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Background and aim: To update our 1996 review on the incidence of subarachnoid haemorrhage (SAH) and assess the relation of incidence with region, age, gender and time period. Methods: We searched for studies on the incidence of SAH published until October 2005. The overall incidences with corresponding 95% confidence intervals were calculated. We determined the relationship between the incidence of SAH and determinants by means of univariate Poisson regression. Results: We included 51 studies (33 new), describing 58 study populations in 21 countries, observing 45 821 896 person-years. Incidences per 100 000 person-years were 22.7 (95% CI 21.9 to 23.5) in Japan, 19.7 (18.1 to 21.3) in Finland, 4.2 (3.1 to 5.7) in South and Central America, and 9.1 (8.8 to 9.5) in the other regions. With age category 45-55 years as the reference, incidence ratios increased from 0.10 (0.08 to 0.14) for age groups younger than 25 years to 1.61 (1.24 to 2.07) for age groups older than 85 years. The incidence in women was 1.24 (1.09 to 1.42) times higher than in men; this gender difference started at age 55 years and increased thereafter. Between 1950 and 2005, the incidence decreased by 0.6% (1.3% decrease to 0.1% increase) per year. Conclusions: The overall incidence of SAH is approximately 9 per 100 000 person-years. Rates are higher in Japan and Finland and increase with age. The preponderance of women starts only in the sixth decade. The decline in incidence of SAH over the past 45 years is relatively moderate compared with that for stroke in general.

IMPORTANCE Subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms is a subset of stroke with high fatality and morbidity. Better understanding of a change in incidence over time and of factors associated with this change could facilitate primary prevention.OBJECTIVE To assess worldwide SAH incidence according to region, age, sex, time period, blood pressure, and smoking prevalence.DATA SOURCES We searched PubMed, Web of Science, and Embase for studies on SAH incidence published between January 1960 and March 2017. Worldwide blood pressure and smoking prevalence data were extracted from the Noncommunicable Disease Risk Factor and Global Burden of Disease data sets. STUDY SELECTION Population-based studies with prospective designs representative of the entire study population according to predefined criteria.DATA EXTRACTION AND SYNTHESIS Two reviewers independently extracted data according to PRISMA guidelines. Incidence of SAH was calculated per 100 000 person-years, and risk ratios (RRs) including 95% CIs were calculated with multivariable random-effects binomial regression. The association of SAH incidence with blood pressure and smoking prevalence was assessed with linear regression. MAIN OUTCOMES AND MEASURES Incidence of SAH.RESULTS A total of 75 studies from 32 countries were included. These studies comprised 8176 patients with SAH were studied over 67 746 051 person-years. Overall crude SAH incidence across all midyears was 7.9 (95% CI, 6.9-9.0) per 100 000 person-years; the RR for women was 1.3 (95% CI, 0.98-1.7). Compared with men aged 45 to 54 years, the RR in Japanese women older than 75 years was 2.5 (95% CI, 1.8-3.4) and in European women older than 75 years was 1.5 (95% CI, 0.9-2.5). Global SAH incidence declined from 10.2 (95% CI, 8.4-12.5) per 100 000 person-years in 1980 to 6.1 (95% CI, 4.9-7.5) in 2010 or by 1.7% (95% CI, 0.6-2.8) annually between 1955 and 2014. Incidence of SAH declined between 1980 and 2010 by 40.6% in Europe, 46.2% in Asia, and 14.0% in North America and increased by 59.1% in Japan. The global SAH incidence declined with every millimeter of mercury decrease in systolic blood pressure by 7.1% (95% CI, 5.8-8.4) and with every percentage decrease in smoking prevalence by 2.4% (95% CI, 1.6-3.3). CONCLUSIONS AND RELEVANCEWorldwide SAH incidence and its decline show large regional differences and parallel the decrease in blood pressure and smoking prevalence. Understanding determinants for regional differences and further reducing blood pressure and smoking prevalence may yield a diminished SAH burden.

Background and Purpose-Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage worsens the prognosis and is difficult to diagnose. We investigated the diagnostic value of noncontrast CT (NCT), CT perfusion (CTP), and CT angiography (CTA) for DCI after clinical deterioration in patients with subarachnoid hemorrhage.

