Post-stroke Dementia Research Articles

Hobby Engagement and Risk of Disabling Dementia.

The association between hobby engagement and risk of dementia reported from a short-term follow-up study for individuals aged ≥65 years may be susceptible to reverse causation. We examined the association between hobby engagement in age of 40-69 years and risk of dementia in a long-term follow-up study among Japanese, including individuals in mid-life, when the majority of individuals have normal cognitive function. A total of 22,377 individuals aged 40-69 years completed a self-administered questionnaire in 1993-1994. The participants answered whether they had hobbies according to the three following responses: having no hobbies, having a hobby, and having many hobbies. Follow-up for incident disabling dementia was conducted with long-term care insurance data from 2006 to 2016. During a median of 11.0 years of follow-up, 3,095 participants developed disabling dementia. Adjusting for the demographic, behavioral, and psychosocial factors, the multivariable hazard ratios of incident disabling dementia compared with "having no hobbies" were 0.82 (95% confidence interval [CI], 0.75-0.89) for "having a hobby" and 0.78 (95% CI, 0.67-0.91) for "having many hobbies". The inverse association was similarly observed in both middle (40-64 years) and older ages (65-69 years). For disabling dementia subtypes, hobby engagement was inversely associated with the risk of dementia without a history of stroke (probably non-vascular type dementia), but not with that of post-stroke dementia (probably vascular type dementia). Hobby engagement in both mid-life and late life was associated with a lower risk of disabling dementia without a history of stroke.

Intravenous thrombolysis for acute ischemic stroke is associated with lower risk of post-stroke dementia: A nationwide cohort study.

Dementia after stroke is common and is a great concern for patients and their caregivers. The objective was to investigate if intravenous thrombolysis (IVT) for acute ischemic stroke (AIS) was associated with lower risk of dementia after stroke. When IVT was introduced in Denmark, not all eligible patients were treated due to restricted access. We conducted a nationwide register-based cohort study of all patients with AIS in Denmark from 2004 to 2011. IVT-treated patients were propensity score-matched with comparable non-treated patients. Cox proportional hazards regression was used to estimate the hazard ratio (HR) for all-cause and vascular dementia 2, 5, and 10 years after stroke. Of the 5919 patients eligible for the study, 2305 IVT-treated patients were propensity score-matched with 2305 non-treated patients. Mean (SD) age was 66.6 (13.3) and 61.2% were male. Rate of all-cause dementia was lower for the IVT-treated 2 years (8.4/1000 person years (PY) vs 13.6/1000 PY, HR 0.63 (0.40-0.99)) and 5 years after stroke (7.3/1000 PY vs 11.4/1000 PY, HR 0.65 (0.46-0.91)). 10 years after stroke, the rates of all-cause dementia remained in favor of IVT (8.0/1000 PY vs 9.8/1000 PY, HR 0.83 (0.64-1.07)). IVT-treated had lower rates of vascular dementia 2 years (2.4/1000 PY vs 7.4/1000 PY, HR 0.33 (0.15-0.71)), 5 years (2.3/1000 PY vs 6.2/1000 PY, HR 0.38 (0.23-0.65)), and 10 years after stroke (3.0/1000 PY vs 5.4/1000 PY, HR 0.56 (0.38-0.81)). IVT treatment was associated with lower long-term risk of both vascular and all-cause dementia after AIS.

Abstract 013: Hippocampal Neuroinflammation Occurs After Focal Cerebral Ischemic Stroke That May Contribute To Post-Stroke Memory Loss

