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Study Design: This is a cross-sectional descriptive study., Objectives: To quantify differences in hand muscle morphology between persons with cervical spinal cord injury (SCI) and uninjured adults., Setting: The study was performed at the Guangdong Work Injury Rehabilitation Hospital., Methods: We quantified hand muscle cross-sectional area (CSA), thickness, and echo intensity (EI) in 18 persons with subacute to chronic SCI and 23 controls using ultrasound imaging., Results: Mean SCI abductor pollicis brevis (APB), abductor digiti minimi (ADM), and first dorsal interosseous (FDI) CSA were ~26%, 43%, and 37% smaller than the control means, the deficit in the APB being less than the ADM (P < 0.05). Muscle thickness was also smaller after SCI, but deficits in ADM (31%) and FDI (20%) thickness were less than the CSA deficits (P < 0.05). In five SCI persons, APB CSA and/or opponens pollicis (OP) thickness were normal despite complete motor paralysis. Mean longitudinal image EI was 40% higher in the OP and 15% higher in the flexor pollicis brevis (FPB) after SCI (P < 0.05), suggesting denervation-induced infiltration of fat and fibrous tissues. OP EI was related to OP thickness (r = -0.6, P = 0.007, n = 18). Mean axial image EI was 10% higher in the APB and ADM after SCI (P < 0.05). There were no significant correlations between muscle morphological properties and clinical features in the SCI participants., Conclusion: Our results indicate significant SCI atrophy and elevated EI that are muscle dependent., (© 2021. The Author(s), under exclusive licence to International Spinal Cord Society.)

After human spinal cord injury (SCI), motoneuron recruitment and firing rate during voluntary and involuntary contractions may be altered by changes in motoneuron excitability. Our aim was to compare F waves in single thenar motor units paralyzed by cervical SCI to those in uninjured controls because at the single-unit level F waves primarily reflect the intrinsic properties of the motoneuron and its initial segment. With intraneural motor axon stimulation, F waves were evident in all 4 participants with C 4 -level SCI, absent in 8 with C 5 or C 6 injury, and present in 6 of 12 Uninjured participants (P < 0.001). The percentage of units that generated F waves differed across groups (C 4 : 30%, C 5 or C 6 : 0%, Uninjured: 16%; P < 0.001). Mean (±SD) proximal axon conduction velocity was slower after C 4 SCI [64 ± 4 m/s (n = 6 units), Uninjured: 73 ± 8 m/s (n = 7 units); P = 0.037]. Mean distal axon conduction velocity differed by group [C 4 : 40 ± 8 m/s (n = 20 units), C 5 or C 6 : 49 ± 9 m/s (n = 28), Uninjured: 60 ± 7 m/s (n = 45); P < 0.001]. Motor unit properties (EMG amplitude, twitch force) only differed after SCI (P ≤ 0.004), not by injury level. Motor units with F waves had distal conduction velocities, M-wave amplitudes, and twitch forces that spanned the respective group range, indicating that units with heterogeneous properties produced F waves. Recording unitary F waves has shown that thenar motoneurons closer to the SCI (C 5 or C 6 ) have reduced excitability whereas those further away (C 4 ) have increased excitability, which may exacerbate muscle spasms. This difference in motoneuron excitability may be related to the extent of membrane depolarization following SCI., New & Noteworthy: Unitary F waves were common in paralyzed thenar muscles of people who had a chronic spinal cord injury (SCI) at the C 4 level compared with uninjured people, but F waves did not occur in people that had SCI at the C 5 or C 6 level. These results highlight that intrinsic motoneuron excitability depends, in part, on how close the motoneurons are to the site of the spinal injury, which could alter the generation and strength of voluntary and involuntary muscle contractions., (Copyright © 2017 the American Physiological Society.)

Spinal cord injury (SCI) results in widespread variation in muscle function. Review of motor unit data shows that changes in the amount and balance of excitatory and inhibitory inputs after SCI alter management of motoneurons. Not only are units recruited up to higher than usual relative forces when SCI leaves few units under voluntary control, the force contribution from recruitment increases due to elevation of twitch/tetanic force ratios. Force gradation and precision are also coarser with reduced unit numbers. Maximal unit firing rates are low in hand muscles, limiting voluntary strength, but are low, normal or high in limb muscles. Unit firing rates during spasms can exceed voluntary rates, emphasizing that deficits in descending drive limit force production. SCI also changes muscle properties. Motor unit weakness and fatigability seem universal across muscles and species, increasing the muscle weakness that arises from paralysis of units, motoneuron death and sensory impairment. Motor axon conduction velocity decreases after human SCI. Muscle contractile speed is also reduced, which lowers the stimulation frequencies needed to grade force when paralysed muscles are activated with patterned electrical stimulation. This slowing does not necessarily occur in hind limb muscles after cord transection in cats and rats. The nature, duration and level of SCI underlie some of these species differences, as do variations in muscle function, daily usage, tract control and fibre-type composition. Exploring this diversity is important to promote recovery of the hand, bowel, bladder and locomotor function most wanted by people with SCI., (© 2013 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.)

