Background: Aspects of neighborhood environment, such as socioeconomic status, air pollution, walkability, and extreme heat, are associated with stroke incidence and severity. Less is known about cumulative and interactive effects of a range of neighborhood environmental features. We evaluated the associations of neighborhood social and environmental burden with incident stroke and initial stroke severity and whether these associations differed by ethnicity. Method: All first-ever Mexican American (MA) and Non-Hispanic White (NHW) stroke cases between 2022-2024 in the Brain Attack Surveillance in Corpus Christi Project across 78 census tracts were included (n=1,215). Stroke severity was measured by National Institute of Health Stroke Severity (NIHSS) score. Census-tract level social vulnerability index (SVI) and environmental burden index (EBI) data came from the CDC in 2022 ( Table 1 ). Cumulative environmental burden was calculated by summing the ranks of SVI and EBI and converting to a percentile score ranging from 0-1 (larger →higher burden). Data on population at risk of stroke by census tracts were from the US Census. Poisson and linear regressions were used to estimate unadjusted and age-sex-ethnicity adjusted associations between three environmental burden indices and their interaction and incident stroke rates and NIHSS score, respectively, accounting for clustering within census tracts. Results: High cumulative burden (index>0.75) existed in 15 tracts ( Figure 1 ). Similar distributions were found for SVI and EBI. Higher SVI was associated with higher incident stroke rates in the fully adjusted model ( Table 2 ), overall (90 th vs 10 th percentile RR 1.32, 95% CI 1.03, 1.69) and among MAs (RR 1.53, 95% CI 1.08, 2.16). Higher EBI was associated with lower incident stroke rates among NHWs (RR 0.78, 95% CI 0.61, 0.99) but not MAs. A multiplicative interaction between SVI and EBI was found (P=0.02) in the full sample. In neighborhoods with high EBI (90 th percentile), higher SVI was associated with higher stroke rates (RR 2.62, 95% CI 1.59, 4.32) but not in neighborhoods with low EBI. No significant association between environmental burden and NIHSS was found. Conclusion: Neighborhood social environmental burden was associated with higher incident stroke rates, particularly among MAs and neighborhoods with high natural and built environment burden. Findings suggest the importance of neighborhood social and environmental burdens in primary prevention of stroke.

BACKGROUND:Poverty is associated with increased stroke risk. It is unclear how this has changed over time. We evaluated temporal trends in stroke incidence and 30-day poststroke mortality by neighborhood socioeconomic status (nSES) from 2000 to 2022. METHODS:All ischemic and hemorrhagic strokes from a population-based stroke surveillance study in Nueces County, Texas from 2000 to 2022 were ascertained and geocoded to census tracts. A composite nSES score was assigned to each tract for each year using data from the US Census Bureau and American Community Survey. Incidence rates at the group level were estimated using Poisson regression. Model 1 included annual nSES percentile, age, sex, and ethnicity. Model 2 added nSES-time, age-time, and ethnicity-time interactions. Trends in 30-day mortality at the individual level were evaluated similarly using multivariable logistic regression, adjusting for clinical and sociodemographic factors. RESULTS:A total of 5536 stroke cases occurred during the study period and were successfully geocoded. Poorer nSES was associated with greater stroke incidence (incidence rate ratio for 10th versus 90th percentile nSES, 1.37 [95% CI, 1.22-1.54]) at the group level. The magnitude of this association changed over time (nSES*time interaction P value=0.019), fluctuating without a consistent unidirectional trend. Thirty-day mortality at the individual level was not associated with nSES (10th versus 90th percentile adjusted odds ratio, 0.96 [95% CI, 0.70-1.43]) and changes in mortality over time did not differ by nSES (no significant nSES-time interaction). CONCLUSIONS:Residents of poorer neighborhoods had an excess risk of incident stroke that fluctuated in magnitude over time. Ongoing stroke prevention efforts are needed, particularly among residents of low SES neighborhoods.

