无痴呆型血管性认知功能障碍的诊断和治疗进展

血管因素是独立于年龄的导致痴呆的第二大危险因素.在血管性认知损害(VCI)早期即无痴呆型血管性认知功能障碍(VCIND)甚至认知损害发生之前,血管性因素以及脑血管病是唯一可治疗的,并且能够延缓甚至逆转痴呆进展的干预靶点.因此早期诊断出VCIND的病例,治疗血管性因素及脑血管病,有利于VCI的一级预防和二级预防.现对VCIND的诊断、预防和治疗的进展作一综述.     

血管性痴呆的临床分析

<正> 血管性痴呆系由于脑血管病引起的痴呆。近年来随着脑血管病发病率的升高,血管性痴呆患者也日益增多。脑血管病的种类,病变部位,再发次数与痴呆密切相关。本文对68例血管性痴呆患者进行了以上三方面的临床分析。     

补肾活血化痰法对血管性痴呆病人智能影响

随着脑血管病患者的增加,血管性痴呆成为威胁老年人健康的严重疾病之一.我们选用补肾活血化痰法对血管性痴呆(VD)患者智能影响进行临床观察,现报道如下.     

血管性认知功能障碍

血管性痴呆(vascular dementia,VD)是指各类脑血管病所致的痴呆综合征,但目前越来越认识到不明显的脑血管病如皮质下白质缺血、小血管疾病和腔隙性梗死也能引起痴呆或认知损害,甚至脑血管病危险因素如高血压和糖尿病等也可引起认知损害进而发生痴呆。     

25例血管性痴呆临床分析

随着人口老龄化脑血管病发病率不断提高,血管性痴呆(VD)发病率也逐渐增加,目前对VD治疗无突破性进展。血管性痴呆一半左右是由血管性认知障碍(VCI)发展过来,早期识别认知功能损害,进行有效的干预,可延缓或预防血管性痴呆的发生。现将我科近5年来收治VD患者的诊疗情况分析如下。     

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>.     

血管性痴呆

血管性痴呆是一常见而某些功能障碍又是可逆的一类疾病。需要一简单而又确实有根据之工具来确诊和随诊血管性痴呆。我们检查了63例已知的缺血性脑血管病患者,发现13例符合血管性痴呆,19例可疑,31例没有痴呆。主要用筛选痴呆病人认识能力30题(CCSR)和社会功能活动调查试验(FAQ),发现此两试验对患者有无痴呆都能鉴别,而且有高度的敏感性和特异性。此两项试验在门诊随诊中都简而易行,容易掌握。     

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。     

血管性痴呆患者脑脊液微量元素的变化

目的探讨血管性痴呆患者脑脊液微量元素铁、铜、锌、铬的变化。方法采用原子分光光度计直接测定６４例血管性痴呆患者脑脊液中上述４种微量元素的含量并与脑血管病无痴呆组及对照组进行比较。结果铁含量在脑血管病时有明显升高。铜在脑血管病时升高不明显,痴呆时明显升高。锌在脑血管病时下降,痴呆时反而上升。铬在３组无差别。结论这些微量元素的改变可作为血管性痴呆的诊断及预后判断的指标     

卡巴拉汀治疗血管性认知障碍的研究现状

血管性认知障碍(vascualr cognitive impairment,VCI)是指由脑血管病危险因素(如高血压病、糖尿病和高脂血症等)、显性(如脑梗死和脑出血等)或非显性脑血管病(如白质疏松和慢性脑缺血)引起的从轻度认知损害到痴呆的一大类综合征[1].该病包括了血管性的认知功能障碍从轻到重的完整的发病病程,依据严重程度可分为非痴呆性血管性认知障碍(vascular cognitive impairment not dementia,VCIND)和血管性痴呆(vascular dementia,VaD)[2].根据国际阿尔茨海默病协会2018年公布的数据[3],全球有5000万人罹患痴呆症,其中VCI占所有痴呆类型的20%~30%,为仅次于阿尔茨海默病(Alzheimer's disease,AD)的第二常见的痴呆类型,给家庭和社会造成较大的经济压力.然而VCI具有可防可治性,因此逐渐成为人们研究热点之一.目前推荐用于治疗VaD的药物有胆碱酯酶抑制剂(主要有多奈哌齐、加兰他敏、卡巴拉汀、石杉碱甲)、美金刚、银杏叶制剂、奥拉西坦等,但部分药物疗效尚存争议[1].     

