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Bradykinesia and Its Progression Are Related to Interhemispheric Beta Coherence
Kevin B Wilkins1, Yasmine M Kehnemouyi1,2, Matthew N Petrucci1,2
1Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, United States.
Increased brain synchrony, specifically in the subthalamic nucleus (STN), correlates with worsening bradykinesia in Parkinson disease (PD) patients undergoing deep brain stimulation (DBS). This suggests bilateral network dysfunction contributes to PD motor symptoms.
Area of Science:
- Neuroscience
- Neurology
- Biomedical Engineering
Background:
- Bradykinesia is a primary motor symptom of Parkinson disease (PD).
- The precise neural mechanisms underlying bradykinesia, especially in relation to subthalamic nucleus (STN) deep brain stimulation (DBS), remain incompletely understood.
- Long-term STN-DBS effects on bradykinesia require further investigation into local and network-level brain dynamics.
Purpose of the Study:
- To investigate the neural correlates of bradykinesia changes after long-term STN-DBS.
- To determine if local STN beta-band (13-30 Hz) activity or broader bilateral network dysfunction is associated with bradykinesia progression.
- To explore the relationship between STN beta-band dynamics and bradykinesia in PD patients over time.
Main Methods:
- A longitudinal study involving 21 PD patients with implanted STN sensing neurostimulators.
- Participants underwent periodic medication withdrawal and DBS 'off' periods over an average of 3 years.
- Bradykinesia was assessed quantitatively using a wrist-flexion extension task, with simultaneous local field potential recordings from the STN to analyze beta power, burst duration, and interhemispheric coherence.
Main Results:
- Higher interhemispheric STN beta coherence, not local beta power or burst duration, was significantly linked to more severe bradykinesia.
- Over time, bradykinesia worsened, and interhemispheric STN-STN beta coherence increased, while local beta power and burst duration remained stable.
- The progression of bradykinesia correlated with increased interhemispheric beta synchrony.
Conclusions:
- Interhemispheric STN beta synchrony serves as a neural marker for the progression of bradykinesia in PD patients receiving chronic STN-DBS.
- These findings suggest that pathological bilateral network dysfunction, characterized by increased interhemispheric synchrony, may contribute to bradykinesia in Parkinson disease.
- Targeting bilateral network dynamics could offer new therapeutic strategies for managing bradykinesia in PD.
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