All patients were derived from the prospectively collected cohort of SAH patients admitted to our hospital. The development cohort originated from a previously described study population of patients admitted between January 1999 and June 2007.9 Three-hundred seventy-one patients met the following inclusion criteria (1) SAH confirmed by computed tomography (CT) or lumbar puncture; (2) aneurysm proven by means of CT/MR-or catheter angiography; (3) admitted within 3 days after onset; (4) at least 1 follow-up scan performed >24 hours after the initial scan; (5) initial CT scan available for review; (6) absence of a large intracerebral hemorrhage Background and Purpose-To develop and validate a risk chart for prediction of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage based on admission characteristics. Methods-For derivation of the risk chart, we studied data from 371 prospectively collected consecutive subarachnoid hemorrhage patients with a confirmed aneurysm admitted between 1999 and 2007. For its validation we similarly studied 255 patients admitted between 2007 and 2009. The predictive value of admission characteristics was tested in logistic regression models with delayed cerebral ischemia-related infarction as primary outcome. Procedure-related infarctions were not included. Performance of the models was tested by discrimination and calibration. On the basis of these models, a risk chart was developed for application in clinical practice. Results-The strongest predictors were clinical condition on admission, amount of blood on computed tomography (both cisternal and intraventricular) and age. A model that combined these 4 predictors had an area under the receiver operating characteristic curve of 0.63 (95% confidence interval, 0.57-0.69). This model improved little by including current smoking and hyperglycemia on admission (area under the receiver operating characteristic curve, 0.65; 95% confidence interval, 0.59-0.71). The risk chart predicted risks of delayed cerebral ischemia-related infarction varying from 12% to 61%. Both low risk (<20% risk) and high risk (>40% risk) were predicted in ≈20% of the patients. Validation confirmed that the discriminative ability was adequate (area under the receiver operating characteristic curve, 0.69; 95% confidence interval, 0.61-0.77). Conclusions-Absolute risks of delayed cerebral ischemia-related infarction can be reliably estimated by a simple risk chart that includes clinical condition on admission, amount of blood on computed tomography (both cisternal and intraventricular), and age. (Stroke. 2013;44:1288-1294.)

Background and Purpose-Early diagnosis of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage is critical but difficult. We analyzed diagnostic threshold values of CT perfusion for use in detection of DCI in patients with subarachnoid hemorrhage. Methods-We prospectively enrolled patients with subarachnoid hemorrhage with CT perfusion on admission and at time of clinical deterioration or after 1 week if no deterioration occurred. The gold standard was the clinical diagnosis of DCI based on all clinical, laboratory, and imaging data except CT perfusion. Patients with failed imaging (nϭ6) and other causes of deterioration (nϭ45) were excluded for the current study. We measured CT perfusion values, including cerebral blood volume, blood flow, mean transit time (MTT), and time to peak in predefined regions of interest and then compared absolute perfusion and perfusion asymmetry for patients with and without DCI. Diagnostic threshold values for DCI were evaluated and sensitivity and specificity calculated for optimal thresholds. Results-Of 85 eligible patients with subarachnoid hemorrhage, 50 had DCI; 35 patients with no clinical deterioration comprised the reference group. Cerebral blood flow was significantly lower, MTT higher, and perfusion asymmetry larger in patients with DCI. We found that largest absolute MTT and the MTT difference between hemispheres were good diagnostic tests. Diagnostic threshold values with optimal sensitivity and specificity were an MTT of 5.9 seconds and an MTT difference of 1.1 second. Conclusion-Thresholds

Background and Purpose— Established predictors of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage are large amounts of extravasated blood and poor clinical condition on admission. The predictive value of other factors is uncertain. Methods— We searched MEDLINE (1960–2012) for clinical, laboratory, and radiological predictors routinely available within 72 hours after subarachnoid hemorrhage. The studies were categorized according to methodological quality. Crude data and effect estimates (odds ratio [OR], hazard ratios, and risk ratio) with 95% CI were extracted, (re-)calculated and pooled if possible. For every potential predictor we assessed all effect estimates on consistency (point estimates in equal direction) and clinical relevance (size and 95% CI). Results— Fifty-two studies on 33 potential predictors were included. There was strong evidence (≥3 high-quality studies) for a higher risk of delayed cerebral ischemia in smokers (pooled OR, 1.2; 95% CI, 1.1–1.4), and moderate evidence (2 high-quality studies) for an increased risk in patients with hyperglycemia (OR, 3.2; 1.8–5.8 and hazard ratios, 1.7; 1.1–2.5), hydrocephalus (OR, 1.3; 1.1–1.5 and OR, 2.6; 1.2–5.5), history of diabetes mellitus (pooled OR, 6.7; 1.7–26), and early systemic inflammatory response syndrome (pooled OR, 2.1; 1.4–3.3). Evidence was limited for increased risk in women (pooled OR, 1.3; 1.1–1.6) and in patients with history of hypertension (pooled OR, 1.5; 1.3–1.7). The evidence on initial loss of consciousness, history of migraine, previous use of selective serotonin reuptake inhibitors, hypomagnesemia, low hemoglobin, or high blood flow on early transcranial Doppler was also limited. Conclusions— There is strong evidence that smoking is a predictor of delayed cerebral ischemia. For several other potential predictions the evidence is moderate, limited, or inconsistent.

Direction of flow into the aneurysm and nonspherical (both elliptical and multilobed) shape may contribute to the risk of rupture, but are related to aneurysm size and may warrant more frequent follow-up.