Lumbar puncture for treating acute hydrocephalus after aneurysmal subarachnoid haemorrhage.

BACKGROUND: External ventricular drainage (EVD) for acute hydrocephalus after aneurysmal subarachnoid haemorrhage (aSAH) carries a risk of complications. We studied the proportion of patients in whom EVD can be avoided by treating acute hydrocephalus with ≥1 lumbar punctures (LP). METHODS: From a prospectively collected database, we retrieved data on all aSAH patients admitted between 2007 and 2017 who developed acute hydrocephalus (i.e. neurological deterioration and ventricular enlargement <72 h after aSAH). Our regime is to consider LP as initial treatment. We calculated the proportions of patients (with corresponding 95% confidence interval (CI)) who improved after the initial LP and the extent of clinical improvement, the proportions of patients who were treated with only ≥1 LP(s), and those of patients needing continuous external ventricular or external lumbar drainage, or permanent ventriculoperitoneal or lumboperitoneal drainage. RESULTS: Of 1391 consecutive aSAH patients, 473 (34%) had acute hydrocephalus, of whom 388 (82%) were treated. Of the 86 patients with LP as initial treatment, 70 (81% [95% CI 72-88]) showed initial improvement (with increase in median Glasgow Coma Score from 10 (IQR 7-12) to 12 (IQR 9-14) after initial LP), 39 (45% [95% CI 35-56]) improved with LP only, 41 (48% [95% CI 37-58]) needed continuous drainage and six (7% [95% CI 3-14]) needed permanent drainage. CONCLUSION: Around half the patients treated with LP for deterioration from acute hydrocephalus after aSAH does not require continuous extraventicular or extralumbar drainage.

Pulsatility Attenuation along the Carotid Siphon in Pseudoxanthoma Elasticum.

We compared velocity pulsatility, distensibility, and pulsatility attenuation along the intracranial ICA and MCA between 50 patients with pseudoxanthoma elasticum and 40 controls. Patients with pseudoxanthoma elasticum had higher pulsatility and lower distensibility at all measured locations, except for a similar distensibility at C4. The pulsatility attenuation over the siphon was similar between patients with pseudoxanthoma elasticum and controls. This finding suggests that other disease mechanisms are the main contributors to increased intracranial pulsatility in pseudoxanthoma elasticum.

Prediction of Outcome Using Quantified Blood Volume in Aneurysmal SAH.

BACKGROUND AND PURPOSE: In patients with SAH, the amount of blood is strongly associated with clinical outcome. However, it is commonly estimated with a coarse grading scale, potentially limiting its predictive value. Therefore, we aimed to develop and externally validate prediction models for clinical outcome, including quantified blood volumes, as candidate predictors. MATERIALS AND METHODS: Clinical and radiologic candidate predictors were included in a logistic regression model. Unfavorable outcome was defined as a modified Rankin Scale score of 4-6. An automatic hemorrhage-quantification algorithm calculated the total blood volume. Blood was manually classified as cisternal, intraventricular, or intraparenchymal. The model was selected with bootstrapped backward selection and validated with the R 2, C-statistic, and calibration plots. If total blood volume remained in the final model, its performance was compared with models including location-specific blood volumes or the modified Fisher scale. RESULTS: The total blood volume, neurologic condition, age, aneurysm size, and history of cardiovascular disease remained in the final models after selection. The externally validated predictive accuracy and discriminative power were high (R 2 = 56% ± 1.8%; mean C-statistic = 0.89 ± 0.01). The location-specific volume models showed a similar performance (R 2 = 56% ± 1%, P = .8; mean C-statistic = 0.89 ± 0.00, P = .4). The modified Fisher models were significantly less accurate (R 2 = 45% ± 3%, P < .001; mean C-statistic = 0.85 ± 0.01, P = .03). CONCLUSIONS: The total blood volume-based prediction model for clinical outcome in patients with SAH showed a high predictive accuracy, higher than a prediction model including the commonly used modified Fisher scale.

Gadolinium Enhancement of the Aneurysm Wall in Unruptured Intracranial Aneurysms Is Associated with an Increased Risk of Aneurysm Instability: A Follow-Up Study.

