Abstract
The global burden of ischaemic strokes is almost 4-fold greater than haemorrhagic strokes. Current evidence suggests that 25–30% of ischaemic stroke survivors develop immediate or delayed vascular cognitive impairment (VCI) or vascular dementia (VaD). Dementia after stroke injury may encompass all types of cognitive disorders. States of cognitive dysfunction before the index stroke are described under the umbrella of pre-stroke dementia, which may entail vascular changes as well as insidious neurodegenerative processes. Risk factors for cognitive impairment and dementia after stroke are multifactorial including older age, family history, genetic variants, low educational status, vascular comorbidities, prior transient ischaemic attack or recurrent stroke and depressive illness. Neuroimaging determinants of dementia after stroke comprise silent brain infarcts, white matter changes, lacunar infarcts and medial temporal lobe atrophy. Until recently, the neuropathology of dementia after stroke was poorly defined. Most of post-stroke dementia is consistent with VaD involving multiple substrates. Microinfarction, microvascular changes related to blood–brain barrier damage, focal neuronal atrophy and low burden of co-existing neurodegenerative pathology appear key substrates of dementia after stroke injury. The elucidation of mechanisms of dementia after stroke injury will enable establishment of effective strategy for symptomatic relief and prevention. Controlling vascular disease risk factors is essential to reduce the burden of cognitive dysfunction after stroke. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock.
Highlights
Stroke as the third leading cause of death is considered an important cause of long-term disability and cognitive impairment
Metabolic syndrome, a clustering of several cardiovascular risk factors may well affect dementia after stroke through ‘metabolic–cognitive syndrome’ [62]. Another longitudinal study [63] showed that patients with dementia after stroke had a higher prevalence of several vascular risk factors including hypertension, diabetes, atrial fibrillation, previous myocardial infarction and history of transient ischaemic attack (Table 2)
There is selective atrophy (30–40%) of pyramidal cells in layers III and V of the dorsolateral prefrontal cortex compared to the anterior cingulate and orbitofrontal cortices of the frontal lobe in subjects with dementia after stroke, vascular dementia (VaD) and, of mixed and Alzheimer's disease (AD) versus normal ageing controls and those who did not have dementia after stroke [99]
Summary
Stroke as the third leading cause of death is considered an important cause of long-term disability and cognitive impairment. This demands enormous resources from healthcare systems [1]. Burden of stroke is likely underestimated by not accounting for silent strokes, transient ischaemic attacks in many cases, vascular dementia (VaD) and long term stroke related disability in case definition. R.N. Kalaria et al / Biochimica et Biophysica Acta 1862 (2016) 915–925 is the most treatable risk factor for both ischaemic and haemorrhagic strokes. Kalaria et al / Biochimica et Biophysica Acta 1862 (2016) 915–925 is the most treatable risk factor for both ischaemic and haemorrhagic strokes It presents a golden opportunity for prevention and reducing the burden of stroke and post-stroke cognitive impairment
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