Levy Richard, Dubois Bruno
Fédération de Neurologie and INSERM U610, Hôpital de la Salpêtrière, Paris, France.
Cereb Cortex. 2006 Jul;16(7):916-28. doi: 10.1093/cercor/bhj043. Epub 2005 Oct 5.
The clinical signs grouped under the concept of apathy are a common feature of prefrontal and basal ganglia lesions or dysfunctions and can therefore help to improve our understanding of the functional anatomy of the prefrontal-basal ganglia system. Apathy is here defined as a quantitative reduction of voluntary, goal-directed behaviors. The underlying mechanisms responsible for apathy can be divided into three subtypes of disrupted processing: 'emotional-affective', 'cognitive' and 'auto-activation'. Apathy due to the disruption of 'emotional-affective' processing refers to the inability to establish the necessary linkage between emotional-affective signals and the ongoing or forthcoming behavior. It may be related to lesions of the orbital-medial prefrontal cortex or to the related subregions (limbic territory) within the basal ganglia (e.g. ventral striatum, ventral pallidum). Apathy due to the disruption of 'cognitive' processing refers to difficulties in elaborating the plan of actions necessary for the ongoing or forthcoming behavior. It may be related to lesions of the dorsolateral prefrontal cortex and the related subregions (associative territory) within the basal ganglia (e.g. dorsal caudate nucleus). The disruption of 'auto-activation' processing refers to the inability to self-activate thoughts or self-initiate actions contrasting with a relatively spared ability to generate externally driven behavior. It is responsible for the most severe form of apathy and in most cases the lesions affect bilaterally the associative and limbic territories of the internal portion of the globus pallidus. It characterizes the syndrome of 'auto-activation deficit' (also known as 'psychic akinesia' or 'athymormia'). This syndrome implies that direct lesions of the basal ganglia output result in a loss of amplification of the relevant signal, consequently leading to a diminished extraction of this signal within the frontal cortex. Likewise, apathy occurring in Parkinson's disease could be interpreted as secondary to the loss of spatial and temporal focalization of the signals transferred to the frontal cortex. In both situations (direct basal ganglia lesions and nigro-striatal dopaminergic loss), the capacity of the frontal cortex to select, initiate, maintain and shift programs of actions is impaired.
归类于淡漠概念下的临床体征是前额叶和基底神经节病变或功能障碍的常见特征，因此有助于增进我们对前额叶 - 基底神经节系统功能解剖学的理解。在此，淡漠被定义为自愿的、目标导向行为的数量减少。导致淡漠的潜在机制可分为三种处理过程中断的亚型：“情感 - 情绪型”、“认知型”和“自我激活型”。因“情感 - 情绪型”处理过程中断导致的淡漠是指无法在情感 - 情绪信号与正在进行或即将发生的行为之间建立必要的联系。它可能与眶额内侧前额叶皮质或基底神经节内相关亚区域（边缘区域）（如腹侧纹状体、腹侧苍白球）的病变有关。因“认知型”处理过程中断导致的淡漠是指在制定正在进行或即将发生的行为所需的行动计划时存在困难。它可能与背外侧前额叶皮质及基底神经节内相关亚区域（联合区域）（如背侧尾状核）的病变有关。“自我激活型”处理过程的中断是指无法自我激活思维或自我发起行动，与之形成对比的是产生外部驱动行为的能力相对保留。它导致最严重形式的淡漠，在大多数情况下，病变双侧累及苍白球内部的联合和边缘区域。它是“自我激活缺陷综合征”（也称为“精神运动不能”或“情感淡漠症”）的特征。该综合征意味着基底神经节输出的直接病变导致相关信号放大丧失，从而导致额叶皮质内该信号的提取减少。同样，帕金森病中出现的淡漠可解释为继发于传递至额叶皮质的信号在空间和时间上的聚焦丧失。在这两种情况下（基底神经节直接病变和黑质 - 纹状体多巴胺能丧失），额叶皮质选择、发起、维持和转换行动计划的能力均受损。
