卒中后痴呆

卒中是老年人死亡的主要原因，卒中后发生痴呆的风险增高。卒中后痴呆涵盖了卒中后的各种痴呆类型，是老年人致残的重要原因，其患病率在卒中后3个月至4年内为31．4％～21．5％，其发病率随卒中后时间的延长而增高。卒中和痴呆有许多共同的危险因素。卒中可以是痴呆的直接原因，也可能促进了变性性疾病的发展而引起痴呆。     

脑梗死存活率影响因素的前瞻性研究

目的研究脑梗死后痴呆对存活率的影响。方法对619例急性脑梗死患者进行人文因素、血管因素、卒中特征资料收集和神经心理检查。在入院及卒中后3个月按美国精神病学会DSM-Ⅳ标准对卒中患者进行痴呆诊断,随访2年,分析痴呆患者的存活率及死亡相关预测因素。结果 卒中后3个月共有146例(23.6％)患者被诊断为痴呆,其中39例为卒中前痴呆,107例为卒中相关痴呆。随访(19.4±8.3)个月,卒中后痴呆患者存活率为49.3％,随访(21.3±9.1)个月,卒中相关性痴呆存活率为53.7％,非痴呆患者存活率为92.0％。多因素分析显示,卒中后痴呆与死亡明显相关,脑梗死后痴呆病死率的独立危险因素是年龄、心房颤动、卒中史、日常生活能力评分、卒中后痴呆和卒中相关痴呆。结论痴呆降低卒中患者存活率,并可作为卒中后存活的一个预测因素。     

脑卒中后血管性痴呆66例临床分析

卒中一直被认为是造成痴呆的重要原因，为探讨卒中后血管性痴呆的相关因素，进一步做好卒中及卒中后痴呆的预防，我们对66例卒中后血管性痴呆患者的临床资料进行了回顾性分析。     

抑郁是85岁老年人首次卒中发生率的一个危险因素

抑郁可能会增加卒中风险.在高龄和痴呆患者中,为数不多的几项研究已对抑郁是否会增高卒中风险进行了研究.德国Dr Horst Schmidt Klinik医院神经内科的Liebetrau等对85岁老年人抑郁与3年首发性卒中发生率之间的联系进行了研究.     

老年心房颤动患者的抗血栓治疗

心房颤动(房颤)是一种十分常见的心律失常.随年龄的增长其发病率明显增高,在年龄＜50岁的人群中发病率低于2%,而70岁以上人群中发病率则增加到13%.由于老年人房颤发病率增高,作为其重要合并症之一的缺血性卒中的发生率也呈增高趋势.风湿性瓣膜病房颤患者卒中的危险性增加17倍,非瓣膜性房颤(NVAF)患者卒中危险性可增加4倍,缺血性卒中已经成为影响老年房颤预后的重要原因之一.抗血栓治疗是预防卒中的有效手段,近年来已有多项大规模临床研究证实抗血栓治疗可以明显降低老年房颤患者卒中发生率,并在适应证、药物选择及并发症预防等方面取得了很大进展.     

正规的吞咽困难筛查方案能够预防卒中后肺炎

肺炎是缺血性卒中的一种重要并发症,可使卒中患者的病死率增高3倍。吞咽困难是卒中后肺炎的一个常见原因,一些卒中治疗指南均建议在患者进食前进行吞咽评价。然而,对吞咽困难筛查的强度和哪些患者应进行筛查还不清楚。美国波士顿圣·伊丽莎白医学中心神经内科的Hinchey等从15家紧急治疗机构前瞻性收集了所有急性缺血性卒中患者的资料,必需收集的资料包括人口统计学特征和4项质量标记指标,可供选择的资料包括卒中严重程度和并发症。对吞咽困难筛查的依从性、筛查类型和院内肺炎进行检测。在2001年12月—2003年1月期间,共收集到2532例患者的…     

