The Risk of Seizure After Surgery for Unruptured Intracranial Aneurysms: A Prospective Cohort Study.

BACKGROUND We aimed to identify a group of patients with a low risk of seizure after surgery for unruptured intracranial aneurysms (UIA). OBJECTIVE To determine the risk of seizure after discharge from surgery for UIA. METHODS A consecutive prospectively collected cohort database was interrogated for all surgical UIA cases. There were 726 cases of UIA (excluding cases proximal to the superior cerebellar artery on the vertebrobasilar system) identified and analyzed. Cox proportional hazards regression models and Kaplan-Meier life table analyses were generated assessing risk factors. RESULTS Preoperative seizure history and complication of aneurysm repair were the only risk factors found to be significant. The risk of first seizure after discharge from hospital following surgery for patients with neither preoperative seizure, treated middle cerebral artery aneurysm, nor postoperative complications (leading to a modified Rankin Scale score >1) was <0.1% and 1.1% at 12 months and 7 years, respectively. The risk for those with preoperative seizures was 17.3% and 66% at 12 months and 7 years, respectively. The risk for seizures with either complications (leading to a modified Rankin Scale score >1) from surgery or treated middle cerebral artery aneurysm was 1.4% and 6.8% at 12 months and 7 years, respectively. These differences in the 3 Kaplan-Meier curves were significant (log-rank P < .001). CONCLUSION The risk of seizures after discharge from hospital following surgery for UIA is very low when there is no preexisting history of seizures. If this result can be supported by other series, guidelines that restrict returning to driving because of the risk of postoperative seizures should be reconsidered. ABBREVIATIONS MCA, middle cerebral arterymRS, modified Rankin ScaleUIA, unruptured intracranial aneurysms.

Computational fluid dynamic analysis of intracranial aneurysm bleb Formation (NS26P)

Purpose: The management of unruptured aneurysms remains controversial as treatment infers potential significant risk to the currently well patient. The decision to treat is based upon aneurysm location, size and abnormal morphology (e.g. bleb formation). A method to predict bleb formation would thus help stratify patient treatment. Our study aims to investigate possible associations between intra-aneurysmal flow dynamics and bleb formation within intracranial aneurysms. Competing theories on aetiology appear in the literature. Our purpose is to further clarify this issue. Methodology: We recruited data from 3D rotational angiograms (3DRA) of 30 patients with cerebral aneurysms and bleb formation. Models representing aneurysms pre-bleb formation were reconstructed by digitally removing the bleb, then computational fluid dynamics simulations were run on both pre and post bleb models. Pulsatile flow conditions and standard boundary conditions were imposed. Results: Aneurysmal flow structure, impingement regions, wall shear stress magnitude and gradients were produced for all models. Correlation of these parameters with bleb formation was sought. Certain CFD parameters show significant inter patient variability, making statistically significant correlation difficult on the partial data subset obtained currently. Conclusion: CFD models are readily producible from 3DRA data. Preliminary results indicate bleb formation appears to be related to regions of high wall shear stress and direct impingement regions of the aneurysm wall.

Distal anterior cerebral artery aneurysms

Objective: Distal anterior cerebral artery (DACA) aneurysms represent about 6% of all intracranial aneurysms. So far, only small series on treatment of these aneurysms have been published. Our aim is to evaluate the anatomic features, microneurosurgical techniques, treatment results, and long-term outcome in patients treated for DACA aneurysms. Patients and methods: We analyzed the clinical and radiological data on 517 consecutive patients diagnosed with DACA aneurysm at two neurosurgical centers serving solely the Southern (Helsinki) and Eastern (Kuopio) Finland in 1936–2007, and used a defined subgroup of the whole study population in each part of the study. Detailed anatomic analysis was performed in 101 consecutive patients from 1998 to 2007. Treatment results were analyzed in 427 patients treated between 1980 to 2005, the era of CT imaging and microneurosurgery. Long-term treatment outcome of ruptured DACA aneurysm(s) was evaluated in 280 patients with a median follow-up of 10 years; no patients were lost to follow-up. Results: DACA aneurysms, found most often (83%) at the A3 segment of the anterior cerebral artery (ACA), were smaller (median 6 mm vs. 8 mm), more frequently associated with multiple aneurysms (35% vs. 18%), and presented more often with intracerebral hematomas (ICHs) (53% vs. 26%) than ruptured aneurysms in general. They were associated with anomalies of the ACA in 23% of the patients. Microsurgical treatment showed similar complication rates (treatment morbidity 15%, treatment mortality 0.4%) as for other ruptured aneurysms. At one year after subarachnoid hemorrhage (SAH), DACA aneurysms had equally favorable outcome (GOS≥4) as other ruptured aneurysms (74% vs. 69%) but their mortality was lower (13% vs. 24%). Factors predicting unfavorable outcome for ruptured DACA aneurysms were advanced age, Hunt&Hess≥3, rebleeding before treatment, ICH, intraventricular hemorrhage, and severe preoperative hydrocephalus. The cumulative relative survival ratio showed 16% excess mortality in patients with ruptured DACA aneurysm during the first three years after SAH compared to the matched general population. From the fourth year onwards, there was no excess mortality during the follow-up. There were four episodes of recurrent SAH, only one due to treated DACA aneurysm, with a 10-year cumulative risk of 1.4%. Conclusions: The special neurovascular features and frequent association with anterior cerebral artery anomalies must be taken into account when planning occlusive treatment of DACA aneurysms. Clipping of DACA aneurysms provides a long-lasting result, with very small rates of rebleeding. After surviving three years from rupture of DACA aneurysm, the long-term survival of these patients becomes similar to that of the matched general population.

