Investigating the brain mechanisms of externally cued sit-to-stand movement in Parkinson's disease

Research overview

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Background: One of the more challenging daily-life actions for a patient with Parkinson’s disease is standing from a sitting position. Parkinson’s patients are known to have difficulty with self-initiated movements and they benefit from external cues. However, brain processes underlying external cueing as an aid are still unknown. With mobile EEG, this can now be investigated in dynamic sit-to-stand movements. Objective: To identify cortical correlates of the mechanisms underlying auditory cued sit-to-stand movement in Parkinson’s disease. Methods: 22 Parkinson’s disease patients and 24 neurotypical participants performed self-initiated and externally cued sit-to-stand movements while cortical activity was recorded through 32-channel mobile EEG. Results: Overall impaired integration of sensory and motor information can be seen in the Parkinson’s disease patients exhibiting less modulation in the theta band during movement compared to neurotypical controls. How Parkinson’s patients utilise external cueing of the sit-to-stand movements can be seen in larger high beta power over sensorimotor brain areas compared to neurotypical controls, signalling sensory integration to support the maintenance of the motor output. This appears to involve the allocation of cognitive resources to update the motor plan, reflected in frontal theta power increases in the Parkinson’s patients when cued. Conclusion: These findings provide the first neural evidence for why and how cueing improves motor function in sit-to-stand movement in Parkinson’s disease. The Parkinson’s patients’ neural correlates indicate that cueing induces a greater activation of motor cortical areas supporting maintenance of a more stable motor output, but involves the allocation of cognitive resources to update the motor plan.

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