Neuropathological diagnosis of Alzheimer disease.
Neuropathological diagnosis of Alzheimer disease.
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DOI：
10.1097/00005072-199009000-00010
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发表时间：
1990-09
影响因子：
3.2
通讯作者：
R. Lindenberg
中科院分区：
文献类型：
--
作者：
R. Lindenberg
The authors of the Editorial on the Neuropathological Diagnosis of Alzheimer Disease missed an important diagnostic key: the gross pathology of Alzheimer's disease (AD)(1). As I stated in 1982 (2), senile dementia of the Alzheimer type (SDAT) and presenile dementia (PDAT or simply AD) are grossly two independent entities in spite of similar histologic features. Each has its own pattern of convolu-tional atrophy, which is as repetitive as the striatum atrophy in Huntington's disease and is, therefore, diagnostically significant. Both entities are system degenerations. In SDAT, structures of the limbic system are affected. In PDAT the cortical association areas, starting with the parieto-occipital and spreading to the temporal and frontal fields are the affected sites. Ball et al (3) proposed defining SDAT as hip-pocampal dementia; I prefer the name limbic Alzheimer dementia. In my 261 cases with this pattern, atrophy always included the amygdaloid complexes, structures of the basal forebrain, the parahippocampal gyri and, sometimes, the limen insulae and temporal poles. Ultimately, the fornices atrophy and the mamillary bodies shrivel as much as they do in Wernicke's encephalopathy (Fig. 1a). If there is shrink-age of the convolutions over the convexity it is moderate and mainly caused by secondary loss of white matter. In PDAT, long known to be as rare as Pick's disease (4), the loss of both cortex and white matter produce the atrophy. It is most striking, when shown side by side with an identical area from a case of limbic AD (Fig. 1b), Additional features of lDAT are: 1. gyri of the cunei and the adjacent posterior one fourth of the cingulate gyri are atrophic, something I have never seen in SDAT or Pick's disease; 2. relative preservation of primary somatosensory, visual and acustic cortex; see illustrations in reference 2. Early signs and symptoms of the two entities correspond to their topical features. It is my clinical experience that limbic AD starts with a failure ofattention power, an inability to deposit new memories and repetitious conversation. Characteristically, the patient is not aware of it and does not worry, The old contents of the patient's memory bank keep the mind busy for quite some time and when memories fade, simple reading and writing are still possible for awhile. In contrast, PDAT does not start with loss of attention; its first signs are agnosias (visual for persons, objects, numbers, letters and tactile) pointing to the parietooccipital lobes. Characteristically, the patient is aware of the breakdown of the intellectual functions and of the depletion of the memory bank and may become frentic, depressed and even suicidal. Since loss of cortical associations are clinical as well as pathological hallmarks of this entity, the term associative Alzheimer dementia appears appropriate, particularly since presenile dementia may commence in the senium and semile dementia in the presenium. Loss of neurons is the cause of the gross atrophy in both entities. Senile plaques which are due to dysoria at sites of transient or permanent blockage of capillaries by blobs of plasma (2), are less instrumental. Why in some cases the limbic and in others the associate system degenerates has never been debated. Perhaps, ongoing genetic research may suggest an answer, The gross findings are certainly of practical value for radiological imaging,
