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.