Adenosine-induced flow arrest to facilitate intracranial aneurysm clip ligation: dose-response data and safety profile.

BACKGROUND: Adenosine-induced transient flow arrest has been used to facilitate clip ligation of intracranial aneurysms. However, the starting dose that is most likely to produce an adequate duration of profound hypotension remains unclear. We reviewed our experience to determine the dose-response relationship and apparent perioperative safety profile of adenosine in intracranial aneurysm patients. METHODS: This case series describes 24 aneurysm clip ligation procedures performed under an anesthetic consisting of remifentanil, low-dose volatile anesthetic, and propofol in which adenosine was used. The report focuses on the doses administered; duration of systolic blood pressure <60 mm Hg (SBP(<60 mm Hg)); and any cardiovascular, neurologic, or pulmonary complications observed in the perioperative period. RESULTS: A median dose of 0.34 mg/kg ideal body weight (range: 0.29-0.44 mg/kg) resulted in a SBP(<60 mm Hg) for a median of 57 seconds (range: 26-105 seconds). There was a linear relationship between the log-transformed dose of adenosine and the duration of a SBP(<60 mm Hg) (R(2) = 0.38). Two patients developed transient, hemodynamically stable atrial fibrillation, 2 had postoperative troponin levels >0.03 ng/mL without any evidence of cardiac dysfunction, and 3 had postoperative neurologic changes. CONCLUSIONS: For intracranial aneurysms in which temporary occlusion is impractical or difficult, adenosine is capable of providing brief periods of profound systemic hypotension with low perioperative morbidity. On the basis of these data, a dose of 0.3 to 0.4 mg/kg ideal body weight may be the recommended starting dose to achieve approximately 45 seconds of profound systemic hypotension during a remifentanil/low-dose volatile anesthetic with propofol induced burst suppression.

Aneurysms increase the risk of rebleeding after stereotactic radiosurgery for hemorrhagic arteriovenous malformations

BACKGROUND AND PURPOSE:
The purpose of this study was to define the risk of rebleeding after stereotactic radiosurgery (SRS) for hemorrhagic arteriovenous malformations with or without associated intracranial aneurysms.

METHODS:
Between 1987 and 2006, we performed Gamma Knife SRS on 996 patients with brain arteriovenous malformations; 407 patients had sustained an arteriovenous malformation hemorrhage. Sixty-four patients (16%) underwent prior embolization and 84 (21%) underwent prior surgical resection. The median target volume was 2.3 mL (range, 0.1-20.7 mL). The median margin dose was 20 Gy (range, 13.5-27 Gy).

RESULTS:
The overall rate of total obliteration defined by angiography or MRI was 56%, 77%, 80%, and 82% at 3, 4, 5, and 10 years, respectively. Before obliteration, 33 patients (8%) sustained an additional hemorrhage after SRS. The overall annual hemorrhage rate until obliteration after SRS was 1.3%. The presence of a patent aneurysm was significantly associated with an increased rehemorrhage risk after SRS (annual hemorrhage rate, 6.4%) compared with patients with a clipped or embolized aneurysm (annual hemorrhage rate, 0.8%; P=0.033).

