
Effects of different scales on evaluating post-stroke cognitive impairment
LIJiarui, LUOBenyan
Chinese Journal of Alzheimer's Disease and Related Disorders ›› 2020, Vol. 3 ›› Issue (2) : 108-112.
Abbreviation (ISO4): Chinese Journal of Alzheimer's Disease and Related Disorders
Editor in chief: Jun WANG
Effects of different scales on evaluating post-stroke cognitive impairment
Objective: To compare the roles of mini-mental state examination (MMSE), Alzheimer's disease assessment scale-cognitive (ADAS-cog) and clinical dementia rating (CDR) in the assessment of post-stroke cognitive impairment (PSCI) based on multi-center large sample clinical data. Methods: The acute stroke patients (n=983) onset within 14 days were assessed by MMSE, ADAS-cog and CDR, and diagnosed according to AHA/ASA guidelines and NINCD-ADRDA criteria. The results, sensitivity, and specificity of these scales were compared. Results: The rates of cognitive dysfunction were 19.33% assayed by MMSE and 28.99% by ADAS-cog. According to CDR, there were 49.38% of suspected dementia, 10.63% of mild dementia, 2.80% of moderate dementia, and 0.90% of severe dementia. The results evaluated by the three scales were significantly different (χ2=2787.64, P< 0.01) and not independent (P< 0.01). The three scales had good efficacy in the diagnosis of PSCI and PSD, but the best demarcation points of MMSE and ADAS-cog were different from the existing conclusions. MMSE and CDR had higher diagnostic efficacy for PSD (P< 0.05). ADAS-cog had no significant difference in the diagnostic efficacy of PSCI and PSD. Conclusion: The impact of demarcation points of MMSE and ADAS-cog should be taken into account when screening of PSCI. MMSE and CDR have advantages in screening for severe PSCI.
Acute stroke / Cognitive impairment / Neuropsychological scales
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中国卒中研究进展迅猛,已整合血管性认知障碍(VaCD) 的临床干预策略。卒中后认知障碍(PSCI) 中国专家共识提出高度关注PSCI 人群,将是整合卒中和认知干预的突破口。PSCI 应作为卒中后综合管理的重点内容之一,基因、影像学等生物标志物的应用将进一步推动PSCI 病因学诊断和分型。
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Reliable data on the prevalence and predictors of post-stroke dementia are needed to inform patients and carers, plan services and clinical trials, ascertain the overall burden of stroke, and understand its causes. However, published data on the prevalence and risk factors for pre-stroke and post-stroke dementia are conflicting. We undertook this systematic review to assess the heterogeneity in the reported rates and to identify risk factors for pre-stroke and post-stroke dementia.Studies published between 1950 and May 1, 2009, were identified from bibliographic databases, reference lists, and journal contents pages. Studies were included if they were on patients with symptomatic stroke, were published in English, reported on a series of consecutive eligible patients or volunteers in prospective cohort studies, included all stroke or all ischaemic stroke, measured dementia by standard criteria, and followed up patients for at least 3 months after stroke. Pooled rates of dementia were stratified by study setting, inclusion or exclusion of pre-stroke dementia, and by first, any, or recurrent stroke. Pooled odds ratios were calculated for factors associated with pre-stroke and post-stroke dementia.We identified 22 hospital-based and eight population-based eligible cohorts (7511 patients) described in 73 papers. The pooled prevalence of pre-stroke dementia was higher (14.4%, 95% CI 12.0-16.8) in hospital-based studies than in population-based studies (9.1%, 6.9-11.3). Although post-stroke (<or=1 year) dementia rates were heterogeneous overall, 93% of the variance was explained by study methods and case mix; the rates ranged from 7.4% (4.8-10.0) in population-based studies of first-ever stroke in which pre-stroke dementia was excluded to 41.3% (29.6-53.1) in hospital-based studies of recurrent stroke in which pre-stroke dementia was included. The cumulative incidence of dementia after the first year was little greater (3.0%, 1.3-4.7) per year in hospital-based studies than expected on the basis of recurrent stroke alone. Medial temporal lobe atrophy, female sex, and a family history of dementia were strongly associated with pre-stroke dementia, whereas the characteristics and complications of the stroke and the presence of multiple lesions in time and place were more strongly associated with post-stroke dementia.After study methods and case mix are taken into account, reported estimates of the prevalence of dementia are consistent: 10% of patients had dementia before first stroke, 10% developed new dementia soon after first stroke, and more than a third had dementia after recurrent stroke. The strong association of post-stroke dementia with multiple strokes and the prognostic value of other stroke characteristics highlight the central causal role of stroke itself as opposed to the underlying vascular risk factors and, thus, the likely effect of optimum acute stroke care and secondary prevention in reducing the burden of dementia.None.
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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.Copyright © 2016 The Authors. Published by Elsevier B.V. All rights reserved.
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