Chronic hypertension is a leading risk factor for ischemic stroke. Post-stroke dementia occurs in up to 80% of stroke survivors, and its prevalence is increasing due to an aging population. Memory is impaired in rodent models of transient middle cerebral artery occlusion (tMCAO). However, the impact of cerebral ischemia on brain regions involved in memory that are distant from the ischemic site, such as the hippocampus, remains unclear, but may involve neuroinflammation that is known to disrupt memory. We tested the hypothesis that neuroinflammation occurs in the hippocampus after tMCAO, contributing to memory dysfunction, and is more severe during chronic hypertension. Adult normotensive male Wistar rats and spontaneously hypertensive rats (SHR) underwent 45 minutes of ischemia induced using the intravascular filament method of tMCAO and seven days of reperfusion (or sham; n=6-8/group). A novel object recognition task was used days 5-7 post-tMCAO, and recognition index calculated to assess long-term memory function. Neuroinflammation in the hippocampal CA1 region of ipsi- and contralesional hemispheres was assessed immunohistochemically: microglial activation using Iba1 staining and neuronal expression of tumor necrosis factor alpha (TNFα). Data are mean ± SEM and comparisons made via a two-way ANOVA to determine the interaction between hypertension and stroke with a post-hoc Tukey test. Sham operated SHR and Wistar rats performed similarly well in the memory task and had recognition indices 0.65-0.70. However, memory was impaired in rats that had tMCAO, with recognition indices decreasing to 0.52±0.02 in Wistar rats and 0.52±0.03 in SHR (F 1,24 =21.60; p<0.01). Ischemia increased the number of TNFα expressing neurons regardless of hypertensive status in hippocampus of ipsi- (F 1,25 =7.87; p<0.01) and contra-lesional hemispheres (F 1,25 =4.22; p<0.05). There was a significant effect of ischemia on microglial activation in the hippocampus of both SHR and Wistar rats that only occurred ipsi-lesionally (F 1,24 =5.48; p<0.05). These findings demonstrate that hippocampal neuroinflammation is present seven days after transient focal cerebral ischemia that may contribute to post-stroke memory impairment.

Bolstering Cognitive and Locomotor Function in Post-Stroke Dementia Using Human-Robotic Interactive Gait Training.

Studies have reported inconclusive results regarding the effectiveness and clinical indications of the exclusive use of human-robotic interactive gait training (HIT) in patients with post-stroke dementia (PSD). This study aimed to compare the effects of human-robotic interactive gait training (HIT) and conventional physiotherapy (CPT) on cognitive and sensorimotor functions, trunk balance and coordination, dynamic and static balance, and activities related to daily living performance in patients with PSD. Forty-eight patients with PSD who received 60-minute therapy sessions three times per week for 6 weeks were assigned to either the CPT (n = 25) or HIT (n = 23) group. The clinical outcomes included the scores of the mini-mental state examination (MMSE), Fugl-Meyer assessment (FMA), trunk impairment scale (TIS), Berg balance scale (BBS), and modified Barthel index (MBI). Friedman tests were conducted at p < 0.05. The Friedman tests showed that HIT had superior effects to CPT in relation to MMSE, FMA, and TIS (p < 0.05), but not in relation to BBS and MBI (p > 0.05). Our results provide promising clinical evidence that HIT significantly improves cognitive and sensorimotor recovery functions, as well as trunk balance and coordination, in patients with PSD who cannot concurrently perform dual cognitive-locomotor tasks.

Cortical superficial siderosis is associated with reactive astrogliosis in cerebral amyloid angiopathy

