Menon Uma, Kelley Roger E
Department of Neurology, LSU Health Sciences Center, Shreveport, Louisiana 71103, USA.
Int Rev Neurobiol. 2009;84:21-33. doi: 10.1016/S0074-7742(09)00402-4.
It has become increasingly apparent, especially with the advent of MRI brain scanning, that a large number of patients develop signal intensity changes in the subcortical white matter and periventricular region as they age. This appears to be accelerated by risk factors for small vessel cerebrovascular disease such as hypertension, smoking, diabetes mellitus and hyperlipidemia. The major question becomes when such changes become clinically significant. It is obvious that subcortical lacunar-type infarction can be identified by the clinical presentation. For example, typical examples of so-called "lacunar syndrome" include pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, clumsy hand-dysarthria, and hemiataxia-hemiparesis. The issue becomes a measure of impact on functional ability. This is influenced by several factors. Baseline IQ and educational level, as well as expectations of age, certainly play a role. A person who develops cognitive impairment and long tract signs in their 50s or 60s is certainly going to be recognized as more impaired than an 80 year old individual who is retired and primarily is engaged in recreational activity. It would be expected that a person born with limited intellectual capacity and/or limited educational opportunity would be less likely to be identified as impaired than a person who has achieved substantial economic achievement through their innate talents. The concept of tissue loss or lesion load becomes important when determining how pronounced the ischemic cerebrovascular changes translate into functional impairment. Correlative pathology may include cortical atrophy and ventricular dilatation. Loss of either cortical or subcortical tissue function is expected to be related to functional compromise. In addition, there are potential features such as the coexistence of small vessel cerebrovascular disease and Alzheimer's disease. Small vessel cerebrovascular disease might also play a contributing factor in patients susceptible to Dementia with Lewy Bodies or patients susceptible to fronto-temporal dementia or any other dementing process. Thus, the concept of tissue loss or lesion burden of disease becomes increasingly important as we recognize the potential for multifactorial issues, including genetic factors, to contribute to the phenotypic expression. The relationships between cognitive impairment, dementia and subcortical vascular lesions are poorly understood. There have been several papers on the different aspects of cerebral insults and their impact on cognition, the various kinds of dementia and different methods of analyzing the impact of the various insults to the brain. This chapter is an attempt to review all pertinent information currently available on the poorly understood condition of "subcortical ischemic cerebrovascular dementia."
越来越明显的是,尤其是随着脑部磁共振成像扫描技术的出现,大量患者随着年龄增长,其皮质下白质和脑室周围区域会出现信号强度变化。诸如高血压、吸烟、糖尿病和高脂血症等小血管脑血管疾病的危险因素似乎会加速这种变化。主要问题变成了这种变化何时具有临床意义。显然,皮质下腔隙性梗死可以通过临床表现来识别。例如,所谓“腔隙综合征”的典型例子包括纯运动性偏瘫、纯感觉性卒中、感觉运动性卒中、笨拙手-构音障碍以及偏身共济失调-偏瘫。问题变成了对功能能力影响程度的衡量。这受到几个因素的影响。基线智商和教育水平,以及年龄预期,当然都起到一定作用。一个在五六十岁时出现认知障碍和长束征的人,肯定会比一个八十岁已退休且主要从事娱乐活动的人被认为受损程度更高。可以预期,一个天生智力有限和/或教育机会有限的人,比一个凭借自身天赋取得巨大经济成就的人,被认定为受损的可能性更小。在确定缺血性脑血管变化在多大程度上转化为功能损害时,组织损失或病变负荷的概念变得很重要。相关病理学表现可能包括皮质萎缩和脑室扩大。皮质或皮质下组织功能的丧失预计与功能受损有关。此外,还存在一些潜在特征,如小血管脑血管疾病与阿尔茨海默病并存。小血管脑血管疾病在易患路易体痴呆的患者或易患额颞叶痴呆或任何其他痴呆过程的患者中,也可能起到促成因素的作用。因此,随着我们认识到包括遗传因素在内的多因素问题导致表型表达的可能性,疾病的组织损失或病变负担的概念变得越来越重要。认知障碍、痴呆与皮质下血管病变之间的关系目前还知之甚少。已经有几篇关于脑损伤的不同方面及其对认知的影响、各种类型的痴呆以及分析各种脑损伤影响的不同方法的论文。本章试图回顾目前所有关于人们了解甚少的“皮质下缺血性脑血管性痴呆”状况的相关信息。