BACKGROUND AND PURPOSE: Previous studies have suggested that gadolinium enhancement of the wall of unruptured intracranial aneurysms on MR imaging may reflect aneurysm wall instability. However, all previous studies were cross-sectional. In this longitudinal study, we investigated whether aneurysm wall enhancement is associated with an increased risk of aneurysm instability. MATERIALS AND METHODS: We included all patients 18 years of age or older with ≥1 unruptured aneurysm from the University Medical Center Utrecht, the Netherlands, who were included in 2 previous studies with either 3T or 7T aneurysm wall MR imaging and for whom it was decided not to treat the aneurysm but to monitor it with follow-up imaging. We investigated the risk of growth or rupture during follow-up of aneurysms with and without gadolinium enhancement of the aneurysm wall at baseline and calculated the risk difference between the 2 groups with corresponding 95% confidence intervals. RESULTS: We included 57 patients with 65 unruptured intracranial aneurysms. After a median follow-up of 27 months (interquartile range, 20-31 months), growth (n = 2) or rupture (n = 2) was observed in 4 of 19 aneurysms (21%; 95% CI, 6%-54%) with wall enhancement and in zero of 46 aneurysms (0%; 95% CI, 0%-8%) without enhancement (risk difference, 21%; 95% CI, 3%-39%). CONCLUSIONS: Gadolinium enhancement of the aneurysm wall on MR imaging is associated with an increased risk of aneurysm instability. The absence of wall enhancement makes it unlikely that the aneurysm will grow or rupture in the short term. Larger studies are needed to investigate whether aneurysm wall enhancement is an independent predictor of aneurysm instability.

The relationship between ischaemic brain lesions and cognitive outcome after aneurysmal subarachnoid haemorrhage.

BACKGROUND: Cerebral ischaemia is thought to be an important determinant of cognitive outcome after aneurysmal subarachnoid haemorrhage (aSAH), but the exact relationship is unclear. We studied the effect of ischaemic brain lesions during clinical course on cognitive outcome 2 months after aSAH. METHODS: We studied 74 consecutive patients admitted to the University Medical Center Utrecht who had MRI post-coiling (3-21 days post-aSAH) and neuropsychological examination at 2 months. An ischaemic lesion was defined as hyperintensity on T2-FLAIR and DWI images. We measured both cognitive complaints (subjective) and cognitive functioning (objective). The relationship between ischaemic brain lesions and cognitive outcome was analysed by logistic regression analyses. RESULTS: In 40 of 74 patients (54%), 152 ischaemic lesions were found. The median number of lesions per patient was 2 (1-37) and the median total lesion volume was 0.2 (0-17.4) mL. No difference was found between the group with and the group without ischaemic lesions with respect to the frequency of cognitive complaints. In the group with ischaemic lesions, significantly more patients (55%) showed poor cognitive functioning compared to the group without ischaemic lesions (26%) (OR 3.4, 95% CI 1.3-9.1). We found no relationship between the number and volume of the ischaemic lesions and cognitive functioning. CONCLUSIONS: Ischaemic brain lesions detected on MRI during clinical course after aSAH is a marker for poor cognitive functioning 2 months after aSAH, irrespective of the number or volume of the ischaemic lesions. Network or connectivity studies are needed to better understand the relationship between location of the ischaemic brain lesions and cognitive functioning.

Effect of magnesium on cognition after aneurysmal subarachnoid haemorrhage in a randomized trial.

BACKGROUND AND PURPOSE: In randomized trials magnesium supplementation did not improve clinical outcome after aneurysmal subarachnoid haemorrhage (aSAH) on handicap scales. After aSAH, many patients have cognitive problems that may not translate into handicap. The effect of magnesium on cognitive outcome after aSAH was studied. METHODS: In total, 209 patients who had been included in the Magnesium for Aneurysmal Subarachnoid Haemorrhage (MASH-2) trial in the University Medical Centre of Utrecht were studied. Patients had been randomized to 64 mmol magnesium sulfate daily or placebo during hospitalization. Three months after aSAH patients underwent a neuropsychological examination (NPE) consisting of six neuropsychological tests or a brief cognitive assessment. Poisson and linear regression analyses were used to analyse the effect of magnesium on cognition. RESULTS: In the magnesium group 53 (49.5%) of the 107 patients and in the placebo group 51 (50.0%) of the 102 patients scored lower than the median cognitive score [relative risk 0.99, 95% confidence interval (CI) 0.76-1.30]. Linear regression analyses showed no significant relationship between intervention and cognition (B = 0.05, 95% CI -0.15 to 0.33). CONCLUSIONS: Treatment with magnesium has no effect on cognitive outcome after aSAH.