CONCLUSIONS:
When an aneurysm is identified in patients with arteriovenous malformations selected for SRS, additional endovascular or surgical strategies should be considered to reduce the risk of bleeding during the latency interval.

Modified abbreviated transcavernous approach to basilar artery aneurysms-Case report

Background: Endovascular procedures and direct surgical clipping, are the main therapeutic modalities for managing of BAAs. Furthermore, giant or wide-necked aneurysms and those that involve the PCA or perforators at its neck usually are not embolized. Case Description: A 55-year-old man presented to the emergency room complaining Of Sudden and intense headache. Neurological examination evidenced meningismus. Computed tomography disclosed a subarachnoid hemorrhage (Fisher grade III). Arteriograms revealed BAA, whose neck was partially obseured by the PCP. A standard pterional craniotomy was performed, followed. by extensive drilling of the greater sphenoid wing. The neck was partially hidden by the PCP, and no proximal control was obtained without drilling the PCP and opening the CS (modified TcA). Drilling of the PCP was begun by cutting the overlying dura and extended caudally as much as possible. Next. opening, of the roof of the CS was performed by incising the dura in the oculomotor trigone medical and parallel 10 the oculomotor nerve and lateral to ICA: the incision progressed posteriorly toward the dorsum sellae. Further resection of the dorsum sellac and clivus was carried out. After performing these steps, proximal control was obtained, aneurysm was deflated, perforators were saved. and aneurysm was clipped. Conclusions: This study has demonstrated the clinical Usefulness of and abbreviated form of the TcA, which led the ""modified TcA."" in approaching complex low-lying, BAA. It provides additional surgical room by removing the PCP and partially, opening the CS, which permits further bone removal and improves exposure. (C) 2009 Elsevier Inc. All rights reserved.

Genome-wide association study of intracranial aneurysm identifies three new risk loci

Saccular intracranial aneurysms are balloon-like dilations of the intracranial arterial wall; their hemorrhage commonly results in severe neurologic impairment and death. We report a second genome-wide association study with discovery and replication cohorts from Europe and Japan comprising 5,891 cases and 14,181 controls with approximately 832,000 genotyped and imputed SNPs across discovery cohorts. We identified three new loci showing strong evidence for association with intracranial aneurysms in the combined dataset, including intervals near RBBP8 on 18q11.2 (odds ratio (OR) = 1.22, P = 1.1 x 10(-12)), STARD13-KL on 13q13.1 (OR = 1.20, P = 2.5 x 10(-9)) and a gene-rich region on 10q24.32 (OR = 1.29, P = 1.2 x 10(-9)). We also confirmed prior associations near SOX17 (8q11.23-q12.1; OR = 1.28, P = 1.3 x 10(-12)) and CDKN2A-CDKN2B (9p21.3; OR = 1.31, P = 1.5 x 10(-22)). It is noteworthy that several putative risk genes play a role in cell-cycle progression, potentially affecting the proliferation and senescence of progenitor-cell populations that are responsible for vascular formation and repair.

Repeated laser-assisted high-flow bypass for recurrent giant intracranial aneurysm

The treatment of intracranial aneurysms is changing as endovascular obliteration possibilities and long-term results are being published in regard to outcome. However, not all aneurysms are amenable to direct endovascular or surgical treatment. In such situations, a high flow bypass for flow preservation can be considered as indirect treatment alternative, enabling a trapping of the aneurysm or occlusion of the feeding artery. We present the case history of a 57 year-old patient suffering of a recurrent giant intracranial carotid aneurysm. The aneurysm could be excluded using a new cerebral high-flow bypass technique for which no temporary occlusion of any intracranial vessels is required. This technique reduces the risks of perioperative neurological complications.

Assessment of flow in perforating arteries during intracranial aneurysm surgery using intraoperative near-infrared indocyanine green videoangiography

