Disconnecting force from money: Effects of basal ganglia damage on incentive motivation

Laboratoire INSERM U610, Institut Fédératif de Recherches en Neurosciences, Université Pierre et Marie Curie (Paris 6), Site Pitié-Salpêtrière, F-75013 Paris, France.
Brain (Impact Factor: 9.2). 06/2008; 131(Pt 5):1303-10. DOI: 10.1093/brain/awn045
Source: PubMed


Bilateral basal ganglia lesions have been reported to induce a particular form of apathy, termed auto-activation deficit (AAD), principally defined as a loss of self-driven behaviour that is reversible with external stimulation. We hypothesized that AAD reflects a dysfunction of incentive motivation, a process that translates an expected reward (or goal) into behavioural activation. To investigate this hypothesis, we designed a behavioural paradigm contrasting an instructed (externally driven) task, in which subjects have to produce different levels of force by squeezing a hand grip, to an incentive (self-driven) task, in which subjects can win, depending on their hand grip force, different amounts of money. Skin conductance was simultaneously measured to index affective evaluation of monetary incentives. Thirteen AAD patients with bilateral striato-pallidal lesions were compared to thirteen unmedicated patients with Parkinson's; disease (PD), which is characterized by striatal dopamine depletion and regularly associated with apathy. AAD patients did not differ from PD patients in terms of grip force response to external instructions or skin conductance response to monetary incentives. However, unlike PD patients, they failed to distinguish between monetary incentives in their grip force. We conclude that bilateral striato-pallidal damage specifically disconnects motor output from affective evaluation of potential rewards.

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Available from: Gilles Lafargue, Oct 11, 2015
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    • "As stated above, bilateral basal ganglia lesions have been reported to induce a particular form of apathy, termed auto-activation deficit, principally defined as a loss of self-driven behavior that is reversible with external stimulation. Schmidt et al. (2008) proposed that bilateral striato-pallidal damage, observed in PD, specifically disconnects motor output from affective evaluation of potential rewards. "
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    ABSTRACT: Apathy, characterized by lack of motivation and loss of initiative, is a non-cognitive symptom that affects a high proportion, but not all, of patients with all forms of dementia. To explore the phenomenon of apathy in people with dementia, we searched the PubMed and Google Scholar electronic databases for original research and review articles on apathetic behaviors in patients with dementia using the search terms "apathy, behavioral and psychological symptoms, dementia, Alzheimer's disease, Frontotemporal dementia, Dementia associated with Parkinson's disease, Huntington's disease, Vascular dementia". Some nosological aspects, neurobiological basis, and assessment of, as well as, potential benefits of non-pharmacologic and pharmacologic interventions for apathy in dementia are discussed. Greater understanding of apathy will improve the identification, intervention, and treatment of this ubiquitous and pernicious syndrome.
    Journal of Nervous & Mental Disease 10/2014; 202(10):718-724. DOI:10.1097/NMD.0000000000000190 · 1.69 Impact Factor
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    • "It may be that clinical groups exhibit a distinctly different pattern of motivational deficits (cf. Schmidt et al., 2008) to the ones we observed in the healthy population. However, our observations appear to echo some of the previously described characteristics of auto-activation deficit: behavioral inertia that is reversed by strong enough external incentives, or solicitors (Levy and Dubois, 2006). "
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    ABSTRACT: Apathy is a common but poorly understood condition with a wide societal impact observed in several brain disorders as well as, to some extent, in the normal population. Hence the need for better characterization of the underlying mechanisms. The processes by which individuals decide to attribute physical effort to obtain rewards might be particularly relevant to relate to apathy traits. Here, we designed two paradigms to assess individual differences in physical effort production and effort-based decision-making and their relation to apathy in healthy people. Apathy scores were measured using a modified version of the Lille Apathy Rating Scale, suitable for use in a non-clinical population. In the first study, apathy scores were correlated with the degree to which stake (reward on offer) and difficulty level impacts on physical effort production. Individuals with relatively high apathy traits showed an increased modulation of effort while more motivated individuals generally exerted greater force across different levels of stake. To clarify the underlying mechanisms for this behavior, we designed a second task that allows independent titration of stake and effort levels for which subjects are willing to engage in an effortful response to obtain a reward. Our results suggest that apathy traits in the normal population are related to the way reward subjectively affects the estimation of effort costs, and more particularly manifest as decreased willingness to exert effort when rewards are small, or below threshold. The tasks we introduce here may provide useful tools to further investigate apathy in clinical populations.
    Journal of Physiology-Paris 04/2014; 109(1-3). DOI:10.1016/j.jphysparis.2014.04.002 · 1.90 Impact Factor
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    • "Our finding that even “off” medication patients improved their ITs with the prospect of monetary incentive (Fig. 2a,b) may perhaps be surprising, but is consistent with previous studies, which demonstrated a preserved ability of PD patients to translate the expectation of reward into generation of faster movements or greater physical force, even when unmedicated. For example, non-apathetic bradykinetic PD patients “off” medication, in the presence of monetary incentive, were able to increase hand grip force [17] or to complete a spatial search task faster [18]. Nevertheless, our results are different from those of Shiner et al. [19], who reported that PD patients “off” dopaminergic treatment failed to modulate movement speed in the face of monetary reward. "
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