Search

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.

Introduction First-degree relatives of patients with familial aneurysmal subarachnoid hemorrhage have an increased risk of unruptured intracranial aneurysms and aneurysmal subarachnoid hemorrhage. We assessed whether the type of kinship of first-degree relatives of aneurysmal subarachnoid hemorrhage patients influences this risk. Patients and methods We used all available data from the prospectively collected database of families consulting our outpatient clinic between 1994-2016. We constructed pedigrees for all families with ≥2 first-degree relatives with aneurysmal subarachnoid hemorrhage or unruptured intracranial aneurysms. The proband was defined as the first family member with aneurysmal subarachnoid hemorrhage who sought medical attention. We compared both the proportion of aneurysmal subarachnoid hemorrhage and unruptured intracranial aneurysms in proband's first-degree relatives by calculating relative risks (RR) with children as the reference. Results We studied 154 families with 1,105 first-degree relatives of whom 146 had aneurysmalsubarachnoid hemorrhage. Unruptured intracranial aneurysms were identified in 63 (19%) of the 326 screened relatives. Siblings had a higher risk of aneurysmal subarachnoid hemorrhage (RR:1.62, 95% CI:1.12–2.38) and parents a lower risk (RR:0.44, 95% CI:0.24–0.81) than children. Siblings also had a higher risk of unruptured intracranial aneurysms (RR:2.28, 95% CI:1.23–4.07, age-adjusted RR:2.04, 95% CI:1.07–3.92) than children. Conclusion: Siblings of patients with aneurysmal subarachnoid hemorrhage have a significanthigher risk of both unruptured intracranial aneurysms and aneurysmal subarachnoid hemorrhage and parents have a lower risk of aneurysmal subarachnoid hemorrhage than children. Discussion: Type of kinship is a relevant factor to consider in risk prediction and screening advice in families with familial aneurysmal subarachnoid hemorrhage.

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.

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.

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.

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.

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 mm 3 (range, 3–51 mm 3 ). The mean difference in volume change for the repeat image analysis was 2 ± 6 mm 3 . 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.

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.

BACKGROUND AND PURPOSE: Comparisons of geometric data of ruptured and unruptured aneurysms may yield risk factors for rupture. Data on changes of geometric measures associated with rupture are, however, sparse, because patients with ruptured aneurysms rarely have undergone previous imaging of the intracranial vasculature. We had the opportunity to assess 3D geometric differences of aneurysms before and after rupture. The purpose of this study was to evaluate possible differences between prerupture and postrupture imaging of a ruptured intracranial aneurysm. MATERIALS AND METHODS: Using high-quality 3D image data, we generated 3D geometric models before and after rupture and compared these for changes in aneurysm volume and displacement. A neuroradiologist qualitatively assessed aneurysm shape change, the presence of perianeurysmal hematoma, and subsequent mass effect exerted on aneurysm and parent vessels. RESULTS: Aneurysm volume was larger in the postrupture imaging in 7 of 9 aneurysms, with a median increase of 38% and an average increase of 137%. Three aneurysms had new lobulations on postrupture imaging; 2 other aneurysms were displaced up to 5 mm and had changed in geometry due to perianeurysmal hematoma. CONCLUSIONS: Geometric comparisons of aneurysms before and after rupture show a large volume increase, origination of lobulations, and displacement due to perianeurysmal hematoma. Geometric and hemodynamic comparison of series of unruptured and ruptured aneurysms in the search for rupture-risk-related factors should be interpreted with caution.

BACKGROUND AND PURPOSE: The total amount of extravasated blood after aneurysmal subarachnoid hemorrhage, assessed with semiquantitative methods such as the modified Fisher and Hijdra scales, is known to be a predictor of delayed cerebral ischemia. However, prediction rates of delayed cerebral ischemia are moderate, which may be caused by the rough and observer-dependent blood volume estimation used in the prediction models. We therefore assessed the association between automatically quantified total blood volume on NCCT and delayed cerebral ischemia. MATERIALS AND METHODS: We retrospectively studied clinical and radiologic data of consecutive patients with aneurysmal SAH admitted to 2 academic hospitals between January 2009 and December 2011. Adjusted ORs with associated 95% confidence intervals were calculated for the association between automatically quantified total blood volume on NCCT and delayed cerebral ischemia (clinical, radiologic, and both). The calculations were also performed for the presence of an intraparenchymal hematoma and/or an intraventricular hematoma and clinical delayed cerebral ischemia. RESULTS: We included 333 patients. The adjusted OR of total blood volume for delayed cerebral ischemia (clinical, radiologic, and both) was 1.02 (95% CI, 1.01–1.03) per milliliter of blood. The adjusted OR for the presence of an intraparenchymal hematoma for clinical delayed cerebral ischemia was 0.47 (95% CI, 0.24–0.95) and of the presence of an intraventricular hematoma, 2.66 (95% CI, 1.37–5.17). CONCLUSIONS: A higher total blood volume measured with our automated quantification method is significantly associated with delayed cerebral ischemia. The results of this study encourage the use of rater-independent quantification methods in future multicenter studies on delayed cerebral ischemia prevention and prediction.

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.

In patients with sudden severe headache and a negative computed tomography (CT) scan, a lumbar puncture (LP) is performed to rule in or out a subarachnoid haemorrhage (SAH), but this procedure is under debate. In a hospital-based series of 30 patients with sudden headache, a negative CT scan but a positive LP (defined as detection of bilirubin >0.05 at wavelength 458 nm), we studied the chance of harbouring an aneurysm and the clinical outcome. Aneurysms were found in none of both patients who presented within 3 days, in 8 of the 18 (44%) who presented within 4–7 days and in 5 of the 10 (50%) who presented within 8–14 days. Of the 13 patients with an aneurysm, 3 (23%) had poor outcome. In patients who present late after sudden headache, the yield in terms of aneurysms is high in those who have a positive lumbar puncture. In patients with an aneurysm as cause of the positive lumbar puncture, outcome is in the same range as in SAH patients admitted in good clinical condition.

