血管性痴呆的生物学标记物研究进展

血管性痴呆与阿尔茨海默病、混合性痴呆的鉴别诊断面临困难。目前应用的血管性痴呆临床诊断标准的敏感度和特异度偏低。近年一些生物学标记物作为病理生理过程的客观指标被应用于与血管性痴呆的诊断和鉴别诊断。这些生物学标记物包括结构影像学、正电子发射断层扫描（positron emission tomography,PET）、脑脊液标记物[淀粉样β多肽（Amyloidβ-peptide,Aβ）和tau蛋白]、血浆细胞因子和脑血管血液动力学检查等。初步的研究结果提示脑脊液Aβ和脑的脱氧葡萄糖-PET显像对于血管性痴呆的诊断和鉴别诊断具有较高的应用价值。     

血管性痴呆诊断标准草案

前言 :随着社会人口的老龄化 ,老年期痴呆的患病率正在逐年增高。血管性痴呆是老年期痴呆第二位重要的疾病 ,对于该疾病的正确诊断 ,建立统一的诊断标准不仅对理解其病理生理和适当的治疗至关重要 ,而且为促进多中心合作、推进血管性痴呆的研究有很大的帮助。中华医学会神经病学分会组织了北京、上海、广州的部分神经科、精神科教授 ,在参照第四次修订诊断与统计手册 (ＤＳＭ Ⅳ )、国立神经病及卒中研究所 国际神经科学研究与教育协会 (ＮＩＮＤＳ ＡＩＲＥＮ)、第 10次修订的国际疾病分类法 (ＩＣＤ 10 )的基础上 ,经多次讨论 ,制订了我…     

血管性痴呆和血管性认知障碍的临床研究进展

血管性认知障碍和痴呆是认知障碍和痴呆领域以及脑血管病领域研究方面的交叉点。本文综述了血管性痴呆和认知障碍的定义、诊断标准和药物治疗进展。在诊断方面重点介绍了血管性痴呆各个亚型的临床特点。在治疗方面重点介绍了血管性痴呆和认知障碍的胆碱能递质代谢障碍以及胆碱酯酶抑制剂治疗的进展。     

血管性痴呆的临床研究进展

血管性痴呆(VAD)已成为临床常见的疾患之一。约20～40％的脑血管病患者伴有程度不同的智能障碍。既往认为,痴呆的发生为脑动脉硬化的结果。Hachinski(1974)经病理研究指出,多发性的双侧半球缺血卒中是导致认识障碍的直接原因,提出“多梗塞性痴呆”(MID)的诊断,并作为一个特殊的临床疾病实体。进一步的研究表明,除MID外,还存在与血管因素有关,而以其它不同形式表现的痴呆者。轻微的卒中,损害了脑重要部位或单一的大片梗塞及皮质下白质的变化,均可导致痴呆而并非决定于脑多梗塞的存     

血管性痴呆的临床与CT改变的研究

目的：探讨血管性痴呆的临床特点及脑部CT的动态变化。方法：应用NINDS－AIREN标准诊断血管性痴呆患者57例,其中34例在确诊痴呆后1－3年内再次住院并有两次以上CT检查结果。30例无痴呆的脑血管病患者亦有两次CT检查结果。对34例血管性痴呆患者和30例无痴呆脑血管病患者脑部CT的动态变化进行比较,结果：血管性痴呆组卒中两次以及上比例高于无痴呆组（P＜0．05）,大小便失禁、意志行为改变、人格改变及妄想在血管性痴呆组的出现明显高于无痴呆组（P＜0．05）。与无痴呆组相比,血管性阁呆组随着病情的发展,脑梗死容积进行性增加,脑萎缩的发展加快（P＜0．05）,脑白质的改变却与对照组无差异（P＞0．05）。结论：血管性痴呆患者的精神症状并少见,血管性痴呆患者的记忆、智力、人格可以相互影响,随着病和的延长血管性痴呆患者脑部梗死容积农渐增加,脑萎缩明显加重。     

56例老年血管性痴呆病人的护理体会

本文对56例老年血管性痴呆病人进行护理,现将护理体会总结如下. 1 临床资料 1.1 一般资料 样本来自我院2007-01～2009-10住院的老年血管性痴呆患者,以Hachinski缺血评分量表>分及长谷川智能量表(HDS)<24分者为老年血管性痴呆诊断标准[1],病程≥3个月;由照料者或知情者提供信息,意识清晰,检查合作,排除其他原因引起的痴呆,入组56例,男31例,女25例,年龄62～76岁,平均(78.2±15.3)岁;其中有高血压和动脉粥样硬化史34例(62.7%),反复卒中进入痴呆38例(32.6%),1次卒中起病7例(8.1%),糖尿病26例(40.7%),高血脂19例(22.1%).     

