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Author Notes:

Amy W. Amara, MD, PhD, University of Colorado, Anschutz Medical Campus, 12631 E 17th Avenue, Mail Stop B185, Aurora, CO 80045, USA. E-mail: amy.amara@cuanschutz.edu

Dr. Adeel Memon received funding from NINDS R25NS079188 Training Fellowship; Dr. Kimberly Wood received funding from NIH: T32 HD071866 Training Fellowship; Dr. Amy W Amara received funding from NIH (K23NS080912 and R01HD100670). Dr. Svjetlana Miocinovic received funding from NIH (K23NS097576). We are grateful to the research participants, without whom this study would not have been possible.

The authors have no conflict of interest to report.

Subject:

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • Parkinson's disease
  • quantitative sleep EEG
  • non-rapid eye movement sleep
  • slow waves
  • sleep spindles
  • phase-amplitude
  • coupling
  • rapid eye movement sleep
  • EYE-MOVEMENT SLEEP
  • SLOW WAVES
  • REM-SLEEP
  • SPINDLES
  • EEG
  • OSCILLATION
  • HIPPOCAMPAL
  • ATROPHY
  • ALPHA

Quantitative Sleep Electroencephalogram in Parkinson's Disease: A Case-Control Study

Tools:

Journal Title:

JOURNAL OF PARKINSONS DISEASE

Volume:

Volume 13, Number 3

Publisher:

, Pages 351-365

Type of Work:

Article | Final Publisher PDF

Abstract:

BACKGROUND: Sleep disorders are common in Parkinson's disease (PD) and include alterations in sleep-related EEG oscillations. OBJECTIVE: This case-control study tested the hypothesis that patients with PD would have a lower density of Scalp-Slow Wave (SW) oscillations and higher slow-to-fast frequencies ratio in rapid eye movement (REM) sleep than non-PD controls. Other sleep-related quantitative EEG (qEEG) features were also examined, including SW morphology, sleep spindles, and Scalp-SW spindle phase-amplitude coupling. METHODS: Polysomnography (PSG)-derived sleep EEG was compared between PD participants (n = 56) and non-PD controls (n = 30). Following artifact rejection, sleep qEEG analysis was performed in frontal and central leads. Measures included SW density and morphological features of SW and sleep spindles, SW-spindle phase-amplitude coupling, and spectral power analysis in Non-REM (NREM) and REM. Differences in qEEG features between PD and non-PD controls were compared using two-tailed Welch's t-tests, and correction for multiple comparisons was performed per the Benjamini-Hochberg method. RESULTS: SW density was lower in PD than in non-PD controls (F = 13.5, p' = 0.003). The PD group also exhibited higher ratio of slow REM EEG frequencies (F = 4.23, p' = 0.013), higher slow spindle peak frequency (F = 24.7, p' < 0.002), and greater SW-spindle coupling angle distribution non-uniformity (strength) (F = 7.30, p' = 0.034). CONCLUSION: This study comprehensively evaluates sleep qEEG including SW-spindle phase amplitude coupling in PD compared to non-PD controls. These findings provide novel insights into how neurodegenerative disease disrupts electrophysiological sleep rhythms. Considering the role of sleep oscillatory activity on neural plasticity, future studies should investigate the influence of these qEEG markers on cognition in PD.

Copyright information:

© 2023 – The authors. Published by IOS Press

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (https://creativecommons.org/licenses/by-nc/4.0/).
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