Background: To investigate the prevalence of cognitive complaints after subarachnoid hemorrhage (SAH) and the relationships between cognitive complaints and cognitive impairments, disability and emotional problems. Methods: Cognitive complaints were assessed with the Checklist for Cognitive and Emotional Consequences following stroke (CLCE-24) in 111 persons who visited our outpatient clinic 3 months after SAH. Associations between cognitive complaints and cognitive functioning, demographic characteristics, disability and emotional problems were examined using Spearman correlations and linear regression analysis. Results: In this study group, 105 patients (94.6%) reported at least one cognitive or emotional complaint that hampered everyday functioning. The most frequently reported cognitive complaints were mental slowness, short-term memory problems and attention deficits. All cognitive domains, disability, depressive symptoms and feelings of anxiety were significantly associated with the CLCE-24 cognition score. In the final regression model, memory functioning (β value –0.21), disability (–0.28) and depressive symptoms (0.40) were significant determinants of cognitive complaints, together explaining 35.4% of the variance. Conclusion: Cognitive complaints are common after SAH and associated with memory deficits, disability and depressive symptoms. Rehabilitation programs should focus on these symptoms and deficits.

BACKGROUND AND PURPOSE: MR angiography (MRA) is increasingly used as a noninvasive imaging technique for the follow-up of coiled intracranial aneurysms. However, the need for contrast enhancement has not yet been elucidated. We compared 3D time-of-flight MRA (TOF-MRA) and contrast-enhanced MRA (CE-MRA) at 3T with catheter angiography. MATERIALS AND METHODS: Sixty-seven patients with 72 aneurysms underwent TOF-MRA, CE-MRA, and catheter-angiography 6 months after coiling. Occlusion status on MRA was classified as adequate (complete and neck remnant) or incomplete by 2 independent observers. For TOF-MRA and CE-MRA, interobserver agreement, intermodality agreement, and correlation with angiography were assessed by kappa statistics. RESULTS: Catheter-angiography revealed incomplete occlusion in 12 (17%) of the 69 aneurysms; 3 aneurysms were excluded due to MR imaging artifacts. Interobserver agreement was good for CE-MRA (kappa = 0.77; 95% confidence interval [CI], 0.55-0.98) and very good for TOF-MRA (kappa = 0.89; 95% CI, 0.75-1.00). Correlation of TOF-MRA and CE-MRA with angiography was good. The sensitivity of TOF-MRA and CE-MRA was 75% (95% CI, 43%-95%); the specificity of TOF-MRA was 98% (95% CI, 91%-100%) and of CE-MRA, 97% (95% CI, 88%-100%). All 5 incompletely occluded aneurysms, which were additionally treated, were correctly identified with both MRA techniques. Areas under the receiver operating characteristic curve for TOF-MRA and CE-MRA were 0.90 (95% CI, 0.79-1.00) and 0.91 (95% CI, 0.79-1.00). Intermodality agreement between TOF-MRA and CE-MRA was very good (kappa = 0.83; 95% CI, 0.65-1.00), with full agreement in 66 (96%) of the 69 aneurysms. CONCLUSIONS: In this study, TOF-MRA and CE-MRA at 3T were equivalent in evaluating the occlusion status of intracranial aneurysms after coiling. Because TOF-MRA does not involve contrast administration, this method is preferred over CE-MRA

BACKGROUND AND PURPOSE: Patients with intracranial aneurysms are at risk for future development of new aneurysms and growth of additional untreated aneurysms. Because in previous long-term studies duration of follow-up varied widely, the time interval after which screening could be effective remains largely unknown. The purpose of this study was to assess the incidence of de novo aneurysm formation and the growth of additional untreated aneurysms in patients with coiled aneurysms followed up with MR angiography (MRA) after a fixed period of 5 years. MATERIALS AND METHODS: In 65 patients with coiled intracranial aneurysms, high-resolution 3T MRA was performed 5.1 ± 0.2 years after coiling. MRA follow-up imaging was compared with MRA or CT angiography at the time of coiling. Additional aneurysms detected at MRA follow-up were classified as unchanged, grown, de novo, or incomparable with previous imaging. RESULTS: In 13 of 65 patients (20%), 24 additional aneurysms were found. Four aneurysms were incomparable with previous imaging and 2 of these were clipped. Of the remaining 20 additional aneurysms, 1 was de novo, 1 had grown slightly, and 18 were unchanged. The incidence of de novo aneurysm formation after 5 years was 1.54% (95% confidence interval, 0.01–9.0%). For additional aneurysms known at the time of initial coiling and for the 1 de novo aneurysm, no treatment was indicated. CONCLUSIONS: MRA screening 5 years after coiling for detection of de novo aneurysms and growth of additional untreated aneurysms has a low yield in terms of finding aneurysms that need to be treated.

