Jellinger K
Acta Neurol Belg. 1976 Mar-Apr;76(2):83-102.
In a large autopsy series of elderly individuals, organic dementia was attributed to (pre-) senile atrophy in 52.8%, to cerebrovascular disease in 22.5%, while 13.6% were of mixed senile and vascular origin, and 1.3% showed communicating hydrocephalus with meningopathies or were of undetermined origin. A survey is given of the morphological criteria of dementia resulting from disorders of cerebral blood supply and CSF circulation. The anatomic basis of vascular dementias are: atherosclerotic encephalopathy with lacunar state or multiple infarcts; granular cortical atrophy resulting from local microcirculation disorders; hypertensive cerebrovascular disease with the common "mixed" cortico-subcortical type, and the rare Binswanger's subcortical type. Atypical cerebral hemorrhage in old individuals rather results from congophilic (amyloid) angiopathy than from hypertensive arteriosclerosis. Multiple infarct dementia may also result from thrombotic microangiopathy, thromboembolic disease or cerebral vasculitides. The anatomical features of dementia associated with communicating "normal-pressure" hydrocephalus (NPH) are meningopathy at the basis or on the convexity, and fibrosis of the choroid plexus and/or arachnoid villi of post-inflammatory or undetermined origin, and other non-specific changes (periventricular gliosis). This condition is also associated with hypertensive cerebrovascular disease and Alzheimer's disease. Cerebral biopsies in NPH as well as in other types of hydrocephalus show enlarged extracellular spaces with otherwise normal neuropil probably resulting from increased transcapillary filtration. In some cases of "idiopathic" NPH no causative anatomical changes are found. The relationship between cerebral tissue changes, abnormal blood and CSF dynamics in these conditions remains to be clarified.
在一项针对老年个体的大型尸检系列研究中,52.8%的器质性痴呆归因于(早)老年性萎缩,22.5%归因于脑血管疾病,13.6%为老年性和血管性混合起源,1.3%表现为交通性脑积水合并脑膜病变或病因不明。本文综述了由脑供血和脑脊液循环障碍导致痴呆的形态学标准。血管性痴呆的解剖学基础包括:伴有腔隙状态或多发性梗死的动脉粥样硬化性脑病;局部微循环障碍导致的颗粒性皮质萎缩;常见的“混合性”皮质 - 皮质下型高血压性脑血管病以及罕见的宾斯旺格皮质下型。老年人的非典型脑出血更多是由嗜刚果红(淀粉样)血管病引起,而非高血压动脉硬化。多发性梗死性痴呆也可能由血栓性微血管病、血栓栓塞性疾病或脑血管炎导致。与交通性“正常压力”脑积水(NPH)相关的痴呆的解剖学特征包括基底或脑凸面的脑膜病变,以及炎症后或病因不明的脉络丛和/或蛛网膜绒毛纤维化,还有其他非特异性改变(脑室周围胶质增生)。这种情况还与高血压性脑血管病和阿尔茨海默病相关。NPH以及其他类型脑积水的脑活检显示细胞外间隙扩大,神经纤维网其他方面正常,这可能是由于跨毛细血管滤过增加所致。在一些“特发性”NPH病例中未发现有因果关系的解剖学改变。这些情况下脑组织变化、异常血液和脑脊液动力学之间的关系仍有待阐明。