无症状卒中研究进展

随着影像学技术的发展,尤其是磁共振弥散加权成像的应用,可以很容易地检测到无症状卒中病灶.无症状卒中的患病率和发病率均高于有症状卒中,年龄、高血压、心房颤动等是其公认的危险因素.尽管按照定义无症状卒中缺乏临床卒中样症状,但仔细检查仍常有轻微的躯体和认知功能障碍.此外,无症状卒中还与随后的有症状卒中、认知功能减退以及痴呆的发生有关.因此,临床医生需予以重视,积极控制其高危因素和改善其预后.     

心房颤动与无症状脑梗死

无症状脑梗死在老年人群中广泛存在,被认为是有症状卒中和认知损害的早期临床阶段.心房颤动和心房颤动消融术后患者无症状脑梗死的发生率较高,尚不清楚抗凝治疗能否预防心房颤动患者的无症状脑梗死和改善认知功能.文章对无症状脑梗死与心房颤动相关的热点问题进行了综述.     

心房颤动和认知功能下降的关系研究

心房颤动(房颤)是老年人常见的心律失常,并随着年龄增长发病率及病死率增高.众多的血管危险因素和血管疾病导致认知功能障碍和痴呆,而年龄亦是认知功能障碍的最主要因素.房颤和认知功能障碍相关的可能机制有:共同危险因素及共患病、缺血性卒中(有症状或无症状)和房颤的促炎状态等.房颤患者窦律的恢复和抗凝治疗有可能降低认知功能障碍的...     

急性卒中患者的无症状梗塞发病率、好发部位、危险因素及临床意义

对首发卒中患者的CT检查,文献报道无症状梗塞(SI)发生率为10％～38％。关于SI的危险因素尚存有争议。尽管SI不引起明确的症状,但可引起或加剧认知和智力障碍。Desemend等人最近报道,即使未发生卒中的人,如有卒中危险因素存在,其认知功能也常受到损害。因此,有理由认为急性卒中患者如有1个或多个SI,则可影响卒中的康复。但是,     

非卒中人群中脑血管疾病危险因素与认知功能的关系

如果存在血管病危险因素而又未发生卒中的老年人有智能缺陷,这种认知功能减退,可能是无症状性卒中所致,也可能就是严重脑血管病的首发症状。 作者对249名非卒中自愿者进行了认知功能测定,其平均年龄为70.8±6.7岁,平均教育年限为12.3±4.6年。调查的主要危险因素包括:高血压、糖尿病、心肌梗塞、心绞痛、高血脂及长期吸烟。同时还收集了诸如人文、服药、嗜酒等其它可能影响认知功能的因素。神经心理测定内容包括:记忆、抽象思维、言语、视觉空间及注意能力。经过逻辑回归处理,在控制人文因素影响之后发现:高血脂是记忆障     

346例无症状性脑梗塞临床分析

对346例无症状性脑梗塞患者的临床资料和CT结果进行分析，发现无症状性脑梗塞患者年龄偏大，常伴有高血压、短暂性脑缺血发作、糖尿病、冠心病或高脂血症，且无卒中史无症状性脑梗塞组与首次卒中无症状性脑梗塞组之间的危险因素无差异（P＞0．05）。无卒中史无症状性脑梗塞组患者常表现为头痛、头晕、智力减退和震颠等主要临床症状、CT共发现非责任梗塞灶497个，大多位于基底节区和半卵圆中心。结果提示，高血压、短暂性脑缺血发作、糖尿病、冠心病、高脂血症和高龄是无症状性脑梗塞的主要危险因素，提出其在临床诊断和防治上具有重要性。     

静止性脑梗死

静止性脑梗死是指临床上无症状或与临床症状不相关或与既往卒中史不相关的梗死灶。其发生率约为１０％～４８％，有关危险因素与糖耐量异常、无症状颈动脉粥样硬化、高血压及增龄等有关。ＣＴ及ＭＲＩ最常显示为腔隙性梗死，多位于深部结构如基底节区白质运动传导束以外。临床表现为认知障碍和精细神经功能缺损，可能是明显临床卒中的潜伏期     

静止性脑梗死

静止性脑梗死是指临床上无症状或与临床症状不相关或与既往卒中史不相关的梗死灶。其发生率约为１０％￣４８％，有关危险因素与糖耐量异常、无症状颈动脉粥样硬化、高血压及增龄等有关。ＣＴ及ＭＲＩ最常显示为腔隙性梗死，多位于深部结构如基底节区白质运动传导束以外。临床表现为认知障碍和精细神经功能缺损，可能是明显临床卒中的潜伏期。     

卒中在普通人群中并不少见——卒中的地理和种族差异原因（REGARDS）研究

相当多的普通人群在脑成像上有临床无症状的卒中,此类损害可能会引起症状。美国阿拉巴马大学流行病学系Howard等在无卒中和短暂性脑缺血发作(transient ischemic attack TIA)人群中对卒中症状的患病率以及卒中症状与由Framingham卒中风险评分评定的危险因素之间的联系进行了研究。     