We thank Dr Darsaut et al 1 for their attention paid to the PHASES score and for sharing their thinking in an opinion paper 2 years after the publication of our article.2 The authors discuss whether or not prediction modeling based on data from previous observational studies is science. Their final conclusion is that the only valid way to decide whether or not unruptured aneurysms should be treated is to compare outcomes in patients eligible for both options (ie, aneurysm occlusion …

Background: Brain arteriovenous malformations (BAVMs) are thought to be sporadic developmental vascular lesions, but familial occurrence has been described. We compared characteristics of patients with familial BAVMs with those of patients with sporadic BAVMs. Methods: We systematically reviewed the literature on patients with familial BAVMs. Three families that were found in our centre were added. Age, sex distribution and clinical presentation of the identified patients were compared with those in population-based series of patients with sporadic BAVMs. Furthermore, we calculated the difference in mean age at diagnosis of parents and children to study possible anticipation. Results: We identified 53 patients in 25 families with BAVMs. Mean age at diagnosis of patients with familial BAVMs was 27 years (range 9 months-58 years), which was younger than in the reference population (difference between means 8 years, 95% confidence interval (CI) 3-13 years). Patients with familial BAVMs did not differ from the reference populations with respect to sex and mode of presentation. In families with BAVMs in successive generations, the age of the child at diagnosis was younger than the age of the parent (difference between means 22 years, 95% CI 13-30 years), which suggests clinical anticipation. Conclusions: Few patients with familial BAVMs have been described. These patients were diagnosed at younger age than sporadic BAVMs whereas their mode of presentation was similar. Although there are indications of anticipation, it remains as yet unclear whether the described families represent accidental aggregation or indicate true familial occurrence of BAVMs.

Induced hypertension is often used to treat delayed cerebral ischaemia (DCI) after aneurysmal subarachnoid haemorrhage (aSAH) by trying to augment cerebral blood flow (CBF) [1]. However, evidence on effectiveness is lacking, since previous studies on the effect of induced hypertension on CBF are scarce, small and without control groups [2–4].

Background and Purpose— Delayed cerebral ischemia (DCI) is an important cause of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). Trials of magnesium treatment starting Methods— Patients were divided into categories according to the delay between symptom onset and start of the study medication: 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 24 hours 1.06 (0.87–1.31), and for DCI, 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.

Background: Delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) is difficult to predict. The authors studied the relation between several parameters of brain perfusion at admission and development of DCI. Methods: The authors analyzed the admission CT perfusion (CTP) scans of 46 patients scanned within 72 hours after SAH. They assessed cerebral blood volume (CBV) and flow (CBF), mean transit time (MTT), and time to peak (TTP) for eight predefined regions of interest. For patients with and without DCI, the authors compared perfusion quantitatively and semiquantitatively. With receiver-operator characteristic (ROC) curves, the authors assessed the relationship between DCI and perfusion parameters. To assess the potential prognostic value, they calculated sensitivity and specificity of optimal threshold values for the semiquantitative data. Results: DCI was not significantly related with quantitative perfusion values. For the semiquantitative data, patients with DCI had significantly more asymmetry in perfusion, and ROC curves indicated a good relation (0.75 to 0.81). Optimal threshold values distinguishing between patients with and without DCI were 0.77 for CBV and 0.72 for CBF ratios, and 0.87 seconds for MTT and 1.0 second for TTP differences. The corresponding sensitivity was 0.75 for all parameters; the specificity was 0.70 for CBV, 0.93 for CBF, 0.70 for MTT, and 0.90 for TTP. Conclusions: Delayed cerebral ischemia (DCI) is related to perfusion asymmetry on admission CT perfusion (CTP). The cerebral blood flow ratio (comparing contralateral regions of interest) seems the best prognosticator for development of DCI. Further studies are needed to investigate the additional value of CTP to other prognosticators for DCI and to validate the chosen threshold values.

Objective: To investigate the relation of endothelial cell activation with delayed cerebral ischaemia (DCI) and outcome after subarachnoid haemorrhage (SAH).Methods: Concentrations of soluble (s) intercellular adhesion molecule-1, sE-selectin, sP-selectin, ED1-fibronectin, von Willebrand Factor (vWf), and vWf propeptide were measured within three days of SAH onset. The associations with poor outcome were investigated at three months in 106 patients. In 90 patients in whom the occurrence of cerebral ischaemia could be dated accurately, two analyses were undertaken: one for all ischaemic events (n = 32), including those related to treatment, and another for spontaneous DCI ( n = 11). Concentrations of markers were dichotomised at their medians. The associations of endothelial cell activation markers with outcome were expressed as odds ratios ( OR) from logistic regression and those with ischaemic events as hazard ratios (HR) derived from Cox regression.Results: Early vWf concentrations were associated with poor outcome ( crude OR = 4.6 (95% CI, 2.0 to 10.9; adjusted OR = 3.3 (1.1 to 9.8). Early levels of vWf were also positively related to occurrence of all ischaemic events ( crude HR = 2.3 ( 1.1 to 4.9); adjusted HR = 1.8 ( 0.8 to 3.9) and with occurrence of spontaneous DCI ( crude HR = 3.5 (0.9 to 13.1); adjusted HR = 2.2 (0.5 to 9.8). None of the other markers showed any associations.Conclusions: Concentrations of sICAM-1, sP-selectin, sE- selectin, and ED1-fibronectin do not predict the occurrence of DCI or outcome. The positive associations of raised early vWf concentrations with ischaemic events and poor outcome after SAH may reflect a predisposition to further ischaemic injury through formation of microthrombi in the cerebral circulation.

So there you are, in the emergency department, on a night shift. You have just seen a young woman with an unremarkable past medical history who had come to hospital because of an excruciating headache. The pain had come on in seconds, or at most two minutes, about three hours beforehand, while she was clearing the kitchen. Even though the examination was normal you have ordered a CT scan, as you are well aware that it can take 6 h or more for neck stiffness to develop after subarachnoid haemorrhage (SAH). To your surprise there is no evidence of subarachnoid blood or other abnormality on any of the CT slices; the radiology resident has the same opinion. Since you may now be feeling a little nonplussed, if only briefly, the next section is meant to help you get quickly back on your feet again. IS THE CT SCAN REALLY NORMAL?