老年人隐性心力衰竭84例误诊分析

慢性心力衰竭是临床常见的综合征,且发病与多种因素相关。近年来,随着我国人口老龄化进程的加快和高血脂、高血压、冠心病、糖尿病等常见病发病率的上升,心力衰竭的患病率逐渐增高。典型的心力衰竭诊断不难,但是老年人隐性心力衰竭因缺乏典型症状、体征,极易误诊,我们收集整理老年人隐性心力衰竭84例,就其误诊原因进行分析,现报道如下。1临床资料1·1一般资料选择1997~2004年我院84例隐性心力衰竭患者,其中男45例,女39例,年龄65~88岁,平均73·5岁。误诊为:慢性支气管炎31例(36·9%),支气管哮喘7例(8·0%),肺炎6例(7·0%),慢性阻塞性肺气肿4…     

老年痴呆86例临床分析

目的　通过分析老年人发生痴呆的原因及临床表现 ,从而提高对老年痴呆的认识。方法　对 86例已确诊为老年痴呆的病人的临床资料进行回顾性分析。结果　 86例病人中血管性痴呆 (VaD) 81例 ,阿尔茨海默病痴呆 (AD) 5例。VaD痴呆全部有卒中史 ,多发性梗死 43例 ,大脑前动脉梗死 4例 ,内囊及其周围的白质梗死 8例 ,Binswanger病 3例 ,出血性卒中 5例。AD痴呆无局灶神经定位体征 ,影像学检查示有脑室增大及不同程度的脑萎缩。结论　脑卒中及阿尔茨海默病是老年痴呆最主要的原因。该两种病可能存在共同的危险因素和发病机制 ,早期干预治疗意义重大。     

为什么卒中患者易发生痴呆?

卒中后发生痴呆的机制仍不清楚。作者通过复习文献,揭示了卒中后易发生痴呆的3种可能的发病机制。(1)卒中后痴呆是脑血管损害的直接后果。尤其在年轻人、冰岛型遗传性脑淀粉样血管病和伴皮质下梗死和白质脑病的常染色体显性遗传性脑动脉病(CADASIL)患者中,若卒中前认知功能正常,则丘脑、角回、尾状核等重要部位的单个梗死灶往往是脑血管病之后发生痴呆的最可能原因。(2)卒中后痴呆可能     

多发性脑梗死后痴呆与头颅CT关系的分析

老年期痴呆是严重危害老年人生活和健康的神经系统疾病 ,随着社会人口的老龄化 ,患者人数逐年增加 ,近年研究发现血管性痴呆发生率比预期高 ,梗死后可使痴呆发生率增加 4～ 12倍 ,本文对37例多发性脑梗死后痴呆的临床资料与头颅CT关系进行分析。1　资料与方法1.1　一般资料　 37例 ,男 30例 ,女 7例。年龄 6 0～ 87岁 ,平均 (6 8 97± 6 8)岁。有高血压、动脉硬化史 32例 ,冠心病史 17例 ,卒中史 14例 ,心房纤颤 5例 ,糖尿病史 12例 ,吸烟 15例 ,饮酒 9例。患者除高级神经活动异常外 ,语言欠清 9例 ,假性球麻痹 2 7例 ,肢体瘫痪 2 1例 ,肢…     

Specificity of stroke in the elderly: clinical characteristics and impact on care

Stroke in the elderly differs from stroke in younger adults in several points. It represents the most frequent consequence of atherothrombotic disease associated with hypertension, diabetes and hypercholesterolemia. It is also the main complication of cardiac arrhythmia. From a clinical point of view, epileptic seizure is frequently observed at the onset, and prognosis is darkened by a high risk of dementia occurrence (20%). Management of stroke in acute phase requires intensive care, which has been shown to decrease mortality and handicap by 20% in Stroke Units. Fibrinolysis with rt-PA can be carried out till 80 years. Primary and secondary prevention are still very efficacious in old patients and decrease not only the risk of stroke, but also the risk of dementia. Moreover, influenzae vaccination has been shown to decrease the risk of stroke in the following year in subjects over 65 years.     

