life assessment. Neurosurgery. 2005; 56: 12–20.CrossrefMedlineGoogle Scholar55 Molyneux A, Kerr R, Stratton I, Sandercock P, Clarke M, Shrimpton J, Holman R; International Subarachnoid Aneurysm Trial (ISAT) Collaborative Group. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. Lancet. 2002; 360: 1267–1274.CrossrefMedlineGoogle Scholar56 Molyneux A, Kerr RSC, Yu L-M, Clarke M, Sneade M, Yarnold JA, Sandercock P; for the International Subarachnoid Aneurysm (ISAT) Collaborative Group. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomized comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet. 2005; 366: 809–817.CrossrefMedlineGoogle Scholar57 Lempert TE, Malek AM, Halback VV, Phatouros CC, Meyers PM, Dowd CF, Higashida RT. Endovascular treatment of ruptured posterior circulation cerebral aneurysms: clinical and angiographic outcomes. Stroke. 2000; 31: 100–110.CrossrefMedlineGoogle Scholar58 Nilsson OG, Saveland H, Ramgren B, Cronqvist M, Brandt L. Impact of coil embolization on overqall management and outcome of patients with aneurysmal subarachnoid hemorrhage. Neurosurgery. 2005; 57: 216–224.CrossrefMedlineGoogle Scholar59 Benetez RP, Silva MT, Klem J, Veznedaroglu RH. Endovascular occlusion of wide-necked aneurysms with a new intracranial microstent (Neuroform) and detachable coils. Neurosurgery. 2004; 54: 1359–1368.CrossrefMedlineGoogle Scholar60 Fiorella D, Albuquerque FC, Deshmukh VR, McDougall CG. Usefulness of the Neuroform stent for the treatment of cerebral aneurysms: results at initial (3–6 mo) follow-up. Neurosurgery. 2005; 56: 1191–1202.CrossrefMedlineGoogle Scholar61 Linfante I, Akkawi NM, Perlow A, Andreone V, Wakhloo AK. Polyclycolid/polyactide-coated platinum coils for patients with ruptured and unruptured cerebral aneurysms: a single-center experience. Stroke. 2005; 35: 1948–1953.Google Scholar62 Henkes H, Fischer S, Wever W, Miloslavski E, Felber S, Brew S, Kuehne D. Endovascular coil occlusion of 1811 intracranial aneurysms: early angiographic and clinical results. Neurosurgery. 2004; 54: 268–285.CrossrefMedlineGoogle Scholar63 Kole MK, Pelz DM, Kalapos P, Lee DH, Gulka IB, Lownie SP. Endovascular coil embolization of intracranial aneurysms: important factors related to rates and outcomes of incomplete occlusion. J Neurosurg. 2005; 102: 607–615.CrossrefMedlineGoogle Scholar64 Murayama Y, Nien YL, Duckwiler G, Gobin YP, Jahan R, Frazee J, Martin N, Vinuela F. Guglielmi detachable coil embolization of cerebral aneurysms: 11 years’ experience. J Neurosurg. 2003; 98: 959–966.CrossrefMedlineGoogle Scholar65 Sluzewski M, van Rooij WJ, Rinkel GJ, Wijnalda D. Endovascular treatment of ruptured intracranial aneurysms with detachable coils: long-term clinical and serial angiographic results. Radiology. 2003; 227: 720–724.CrossrefMedlineGoogle Scholar66 Niskanen M, Koivisto T, Ronkainen A, Rinne J, Ruokonen E. Resource use after subarachnoid hemorrhage: comparison between endovascular and surgical treatment. Neurosurgery. 2004; 54: 1081–1088.CrossrefMedlineGoogle Scholar67 Javadpour" @default.
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• W1987601332 cites W1923366023 @default.
• W1987601332 cites W1973450490 @default.
• W1987601332 cites W1974180918 @default.
• W1987601332 cites W1974450637 @default.
• W1987601332 cites W1981284141 @default.
• W1987601332 cites W1983467310 @default.
• W1987601332 cites W1983924397 @default.
• W1987601332 cites W1990316520 @default.
• W1987601332 cites W1991385448 @default.
• W1987601332 cites W1992575721 @default.
• W1987601332 cites W1994033557 @default.
• W1987601332 cites W1994216904 @default.
• W1987601332 cites W1995898225 @default.
• W1987601332 cites W2003247460 @default.
• W1987601332 cites W2005240242 @default.
• W1987601332 cites W2009065888 @default.
• W1987601332 cites W2014420014 @default.
• W1987601332 cites W2015178727 @default.
• W1987601332 cites W2018814421 @default.
• W1987601332 cites W2027065303 @default.
• W1987601332 cites W2031208650 @default.
• W1987601332 cites W2031955337 @default.
• W1987601332 cites W2035835935 @default.
• W1987601332 cites W2037159550 @default.
• W1987601332 cites W2038450148 @default.
• W1987601332 cites W2038680419 @default.
• W1987601332 cites W2041598904 @default.
• W1987601332 cites W2044313202 @default.
• W1987601332 cites W2047191049 @default.
• W1987601332 cites W2049347141 @default.
• W1987601332 cites W2059089859 @default.
• W1987601332 cites W2062301318 @default.
• W1987601332 cites W2062553731 @default.
• W1987601332 cites W2062862876 @default.
• W1987601332 cites W2065894324 @default.
• W1987601332 cites W2067970364 @default.
• W1987601332 cites W2073958700 @default.
• W1987601332 cites W2079405518 @default.
• W1987601332 cites W2082180627 @default.
• W1987601332 cites W2085502908 @default.
• W1987601332 cites W2087938242 @default.
• W1987601332 cites W2100460925 @default.
• W1987601332 cites W2107655025 @default.
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