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Published on: May 31, 2016
Subthalamic Nucleus Deep Brain Stimulation Enhanced Long-Latency Reflex II in Parkinson's Disease Through Rapid
Kai-Hsiang Stanley Chen1, Yih-Chih Jacinta Kuo2, Chang-Yu Jeng1
1Department of Neurology, National Taiwan University Hospital Hsinchu Branch, Hsinchu, Taiwan.
Summary
Long-latency reflex II (LLR II) is modulated by effective subthalamic nucleus deep brain stimulation (STN-DBS) parameters in Parkinson's disease. LLR II serves as a biomarker for STN-DBS sensorimotor circuit modulation, independent of medication.
Area of Science:
- Neuroscience
- Biomarkers
- Movement Disorders
Background:
- The long-latency reflex II (LLR II), a transcortical reflex, may indicate cortical-subcortical excitability.
- Its potential as a biomarker for optimizing subthalamic nucleus deep brain stimulation (STN-DBS) in Parkinson's disease (PD) is not well-established.
Purpose of the Study:
- To investigate if STN-DBS parameters and dopaminergic medication modulate LLR II responses.
- To explore mechanisms of STN-DBS-related motor improvement in Parkinson's disease.
Main Methods:
- Assessed LLR II in 13 PD patients with STN-DBS using median nerve stimulation and electromyography (EMG).
- Varied stimulation intensity, contacts, and frequencies (60 Hz, 130 Hz, energy-matched).
- Tested single DBS pulse effects and compared LLR II in 16 PD patients with/without medication.
Main Results:
- LLR II was significantly higher with effective STN-DBS intensity, contacts, and frequency compared to DBS-off.
- A single DBS pulse increased LLR II at a specific timing (T2) relative to the N20 response.
- No significant difference in LLR II was observed between medication-on and medication-off states.
Conclusions:
- Clinically effective STN-DBS parameters modulate LLR II, suggesting its role as a biomarker for sensorimotor circuit changes.
- LLR II modulation by STN-DBS is independent of dopaminergic medication.
- Findings suggest the hyperdirect pathway may be involved in STN-DBS-related motor improvements.