BackgroundCortical superficial siderosis (cSS) has recently emerged as one of the most important predictors of symptomatic intracerebral hemorrhage and is a risk factor for post-stroke dementia in cerebral amyloid angiopathy (CAA). However, it remains unknown whether cSS is just a marker of severe CAA pathology or may itself contribute to intracerebral hemorrhage risk and cognitive decline. cSS is a chronic manifestation of convexal subarachnoid hemorrhage and is neuropathologically characterized by iron deposits in the superficial cortical layers. We hypothesized that these iron deposits lead to local neuroinflammation, a potentially contributory pathway towards secondary tissue injury.MethodsAccordingly, we assessed the distribution of inflammatory markers in relation to cortical iron deposits in post-mortem tissue from CAA cases. Serial sections from the frontal, parietal, temporal, and occipital lobes of nineteen autopsy cases with CAA were stained with Perls’ Prussian blue (iron) and underwent immunohistochemistry against glial fibrillary acidic protein (GFAP, reactive astrocytes) and cluster of differentiation 68 (CD68, activated microglia/macrophages). Digitized sections were uploaded to the cloud-based Aiforia® platform, where deep-learning algorithms were utilized to detect tissue, iron deposits, and GFAP-positive and CD68-positive cells.ResultsWe observed a strong local relationship between cortical iron deposits and reactive astrocytes. Like cSS-related iron, reactive astrocytes were mainly found in the most superficial layers of the cortex. Although we observed iron within both astrocytes and activated microglia/macrophages on co-stains, there was no clear local relationship between the density of microglia/macrophages and the density of iron deposits.ConclusionIron deposition resulting from cSS is associated with local reactive astrogliosis.

Determinants of post-stroke cognitive impairment and dementia: association with objective measures and patient-reported outcomes

BackgroundPost-stroke cognitive impairment and dementia (PSCID) is a sequel of ischemic stroke (IS), highly prevalent and linked to poor long-term outcomes. Thus, early recognition of the clinical determinants of PSCID is urgent for identifying high-risk individuals who are susceptible to PSCID. And investigating objective measures of PSCID in relation to patient-reported outcome measures (PROMs) is essential for understanding the impact of IS. Here we identify the clinical determinants associated with PSCID and the relationship of PSCID to patient-reported outcomes in a population with IS.MethodsThis was a cohort study. We enrolled 138 patients who were admitted to our hospital between February 2017 and February 2020, with IS and no pre-stroke diagnosis of dementia. Clinical variables were acquired on admission. At 3 months, patients underwent a follow-up evaluation including the Telephone Interview for Cognitive Status (TICS), modified Rankin scale (mRS), Barthel Index (BI), and PROMs, using the Patient-Reported Outcomes Measurement information System Global Health (PROMIS GH). MCI/Dementia was defined as a TICS score of &amp;lt;36. Regression analyses were used to identify clinical, functional, and patient-reported outcome determinants of the 3-month TICS score. Analyses were adjusted for age, stroke severity, and prior IS.ResultsAt follow-up, 113 participants (82%) were found to have MCI/Dementia. Patients with PSCID were more likely to be older, and at 3-months post-stroke they had lower rates of PROMIS GH T Mental (mean 47.69 vs. 52.13) and T Physical (mean 46.75 vs. 50.64). In multivariable linear regression analyses, increasing age (β = −0.07, p = 0.03) and Peripheral Artery Disease (PAD; β = −3.60, p = 0.03) were independently associated with a lower TICS score. Functional and patient-reported outcomes were also associated with worse TICS, including mRS ≥ 2, BI, T Mental, Global Mental, T Physical, and Global Physical in adjusted analyses. Individual components of PROMs were also associated with TICS, including quality of life, mental health, social satisfaction, and physical activities.ConclusionsIn patients with IS, increased age and a pre-admission diagnosis of PAD are independently associated with worse objective measures of PSCID. Worse functional and patient-reported outcomes are also strongly linked to PSCID.

Direct Thrombectomy versus Bridging Thrombectomy within 6 Hours of Stroke Onset: A Prospective Cohort Study on Cognitive and Physical Function Outcomes