多奈哌齐联合脑复康治疗血管性痴呆45例疗效观察

本文观察多奈哌齐与脑复康联合治疗血管性痴呆的临床效果,现报告如下。1资料和方法1.1一般资料选择我院2009-10—2011-10血管性痴呆患者90例,符合第4版美国精神疾病诊断和统计手册中血管性痴呆的诊断标准,同时排除其他原因导致的痴呆、合并肝     

非痴呆的血管性认知障碍

回顾历史,我们可以发现血管性痴呆(vascular dementia,VaD)和血管性认知障碍(vascular cognitive impalrment,VCI)的概念在近百年来处于演变之中。早在1896年Emil Kraepelin在其编写的教科书中提出"动脉硬化性痴呆"的概念,掀开了VaD研究的帷幕。1974年Hachinski等提出了"多发梗死性痴呆"的概念以及著名的Hachinski缺血量表。1993年Hachinski和Bowler等提出了涵盖更广泛的"VCI"的概念,其中包括VaD、伴血管病变的阿尔茨海默病和非痴呆的VCI等。尽管已经有了关于VCI的共识性标准,但是对于VCI仍缺乏明确的定义。关于VaD的国际性诊断标准虽然有多种,但临床病理研究提示这些常用临床诊断标准对于病理诊断的阳性和阴性预测率都较低。迄今对于VaD和VCI的治疗也没有形成统一的具有充分循证医学证据的指南。这些令神经病学家们困惑难题的根源很大程度上是由于我们对于VCI和VaD的发病机制缺乏充分认识。近年许多学者都指出VCI和VaD具有显著的临床异质性和病理异质性,基于不同脑血管病亚型有着不同病理生理过程。有关VCI和VaD的研究进展主要集中在下列方面:①将VaD的概念延伸到VCI,将血管性病变导致痴呆的干预时机适当提前,这将有赖于在疾病早期快速准确地筛查出VCI或者VaD从而进行有效的防治。②将VaD进行分型研究。迄今只有两种类型的血管病变(融合性白质病变以及腔隙性病灶)与认知下降有明确的相关性;而包括微栓子、血管病变导致的脑萎缩、新型影像技术显示的脑结构改变等尚未能明确与认知障碍程度和进展的相关性。在VaD的亚型中,皮层下VaD表现出与多发梗死性痴呆不同的发病机制,在其诊断、预防、治疗方面应有不同的策略。③关注脑血管病与退行性病变(特别是阿尔茨海默病)的相互作用。基于临床病理研究以及神经生化、神经影像标记物(特别是分子影像技术)的研究提示大多数痴呆实际上是神经系统退行性病变与血管性病变共同作用的结果,将痴呆截然分类为退行性病变和VCI碍可能是不恰当的。④VaD和VCI的诊断标准有待更新,将VCI从时髦的概念发展为明确定义的疾病。本期发表了一系列有关VaD和VCI发病机制、诊断等方面的论著和综述,将有助于我们在上述四个方面扩展视野、加深认识。冯涛     

盐酸多奈哌齐治疗血管性痴呆的疗效观察

本研究观察盐酸多奈哌齐(安理申)治疗血管性痴呆(VD)的临床疗效. 1 对象与方法 1.1 对象系2006年1月～2008年7月住我院神经内科治疗的VD患者56例,脑血管病诊断符合全国第四届脑血管病学术会议修订的标准;VD诊断符合中华医学会神经病学分会<血管性痴呆诊断标准草案>.     

脑卒中后痴呆39例临床分析

痴呆是脑卒中的常见后果，是影响患者肢体功能恢复和生活质量改善的重要因素。本文观察了首次发生脑卒中患者卒中后痴呆的发病情况，报道如下。１　资料１１　一般资料：选自１９９５年１月～１９９６年１２月本院和省人民医院脑血管病房首次卒中，生存时间大于３０天的１５１例病人为研究对象，在卒中后３个月内进行评定。所有病人经ＣＴ或ＭＲＩ证实存在大脑半球梗死或出血，无痴呆个人史及家族史，痴呆诊断符合美国立神经系统疾病与卒中研究所和瑞士神经科学研究协会（ＮＩＮＤＳＡＩＲＥＮ）１９９３年制订的血管性痴呆诊断标准。１…     

Clinicopathological validation study of four sets of clinical criteria for vascular dementia.