Experience of a single center in the conservative approach of 20 consecutive cases of asymptomatic extracranial carotid artery aneurysms.

BACKGROUND AND PURPOSE: The clinical course and optimal treatment strategy for asymptomatic extracranial carotid artery aneurysms (ECAAs) are unknown. We report our single-center experience with conservative management of patients with an asymptomatic ECAA. METHODS: A search in our hospital records from 1998 to 2013 revealed 20 patients [mean age 52 (SD 12.5) years] with 23 ECAAs, defined as a 150% or more fusiform dilation or any saccular dilatation compared with the healthy internal carotid artery. None of the aneurysms were treated and we had no pre-defined follow-up schedule for these patients. The primary study end-point was the yearly rate for ipsilateral ischemic stroke. Secondary end-points were ipsilateral transient ischemic attack, any stroke-related death, other symptoms related to the aneurysm or growth defined as any diameter increase. RESULTS: The ECAA was either fusiform (n = 6; mean diameter 10.2 mm) or saccular (n = 17; mean diameter 10.9 mm). Eleven (55%) patients with 13 ECAAs received antithrombotic medication. During follow-up [median 46.5 (range 1-121) months], one patient died due to ipsilateral stroke and the ipsilateral cerebral stroke rate was 1.1 per 100 patient-years (95% confidence interval, 0.01-6.3). Three patients had ECAA growth, two of whom were asymptomatic and one was the patient who suffered a stroke. CONCLUSIONS: In this retrospective case series of patients with an asymptomatic ECAA, the risk of cerebral infarction is small but not negligible. Conservative management seems justified, in particular in patients without growth. Large prospective registry data are necessary to assess follow-up imaging strategies and the role of antiplatelet therapy.

Association of Quantified Location-Specific Blood Volumes with Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND AND PURPOSE: Delayed cerebral ischemia is a severe complication of aneurysmal SAH and is associated with a high case morbidity and fatality. The total blood volume and the presence of intraventricular blood on CT after aneurysmal SAH are associated with delayed cerebral ischemia. Whether quantified location-specific (cisternal, intraventricular, parenchymal, and subdural) blood volumes are associated with delayed cerebral ischemia has been infrequently researched. This study aimed to associate quantified location-specific blood volumes with delayed cerebral ischemia. MATERIALS AND METHODS: Clinical and radiologic data were collected retrospectively from consecutive patients with aneurysmal SAH with available CT scans within 24 hours after ictus admitted to 2 academic centers between January 2009 and December 2011. Total blood volume was quantified using an automatic hemorrhage-segmentation algorithm. Segmented blood was manually classified as cisternal, intraventricular, intraparenchymal, or subdural. Adjusted ORs with 95% confidence intervals for delayed cerebral ischemia per milliliter of location-specific blood were calculated using multivariable logistic regression analysis. RESULTS: We included 282 patients. Per milliliter increase in blood volume, the adjusted OR for delayed cerebral ischemia was 1.02 (95% CI, 1.01-1.04) for cisternal, 1.02 (95% CI, 1.00-1.04) for intraventricular, 0.99 (95% CI, 0.97-1.02) for intraparenchymal, and 0.96 (95% CI, 0.86-1.07) for subdural blood. CONCLUSIONS: Our findings suggest that in patients with aneurysmal subarachnoid hemorrhage, the cisternal blood volume has a stronger relation with delayed cerebral ischemia than the blood volumes at other locations in the brain.

Quantification of Intracranial Aneurysm Volume Pulsation with 7T MRI.

