Bodis-Wollner Ivan
Downstate Medical Centre, State University of New York, Kings County Hospital Center and SUNY, 450 Clarkson Avenue, Box 1213 Brooklyn, NY 11203, USA.
Parkinsonism Relat Disord. 2003 Aug;9 Suppl 2:S83-9. doi: 10.1016/s1353-8020(03)00022-1.
Neuropsychiatric, perceptual and cognitive deficits are increasingly recognized as non-motor manifestations of Parkinson's Disease (PD).The premorbid personality profile of PD patients is characterized by a number of traits which figure prominently after the disease becomes manifest. In particular, less novelty seeking is one premorbid trait providing an understanding of later cognitive deficits. Anxiety and depression have been shown to precede in some patients motor manifestations and cannot be attributed to anti-parkinsonian therapy. Some neuropsychiatric manifestations and in particular hallucinosis are linked to select perceptual and cognitive changes. Cognitive deficits are common in PD, in particular in younger onset patients. Current animal studies link genetic differences in the dopamine transporter and dopamine catabolic enzyme system to select cognitive impairments attributed to frontal lobe dysfunction.Visuo-cognitive impairment is prevalent in PD. Retinal dopaminergic deficiency has been shown in patients and in the animal model of PD. Visuo-spatial deficits, however, are not simply passive reflections of retinal deficiency. In addition to vision, saccadic eye movements are affected in PD whether they contribute to visuo-spatial dysfunction is unknown. However, recent functional Magnetic Resonance Imaging (fMRI) and electroencephalogram (EEG) studies show an essential role of the occipital cortex in saccadic eye movements and positron emission tomography (PET) studies show occipital hypometabolism in PD. Visual and eye movement studies suggest that certain neuropsychiatric and cognitive deficits in PD are linked to the visual system. Synchrony of signals are essential for the co-operation of distributed neuronal network engaged in sensory-motor coordination. Local, dopaminergic neuronal groups in the retina, basal ganglia and frontal cortical memory system are affected in PD. These connections may not primarily rely on dopamine as a neurotransmitter. It is suggested that to understand visuocognitive changes we should consider pathology affecting neuronal connections, necessary for binding parallel distributed networks.
神经精神、感知和认知缺陷日益被视为帕金森病（PD）的非运动表现。PD患者病前的人格特征表现为一些在疾病显现后显著出现的特质。特别是，较少寻求新奇事物是一种病前特质，有助于理解后期的认知缺陷。在一些患者中，焦虑和抑郁在运动表现之前就已出现，且不能归因于抗帕金森治疗。一些神经精神表现，尤其是幻觉，与特定的感知和认知变化有关。认知缺陷在PD中很常见，尤其是在发病年龄较轻的患者中。目前的动物研究将多巴胺转运体和多巴胺分解代谢酶系统的基因差异与归因于额叶功能障碍的特定认知障碍联系起来。视觉认知障碍在PD中很普遍。PD患者及其动物模型均已显示视网膜多巴胺能缺乏。然而，视觉空间缺陷并非仅仅是视网膜缺陷的被动反映。除了视觉外，PD患者的眼球扫视运动也受到影响，但其是否导致视觉空间功能障碍尚不清楚。然而，最近的功能磁共振成像（fMRI）和脑电图（EEG）研究表明枕叶皮质在眼球扫视运动中起重要作用，正电子发射断层扫描（PET）研究显示PD患者枕叶代谢减退。视觉和眼球运动研究表明，PD中的某些神经精神和认知缺陷与视觉系统有关。信号同步对于参与感觉运动协调的分布式神经元网络的协作至关重要。视网膜、基底神经节和额叶皮质记忆系统中的局部多巴胺能神经元群在PD中受到影响。这些连接可能并不主要依赖多巴胺作为神经递质。有人认为，为了理解视觉认知变化，我们应该考虑影响神经元连接的病理学，这对于绑定并行分布式网络是必要的。
