Session Time: 1:15pm-2:45pm
Location: Hall 3FG
Objective: To investigate the relationship between slow wave activity (SWA) of non-rapid eye movement (NREM) sleep, which underlies adjustment of cortical excitability, and levodopa-induced dyskinesias (LIDs)
Background: The spectrum of clinical symptoms in Parkinson’s disease is susceptible to changes through the course of the disease. Levodopa therapy successfully controls motor symptoms for several years and then induces motor fluctuation and abnormal involuntary movements, i.e., levodopa-induced dyskinesias (LIDs) that have been associated with abnormal cortical plasticity
Methods: Thirty-six patients with different stages of Parkinson’s disease underwent whole-night video polysomnography high density EEG (vPSG-hdEEG), preceded by 1-week actigraphy. To represent the broad spectrum of the disease, patients were divided into three groups by disease stage-(i) de novo (DNV; n = 9), (ii) advanced (ADV; n = 13), and (iii) dyskinetic (DYS; n = 14)-and were compared to an age-matched control group (CTL; n = 12). The SWA-NREM content of the PSG-hdEEG was subdivided into 10 equal segments. The 2nd, 3rd, and 4th segments and the 7th, 8th, and 9th segments were designated as early and late sleep
Results: There was a negative correlation between both total sleep time (TST) and sleep efficiency (SE) and disease duration in all patients. Of note, slow wave sleep (SWS) and disease duration were positively correlated in the DNV and ADV groups and negatively correlated in the DYS group. TST and SE were negatively correlated with the levodopa-equivalent daily dose (LEDD) in all patients with motor fluctuations (ADV and DYS). SE and SWS were also negatively correlated with LEDD in the DYS group. There was a negative correlation between dyskinesia severity and the estimated TST (eTST) over the 1-week actigraphy recording. In the early sleep, control subjects showed a significant greater amount of SWA, diffused over the whole scalp, compared to Parkinson’s disease patients. All groups, except the DYS group, manifested a clear-cut SWA decrease between early and late sleep.
Conclusions: Our data underline a strong pathophysiological association between sleep and Parkinson’s disease. 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 LIDs
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To cite this abstract in AMA style:N. Amato, M. Manconi, J.C. Möller, S. Sarasso, P. Stanzione, C. Städler, A. Kaelin-Lang, S. Galati. Levodopa-induced dyskinesia in Parkinson’s disease: Sleep matters [abstract]. Mov Disord. 2018; 33 (suppl 2). https://www.mdsabstracts.org/abstract/levodopa-induced-dyskinesia-in-parkinsons-disease-sleep-matters/. Accessed December 2, 2023.
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