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Apathy: a neurocircuitry model based on frontotemporal dementia
  1. Simon Ducharme1,2,
  2. Bruce H Price3,
  3. Bradford C Dickerson4
  1. 1 Department of Psychiatry, Montreal Neurological Institute and McGill University Health Centre, Montreal, Québec, Canada
  2. 2 Department of Neurology and Neurosurgery, McGill University, Montreal, Québec, Canada
  3. 3 Department of Neurology, Harvard University, McLean Hospital, Boston, Massachusetts, USA
  4. 4 Department of Neurology, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts, USA
  1. Correspondence to Dr Simon Ducharme, Department of Psychiatry, Montreal Neurological Institute and McGill University Health Centre, Montreal, QC H3A 2B4, Canada; simon.ducharme{at}


Apathy is a symptom shared among many neurological and psychiatric disorders. However, the underlying neurocircuitry remains incompletely understood. Apathy is one of the core features of behavioural variant frontotemporal dementia (bvFTD), a neurodegenerative disease presenting with heterogeneous combinations of socioaffective symptoms and executive dysfunction. We reviewed all neuroimaging studies of apathy in frontotemporal dementia (FTD) attempting to refine a neurocircuitry model and inform clinical definitions. Levels of apathy have been consistently shown to correlate with the severity of executive dysfunctions across a wide range of diseases, including FTD. Some authors view ‘energisation’—the loss of which is central in apathy—as a core executive function. Apathy in FTD is most robustly associated with atrophy, hypometabolism and/or hypoperfusion in the dorsolateral prefrontal cortex, the anterior and middle cingulate cortex, the orbitofrontal cortex and the medial and ventromedial superior frontal gyri. Data also suggest that abnormalities in connecting white matter pathways and functionally connected more posterior cortical areas could contribute to apathy. There is a lack of consistency across studies due to small samples, lenient statistical thresholds, variable measurement scales and the focus on apathy as a unitary concept. Integrating findings across studies, we revise a neurocircuitry model of apathy divided along three subcomponents (cognition/planning, initiation, emotional-affective/motivation) with specific neuroanatomical and cognitive substrates. To increase consistency in clinical practice, a recommendation is made to modify the bvFTD diagnostic criteria of apathy/inertia. More generally, we argue that bvFTD constitutes a disease model to study the neurocircuitry of complex behaviours as a ‘lesion-based’ approach to neuropsychiatric symptoms observed across diagnostic categories.

  • neuroimaging

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  • Contributors SD has contributed to the design of study, literature review, interpretation of data, preparation of the manuscript and editing of the manuscript. BHP has contributed to the design of study and editing of the manuscript. BCD has contributed to the design of study, interpretation of data and editing of the manuscript.

  • Funding Dr Ducharme receives salary funding from the Fonds de Recherche du Québec - Santé. Authors would like to thank The Sidney R Baer, Jr Foundation for their support.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.