OBJECTIVE: The authors' goal was to validate the clinical criteria for vascular dementia of the State of California Alzheimer's Disease Diagnostic and Treatment Centers (ADDTC), the National Institute for Neurological Disorders and Stroke-Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN), DSM-IV, and ICD-10. METHOD: Sensitivity and specificity were assessed by comparing the clinical with the neuropathological diagnosis of 89 autopsied patients with dementia from a geriatric and psychiatric hospital. All cases were reviewed by a clinician and a neuropathologist who were blind to each other's findings. RESULTS: Neuropathologically there were 20 cases of vascular dementia, 23 cases of mixed dementia, and 46 cases of Alzheimer's disease among the autopsied patients. The sensitivity was 0.50 for DSM-IV criteria for vascular dementia, 0.70 for ADDTC criteria for possible vascular dementia, 0.55 for NINDS-AIREN criteria for possible vascular dementia, 0.20 for ICD-10 criteria for vascular dementia, 0.25 for ADDTC criteria for probable vascular dementia, and 0.20 for NINDS-AIREN criteria for probable vascular dementia. Specificity was 0.84, 0.78, 0.84, 0.94, 0.91, and 0.93, respectively. The proportion of cases clinically classified as vascular dementia ranged from 0% to 13% for neuropathologically confirmed cases of Alzheimer's disease and 9% to 39% for neuropathologically confirmed cases of mixed dementia. There was no statistically significant relationship between the neuropathological diagnosis and three of the clinical criteria sets studied (ICD-10 criteria for vascular dementia and ADDTC and NINDS-AIREN criteria for probable vascular dementia). CONCLUSIONS: Clinical criteria for vascular dementia are not interchangeable. The ADDTC criteria for possible vascular dementia are the most sensitive for the detection of vascular dementia; however, the DSM-IV criteria for vascular dementia and the NINDS-AIREN criteria for possible vascular dementia may be more effective in excluding mixed dementia. Given their inability to detect the vast majority of cases of vascular dementia, the ICD-10 criteria for vascular dementia and the ADDTC and NINDS-AIREN criteria for probable vascular dementia should be revised.     

Vascular dementias

Cerebrovascular disorders are the second most frequent cause of dementia in late life next to Alzheimer's disease. A recent community-based autopsy study has demonstrated that relevant cerebrovascular changes are much more prevalent in individuals aged 70+ years than previously assumed. Furthermore, the combination between cerebrovascular lesions and Alzheimer-type pathology is the most common neuropathological finding in elderly patients with dementia. There is still some uncertainty about which types of cerebrovascular changes are most likely to cause cognitive impairment including dementia and which pathogenetic mechanisms are involved. Without doubt, however, the vascular dementias are a heterogeneous group of diseases in terms of etiology, histopathology, and clinical appearance. According to the vessel calibres and perfusion territories that are preferentially affected a distinction is commonly made between the frequent subcortical small-vessel disease and the rare cortical large-vessel disease. With these morphological subtypes three major clinical variants are associated: dementia due to subcortical lacunes and white matter changes including Binswanger's disease, multi-infarct-dementia, and dementia due to singular strategic infarcts. In most cases of dementia of cerebrovascular origin the pattern of intellectual impairment is frontal or subcortical, in contrast to the typical cortical presentation of Alzheimer's disease. Deterioration of executive function and attention as well as changes in personality, rather than memory loss, are the predominant symptoms. Therefore the current diagnostic criteria for dementia are poorly suited for the detection of vascular dementias. None of the criteria that have been specifically proposed for the diagnosis of vascular dementias provide clear guidelines for evaluating the causal relationship between cerebrovascular lesions and psychopathological findings. Further research will reveal whether clinical diagnosis can be improved by taking into account the heterogeneity of cerebrovascular diseases. A large proportion of dementias of cerebrovascular origin may be preventable by treating the risk-factors for stroke. Once significant cognitive impairment has occurred, however, there is no established pharmacological treatment for the vascular dementias to date. Only recently results of placebo-controlled clinical trials have become available showing that cholinergic treatment strategies are effective in vascular dementia and in dementia due to combined vascular and neurodegenerative pathologies.     

