Post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI) may affect up to one third of stroke survivors. Various definitions of PSCI and PSD have been described. We propose PSD as a label for any dementia following stroke in temporal relation. Various tools are available to screen and assess cognition, with few PSD-specific instruments. Choice will depend on purpose of assessment, with differing instruments needed for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic formulation (e.g., NINDS VCI battery). A comprehensive evaluation should include assessment of pre-stroke cognition (e.g., using Informant Questionnaire for Cognitive Decline in the Elderly), mood (e.g., using Hospital Anxiety and Depression Scale), and functional consequences of cognitive impairments (e.g., using modified Rankin Scale). A large number of biomarkers for PSD, including indicators for genetic polymorphisms, biomarkers in the cerebrospinal fluid and in the serum, inflammatory mediators, and peripheral microRNA profiles have been proposed. Currently, no specific biomarkers have been proven to robustly discriminate vulnerable patients (‘at risk brains’) from those with better prognosis or to discriminate Alzheimer’s disease dementia from PSD. Further, neuroimaging is an important diagnostic tool in PSD. The role of computerized tomography is limited to demonstrating type and location of the underlying primary lesion and indicating atrophy and severe white matter changes. Magnetic resonance imaging is the key neuroimaging modality and has high sensitivity and specificity for detecting pathological changes, including small vessel disease. Advanced multi-modal imaging includes diffusion tensor imaging for fiber tracking, by which changes in networks can be detected. Quantitative imaging of cerebral blood flow and metabolism by positron emission tomography can differentiate between vascular dementia and degenerative dementia and show the interaction between vascular and metabolic changes. Additionally, inflammatory changes after ischemia in the brain can be detected, which may play a role together with amyloid deposition in the development of PSD. Prevention of PSD can be achieved by prevention of stroke. As treatment strategies to inhibit the development and mitigate the course of PSD, lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents have all been studied without convincing evidence of efficacy. Lifestyle interventions, physical activity, and cognitive training have been recently tested, but large controlled trials are still missing.

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URL: https://www.clinicaltrials.gov. Unique identifier: NCT01467206.

We could not demonstrate cognitive effects of an intensive risk factor intervention at one-year poststroke. Longer follow-up and a more heterogeneous study sample might have lead to larger effects. More effective methods for managing the risk of further cognitive decline after stroke are needed.

Background: Post-stroke dementia is defined as any dementia occurring after stroke, and includes vascular, degenerative and mixed dementia. The aim of this study was to assess the incidence of dementia and mild cognitive impairment (MCI) one year after stroke in a population free from pre-stroke cognitive decline, and to investigate the different aetiological subtypes of post-stroke dementia and MCI, using a novel method of subclassification in order to separate vascular causes of MCI or dementia from a neurodegenerative disease. Methods: All patients with a first-ever stroke and TIA admitted to the stroke unit of Asker and Bærum Hospital were invited. After 12 months, dementia and MCI were diagnosed. Sub-classification was made using MRI findings, the results of biomarkers in cerebrospinal fluid and the patients’ clinical cognitive profile. Results: 36 (19.6%) patients developed dementia during the first year after stroke and 69 (37.5%) developed MCI. Fourteen (13.3%) were diagnosed as suffering from degenerative cognitive disease, 34 (32.4%) from vascular cognitive disease, and 57 (54.3%) from mixed disease. Conclusion: Fifty-seven percent suffered from cognitive impairment one year after stroke and only one third from isolated vascular cognitive disease. Post-stroke cognitive impairment is complex with a high coexistence of vascular and degenerative changes.

