Uitti R J, Calne D B
University of British Columbia, Neurodegenerative Disorders Centre, Vancouver, Canada.
Eur Neurol. 1993;33 Suppl 1:6-23. doi: 10.1159/000118533.
Idiopathic parkinsonism (Parkinson's disease) makes up the largest diagnostic subgroup of patients with parkinsonism. Various hypotheses exist regarding the pathogenesis of idiopathic parkinsonism: these include genetic predilection aging, environmental factors, oxidative stress, excitotoxicity, autoimmunity, and trauma. We suggest that the pathogenesis of idiopathic parkinsonism is likely to be multifactorial, deriving from environmental factor(s) acting upon a genetically predisposed individual. Because of the compelling evidence indicating common clinical and pathological findings in idiopathic parkinsonism, Alzheimer's disease, and amyotrophic lateral sclerosis, we believe that these conditions result from pathological processes with more similarity than diversity. A primary glutamatergic cell neocortical abnormality provides an attractive unifying explanation which may explain the overlapping abnormalities found in idiopathic parkinsonism, Alzheimer's disease, and amyotrophic lateral sclerosis.
特发性帕金森症（帕金森病）是帕金森症患者中最大的诊断亚组。关于特发性帕金森症的发病机制存在多种假说：这些包括遗传易感性、衰老、环境因素、氧化应激、兴奋性毒性、自身免疫和创伤。我们认为特发性帕金森症的发病机制可能是多因素的，源于作用于具有遗传易感性个体的环境因素。由于有令人信服的证据表明特发性帕金森症、阿尔茨海默病和肌萎缩侧索硬化症存在共同的临床和病理表现，我们相信这些病症是由相似而非不同的病理过程导致的。原发性谷氨酸能细胞新皮质异常提供了一个有吸引力的统一解释，这可能解释了在特发性帕金森症、阿尔茨海默病和肌萎缩侧索硬化症中发现的重叠异常。