Objectives: Several models for prediction of short term outcome after intracerebral haemorrhage (ICH) have been published, however, these are rarely used in clinical practice for treatment decisions. This study was conducted to identify current models for prediction of short term outcome after ICH and to evaluate their clinical applicability and relevance in treatment decisions. Methods: MEDLINE was searched from 1966 to June 2003 and studies were included if they met predefined criteria. Regression coefficients of multivariate models were extracted. Two neurologists independently evaluated the models for applicability in clinical practice. To assess clinical relevance and accuracy of each model, in a validation series of 122 patients the proportion with a ⩾95% probability of death or poor outcome and the actual 30 day case fatality in these patients were calculated. Receiver operator characteristic (ROC) curves were computed for assessment of discriminatory power. Results: A total of 18 prognostic models were identified, of which 14 appeared easy to apply. In the validation series, the proportion of patients with a ⩾95% probability of death or poor outcome ranged from 0% to 43% (median 23%). The 30 day case fatality in these patients ranged from 75% to 100% (median 93%). The area under the ROC curves ranged from 0.81 to 0.90. Conclusions: Most models are easy to apply and can generate a high probability of death or poor outcome. However, only a small proportion of patients have such a high probability, and 30 day case fatality is not always correctly predicted. Therefore, current models have limited relevance in triage, but can be used to estimate the chances of survival of individual patients.

Objectives Initial and secondary ischaemia are important determinants of outcome after subarachnoid haemorrhage (SAH). Cerebral ischaemia is a potent stimulus for expression of genes that may influence recovery. We investigated whether functional polymorphisms in the apolipoprotein E ( APOE), insulin-like growth factor-1 (IGF-1), tumor necrosis factor-A (TNF-A), interleukin-1A (IL-1A), interleukin-1B (IL-1B), and interleukin-6 (IL-6) genes are related with outcome after aneurysmal SAH. Methods Genotyping of the polymorphisms was performed in a consecutive series of 167 patients with aneurysmal SAH. The risk of a poor outcome was analysed with logistic regression with adjustment for prognostic factors for outcome after SAH, using the homozygotes for the wild type alleles as a reference. Results Patients carrying any IGF-1 non-wild type allele had a lower risk of a poor outcome ( OR 0.4, 95% CI 0.2 - 1.0), while carriers of the TNF-A non-wild type allele had a higher risk ( OR 2.3, 95% CI 1.0 - 5.4). We could not demonstrate an association with outcome for APOE ( APOE epsilon 4 OR 0.4, 95% CI 0.1 - 1.2; APOE epsilon 2 OR 0.7, 95% CI 0.2 - 2.4), IL-1A ( OR 1.8, 95% CI 0.8 - 4.0), IL-1B ( OR 0.7, 95% CI 0.3 - 1.5) and IL-6 ( OR 0.7, 95% CI 0.3 - 1.8) polymorphisms. Conclusions Variation in some genes that are expressed after cerebral ischaemia may partly explain the large differences in outcome between patients with aneurysmal SAH. SAH patients homozygote for the IGF-1 wild type allele or carriers of the TNF-A non-wild type allele have a higher risk of poor outcome. Additional studies in other populations are needed to assess the generalisability of our results.

BACKGROUND: Magnesium is a neuroprotective agent that might prevent or reverse delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage (SAH). We are presently running a randomized, placebo-controlled, double blind trial with magnesium sulphate (64 mmol/day intravenously). We studied whether this treatment regime resulted in our target serum magnesium levels of 1.0-2.0 mmol/L. METHODS: Magnesium sulphate was administered intravenously as soon as possible after admission and continued until 14 days after occlusion of the aneurysm. Serum magnesium measurements were done at baseline and at least every 2 days during administration of trial medication. For comparison we used the serum magnesium levels of the placebo-treated patients. RESULTS: Magnesium therapy was begun in 94 patients. The mean magnesium level in the treatment period was 1.47 +/- 0.32 mmol/L. In 81 patients serum magnesium stayed within target levels during the entire treatment period. One patient had a serum magnesium level below 1.0 mmol/L (0.91 mmol/L) in a single measurement and 10 patients had serum magnesium levels above 2.0 mmol/L at one or more measurements. In six patients magnesium therapy was discontinued: in three because of nausea, headache, or both in combination with serum magnesium levels above 2.0 mmol/L and in the other three because of hypotension, phlebitis and renal failure. CONCLUSIONS: With an intravenous dosage schedule of 64 mmol magnesium sulphate a day, serum magnesium levels of 1.0-2.0 mmol/L can easily be maintained without severe side effects for an extended period in a vast majority of patients with SAH.

Background and Purpose— A locus containing the elastin gene has been linked to familial intracranial aneurysms in 2 distinct populations. We investigated the association of single-nucleotide polymorphisms (SNPs) and haplotypes of SNPs in the elastin gene with the occurrence of subarachnoid hemorrhage (SAH) from sporadic aneurysms in the Netherlands. Methods— We genotyped 167 SAH patients and 167 matching controls for 18 exonic and intronic SNPs in the elastin gene. A Bonferroni correction was applied for multiple comparisons with all novel associations, with a correction factor derived from the number of SNPs tested ( P value after Bonferroni correction [ P corr ]). Results— SAH was statistically significant associated with an SNP in exon 22 of the elastin gene (minor allele frequency was 0.000 in patients and 0.028 in controls; odds ratio [OR], 0.0; 95% CI, 0.0 to 0.7; P =0.004; P corr =0.05) and possibly with an SNP in intron 5 (minor allele frequency was 0.062 in patients and 0.128 in controls; OR, 0.5; 95% CI, 0.2 to 0.8; P =0.007; P corr =0.08). Haplotypes of intron 5/exon 22 ( P corr =0.002), intron 4/exon 22 ( P corr =0.02), and intron 4/intron 5/exon 22 ( P =9.0×10 −9 ) were also associated with aneurysmal SAH. Conclusions— Variants and haplotypes within the elastin gene are associated with the risk of sporadic SAH in Dutch patients. Gradual increase of statistical power with the inclusion of 2 or 3 SNPs in the studied haplotypes supports the validity of our conclusion that the elastin gene is a susceptibility locus for SAH.

