Stroke injury, cognitive impairment and vascular dementia.
Stroke injury, cognitive impairment and vascular dementia.
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DOI：
10.1016/j.bbadis.2016.01.015
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发表时间：
2016-05
期刊：
影响因子：
--
通讯作者：
Ihara M
中科院分区：
文献类型：
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作者：
Kalaria RN;Akinyemi R;Ihara M
缺血性卒中的全球负担几乎是出血性卒中的4倍。目前的证据表明，25-30%的缺血性卒中幸存者发展为即刻或迟发性血管性认知障碍（VCI）或血管性痴呆（VaD）。中风损伤后的痴呆可能包括所有类型的认知障碍。在中风前痴呆的保护伞下描述了指数中风前的认知功能障碍的状态，这可能需要血管变化以及潜伏的神经退行性过程。卒中后认知障碍和痴呆的风险因素是多因素的，包括年龄较大、家族史、遗传变异、教育程度低、血管合并症、既往短暂性脑缺血发作或复发性卒中和抑郁症。脑卒中后痴呆的神经影像学决定因素包括无症状脑梗死、白色改变、腔隙性梗死和内侧颞叶萎缩。直到最近，脑卒中后痴呆的神经病理学定义不明确。大多数卒中后痴呆与涉及多种底物的VaD一致。微梗死、与血脑屏障损伤相关的微血管变化、局灶性神经元萎缩和共存神经退行性病理学的低负担似乎是中风损伤后痴呆的关键基质。阐明脑卒中后痴呆的发病机制将有助于建立有效的缓解和预防策略。控制血管疾病危险因素对于减轻卒中后认知功能障碍的负担至关重要。这篇文章是由M。作者：Paul Murphy，Roderick A. Corriveau和Donna M.威尔科克缺血性损伤在长期中风幸存者中很常见。约25%的中风幸存者发展为痴呆，其中更大比例的人发展为认知障碍。中风后痴呆的风险因素包括年龄较大，血管合并症，既往卒中和卒中前损害目前的成像和病理学研究表明，脑卒中后痴呆的病因是血管性痴呆。缺血性损伤后后遗症严重的白色改变和内侧颞叶萎缩是痴呆的基础。与生活方式因素相关的策略将减少中风后痴呆
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. Ischaemic injury is common among long-term stroke survivors About 25% stroke survivors develop dementia with a much greater proportion developing cognitive impairment Risk factors of dementia after stroke include older age, vascular comorbidities, prior stroke and pre-stroke impairment Current imaging and pathological studies suggest 70% of dementia after stroke is vascular dementia Severe white matter changes and medial temporal lobe atrophy as sequelae after ischaemic injury are substrates of dementia Controlling vascular risk factors and prevention strategies related to lifestyle factors would reduce dementia after stroke