BACKGROUND: This study aims to perform a comprehensive analysis of stroke burden from the Global Burden of Disease 2021. METHODS: We conducted a comprehensive analysis of the burden, including prevalence, incidence, mortality, and disability-adjusted life year rates, for stroke across 204 countries and regions from 1990 to 2021 using data from the Global Burden of Disease 2021. We calculated the estimated annual percentage change (EAPC) and performed a joinpoint regression analysis to identify the trends. We also explored the association between the stroke burden and sociodemographic index. RESULTS: The age-standardized prevalence, incidence, mortality, and disability-adjusted life year rates for stroke were 1099.310, 141.553, 87.454, and 1886.196 per 100 000 persons in 2021, respectively. The general stroke burden trends declined in EAPC analysis (age-standardized prevalence: EAPC, −0.37; age-standardized incidence: EAPC, −0.99; age-standardized mortality: EAPC, −1.81; and disability-adjusted life year: EAPC, −1.76). However, we found an increasing burden of stroke in East Asia and Southern Sub-Saharan Africa (EAPC >0). The global burdens of intracerebral hemorrhage, subarachnoid hemorrhage, and ischemic stroke showed a similar trend. The stroke, intracerebral hemorrhage, and ischemic stroke burdens were heavier in men than in women, except for that of subarachnoid hemorrhage in women. Our joinpoint regression analysis revealed that the age-standardized burden rates of stroke decreased from 1990 to 2021 (average annual percent change 0). The burden of stroke was inversely proportional to the sociodemographic index ( P <0.05), except in the case of subarachnoid hemorrhage. The actual stroke burden showed an increasing trend for stroke, intracerebral hemorrhage, subarachnoid hemorrhage, and ischemic stroke in 2021 (during the coronavirus pandemic). CONCLUSIONS: We found age-standardized rates of stroke burden declining over time, but some areas exhibited a notable increase in the prevalence, incidence, mortality, and disability-adjusted life year rates.

This study aims to assess the burden of young-onset dementia worldwide, regionally, and nationally during 1990–2021. Prevalence, incidence, mortality, and disability adjusted life years (DALYs) rates were used to estimate burden of the young-onset dementia. The average annual percentage was utilized to evaluate the trends during 1990–2021. Decomposition analysis was performed to explore driving factors behind changes. Age-period-cohort modeling was used to estimate local drift, age, period and cohort effects. Global age standardized prevalence and incidence of dementia among people under 65 years increased from 93.39 and 16.24 per 100,000 persons in 1990 to 96.09 and 17.16 per 100,000 persons in 2021; mortality increased from 0.89 per 100,000 population to 0.91 per 100,000 population; and age standardized DALYs increased from 45.60 per 100,000 persons to 46.78 per 100,000 persons. Countries with a high, high-middle, and middle SDI experienced an upward trend of prevalence and incidence, and the mortality and DALYs of young-onset dementia in countries with a low-middle and low sociodemographic index was a higher level. Smoking, high body-mass index and high fasting plasma glucose levels were main risk factors. Population growth was the largest factor for the increasing young-onset dementia in all regions. Globally, prevalence, incidence, and DALYs rate of young-onset dementia increased with age, period effects showing a decreasing risk and then an increasing risk. Cohort effects of prevalence and DALYs began to decline after the 1950s. Young-onset dementia presents a growing global health challenge in the age, period and cohort across SDI regions, countries.

Background and purpose: The causal association between inflammatory cytokines and the development of intracranial aneurysm (IA), unruptured IA (uIA) and subarachnoid hemorrhage (SAH) lacks clarity.Methods: The summary‐level datasets for inflammatory cytokines were extracted from a genome‐wide association study of the Finnish Cardiovascular Risk in Young Adults Study and the FINRISK survey. The summary statistics datasets related to IA, uIA and SAH were obtained from the genome‐wide association study meta‐analysis of the International Stroke Genetics Consortium and FinnGen Consortium. The primary method employed for analysis was inverse variance weighting (false discovery rate), supplemented by sensitivity analyses to address pleiotropy and enhance robustness.Results: In the International Stroke Genetics Consortium, 10, six and eight inflammatory cytokines exhibited a causal association with IA, uIA and SAH, respectively (false discovery rate, p < 0.05). In FinnGen datasets, macrophage Inflammatory Protein‐1 Alpha (MIP_1A), MIP_1A and interferon γ‐induced protein 10 (IP_10) were verified for IA, uIA and SAH, respectively. In the reverse Mendelian randomization analysis, the common cytokines altered by uIA and SAH were vascular endothelial growth factor (VEGF), MIP_1A, IL_9, IL_10 and IL_17, respectively. The meta‐analysis results show that MIP_1A and IP_10 could be associated with the decreased risk of IA, and MIP_1A and IP_10 were associated with the decreased risk of uIA and SAH, respectively. Notably, the levels of VEGF, MIP_1A, IL_9, IL_10 and TNF_A were increased with uIA. Comprehensive heterogeneity and pleiotropy analyses confirmed the robustness of these results.Conclusion: Our study unveils a bidirectional association between inflammatory cytokines and IA, uIA and SAH. Further investigations are essential to validate their relationship and elucidate the underlying mechanisms.

