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J Neurol. 2015 Dec;262(12):2653-61. doi: 10.1007/s00415-015-7892-3. Epub 2015 Sep 26.

Morphometric changes in the reward system of Parkinson's disease patients with impulse control disorders.

Author information

1
Division of Brain Sciences, Neurology Imaging Unit, Centre of Neuroinflammation and Neurodegeneration, Hammersmith Campus, Imperial College London, London, UK.
2
Department of Neuroscience, Mental Health and Sensory Organs-(NESMOS), Sapienza University, Rome, Italy.
3
Neurodegeneration Imaging Group, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, 1 Windsor Walk, London, SE5 8AF, UK.
4
Reta Lila Weston Institute of Neurological Studies, University College London, London, UK.
5
Cardiff University Brain Research Imaging Centre (CUBRIC) and School of Psychology, Cardiff University, Cardiff, UK.
6
Division of Brain Sciences, Neurology Imaging Unit, Centre of Neuroinflammation and Neurodegeneration, Hammersmith Campus, Imperial College London, London, UK. marios.politis@kcl.ac.uk.
7
Neurodegeneration Imaging Group, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, 1 Windsor Walk, London, SE5 8AF, UK. marios.politis@kcl.ac.uk.

Abstract

Impulse control disorders (ICDs) occur in a subset of patients with Parkinson's disease (PD) who are receiving dopamine replacement therapy. In this study, we aimed to investigate structural abnormalities within the mesocortical and limbic cortices and subcortical structures in PD patients with ICDs. We studied 18 PD patients with ICDs, 18 PD patients without ICDs and a group of 24 age and sex-matched healthy controls. Cortical thickness (CTh) and subcortical nuclei volume analyses were carried out using the automated surface-based analysis package FreeSurfer (version 5.3.0). We found significant differences in MRI measures between the three groups. There was volume loss in the nucleus accumbens of both PD patients with ICDs and without ICDs compared to the control group. In addition, PD patients with ICDs showed significant atrophy in caudate, hippocampus and amygdala compared to the group of healthy controls. PD patients with ICDs had significant increased cortical thickness in rostral anterior cingulate cortex and frontal pole compared to PD patients without ICDs. Cortical thickness in rostral anterior cingulate and frontal pole was increased in PD patients with ICDs compared to the control group, but the differences failed to reach corrected levels of statistical significance. PD patients with ICDs showed increased cortical thickness in medial prefrontal regions. We speculate that these findings reflect either a pre-existing neural trait vulnerability to impulsivity or the expression of a maladaptive synaptic plasticity under non-physiological dopaminergic stimulation.

KEYWORDS:

Cortical thickness; Impulse control disorders; MRI; Parkinson’s disease

PMID:
26410743
DOI:
10.1007/s00415-015-7892-3
[Indexed for MEDLINE]

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