无症状脑血管病患者的卒中预防美国心脏协会/美国卒中协会对医疗卫生专业人员发布的科学声明

最近20年的流行病学研究表明,无症状脑血管病很常见,且与未来发生卒中和痴呆的风险相关.它是脑部扫描时最为常见的偶然发现.为了总结无症状脑血管病的诊断和管理对卒中预防意义的相关证据,美国心脏协会卒中委员会召集了一个编写委员会来评估现有的证据,讨论临床思路,并为有关三大主要表现的无症状脑血管病患者(无症状脑梗死、推测为血管源性的MRI白质高信号、脑微出血)卒中预防的将来研究方向提供建议.编写委员会发现,有强烈的证据显示无症状脑血管病是衰老过程中的常见问题,无症状脑梗死和白质高信号与未来发生有症状卒中的风险相关,而且独立于其他血管危险因素.有证据表明,伴有脑微出血的急性缺血性卒中患者接受溶栓治疗后发生有症状颅内出血的风险略增高,但几乎没有前瞻性研究探讨抗凝治疗对这类患者发生有症状出血的风险.目前尚未专门针对无症状脑血管病患者的卒中预防进行过随机对照试验.无症状脑梗死、白质高信号和脑微出血均是卒中一级预防的指征.采用以往美国心脏协会/美国卒中协会声明或专家共识中提供的关于无症状脑血管病的标准术语和定义将有利于疾病的诊断以及放射科医生与神经科医生之间对于检查结果的交流.     

Functional and cognitive consequences of silent stroke discovered using brain magnetic resonance imaging in an elderly population

OBJECTIVES: To evaluate the prevalence of silent stroke and its associated consequences on physical, cognitive, and emotional functioning in an elderly population. DESIGN: Population-based cross-sectional survey. SETTING: The Memory and Morbidity in Augsburg Elderly project in the Augsburg region of southern Germany. PARTICIPANTS: Two hundred sixty-seven community-dwelling persons aged 65 to 83. MEASUREMENTS: The presence of silent stroke was determined using magnetic resonance imaging brain scan and a single question asking for physician-diagnosed stroke in each participant. The health effect of silent stroke was assessed using rating scales for self-perceived health status (36-item short-form health survey), activities of daily living (ADLs) and instrumental ADLs, cognitive function, and depression (Center for Epidemiologic Studies Depression scale). RESULTS: Just fewer than 13% (12.7%) of participants were affected by silent stroke. Silent stroke was associated with a history of hypertension, heart surgery, and elevated C-reactive protein. Individuals with silent stroke showed impairments on the Mini-Mental State Examination test and in the cognitive domains of memory, procedural speed, and motor performance. CONCLUSION: The presence of silent stroke has a considerable effect on cognitive performance in those affected. Determining the presence of silent stroke using brain imaging may contribute to identifying individuals at risk for developing gradual neurological deficits.     

Mechanisms and Clinical Manifestations of Cognitive Decline in Atrial Fibrillation Patients: Potential Implications for Preventing Dementia

Atrial fibrillation (AF) patients face an approximate 1.5-fold increased risk of cognitive decline compared with the general population. Among poststroke AF patients, the risk of cognitive decline is even higher with an estimated threefold increase. This article provides a narrative review on the current evidence and highlights gaps in knowledge and areas for future research. Although earlier studies hypothesized that the association between AF and cognitive decline is mainly a consequence of previous ischemic strokes, more recent evidence also suggests such an association in AF patients without a history of clinical stroke. Because AF and cognitive decline mainly occur among elderly individuals, it is not surprising that both entities share multiple risk factors. In addition to clinically overt ischemic strokes, silent brain infarcts and other brain injury are likely mechanisms for the increased risk of cognitive decline among AF patients. Oral anticoagulation for stroke prevention in AF patients with additional stroke risk factors is one of the only proven therapies to prevent brain injury. Whether a broader use of oral anticoagulation, or more intense anticoagulation in some patients are beneficial in this context needs to be addressed in future studies. Although direct studies are lacking, it is reasonable to recommend optimal treatment of comorbidities and risk factors for the prevention of cognitive decline and dementia.     

Clinical implications for diffusion‐weighted MRI brain lesions associated with transcatheter aortic valve replacement

Transcatheter aortic valve replacement (TAVR) is increasingly used to treat patients with aortic stenosis deemed high or extreme surgical risk candidates. Despite improved survival and quality of life following the procedure, TAVR is not without its complications. Stroke is a major source of morbidity and mortality in patients undergoing the procedure, with rates similar to and often higher than those associated with surgery. Most studies show a consistent link between TAVR and embolic lesions visualized on diffusion‐weighted magnetic resonance imaging. The question of whether these lesions lead to long‐term cognitive consequences remains open, but given the large literature on silent strokes and cognition, this association is probable. Initial studies implementing cerebral embolic protection devices in TAVR have yielded promising results with decreased neurological complications and appearance of new lesions on imaging. In this article, we will review the evidence linking silent stroke with cognitive decline, and potential therapeutic options to prevent stroke related to TAVR, including cerebral protection devices currently under investigation. © 2013 Wiley Periodicals, Inc.     