BACKGROUND AND PURPOSE: Aneurysm volume pulsation is a potential predictor of intracranial aneurysm rupture. We evaluated whether 7T MR imaging can quantify aneurysm volume pulsation. MATERIALS AND METHODS: In Stage I of the study, 10 unruptured aneurysms in 9 patients were studied using a high-resolution (0.6-mm, isotropic) 3D gradient-echo sequence with cardiac gating. Semiautomatic segmentation was used to measure aneurysm volume (in cubic millimeters) per cardiac phase. Aneurysm pulsation was defined as the relative increase in volume between the phase with the smallest volume and the phase with the largest volume. The accuracy and precision of the measured volume pulsations were addressed by digital phantom simulations and a repeat image analysis. In Stage II, the imaging protocol was optimized and 9 patients with 9 aneurysms were studied with and without administration of a contrast agent. RESULTS: The mean aneurysm pulsation in Stage I was 8% ± 7% (range, 2%-27%), with a mean volume change of 15 ± 14 mm3 (range, 3-51 mm3). The mean difference in volume change for the repeat image analysis was 2 ± 6 mm3. The artifactual volume pulsations measured with the digital phantom simulations were of the same magnitude as the volume pulsations observed in the patient data, even after protocol optimization in Stage II. CONCLUSIONS: Volume pulsation quantification with the current imaging protocol on 7T MR imaging is not accurate due to multiple imaging artifacts. Future studies should always include aneurysm-specific accuracy analysis.

Prevalence of extracranial carotid artery aneurysms in patients with an intracranial aneurysm.

BACKGROUND AND PURPOSE: Aneurysms in various arterial beds have common risk- and genetic factors. Data on the correlation of extracranial carotid artery aneurysms (ECAA) with aneurysms in other vascular territories are lacking. We aimed to investigate the prevalence of ECAA in patients with an intracranial aneurysm (IA). METHODS: We used prospectively collected databases of consecutive patients registered at the University Medical Center Utrecht with an unruptured intracranial aneurysm (UIA) or aneurysmal Subarachnoid hemorrhage (SAH). The medical files of patients included in both databases were screened for availability of radiological reports, imaging of the brain and of the cervical carotid arteries. All available radiological images were then reviewed primarily for the presence of an ECAA and secondarily for an extradural/cavernous carotid or vertebral artery aneurysm. An ECAA was defined as a fusiform dilation ≥150% of the normal internal or common carotid artery or a saccular distention of any size. RESULTS: We screened 4465 patient records (SAH database n = 3416, UIA database n = 1049), of which 2931 had radiological images of the carotid arteries available. An ECAA was identified in 12/638 patients (1.9%; 95% CI 1.1-3.3) with completely imaged carotid arteries and in 15/2293 patients (0.7%; 95% CI 0.4-1.1) with partially depicted carotid arteries. Seven out of 27 patients had an additional extradural (cavernous or vertebral artery) aneurysm. CONCLUSIONS: This comprehensive study suggests a prevalence for ECAA of approximately 2% of patients with an IA. The rarity of the disease makes screening unnecessary so far. Future registry studies should study the factors associated with IA and ECAA to estimate the prevalence of ECAA in these young patients more accurately.

A strategy to expeditious invasive treatment improves clinical outcome in comatose patients with aneurysmal subarachnoid haemorrhage.

BACKGROUND: In patients with poor clinical condition after aneurysmal subarachnoid haemorrhage (aSAH), treatment is often deferred until patients show signs of improvement. Early external ventricular drainage and aneurysm occlusion may improve prognosis also in poor grade patients. The clinical outcome of an expeditious approach was compared with that of a conservative approach. METHODS: In all, 285 consecutive World Federation of Neurological Surgeons (WFNS) grade V aSAH patients admitted to three university hospitals between January 2000 and June 2007 were included. Two hospitals followed an expeditious approach, one a more conservative approach. Groups were compared with respect to demographic and clinical characteristics and outcome. Univariable and multivariable analyses were performed to determine the associations with good outcome (Glasgow Outcome Scale scores 4-5), using logistic regression models. RESULTS: Good outcome was seen more often in expeditiously treated patients [22% vs. 11%; odds ratio (OR) 2.24, 95% confidence interval (CI) 1.17-4.27]. Expeditiously treated patients more often underwent aneurysm occlusion than conservatively treated patients (64% vs. 27%; OR 4.86, 95% CI 2.93-8.05) and placement of an external ventricular catheter (82% vs. 31%; OR 10.05, CI 5.72-10.66). There was no significant difference in rebleeding between patient groups. Occlusion of the aneurysm was the only variable that remained significant in the multivariable model with an OR of 43.73 (95% CI 10.34-184.97). CONCLUSIONS: An expeditious invasive treatment strategy in WFNS grade V aSAH patients can lead to a better outcome. Hesitance in the early stages seems a self-fulfilling prophecy for a poor outcome.

