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冷漠与基底神经节。

Apathy and the basal ganglia.

作者信息

Levy Richard, Czernecki Virginie

机构信息

Department of Neurology and INSERM U 0.610, Hôpital de la Salpêtrière, Paris, France.

出版信息

J Neurol. 2006 Dec;253 Suppl 7:VII54-61. doi: 10.1007/s00415-006-7012-5.

Abstract

We should like to emphasize the following points: 1. Apathy is defined here as a quantified and observable behavioral syndrome consisting in a quantitative reduction of voluntary (or goal-directed) behaviors; 2. Therefore, apathy occurs when the systems that generate and control voluntary actions are altered; 3. These systems are mostly represented by the different subregions embedded in the Prefrontal cortex (PFC) and in the basal ganglia regions that are closely connected with the PFC; 4. In consequence, clinically, apathy is a prefrontal syndrome either due to direct lesions of the PFC or to lesions of basal ganglia areas that are closely related to the PFC; 5. Apathy is not a single entity but rather heterogeneous. Several different mechanisms may lead to apathy; Because there are several anatomical-functional prefrontal-basal ganglia circuits, the underlying mechanisms responsible for apathy may differ according to which prefrontal-basal ganglia circuit is affected; 6. In this context, apathy is the macroscopic results of the disruption of one or several elementary steps necessary for goal-directed behavior that are subserved by different prefrontal-basal ganglia circuits; 7. Intense apathy is related to caudate nucleus and GPi, disrupting associative and limbic pathways from/to the PFC; 8. in progressive supranuclear palsy (PSP) and focal lesions (caudate nuclei, GPi), apathy may be due to a loss of PFC activation; 9. In Parkinson's disease (PD), apathy may be due to a loss of signal focalization; 10. More globally, we propose that apathy may be explained by the impact of lesions or dysfunctions of the BG, because these lesions or dysfunctions lead to a loss of amplification of the relevant signal and/or to a loss of temporal and spatial focalization, both of which result in a diminished extraction of the relevant signal within the frontal cortex, thereby inhibiting the capacity of the frontal cortex to select, initiate, maintain and shift programs of action.

摘要

我们谨强调以下几点

  1. 在此,淡漠被定义为一种可量化且可观察到的行为综合征,其表现为自主(或目标导向)行为在数量上的减少;2. 因此,当产生和控制自主行动的系统发生改变时,淡漠就会出现;3. 这些系统主要由前额叶皮质(PFC)中不同的亚区域以及与PFC紧密相连的基底神经节区域所代表;4. 因此,在临床上,淡漠是一种前额叶综合征,要么是由于PFC的直接损伤,要么是由于与PFC密切相关的基底神经节区域的损伤;5. 淡漠并非单一实体,而是具有异质性。几种不同的机制可能导致淡漠;由于存在多个解剖 - 功能上前额叶 - 基底神经节回路,导致淡漠的潜在机制可能因受影响的前额叶 - 基底神经节回路不同而有所差异;6. 在这种情况下,淡漠是由不同前额叶 - 基底神经节回路所支持的目标导向行为所需的一个或几个基本步骤中断的宏观结果;7. 强烈的淡漠与尾状核和苍白球内侧部(GPi)有关,破坏了与PFC之间的联合和边缘通路;8. 在进行性核上性麻痹(PSP)和局灶性病变(尾状核、GPi)中,淡漠可能是由于PFC激活缺失所致;9. 在帕金森病(PD)中,淡漠可能是由于信号聚焦缺失所致;

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