Dementia and Atrial Fibrillation: Pathophysiological Mechanisms and Therapeutic Implications

Atrial fibrillation increases the risk of stroke by a factor of four- to fivefold, and dementia is a common consequence of stroke. However, atrial fibrillation has been associated with cognitive impairment and dementia, even in patients without prior overt stroke. Nonischemic mechanisms include cerebral hypoperfusion, vascular inflammation, brain atrophy, genetic factors, and shared risk factors such as age or hypertension. Critical appraisal of studies evaluating the association between atrial fibrillation and dementia in stroke-free patients reveals that several suffer from methodological issues, such as not including silent stroke or anticoagulation therapy in multivariate analyses. Some studies show a close relationship between atrial fibrillation and dementia due to silent stroke, in the absence of overt stroke. Evidence is accumulating that anticoagulation may be effective to decrease the risk of dementia in atrial fibrillation patients. Overall, the pathogenesis linking atrial fibrillation to dementia is likely multifactorial. Cerebral infarctions, including silent stroke, play a central role. These findings underscore the importance of stroke prevention measures in atrial fibrillation patients.     

Nocturnal Blood Pressure, Morning Blood Pressure Surge, and Cerebrovascular Events

Cerebrovascular disease is a common cause of death and major cause of disability worldwide. Even in silent cases (e.g., silent cerebral infarction, white matter lesion), cerebrovascular disease can lead to physical and cognitive impairment, thereby substantially reducing the activities of daily living. Accordingly, the earliest possible action to prevent not only symptomatic but also silent cerebrovascular disease has become a major public health challenge. Hypertension is a potent risk factor for both symptomatic and silent cerebrovascular disease. Twenty-four-hour blood pressure (BP) rather than office BP is closely associated with cerebrovascular disease and/or poor physical and cognitive function. In particular, nocturnal BP and morning BP surge have attracted much attention as risk factors for cerebrovascular diseases independently of 24-h BP level. This review is an attempt to summarize some of the evidence on nocturnal BP level or nocturnal BP dipping status, and morning BP surge as potent risk factors for cerebrovascular disease.     

Atrial Fibrillation and Cognitive Function: JACC Review Topic of the Week

Numerous vascular risk factors and vascular diseases contribute to cognitive impairment and dementia. Many studies and registries show an association of atrial fibrillation (AF) with cognitive impairment, cognitive decline, and dementia. This is true for vascular dementia and Alzheimer's disease. The assumed multifactorial mechanisms include ischemic stroke, both apparent and silent, cerebral microinfarcts, cerebral hemorrhage, and reduced cerebral blood flow. A number of retrospective observational and prospective studies support that anticoagulation in patients with AF may reduce the risk of cognitive decline and dementia. This holds for both vitamin K antagonists (e.g., warfarin) and direct oral anticoagulants. However, it still remains unproven if anticoagulation reduces cognitive decline and dementia in AF patients based on randomized trials.     

Longitudinal changes in brain magnetic resonance imaging findings in children with sickle cell disease

Children with sickle cell anemia (HbSS) are at high risk for neurologically overt cerebral infarcts associated with stroke and neurologically silent cerebral infarcts correlated with neuropsychometric deficit. We used complete magnetic resonance imaging (MRI) histories from 266 HbSS children, aged 6 through 19 years, who were enrolled in the Cooperative Study of Sickle Cell Disease (CSSCD) to examine silent infarct prevalence, localization, recurrence, and progression. We report a baseline prevalence of 21.8%, marginally higher than previously reported due to improved imaging technologies. Although we observed no overall sex difference in prevalence, most lesions in girls occurred before age 6, whereas boys remained at risk until age 10. Silent infarcts were significantly smaller and less likely to be found in the frontal or parietal cortex than were infarcts associated with stroke. Children with silent infarct had an increased incidence of new stroke (1.03/100 patient-years) and new or more extensive silent infarct (7.06/100 patient-years) relative to stroke incidence among all children in our cohort (0.54/100 patient-years). Both events were substantially less frequent than the risk of stroke recurrence among children not provided chronic transfusion therapy. Although chronic transfusion is known to decrease occurrence of new silent infarcts and strokes in children with elevated cerebral arterial blood flow velocity, further study is required to determine its risk-benefit ratio in children with silent infarct and normal velocities. Until safe and effective preventive strategies against infarct recurrence are discovered, MRI studies are best reserved for children with neurologic symptoms, neuropsychometric deficits, or elevated cerebral artery velocities.