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Updated: Jan 6, 2026

Dynamic Digital Biomarkers of Motor and Cognitive Function in Parkinson's Disease
Published on: July 24, 2019
Motor segmentation: a key neuromuscular impairment in people with parkinson's disease
Rebecca J Daniels1, Christopher A Knight2
1Department of Kinesiology and Applied Physiology, University of Delaware, 100 Discovery Blvd , Newark, DE, 19713, USA. rdaniels@udel.edu.
Abstract:
Healthy adults (OA) achieve rapid isometric force production with a brief, high amplitude burst of neural excitation. In some people with Parkinson's disease (PwPD), transient reductions in neural excitation (motor segmentation) reduce rates of force development (RFD) and prolong contractions. Segmentation has strong relationships with time and rate-based measures of slowing in rapid contractions and is reliably measured from the second derivative of force (F"(t)). We sought more information about how segmentation affects neuromuscular control in PwPD. Aim 1 was to determine the prevalence of PwPD with segmentation (PDSeg). Aim 2 was to determine how force performance differs in PDSeg, PwPD without segmentation (PDNoSeg), and OA. Aim 3 was to quantify force segment durations. Fifty-seven PwPD ON medication and 22 OA performed rapid isometric finger abduction contractions to 20-60% of maximal voluntary contraction force. The median number of force segments to 90% of peak force were measured from F"(t) zero crossings. Additional outcomes included median times to peak force (tPF) and peak RFD (tRFD), and peak RFD (RFDpk). 68% of PwPD had segmentation (median segments ≥ 2, 95% CI [0.55 0.80]). PDSeg had slower tPF, tRFD and RFDpk than PDNoSeg and OA (all p ≤ 0.012, 0.38 ≤ r ≤ 0.85). PDNoSeg and OA did not have statistically different tPF, tRFD, or RFDpk (p > 0.05). PDSeg had consistent segment durations (coefficient of variation ≤ 25.5%) and shorter first segment durations compared to PDNoSeg and OA (p < 0.001, r ≥ 0.68), indicating PDSeg had reduced neuromuscular excitation prior to peak force. Segmentation identifies specific pathophysiology in neuromuscular control that exacerbates slowing in isometric force production.
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