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Stroke is a disease of disparities, with tremendous racial and ethnic inequities in incidence, prevalence, treatment, and outcomes. The accumulating literature on the relationship between stroke and social determinants of health (ie, the structural conditions of the places where people live, learn, work, and play) contributes to our understanding of stroke inequities. Several interventions have been tested concurrently to reduce racial and ethnic inequities in stroke preparedness, care, recovery, and risk factor control. It is regrettable that no common theoretical framework has been used to facilitate comparison of interventions. In this scientific statement, we summarize, across the stroke continuum of care, trials of interventions addressing racial and ethnic inequities in stroke care and outcomes. We reviewed the literature on interventions to address racial and ethnic inequities to identify gaps and areas for future research. Although numerous trials tested interventions aimed at reducing inequities in prehospital, acute care, transitions in care, and poststroke risk factor control, few addressed inequities in rehabilitation, recovery, and social reintegration. Most studies addressed proximate determinants (eg, medication adherence, health literacy, and health behaviors), but upstream determinants (eg, structural racism, housing, income, food security, access to care) were not addressed. A common theoretical model of social determinants can help researchers understand the heterogeneity of social determinants, inform future directions in stroke inequities research, support research in understudied areas within the continuum of care, catalyze implementation of successful interventions in additional settings, allow for comparison across studies, and provide insight into whether addressing upstream or downstream social determinants has the strongest effect on reducing inequities in stroke care and outcomes.

Purpose: Cognitive impairment is a common consequence of stroke and has direct implications for poststroke functioning and quality of life, including the ability to maintain a job, live independently, sustain interpersonal relationships, and drive a vehicle. In this scientific statement, we critically appraise the literature on the prevalence, diagnosis, and management of poststroke cognitive impairment (PSCI) and provide a framework for clinical care while highlighting gaps that merit further study., Methods: We performed a scoping literature review of randomized controlled clinical trials, prospective and retrospective cohort studies, case-control studies, clinical guidelines, review articles, and editorials on the incidence and prevalence, natural history, diagnosis, and management of PSCI. Scoping reviews determine the scope of a body of literature on a given topic to indicate the volume of literature and the studies currently available and provide an overview of its focus., Results: PSCI is common after stroke, especially in the first year, and ranges from mild to severe. Although cognitive impairment is reversible in some cases early after stroke, up to one-third of individuals with stroke develop dementia within 5 years. The pathophysiology is not yet fully elucidated but is likely attributable to an acute stroke precipitating a series of pathological events, often in the setting of preexisting microvascular and neurodegenerative changes. Screening for associated comorbidities and interdisciplinary management are integral components of the care of individuals with PSCI. There is a need for prospective studies evaluating the individual trajectory of PSCI and the role of the acute vascular event in the predisposition for Alzheimer disease and related dementias, as well as high-quality, randomized clinical trials focused on PSCI management.

Background: Post-stroke depression and anxiety are common and are associated with worse post-stroke outcomes. Even though checking for depression during stroke hospitalization has become a common practice, the prognostic value of a positive in-hospital depression screen following stroke remains unclear., Methods: This is a retrospective cohort study of patients with stroke or TIA discharged home from a tertiary care center. We examined the association between premorbid history of depression and in-hospital anxiety/depressive symptoms, with anxiety/depressive symptoms and functional outcome at 3-months post-stroke. Logistic regression models were generated using two different main predictors: 1) pre-hospital history of depression (N = 117) and 2) in-hospital depression/anxiety measured by the EQ-5D-3L (N = 66)., Results: In the cohort of 117 patients, the mean age was 66 years, with median NIHSS 2;44% were women and 70% White. A history of pre-stroke depression was reported by 7% (8/117). Anxiety/depression on ED-5D-3L was reported by 29/66 (43%) in the hospital and by 22/66 (33%) at three months' post-stroke. In the first adjusted model, previous history of depression was associated with 3 months EQ-5D-3L anxiety/depression (OR = 10.2;95%CI:1.12-90.9, p = 0.038). In the second adjusted model, in-hospital anxiety/depression was associated with 3-month EQ-5D-3L anxiety/depression (OR = 3.9; 95% CI:1.16-13.1, p = 0.027). In-hospital anxiety/depression was associated with a higher mRS at 3 months but not after adjusting for covariates., Conclusion: A previous history of depression and in-hospital anxiety/depression symptoms are associated with anxiety/depression symptoms 3-months post-stroke but not with functional outcome. Screening stroke patients for both during hospitalization is warranted because of the association with later symptoms., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Stroke contributes an estimated $28 billion to US health care costs annually, and alternative payment models aim to improve outcomes and lower spending over fee-for-service by aligning economic incentives with high value care. This systematic review evaluates historical and current evidence regarding the impacts of alternative payment models on stroke outcomes, spending, and utilization. Included studies evaluated alternative payment models in 4 categories: pay-for-performance (n=3), prospective payments (n=14), shared savings (n=5), and capitated payments (n=14). Pay-for-performance models were not consistently associated with improvements in clinical quality indicators of stroke prevention. Studies of prospective payments suggested that poststroke spending was shifted between care settings without consistent reductions in total spending. Shared savings programs, such as US Medicare accountable care organizations and bundled payments, were generally associated with null or decreased spending and service utilization and with no differences in clinical outcomes following stroke hospitalizations. Capitated payment models were associated with inconsistent effects on poststroke spending and utilization and some worsened clinical outcomes. Shared savings models that incentivize coordination of care across care settings show potential for lowering spending with no evidence for worsened clinical outcomes; however, few studies evaluated clinical or patient-reported outcomes, and the evidence, largely US-based, may not generalize to other settings.