Thinner Regions of Intracranial Aneurysm Wall Correlate with Regions of Higher Wall Shear Stress: A 7T MRI Study.

BACKGROUND AND PURPOSE: Both hemodynamics and aneurysm wall thickness are important parameters in aneurysm pathophysiology. Our aim was to develop a method for semi-quantitative wall thickness assessment on in vivo 7T MR images of intracranial aneurysms for studying the relation between apparent aneurysm wall thickness and wall shear stress. MATERIALS AND METHODS: Wall thickness was analyzed in 11 unruptured aneurysms in 9 patients who underwent 7T MR imaging with a TSE-based vessel wall sequence (0.8-mm isotropic resolution). A custom analysis program determined the in vivo aneurysm wall intensities, which were normalized to the signal of nearby brain tissue and were used as measures of apparent wall thickness. Spatial wall thickness variation was determined as the interquartile range in apparent wall thickness (the middle 50% of the apparent wall thickness range). Wall shear stress was determined by using phase-contrast MR imaging (0.5-mm isotropic resolution). We performed visual and statistical comparisons (Pearson correlation) to study the relation between wall thickness and wall shear stress. RESULTS: 3D colored apparent wall thickness maps of the aneurysms showed spatial apparent wall thickness variation, which ranged from 0.07 to 0.53, with a mean variation of 0.22 (a variation of 1.0 roughly means a wall thickness variation of 1 voxel [0.8 mm]). In all aneurysms, apparent wall thickness was inversely related to wall shear stress (mean correlation coefficient, -0.35; P < .05). CONCLUSIONS: A method was developed to measure the wall thickness semi-quantitatively, by using 7T MR imaging. An inverse correlation between wall shear stress and apparent wall thickness was determined. In future studies, this noninvasive method can be used to assess spatial wall thickness variation in relation to pathophysiologic processes such as aneurysm growth and rupture.

Early Magnesium Treatment After Aneurysmal Subarachnoid Hemorrhage: Individual Patient Data Meta-Analysis.

BACKGROUND AND PURPOSE: Delayed cerebral ischemia (DCI) is an important cause of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). Trials of magnesium treatment starting <4 days after symptom onset found no effect on poor outcome or DCI in SAH. Earlier installment of treatment might be more effective, but individual trials had not enough power for such a subanalysis. We performed an individual patient data meta-analysis to study whether magnesium is effective when given within different time frames within 24 hours after the SAH. METHODS: Patients were divided into categories according to the delay between symptom onset and start of the study medication: <6, 6 to 12, 12 to 24, and >24 hours. We calculated adjusted risk ratios with corresponding 95% confidence intervals for magnesium versus placebo treatment for poor outcome and DCI. RESULTS: We included 5 trials totaling 1981 patients; 83 patients started treatment<6 hours. For poor outcome, the adjusted risk ratios of magnesium treatment for start <6 hours were 1.44 (95% confidence interval, 0.83-2.51); for 6 to 12 hours 1.03 (0.65-1.63), for 12 to 24 hours 0.84 (0.65-1.09), and for >24 hours 1.06 (0.87-1.31), and for DCI, <6 hours 1.76 (0.68-4.58), for 6 to 12 hours 2.09 (0.99-4.39), for 12 to 24 hours 0.80 (0.56-1.16), and for >24 hours 1.08 (0.88-1.32). CONCLUSIONS: This meta-analysis suggests no beneficial effect of magnesium treatment on poor outcome or DCI when started early after SAH onset. Although the number of patients was small and a beneficial effect cannot be definitively excluded, we found no justification for a new trial with early magnesium treatment after SAH.

Outcome after intracranial haemorrhage from dural arteriovenous fistulae; a systematic review and case-series.