Vascular dementia: a diagnostic challenge

Although vascular dementia was described over a century ago, it remains a difficult and challenging diagnosis. Several sets of clinical criteria have been published in an effort to establish the presence or absence of vascular dementia in a standardized fashion. Clinical studies have demonstrated that they identify different groups of patients and are thus not interchangeable. Retrospective clinicopathological correlations have shown that most are insufficiently sensitive, although they are generally relatively specific. They accurately exclude pure Alzheimer's disease but may include 9% to 39% of mixed dementia cases (Alzheimer's disease and vascular dementia combined). Further studies are needed to develop better performing criteria that could lead to a broad consensus on the clinical diagnosis of vascular and mixed dementia.     

Impact of applying NINDS-AIREN criteria of probable vascular dementia to clinical and radiological characteristics of a stroke cohort with dementia

BACKGROUND: There are no data concerning the relative representation of clinical vascular risk factors and radiological lesions in cases that have been ruled in and ruled out for probable vascular dementia (VaD) according to NINDS-AIREN criteria. METHODS: Three months after their index stroke, a psychiatrist interviewed patients and made a diagnosis of VaD according to both DSM-IV and NINDS-AIREN criteria for probable VaD. Patients who fulfilled the DSM-IV criteria for VaD were divided into two groups: those who were ruled in and ruled out according to NINDS-AIREN criteria as probable VaD. Demographic characteristics, vascular risk factors, clinical features of the index stroke and radiological findings were then compared between the two groups. RESULTS: Of the 297 patients screened, 56 (18.8%) had a DSM-IV diagnosis of dementia. Among these demented patients, 55 (98.2%) and 22 (39.3%) fulfilled DSM-IV and NINDS-AIREN diagnosis of VaD, respectively. The concordance and level of agreement (kappa statistic) between DSM-IV and NINDS-AIREN diagnoses were 40% and 0.02, respectively. Reasons of failure to meet NINDS-AIREN criteria included the lack of temporal relationship between dementia and stroke (n = 20), the absence of focal neurological signs and/or radiological evidence of stroke (n = 6) and both of the above (n = 7). There was no significant difference between the above two groups in terms of demographic data, features of index stroke, vascular risk factors and CT scan findings, except that leukoaraiosis (p = 0.021) and bilateral lesions (p = 0.015) were more frequent in subjects diagnosed according to NINDS-AIREN criteria of probable VaD. The difference between these two groups with respect to the number of lesions was borderline for significance (p = 0.052). CONCLUSIONS: The use of NINDS-AIREN criteria for VaD for case selection in poststroke dementia research may exclude a number of subjects with VaD.     

Alzheimer's disease and brain infarcts in the elderly. Agreement with neuropathology

Clarifying the etiology of dementia is one of the most difficult diagnostic challenges, especially in the elderly. We examined the accuracy of clinical criteria to distinguish Alzheimer's disease (AD) and dementia associated with infarcts of the brain, either isolated (vascular dementia) or associated with degenerative lesions (mixed dementia). We carried out a prospective clinico-neuropathological study in a selected series of hospitalized patients. We evaluated the clinical aspects of 33 patients aged over 75 years by use of the criteria and scores of DSMIII, NINCDS-ADRDA, Loeb and Gandolfo, ADDTC and NINDS-AIREN and the Hachinski Ischemic Score. The neuropathological diagnosis was considered to be the gold standard. When comparing clinical criteria and neuropathology, the agreement was moderate for Hachinski's score (0.50) and Loeb's score (0.43) and substantial for the ADDTC (0.63) and the NINDS-AIREN (0.67). When mixed dementias were excluded, the agreement between all clinical criteria and scores and the pathological diagnosis rose to 0.88. Hachinski's score was the most sensitive (0.89) and the NINDS-AIREN the most specific (0.86) for the diagnosis of vascular dementia. In conclusion, all sets of clinical criteria distinguished pure AD from vascular dementia with a high accuracy whereas mixed dementia was clinically under-recognized. The NINDS-AIREN criteria were the most discriminating for the accurate identification of patients with mixed dementia. Received: 17 November 2001, Received in revised form: 14 May 2002, Accepted: 22 May 2002 Correspondence to Pr. Jean-Jacques Hauw     

