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Background There are multiple stroke guidelines globally. To synthesize these and summarize what existing stroke guidelines recommend about the management of people with stroke, the World Stroke Organisation (WSO) Guideline committee, under the auspices of the WSO, reviewed available guidelines. They identified areas of strong agreement across guidelines, and their global coverage. Aims To systematically review the literature to identify stroke guidelines (excluding primary stroke prevention and subarachnoid haemorrhage) since 1st January 2011, evaluate quality (AGREE II), tabulate strong recommendations, and judge applicability according to stroke care available (minimal, essential, advanced). Summary of review Searches identified 15400 titles, 911 texts were retrieved, 203 publications scrutinized by the three subgroups (acute, secondary prevention, rehabilitation), and recommendations extracted from most recent version of relevant guidelines. For acute treatment, there were more guidelines about ischaemic stroke than intracerebral haemorrhage; recommendations addressed pre-hospital, emergency, and acute hospital care. Strong recommendations were made for reperfusion therapies for acute ischaemic stroke. For secondary prevention, strong recommendations included establishing aetiological diagnosis, management of hypertension, weight, diabetes, lipids, lifestyle modification; and for ischaemic stroke: management of atrial fibrillation, valvular heart disease, left ventricular and atrial thrombi, patent foramen ovale, atherosclerotic extracranial large vessel disease, intracranial atherosclerotic disease, antithrombotics in non-cardioembolic stroke. For rehabilitation there were strong recommendations for organized stroke unit care, multidisciplinary rehabilitation, task specific training, fitness training, and specific interventions for post-stroke impairments. Most recommendations were from high income countries, and most did not consider comorbidity, resource implications and implementation. Patient and public involvement was limited. Conclusions The review identified a number of areas of stroke care in there was strong consensus. However there was extensive repetition and redundancy in guideline recommendations. Future guidelines groups should consider closer collaboration to improve efficiency, include more people with lived experience in the development process, consider comorbidity, and advise on implementation.

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Background: Ischemic and hemorrhagic stroke onset exhibit is known to exhibit diurnal variation throughout the 24-hour cycle. But whether this variation differs on weekdays compared with weekends/holidays has not been well delineated. Methods: We evaluated consecutive patients with acute cerebral ischemia [(ACI), including ischemic stroke (IS) and transient ischemic attack (TIA)] and intraparenchymal hemorrhage (IPH) enrolled during ambulance transport to 60 receiving stroke centers in the NIH FAST-MAG trial. Enrollment required onset within the prior 2 hours, excluding confounding by wake-up and unwitnessed onset strokes. The patterns of time of onset were analyzed: 1) hourly, 2) in 4-hour increments, and 3) daytime (08:00-19:59) vs. night-time (20:00-07:59). Diurnal variation in presenting demographic/clinical features were assessed using ANOVA, Kruskal-Wallis, t-tests, and Wilcoxon Rank-Sum. Results: Among 1615 patients (1202 enrolled on weekdays and 442 on weekends/holidays), 64% had IS, 12.5% TIA, and 23.5% IPH. ACI patients had different patterns of onset time (Figure). During weekdays, a broad plateau of highest rates of onset occurred 09:00-22:00. Conversely, during weekends/holidays, a unimodal peak was observed between 14:00-16:00. In contrast, patterns of onset time in IPH patients were broadly similar, with bimodal peaks on both weekdays and weekends/holidays. However, the first peak occurred earlier on weekdays (09:00-12:00 vs. 11:00-13:00), with the second peak occurring within 17:00-20:00 in both groups. Conclusion: Acute cerebral ischemia shows marked, and intraparenchymal hemorrhage minor, pattern differences in onset times on weekdays vs. weekends/holidays, likely related to variations in times of greater physical activity and stress. These findings can inform EMS resource allocation to stroke, aligned with weekday vs. weekend/holiday onset patterns.

Introduction: Stroke and traumatic brain injury (TBI) accounts for 70% of secondary epilepsy in the adult population. The genetic architecture of epilepsy secondary to TBI or stroke is poorly understood. Objective: We undertook a systematic review to test the association of single nucleotide polymorphisms (SNPs) with the risk of posttraumatic epilepsy (PTE) and post-stroke epilepsy (PSE). Methods: We conducted a comprehensive literature search until 5 July 2022 in PubMed, Embase, PsycINFO, Web of Science, and Google Scholar. We preregistered the protocol of this systematic review on PROSPERO (CRD42022325617). We collated the association statistics from the articles to assess the association of SNPs with the risk of epilepsy amongst TBI or stroke patients. We assessed the study quality using the Quality of Genetic Association (Q-Genie) tool. We report Odds Ratio (OR) and Hazard Ratio (HR) with a 95% confidence interval (CI), including combined OR where a meta-analysis was possible. Results: The literature search yielded 420 articles, of which 16 were included in our systematic review. Q-Genie-based assessment of the literature found that 58% of the included studies were of poor quality. We examined published data on 127 SNPs from 32 genes identified in PTE and PSE patients. Twelve studies reported that 718 TBI patients (21%) suffered from PTE. Four studies reported PSE in 1192 stroke patients (50%). Eleven SNPs were associated with an increased risk of PTE. Three SNPs, TRMP6 rs2274924, ALDH2 rs671, CD40 -1C/T, were significantly associated with an increased risk of PSE, while two SNPs, AT1R rs12721273 and rs55707609, were significantly associated with reduced risk. Only two studies tested the association of APOE E4 with PTE; no other studies validated previously reported genetic association data. Hence, the limited data precluded meta-analysis of all but one SNP, i.e., the APOE E4 allele. The meta-analysis for the association of the APOE E4 allele with PTE was non-significant (OR 1.8, CI 0.6-5.6). Conclusions: The current evidence on the association of genetic polymorphisms in epilepsy secondary to TBI or stroke is of low quality and lacks validation. A collaborative effort to pool genetic data linked to epileptogenesis in stroke and TBI patients is warranted.