ArticleJournal of clinical neurology (Seoul, Korea)2023
Temporal Investigations of the Changes in Presynaptic Inhibition Associated With Subthalamic Nucleus-Deep-Brain Stimulation.
Article in Journal of clinical neurology (Seoul, Korea), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Motoric cognitive risk syndrome: A review of fall risk assessment and management strategies.World journal of psychiatry · 2025Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThere are controversies regarding the role of presynaptic inhibition (PSI) in the mechanisms underlying the efficacy of deep-brain stimulation (DBS) in Parkinson's disease (PD). We sought to determine the involvement of PSI in DBS-related mechanisms and clinical correlates.
methodsWe enrolled PD subjects who had received subthalamic nucleus DBS (STN-DBS) therapy and had been admitted to our clinic between January 2022 and March 2022. The tibial H-reflex was studied bilaterally during the medication-off state, and all tests were repeated 10 and 20 minutes after the simulation was turned off. Simultaneous evaluations based on the Movement-Disorder-Society-sponsored revision of the Unified Parkinson's Disease Rating Scale part III (MDS-UPDRS-III) were performed in all of the patients.
resultsUltimately we enrolled 18 patients aged 58.7±9.3 years (mean±standard deviation, 10 females). Fifty percent of the patients showed a decrease in the MDS-UPDRS-III score of more than 60% during the stimulation-on period. Comparative analyses of the repeated measurements made according to the stimulation status revealed significant differences only in the left H-reflex/M-response amplitude ratio (H/M ratio). However, no difference in the left H/M ratio was found in the subgroup of patients with a prominent clinical response to stimulation (
conclusionsWe found evidence of PSI recovery on the less-affected side of our PD subjects associated with STN-DBS. We hypothesize that the involvement of this spinal pathway and its contribution to the mechanisms of DBS differ between individuals based on the severity of the disease and which brainstem regions and descending tracts are involved.
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