Background and Purpose— Familial occurrence of intracranial aneurysms suggests a genetic factor in the development of these aneurysms. In this study, we present the identification of a susceptibility locus for the development of intracranial aneurysms detected by a genome-wide linkage approach in a large consanguineous pedigree. Methods— Patients with clinical signs and symptoms of intracranial aneurysms, confirmed by radiological, surgical, or postmortem investigations, were included in the study. Magnetic resonance angiography was used to detect asymptomatic aneurysms in relatives. Results— Seven out of 20 siblings had an intracranial aneurysm. Genome-wide multipoint linkage analysis showed a significant logarithm of the odds score of 3.55. Conclusion— In a large consanguineous pedigree intracranial aneurysms are linked to chromosome 2p13 in a region between markers D2S2206 and D2S2977.

Background: Relatively high rates of complications occur after operation for unruptured intracranial aneurysms. Published data on endovascular treatment suggest lower rates of complications. We measured the impact of treatment of unruptured aneurysms by clipping or coiling on functional health, quality of life, and the level of anxiety and depression. Methods: In three centres, we prospectively collected data on patients with an unruptured aneurysm who were treated by clipping or coiling. Treatment assignment was left to the discretion of the treating physicians. Before, 3 and 12 months after treatment, we used standardised questionnaires to assess functional health (Rankin Scale score), quality of life (SF-36, EuroQol), and the level of anxiety and depression (Hospital Anxiety and Depression Scale). Results: Nineteen patients were treated by coiling and 32 by clipping. In the surgical group, 4 patients (12%) had a permanent complication; 36 of all 37 aneurysms (97%) were successfully clipped. Three months after operation, quality of life was worse than before operation; 12 months after operation, it had improved but had not completely returned to baseline levels. Scores for depression were higher than in the general population. In the endovascular group, no complications with permanent deficits occurred; 16 of 19 aneurysms (84%) were occluded by more than 90%. One patient died from rupture of the previously coiled aneurysm. In the others, quality of life after 3 months and after 1 year was similar to that before treatment. Conclusions: In the short term, operation of patients with an unruptured aneurysm has a considerable impact on functional health and quality of life. After 1 year, recovery occurs but it is incomplete. Coil embolisation does not affect functional health and quality of life.

Patients with a ruptured intracranial aneurysm should be treated as soon as possible after the haemorrhage to prevent rebleeding and to allow vigorous treatment of ischemic events in case of vasospasm. The choice of treatment, endovascular or surgical, should be based on the angio-architectural aspects of the aneurysm. 3D rotational subtraction angiography will more clearly show the aneurysm morphology and will therefore help in the decision-making process. If an aneurysm is suitable for endovascular treatment ('coiling'), this should be the treatment of first choice, as has been clarified in the ISAT study. Location of the aneurysm only influences the treatment decision in aneurysms located at the basilar artery bifurcation. These aneurysms are preferably treated by endovascular means. The long-term results of endovascular and surgical treatment are still the subject of debate. For both treatment modalities, re-growth of the treated aneurysm has been described, but solid comparative data is missing. In analogy with the ISAT, referral of patients with a ruptured intracranial aneurysm should be performed as soon as possible after the haemorrhage. Preferably, this should be a hospital where neurosurgeons, interventional neuroradiologists, as well as neurologists (with expertise on medical treatment of patients with a subarachnoid haemorrhage) collaborate.

BACKGROUND: Magnesium is a neuroprotective agent which might prevent or reverse delayed cerebral ischemia (DCI) after aneurysmal subarachnoid haemorrhage (SAH). Although the dosage for short-term magnesium therapy is well established, there is lack of knowledge on the dosage for extended use of magnesium. Our aim was to find a dosage schedule of magnesium sulphate to maintain a serum magnesium level of 1.0-2.0 mmol/L for 14 days to cover the period of DCI. METHODS: We prospectively studied 14 patients admitted within 48 hours after aneurysmal subarachnoid haemorrhage (SAH) to our hospital. Magnesium sulphate was administrated intravenously for 14 days, using 3 different dosage schedules. Group A (n=3) received a bolus injection of 16 mmol magnesium sulphate followed by a continuous infusion of 16 mmol/daily; group B (n=6) a continuous infusion of 30 mmol/daily; and group C (n=5) a continuous infusion of 64 mmol/daily. Serum magnesium was measured at least every two days and all patients were under continuous observation during magnesium treatment. Renal magnesium excretion was measured only in group C. FINDINGS: In treatment group A the mean serum magnesium level during treatment was 1.03+/-0.14 (range 0.82-1.34) mmol/L, in group B 1.10+/-0.15 (range 0.87-1.43) mmol/L, and in group C 1.38+/-0.18 (range 1.11-1.98) mmol/L. The renal magnesium excretion in group C was equal to the administrated doses within 48 hours after treatment had started. All patients in group A reported a flushing sensation during the bolus injection; no other side effects were noted. INTERPRETATION: With a continuous intravenous dosage of 64 mmol/L per day, serum magnesium levels maintained within the range of 1.0-2.0 mmol/L for 14 days.

