Non-Invasive Brain Stimulation Unit, IRCCS Santa Lucia Foundation, Via Ardeatina, 306, 00179, Rome, Italy.
Department of System Medicine, University of Rome Tor Vergata, Via Montpellier, 1, 00133, Rome, Italy.
J Neurol. 2018 Sep;265(9):2088-2096. doi: 10.1007/s00415-018-8945-1. Epub 2018 Jul 6.
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.
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.
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.
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.
在帕金森病中，慢性多巴胺替代疗法可引起副作用，如左旋多巴诱导的运动障碍和冲动控制障碍。抑制性脑网络功能障碍与这两种疾病都有关；然而，没有明确的行为证据支持这一假说。我们旨在确定是否患有左旋多巴诱导的运动障碍的帕金森病患者是否表现出冲动性增加的特征，同时伴有运动抑制的改变。
两组帕金森病患者（伴有或不伴有左旋多巴诱导的运动障碍，每组 14 例）和对照组（10 例）参与了这项研究。所有组均通过巴瑞特冲动量表-11 评估冲动特质。此外，参与者还进行了停止信号任务来评估反应性运动抑制，以及 Go/NoGo 任务来评估主动性抑制控制。帕金森病患者在停用和启用左旋多巴药物时均接受测试。
患有左旋多巴诱导的运动障碍的帕金森病患者的冲动性评分高于没有左旋多巴诱导的运动障碍的帕金森病患者。运动障碍患者的停止信号反应时间也延迟，表明反应抑制能力较差。抑制运动指令的速度与冲动性评分相关。此外，在运动障碍组中，停止反应时间与不自主运动的严重程度呈正相关。在左旋多巴的作用下，所有患者的反应速度都加快，但运动障碍患者在主动性抑制方面的准确性显著降低。
运动障碍患者的抑制控制能力受损，同时冲动性增加，这揭示了帕金森病患者在患有左旋多巴诱导的运动障碍时，运动和行为抑制控制受损。
