Apathy: a pathology of goal-directed behaviour: a new concept of the clinic and pathophysiology of apathy

Abstract

We propose to defined apathy as a quantitative reduction of goal-directed behaviour. As such, the neural bases of apathy rely on lesions or dysfunctions of the brain structures that generate and control goal-directed behaviour: the frontal lobes, the basal ganglia and the frontal-basal ganglia circuits. Lesions or dysfunctions of the limbic territories of the frontal lobes (the orbital-mesial prefrontal cortex) and the basal ganglia (e.g., the ventral striatum) lead to apathy through difficulties to provide the affective value of a given behavioural context. We also suggest that lesions or dysfunctions of the associative ("cognitive") territories of the frontal lobes (the dorsal prefrontal cortex) and the basal ganglia (e.g., the dorsal caudate) contribute to apathy via a "cognitive inertia" - an inability to generate or activate strategies required to successfully complete a given program of actions. The most severe forms of apathy ("auto-activation deficit" syndrome), due to bilateral lesions in the prefrontal-basal ganglia circuits can be explained either by the addition of lesions in the cognitive and limbic territories or by a more general and elementary impairment that mirrored the presumed normal functions of the prefrontal-basal ganglia circuits, that is to selectively amplified the behaviour that one considers as the most adapted to one's personal needs or environmental demands. These lesions may limit the selective amplification of the signal that represents relevant thoughts and actions, leading to difficulties to disambiguate decision-making at the level of the prefrontal cortex.