Lévy Richard, Pillon Bernard
Inserm U 610 et Fédération de neurologie, Hôpital de la Salpêtrière, Paris.
Psychol Neuropsychiatr Vieil. 2006 Dec;4 Spec No 1:S25-34.
The cognitive disorders observed in non-demented Parkinsonian patients are frequent but subtle. They mostly result from difficulties to control attentional resources. These deficits particularly disturb the strategies involved in planning as well as in encoding and retrieval processing of memory, whereas consolidation of the mnemonic traces and instrumental functions are relatively spared. These deficits can be related to the striatal dopamine depletion (in particular in the caudate nuclei) which seems sufficient to account for the cognitive disorders that appear early in the course of the disease. In particular, the caudate dopamine depletion induces a cascade of dysfunction within the basal ganglia, downstream of the striatum, which ultimately affects the prefrontal functions. It is likely that, in the course of the disease, lesions of other ascending systems of neurotransmission (cholinergic, serotoninergic and noradrenergic pathways) contribute to worsen the cognitive disorders and also to modify their clinical pattern. The impact of direct cortical lesions can also be discussed but it seems that these lesions mostly contribute to the cognitive deficits in the late stages of Parkinson's disease.
在非痴呆帕金森病患者中观察到的认知障碍很常见但很细微。它们主要是由于难以控制注意力资源所致。这些缺陷尤其会干扰计划以及记忆编码和检索过程中所涉及的策略，而记忆痕迹的巩固和工具性功能相对未受影响。这些缺陷可能与纹状体多巴胺耗竭（特别是在尾状核中）有关，这似乎足以解释在疾病早期出现的认知障碍。特别是，尾状核多巴胺耗竭会在纹状体下游的基底神经节内引发一系列功能障碍，最终影响前额叶功能。在疾病过程中，其他上行神经传递系统（胆碱能、5-羟色胺能和去甲肾上腺素能通路）的损伤可能会导致认知障碍恶化，并改变其临床模式。也可以讨论直接皮质损伤的影响，但似乎这些损伤主要在帕金森病晚期导致认知缺陷。
