Basal Ganglia Activity Associated With REM Sleep Behavior Disorder in Parkinson Disease


In a recent study assessing basal ganglia activity during REM sleep, results revealed that elevated beta power may be correlated with the severity of REM sleep behavior disorder in Parkinson disease.

Jian-Guo Zhang, MD, PhD  (Credit: Capital Medical University)

Jian-Guo Zhang, MD, PhD

(Credit: Capital Medical University)

Newly published in the Journal of Neurology, Neurosurgery and Psychiatry, findings showed that basal ganglia activities are associated with if not directly contribute to the occurrence of REM sleep behavior disorder (RBD) in Parkinson disease (PD). Investigators concluded that these results expand the understanding of the role of basal ganglia in RBD and may lead to enhanced therapies for RBD by interrupting the basal ganglia-muscular communication during REM sleep in PD.1

In the study, investigators observed that patients with PD who received deep brain stimulation targeting the globus pallidus internus (GPi- DBS, n = 11) or subthalamic nucleus (STN-DBS, n = 17) had significantly higher proportions of REM sleep without atonia (RSWA) episodes than patients with dystonia who received GPi-DBS (n = 12)(27.0 [±19.0%] vs 7.9 [±5.8%]; P =3.55×10−4, respectively). In basal ganglia spectra, beta power revealed significantly higher in loss of atonia episodes in patients with PD, both for the GPi (P = .004) and STN (P = 3.81×10−5) PD groups but not in patients with dystonia.

Top Clinical Takeaways

  • Basal ganglia beta power elevation during REM sleep shows an association with the severity of REM sleep behavior disorder (RBD) in patients with Parkinson disease (PD).
  • This study provides insights into the distinct basal ganglia oscillatory patterns in PD-related RBD compared to dystonia, suggesting a specific role in PD pathology.
  • Potential therapeutic interventions targeting basal ganglia-muscular communication during REM sleep could offer new avenues for treating RBD in patients with PD.

In parallel with whole-night video polysomnography, investigators recorded local field potentials from 2 major basal ganglia structures, the GPi and STN, in 2 cohorts of patients with PD who had varied severity of RBD. Conducted by senior author Jian-Guo Zhang, MD, PhD, director of department of stereotactic and functional neurosurgery at Beijing Tiantan Hospital & Beijing Neurosurgery Institute, Capital Medical University, and colleagues, basal ganglia oscillatory patterns during RBD and REM sleep without atonia were evaluated and compared with another age-matched cohort of patients with dystonia who served as the controls.

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Authors also identified a significant positive correlation between average basal ganglia beta power and integrated electromyogram (EMG) for both the GPi (P = .003) and STN (P = 0.010) in patients with PD but not in those with dystonia. A time-lagged cross correlation revealed that the average time-lagged connectivity peaked at around −200 ms favoring basal ganglia beta leading EMGs in both the PD groups. Investigators observed no correlation between REM sleep beta power and the RBD-Screening Questionnaire (RBDSQ) score for both the GPi (ρ = .200, P = .554) and STN (ρ = −0.026, P = .921) groups. Additionally, the integrated EMG in REM sleep did not correlate with the RBD-Screening Questionnaire (ρ = 0.232, P = 0.235) but authors reported that in patients with PD who had a clinical diagnosis of RBD, the magnitude of basal ganglia beta-EMG connectivity as assessed using envelope correlation was significantly higher than in patients without RBD (P = .017).

In terms of limitations, 2 of the PD patient populations included in the study might have had different disease profiles in severity, which potentially impaired the comparability between the groups. Investigators also did not exclude patients with PD based on their age at onset and noted that the 4 patients with young-onset PD included in the analysis could have had different clinical features and basal ganglia electrophysiological profiles from late-onset PD.2 Additionally, authors noted that they did not conduct event-related analysis on the dream-enactment event because of the limited number of events captured and they only used the chin EMG to quantify the loss of REM atonia.

1. Yin Z, Yuan T, Yang A, et al. Contribution of basal ganglia activity to REM sleep disorder in Parkinson's disease. J Neurol Neurosurg Psychiatry. Published online April 19, 2024. doi:10.1136/jnnp-2023-332014
2. Wu D, Zhao B, Xie H, et al. Profiling the low-beta characteristics of the subthalamic nucleus in early- and late-onset Parkinson's disease. Front Aging Neurosci. 2023;15:1114466. Published 2023 Feb 16. doi:10.3389/fnagi.2023.1114466
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