Background: Post-stroke cognitive impairment (PSCI) is common, but evidence of cognitive symptom profiles, course over time, and pathogenesis is scarce. We investigated the significance of time and etiologic stroke subtype for the probability of PSCI, severity, and cognitive profile. Methods: Stroke survivors (n = 617) underwent cognitive assessments of attention, executive function, memory, language, perceptual-motor function, and the Montreal Cognitive Assessment (MoCA) after 3 and/or 18 months. PSCI was classified according to DSM-5 criteria. Stroke severity was assessed with the National Institutes of Health Stroke Scale (NIHSS). Stroke subtype was categorized as intracerebral hemorrhage (ICH), large artery disease (LAD), cardioembolic stroke (CE), small vessel disease (SVD), or un-/other determined strokes (UD). Mixed-effects logistic or linear regression was applied with PSCI, MoCA, and z-scores of the cognitive domains as dependent variables. Independent variables were time as well as stroke subtype, time, and interaction between these. The analyses were adjusted for age, education, and sex. The effects of time and stroke subtype were analyzed by likelihood ratio tests (LR). Results: Mean age was 72 years (SD 12), 42% were females, and mean NIHSS score at admittance was 3.8 (SD 4.8). Probability (95% CI) for PSCI after 3 and 18 months was 0.59 (0.51-0.66) and 0.51 (0.52-0.60), respectively and remained constant over time. Global measures and most cognitive domains were assessed as impaired for the entire stroke population and for most stroke subtypes. Executive function and language improved for the entire stroke population (LR) = 9.05, p = 0.003, and LR = 10.38, p = 0.001, respectively). After dividing the sample according to stroke subtypes, language Aam et al. Post-stroke Cognitive Impairment improved for ICH patients (LR = 18.02, p = 0.003). No significant differences were found in the severity of impairment between stroke subtypes except for attention, which was impaired for LAD and CE in contrast to no impairment for SVD (LR = 56.58, p < 0.001). Conclusions: In this study including mainly minor strokes, PSCI is common for all subtypes, both early and long-term after stroke, while executive function and language improve over time. The findings might contribute to personalizing follow-up and offer new insights into underlying mechanisms. Further research is needed on underlying mechanisms, PSCI prevention and treatment, and relevance for rehabilitation.

Physical activity may help to keep the brain healthier and preserve cognitive ability and mood years after a stroke. In The Life After STroke (LAST) study, stroke survivors were allocated into 2 groups. A training group was encouraged to perform physical activity for 30 min daily, and 45-60 min of moderate-to-intense physical exercise every week. A control group was followed by their general practitioner as usual. This study aimed to measure the effect on cognitive and emotional function in both groups after 18 months. Of the 362 participants, almost half were in the training group. The mean age was 72 years and 40% were female. There were no differences between the groups regarding effect on cognitive or emotional function. In conclusion, this study did not show an effect of the physical training programme on cognition or mood after stroke. Objective: To examine the effects of individualized regular coaching and exercise on post-stroke cognitive and emotional function. Methods: The Life After STroke (LAST) study investigated the differences between intervention and care-as-usual between 3 and 21 months post-stroke. Outcome measures were the Trail Making Test (TMT) A and B, Mini Mental State Examination (MMSE), Hospital Anxiety and Depression Scale (HADS), and adherence to the intervention. Results: Of the 362 patients included in the study, 177 were assigned to the intervention. The mean age was 71.7 years (SD 11.3) and 39.5% were female. The adjusted mean difference between groups for TMT A was 8.54 (95% CI 0.7 to 6.3), p = 0.032, for TMT B 8.6 (95% CI-16.5 to 33.6), p = 0.50, for MMSE-0.1 (95% CI-0.8 to 0. 6), p = 0.77, for HADS A-0.2 (95% CI-0.9 to 0.5), p = 0.56 and for HADS D-0.1 (95% CI-0.7 to 0.5), p = 0.76). A higher level of adherence to the intervention was significantly associated with increased MMSE (B = 0.030 (95% CI 0.005-0.055), p = 0.020). Conclusion: No clinically relevant effects on cognitive or emotional function were found of individualized regular coaching for physical activity and exercise. However, increased adherence to the intervention was associated with improved cognitive function.

Introduction: Post-stroke neurocognitive disorder (NCD) is common; prevalence varies between studies, partially related to lack of consensus on how to identify cases. The aim was to compare the prevalence of post-stroke NCD using only cognitive assessment (model A), DSM-5 criteria (model B), and the Global Deterioration Scale (model C) and to determine agreement among the three models. Methods: In the Norwegian Cognitive Impairment After Stroke study, 599 patients were assessed 3 months after suffering a stroke. Results: The prevalence of mild NCD varied from 174 (29%) in model B to 83 (14%) in model C; prevalence of major NCD varied from 249 (42%) in model A to 68 (11%) in model C. Cohen's kappa and Cohen's quadratic weighted kappa showed fair to very good agreement among models; the poorest agreement was found for identification of mild NCD.