OBJECTIVE: Perforating arteries are commonly involved during the surgical dissection and clipping of intracranial aneurysms. Occlusion of perforating arteries is responsible for ischemic infarction and poor outcome. The goal of this study is to describe the usefulness of near-infrared indocyanine green videoangiography (ICGA) for the intraoperative assessment of blood flow in perforating arteries that are visible in the surgical field during clipping of intracranial aneurysms. In addition, we analyzed the incidence of perforating vessels involved during the aneurysm surgery and the incidence of ischemic infarct caused by compromised small arteries. METHODS: Sixty patients with 64 aneurysms were surgically treated and prospectively included in this study. Intraoperative ICGA was performed using a surgical microscope (Carl Zeiss Co., Oberkochen, Germany) with integrated ICGA technology. The presence and involvement of perforating arteries were analyzed in the microsurgical field during surgical dissection and clip application. Assessment of vascular patency after clipping was also investigated. Only those small arteries that were not visible on preoperative digital subtraction angiography were considered for analysis. RESULTS: The ICGA was able to visualize flow in all patients in whom perforating vessels were found in the microscope field. Among 36 patients whose perforating vessels were visible on ICGA, 11 (30%) presented a close relation between the aneurysm and perforating arteries. In one (9%) of these 11 patients, ICGA showed occlusion of a P1 perforating artery after clip application, which led to immediate correction of the clip confirmed by immediate reestablishment of flow visible with ICGA without clinical consequences. Four patients (6.7%) presented with postoperative perforating artery infarct, three of whom had perforating arteries that were not visible or distant from the aneurysm. CONCLUSION: The involvement of perforating arteries during clip application for aneurysm occlusion is a usual finding. Intraoperative ICGA may provide visual information with regard to the patency of these small vessels.

Sequencing of TGF-beta pathway genes in familial cases of intracranial aneurysm.

BACKGROUND AND PURPOSE: Familial aggregation of intracranial aneurysms (IA) strongly suggests a genetic contribution to pathogenesis. However, genetic risk factors have yet to be defined. For families affected by aortic aneurysms, specific gene variants have been identified, many affecting the receptors to transforming growth factor-beta (TGF-beta). In recent work, we found that aortic and intracranial aneurysms may share a common genetic basis in some families. We hypothesized, therefore, that mutations in TGF-beta receptors might also play a role in IA pathogenesis. METHODS: To identify genetic variants in TGF-beta and its receptors, TGFB1, TGFBR1, TGFBR2, ACVR1, TGFBR3, and ENG were directly sequenced in 44 unrelated patients with familial IA. Novel variants were confirmed by restriction digestion analyses, and allele frequencies were analyzed in cases versus individuals without known intracranial disease. Similarly, allele frequencies of a subset of known SNPs in each gene were also analyzed for association with IA. RESULTS: No mutations were found in TGFB1, TGFBR1, TGFBR2, or ACVR1. Novel variants identified in ENG (p.A60E) and TGFBR3 (p.W112R) were not detected in at least 892 reference chromosomes. ENG p.A60E showed significant association with familial IA in case-control studies (P=0.0080). No association with IA could be found for any of the known polymorphisms tested. CONCLUSIONS: Mutations in TGF-beta receptor genes are not a major cause of IA. However, we identified rare variants in ENG and TGFBR3 that may be important for IA pathogenesis in a subset of families.

Is intracranial aneurysm rupture related to solar activity?

Objective: A number of intrinsic and extrinsic risk factors for the rupture of intracranial aneurysms have been identified. Still, the cause precipitating aneurysm rupture remains unknown in many cases. In addition, it has been observed that aneurysm ruptures are clustered in time but the trigger mechanism remains obscure. As solar activity has been associated with cardiovascular mortality and morbidity we decided to study ist association to aneurysm rupture in the Swiss population. Method: Patient data was extracted from the Swiss SOS database, at time of analysis covering 918 patients with angiography-proven aSAH treated at seven Swiss neurovascular centers between 01/01/2009 – 12/31/2011. The number of aneurysm rupture per day, week, month (Daily/Weekly/Monthly Rupture Frequency = RF) was measured and correlated to the absolute amount and the change in various parameters of interest representing continuous measurements of solar activity (radioflux (F10.7 index), solar proton flux, solar flare occurrence, planetary K-index/planetary A-index) using Poisson regression analysis. Results: Of a consecutive series of 918 cases of SAH, precise determination of the date of symptom onset was possible in 816 (88.9%). During the period of interest there were 517 days without recorded aneurysm rupture. There were 398, 139, 27 and 12 days with 1, 2, 3, and 4 ruptures per day. Five or 6 ruptures were only noted on a single day each. Poisson regression analysis demonstrated a significant correlation of F10.7 index and aneurysm rupture (incidence rate ratio (IRR) = 1.006303; standard error (SE) 0.0013201; 95% confidence interval (CI) 1.003719 – 1.008894; p<0.001), according to which every 1-unit increase of the F10.7 index increased the count for an aneurysm to rupture by 0.63%. As the F10.7 index is known to correlate well with the Space Environment Services Center (SESC) sunspot number, we performed additional analyses on SESC sunspot number and sunspot area. Here, a likewise statistically significant relationship of both the SESC sunspot number (IRR 1.003413; SE 0.0007913; 95%CI 1.001864 – 1.004965; p<0.001) and the sunspot area (IRR 1.000419; SE 0.0000866; 95%CI 1.000249 – 1.000589; p<0.001) emerged. All other variables analyzed showed no correlation with RF. Conclusions: Using valid methods, we found higher radioflux, sunspot number and sunspot area to be associated with an increased count of aneurysm rupture. Since we were using rupture frequencies rather than incidences and because we cannot explain the physiological basis of this statistical association, the clinical meaningfulness of this statistical association must be interpreted carefully. Future studies are warranted to rule out a type-1 error.