PurposeTo evaluate the physical and cognitive functions of patients with stroke who underwent either direct or bridging thrombectomy within 6 hours of stroke onset. Materials and MethodsPatients with large vessel occlusion in anterior circulation treated with direct (direct group) or bridging thrombectomy (bridging group) were prospectively analyzed between June 2020 and February 2022. The efficacy outcome was the 3-month modified Rankin Scale (mRS) score, the safety outcome was symptomatic intracranial hemorrhage (sICH), and cognitive function was assessed using the Clinical Dementia Rating (CDR) scale at 6 months after stroke. ResultsA total of 125 patients (direct group, n = 75; bridging group, n = 50) who had completed follow-up at 3 months by telephone call were included. No significant differences were observed between the direct and bridging groups in terms of an mRS score of 0–2 (25.3% vs 22.0%, respectively; P = .83), an mRS score of 0–3 (37.3% vs 44.0%, respectively; P = .58), sICH (17.3% vs 14.0%, respectively; P = .80), or 3-month all-cause mortality (36.3% vs 30.0%, respectively; P = .34). Sixty-nine patients (direct group, n = 38; bridging group, n = 31) completed the CDR assessment at 6 months after stroke. There was no significant difference in poststroke dementia, defined as a CDR score of ≥1 point between the direct group (42.1%) and bridging group (22.6%) (P = .12). Ordinal regression analyses showed that the CDR score at 6 months was not associated with treatment type (direct thrombectomy vs bridging thrombectomy). ConclusionsWith regard to physical and cognitive functions at 3 and 6 months, direct thrombectomy was comparable with bridging thrombectomy in patients who were treated within 6 hours of stroke onset.

The role of gut microbiota in cerebrovascular disease and related dementia.

In recent years, increasing evidence suggests that commensal microbiota may play an important role not only in health but also in disease including cerebrovascular disease. Gut microbes impact physiology, at least in part, by metabolizing dietary factors and host-derived substrates and then generating active compounds including toxins. The purpose of this current review is to highlight the complex interplay between microbiota, their metabolites. and essential functions for human health, ranging from regulation of the metabolism and the immune system to modulation of brain development and function. We discuss the role of gut dysbiosis in cerebrovascular disease, specifically in acute and chronic stroke phases, and the possible implication of intestinal microbiota in post-stroke cognitive impairment and dementia, and we identify potential therapeutic opportunities of targeting microbiota in this context. LINKED ARTICLES: This article is part of a themed issue From Alzheimer's Disease to Vascular Dementia: Different Roads Leading to Cognitive Decline. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.6/issuetoc.

Myeloid cells in vascular dementia and Alzheimer's disease: Possible therapeutic targets?

Growing evidence supports the suggestion that the peripheral immune system plays a role in different pathologies associated with cognitive impairment, such as vascular dementia (VD) or Alzheimer's disease (AD). The aim of this review is to summarize, within the peripheral immune system, the implications of different types of myeloid cells in AD and VD, with a special focus on post-stroke cognitive impairment and dementia (PSCID). We will review the contributions of the myeloid lineage, from peripheral cells (neutrophils, platelets, monocytes and monocyte-derived macrophages) to central nervous system (CNS)-associated cells (perivascular macrophages and microglia). Finally, we will evaluate different potential strategies for pharmacological modulation of pathological processes mediated by myeloid cell subsets, with an emphasis on neutrophils, their interaction with platelets and the process of immunothrombosis that triggers neutrophil-dependent capillary stall and hypoperfusion, as possible effector mechanisms that may pave the way to novel therapeutic avenues to stop dementia, the epidemic of our time. LINKED ARTICLES: This article is part of a themed issue From Alzheimer's Disease to Vascular Dementia: Different Roads Leading to Cognitive Decline. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.6/issuetoc.

Cerebral Small Vessel Disease Burden: An Independent Biomarker for Anomia Treatment Responsiveness in Chronic Stroke Patients With Aphasia

