Objective: To investigate latencies and distribution of evoked cortical potentials (ECPs) based on high-resolution electroencephalography (EEG) recordings and neuroimaging analyses in subthalamic nucleus deep brain stimulation (STN-DBS).

Background: STN-DBS is a well-established treatment for people with Parkinson’s disease (PwP). Due to increasing complexity of DBS programming, electrophysiological biomarkers to predict clinical improvement are needed. Low-frequency DBS pulses lead to ECPs in various cortical locations at different latencies [1]. Specifically, short-latency ECPs have been associated with antidromic activation of the hyperdirect pathway (HDP) from the cortex to the STN [2]. Activation of the HDP has been linked to clinical improvement in PwP, thus short-latency ECPs might serve as a promising biomarker for clinical efficacy [3-5]. Contrarily, long-latency ECPs have been associated with nigral stimulation and earlier side effects [4,5].

Method: So far, 18 PwP were enrolled in the study. We performed 64-channel EEG-recordings at a sampling rate of 50 kHz during low-frequency monopolar contact stimulation (10 Hz, 60 µs) in the STN for each contact of a directional lead (n = 33 hemispheres, n = 264 stimulation locations) with three different amplitudes (0.5, 2.0, 4.0 mA). Based on postoperative electrode reconstruction, origins of ECPs were mapped into the patient’s individual space and transformed into MNI space. Voxel- and fiber-wise probabilistic mapping were performed to identify anatomical regions and connections associated with the occurrence and propagation of different ECPs.

Results: Our preliminary results indicate that ECPs of different latencies originate from different regions within the STN area.

Conclusion: The occurrence of different DBS evoked cortical potentials offers insight into which part of the STN area was stimulated. Thus, the use of ECPs as DBS biomarkers should be explored further.

References: 1. Dale J, Schmidt SL, Maitchell K, et al. Evoked potentials generated by deep brain stimulation for Parkinson’s disease. Brain Stimul. 2022 Sep-Oct;15(5):1040-1047. doi: 10.1016/j.brs.2022.07.048.
2. Miocinovic S, de Hemptinne C, Chen W, et al. Cortical Potentials Evoked by Subthalamic Stimulation Demonstrate a Short Latency Hyperdirect Pathway in Humans. J Neurosci. 2018 Oct 24;38(43):9129-9141. doi: 10.1523/JNEUROSCI.1327-18.2018.
3. Chen Y, Ge S, Li Y, et. al. Role of the Cortico-Subthalamic Hyperdirect Pathway in Deep Brain Stimulation for the Treatment of Parkinson Disease: A Diffusion Tensor Imaging Study. World Neurosurg. 2018 Jun:114:e1079-e1085. doi: 10.1016/j.wneu.2018.03.149.
4. Peeters J, van Bogaert T, Boogers A, et al. EEG-based biomarkers for optimizing deep brain stimulation contact configuration in Parkinson’s disease. Front Neurosci. 2023 Oct 5:17:1275728. doi: 10.3389/fnins.2023.1275728.
5. Peeters J, Boogers A, Van Bogaert T, et. al. Towards biomarker-based optimization of deep brain stimulation in Parkinson’s disease patients. Front Neurosci. 2023 Jan 11:16:1091781.doi: 10.3389/fnins.2022.1091781.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/pooling-event-related-potentials-with-anatomy-and-lead-localization-in-subthalamic-deep-brain-stimulation/