Baclofen, a gamma-aminobutyric acid receptor(B) agonist, is used to reduce symptoms of spasticity (hyperreflexia, increases in muscle tone, involuntary muscle activity), but the long-term effects of sustained baclofen use on skeletal muscle properties are unclear. The aim of our study was to evaluate whether baclofen use and paralysis due to cervical spinal cord injury change the contractile properties of human thenar motor units more than paralysis alone. Evoked electromyographic activity and force were recorded in response to intraneural stimulation of single motor axons to thenar motor units. Data from three groups of motor units were compared: 23 paralysed units from spinal cord injured subjects who take baclofen and have done so for a median of 7 years, 25 paralysed units from spinal cord injured subjects who do not take baclofen (median: 10 years) and 45 units from uninjured control subjects. Paralysed motor unit properties were independent of injury duration and level. With paralysis and baclofen, the median motor unit tetanic forces were significantly weaker, twitch half-relaxation times longer and half maximal forces reached at lower frequencies than for units from uninjured subjects. The median values for these same parameters after paralysis alone were comparable to control data. Axon conduction velocities differed across groups and were slowest for paralysed units from subjects who were not taking baclofen and fastest for units from the uninjured. Greater motor unit weakness with long-term baclofen use and paralysis will make the whole muscle weaker and more fatigable. Significantly more paralysed motor units need to be excited during patterned electrical stimulation to produce any given force over time. The short-term benefits of baclofen on spasticity (e.g. management of muscle spasms that may otherwise hinder movement or social interactions) therefore have to be considered in relation to its possible long-term effects on muscle rehabilitation. Restoring the strength and speed of paralysed muscles to pre-injury levels may require more extensive therapy when baclofen is used chronically.

Little is known about how human motor units respond to chronic paralysis. Our aim was to record surface electromyographic (EMG) signals, twitch forces, and tetanic forces from paralyzed motor units in the thenar muscles of individuals (n = 12) with chronic (1.5-19 yr) cervical spinal cord injury (SCI). Each motor unit was activated by intraneural stimulation of its motor axon using single pulses and trains of pulses at frequencies between 5 and 100 Hz. Paralyzed motor units (n = 48) had small EMGs and weak tetanic forces (n = 32 units) but strong twitch forces, resulting in half-maximal force being achieved at a median of only 8 Hz. The distributions for cumulative twitch and tetanic forces also separated less for paralyzed units than for control units, indicating that increases in stimulation frequency made a smaller relative contribution to the total force output in paralyzed muscles. Paralysis also induced slowing of conduction velocities, twitch contraction times and EMG durations. However, the elevated ratios between the twitch and the tetanic forces, but not contractile speed, correlated significantly with the extent to which unit force summated in response to different frequencies of stimulation. Despite changes in the absolute values of many electrical and mechanical properties of paralyzed motor units, most of the distributions shifted uniformly relative to those of thenar units obtained from control subjects. Thus human thenar muscles paralyzed by SCI retain a population of motor units with heterogeneous contractile properties because chronic paralysis influenced all of the motor units similarly.

Human muscles paralysed chronically by spinal cord injury (SCI) fatigue excessively. Whether these reductions in force reflect a decrease in the fatigue resistance of the motor units is unknown. Our aim was to determine the fatigability of thenar motor units paralysed chronically (10 +/- 2 years) by cervical SCI. Surface electromyographic activity (EMG) and force were recorded from 17 paralysed motor units (n = 7 subjects) in response to intraneural motor axon stimulation (13 pulses at 40 Hz, 1 s(-1) for 2 min). Unit force decreased progressively, reaching 8-60% of initial after 2 min, whereas both the amplitude and area of the first EMG potentials in the trains increased significantly (both P < 0.05). Thus, transmission of neural signals to the sarcolemma was effective and the reduction in force must reflect impaired processes in the muscle fibres. The median fatigue index for paralysed units (0.31), the ratio of the force at 2 min compared to the initial force, was significantly lower than that for units from control subjects (0.85, P < 0.05), but the distribution of fatigue indices for each population had a similar shape (ranges: 0.08-0.60 and 0.41-0.95, respectively). Hence, chronic paralysis did not limit the range of fatigability typically found for thenar units, only its magnitude. These findings suggest that all paralysed units underwent similar reductions in fatigue resistance. After fatigue, paralysed unit forces were reduced at all frequencies (1-100 Hz, P < 0.05). Twitch contraction and half-relaxation times were increased, as was the frequency needed to produce half maximal force (P < 0.05). Thus, stimulation protocols used to produce functional movements in paralysed muscles need to accommodate the significant and rapid fatigue of the motor units.