Objective: The objective was to assess the risk of aneurysmal subarachnoid hemorrhage (aSAH) in the initial 15 years after negative aneurysm screening in persons with one first-degree relative with aSAH. Methods: From a cohort of first-degree relatives of patients with aSAH who underwent screening between 1995 and 1997 (n = 626), we included those with a negative screening (n = 601). We retrieved all causes of death and sent a questionnaire to screenees who were still alive. If aSAH was reported, we reviewed all medical data. We assessed the incidence of aSAH in this cohort with survival analysis and calculated an incidence ratio by dividing the observed incidence with the age- and sex-adjusted incidence in the general population. Results: Of the 601 screenees, 3 had aSAH during 8,938 follow-up patient-years (mean 14.9 years). After 15 years, the cumulative incidence was 0.50% (95% confidence interval: 0.00%–1.06%) with an incidence rate of 33.6 per 100,000 person-years; the incidence rate ratio was 1.7 (95% confidence interval: 0.3–5.7). Conclusions: In the first 15 years after a negative screening, the risk of aSAH in persons with one first-degree relative with aSAH is not nil, but in the range of that in the general population, or even higher. Whether this finding justifies serial aneurysm screening in this population requires further study.

Article abstract— Objective: To assess the time course of secondary ischemia and first rebleeding and the relation between the timing of operation and the time course of secondary ischemia in a consecutive series of patients with aneurysmal subarachnoid hemorrhage (SAH). Methods: Life table methods were used to assess the daily rates of ischemia and of rebleeding on day 0, day 1 to 3, day 4 to 10, day 11 to 14, and day 15 to 21. The authors compared the time course of secondary ischemia between patients operated within 4 days of SAH and those operated after 10 days. Results: Of 346 patients included, 220 were operated, 131 within 4 days and 74 after 10 days. The rebleed rate was highest on the day of the initial hemorrhage, then diminished, and increased slightly again during the second week. The rate of secondary ischemia was highest on day 4, diminished after day 10, but peaked again from day 14 to 18 for patients who were operated later than 10 days after aneurysmal rupture. The peak rate of ischemia was much higher after early than after late operation. Although patients with early operation were in a better clinical condition on admission, with a relatively low risk of secondary ischemia, the overall rate of secondary ischemia was as high as in patients with delayed operation. From day 11 to 21 the rebleed rate was higher than the rate of secondary ischemia. Conclusions: These results indicate that operation is a risk factor for ischemia, especially when performed early. If operation is postponed, it should be planned soon after day 10, because of the relatively high rebleed rate from day 11 to 21.

Background and Purpose —Delayed cerebral ischemia (DCI) is a major cause of death and disability in patients with aneurysmal subarachnoid hemorrhage. We studied the prognostic value for DCI of 2 factors: the duration of unconsciousness after the hemorrhage and the presence of risk factors for atherosclerosis. Methods —In 125 consecutive patients admitted within 4 days after hemorrhage, we assessed the presence and duration of unconsciousness after the hemorrhage, the neurological condition on admission, the amount of subarachnoid blood, the size of the ventricles, and a history of smoking, hypertension, stroke, or myocardial infarction. The relationship between these variables and the development of DCI was analyzed by means of the Cox proportional hazards model. Results —The univariate hazard ratio (HR) for the development of DCI in patients who had lost consciousness for >1 hour was 6.0 (95% CI 3.0 to 12.0) compared with patients who had no loss or a Conclusions —The duration of unconsciousness after subarachnoid hemorrhage is a strong predictor for the occurrence of DCI. This observation may contribute to a better understanding of the pathogenesis of DCI and increased attention for patients at risk.

Background and Purpose: It has been reported that nimodipine reduces the frequency of secondary ischemia and improves outcome after aneurysmal SAH, but definitive evidence concerning all available calcium antagonists is lacking. Methods: Systematic overview of randomized trials that were completed by January 1996 compared calcium antagonists with control and started treatment within 10 days after onset of subarachnoid hemorrhage (SAH) was performed. All calcium antagonists studied thus far (nimodipine, nicardipine, and AT877) were included. Results: We analyzed 10 trials totaling 2756 patients. The relative risk (RR) reduction of poor outcome (death or dependency) was 16% (95% CI, 6 to 27%) and that of case fatality was 10% (95% CI, -6 to 25%). To prevent one poor outcome, 19 (12 to 59) patients need to be treated. Calcium antagonists give a 33% (95%, CI 25 to 41) RR reduction in the frequency of ischemic neurologic deficit and a 20% (95% CI, 11 to 28) RR reduction in the frequency of CT-scan documented cerebral infarction. Eight (6 to 11) patients need to be treated to prevent one ischemic neurologic deficit. In the analyses for nimodipine only, treatment was associated with a 24% RR reduction of poor outcome (95% CI, 12 to 38). To prevent one poor outcome, 13 (8 to 30) patients need to be treated with nimodipine. The RR reduction of angiographically detected cerebral vasospasm was statistically significant for AT877 (38%; 95% CI, 17 to 54%) and nicardipine (21%; 95% CI, 6 to 34%) but not for nimodipine (9%; 95% CI, -2 to 19%). Conclusion: Calcium antagonists reduce the proportion of ischemic neurologic deficits and nimodipine improves overall outcome within 3 months of aneurysmal SAH; evidence for a reduction of poor outcome from all causes by nicardipine and AT877 is inconclusive. The intermediate factors by which nimodipine exerts its beneficial effect remain uncertain.

