Post-stroke dementia - a comprehensive review.
Post-stroke dementia - a comprehensive review.
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中风后痴呆 - 全面回顾。
DOI：
10.1186/s12916-017-0779-7
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发表时间：
2017-01-18
期刊：
影响因子：
9.3
通讯作者：
Bornstein NM
中科院分区：
文献类型：
--
作者：
Mijajlović MD;Pavlović A;Brainin M;Heiss WD;Quinn TJ;Ihle-Hansen HB;Hermann DM;Assayag EB;Richard E;Thiel A;Kliper E;Shin YI;Kim YH;Choi S;Jung S;Lee YB;Sinanović O;Levine DA;Schlesinger I;Mead G;Milošević V;Leys D;Hagberg G;Ursin MH;Teuschl Y;Prokopenko S;Mozheyko E;Bezdenezhnykh A;Matz K;Aleksić V;Muresanu D;Korczyn AD;Bornstein NM
中风后痴呆（PSD）或中风后认知障碍（PSCI）可能影响多达三分之一的中风幸存者。PSCI和PSD的各种定义已经被描述。我们建议将PSD作为中风后痴呆的时间关系标签。有各种各样的工具可用于筛选和评估认知，很少有psd特定的工具。选择将取决于评估目的，需要不同的工具进行简短筛查（例如，蒙特利尔认知评估）或诊断配方（例如，NINDS VCI电池）。全面的评估应包括中风前的认知评估（例如，使用老年人认知能力下降的信息调查表），情绪评估（例如，使用医院焦虑和抑郁量表），以及认知障碍的功能后果评估（例如，使用改进的Rankin量表）。大量PSD的生物标志物，包括遗传多态性指标、脑脊液和血清中的生物标志物、炎症介质和外周microRNA谱已经被提出。目前，还没有特定的生物标志物被证明可以有效地区分易感患者（“风险大脑”）和预后较好的患者，或者区分阿尔茨海默病痴呆和PSD。此外，神经影像学是PSD的重要诊断工具。计算机断层扫描的作用仅限于显示潜在原发病变的类型和位置，并指示萎缩和严重的白质改变。磁共振成像是关键的神经成像方式，对检测病理变化，包括小血管疾病具有很高的灵敏度和特异性。先进的多模态成像包括用于光纤跟踪的扩散张量成像，通过它可以检测网络的变化。通过正电子发射断层扫描定量成像脑血流和代谢可以区分血管性痴呆和退行性痴呆，并显示血管和代谢变化之间的相互作用。脑缺血后可见炎性改变，可能与淀粉样蛋白沉积共同参与PSD的发生发展。预防PSD可以通过预防中风来实现。作为抑制PSD发展和缓解病程的治疗策略，降压、他汀类药物、神经保护药物、抗炎药物等均被研究过，但没有令人信服的疗效证据。最近对生活方式干预、体育活动和认知训练进行了测试，但仍缺少大型对照试验。
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.