Dural arteriovenous fistulae (DAVFs) are a rare cause of intracranial haemorrhage. We aimed to investigate outcome of patients with intracranial haemorrhage from a DAVF. We performed a systematic literature search for studies reporting outcome after intracranial haemorrhage caused by a DAVF. We used predefined selection criteria and assessed the quality of the studies. In addition, we studied outcome in all patients with DAVF who had presented with intracranial haemorrhage at two university centers in the Netherlands, between January 2007 and April 2012. We calculated case fatality and proportions of patients with poor outcome (defined as modified Rankin Scale ≥ 3 or Glasgow Outcome Scale ≤ 3) during follow-up. We investigated mean age, sex, mid-year of study and percentage of patients with parenchymal haemorrhage as determinants of case fatality and poor outcome. The literature search yielded 16 studies, all but two retrospective and all hospital-based. Combined with our cohort of 29 patients the total number of patients with DAVF-related intracranial haemorrhage was 326 (58% intracerebral haemorrhage). At a median follow-up of 12 months case fatality was 4.7% (95% CI 2.5-7.5; 17 cohorts) and the proportion of patients with poor outcome 8.3% (95% CI 3.1-15.7; nine cohorts). We found no effect of mean age, sex, mid-year of the cohorts and percentage of patients with parenchymal haemorrhage on either outcome. Hospital based case-series suggest a relatively low risk of death and poor outcome in patients with intracranial haemorrhage due to rupture of a DAVF. These risks may be underestimated because of bias.

Additional Value of Intra-Aneurysmal Hemodynamics in Discriminating Ruptured versus Unruptured Intracranial Aneurysms.

BACKGROUND AND PURPOSE: Hemodynamics are thought to play an important role in the rupture of intracranial aneurysms. We tested whether hemodynamics, determined from computational fluid dynamics models, have additional value in discriminating ruptured and unruptured aneurysms. Such discriminative power could provide better prediction models for rupture. MATERIALS AND METHODS: A cross-sectional study was performed on patients eligible for endovascular treatment, including 55 ruptured and 62 unruptured aneurysms. Association with rupture status was tested for location, aneurysm type, and 4 geometric and 10 hemodynamic parameters. Patient-specific spatiotemporal velocities measured with phase-contrast MR imaging were used as inflow conditions for computational fluid dynamics. To assess the additional value of hemodynamic parameters, we performed 1 univariate and 2 multivariate analyses: 1 traditional model including only location and geometry and 1 advanced model that included patient-specific hemodynamic parameters. RESULTS: In the univariate analysis, high-risk locations (anterior cerebral arteries, posterior communicating artery, and posterior circulation), daughter sacs, unstable inflow jets, impingements at the aneurysm body, and unstable complex flow patterns were significantly present more often in ruptured aneurysms. In both multivariate analyses, only the high-risk location (OR, 3.92; 95% CI, 1.77-8.68) and the presence of daughter sacs (OR, 2.79; 95% CI, 1.25-6.25) remained as significant independent determinants. CONCLUSIONS: In this study population of patients eligible for endovascular treatment, we found no independent additional value of aneurysmal hemodynamics in discriminating rupture status, despite high univariate associations. Only traditional parameters (high-risk location and the presence of daughter sacs) were independently associated with ruptured aneurysms.

Hemodynamic Differences in Intracranial Aneurysms before and after Rupture.

BACKGROUND AND PURPOSE: Rupture risk of intracranial aneurysms may depend on hemodynamic characteristics. This has been assessed by comparing hemodynamic data of ruptured and unruptured aneurysms. However, aneurysm geometry may change before, during, or just after rupture; this difference causes potential changes in hemodynamics. We assessed changes in hemodynamics in a series of intracranial aneurysms, by using 3D imaging before and after rupture. MATERIALS AND METHODS: For 9 aneurysms in 9 patients, we used MRA, CTA, and 3D rotational angiography before and after rupture to generate geometric models of the aneurysm and perianeurysmal vasculature. Intra-aneurysmal hemodynamics were simulated by using computational fluid dynamics. Two neuroradiologists qualitatively assessed flow complexity, flow stability, inflow concentration, and flow impingement in consensus, by using flow-velocity streamlines and wall shear stress distributions. RESULTS: Hemodynamics changed in 6 of the 9 aneurysms. The median time between imaging before and after rupture was 678 days (range, 14-1461 days) in these 6 cases, compared with 151 days (range, 34-183 days) in the 3 cases with unaltered hemodynamics. Changes were observed for flow complexity (n = 3), flow stability (n = 3), inflow concentration (n = 2), and region of flow impingement (n = 3). These changes were in all instances associated with aneurysm displacement due to rupture-related hematomas, growth, or newly formed lobulations. CONCLUSIONS: Hemodynamic characteristics of intracranial aneurysms can be altered by geometric changes before, during, or just after rupture. Associations of hemodynamic characteristics with aneurysm rupture obtained from case-control studies comparing ruptured with unruptured aneurysms should therefore be interpreted with caution.