There are a plethora of cognitive sequelae in addition to neglect and extinction that arise with unilateral right hemispheric stroke (RHS). Cognitive deficits following non-dominant (right) hemisphere stroke are common with unilateral neglect and extinction being the most recognized examples. The severity of RHS is usually underestimated by the National Institutes of Health Stroke Scale (NIHSS), which in terms of lateralized right hemisphere cognitive deficits, tests only for visual inattention/extinction. They account for 2 out of 42 total possible points. Additional neuropsychiatric sequelae include but are not limited to deficiencies in affective prosody comprehension and production (aprosodias), understanding and expressing facial emotions, empathy, recognition of familiar faces, anxiety, mania, apathy, and psychosis. These sequelae have a profound impact on patients' quality of life; affecting communication, interpersonal relationships, and the ability to fulfill social roles. They also pose additional challenges to recovery. There is presently a gap in the literature regarding a cohesive overview of the significant cognitive sequelae following RHS. This paper serves as a narrative survey of the current understanding of the subject, with particular emphasis on neuropsychiatric poststroke syndromes not predominantly associated with left hemisphere lesions (LHL), bilateral lesions, hemiplegia, or paralysis. A more comprehensive understanding of the neuropsychological consequences of RHS extending beyond the typical associations of unilateral neglect and extinction may have important implications for clinical practice, including the ways in which clinicians approach diagnostics, treatment, and rehabilitation., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background: African-Americans (AA) are 3 times more likely to have small-vessel-type ischemic strokes (SVS) than Whites. Small vessel strokes are associated with cognitive impairment, a relationship incompletely explained by white matter hyperintensity (WMH) burden. We examined whether inflammatory/endothelial dysfunction biomarkers are associated with cognition after SVS in AAs., Methods: Biomarkers were obtained in 24 subjects (median age 56.5 years, 54% women, median 12 years education). Cognition was assessed more than 6 weeks poststroke using the memory composite score (MCS), which was generated using recall from the Hopkins Verbal Learning Test-II and Brief Visuospatial Memory Test-Revised. A semi-automated, volumetric protocol was used to quantify WMH volume (WMHv) on clinical MRI scans. Potential biomarkers including vascular cell adhesion molecule-1 (VCAM-1), interleukin-1 receptor antagonist, interleukin-6, interleukin-8, interleukin-10, interferon gamma, and thrombin-antithrombin (TAT) were log-transformed and correlated with MCS with adjustment for potential confounders., Results: Among serum biomarkers, only VCAM-1-correlated with poorer memory based on the MCS (r = -.659; P = .0006). VCAM-1 (r = .554; P = .005) and age (r = .479; P = .018) correlated with WMHv; VCAM-1 was independently associated with MCS after adjustment for WMHv, age, and education (P = .023)., Conclusions: The findings of this exploratory analysis suggest that endothelial dysfunction and inflammation as reflected by VCAM-1 levels may play a role in poststroke cognitive impairment. Additional studies are needed to validate this observation and to evaluate this relationship in non-AAs and with other stroke types and compare this finding to cognitive impairment in nonstroke populations., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background and Purpose- Kidney dysfunction is common among patients hospitalized for ischemic stroke. Understanding the association of kidney disease with poststroke outcomes is important to properly adjust for case mix in outcome studies, payment models and risk-standardized hospital readmission rates. Methods- In this cohort study of fee-for-service Medicare patients admitted with ischemic stroke to 1579 Get With The Guidelines-Stroke participating hospitals between 2009 and 2014, adjusted multivariable Cox proportional hazards models were used to determine the independent associations of estimated glomerular filtration rate (eGFR) and dialysis status with 30-day and 1-year postdischarge mortality and rehospitalizations. Results- Of 204 652 patients discharged alive (median age [25th-75th percentile] 80 years [73.0-86.0], 57.6% women, 79.8% white), 48.8% had an eGFR ≥60, 26.5% an eGFR 45 to 59, 16.3% an eGFR 30 to 44, 5.1% an eGFR 15 to 29, 0.6% an eGFR <15 without dialysis, and 2.8% were receiving dialysis. Compared with eGFR ≥60, and after adjusting for relevant variables, eGFR <45 was associated with increased 30-day mortality with the risk highest among those with eGFR <15 without dialysis (hazard ratio [HR], 2.09; 95% CI, 1.66-2.63). An eGFR <60 was associated with increased 1-year poststroke mortality that was highest among patients on dialysis (HR, 2.65; 95% CI, 2.49-2.81). Dialysis was also associated with the highest 30-day and 1-year rehospitalization rates (HR, 2.10; 95% CI, 1.95-2.26 and HR, 2.55; 95% CI, 2.44-2.66, respectively) and 30-day and 1-year composite of mortality and rehospitalization (HR, 2.04; 95% CI, 1.90-2.18 and HR, 2.46; 95% CI, 2.36-2.56, respectively). Conclusions- Within the first year after index hospitalization for ischemic stroke, eGFR and dialysis status on admission are associated with poststroke mortality and hospital readmissions. Kidney function should be included in risk-stratification models for poststroke outcomes.

