Diehl Janine, Kurz A
Klinik für Psychiatrie und Psychotherapie, Technische Universität München, Germany.
Fortschr Neurol Psychiatr. 2002 Mar;70(3):145-54. doi: 10.1055/s-2002-20502.
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.
脑血管疾病是老年期仅次于阿尔茨海默病的第二常见痴呆病因。最近一项基于社区的尸检研究表明，相关脑血管变化在70岁及以上人群中比之前认为的更为普遍。此外，脑血管病变与阿尔茨海默型病理的结合是老年痴呆患者最常见的神经病理学发现。关于哪种类型的脑血管变化最有可能导致包括痴呆在内的认知障碍以及涉及哪些致病机制，仍存在一些不确定性。然而，毫无疑问，血管性痴呆在病因、组织病理学和临床表现方面是一组异质性疾病。根据优先受累的血管口径和灌注区域，通常将常见的皮质下小血管疾病与罕见的皮质大血管疾病区分开来。与这些形态学亚型相关的有三种主要临床变体：由皮质下腔隙和白质变化导致的痴呆，包括宾斯旺格病、多发梗死性痴呆以及由单个关键梗死导致的痴呆。在大多数脑血管性痴呆病例中，智力损害模式为额叶或皮质下型，这与阿尔茨海默病典型的皮质型表现形成对比。执行功能和注意力的恶化以及人格改变，而非记忆丧失，是主要症状。因此，目前的痴呆诊断标准不太适合检测血管性痴呆。专门为诊断血管性痴呆而提出的标准中，没有一个能为评估脑血管病变与精神病理学发现之间的因果关系提供明确指导。进一步的研究将揭示，考虑到脑血管疾病的异质性是否能改善临床诊断。通过治疗中风的危险因素，很大一部分脑血管性痴呆可能是可预防的。然而，一旦出现严重认知障碍，迄今为止尚无针对血管性痴呆的确立的药物治疗方法。直到最近，安慰剂对照临床试验的结果才表明，胆碱能治疗策略对血管性痴呆以及由血管和神经退行性病变共同导致的痴呆有效。
