ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020
Direct Activation of Primary Motor Cortex during Subthalamic But Not Pallidal Deep Brain Stimulation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- Acute unilateral DBS of the basolateral amygdala does not affect motricity, anxiety-like behavior, or fear memory consolidation in rats.Experimental brain research · 2026Article
- Nonlinear dynamics and multiscale mechanisms of deep brain stimulation.Frontiers in neuroscience · 2026Review
- Differential synaptic depression mediates the therapeutic effect of deep brain stimulation.Nature neuroscience · 2025Article
- Deep Brain Stimulation: Mechanisms, Cost-Effectiveness, and Precision Applications Across Neurology and Psychiatry.Biomedicines · 2025Review
- Electrophysiological signatures predict the therapeutic window of deep brain stimulation electrode contacts.NPJ digital medicine · 2025Article
- Parkinsonism disrupts the balance between excitatory and inhibitory activity within the primary motor cortex during movement.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Subthalamic Nucleus Oscillatory Characteristics in Meige, Cervical Dystonia and Generalized Dystonia.Annals of clinical and translational neurology · 2025Article
- The simulation and experimental validation of a novel noninvasive multi-target electrical stimulation method.Scientific reports · 2025Article
- Neural pathway activation in the subthalamic region depends on stimulation polarity.Brain communications · 2025Article
- Impairment of neuronal activity in the dorsolateral prefrontal cortex occurs early in parkinsonism.Frontiers in neuroscience · 2025Article
- A framework for translational therapy development in deep brain stimulation.NPJ Parkinson's disease · 2024Review
- Clinical and Brain Morphometry Predictors of Deep Brain Stimulation Outcome in Parkinson's Disease.Brain topography · 2024Article
- Dysfunction of motor cortices in Parkinson's disease.Cerebral cortex (New York, N.Y. : 1991) · 2024Review
- A longitudinal electrophysiological and behavior dataset for PD rat in response to deep brain stimulation.Scientific data · 2024Article
- Quantitative analysis of noninvasive deep temporal interference stimulation: A simulation and experimental study.Heliyon · 2024Article
- Neural signatures of indirect pathway activity during subthalamic stimulation in Parkinson's disease.Nature communications · 2024Article
- Case report: Improvement of gait with adaptive deep brain stimulation in a patient with Parkinson's disease.Frontiers in bioengineering and biotechnology · 2024Article
- Neuronal and synaptic adaptations underlying the benefits of deep brain stimulation for Parkinson's disease.Translational neurodegeneration · 2023Review
- Neurophysiological mechanisms of deep brain stimulation across spatiotemporal resolutions.Brain : a journal of neurology · 2023Review
- Substantia Nigra Pars Reticulata Projections to the Pedunculopontine Nucleus Modulate Dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2023Article
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6 authors.
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Abstract
Deep brain stimulation (DBS) of the subthalamic nucleus (STN) and globus pallidus internus (GPi) is an effective treatment for parkinsonian motor signs. Though its therapeutic mechanisms remain unclear, it has been suggested that antidromic activation of the primary motor cortex (M1) plays a significant role in mediating its therapeutic effects. This study tested the hypothesis that antidromic activation of M1 is a prominent feature underlying the therapeutic effect of STN and GPi DBS. Single-unit activity in M1 was recorded using high-density microelectrode arrays in two parkinsonian nonhuman primates each implanted with DBS leads targeting the STN and GPi. Stimulation in each DBS target had similar therapeutic effects, however, antidromic activation of M1 was only observed during STN DBS. Although both animals undergoing STN DBS had similar beneficial effects, the proportion of antidromic-classified cells in each differed, 30 versus 6%. Over 4 h of continuous STN DBS, antidromic activation became less robust, whereas therapeutic benefits were maintained. Although antidromic activation waned over time, synchronization of spontaneous spiking in M1 was significantly reduced throughout the 4 h. Although we cannot discount the potential therapeutic role of antidromic M1 activation at least in the acute phase of STN DBS, the difference in observed antidromic activation between animals, and target sites, raise questions about its hypothesized role as the primary mechanism underlying the therapeutic effect of DBS. These results lend further support that reductions in synchronization at the level of M1 are an important factor in the therapeutic effects of DBS.
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