Erkinjuntti T, Bowler J V, DeCarli C S, Fazekas F, Inzitari D, O'Brien J T, Pantoni L, Rockwood K, Scheltens P, Wahlund L O, Desmond D W
Department of Clinical Neurosciences, Helsinki University Central Hospital, Finland.
Alzheimer Dis Assoc Disord. 1999 Oct-Dec;13 Suppl 3:S81-90.
Vascular dementia (VaD) relates to different vascular mechanisms and changes in the brain and has different causes and clinical manifestations, reflecting complex interactions between vascular etiologies, changes in the brain, host factors, and cognition. Critical elements to the concept and diagnosis of VaD are defining the vascular causes, the vascular etiologies, and changes in the brain. Verifying the relation between brain lesions and cognition (i.e., the extent to which brain changes cause, compound, or coexist with cognitive impairment) and establishing the types, extent, side, site, and tempo of brain lesions that relate to incident cognitive impairment are major diagnostic challenges. Previous work on interactions between brain lesion and cognition in to cerebrovascular disease (CVD) have shown variation in the definitions and measures of cognitive impairment, in the techniques and methods used to reveal different brain changes, and in the selection of patient populations. Furthermore, small sample sizes and the absence of multivariate statistics have been design limitations. Accordingly, the different sets of criteria used and methods applied identify different numbers and clusters of subjects and different distribution of brain changes. Furthermore, this heterogeneity is reflected in variation in natural history such as the rate of progression of decline in different cognitive domains over time. All these factors have hampered optimal designs of clinical drug trials. A summary of generalizations regarding lesion and cognition interaction in VaD can be made. (1) Not a single feature, but a combination of infarct features--extent and type of white matter lesions (WMLs), degree and site of atrophy, and host factor characteristics--constitues correlates of VaD. (2) Infarct features favoring VaD include bilaterality, multiplicity (>1), location in the dominant hemisphere, and location in the limbic structures (fronto- and mediolimbic). (3) WML features favoring VaD are extensive WMLs (extensive periventricular WMLs and confluent to extensive WMLs in the deep WM). (4) It is doubtful that only a single small lesion could provide imaging evidence for a diagnosis of VaD. (5) Absence of CVD lesions on computed tomography or magnetic resonance imaging is strong evidence against a diagnosis of VaD. In forthcoming protocols on CVD-associated cognitive impairment, the following brain imaging features should be specified: detailed characterization of brain changes; use of possible predefined subtypes based on brain imaging; use of rating of vascular burden; defining the type and extent of WMLs favoring a diagnosis of VaD; defining the extent of medial temporal lobe atrophy disfavoring a diagnosis of VaD; and technical harmonization of methods of scanning and analysis.
血管性痴呆（VaD）与不同的血管机制及脑部变化相关，具有不同的病因和临床表现，反映了血管病因、脑部变化、宿主因素和认知之间复杂的相互作用。VaD概念和诊断的关键要素是明确血管病因、血管病变以及脑部变化。验证脑部病变与认知之间的关系（即脑部变化导致、加重或与认知障碍共存的程度），并确定与新发认知障碍相关的脑部病变的类型、范围、侧别、部位和发展速度，是主要的诊断挑战。先前关于脑血管疾病（CVD）中脑病变与认知相互作用的研究表明，在认知障碍的定义和测量、用于揭示不同脑部变化的技术和方法以及患者人群的选择方面存在差异。此外，样本量小和缺乏多变量统计一直是设计上的局限。因此，所使用的不同标准集和应用的方法识别出不同数量和组群的受试者以及不同的脑部变化分布。此外，这种异质性反映在自然病程的变化中，例如不同认知领域随时间下降的进展速度。所有这些因素都阻碍了临床药物试验的优化设计。可以对VaD中病变与认知相互作用的一般情况进行总结。（1）构成VaD相关因素的不是单一特征，而是梗死特征的组合——白质病变（WMLs）的范围和类型、萎缩的程度和部位以及宿主因素特征。（2）有利于VaD的梗死特征包括双侧性、多发性（>1个）、位于优势半球以及位于边缘结构（额叶和内侧边缘叶）。（3）有利于VaD的WML特征是广泛的WMLs（广泛的脑室周围WMLs以及深部白质中融合至广泛的WMLs）。（4）仅一个小病变就能为VaD诊断提供影像学证据，这一点值得怀疑。（5）计算机断层扫描或磁共振成像上无CVD病变是反对VaD诊断的有力证据。在即将出台的关于CVD相关认知障碍的方案中，应明确以下脑成像特征：脑部变化的详细特征描述；基于脑成像使用可能的预定义亚型；血管负担评分的使用；定义有利于VaD诊断的WMLs的类型和范围；定义不利于VaD诊断的内侧颞叶萎缩的范围；以及扫描和分析方法的技术协调。
