Charlotte Spay1, Garance Meyer1, Guillaume Lio2, Gianni Pezzoli3, Bénédicte Ballanger1, Roberto Cilia3, Philippe Boulinguez4. 1. Université de Lyon, 92 rue Pasteur, 69007 Lyon, France; Université Lyon 1, 43 boulevard du 11 novembre 1918, 69622 Villeurbanne, France; INSERM, U 1028, Lyon Neuroscience Research Center, 95 boulevard Pinel, 69500 Bron, France; CNRS, UMR 5292, Lyon Neuroscience Research Center, 95 boulevard Pinel, 69500 Bron, France. 2. Centre de Neuroscience Cognitive, UMR 5229, 67 boulevard Pinel, 69675 Bron, France. 3. Parkinson Institute, ASST Gaetano Pini-CTO, Via bignami 1, 20126 Milan, Italy. 4. Université de Lyon, 92 rue Pasteur, 69007 Lyon, France; Université Lyon 1, 43 boulevard du 11 novembre 1918, 69622 Villeurbanne, France; INSERM, U 1028, Lyon Neuroscience Research Center, 95 boulevard Pinel, 69500 Bron, France; CNRS, UMR 5292, Lyon Neuroscience Research Center, 95 boulevard Pinel, 69500 Bron, France. Electronic address: philippe.boulinguez@univ-lyon1.fr.
Abstract
OBJECTIVES: Impulse control disorders (ICDs) in Parkinson's disease (PD) have been associated with cognitive impulsivity and dopaminergic dysfunction and treatment. The present study tests the neglected hypothesis that the neurofunctional networks involved in motor impulsivity might also be dysfunctional in PD-ICDs. METHODS: We performed blind spectral analyses of resting state electroencephalographic (EEG) data in PD patients with and without ICDs to probe the functional integrity of all cortical networks. Analyses were performed directly at the source level after blind source separation. Discrete differences between groups were tested by comparing patients with and without ICDs. Gradual dysfunctions were assessed by means of correlations between power changes and clinical scores reflecting ICD severity (QUIP score). RESULTS: Spectral signatures of ICDs were found in the medial prefrontal cortex, the dorsal anterior cingulate and the supplementary motor area, in the beta and gamma bands. Beta power changes in the supplementary motor area were found to predict ICDs severity. CONCLUSION: ICDs are associated with abnormal activity within frequency bands and cortical circuits supporting the control of motor response inhibition. SIGNIFICANCE: These results bring to the forefront the need to consider, in addition to the classical interpretation based on aberrant mesocorticolimbic reward processing, the issue of motor impulsivity in PD-ICDs and its potential implications for PD therapy.
OBJECTIVES: Impulse control disorders (ICDs) in Parkinson's disease (PD) have been associated with cognitive impulsivity and dopaminergic dysfunction and treatment. The present study tests the neglected hypothesis that the neurofunctional networks involved in motor impulsivity might also be dysfunctional in PD-ICDs. METHODS: We performed blind spectral analyses of resting state electroencephalographic (EEG) data in PDpatients with and without ICDs to probe the functional integrity of all cortical networks. Analyses were performed directly at the source level after blind source separation. Discrete differences between groups were tested by comparing patients with and without ICDs. Gradual dysfunctions were assessed by means of correlations between power changes and clinical scores reflecting ICD severity (QUIP score). RESULTS: Spectral signatures of ICDs were found in the medial prefrontal cortex, the dorsal anterior cingulate and the supplementary motor area, in the beta and gamma bands. Beta power changes in the supplementary motor area were found to predict ICDs severity. CONCLUSION: ICDs are associated with abnormal activity within frequency bands and cortical circuits supporting the control of motor response inhibition. SIGNIFICANCE: These results bring to the forefront the need to consider, in addition to the classical interpretation based on aberrant mesocorticolimbic reward processing, the issue of motor impulsivity in PD-ICDs and its potential implications for PD therapy.