从血管性痴呆到血管性认知功能损害

本文通过回顾血管性痴呆的提出及争议，引出血管性认知功能损害提出的背景及其必要性，阐述了其诊断标准目前存在的问题及新近的研究进展，旨在通过比较血管性痴呆到血管性认知功能损害定义的演变说明血管性认知功能损害这一定义的重要性，指出寻找血管性认知功能损害特异性的神经心理学表现、影像学特点、生物学标记以及病理学特点将是今后。     

Neuropathology of vascular cognitive impairment and vascular dementia

Understanding of vascular substrates of cognitive decline in the elderly is evolving to include a major emphasis on the impact of small vessel disease (SVD). While existing concepts of multi-infarct dementia and strategic infarct dementia remain valid, they present difficulty in generalizing clinicopathological correlations from patient to patient. The range and significance of lesions that should be included as manifestations of SVD are unresolved, as is their impact on, and association with, neurodegenerative changes. This mini-review summarizes the authors' views on SVD substrates leading to cognitive decline and proposes priorities for pathological investigations of human cerebrovascular mechanisms leading to cognitive decline.     

Behavioral symptoms in vascular cognitive impairment and vascular dementia

Noncognitive or behavioral and psychological symptoms (BPSD) are common in vascular dementia. Many occur with the same frequency as in Alzheimer's disease, though depression, emotional lability, and apathy may be more common and psychosis less so. There is a particularly strong relationship between cerebrovascular disease and depression.     

The enigma of vascular cognitive disorder and vascular dementia

The prevalence, morphology and pathogenesis of vascular dementia (VaD), recently termed vascular cognitive impairment, are a matter of discussion, and currently used clinical diagnostic criteria show moderate sensitivity (average 50%) and variable specificity (range 64–98%). In Western clinic-based series, VaD is suggested in 8–10% of cognitively impaired aged subjects. Its prevalence in autopsy series varies from 0.03 to 58%, with reasonable values of 8–15%, while in Japan it is seen in 22–35%. Neuropathologic changes associated with cognitive impairment include multifocal and/or diffuse disease and focal lesions: multi-infarct encephalopathy, white matter lesions or arteriosclerotic subcortical (leuko)encephalopathy, multilacunar state, mixed cortico-subcortical type, borderline/watershed lesions, rare granular cortical atrophy, post-ischemic encephalopathy and hippocampal sclerosis. They result from systemic, cardiac and local large or small vessel disease. Recent data indicate that cognitive decline is commonly associated with widespread small ischemic/vascular lesions (microinfarcts, lacunes) throughout the brain with predominant involvement of subcortical and functionally important brain areas. Their pathogenesis is multifactorial, and their pathophysiology affects neuronal networks involved in cognition, memory, behavior and executive functioning. Vascular lesions often coexist with Alzheimer disease (AD) and other pathologies. Minor cerebrovascular lesions, except for severe amyloid angiopathy, appear not essential for cognitive decline in full-blown AD, while both mild Alzheimer pathology and small vessel disease may interact synergistically. The lesion pattern of “pure” VaD, related to arteriosclerosis and microangiopathies, differs from that in mixed-type dementia (AD with vascular encephalopathy), more often showing large infarcts, which suggests different pathogenesis of both types of lesions. Due to the high variability of cerebrovascular pathology and its causative factors, no validated neuropathologic criteria for VaD are available, and a large variability across laboratories still exists in the procedures for morphologic examination and histology techniques. After a lecture at the XI International Congress of Neuropathology, San Francisco, CA, on 11 September 2006. Addendum In a recent clinicopathological evaluation of 79 autopsy cases derived from a prospective longitudinal study of subcortical ischemic vascular disease (SIVD) and Alzheimer disease (AD), Chui et al. [555] found significant cerebrovascular lesions (CVL) in 30%, AD pathology in 54%, and hippocampal sclerosis (HS) in 18%. Statistical assessment showed that all three pathology variables contributed independently to cognitive status, but only the neuritic Braak scores contributed significantly to cognitive impairment, indicating that advancing AD pathology overwhelms the effects of the two other factors that, in the absence of considerable AD, contribute to mild cognitive impairment. A recent histologic-neuroimaging study in two patients with SIVD showed correspondence between subinsular T2 hyperintensive lesions and demyelination, gliosis, and dilated perivascular spaces [556].     

Subcortical vascular dementia

Vascular dementia (VaD) incorporates different vascular mechanisms and changes in the brain, and has different causes and clinical manifestations. Current criteria for VaD select an aetiologically and clinically heterogeneous group and this definitional heterogeneity has affected clinical trial results. Focus on a more homogeneous group, such as that with subcortical (ischaemic) VaD, could be an alternative in clinical drug trials. This subtype incorporates two small vessel clinical entities - 'Binswanger's disease' and 'the lacunar state'. It comprises small vessel disease as the primary vascular aetiology, lacunar infarct(s) and ischaemic white matter lesions as the primary type of brain lesions, subcortical location as the primary location of lesions, and the subcortical clinical syndrome as the primary clinical manifestation. Subcortical VaD is expected to show a more predictable clinical picture, natural history, outcome and treatment responses.