ObjectiveTo determine whether MRI-based cerebral small vessel disease (cSVD) burden predicts treatment-induced aphasia recovery in chronic stroke patients above and beyond initial aphasia severity and stroke-lesion volume. DesignRetrospective. Four cSVD neuroimaging markers were rated using validated visual scales: white matter hyperintensities, enlarged perivascular spaces, lacunes, and global cortical atrophy. We also calculated a cSVD total score. We employed linear regression models to model treatment response as a function of cSVD burden. We also ran correlation analyses to determine the association among cSVD burden and pre-treatment linguistic and non-linguistic cognition. SettingResearch clinic. ParticipantsThe study includes data from 30 chronic stroke patients with aphasia who received treatment for word finding difficulties and completed additional pre-treatment neuroimaging and behavioral assessments (N=30). Interventions120-minute sessions of anomia treatment 2 times per week for up to 12 weeks. Main Outcome MeasuresChange in accuracy on the treatment probes measured as a percentage (ie, change in accuracy percentage score=post-treatment accuracy percentage minus pre-treatment accuracy percentage). ResultsBaseline cSVD burden predicted response to anomia treatment independently from demographic and stroke-related factors. Patients with lower cSVD burden exhibited enhanced rehabilitation response compared with those with higher cSVD burden (β=-6.816e-02, P=.019). cSVD burden was highly associated with nonverbal executive function at baseline (r=-0.49, P=.005): patients with lower cSVD burden exhibited higher performance on nonverbal executive function tasks compared with participants with higher cSVD burden. No association was observed among cSVD burden and performance on language tasks at the baseline. ConclusionscSVD, a marker of brain reserve and a robust risk factor for post-stroke dementia, may be used as a biomarker for distinguishing patients who are more likely to respond to anomia therapy from those who are less likely to do so and for individualizing treatment parameters (eg, targeting both linguistic and nonlinguistic cognition in severe cSVD).

Educational Attainment and Dementia: Mediation by Mid-Life Vascular Risk Factors.

Lower education is associated with higher burden of vascular risk factors in mid-life and higher risk of dementia in late life. We aim to understand the causal mechanism through which vascular risk factors potentially mediate the relationship between education and dementia. In a cohort of 13,368 Black and White older adults in the Atherosclerosis Risk in Communities Study, we assessed the relationship between education (grade school, high school without graduation, high school graduate or equivalent, college, graduate/professional school) and dementia among all participants and among those with incident stroke. Cox models were adjusted for age, race-center (a variable stratified by race and field center), sex, apolipoprotein E (APOE) ε4 genotype, and family history of cardiovascular disease. Causal mediation models assessed mediation by mid-life systolic blood pressure, fasting blood glucose, body mass index, and smoking. More education was associated with 8 to 44% lower risk of dementia compared to grade school-level education in a dose-response pattern, while the relationship between education and post-stroke dementia was not statistically significant. Up to 25% of the association between education and dementia was mediated through mid-life vascular risk factors, with a smaller percentage mediated for lower levels of education. A substantial proportion of the relationship between education and dementia was mediated through mid-life vascular risk factors. However, risk factor modification is unlikely to fully address the large educational disparities in dementia risk. Prevention efforts must also address disparities in socioeconomic resources leading to divergent early-life education and other structural determinants of mid-life vascular risk factors. ANN NEUROL 2023;94:13-26.

Importance of Retesting for the Final Diagnosis of Post-Stroke Cognitive Impairment

Background and Objectives: Post-stroke cognitive impairment (PSCI) has been defined as all problems in cognitive function that occur following a stroke. Studies published thus far on the prevalence of PSCI and post-stroke dementia (PSD) have shown conflicting estimates. The aim of this study was screening for cognitive impairment (CogI) in patients with an ischaemic stroke and finding the relationship between CogI (and its changes) and cardiovascular risk factors and imaging procedures-CT/MRI. Materials and Methods: We prospectively included patients with an ischaemic stroke admitted in the period from October 2019 to May 2022. In this period, 1328 patients were admitted, 305 of whom met the established inclusion criteria and underwent an examination of cognitive functions using the Montreal Cognitive Assessment (MoCA). Of these, 50 patients appeared for the control examination after 6 months. Results: In the retested group, CogI at discharge was diagnosed in 37 patients (74%). In follow-up testing after 6 months, CogI was present in 30 patients (60%). Only arterial hypertension (OR: 15; 95% CI; Pearson r: 0.001), lower education level (less than 13 years) (OR: 9.7; 95% CI 2.0-48.5; Pearson r: 0.002), and higher age were significantly associated with CogI after stroke. Conclusions: We established the prevalence of CogI and its course after 6 months in a well-defined group of patients after a mild ischaemic stroke (mean NIHSS: 2 and mean mRS: 1 at the discharge). Our results show that the prevalence of CogI after an ischaemic stroke at discharge is relatively high (74%), and it tends to be a spontaneous reduction. Cognitive functions were changed in 35% of patients. The definition of PSCI was completed in only 24% of individuals. Only an examination several months after a stroke can give us more accurate information about the true prevalence of persistent CogI after a stroke.