Background: We investigated the independent association of depression status at 3 and 12 months after stroke and functional decline., Methods: Data were obtained as part of the multicenter Adherence eValuation After Ischemic stroke Longitudinal (AVAIL) registry. Depression was assessed with the Patient Health Questionnaire-8 (depression, PHQ-8 ≥ 10), and functional status was assessed with the modified Rankin score (mRS) at 3 and 12 months following hospitalization for ischemic stroke. We used logistic regression analyses to evaluate the independent association between the change in depression rating and the change in mRS., Results: Among 1444 patients, 75% did not have depression at either time point, 9.2% had persistent depression, 8.7% had resolving depression, and 7% had incident depression at 12 months. After covariate adjustment, depression status at 3 and 12 months remained associated with worsening mRS (P = .01). Compared with patients without depression, those with resolving depression were less likely to have a worsening mRS (odds ratio [OR] = .49, 95% confidence interval [CI]: .29-0.83). There was no difference in functional decline between those with no depression and those with persistent depression; however, those with persistent depression had worse mRS at both time points (median mRS: 2.5 [Q1-Q3: 2-3] at 3 months; 2 [2-3] at 12 months) than those with no depression (mRS: 1 [0-2] at both 3 and 12 months), P < .0001., Conclusions: Patients with resolving depression in the first year after stroke were less likely to have functional deterioration than those without depression. Greater functional impairment was present in the setting of depression., (Copyright © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Poststroke depression (PSD) is common, affecting approximately one third of stroke survivors at any one time after stroke. Individuals with PSD are at a higher risk for suboptimal recovery, recurrent vascular events, poor quality of life, and mortality. Although PSD is prevalent, uncertainty remains regarding predisposing risk factors and optimal strategies for prevention and treatment. This is the first scientific statement from the American Heart Association on the topic of PSD. Members of the writing group were appointed by the American Heart Association Stroke Council's Scientific Statements Oversight Committee and the American Heart Association's Manuscript Oversight Committee. Members were assigned topics relevant to their areas of expertise and reviewed appropriate literature, references to published clinical and epidemiology studies, clinical and public health guidelines, authoritative statements, and expert opinion. This multispecialty statement provides a comprehensive review of the current evidence and gaps in current knowledge of the epidemiology, pathophysiology, outcomes, management, and prevention of PSD, and provides implications for clinical practice., (© 2016 American Heart Association, Inc.)