Background: Aspects of neighborhood environment, such as socioeconomic status, air pollution, walkability, and extreme heat, are associated with stroke incidence and severity. Less is known about cumulative and interactive effects of a range of neighborhood environmental features. We evaluated the associations of neighborhood social and environmental burden with incident stroke and initial stroke severity and whether these associations differed by ethnicity. Method: All first-ever Mexican American (MA) and Non-Hispanic White (NHW) stroke cases between 2022-2024 in the Brain Attack Surveillance in Corpus Christi Project across 78 census tracts were included (n=1,215). Stroke severity was measured by National Institute of Health Stroke Severity (NIHSS) score. Census-tract level social vulnerability index (SVI) and environmental burden index (EBI) data came from the CDC in 2022 ( Table 1 ). Cumulative environmental burden was calculated by summing the ranks of SVI and EBI and converting to a percentile score ranging from 0-1 (larger →higher burden). Data on population at risk of stroke by census tracts were from the US Census. Poisson and linear regressions were used to estimate unadjusted and age-sex-ethnicity adjusted associations between three environmental burden indices and their interaction and incident stroke rates and NIHSS score, respectively, accounting for clustering within census tracts. Results: High cumulative burden (index>0.75) existed in 15 tracts ( Figure 1 ). Similar distributions were found for SVI and EBI. Higher SVI was associated with higher incident stroke rates in the fully adjusted model ( Table 2 ), overall (90 th vs 10 th percentile RR 1.32, 95% CI 1.03, 1.69) and among MAs (RR 1.53, 95% CI 1.08, 2.16). Higher EBI was associated with lower incident stroke rates among NHWs (RR 0.78, 95% CI 0.61, 0.99) but not MAs. A multiplicative interaction between SVI and EBI was found (P=0.02) in the full sample. In neighborhoods with high EBI (90 th percentile), higher SVI was associated with higher stroke rates (RR 2.62, 95% CI 1.59, 4.32) but not in neighborhoods with low EBI. No significant association between environmental burden and NIHSS was found. Conclusion: Neighborhood social environmental burden was associated with higher incident stroke rates, particularly among MAs and neighborhoods with high natural and built environment burden. Findings suggest the importance of neighborhood social and environmental burdens in primary prevention of stroke.

Postoperative Nausea and Vomiting (PONV) is a potential complication in all people undergoing general anesthesia (GA), causing significant discomfort and potentially leading to serious complications. Despite decades of research and the implementation of various preventive drugs and measures, complete prevention via traditional guidelines continues to pose challenges in clinical settings. This article will review mechanisms, influencing factors (including patient-related, surgery-related, and anesthesia-related factors), and strategies for prevention and treatment, both pharmacological and non-pharmacological, for PONV in adultsunder GA. This manuscript also summarizes randomized trials investigating the incidence of PONV in adults receiving opioid-sparing or opioid-free perioperative GA-based protocols. This review aims to summarize evidence-based guidance amidst traditional guidance, and other recent considerations, for optimizing anesthetic management strategies in clinical practice.

BACKGROUND AND OBJECTIVES:Given the growing number of US stroke survivors, especially female survivors, understanding contemporary trajectories of stroke outcomes by sex is crucial. Yet, such data are rare. We estimated sex-specific changes in poststroke functional, neurologic, quality of life, and cognitive outcomes. METHODS:This cohort study included first-ever ischemic strokes (ISs) ascertained from the Brain Attack Surveillance in Corpus Christi Project (south Texas, 2014-2019). Data were from medical records (e.g., age, sex) and interviews (baseline, 3, 6, and 12 months after stroke), including functional (activities of daily living/instrumental activities of daily living score [ADL/IADL]), neurologic (NIH Stroke Scale), quality of life (abbreviated Stroke-specific Quality of Life scale), and cognitive (Modified Mini-Mental State Examination [3MSE]) outcomes. Multivariable adjusted linear mixed effects models including interactions between sex and time were used to estimate sex differences at each time point and sex-specific changes in outcomes. RESULTS:Among the 1,046 IS (mean age 66, 47.6% female survivors), female survivors had higher adjusted mean ADL/IADL scores than male survivors at 3, 6, and 12 months, despite a decrease in ADL/IADL scores from 3 to 12 months only among female survivors (adjusted mean difference in ADL/IADL scores -0.08, 95% CI -0.14 to -0.03). While no significant sex differences were observed for other outcomes, both sexes experienced an improvement in neurologic outcome, and an improvement in cognition was only found among male survivors (adjusted mean difference in 3MSE scores 0.97, 95% CI 0.09-1.85). Improvements were primarily driven by recoveries from 3 to 6 months. DISCUSSION:Female survivors had worse functional outcome but not other outcomes than male survivors up to 12 months after stroke. Although outcomes generally continued improving after 3 months poststroke for both sexes, the recovery pattern differed by sex. These results suggest that early and continued assessments of functional outcome after stroke may be needed, particularly for female survivors to reduce the sex differences, and that future interventions designed to improve outcomes in the chronic phase of stroke should consider the sex-specific recovery patterns. The generalizability may be limited by our single community study population, and results should be replicated in other populations.

