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Updated: Apr 23, 2026

Controlling Parkinson's Disease With Adaptive Deep Brain Stimulation
Published on: July 16, 2014
GABA-mediated changes in inter-hemispheric beta frequency activity in early-stage Parkinson's disease
S D Hall1, E J Prokic2, C J McAllister2
1Aston Brain Centre, Aston University, Birmingham, West Midlands, UK; School of Psychology, Plymouth University, Devon, UK.
Low-dose zolpidem reduces beta power in Parkinson's disease (PD) motor cortex, improving symptoms. This GABAA receptor modulator rebalances brain activity between hemispheres, correlating with reduced motor impairment in PD patients.
Area of Science:
- Neuroscience
- Neurology
- Pharmacology
Background:
- Elevated beta power in motor networks is linked to Parkinson's disease (PD) symptoms.
- GABAA receptor modulation has shown potential for symptomatic improvement in PD.
Purpose of the Study:
- To investigate the effects of low-dose zolpidem on neuronal network activity in PD patients.
- To characterize changes in beta power and oscillations in the motor cortex following zolpidem administration.
Main Methods:
- Whole-head magnetoencephalography (MEG) was used to record brain activity in PD patients and controls.
- A beamforming 'virtual electrode' approach reconstructed oscillatory power in the primary motor cortex (M1).
- Recordings were taken before and after administration of low-dose zolpidem (0.05mg/kg).
Main Results:
- PD patients exhibited greater beta power in the contralateral M1 compared to the ipsilateral M1.
- Zolpidem significantly reduced contralateral M1 beta power and increased ipsilateral M1 beta power, balancing the hemispheric ratio.
- The changes in hemispheric beta power ratio strongly correlated with improvements on the Unified Parkinson's Disease Rating Scale (UPDRS).
Conclusions:
- Low-dose zolpidem effectively rebalances M1 network oscillations between hemispheres in PD patients.
- These neurophysiological changes induced by zolpidem are associated with symptomatic relief in Parkinson's disease.
- Zolpidem's modulation of GABAA receptors offers a potential therapeutic avenue for PD.
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