Background and Purpose: Kidney disease is a frequent comorbidity in patients presenting with acute ischemic stroke. We evaluated whether the estimated glomerular filtration rate (eGFR) on admission is associated with poststroke in-hospital mortality or discharge disposition., Methods: In this cohort study, data from ischemic stroke patients in Get With The Guidelines-Stroke linked to fee-for-service Medicare data were analyzed. The Modification of Diet in Renal Disease study equation was used to calculate the eGFR (mL/min/1.73 m 2 ). Dialysis was identified by International Classification of Diseases, Ninth Revision codes. Adjusted multivariable Cox proportional hazards models were used to determine the independent associations of eGFR with discharge disposition and in-hospital mortality. Adjusted individual models also examined whether the association of clinical and demographic factors with outcomes varied by eGFR level., Results: Of 232 236 patients, 47.3% had an eGFR ≥60, 26.6% an eGFR 45 to 59, 16.8% an eGFR 30 to 44, 5.6% an eGFR 15 to 29, 0.7% an eGFR<15 without dialysis, and 2.8% were receiving dialysis. Of the total cohort, 11.8% died during the hospitalization or were discharged to hospice, and 38.6% were discharged home. After adjusting for other relevant variables, renal dysfunction was independently associated with an increased risk of in-hospital mortality that was highest among those with eGFR <15 without dialysis (odds ratio, 2.52; 95% confidence interval, 2.07-3.07). An eGFR 15 to 29 (odds ratio, 0.82; 95% confidence interval, 0.78-0.87), eGFR <15 (odds ratio, 0.72; 95% confidence interval, 0.61-0.86), and dialysis (odds ratio, 0.86; 95% confidence interval, 0.79-0.94) remained associated with lower odds of being discharged home. In addition, the associations of several clinical and demographic factors with outcomes varied by eGFR level., Conclusions: eGFR on admission is an important predictor of poststroke short-term outcomes., Competing Interests: Conflicts of interest/Disclosures: Christine Ju: Nothing to disclose Dr. Schwamm: Nothing to disclose Dr. Schulte: Nothing to disclose Dr. Xian: Nothing to disclose Dr. Goldstein: Nothing to disclose, (© 2016 American Heart Association, Inc.)

Chronic kidney disease (CKD) is associated with an increased risk of both ischemic and hemorrhagic stroke. In addition to shared risk factors, this higher cerebrovascular risk is mediated by several CKD-associated mechanisms including platelet dysfunction, coagulation disorders, endothelial dysfunction, inflammation, and increased risk of atrial fibrillation. CKD can also modify the effect of treatments used in acute stroke and in secondary stroke prevention. We review the epidemiology and pathophysiology that link CKD and stroke and the impact of CKD on stroke outcomes. Interdisciplinary collaboration between nephrologists, pharmacists, hematologists, nutrition therapists, primary care physicians, and neurologists in providing care to these subjects may potentially improve outcomes., (Copyright © 2014 National Kidney Foundation, Inc. All rights reserved.)

A number of neuroendocrine changes have been described after stroke, which may serve adaptive or deleterious functions. The neuroendocrine changes include activation of the hypothalamo-pituitary-adrenal axis, sympathetic nervous system and alterations of several hormonal levels. Alterations of the HPA axis, increased catecholamines, natriuretic peptides and, decreased melatonin and IGF-1 levels are associated with poor post-stroke outcome, although there is no definitive proof of causality. Therefore, it remains to be established whether alteration of neuroendocrine responses could be used as a potential therapeutic target to improve stroke outcome. This article gives an overview of the major neuroendocrine pathways altered by stroke and highlights their potential for clinical use and further neurotherapeutic development by summarizing the evidence for their association with stroke outcome including functional outcome, post-stroke infection, delirium, depression and stroke-related myocardial injury.

Stroke rapid-response ("code stroke") teams facilitate the evaluation and treatment of patients presenting to emergency departments (EDs). Little is known about the usefulness of code stroke systems for patients hospitalized primarily for other conditions. We hypothesized that the yield of code stroke evaluations would be lower in hospitalized than in ED patients, and sought to identify potential targets for quality improvement efforts. Diagnoses and management of in-hospital and ED code stroke patients were assessed retrospectively in a Joint Commission-certified primary stroke center over a 1-year period. A total of 93 in-hospital and 204 ED code strokes were identified during this period. Compared with the ED patients, the hospitalized patients were less likely to have had a stroke/transient ischemic attack (26.8% vs 51.4%; P < .0001) and less likely to have been treated with a thrombolytic agent (odds ratio, 0.27; 95% confidence interval, 0.07-0.97: P = .03). Conditions not necessitating immediate neurologic care accounted for 63.4% of in-hospital strokes, compared with 31.3% of ED code strokes (P < .0001). "Altered mental status" was the sole presenting symptom in 48% of the hospitalized patients, compared with only 10% of ED patients (P < .0001), and was the only clinical feature independently associated with a stroke mimic in the hospitalized patients (odds ratio, 63.52; 95% confidence interval, 7.37-547.69; P = .0002). There was no association between a final diagnosis of a stroke mimic and patient age, sex or race-ethnicity or nursing shift. The proportions of patients with acute ischemic stroke and patients treated with thrombolytics after activation of in-hospital code stroke were small, and were lower than those of patients with ED code stroke in the same hospital over the same time period. Developing a standardized assessment protocol for hospitalized patients with altered mental status may improve the efficacy of care., (Published by Elsevier Inc.)