PURPOSE:To estimate temporal trends in post-stroke outcomes in Mexican Americans (MAs) and non-Hispanic whites (NHWs). METHODS:We included first-ever ischemic strokes from a population-based study in South Texas (n = 5343, 2000-2019). We applied an illness-death model with three jointly specified Cox-type models to estimate ethnic differences and ethnic-specific temporal trends in recurrence (first stroke to recurrence), recurrence-free mortality (first stroke to death without recurrence), recurrence-affected mortality (first stroke to death with recurrence), and postrecurrence mortality (recurrence to death). RESULTS:MAs had higher rates of postrecurrence mortality than NHWs in 2019 but lower rates in 2000. One-year risk of this outcome increased in MAs and decreased in NHWs, resulting in ethnic differences changing from -14.9% (95% CI -35.9%, -2.8%) in 2000 to 9.1% (1.7%, 18.9%) in 2018. For recurrence-free mortality, lower rates were observed in MAs until 2013. Ethnic differences in 1-year risk changed from -3.3% (95% CI -4.9%, -1.6%) in 2000 to -1.2% (-3.1%, 0.8%) in 2018. For stroke recurrence and recurrence-affected mortality, significant ethnic disparities persisted over the study period. CONCLUSIONS:An ethnic disparity in postrecurrence mortality was newly identified, driven by the increasing trend in MAs but a decreasing trend in NHWs.

ETHNOPHARMACOLOGICAL RELEVANCE:Vascular dementia (VaD) is the common cognitive disorder derived mainly from lacunar stroke (LS). The oxidative stress induced neurovascular coupling (NVC) dysfunction involves in the pathogenesis of VaD. Currently, there is no specific drug for VaD. Ling-Yang-Gou-Teng -Decoction (LG), a well-known traditional Chinese formula, has been used for preventing VaD in clinic. AIM OF THE STUDY:In this study, we aimed to investigate the underlying mechanism of LG on VaD in rats. MATERIALS AND METHOD:VaD was replicated with autologous micro-thrombi against the background of hypercholesterolemia induced with high fatty diet. PTX (68.90 mg/kg/day), LG with three dosages (2.58, 8.14, 25.80 g/kg/day) was orally administrated to VaD rats, respectively. The NVC sensitivity was defined as the ratio of the microcirculative cerebral blood velocity (CBV) to the electroencephalograph (EEG) before and after penicillin stimulation. Behavioral performance, pathological changes of brain and oxidation related molecules were detected to assess the effects of LG on VaD. RESULTS:LG exhibited beneficial effects on the VaD, which was demonstrated as improved exploratory, learning and memory abilities, relieved vascular or neural pathological changes in cerebral cortex or hippocampus. LG maintained NVC sensitivity, which was confirmed as significantly increased ΔCBV and the elevated ratio of ΔCBV/ΔqEEG. The underlying mechanisms of LG was associated with antioxidant effects, which was confirmed as significantly decreased nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) expression, and increased superoxide dismutase 3 (SOD3) expression. LG also reduced iNOS, increased nNOS and eNOS expression to restore NO bioavailability. CONCLUSIONS:The results suggested that LG prevented VaD may associate with inhibiting oxidative stress, protecting NO bioavailability, and then maintaining NVC sensitivity.

Vascular dementia (VaD) is the common cognitive disorder derived mainly from lacunar stroke. The neurovascular coupling (NVC) dysfunction involves in its pathogenesis. VaD lacks suitable animal models for developing preventive therapies. This study aimed to confirm a model for preventing VaD via maintaining NVC sensitivity in rats. The model was replicated with autologous microthrombi against the background of hypercholesterolemia. A phosphodiesterase inhibitor (pentoxyfylline) was preventively administrated to confirm the role of NVC sensitivity. Cognitive function was evaluated as exploratory, learning and memorizing abilities. NVC sensitivity was defined as the ratio of microcirculative cerebral blood flow (∆CBF) to the quantitative electroencephalograph (∆qEEG) before and after penicillin stimulation. The pathogenesis of NVC dysfunction was explored as expressions of neuronal (nNOS), inducible (iNOS) and endothelial nitric oxide synthase (eNOS) in cerebral cortex. The model rats showed cognitive impairment, microvascular edema (2.54 ± 0.30%, P < 0.01), neuronal edema (1.24 ± 0.48%, P < 0.01) and nissl body loss (0.03 ± 0.003%, P < 0.01) in cerebral cortex, and neuronal necrosis in hippocampal CA1 region (neuronal cell number 41.76 ± 10.04 cells, P < 0.01) compared with sham group. The NVC dullness in model rats was confirmed as significantly decreased ratio of ∆CBF/∆qEEG (0.05 ± 0.02%, P < 0.01) compared with sham group (0.20 ± 0.06%). The underlying mechanism of NVC dysfunction was found as imbalanced NOS expressions (decreased nNOS and eNOS, while increased iNOS levels in cerebral cortex). The NVC dullness was significantly relieved in pentoxyfylline administrated rats (0.12 ± 0.06%, P < 0.01). It indicated that this model was suitable to evaluate candidates for preventing VaD via maintaining NVC sensitivity.

To develop a new model of vascular dementia for evaluating Chinese medicine prescriptions.