MAR 16, 2016 1:30 PM PDT

Impulse control disorders (behavioural addictions): insights from dopaminergic medication-related behaviours in Parkinson's disease

Presented at: Neuroscience
Speaker
  • Neuropsychiatrist and Principal Investigator, Department of Psychiatry, Behavioural and Clinical Neuroscience Institute, University of Cambridge
    Biography
      Valerie Voon is a neuropsychiatrist and neuroscientist at the University of Cambridge. She is a Medical Research Council Senior Clinical Fellow. She completed her psychiatry residency at the University of Toronto, a research fellowship at the National Institute of Neurological Disorders and Stroke and a PhD in neuroscience through the University College London. Her research group uses multimodal approaches to understand mechanisms underlying impulsivity and compulsivity across repetitive behaviours.

      Dr. Voon's research group focuses on mechanisms underlying impulsivity and compulsivity and relevance to disorders of addiction across both drug and natural rewards. She uses a multimodal approach including anatomical and functional MRI, PET, pharmacological challenges, computational modelling and cognitive neuroscience. She has published extensively with over 100 peer-reviewed publications including in high impact journals such as Neuron, Molecular Psychiatry, Lancet Neurology, Annals of Neurology, Brain and Biological Psychiatry. She is a Fellow of the American Neuropsychiatric Association.

    Abstract

    Impulse control disorders (ICDs), also known as behavioural addictions, are common in the general population and can have marked consequences.  ICDs can also commonly occur with exposure to dopamine agonists and Levodopa used in the treatment of Parkinson’s disease and provide an intriguing pathophysiological insight.  These behaviours include pathological gambling, compulsive sexual behaviors, binge eating and compulsive shopping.  That the behaviours only occur in a subset of individuals argues for an interaction between the exogenous dopaminergic activity and either an individual vulnerability for addictions or a role for Parkinson’s disease.  Here I discuss evidence from rodent and human studies that chronic exogenous dopamine may interfere with physiological functions of dopamine and link preclinical and clinical data.  Where relevant I compare with behavioural and substance addictions in the general population. 
     
    Enhanced ventral striatal dopaminergic activity is observed within specific contexts; this may be related to decreases in striatal dopamine transporter levels and presynaptic D2 autoreceptor sensitivity enhancing physiological dopaminergic activity or chronic Levodopa increasing dopaminergic gain.  Chronic D2 receptor stimulation is hypothesized to impair detection of negative prediction errors.  Converging evidence highlights the relative imbalance of ventral and dorsal striatal systems.  The reinforcing properties of dopaminergic medications are enhanced in rodent parkinsonian models.   In humans, this imbalance is captured in the better fit with ventral striatal critic models reliant on stimulus value rather than dorsal striatal actor models.  Greater impulsivity in the decisional rather than the motoric domain further reinforces this imbalance.  Stimulation of the subthalamic nucleus appears to moderate these behaviours, likely related to changes in dopaminergic medications but also possibly to an influence on cognitive mechanisms.  Understanding mechanisms underlying dopaminergic medication-induced ICDs provides critical insights into the role of dopamine on cognitive processes and the emerging conceptualization of behavioural addictions.
     
    Learning goals:

    1. To understand the role of exogenous dopamine on cognitive processes
    2. To facilitate a discussion between similarities and differences of these behaviours and behavioural and substance addictions in the general population.

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