BACKGROUND: Iron status has been associated with functional outcomes after ischemic stroke (IS). Nonetheless, this association may be affected by confounders. We perform Mendelian randomization to clarify the causal association between iron status and functional outcome after IS. METHODS: We obtained summary-level statistics related to iron status biomarkers from a meta-analysis of a gene-wide association study conducted by the Genetics of Iron Status Consortium, which included 11 discovery cohorts and 8 replication cohorts. We also took genetic variants related to 4 biomarkers of iron status from combining gene-wide association study results of Iceland, the United Kingdom, and Denmark to perform a replicate Mendelian randomization analysis. This data set included 4 iron status biomarkers, namely, ferritin, total iron binding capacity, iron, and transferrin saturation (TSAT). The confounders in these data sets have been adjusted to mitigate the collider bias. We acquired summary statistics data sets for functional outcomes following IS from the gene-wide association study meta-analysis conducted by the Genetics of Ischemic Stroke Functional Outcome Consortium. The genetic estimates for functional outcomes at 90 days after IS were evaluated by the modified Rankin Scale score, including 3741 cases with good functional outcomes (modified Rankin Scale score, 0–2) and 2280 subjects with poor functional outcomes poststroke (modified Rankin Scale score, 3–6). Inverse variance weighting was used as the primary method, complemented by sensitivity analyses for pleiotropy and increasing robustness. RESULTS: Reported with odds ratios (ORs) of stroke outcome with per SD unit increase in genetically determined iron status biomarker, TSAT and iron were associated with poor functional outcome after IS (TSAT: OR, 1.36 [95% CI, 1.23–1.50]; P =2.27×10 ^{− 9} ; iron: OR, 1.44 [95% CI, 1.13–1.85]; P =0.0033). In replicate Mendelian randomization analysis, the detrimental effects of iron on poor functional outcome after IS remained stable (OR, 1.60 [95% CI, 1.24–2.08]; P =0.0003). In the meta-analysis, iron and TSAT were associated with poor functional outcomes after IS (TSAT: OR _meta , 1.35 [95% CI, 1.23–1.48]; iron: OR _meta , 1.51 [95% CI, 1.27–1.81]). Through sensitivity analyses and reverse Mendelian randomization analyses, we confirmed the robustness of the results. CONCLUSIONS: Our study provides evidence suggesting a potential causal relationship between iron status and poor functional outcomes after IS. Future studies are required to illuminate the underlying mechanism.

Background: Among the histiocytic disorders, anaplastic lymphoma kinase (ALK)-positive histiocytosis emerged in 2008. As more and more cases of the novel entity are reported, our understanding of it is deepened. However, only a few cases with central nervous system (CNS) involvement have been reported. Furthermore, the lesion in the suprasellar region has not been documented. Case presentation: We presented a case of ALK-positive histiocytosis involving the suprasellar region of a one-year-and-four-month-old boy. Through clinical, neuropathological, and genomic analyses, the patient was diagnosed with ALK-positive histiocytosis. After lesions were resected he started treatment with a combination of the three compounds vincristine, prednisolone, and crizotinib, but they did not work. Cytarabine was then added as an additional chemotherapy drug for him, and the lesions in the brain and lungs were shrunk by combining treatment of crizotinib, dexamethasone, vincristine, and cytarabine according to the RECIST (esponse Evaluation Criteria In Solid Tumours). Conclusions: Additional adjuvant chemotherapy drugs are needed when ALK-inhibitor treatment is ineffective.

Introduction Primary pontine haemorrhage (PPH) is the most devastating subtype of intracerebral haemorrhage and is associated with poor prognosis, especially for the severe patients. Although medical treatment (MT) is widely accepted, a large number of studies have shown surgical haematoma evacuation (HE) might dramatically reduce mortality and improve prognosis outcome in severe PPH (sPPH). However, evidence to clarify the safety of HE remains insufficient. Methods and analysis The Safety of surgical Treatment In severe primary Pontine haemorrhage Evacuation study is a multi-centre, randomised, controlled, open-label trial, conducted from January 2022 to November 2024 in 20 tertiary hospitals in China. A total of 64 patients with sPPH will be randomly assigned to MT or HE group. Eligible patients will receive the corresponding treatment according to the result of randomisation. The primary outcomes are related to the safety of surgery including rate of symptomatic rebleeding at 3 days and rate of mortality and intracranial infection at 30 days. The secondary outcomes are the neurological function indexes following up at 30 days, 90 days, 180 days and 365 days. Ethics and dissemination The clinical trial has been approved by the Biomedical Research Ethics Committee of West China Hospital of Sichuan University (unique identifiers: No. 2020-894). All results of the trial will be published in international peer-reviewed scientific journals and will be disseminated through scientific conferences. Academic dissertation will be published in a peer-reviewed journal. Trial registration numbers NCT04647162, ChiCTR2000039679.