38 research outputs found

    Pathological gambling and other addictive behaviours in Parkinson's disease

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    The phenomenology of impulsive compulsive behaviours in patients with Parkinson’s disease (PD) treated with dopaminergic therapy has been reviewed. Neuropsychological studies have been conducted to explore the behavioural mechanisms responsible for these socially devastating disorders, which affect a substantial proportion of treated patients. Results demonstrated that poor information sampling and impaired working memory capacity, especially when mental manipulation of information was required, distinguish PD patients with impulsive compulsive behaviours from those without. A direct comparison to non PD-patients with addictions revealed that impulsive PD patients closely resembled illicit drug abusers, whereas non-impulsive PD patients treated with a dopamine agonist performed similarly to pathological gamblers. PD patients who were not taking dopamine agonists performed as well as healthy volunteers, even when treated with deep brain stimulation. Therefore, dopamine agonists are the single most important risk factor for impulsive choice in PD. Conversely, response inhibition and feedback learning were intact in medicated PD patients with impulsive compulsive behaviours. Furthermore, all PD patients became more risk prone after dopaminergic medication, but greater salivary cortisol release only correlated with risk taking behaviour in the PD group with behavioural addictions. Cortisol plays also a prominent role in stress regulation. Therefore, the literature was reviewed to explore links between emotional stress and PD

    Phenomenology and epidemiology of impulsive-compulsive behaviours in Parkinson's disease, atypical Parkinsonian disorders and non-Parkinsonian populations

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    Impulsive-compulsive behaviours are common, quality of life affecting consequences of dopamine replacement therapy which are well recognized in patients with idiopathic Parkinson's disease. Details of the occurrence and nature of these disorders in the atypical parkinsonian neurodegenerative disorders, and in non-Parkinson's patients prescribed dopaminergic stimulation for other disease processes, are slowly emerging. Here we review what is known about the phenomenology, epidemiology and risk factors for impulsive-compulsive behaviours in Parkinson's disease and in other, less well studied, patient groups. By analyzing the available published data, this review identifies potential clues as to the underlying neurobiological mechanism of these disorders, and further identifies critical gaps yet to be addressed

    Salivary cortisol levels in Parkinson's disease and its correlation to risk behaviour

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    Objective To investigate salivary cortisol samples in patients with Parkinson's disease (PD) with and without impulsive compulsive behaviours (ICB) during a risk task.Methods Salivary cortisol levels were measured in 13 PD patients without ICB (PD-ICB) and in 15 PD patients with ICB (PD+ICB) before, after medication and throughout the day, and were compared with results with 14 healthy controls. All participants also performed a gambling task to assess risk taking behaviour.Results Significantly higher diurnal cortisol levels were found in the PD-ICB group compared with healthy controls but no differences were seen between the PD+ICB and the control group. Increased cortisol levels were significantly correlated with increased risk taking in PD+ICB patients but no interaction was found in the PD-ICB group.Conclusions The findings are in keeping with previous studies which have linked low cortisol levels with antisocial behaviour. The higher cortisol levels during the risk task in the PD+ICB group are consistent with reports in pathological gamblers during gambling and addicts during drug abuse. The results support the hypothesis that cortisol plays an important role in risk taking in ICBs

    Saccadic Direction Errors are Associated with Impulsive Compulsive Behaviours in Parkinson's Disease Patients.

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    Fifteen individuals with Parkinson's disease (PD) and impulsive compulsive behaviours (PD+ICB) were compared to 15 PD patients without ICBs (PD-ICB) and 15 healthy controls (HC) on a pro-saccades and an anti-saccades task to assess if ICBs are associated with distinct saccadic abnormalities. PD+ICB made shorter saccades than HC and more direction errors in the anti-saccades task than PD-ICB and HC, suggesting that patients with ICBs have greater difficulty in suppressing automatic saccades towards a given target. Saccadic assessment has the potential to evolve into a marker to guide therapeutic decisions in patients at risk of developing ICBs

    Effects of Dopamine on Sensitivity to Social Bias in Parkinson's Disease

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    Patients with Parkinson's disease (PD) sometimes develop impulsive compulsive behaviours (ICBs) due to their dopaminergic medication. We compared 26 impulsive and 27 non-impulsive patients with PD, both on and off medication, on a task that examined emotion bias in decision making. No group differences were detected, but patients on medication were less biased by emotions than patients off medication and the strongest effects were seen in patients with ICBs. PD patients with ICBs on medication also showed more learning from negative feedback and less from positive feedback, whereas off medication they showed the opposite effect

    Behavioral results.

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    <p>All error bars are 1 s.e.m. A. Emotion bias for each group. B. Evidence vs. choice curve showing increased selection of happy faces when evidence supports angry face. C. Percent correct for each group.</p

    Learning from positive vs. negative feedback.

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    <p>Error bars show 1 s.e.m. A. Parameter values from the Bayesian model in PD+ICBs. B. Parameter values in PDs.</p

    Demographic characteristics.

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    <p>UPDRS = Unified Parkinson's Disease Rating Scale; LEU = L-dopa equivalent units; DA = dopamine agonists. All values are mean ± SD. Significant differences are labelled with “*”. P-values refer to columns indicated in brackets. Controls (column 1), PD+ICB (column 2), PD−ICB (column 3).</p
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