Targeting BACE1-mediated production of amyloid beta improves hippocampal synaptic function in an experimental model of ischemic stroke

Post-stroke cognitive impairment and dementia (PSCID) affects many survivors of large vessel cerebral ischemia. The molecular pathways underlying PSCID are poorly defined but may overlap with neurodegenerative pathophysiology. Specifically, synaptic dysfunction after stroke may be directly mediated by alterations in the levels of amyloid beta (Aβ), the peptide that accumulates in the brains of Alzheimer’s disease (AD) patients. In this study, we use the transient middle cerebral artery occlusion (MCAo) model in young adult mice to evaluate if a large vessel stroke increases brain soluble Aβ levels. We show that soluble Aβ40 and Aβ42 levels are increased in the ipsilateral hippocampus in MCAo mice 7 days after the injury. We also analyze the level and activity of β-site amyloid precursor protein cleaving enzyme 1 (BACE1), an enzyme that generates Aβ in the brain, and observe that BACE1 activity is increased in the ipsilateral hippocampus of the MCAo mice. Finally, we highlight that treatment of MCAo mice with a BACE1 inhibitor during the recovery period rescues stroke-induced deficits in hippocampal synaptic plasticity. These findings support a molecular pathway linking ischemia to alterations in BACE1-mediated production of Aβ, and encourage future studies that evaluate whether targeting BACE1 activity improves the cognitive deficits seen with PSCID.

A systematic review of auricular therapy for poststroke cognitive impairment and dementia: A protocol for systematic review and meta-analysis.

Post-stroke cognitive impairment and dementia (PSCID) is the main source of morbidity and mortality after stroke worldwide. It is one consequence of ischemic stroke, intracerebral hemorrhage, or subarachnoid hemorrhage. Cognitive impairment and dementia after the clinical stroke may contribute to the clinical expression of PSCID, which are prevalent clinical symptoms, especially in the elderly. Current problems in the field of PSCID are related to a lack of harmonization of the classification and definition, deficiency of well-defined diagnosis, deficiency of standardized and objective treatment plans, etc. Auricular therapy can effectively improve the symptoms of patients with PSCID. However, there has been no systematic review of auricular therapy for PSCID. This study aimed to evaluate the efficacy and safety of auricular therapy in patients with PSCID. Before December 2022, a systematic literature search was conducted using the following databases: PubMed, Embase, SinoMed (previously called the Chinese Biomedical Database), Web of Science, Chinese National Knowledge Infrastructure, and Wanfang Database. Review Manager software (version 5.3) will be used for statistical analysis; otherwise, descriptive analysis or subgroup analysis will be conducted. The quality of evidence for outcomes will be assessed with the Grading of Recommendations Assessment, Development and Evaluation approach. This meta-analysis further confirmed the beneficial effects of auricular therapy in patients with PSCID. This study investigated the efficacy and safety of auricular therapy in patients with PSCID, providing clinicians and patients with additional options for this disease.

