BackgroundPrevious studies have not shown any significant effect on stroke incidence during Ramadan. We aimed to investigate the association between ischemic stroke incident hospitalizations and Ramadan, accounting for seasonality and temperature.Methods and ResultsThis retrospective cohort study included all patients admitted with acute ischemic stroke to Soroka University Medical Center from June 2012 to June 2016. We obtained daily mean temperatures and relative humidity rates from 2 monitoring stations in South Israel. We analyzed the association between stroke incidence and Ramadan month, adjusting for weekly temperature and seasonality using Poisson regression models. We compared the first versus the last Ramadan fortnight. We performed an effect specificity analysis by assessing stroke incidence in the non‐Bedouin population. We identified 4727 cases of ischemic stroke, 564 cases of which were Bedouin Arabs. Fifty‐one cases occurred during Ramadan. Ramadan was significantly associated with an increased risk for ischemic stroke (RR 1.48; 95% confidence interval, 1.04–2.09), mainly during the first fortnight (RR 1.73, 95% confidence interval, 1.13–2.66) when compared with non‐Ramadan periods. Mean weekly temperatures and the summer season were not associated with stroke incidence among Bedouin Arabs (RR 0.98; 95% confidence interval, 0.82–1.18 and RR 0.77; confidence interval 0.56–1.06 accordingly). Such association was not observed in the non‐Bedouin population.ConclusionThe Ramadan month, particularly in its first 2 weeks, is an independent and ethnicity specific risk factor for ischemic stroke hospitalizations among the Bedouin Arab fasting population.

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OBJECTIVE Retrospective patient cohort studies have identified risk factors associated with recurrent focal neurological events in patients with symptomatic cerebral cavernous malformations (CCMs). Using a prospectively maintained database of patients with CCMs, this study identified key risk factors for recurrent neurological events in patients with symptomatic CCM. A simple scoring system and risk stratification calculator was then created to predict future neurological events in patients with symptomatic CCMs. METHODS This was a dual-center, prospectively acquired, retrospectively analyzed cohort study. Adult patients who presented with symptomatic CCMs causing focal neurological deficits or seizures were uniformly treated and clinically followed from the time of diagnosis onward. Baseline variables included age, sex, history of intracerebral hemorrhage, lesion multiplicity, location, eloquence, size, number of past neurological events, and duration since last event. Stepwise multivariable Cox regression was used to derive independent predictors of recurrent neurological events, and predictive accuracy was assessed. A scoring system based on the relative magnitude of each risk factor was devised, and Kaplan-Meier curve analysis was used to compare event-free survival among patients with different score values. Subsequently, 1-, 2-, and 5-year neurological event rates were calculated for every score value on the basis of the final model. RESULTS In total, 126 (47%) of 270 patients met the inclusion criteria. During the mean (interquartile range) follow-up of 54.4 (12–66) months, 55 patients (44%) experienced recurrent neurological events. Multivariable analysis yielded 4 risk factors: bleeding at presentation (HR 1.92, p = 0.048), large size ≥ 12 mm (HR 2.06, p = 0.016), eloquent location (HR 3.01, p = 0.013), and duration ≤ 1 year since last event (HR 9.28, p = 0.002). The model achieved an optimism-corrected c-statistic of 0.7209. All factors were assigned 1 point, except duration from last event which was assigned 2 points. The acronym BLED2 summarizes the scoring system. The 1-, 2-, and 5-year risks of a recurrent neurological event ranged from 0.6%, 1.2%, and 2.3%, respectively, for patients with a BLED2 score of 0, to 48%, 74%, and 93%, respectively, for patients with a BLED2 score of 5. CONCLUSIONS The BLED2 risk score predicts prospective neurological events in symptomatic CCM patients.

Background Blast-explosion may cause traumatic brain injury (TBI), leading to post-concussion syndrome (PCS). In studies on military personnel, PCS symptoms are highly similar to those occurring in post-traumatic stress disorder (PTSD), questioning the overlap between these syndromes. In the current study we assessed PCS and PTSD in civilians following exposure to rocket attacks. We hypothesized that PCS symptomatology and brain connectivity will be associated with the objective physical exposure, while PTSD symptomatology will be associated with the subjective mental experience. Methods Two hundred eighty nine residents of explosion sites have participated in the current study. Participants completed self-report of PCS and PTSD. The association between objective and subjective factors of blast and clinical outcomes was assessed using multivariate analysis. White-matter (WM) alterations and cognitive abilities were assessed in a sub-group of participants (n = 46) and non-exposed controls (n = 16). Non-parametric analysis was used to compare connectivity and cognition between the groups. Results Blast-exposed individuals reported higher PTSD and PCS symptomatology. Among exposed individuals, those who were directly exposed to blast, reported higher levels of subjective feeling of danger and presented WM hypoconnectivity. Cognitive abilities did not differ between groups. Several risk factors for the development of PCS and PTSD were identified. Conclusions Civilians exposed to blast present higher PCS/PTSD symptomatology as well as WM hypoconnectivity. Although symptoms are sub-clinical, they might lead to the future development of a full-blown syndrome and should be considered carefully. The similarities between PCS and PTSD suggest that despite the different etiology, namely, the physical trauma in PCS and the emotional trauma in PTSD, these are not distinct syndromes, but rather represent a combined biopsychological disorder with a wide spectrum of behavioral, emotional, cognitive and neurological symptoms.