Post-stroke dementia – a comprehensive review

Abstract

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.

Longitudinal Effect of Stroke on Cognition: A Systematic Review

“…Our review, however, shows that cognitive decline seems to become more apparent over a longer follow‐up period, and thus new models could be developed to predict poststroke cognitive impairment and dementia over longer time periods. Currently there are no specific biomarkers that can help discriminate between those at risk and those with better prognosis 38. There is evidence, however, of a strong relationship between inflammation markers and cognitive performance,39 and this will need further evaluation before being used in potential risk models.…”

Burden and Predictors of Poststroke Cognitive Impairment in a Sample of Ghanaian Stroke Survivors

“…And although it was not feasible, due to the cross-sectional study design, to examine the trajectory of vascular cognitive dysfunction from our study, data from pooled prospective cohorts suggest a linear increase in Post-stroke dementia rates of 3% and 1.7% per year in hospital- and community-based studies respectively (10). More recently, it has been postulated that stroke survivors may exhibit different cognitive trajectories and that these trajectories could change over time (39). A host of variables including demographic factors (such as age, educational level), pre-stroke factors (such as physical impairment, cognitive impairment), index stroke factors (including hemorrhagic stroke, recurrent strokes), post-stroke factors (such as infection, delirium, early seizures) and neuroimaging predictors (example cerebral small-vessel disease, cortical atrophy) may all conspire to differentially influence the trajectory of post-stroke dementia.…”

Cognitive and Mood Assessment Tools for Use in Stroke

“…1 Thankfully the landscape is changing, there is an increasing recognition of the importance of the psychological consequences of stroke and a growing evidence base and standardisation around assessment. 2,3,4 The stroke physician cannot be expected to take on the role of the neuropsychology specialist and there will always be cases where expert input is required. However, a basic appreciation of how to approach cognitive and mood assessment should now be mandatory for all working in stroke care.…”

“…We have drawn on evidence from recent research, particularly systematic review. 3 We do not offer a comprehensive critique of all cognitive and mood assessment tools. Rather, we suggest a framework for assessment that emphasises the need for differing approaches to testing at differing points in the stroke pathway.…”