Disconnecting force from money: effects of basal ganglia damage on incentive motivation.
Identifieur interne : 000C94 ( PubMed/Corpus ); précédent : 000C93; suivant : 000C95Disconnecting force from money: effects of basal ganglia damage on incentive motivation.
Auteurs : Liane Schmidt ; Baudouin Forgeot D'Arc ; Gilles Lafargue ; Damien Galanaud ; Virginie Czernecki ; David Grabli ; Michael Schüpbach ; Andreas Hartmann ; Richard Lévy ; Bruno Dubois ; Mathias PessiglioneSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2008.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Basal Ganglia (physiopathology), Basal Ganglia Diseases (pathology), Basal Ganglia Diseases (physiopathology), Basal Ganglia Diseases (psychology), Brain Mapping (methods), Female, Galvanic Skin Response, Hand Strength, Humans, Magnetic Resonance Imaging (methods), Male, Middle Aged, Motivation, Parkinson Disease (pathology), Parkinson Disease (physiopathology), Parkinson Disease (psychology), Psychomotor Disorders (etiology), Psychomotor Disorders (pathology), Psychomotor Disorders (physiopathology), Psychomotor Performance, Reward, Severity of Illness Index.
- MESH :
- etiology : Psychomotor Disorders.
- methods : Brain Mapping, Magnetic Resonance Imaging.
- pathology : Basal Ganglia Diseases, Parkinson Disease, Psychomotor Disorders.
- physiopathology : Basal Ganglia, Basal Ganglia Diseases, Parkinson Disease, Psychomotor Disorders.
- psychology : Basal Ganglia Diseases, Parkinson Disease.
- Adult, Aged, Aged, 80 and over, Female, Galvanic Skin Response, Hand Strength, Humans, Male, Middle Aged, Motivation, Psychomotor Performance, Reward, Severity of Illness Index.
Abstract
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.
DOI: 10.1093/brain/awn045
PubMed: 18344560
Links to Exploration step
pubmed:18344560Le document en format XML
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<front><div type="abstract" xml:lang="en">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.</div>
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<Abstract><AbstractText>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.</AbstractText>
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