血管性痴呆危险因素的研究

目的研究脑梗死后痴呆的危险因素。方法本研究纳入546例脑梗死急性期住院患者,完成随访434例,于住院期间和脑卒中3个月后进行神经心理测试,其中痴呆组118例,非痴呆组316例。运用t检验、χ2检验和logistic回归法分析血管性痴呆的发生率和危险因素。结果本研究中血管性痴呆的发生率为27.2%。单因素分析表明,血管性痴呆组的年龄比非痴呆组高8.5岁,在低教育水平(小学以下)、每日饮酒、脑卒中史等方面的比例显著高于非痴呆组。logistic回归分析表明,年龄、低教育水平、每日饮酒和脑卒中史与血管性痴呆相关。结论血管性痴呆是血管因素和退行性因素共同作用的结果,其中血管因素在血管性痴呆发病机制中起主导作用。年龄、低教育水平、每日饮酒和脑卒中史是血管性痴呆的危险因素。     

Stroke-related depression

Stroke represents a major health problem in the United States and most European and Asian countries. Depression is probably the most common and serious emotional disorder following stroke. Post-stroke depression (PSD) has frequently been overlooked and left untreated. Prevention of PSD or successful intervention in the early phase may prevent premature deaths as well as facilitate rehabilitation, reduce costs, and improve quality of life. Stroke is clearly a risk factor for depression, and recent evidence suggests that depression increases the risk for stroke, although the mechanisms by which depression leads to stroke remain to be clarified. Once PSD has developed, numerous studies have documented its adverse effect on cognitive recovery, physical recovery, and mortality. Taken together, these studies support the necessity of identifying and treating this condition.     

The Effects of Statins on Prevention of Stroke and Dementia: A REVIEW

Stroke is the third leading cause of death in the United States and places a heavy toll on health care spending, especially in the elderly population. The prevalence of stroke increases with increasing age. Over the last 2 decades, there have been substantial data supporting the use of statins in the primary, as well as secondary, prevention of stroke. Although most of these studies were designed to evaluate cerebrovascular accidents (CVA) only as secondary endpoints, the data show a significant reduction in strokes associated with statin use. There have been numerous studies that have demonstrated the relationship between serum cholesterol levels, specifically low-density lipoprotein cholesterol, on CVA and the beneficial effects of statins in this setting. Furthermore, in addition to the lipid-lowering properties of statins, these drugs have also been shown to possess cholesterol-independent pleotropic properties that have been associated with neuroprotection. Finally, the role of statins for the prevention of dementia is still highly debatable. We examine the role of this class of drugs in the setting of dementia, particularly from vascular causes and stroke.     

Potential for antihypertensive treatment with an AT(1)-receptor blocker to reduce dementia in the elderly

Hypertension is an established risk factor for stroke and other cerebrovascular disorders. Both stroke and small lacunar infarcts or white matter lesions can cause cognitive impairment and dementia, and there is evidence that vascular risk factors play a major role in the development of both Alzheimer's disease and vascular dementia. Several large epidemiological studies have shown that raised blood pressure in midlife is a strong risk factor for dementia later in life; however, blood pressure often decreases following the development of dementia. The cognitive function hypothesis proposes that elevated blood pressure increases the risk of decline of cognitive function, and that this can be reversed by active lowering of blood pressure. Evidence in support of this hypothesis comes from the Syst-Eur Dementia project, and from a number of smaller studies. SCOPE (Study on Cognition and Prognosis in the Elderly) is a large prospective study involving almost 5000 elderly patients (age 70-89 years), who are randomised to receive candesartan cilexetil, 8-16 mg, or placebo. Candesartan was chosen for this study because it is effective and well tolerated in elderly patients. SCOPE should provide important information on the long-term effects of AT(1)-receptor blocker treatment with candesartan on morbidity-including effects on cognitive function-and cardiovascular mortality in elderly hypertensive patients.     

NEUROIMAGING PREDICTORS OF DEMENTIAIN STROKE PATIENTS

The risk of dementia is increased in stroke patients. Dementia syndromes associated with cerebrovascular diseases were commonly recognized as an immediate consequence of stroke. However, more and more data suggest that degenerative pathology and white matter changes (WMC) may play a role in the development of dementia in stroke patients. The aim of this paper was to review the literature concerning the neuroimaging predictors of dementia in stroke patients. From the literature data, it appears that although vascular lesions alone may lead to dementia, in stroke patients, no clear association between stroke location and size has yet been identified, even if the role of the left hemisphere has been suggested. The influence of silent infarcts remains undetermined while more and more data suggest that global cerebral atrophy and WMC are predictive factors of post-stroke dementia (PSD). The influence of medial temporal lobe atrophy on the risk of PSD has until now never been evaluated.     

