Harrison P J
University Department of Psychiatry, Warneford Hospital, Oxford.
Neurodegeneration. 1995 Mar;4(1):1-12. doi: 10.1006/neur.1995.0001.
The neuropathology of schizophrenia has begun to emerge following renewed investigation in the past 20 years. However, there remain inconsistencies in the data and their interpretation. In particular, although the brains of schizophrenics have been reported to show an excess of neurodegenerative changes, especially astrocytic gliosis and Alzheimer's disease, it is unclear whether these features are an intrinsic part of the neuropathology of schizophrenia. Nor is it apparent how they relate to the symptoms of dementia which afflict a proportion of schizophrenics. This review focuses upon these questions. Two main conclusions are drawn. Firstly, the neuropathological features of schizophrenia together support a neurodevelopmental pathogenesis wherein the aforementioned degenerative changes are either epiphenomenal, artefactual, or are limited to a subgroup of cases which are otherwise indistinguishable clinically or pathologically. Secondly, the dementia of schizophrenia is not attributable to Alzheimer's disease nor to any other recognized neuropathological substrate.
在过去20年重新开展的研究之后，精神分裂症的神经病理学已开始显现。然而，数据及其解释仍存在不一致之处。特别是，尽管有报道称精神分裂症患者的大脑显示出过多的神经退行性变化，尤其是星形细胞胶质增生和阿尔茨海默病，但尚不清楚这些特征是否是精神分裂症神经病理学的固有组成部分。也不清楚它们与折磨一部分精神分裂症患者的痴呆症状有何关联。本综述聚焦于这些问题。得出了两个主要结论。首先，精神分裂症的神经病理学特征共同支持一种神经发育发病机制，其中上述退行性变化要么是附带现象、人为现象，要么仅限于在临床或病理上无法区分的病例亚组。其次，精神分裂症所致的痴呆既不归因于阿尔茨海默病，也不归因于任何其他公认的神经病理学基质。
