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Objective: The spectrum of clinical symptom changes during the course of Parkinson disease (PD). Levodopa therapy, while offering remarkable control of classical motor symptoms, causes abnormal involuntary movements as the disease progresses. This levodopa-induced dyskinesia (LID) has been associated with abnormal cortical plasticity. Because slow wave activity (SWA) of nonrapid eye movement (NREM) sleep underlies adjustment of cortical excitability, we sought to elucidate the relationship between this physiological process and LID. Methods: Thirty-six patients at different stages of PD underwent whole-night video polysomnography-high-density electroencephalography (vPSG-hdEEG), preceded by 1 week of actigraphy. To represent the broad spectrum of the disease, patients were divided into 3 groups by disease stage-(1) de novo (n = 9), (2) advanced (n = 13), and (3) dyskinetic (DYS; n = 14)-were compared to an age-matched control group (n = 12). The SWA-NREM content of the vPSG-hdEEG was then temporally divided into 10 equal parts, from T1 to T10, and power and source analyses were performed. T2-T3-T4 were considered early sleep and were compared to T7-T8-T9, representing late sleep. Results: We found that all groups, except the DYS group, manifested a clear-cut SWA decrease between early and late sleep. Interpretation: Our data demonstrate a strong pathophysiological association between sleep and PD. Given that SWA may be a surrogate for synaptic strength, our data suggest that DYS patients do not have adequate synaptic downscaling. Further analysis is needed to determine the effect of drugs that can enhance cortical SWA in LID.

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Study Objectives Sleep-related slow-wave activity (SWA) has been recognized as a marker of synaptic plasticity. In children affected by attention deficit hyperactivity disorder (ADHD), SWA is mainly located in the central rather than frontal regions, reflecting a maturational delay. A detailed subjective and objective sleep investigation, including a full night video-polysomnography (PSG-HD-EEG), was performed on 30 consecutive drug naïve outpatients with a diagnosis of ADHD. They received a diagnosis of sleep disorders in 29/30 cases, and most of them had a past history of sleep problems. They had a higher apnea–hypopnea index at PSG, and slept less than 9 hr at actigraphy. We aimed to describe the SWA behavior in the same group of children with ADHD. Materials and Methods The full-night PSG-HD EEG of children with ADHD was compared with the one of the 25 healthy controls. The scalp SWA mapping, the decrease of SWA during the night, and the EEG source of SWA were analyzed. Results At scalp topography, the focus of SWA was observed over the centro–parietal–occipital regions in participants with ADHD (p < 0.01), which remained significant in the subgroups divided between subgroups according to the sleep diagnosis (p < 0.01). The physiological decrease in SWA was more evident in control participants. The source analysis revealed a greater delta power over the posterior cingulate in participants with ADHD (p < 0.01). Conclusions Our results confirm static and dynamic changes in SWA behavior in children with ADHD, which may reflect a maturational delay occurring at a vulnerable age, as a consequence of chronic sleep deprivation.

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