Objective: This study aimed to assess phase-amplitude coupling (PAC) between two local field potential (LFPs) signals captured from both wide- and close-spaced contact pairs (i.e. LFP03 and LFP12) in the subthalamic nuclei (STN), before and after Levodopa administration in Parkinson’s disease (PD) patients.

Background: PAC reflects whether and how different frequency bands, spoken by different neuronal populations or basal ganglia networks, interact each other. Despite the correlation of β phase- high frequency (200-500Hz) amplitude coupling with PD symptoms [1-8], whether PAC changes are consistent with different electrodes geometry/disposition is still not clear. Yet, no studies have systematically characterized differences between close- and wide-spaced electrode pairs in the subthalamic nucleus.

Method: LFP12 and LFP03 were recorded from 20 PD patients. We evaluated phase-amplitude coupling between close- and wide spaced electrodes within STN.

Results: Before levodopa, LFP12 showed a strong β-HFO PAC, while after levodopa β-LFO coupling increased and β-HFO decreased in comparison to before levodopa. LFP03 also showed a marked β-HFO PAC before levodopa and after levodopa we found a decrease in β-HFO PAC in comparison to before levodopa condition. Moreover, we found PAC differing between LFP12 and LFP03. Either before and after levodopa LFP03 had lower level of β-LFO and β-HFO coupling than LFP12.

Conclusion: This study discloses the differences in PAC between LFP12 and LFP03 and reveals that levodopa increases β-LFO (15-45 Hz) coupling. low-β-low-γ PAC is a normal mechanism by which a pro-kinetic rhythm is controlled in the GPi [8], possibly accounting the increased β-LFO coupling found in STN following dopaminergic stimulation. This finding may have important implications for adaptive DBS (aDBS) in PD possibly suggesting novel electrophysiological control signals.

References: References [1] B. C. van Wijk et al., “Subthalamic nucleus phase–amplitude coupling correlates with motor impairment in Parkinson’s disease,” Clinical Neurophysiology, vol. 127, no. 4, pp. 2010-2019, 2016. [2] C. De Hemptinne et al., “Exaggerated phase–amplitude coupling in the primary motor cortex in Parkinson disease,” Proceedings of the National Academy of Sciences, p. 201214546, 2013. [3] J. López-Azcárate et al., “Coupling between beta and high-frequency activity in the human subthalamic nucleus may be a pathophysiological mechanism in Parkinson’s disease,” Journal of Neuroscience, vol. 30, no. 19, pp. 6667-6677, 2010. [4] J.-S. Brittain and P. Brown, “Oscillations and the basal ganglia: motor control and beyond,” Neuroimage, vol. 85, pp. 637-647, 2014. [5] A. A. Kühn, A. Kupsch, G. H. Schneider, and P. Brown, “Reduction in subthalamic 8–35 Hz oscillatory activity correlates with clinical improvement in Parkinson’s disease,” European Journal of Neuroscience, vol. 23, no. 7, pp. 1956-1960, 2006. [6] A. A. Kuhn et al., “Pathological synchronisation in the subthalamic nucleus of patients with Parkinson’s disease relates to both bradykinesia and rigidity,” Exp Neurol, vol. 215, no. 2, pp. 380-7, Feb 2009, doi: 10.1016/j.expneurol.2008.11.008. [7] M. Weinberger, W. D. Hutchison, and J. O. Dostrovsky, “Pathological subthalamic nucleus oscillations in PD: can they be the cause of bradykinesia and akinesia?,” Exp Neurol, vol. 219, no. 1, pp. 58-61, Sep 2009, doi: 10.1016/j.expneurol.2009.05.014. [8] C. Tsiokos, M. Malekmohammadi, N. AuYong, and N. Pouratian, “Pallidal low β-low γ phase-amplitude coupling inversely correlates with Parkinson disease symptoms,” Clinical Neurophysiology, vol. 128, no. 11, pp. 2165-2178, 2017.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/inter-electrode-distance-influences-the-phase-amplitude-coupling-pac-of-bipolar-subthalamic-local-field-potentials-recordings-in-parkinsons-disease/