Objective: To evaluate the impact of chronic STN-DBS on sleep architecture and REM-related phenomena, and to identify subcortical signatures of sleep using synchronized local field potentials (LFPs).

Background: Sleep and circadian disturbances are prevalent and impacting non-motor features of Parkinson’s disease (PD), including altered sleep architecture and REM sleep behavior disorder (RBD) [1,2]. Subthalamic nucleus deep brain stimulation (STN-DBS) can influence sleep, but objective neurophysiological in vivo evidence remains limited [3].

Method: 38 PD patients undergoing bilateral STN-DBS were longitudinally recruited. Twenty patients completed pre- and post-surgery full-night video-polysomnography (vPSG) with synchronized STN-LFP recording 6 months post-surgery, under stable DBS settings and dopaminergic therapy. Sleep variables were assessed according to international guidelines [4]. LFP power spectral density were analysed across sleep stages, arousals, and REM motor phenomena.

Results: After STN-DBS, N3 sleep increased (T0: 20.3±10.3%; T2: 28.9±11.9%; p=0.017), with a corresponding reduction in N2 (p=0.039), while total sleep time, sleep efficiency, and fragmentation indices remained unchanged. Mean HR decreased during wake (p=0.003) and sleep (p=0.021). RSWA did not significantly change, whereas RBE were reduced (median 44 [16–78] vs.25 [18–52]; p=0.022). LFPs showed increased delta and theta power from wake to non-REM sleep (p<0.001) and marked beta suppression in N2–N3 (p<0.001) and beta peak reduction. Micro-arousals were associated with alpha and beta power increases (p=0.045 and p=0.022), with concurrent beta peak enhancement (p=0.003). During REM sleep, RSWA was characterized by higher alpha, beta, and gamma power with lower delta versus atonic REM (p=0.015), while RBD episodes further increased theta, beta, gamma, and total power (p=0.040).

Conclusion: Chronic STN-DBS selectively modulates sleep architecture and subcortical sleep-related electrophysiology. Synchronized vPSG–LFP recordings reveal reproducible biomarkers of sleep stages, arousals, and REM motor phenomena, supporting both real-world sleep monitoring and the future development of sleep-aware adaptive DBS [5].

References: [1] Chahine LM, Amara AW, Videnovic A. A systematic review of the literature on disorders of sleep and wakefulness in Parkinson’s disease from 2005 to 2015. Sleep Med Rev. 2017 Jun;35:33–50. doi: 10.1016/j.smrv.2016.08.001. Epub 2016 Aug 9. PMID: 27522554.
[2] Arnulf I, Bejjani BP, Garma L, Bonnet AM, Houeto JL, Damier P, et al. Improvement of sleep architecture in Parkinson’s disease with subthalamic nucleus stimulation. Neurology. 2000 Dec 12;55(11):1732–1734. doi: 10.1212/wnl.55.11.1732. PMID: 11113233.
[3] Thompson JA, Lanctin D, Ince NF, Abosch A. Sleep patterns in Parkinson’s disease: Direct recordings from the subthalamic nucleus. J Neurol Neurosurg Psychiatry. 2018 Jan;89(1):95–104. doi: 10.1136/jnnp-2017-316161. Epub 2017 Jul 27. PMID: 28751406.
[4] Cesari M, Heidbreder A, Videnovic A, et al. Video-polysomnography procedures for diagnosis of rapid eye movement sleep behavior disorder (RBD) and the identification of its prodromal stages: Guidelines from the International RBD Study Group. Sleep. 2022 Mar 9;45(3):zsab257. doi: 10.1093/sleep/zsab257. PMID: 34849790.
[5] Smyth C, Jain S, O’Callaghan C, et al. Adaptive deep brain stimulation for sleep stage targeting in Parkinson’s disease.
Brain Stimul. 2023 Sep–Oct;16(5):1292–1296. doi: 10.1016/j.brs.2023.08.004. Epub 2023 Aug 10. PMID: 37572221.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/modulation-and-subcortical-signatures-of-sleep-in-parkinsons-disease-under-chronic-stn-dbs-insights-from-synchronized-deep-brain-sensing-and-nocturnal-videopolysomnography/