Analyse fonctionnelle de la polycystine-1 et de son domaine intracellulaire dans le développement de la polykystose rénale autosomique dominante

La polykystose rénale autosomique dominante (PKRAD) est la maladie génétique rénale la plus commune touchant 1/500 personnes. Elle se caractérise principalement par la formation de kystes rénaux dans tous les segments du néphron, entraînant l’insuffisance rénale, et par des manifestations extrarénales kystiques (foie, pancréas, rate) et non-kystiques (anomalies cardiaques, vasculaires et cérébrales). Deux gènes, PKD1 et PKD2, sont responsables de 85 et 15% des cas respectivement. Ces gènes encodent les polycystine-1 (PC-1) et -2 (PC-2) qui forment un complexe à la membrane plasmique et ciliaire des cellules épithéliales rénales. PC-1 est une protéine transmembranaire de 4302 acides aminés possédant un court domaine intracellulaire incluant un motif coiled-coil impliqué dans l’interaction entre PC-1 et PC-2 in-vitro. L’importance du coiled-coil est démontrée par des mutations affectant spécifiquement ce motif chez des patients PKRAD. Le mécanisme pathogénétique responsable de la PKRAD est indéterminé. Chez la souris, la PKRAD se développe suite à l’ablation (Pkd1-/-) ou lors de la surexpression (SBPkd1TAG) de Pkd1, ce qui suggère un effet de dosage. Des anomalies ciliaires sont aussi souvent associées à PKRAD. Mon objectif était de déterminer in-vivo le mécanisme pathogénétique de la polycystine-1 dans le développement des symptômes PKRAD rénaux et extrarénaux et plus spécifiquement, le rôle du motif coiled-coil dans le mécanisme de kystogenèse. Pour ce faire, nous avons généré deux constructions, Pkd1 sauvage (Pkd1TAG) et Pkd1 tronquée de son motif coiled-coil (Pkd1ΔCoiled-coil), par recombinaison homologue à partir du BAC-Pkd1 sauvage comprenant la séquence murine entière de Pkd1. Trois lignées de souris Pkd1TAG générées par microinjection démontrent un niveau d’expression de Pkd1 qui corrèle avec le nombre de copie du transgène (2, 5 et 15 copies). Les souris Pkd1TAG reproduisent la PKRAD en développant des kystes rénaux dans toutes les parties du néphron et des cils primaires plus longs que les contrôles non transgéniques. Les analyses physiologiques supportent que les souris Pkd1TAG développent une insuffisance rénale et démontrent une augmentation du volume urinaire de même qu’une diminution de l’osmolalité, de la créatinine et des protéines urinaires. De plus, les souris Pkd1TAG développent des kystes hépatiques, des anomalies cardiaques associées à des dépôts de calcium et des anévrismes cérébraux. La sévérité du phénotype augmente avec l’expression de Pkd1 appuyant l’hypothèse d’un mécanisme de dosage. Nous avons aussi déterminé que l’expression du transgène Pkd1TAG complémente le phénotype létal-embryonnaire des souris Pkd1-/-. D’autre part, nous avons générés 4 lignées de souris Pkd1ΔCoiled-coil (2 et 15 copies du transgène) dont le nombre de copies corrèle avec le niveau d’expression du transgène. Ces souris Pkd1ΔCoiled-coil, contrairement aux Pkd1TAG de même âge, ne développent pas de kystes et possèdent des cils primaires de longueur normale. Afin d’évaluer le rôle du motif coiled-coil en absence de polycystine-1 endogène, nous avons croisé les souris Pkd1ΔCoiled-coil avec les souris Pkd1-/-. Contrairement aux souris Pkd1-/- qui meurent in-utéro, les souris Pkd1ΔCoiled-coil; Pkd1-/- survivent ~10 à 14 jours après la naissance. Elles démontrent des kystes rénaux et pancréatiques sévères, un retard de croissance et des anomalies pulmonaires. Tous les segments du néphron sont affectés. Mon projet démontre que la surexpression de Pkd1 est un mécanisme pathogénique de la PKRAD tant au niveau rénal qu’extrarénal. De plus, il démontre que le motif coiled-coil est un élément déterminant dans la kystogenèse/PKRAD in-vivo.