Neuroimaging predictors of dementia in stroke patients

The risk of dementia is increased in stroke patients. Dementia syndromes associated with cerebrovascular diseases were commonly recognized as an immediate consequence of stroke. However, more and more data suggest that degenerative pathology and white matter changes (WMC) may play a role in the development of dementia in stroke patients. The aim of this paper was to review the literature concerning the neuroimaging predictors of dementia in stroke patients. From the literature data, it appears that although vascular lesions alone may lead to dementia, in stroke patients, no clear association between stroke location and size has yet been identified, even if the role of the left hemisphere has been suggested. The influence of silent infarcts remains undetermined while more and more data suggest that global cerebral atrophy and WMC are predictive factors of post-stroke dementia (PSD). The influence of medial temporal lobe atrophy on the risk of PSD has until now never been evaluated.     

Epidemiology of vascular dementia.

Although epidemiological studies are limited by diagnostic uncertainties, they suggest that stroke increases the risk of dementia. The mortality rate is higher in vascular dementia (VaD) than in Alzheimer's disease (AD). Community-based studies have provided several consistent findings: (i) age dependence with prevalence rates doubling every 5 years, (ii) a higher frequency in men and (iii) nation-to-nation differences. The prevalence of VaD ranges from 2.2% in 70- to 79-year-old women, to 16.3% in men >80 years. One sixth of acute stroke patients have preexisting dementia. The incidence of VaD has been studied much less extensively than that of AD, and substantial variations in the incidence rates have been observed: annual incidence rates (per 100,000) range from 20 to 40 between 60 and 69 years of age and from 200 to 700 over 80. The incidence rate of VaD declined over the last 2 decades, probably as a consequence of effective stroke prevention. It is generally assumed that risk factors for VaD are those of stroke, with arterial hypertension as leading factor, followed by atherosclerotic disease, low education level, alcohol abuse and heart disease. Stroke characteristics, such as lacunar infarction and left-sided hemispheric lesions, are major determinants of VaD. The cerebrovascular lesions are likely to be the only cause of dementia in strategic infarcts, in lacunar state, in hereditary cystatin C amyloid angiopathy and in CADASIL. However, white matter changes, and associated Alzheimer pathology, which are both frequent in this age category, may also contribute to the cognitive decline.     

Role of platelet activation in dementia.

Platelets play an important role in atherosclerosis, and increased platelet activation is associated with stroke. Stroke is an important risk factor for dementia, as approximately 25% of the patients are demented after stroke. In this review, we describe platelet activation studies in patients with stroke and with dementia. In addition, we review the few studies that have investigated the effect of antiplatelet medication such as aspirin and non-steroidal anti-inflammatory drugs on cognitive function and the occurrence of dementia. We conclude that further studies are needed to characterize the mechanisms and determinants of platelet activation in relation to the development of dementia. Furthermore, the efficacy and safety of antiplatelet intervention will have to be assessed in properly designed randomized trials.     

Stroke in diabetic patients

Stroke is the leading cause of disability and the second most frequent cause of death worldwide. On the one hand, diabetic patients have a 1.5 to 3-times higher risk of stroke, especially cerebral infarction, than non-diabetic subjects. This excess risk, which is particularly pronounced in younger individuals and women, can be reduced by effective therapeutic strategies aimed at improving glycaemic control and the management of co-morbid conditions such as hypertension and dyslipidaemia. On the other hand, the prevalence of diabetes in stroke patients is between 10 and 20%, and has been increasing over the last 20 years, probably in response to rising rates of overweight and obesity in the general population and other factors such as a sedentary lifestyle. Even though diabetes has long been considered a specific risk factor of lacunar stroke, recent epidemiological studies have demonstrated that this risk factor was in fact not associated with any ischemic stroke subtype. Finally, it has been suggested that diabetic stroke patients have poorer motor and functional outcomes, and are at a higher risk of dementia, recurrent stroke and death.