Leukoaraiosis as a Predictor of Depression and Cognitive Impairment among Stroke Survivors: A Systematic Review

Stroke survivors are at increased risk of developing depression and cognitive decline. Thus, it is crucial for both clinicians and stroke survivors to be provided with timely and accurate prognostication of post-stroke depression (PSD) and post-stroke dementia (PSDem). Several biomarkers regarding stroke patients' propensity to develop PSD and PSDem have been implemented so far, leukoaraiosis (LA) being among them. The purpose of the present study was to review all available work published within the last decade dealing with pre-existing LA as a predictor of depression (PSD) and cognitive dysfunction (cognitive impairment or PSDem) in stroke patients. A literature search of two databases (MEDLINE and Scopus) was conducted to identify all relevant studies published between 1 January 2012 and 25 June 2022 that dealt with the clinical utility of preexisting LA as a prognostic indicator of PSD and PSDem/cognitive impairment. Only full-text articles published in the English language were included. Thirty-four articles were traced and are included in the present review. LA burden, serving as a surrogate marker of "brain frailty" among stroke patients, appears to be able to offer significant information about the possibility of developing PSD or cognitive dysfunction. Determining the extent of pre-existing white matter abnormalities can properly guide decision making in acute stroke settings, as a greater degree of such lesioning is usually coupled with neuropsychiatric aftermaths, such as PSD and PSDem.

Abstract TP189: Identifying Stroke Patients At Risk For Cognitive Impairment And Dementia Using Electronic Health Record Data And Machine Learning

Background: Stroke patients are at high risk of developing cognitive impairment and dementia. Failure to identify cognitive impairment in time could hasten the progression of dementia and impact the rehabilitation plan. Therefore, a reliable method is needed to determine a stroke survivor’s susceptibility to post-stroke cognitive impairment and dementia (PSCID). Method: We conducted a retrospective cohort study of cryptogenic stroke (CS) patients from January 1, 2017, to February 28, 2022, using EHR data to query for PSCID onset. A machine learning (ML) model was created to forecast the occurrence of PSCID during follow-up. The features used in the model included elements from EHR that were found to be associated with PSCID in other studies, including sociodemographic, medical, and mental morbidities. Logistic Regression, Random Forest (RF) Classifier, and Gradient Boosting are examples of ML algorithms that were used. The final model used RF Classifier due to its superior performance. Results: Of 390 CS patients (62±16 years, 56.4% male) included in the analysis, 110 (28.2%) had documented PSCID in EHR following the initial stroke. We evaluated our model in a repeated (n=100) 10-fold cross validation scheme and used Synthetic Minority Oversampling Technique (SMOTE) to compensate for class imbalance. We identified the most informative ten features using an Extra Tree classifier, which are age, transient ischemic attack, sex, smoking, diabetes, hypertension, atherosclerosis, anemia, and atrial fibrillation. Using these features, our RF classifier reached a performance of 71.2±6.5% accuracy, 70±4.9% precision, 75±12% recall, and 0.777±0.082 AUC. Conclusion: Our model could predict the CS patients at risk for PSCID with reasonable accuracy using only ten features. Future work should involve a larger cohort along with more advanced machine learning algorithms to enhance the prediction performance.

Is cognitive reserve associated with the prevention of cognitive decline after stroke? A Systematic review and meta-analysis.

To conduct a systematic review and meta-analyses of the effect of socio-behavioral cognitive reserve (CR) proxies on cognitive decline after stroke. Three journal search and indexing databases (PubMed, Scopus and Web of Sciences) were crossed to examine the scientific evidence systematically. In addition, meta-analytic techniques, using mixed-effect methods, were carried out to estimate the impact (pooled effect size) of CR proxies on either dementia incidence or cognitive decline after stroke. Twenty-two studies were included in the systematic revision, whereas nineteen of them were eligible for the meta-analysis. The findings showed that high education is associated with a decreased rate of post-stroke dementia. Moreover, other CR proxies (e.g., occupation, bilingualism or social interaction) demonstrate a protective effect against non-dementia cognitive decline after stroke, although some inconsistencies were found in the literature. Regarding the meta-analysis, occupational attainment and education) showed a protective effect against post-stroke cognitive impairment diagnosis in comparison with a mixed category of different CR proxies. Second, a main cognitive change effect was found, pointing to greater cognitive change after stroke in those with low vs. high CR. Our findings emphasize that CR may prevent cognitive decline after stroke, but this effect can be modulated by different factors such the CR proxy and individual characteristics such as age or type of lesion. The methodological divergences of the studies (i.e., follow-up intervals, cognitive outcomes) need unification to diminish external sources of variability for predicting rates of cognitive decline after stroke.