Grados altos en la Escala de Fisher predicen el desarrollo de hidrocefalia en pacientes con hemorragia subaracnoidea espontanea

Objetive. To determine if high grades of Fisher scale are useful to predict the development of hydrocephalus in consecutive Colombian patients with spontaneous subarachnoid hemorrhage (SAH) assessed from January 2005 to April 2012 with 12 month follow-up. Methods. 251 patients were included in a restrospective manner. The association between Fisher scale and hydrocephalus was analyzed bivariate and multivariate analysis. In addition, a systematic literature review (SLR) was done. Results. In our cohort of patients, the etiology of SAH was due to aneurysms; 78,5%. The prevalence of hydrocephalus was found to be of 27,1%. Overall survival with a 12 month follow-up was of 65,7%. Average age of included patients was 55,5 ± 15 years, and most of them were women; 65,7%. Having Fisher 4 and Hunt-Hess III are significantly associated with hydrocephalus: adjusted OR: 2.93 95% CI: 1.51-5.65, P <0.001, adjusted OR: 2.83 95% CI: 1.31-6.17 P=0.008 respectively. The SRL showed an overall prevalence of hydrocephalus between 17 and 68% and mortality varied between 3.0% and 33%. 50% of the included studies significantly associated intraventricular hemorrhage ( Fisher 4) with hydrocephalus. Conclusion. Our results confirm current concepts on post-SAH hydrocephalus and the fact that is obstructive and secondary to Fisher 4 and having neurological impairment on admission (Hunt and Hess III).

Tratamiento de la hipertensión arterial en accidente cerebrovascular

Revisión sistemática de la literatura en la que se discuten las controversias del manejo de la presión arterial en las emergencias neurológicas agudas cerebrovasculares como accidente cerebrovascular isquémico, hemorrágico y hemorragia subaracnoidea.

Escala de Fisher como factor predictor de hidrocefalia en hemorragia subaracnoidea espontanea

Objetivo. Determinar si la cantidad de sangre y su localización es el espacio subaracnoideo, medible con la escala de Fisher en las primeras 24 horas de ocurrido el ictus hemorrágico, es un factor predictor para el desarrollo de hidrocefalia en pacientes con diagnóstico de hemorragia subaracnoidea (HSA) espontánea, vistos en el Hospital Universitario Clínica San Rafael (HUCSR) con seguimiento de 12 meses. Métodos. 251 pacientes fueron incluidos en una cohorte retrospectiva. La asociación entre la escala de Fisher y el desarrollo de hidrocefalia en pacientes con HSA espontánea fue analizada a través de un análisis bivariado y multivariado. Resultados. La edad promedio de los pacientes fue de 55,5 ± 15 años; con predominancia en el sexo femenino 65,7%. La prevalencia de hidrocefalia fue de 27,1% en la cohorte y la etiología de la HSA fue en su mayoría por ruptura de aneurismas de arterias cerebrales; 78,5%. La sobrevida a 12 meses fue de 65,7%. Tanto el grado 4 en la escala de Fisher como Hunt-Hess III se asocian con el desarrollo de hidrocefalia: ORA; 2.93 IC 95%: 1.51-5.65, P <0.001, ORA 2.83 IC 95%: 1.31-6.17 P=0.008 respectivamente. Conclusión. La presencia de sangrado Intraventricular o intraparenquimatoso ( Fisher 4) en las primeras 24 horas, asociado a un deterioro neurológico al ingreso Hunt-Hess III están asociados con el desarrollo de hidrocefalia en los 251 pacientes evaluados con diagnóstico de HSA espontánea; hallazgos consistentes con lo reportado en la literatura mundial.