Bousser M G
Encephale. 1977;3(4):357-72.
The incidence of both atherosclerosis and demential increases with age and therefore the terms "cerebral atherosclerosis" or "cerebro-vascular dementia" are commonly used for any mental deterioration in elderly persons. These names depend on the proposition of a gradual narrowing of cerebral arteries as an inevitable accompaniement of ageing which ends in dementia through a progressive reduction of cerebral blood flow. This apparently reasonnable hypothesis has now been shown to be wrong. ;t has been established that first, senile dementia is not due to cerebral atherosclerosis in spite of the frequent coexistence of degenerative and vascular lesions; and secondly, true cerebro vascular dementia results from the destruction of brain tissue following cerebral infarction; hence the proper term is "multi-infarct dementia". This neuronal destruction leads to decrease in cerebral metabolism and blood flow and to intellectual deterioration. The diagnostic criteria are therefore those of cerebral infarcts i.e: arterial hypertension and/or signs of atherosclerosis, sudden onset and/or stepwise progression, and focal neurological signs. If one follow those criteria, multi-infarct dementia accounts for only about 10% of all dementias; if one does not, the diagnosis will continue to be made to the exclusion of other potentially curable causes of dementias. Five clinico-pathological forms can be distinguished according to the size, number and site of the infarcts: lacunar state, large multiple infarcts, watershed infarction, single infarct and Binswanger's encephalopathy. This distinction is always arbitrary because the association of lacunes and large infarcts is very common in multi-infarct dementia. The almost invariable failure of all therapeutic measures once multi-infarct dementia has been established stresses the importance of prevention. This depends on prevention of cerebral infarcts, i.e. on the correction of risk factors amongst which arterial hypertension is by far, the most important. Some cases benefit also from carotid surgery, anticoagulants, and antiplatelet drugs but antihypertensive drugs are the most essential part. It is very likely that if all cases of arterial hypertension are properly treated, the incidence of multi-infarct dementia will decrease greatly.
动脉粥样硬化和痴呆的发病率均随年龄增长而增加,因此“脑动脉粥样硬化”或“脑血管性痴呆”这两个术语通常用于描述老年人的任何精神衰退。这些名称基于这样一种观点,即脑动脉逐渐变窄是衰老不可避免的伴随现象,最终会因脑血流量逐渐减少而导致痴呆。现在已经证明这个看似合理的假设是错误的。已经确定,首先,尽管退行性病变和血管病变经常同时存在,但老年痴呆并非由脑动脉粥样硬化引起;其次,真正的脑血管性痴呆是由脑梗塞后脑组织破坏所致;因此,恰当的术语是“多发性梗塞性痴呆”。这种神经元破坏会导致脑代谢和血流量减少,进而导致智力衰退。因此,诊断标准是脑梗塞的标准,即:动脉高血压和/或动脉粥样硬化体征、突然发病和/或逐步进展以及局灶性神经体征。如果遵循这些标准,多发性梗塞性痴呆仅占所有痴呆病例的约10%;如果不遵循,就会继续做出该诊断,而排除其他可能可治愈的痴呆病因。根据梗塞的大小、数量和部位,可以区分出五种临床病理形式:腔隙状态、多发性大面积梗塞、分水岭梗塞、单个梗塞和宾斯旺格脑病。这种区分总是人为的,因为在多发性梗塞性痴呆中,腔隙和大面积梗塞同时存在的情况非常常见。一旦确诊为多发性梗塞性痴呆,几乎所有治疗措施都几乎无一例外地失败,这凸显了预防的重要性。这取决于预防脑梗塞,即纠正危险因素,其中动脉高血压是迄今为止最重要的因素。一些病例也受益于颈动脉手术、抗凝剂和抗血小板药物,但抗高血压药物是最重要的部分。很有可能,如果所有动脉高血压病例都得到妥善治疗,多发性梗塞性痴呆的发病率将大幅下降。