Wolters E C
Graduate School of Neurosciences, Department of Neurology, University of Amsterdam, Netherlands.
J Neural Transm Suppl. 2000(60):291-302. doi: 10.1007/978-3-7091-6301-6_20.
Parkinson's disease (PD) is caused by an abnormal degeneration of the dopamine (DA) producing cells in the substantia nigra (SN) and ventral tegmentum area (VTA) in combination with a varying decay of the noradrenergic (locus coeruleus), cholinergic forebrain (nucleus basalis of Meynert) and serotoninergic (dorsal raphe nuclei) systems, leading to a multitude of motor and non-motor behavioral disturbances, known as parkinsonism. Normally, main dopamine depletion is restricted to the SN region with manifest (non)motor behavioral abnormalities caused by the inability to spontaneously switch between intern-cued cortical behavioral programmes. Clinical symptoms comprise motoric abnormalities, though subtle cognitive disturbances as well as psychological dysfunction with loss of mental flexibility and reactive depressive symptoms might be seen. These symptoms might be compensated in part by externally-cued behavior.
帕金森病（PD）是由黑质（SN）和腹侧被盖区（VTA）中产生多巴胺（DA）的细胞异常退化，以及去甲肾上腺素能（蓝斑）、胆碱能前脑（Meynert基底核）和5-羟色胺能（中缝背核）系统不同程度的衰退引起的，导致多种运动和非运动行为障碍，即帕金森综合征。通常，主要的多巴胺耗竭局限于SN区域，由于无法在内部提示的皮层行为程序之间自发切换而导致明显的（非）运动行为异常。临床症状包括运动异常，不过也可能出现细微的认知障碍以及心理功能障碍，如思维灵活性丧失和反应性抑郁症状。这些症状可能会通过外部提示行为得到部分代偿。
