Silvia Picazio1, Viviana Ponzo1, Carlo Caltagirone1,2, Livia Brusa3, Giacomo Koch4,5. 1. Non-Invasive Brain Stimulation Unit, IRCCS Santa Lucia Foundation, Via Ardeatina, 306, 00179, Rome, Italy. 2. Department of System Medicine, University of Rome Tor Vergata, Via Montpellier, 1, 00133, Rome, Italy. 3. UOC Neurologia, Ospedale S. Eugenio, Piazzale dell'Umanesimo, 10, 00144, Rome, Italy. 4. Non-Invasive Brain Stimulation Unit, IRCCS Santa Lucia Foundation, Via Ardeatina, 306, 00179, Rome, Italy. g.koch@hsantalucia.it. 5. Stroke Unit, Department of Neuroscience, Policlinic Tor Vergata, Via Montpellier, 1, 00133, Rome, Italy. g.koch@hsantalucia.it.
Abstract
INTRODUCTION: Chronic dopamine replacement therapies in Parkinson's disease can induce side effects, such as levodopa-induced dyskinesias and impulse control disorders. A dysfunction of inhibitory brain networks has been related to both disorders; however, there is no clear behavioral evidence supporting this hypothesis. We aimed to determine whether PD patients with levodopa-induced dyskinesias show features of increased impulsivity in parallel with altered motor inhibition. METHODS: Two matched samples of Parkinson's disease patients with (n = 14) or without (n = 14) levodopa-induced dyskinesias and a control group (n = 10) participated in the study. All groups were evaluated by the Barratt Impulsiveness Scale-11 to assess impulsivity traits. Furthermore, participants performed a stop signal task to evaluate reactive-motor inhibition and a Go/NoGo task to evaluate proactive-inhibitory control. PD patients were tested both in OFF and ON levodopa medication. RESULTS: Parkinson's disease patients with levodopa-induced dyskinesias showed higher impulsivity scores than PD patients without levodopa-induced dyskinesias. Dyskinetic patients presented also delayed stop signal reaction times indicating a worse performance in reactive inhibition. The slowness in inhibiting a motor command correlated with the impulsiveness scores. Furthermore, in the dyskinetic group, a positive correlation was found between stop reaction times and the severity of involuntary movements. Under the effect of levodopa, all patients were faster but dyskinetic patients were significantly less accurate in proactive inhibition. CONCLUSION: Inhibitory control is compromised in dyskinetic patients in parallel with increased impulsivity, revealing an impairment of motor and behavioral inhibitory control in Parkinson's disease patients with levodopa-induced dyskinesias.
INTRODUCTION: Chronic dopamine replacement therapies in Parkinson's disease can induce side effects, such as levodopa-induced dyskinesias and impulse control disorders. A dysfunction of inhibitory brain networks has been related to both disorders; however, there is no clear behavioral evidence supporting this hypothesis. We aimed to determine whether PDpatients with levodopa-induced dyskinesias show features of increased impulsivity in parallel with altered motor inhibition. METHODS: Two matched samples of Parkinson's diseasepatients with (n = 14) or without (n = 14) levodopa-induced dyskinesias and a control group (n = 10) participated in the study. All groups were evaluated by the Barratt Impulsiveness Scale-11 to assess impulsivity traits. Furthermore, participants performed a stop signal task to evaluate reactive-motor inhibition and a Go/NoGo task to evaluate proactive-inhibitory control. PDpatients were tested both in OFF and ON levodopa medication. RESULTS:Parkinson's diseasepatients with levodopa-induced dyskinesias showed higher impulsivity scores than PDpatients without levodopa-induced dyskinesias. Dyskineticpatients presented also delayed stop signal reaction times indicating a worse performance in reactive inhibition. The slowness in inhibiting a motor command correlated with the impulsiveness scores. Furthermore, in the dyskinetic group, a positive correlation was found between stop reaction times and the severity of involuntary movements. Under the effect of levodopa, all patients were faster but dyskineticpatients were significantly less accurate in proactive inhibition. CONCLUSION: Inhibitory control is compromised in dyskineticpatients in parallel with increased impulsivity, revealing an impairment of motor and behavioral inhibitory control in Parkinson's diseasepatients with levodopa-induced dyskinesias.
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