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Research paper
Impulse control disorders in Parkinson's disease: decreased striatal dopamine transporter levels
  1. Valerie Voon1,2,3,
  2. Alexandra Rizos4,
  3. Riddhika Chakravartty4,5,
  4. Nicola Mulholland4,5,
  5. Stephanie Robinson4,
  6. Nicholas A Howell1,6,
  7. Neil Harrison6,
  8. Gill Vivian5,
  9. K Ray Chaudhuri4
  1. 1Department of Psychiatry, University of Cambridge, Cambridge, UK
  2. 2Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK
  3. 3Cambridgeshire and Peterborough NHS Foundation Trust, Cambridge, UK
  4. 4National Parkinson Foundation Centre of Excellence, Kings College Hospital, and Kings College, London, UK
  5. 5Department of Nuclear Imaging, Kings College Hospital, London, UK
  6. 6University of Toronto, Toronto, Canada
  7. 7University of Sussex, Brighton, UK
  1. Correspondence to Dr Valerie Voon, Department of Psychiatry, University of Cambridge, Addenbrookes Hospital, Level E4, Box 189, Hills Road, Cambridge CB2 0QQ, UK; voonval{at}


Objective Impulse control disorders are commonly associated with dopaminergic therapy in Parkinson's disease (PD). PD patients with impulse control disorders demonstrate enhanced dopamine release to conditioned cues and a gambling task on [11C]raclopride positron emission tomography (PET) imaging and enhanced ventral striatal activity to reward on functional MRI. We compared PD patients with impulse control disorders and age-matched and gender-matched controls without impulse control disorders using [123I]FP-CIT (2β-carbomethoxy-3β-(4-iodophenyl)tropane) single photon emission computed tomography (SPECT), to assess striatal dopamine transporter (DAT) density.

Methods The [123I]FP-CIT binding data in the striatum were compared between 15 PD patients with and 15 without impulse control disorders using independent t tests.

Results Those with impulse control disorders showed significantly lower DAT binding in the right striatum with a trend in the left (right: F(1,24)=5.93, p=0.02; left: F(1,24)=3.75, p=0.07) compared to controls.

Conclusions Our findings suggest that greater dopaminergic striatal activity in PD patients with impulse control disorders may be partly related to decreased uptake and clearance of dopamine from the synaptic cleft. Whether these findings are related to state or trait effects is not known. These findings dovetail with reports of lower DAT levels secondary to the effects of methamphetamine and alcohol. Although any regulation of DAT by antiparkinsonian medication appears to be modest, PD patients with impulse control disorders may be differentially sensitive to regulatory mechanisms of DAT expression by dopaminergic medications.

  • Behavioural Disorder
  • Functional Imaging
  • Neuropsychiatry
  • Spect
  • Movement Disorders

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