Poststroke cognitive impairment and dementia

Abstract

More than half of stroke survivors experience post-stroke cognitive impairment and dementia (PSCID) with cognitive impairment no dementia in two-thirds of cases and post-stroke dementia in one-third of cases. Various tools are available to screen and assess cognition: for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic evaluation (e.g., NINDS VCI battery). Risk factors for PSCID are multifactorial including older age, family history, genetic variants, low educational status, vascular multi-morbidities, prior transient ischaemic attack, recurrent stroke and depressive illness. Neuroimaging determinants of PSCID comprise silent brain infarcts, white matter changes, lacunar infarcts, medial temporal lobe atrophy and global brain atrophy. 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. Microvascular changes including white matter lesions (WMLs), microinfarcts, cerebral microbleeds (CMBs), blood-brain barrier damage, focal neuronal atrophy and low burden of co-existing neurodegenerative pathology are key pathological substrates of PSCID. Biomarkers in the cerebrospinal fluid and in the serum including inflammatory mediators and peripheral microRNAs have been implicated. Treatment strategies to inhibit the development and mitigate the course of PSCID include lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents while lifestyle interventions, physical activity, and cognitive training have been also tested, but large controlled trials are needed.