Background: Subarachnoid haemorrhage (SAH) from a ruptured intracranial aneurysm accounts for approximately 5% of all strokes. Post-traumatic stress disorder (PTSD) is common in the early phase after recovery from aneurysmal SAH. The aim of our study was to examine the prevalence of PTSD 3 years after SAH, its predictors, and relationship with health-related quality of life (HRQoL) in patients living independently in the community. Methods: From a prospectively collected cohort of 143 patients with aneurysmal SAH who visited our outpatient clinic 3 months after SAH, 94 patients (65.7%) completed a mailed questionnaire 3 years after SAH. We assessed PTSD with the Impact of Event Scale and HRQoL with the Stroke-Specific Quality of Life Scale (SS-QoL). The χ2 and t tests were used to investigate if patients who returned the questionnaires were different from those who did not reply. Non-parametric tests (χ2 and Mann-Whitney tests) were used to test for differences between patients with and without PTSD. Relative risks and 95% confidence intervals were calculated. Results: No relevant differences in demographic (age, sex, education) or SAH characteristics (clinical condition on admission, complication, location of aneurysm, Glasgow Outcome Scale score at 3 months) were seen between participants and drop-outs. In 24 patients (26%), Impact of Event Scale scores indicated PTSD. Passive coping style (relative risk, 5.7; 95% confidence interval, 2.1-15.3), but none of the demographic or SAH-related factors, predicted PTSD. The mean SS-QoL total score was 4.2 (SD 1.1), indicative of a relatively satisfactory HRQoL. PTSD was associated with lower HRQoL (p < 0.001), a mean SS-QoL score of 4.4 (SD 1.0) without PTSD, and a mean SS-QoL score of 3.5 (SD 1.1) with PTSD. Conclusions: Even 3 years after SAH, 1 out of 4 patients had PTSD, which was associated with reduced HRQoL. Passive coping style was the most important predictor. There is a need to organize SAH care with more attention to and treatment of PTSD. Strategies shown to reduce PTSD in other conditions should be tested for effectiveness in SAH patients.

Background Intracranial aneurysms are life threatening conditions and occur in 3-6% of the population. The annual rupture rate is approximately 2% associated with significant morbidity and mortality. Hemodynamic information obtained by 4D flow MRI may contribute to the assessment of rupture risk of intracranial aneurysms. However, the small sizes of intracranial aneurysms require high spatial resolution to accurately capture complex intra-aneurysmal flow. Increasing spatial resolution, however, decreases signal-to-noise ratio (SNR) and thus velocity-to-noise ratio in flow images. Performing 4D flow at 7T has high potential to overcome low SNR limits and enable higher spatial resolution in 4D flow acquisitions. In this study 4D flow in intracranial aneurysms at 7T was compared with 4D flow at 3T.

Many studies have assessed the relationships between seasonal or meteorological determinants and the occurrence of aneurysmal subarachnoid hemorrhage (SAH), but the data are conflicting. We systematically searched the literature and meta-analyzed data from all relevant articles when possible. We searched MEDLINE (1966-2011), EMBASE (1980-2011) and the Cochrane Library to identify all observational studies examining the relationship between seasonal and meteorological determinants (temperature, atmospheric pressure and relative humidity) and the occurrence of SAH. Two authors independently extracted data from articles that were included based on predefined criteria. We pooled relative risks (RR's) with corresponding 95 % confidence intervals (CI's) from the individual studies on season and month by means of the random effects method. We included 48 articles, totaling 72,694 patients. SAH occurred less often in summer than in winter (RR 0.89, 95 % CI 0.83-0.96), and was statistically significant more often in January than in the summer months of June-September. For atmospheric pressure seven of 17 studies found a significant association, six of 18 studies were significant for temperature, and three of 15 studies were significant for humidity, but the direction of these associations was conflicting and data on these determinants were too heterogeneous to pool. Seasons influence the occurrence of SAH, with SAH occurring less often in summer than in winter, and most often in January. The explanation for the seasonal differences remains uncertain, due to the lack of sound data on the influence of meteorological factors on SAH occurrence.

BACKGROUND AND PURPOSE: ISHs and ICHs from ruptured MCA aneurysms can be difficult to distinguish on NCE-CT but may have a different impact on admission status and outcome. The presence of IHCEV on CTA may differentiate ISHs and ICHs. MATERIALS AND METHODS: Two observers independently reviewed non-contrast-enhanced CT scans and CTAs of 71 patients with MCA aneurysm hematomas for the site of the hematoma, according to predefined characteristics, and for the presence of IHCEV. We compared CTAs with NCE-CT scans in which both observers were confident about hematoma localization. We calculated κ statistics for interobserver agreement, and RRs for poor clinical condition and poor outcome. RESULTS: Agreement for IHCEV was almost perfect (κ, 0.87; 95% CI, 0.74–0.99). After consensus reading, 30 of 71 patients had IHCEV. In 28 of the 71 NCE-CT scans, both observers were confident as to the the site of the hematoma (κ, 0.55; 95% CI, 37%–73%). IHCEV were present in 10 of these 28 patients, of whom 9 had an ISH based on NCE-CT (positive predictive value, 90%; 95% CI, 55%–100%). In all 18 of 28 patients without IHCEV, the hematoma was not intra-Sylvian (negative predictive value, 100%; 95% CI, 82%–100%). Poor admission status occurred in 50% of patients with IHCEV and in 60% without IHCEV (RR, 1.2; 95% CI, 0.8–1.9). Poor outcome occurred in 63% of patients with IHCEV and in 65% without IHCEV (RR, 1.0; 95% CI, 0.7–1.5). CONCLUSIONS: Although CTA could reliably and accurately differentiate the hematoma types, admission status and outcome were similar for both groups.

