The Iowa Gambling Task in Parkinson's disease: A meta-analysis on effects of disease and medication

Evens, Ricarda; Hoefler, M.; Biber, Karolina; Lueken, Ulrike

doi:10.1016/j.neuropsychologia.2016.07.032

Cited by 38 publications

(30 citation statements)

References 50 publications

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“…In other words, the availability of reward may have caused PD patients to collapse under pressure. Support for this hypothesis comes from studies demonstrating impaired Iowa gambling task (IGT) performance and elevated impulsivity in medicated PD patients (Cools, Barker, Sahakian, & Robbins, 2003;Evens, Hoe, Biber, & Lueken, 2016). In our study, patients with PD experienced numerically faster response times during training compared to HCs.…”

Section: Comparison To Previous Studies Of Reward and Parkinson's Dissupporting

confidence: 55%

Separating the effect of reward from corrective feedback during learning in patients with Parkinson’s disease

Freedberg

Schacherer

Chen

et al. 2017

Cogn Affect Behav Neurosci

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Parkinson's disease (PD) is associated with procedural learning deficits. Nonetheless, studies have demonstrated that reward-related learning is comparable between patients with PD and controls (Bódi et al., Brain, 132(9), 2385-2395 Frank, Seeberger, & O'Reilly, Science, 306(5703), 1940-1943, 2004; Palminteri et al., Proceedings of the National Academy of Sciences of the United States of America, 106(45), 19179-19184, 2009). However, because these studies do not separate the effect of reward from the effect of practice, it is difficult to determine whether the effect of reward on learning is distinct from the effect of corrective feedback on learning. Thus, it is unknown whether these group differences in learning are due to reward processing or learning in general. Here, we compared the performance of medicated PD patients to demographically matched healthy controls (HCs) on a task where the effect of reward can be examined separately from the effect of practice. We found that patients with PD showed significantly less reward-related learning improvements compared to HCs. In addition, stronger learning of rewarded associations over unrewarded associations was significantly correlated with smaller skin-conductance responses for HCs but not PD patients. These results demonstrate that when separating the effect of reward from the effect of corrective feedback, PD patients do not benefit from reward.

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Section: Comparison To Previous Studies Of Reward and Parkinson's Dissupporting

confidence: 55%

Separating the effect of reward from corrective feedback during learning in patients with Parkinson’s disease

Freedberg

Schacherer

Chen

et al. 2017

Cogn Affect Behav Neurosci

View full text Add to dashboard Cite

show abstract

“…This is not only the case of some motor tasks, such as motor sequence performance (Vaillancourt, Schonfeld, Kwak, Bohnen, & Seidler, ), but also of some cognitive abilities, such as reversal learning (Frank, ; Vaillancourt et al., ). Furthermore, often medicated PD patients show signs of impulsivity, like gambling (Evens, Hoefler, Biber, & Lueken, ), surprisingly connected to the treatment of the pathophysiology itself. Although we did not address these aspects explicitly within the model, according to the previous scenario our simulations show that, in PD patients, dyskinesia can easily occur at high DA levels.…”

Section: Discussionmentioning

confidence: 99%

Aberrant learning in Parkinson's disease: A neurocomputational study on bradykinesia

Ursino

Baston

2018

Eur J of Neuroscience

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Parkinson's disease (PD) is a neurodegenerative disorder characterized by a progressive decline in motor functions, such as bradykinesia, caused by the pathological denervation of nigrostriatal dopaminergic neurons within the basal ganglia (BG). It is acknowledged that dopamine (DA) directly affects the modulatory role of BG towards the cortex. However, a growing body of literature is suggesting that DA-induced aberrant synaptic plasticity could play a role in the core symptoms of PD, thus recalling for a "reconceptualization" of the pathophysiology. The aim of this work was to investigate DA-driven aberrant learning as a concurrent cause of bradykinesia, using a comprehensive, biologically inspired neurocomputational model of action selection in the BG. The model includes the three main pathways operating in the BG circuitry, that is the direct, indirect and hyperdirect pathways, and use a two-term Hebb rule to train synapses in the striatum, based on previous history of rewards and punishments. Levodopa pharmacodynamics is also incorporated. Through model simulations of the Alternate Finger Tapping motor task, we assessed the role of aberrant learning on bradykinesia. The results show that training under drug medication (levodopa) provides not only immediate but also delayed benefit lasting in time. Conversely, if performed in conditions of vanishing levodopa efficacy, training may result in dysfunctional corticostriatal synaptic plasticity, further worsening motor performances in PD subjects. This suggests that bradykinesia may result from the concurrent effects of low DA levels and dysfunctional plasticity and that training can be exploited in medicated subjects to improve levodopa treatment.

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“…Dopamine agonist therapy for neurological disorders provides excellent motor benefits, but it is associated with the emergence of disorders related to impulse control and compulsiveness in some treated patients (Grall-Bronnec et al, 2018). There is considerable debate regarding what features of dopamine transmission are responsible for the various behaviors, and what are the roles of therapy, pathology, or neuroplasticity in the behavioral manifestations (Lawrence et al, 2003;Napier et al, 2015;Brusa et al, 2016;Evens et al, 2016;Houeto et al, 2016;Morgante et al, 2016;Maloney et al, 2017;Vriend, 2018). Adding to the conundrum are reports of these disorders emerging during therapy with dopamine receptor partial agonists used to treat (e.g.)…”

Section: Introductionmentioning

confidence: 99%

Pharmacological insights into impulsive‐compulsive spectrum disorders associated with dopaminergic therapy

Napier

Persons

2018

Eur J of Neuroscience

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Impulsive‐compulsive spectrum disorders are associated with dopamine agonist therapy in some patients. These untoward outcomes occur with direct‐acting, full and partial agonists at D2 dopamine family receptors. The disorders typically emerge during chronic treatment, and exhibit common features that are independent of the neurological or psychiatric pathology for which the initial therapy was indicated. It is well‐documented that the brain is ‘plastic’, changing in response to alterations to internal factors (e.g., disease processes), as well as external factors (e.g., therapies). The complexities of these clinical scenarios have eluded a clear depiction of the neurobiology for impulsive‐compulsive spectrum disorders and engendered considerable debate regarding the mechanistic underpinnings of the disorders. In this opinion, we use pharmacological concepts related to homeostatic compensation subsequent to chronic receptor activation to provide a unifying construct. This construct helps explain the occurrence of impulsive‐compulsive spectrum disorders across disease states, and during therapy with full and partial agonists.

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The Iowa Gambling Task in Parkinson's disease: A meta-analysis on effects of disease and medication

Cited by 38 publications

References 50 publications

Separating the effect of reward from corrective feedback during learning in patients with Parkinson’s disease

Separating the effect of reward from corrective feedback during learning in patients with Parkinson’s disease

Aberrant learning in Parkinson's disease: A neurocomputational study on bradykinesia

Pharmacological insights into impulsive‐compulsive spectrum disorders associated with dopaminergic therapy

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