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Cerebral Cortex Advance Access originally published online on October 5, 2005
Cerebral Cortex 2006 16(7):916-928; doi:10.1093/cercor/bhj043
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.

Apathy and the Functional Anatomy of the Prefrontal Cortex–Basal Ganglia Circuits

Richard Levy and Bruno Dubois

Fédération de Neurologie and INSERM U610, Hôpital de la Salpêtrière, Paris, France

Address correspondence to Richard Levy, Fédération de Neurologie, Hôpital de la Salpêtrière, 47, bd de l'hôpital, 75651 Paris cedex 13, France. Email: richard.levy{at}psl.aphp.fr.

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.


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