Hypokinesia and bradykinesia in Parkinson’s disease are consistent with reduced motor vigour, not an impaired capacity to generate and transmit neural drive to muscle

Abstract Hypokinesia and bradykinesia in Parkinson’s disease have been attributed to reduced motor vigour, an account that assumes the neural drive to muscle is intact but inappropriately scaled; an alternative is that generation of the drive is itself impaired. We recorded high-density surface EMG in 12 people with Parkinson’s disease treated with subthalamic deep brain stimulation and 10 age-matched controls. During ballistic isometric contractions to 10, 30 and 50% of maximum voluntary force, controls usually reached the target with a single burst of motor unit activity (1.41 ± 0.10 bursts), whereas patients used multiple smaller bursts (2.57 ± 0.26), increasing further when stimulation was switched off (2.90 ± 0.30) alongside worsening bradykinesia. Interestingly, the first burst at 30 and 50% was large enough to have achieved the 10 and 30% targets, indicating that patients could, but did not, generate appropriately sized neural drives. Motor unit discharge rate and variability during both ballistic and repetitive contractions did not differ between groups or stimulation conditions, indicating preserved mechanisms to generate and transmit neural drive to muscle. Because successive bursts are separated by delays, patients reached target forces ~ 230 ms later than controls. Slowness therefore reflects underscaled motor commands rather than deficient neural drive, consistent with the motor vigour hypothesis.