Strokes resulting from cardiac diseases, and cardiac abnormalities associated with neuromuscular disorders are examples of the many points of contact between neurology and cardiology. Approximately 20-30% of strokes are related to cardiac diseases, including atrial fibrillation, congestive heart failure, bacterial endocarditis, rheumatic and nonrheumatic valvular diseases, acute myocardial infarction with left ventricular thrombus, and cardiomyopathies associated with muscular dystrophies, among others. Strokes can also occur in the setting of cardiac interventions such as cardiac catheterization and coronary artery bypass procedures. Treatment to prevent recurrent stroke in any of these settings depends on the underlying etiology. Whereas anticoagulation with vitamin K antagonists is proven to be superior to acetylsalicylic acid for stroke prevention in atrial fibrillation, the superiority of anticoagulants has not been conclusively established for stroke associated with congestive heart failure and is contraindicated in those with infective endocarditis. Ongoing trials are evaluating management strategies in patients with atrial level shunts due to patent foramen ovale. Cardiomyopathies and conduction abnormalities are part of the spectrum of many neuromuscular disorders including mitochondrial disorders and muscular dystrophies. Cardiologists and neurologists share responsibility for caring for patients with or at risk for cardiogenic strokes, and for screening and managing the heart disease associated with neuromuscular disorders., (Copyright © 2010 Sociedad Española de Cardiología. Published by Elsevier Espana. All rights reserved.)

Background: The National Stroke Project (NSP) was a retrospective cohort study of US Medicare beneficiaries hospitalized with stroke or transient ischemic attack (TIA). The NSP included a simple assessment of stroke severity (NSP-Stroke Scale, NSP-SS). Used for risk adjustment in outcome studies, the reliability and validity of the NSP-SS have not been assessed. We determined the reliability, concurrent and construct validity of the NSP-SS., Methods: The initial neurologic examinations of 100 consecutive patients hospitalized with ischemic stroke/TIA in a single academic medical center were reviewed. The NSP-SS was retrospectively scored twice by the same rater and independently by a second rater to assess reliability. The National Institutes of Health Stroke Scale (NIH-SS) was also scored retrospectively and used as the criterion standard for concurrent validity. Construct validity was based on discharge status., Results: The NSP-SS had moderate-substantial inter-rater (weighted kappa, κ(w) = 0.66, 95% CI 0.55-0.77) and intra-rater (κ(w) = 0.63, 95% CI 0.52-0.75) reliability. Correlation between NSP-SS and NIH-SS scores was moderate (Spearman r = 0.65, 95% CI 0.52-0.75, p < 0.0001) but some categorizations in the NSP-SS seemed inappropriate reflecting poor content validity. Each NSP-SS point was associated with a greater likelihood of poor outcome (OR = 2.1, 95% CI 1.1-3.7, p = 0.016). Based on dichotomized scores (NSP 0-2 and NIH-SS <6; mild deficits), the NSP-SS sensitivity was 70.9% (95% CI 57.9-81.2%), specificity 82.2% (95% CI 68.7-90.7%), likelihood ratio for severe stroke 4.0 (95% CI 2.1-7.6) and likelihood ratio for mild stroke 0.3 (95% CI 0.20-0.5). The dichotomized NSP-SS and NIH-SS similarly predicted poor outcome (NSP-SS >2, OR = 4.7, 95% CI 1.7-13.0, p = 0.003 vs. NIH-SS ≥6, OR = 4.4, 95% CI 1.5-13.0, p = 0.006) with excellent discrimination (C = 0.827 and 0.826, respectively)., Conclusion: The NSP-SS has moderate-substantial reliability but poor content validity and poor to moderate concurrent validity as compared with the NIH-SS. In addition, it is not clear that the NSP-SS is easier to extract from medical records than the NIH-SS. Given this, and its other limitations, the utility of this scale for risk adjustment in future stroke outcome studies is questionable., (Copyright © 2011 S. Karger AG, Basel.)

Identifying a biomarker or panel of biomarkers of cerebral ischemia would have a major impact on the care of stroke patients by facilitating early management decisions and individualization of care. Biochemical surrogates of cerebral ischemia might also play an important role by identifying relevant pathways for novel therapeutic strategies and by facilitating early clinical trials in cerebrovascular disease. Serum biomarkers related to pathways of hemostasis, oxidation and inflammation, or alterations in glial and neuronal proteins, have been identified but none have been recommended for routine clinical use. This review describes the most promising biomarkers of cerebrovascular disease and the context and limitations in which they have been studied.