Diagnosis,risk factors,and treatment of vascular dementia

Although the introduction of modern neuroimaging techniques and standardized clinical evaluations has improved the identification of cerebrovascular disease, the clinical diagnosis of vascular dementia (VaD) is still problematic. Neuropathologic studies have found the current clinical criteria for VaD had low sensitivity with high specificity, suggesting that cerebrovascular disease of sufficient severity to cause cognitive deficits is frequently associated with other disease processes (eg, Alzheimer’s disease). The critical factors about the diagnosis of VaD are centered on two issues: definition of dementia and determination of vascular disease. The current clinical criteria for VaD have different definitions of dementia, which are mainly based on an Alzheimer’s disease-like presentation, and severe vascular disease can present with or without history of clinical strokes. Therefore, there is a need for a better definition of VaD. This is extremely important to better understand its risk factors, as well as to create homogenous cohorts suitable for drug trials.     

Specificity of the clinical diagnosis of dementia.

The specificity of anatomo-clinical observations were investigated on 776 out of 982 consecutive persons hospitalized at the University Psychiatric Clinic of Geneva. Discriminant function analysis shows that most of the anatomical classes (no dementia, senile dementia, Alzheimerized senile dementia and Alzheimer's presenile dementia, vascular dementia, combined dementia nnd undefined form of encephalopathy) are at least partially separable (less than 50% overlap). On the basis of anatomical criteria, Alzheimer's presenile dementia is not separable from Alzheimerized senile dementia, and senile dementia is not separable from combined dementia. Differentiation between the anatomical classes is improved by a preliminary analysis based on clinical diagnosis. Senile plaques account for 43.4% of the total variation between the anatomical classes. The coefficient of agreement between anatomical and clinical diagnosis is 0.27, which is highly significant. The diagnosis of senile dementia has a poor specificity, while the diagnosis of senile Alzheimerized dementia has a better one. The diagnosis of combined dementia has to be reserved for cases with a similar intensity of vascular and degenerative changes. Alzheimer's presenile dementia has a distinct dominant hereditary pattern and must be considered a separate entity. The high specificity of the diagnosis of Alzheimer's presenile dementia makes it possible to conduct epidemiologic and genetic surveys based on clinical data.     

血管性痴呆的可能心理社会危险因素

目的探索血管性痴呆(VD)可能的心理社会危险因素。方法在城市社区中分层整群抽样,10年间完成两次二阶段法调查的55岁及以上人群共5055人。工具为“上海市老年研究访问卷”中有关内容。1987年第一次调查非痴呆4896名老人多方面的心理社会因素资料,以及进行MMSE和ADL量表评定。10后复访,按DSM-Ⅲ-R和Hachinski缺血指数作出痴呆和VD的临床诊断,计算VD年发病率,以Logistic回归法分析VD老人10年前那些心理社会因素对10年后VD疾病发生产生可能的影响。结果10年后访到1206名老年人中有新发痴呆124名,其中VD36名。经统计分析相对危险度(RR),发现VD的心理社会危险因素主要有不参加集体活动、对生活不满意、有不良生活事件和抑郁等4项(RR＞1);此外,ADL总分有较好预测VD的作用。结论心理社会危险因素在VD的发生和发展中可能有一定的影响作用。     

Effect of apolipoprotein E status on clinical features of dementia

Objective. The aims of this study were (a) to determine the frequency of APOE genotypes in dementia, (b) to relate e4 allele frequency to clinical symptomatology of dementia and (c) to relate e4 and assess risk factors for different types of dementia. Design. Prospective clinical study setting older patients with dementia known to a community-based old age psychiatry service. Sample. 101 patients fulfilling ICD 10 criteria for dementia. Results. Replication of previous findings of an association between APOE4 and Alzheimer's disease: younger age of onset of dementia; family history of dementia; persecutory ideation; and (retrospectively determined) rate of competent decline. No association was found between APOE4 and vascular dementia. The association between APOE4 and ‘mixed dementia’ was intermediate between that of pure Alzheimer's disease and pure vascular dementia. Conclusion. The results confirm the relationship between clinical features of dementia and APOE4 status. It may be that APOE can be used as an adjunct to clinical diagnosis. © 1998 John Wiley & Sons, Ltd.