For studies on chronic risk factors and trigger (i.e. acute risk) factors, stroke researchers often have to rely on proxies. The reliability of proxy responses regarding trigger factors for stroke is unknown.Thirty patients with stroke and their proxies were interviewed about chronic risk factors and trigger factors. We assessed the completeness of proxy-derived data by calculating the level of non-response and the level of agreement using Cohen kappa statistics.For most chronic risk factors and trigger factors, the response rate to whether or not exposure had taken place in the past year was 87% or higher. If couples agreed on exposure, patient and proxy could also provide a comparable estimate of the average frequency of exposure. Although the non-response on last time of exposure was higher, proxies who could answer provide a reasonably good estimate for most trigger factors.Proxies provide reliable information on exposure to chronic risk factors and trigger factors for stroke. For exposure and average frequency of exposure, non-response is low and the level of agreement is high for most chronic risk factors; for last time of exposure non-response is higher, but proxies who could respond provided reliable estimates of last time of exposure to most trigger factors.

Background and purpose: Several risk factors for aneurysmal subarachnoid haemorrhage have been identified but it is not known whether some sites of aneurysms are linked to a specific risk factor. In a series of patients with aneurysmal subarachnoid haemorrhage, we compared risk factors according to the site of the ruptured aneurysm at the circle of Willis. Methods: From our prospectively collected database of patients with aneurysmal subarachnoid haemorrhage admitted to our hospital between 2003 and 2007, we retrieved 304 patients with saccular aneurysms on the anterior communicating artery, middle cerebral artery, posterior communicating artery, basilar artery and vertebral artery. Risk factors (age, gender, smoking, no or excessive alcohol intake, hypertension and familial preponderance) were assessed per aneurysm location and compared with the anterior communicating artery as reference. We calculated odds ratios (ORs) and corresponding 95% CI. Results: In comparison with aneurysms at the anterior communicating artery, those at the middle cerebral artery were less associated with age >55 years (OR 0.4; 95% CI 0.2 to 0.8), those at the posterior communicating artery were less associated with male gender (OR 0.4; 95% CI 0.2 to 0.9) and those at the basilar artery were more associated with no alcohol consumption (OR 5.8; 95% CI 1.1 to 29.9). Conclusion: Risk factors differ according to the site of aneurysm. This heterogeneity should be kept in mind in studies on the aetiology of aneurysms, such as genetic studies.

BACKGROUND AND PURPOSE: Acute hydrocephalus after aneurysmal subarachnoid hemorrhage (SAH) may decrease cerebral perfusion by increasing intracranial pressure. We studied cerebral perfusion in patients with and without acute hydrocephalus after SAH. MATERIALS AND METHODS: We performed noncontrast CT scans, CT perfusion (CTP), and CT angiography on admission in all patients with aneurysmal SAH. Patients were dichotomized at a relative bicaudate index of 1 for the presence or absence of hydrocephalus. Cerebral perfusion was measured in the cortex, basal ganglia, and periventricular white matter. Mean CTP parameters were compared between patients with and without acute hydrocephalus (ie, within 3 days after SAH). RESULTS: We included 138 consecutive patients with successful CTP measurements, of whom 49 (36%) had acute hydrocephalus. Mean cerebral blood flow (CBF) was lower in patients with hydrocephalus than in those without in the basal ganglia (difference of means, 6.8; 95% CI, 1.6–11.0 mL/100 g/min) and periventricular white matter (difference of means, 3.8; 95% CI, 0.9–6.8 mL/100 g/min) but not in the cortex (difference of means, 1.8; 95% CI, −2.8 to 6.4 mL/100 g/min). In all regions studied, mean transit time (MTT) and time-to-peak (TTP) were statistically significantly longer in patients with hydrocephalus, but cerebral blood volume (CBV) values were similar. CONCLUSIONS: Acute hydrocephalus after SAH reduces CBF in the deep gray matter and periventricular white matter and delays MTT and TTP in all investigated brain areas. The negative effect of acute hydrocephalus on cerebral perfusion in patients with SAH seems more pronounced in the vicinity of the ventricles than in remote sites.

Patients with aneurysmal subarachnoid haemorrhage (SAH) often have disturbed autoregulation of cerebral blood flow. A reduction in systemic blood pressure during surgery may therefore lead to delayed cerebral ischaemia (DCI). To assess the incidence and severity of intra-operative hypotension, we performed a retrospective cohort study in 164 patients with recent SAH and surgical clipping of the aneurysm.Intra-operative hypotension was defined in three levels of severity, as a decrease in mean arterial pressure (DeltaMAP) of more than 30%, 40% or 50% compared with the pre-operative pressure. For each patient the total amount of time with intra-operative hypotension was retrieved. Logistic regression analysis was performed to study the relation between intra-operative hypotension and the occurrence of DCI and poor outcome.A period with DeltaMAP30% occurred in 128 patients (78%) with a median duration of this period of 105 min (25-75 per thousand 50-171 min). DeltaMAP40% occurred in 88 patients (54%) and DeltaMAP50% occurred in 22 patients (13%). In univariate analysis, DeltaMAP50% was associated with poor outcome. After adjusting for age and World Federation of Neurological Surgeons grade, the association with poor outcome was no longer statistically significant [odds ratio (OR) 1.018; 95% CI 0.996-1.041].Hypotension during surgical clipping of intracranial aneurysms occurred frequently. In our study population of patients mostly in good clinical condition, hypotension was not confirmed as an independent risk factor for DCI or poor outcome. Anaesthesia may have had a cerebral protective effect.