Post-Stroke Neuropsychiatric Complications: Types, Pathogenesis, and Therapeutic Intervention.

Almost all stroke survivors suffer physical disabilities and neuropsychiatric disturbances, which can be briefly divided into post-stroke neurological diseases and post-stroke psychiatric disorders. The former type mainly includes post-stroke pain, post-stroke epilepsy, and post-stroke dementia while the latter one includes post-stroke depression, post-stroke anxiety, post-stroke apathy and post-stroke fatigue. Multiple risk factors are related to these post-stroke neuropsychiatric complications, such as age, gender, lifestyle, stroke type, medication, lesion location, and comorbidities. Recent studies have revealed several critical mechanisms underlying these complications, namely inflammatory response, dysregulation of the hypothalamic pituitary adrenal axis, cholinergic dysfunction, reduced level of 5-hydroxytryptamine, glutamate-mediated excitotoxicity and mitochondrial dysfunction. Moreover, clinical efforts have successfully given birth to many practical pharmaceutic strategies, such as anti-inflammatory medications, acetylcholinesterase inhibitors, and selective serotonin reuptake inhibitors, as well as diverse rehabilitative modalities to help patients physically and mentally. However, the efficacy of these interventions is still under debate. Further investigations into these post-stroke neuropsychiatric complications, from both basic and clinical perspectives, are urgent for the development of effective treatment strategies.

Cognitive Recovery After Stroke: Memory.

Memory impairment occurs in over a third of patients after symptomatic stroke. Memory deficits rarely occur in isolation but are an important component of the poststroke cognitive syndrome because of the strong relationship with the risk of poststroke dementia. In this review, we summarize available data on impairment of episodic memory, with a particular emphasis on the natural history of memory impairment after stroke and the factors influencing trajectory informed by an updated systematic review. We next discuss the pathophysiology of memory impairment and mechanisms of both decline and recovery of function. We then turn to the practical issue of measurement of memory deficits after stroke, emerging biomarkers, and therapeutic approaches. Our review identifies critical gaps, particularly in studies of the natural history that properly map the long-term trajectory of memory and the associations with factors that modulate prognosis. Few studies have used advanced neuroimaging and this, in conjunction with other biomarker approaches, has the potential to provide a much richer understanding of the mechanisms at play and promising therapeutic avenues.

Post‐stroke dementia and its determinant factors among Ethiopian stroke survivors: A cross‐sectional study

AbstractBackgroundStroke and dementia convene risks for each other and share some of the same, largely modifiable, risk factors.MethodAdult stroke survivors, who visited the outpatient stroke clinic in Tikur Anbessa Specialized Teaching Hospital in Addis Ababa University, Ethiopia was assessed for cognitive decline. Beside Montreal Cognitive Assessment‐Basic (MOCA‐B) tool, functional recovery and depression were measured using modified Rankin Scale (mRS) and Patient Health Questionnaire (PHQ‐9).ResultFrom 67 stroke survivors (mean age: 52.1 ± 12.7 years, 40.3 % female, 25.3% illiterate, rural dwellers 32.8%, 37.3% stoke onset &lt; 45‐year), 68.7% had cognitive impairment in at least one domain and 25.3% had dementia. Hospitalization [OR = 0.22 (0.06 ‐0.74)], right hemisphere stroke location [OR = 0.21 (0.06‐0.77)] and poor function recovery with mRS ³3 [OR = 1.4 (1.06‐1.74)] were independently associated with post stroke cognitive impairment and dementia.ConclusionThe frequency of post stroke dementia was high in Ethiopia and poor functional recovery negatively impact cognitive outcome.