Management of extracranial carotid artery aneurysm.

INTRODUCTION: Aneurysms of the extracranial carotid artery (ECAA) are rare. Several treatments have been developed over the last 20 years, yet the preferred method to treat ECAA remains unknown. This paper is a review of all available literature on the risk of complications and long-term outcome after conservative or invasive treatment of patients with ECAA. METHODS: Reports on ECAA treatment until July 2014 were searched in PubMed and Embase using the key words aneurysm, carotid, extracranial, and therapy. RESULTS: A total of 281 articles were identified. Selected articles were case reports (n = 179) or case series (n = 102). Papers with fewer than 10 patients were excluded, resulting in the final selection of 39 articles covering a total of 1,239 patients. Treatment consisted of either conservative treatment in 11% of the cases or invasive treatment in 89% of the cases. Invasive treatment comprised surgery in 94%, endovascular approach in 5%, and a hybrid approach in 1% of the patients. The most common complication described after invasive therapy was cranial nerve damage, which occurred in 11.8% of patients after surgery. The 30 day mortality rate and stroke rate in conservatively treated patients was 4.67% and 6.67%, after surgery 1.91% and 5.16%. Information on confounders in the present study was incomplete. Therefore, adjustments to correct for confounding by indication could not be done. CONCLUSIONS: This review summarizes the largest available series in the literature on ECAA management. The number of ECAAs reported in current literature is scarce. The early and long-term outcome of invasive treatment in ECAA is favorable; however, cranial nerve damage after surgery occurs frequently. Unfortunately, due to limitations in reporting of results and confounding by indication in the available literature, it was not possible to determine the optimal treatment strategy. There is a need for a multicenter international registry to reveal the optimal treatment for ECAA.

Evaluation of genetic risk loci for intracranial aneurysms in sporadic arteriovenous malformations of the brain.

BACKGROUND: In genome-wide association studies (GWAS) five putative risk loci are associated with intracranial aneurysm. As brain arteriovenous malformations (AVM) and intracranial aneurysms are both intracranial vascular diseases and AVMs often have associated aneurysms, we investigated whether these loci are also associated with sporadic brain AVM. METHODS: We included 506 patients (168 Dutch, 338 American) and 1548 controls, all Caucasians. Controls had been recruited as part of previous GWAS. Dutch patients were genotyped by KASPar assay and US patients by Affymetrix SNP 6.0 array. Associations in each cohort were tested by univariable logistic regression modelling, with subgroup analysis in 205 American cases with aneurysm data. Meta-analysis was performed by a Mantel-Haenszel fixed-effect method. RESULTS: In the Dutch cohort none of the single nucleotide polymorphisms (SNPs) were associated with AVMs. In the American cohort, genotyped SNPs near SOX-17 (OR 0.74; 95% CI 0.56-0.98), RBBP8 (OR 0.76; 95% CI 0.62-0.94) and an imputed SNP near CDKN2B-AS1 (OR 0.79; 95% CI 0.64-0.98) were significantly associated with AVM. The association with SNPs near SOX-17 and CDKN2B-AS1 but not RBBP8 were strongest in patients with AVM with associated aneurysms. In the meta-analysis we found no significant associations between allele frequencies and AVM occurrence, but rs9298506, near SOX-17 approached statistical significance (OR 0.77; 95% CI 0.57-1.03, p=0.08). CONCLUSIONS: Our meta-analysis of two Caucasian cohorts did not show an association between five aneurysm-associated loci and sporadic brain AVM. Possible involvement of SOX-17 and RBBP8, genes involved in cell cycle progression, deserves further investigation.