Surface Motor Unit Potentials Research Articles

The reliability of methods to estimate the number and size of human motor units and their use with large limb muscles

PurposeCurrent methods for estimating muscle motor unit (MU) number provide values which are remarkably similar for muscles of widely differing size, probably because surface electrodes sample from similar and relatively small volumes in each muscle. We have evaluated an alternative means of estimating MU number that takes into account differences in muscle size.MethodsIntramuscular motor unit potentials (MUPs) were recorded and muscle cross-sectional area (CSA) was measured using MRI to provide a motor unit number estimate (iMUNE). This was compared to the traditional MUNE method, using compound muscle action potentials (CMAP) and surface motor unit potentials (sMUPs) recorded using surface electrodes. Data were collected from proximal and distal regions of the vastus lateralis (VL) in young and old men while test–retest reliability was evaluated with VL, tibialis anterior and biceps brachii.ResultsMUPs, sMUPs and CMAPs were highly reliable (r = 0.84–0.91). The traditional MUNE, based on surface recordings, did not differ between proximal and distal sites of the VL despite the proximal CSA being twice the distal CSA. iMUNE, however, gave values that differed between young and old and were proportional to the muscle size.ConclusionWhen evaluating the contribution that MU loss makes to muscle atrophy, such as in disease or ageing, it is important to have a method such as iMUNE, which takes into account any differences in total muscle size.

Effect of very old age on anconeus motor unit loss and compensatory remodelling.

It is not known how the process of compensatory remodeling through collateral reinnervation continues into very old age (>80 years) or whether there is a limit to effective motor unit (MU) reinnervation. Therefore, we explore electrophysiological properties related to motor unit number estimates (MUNEs) in very old participants (79-90 years of age) compared with young controls (25-29 years of age). Decomposition-enhanced spike-triggered averaging was used to collect surface and intramuscular electromyography information from the anconeus to derive a MUNE. Young participants had a MUNE of ∼38 and ∼25 at 30% and 50% root mean squared maximum voluntary contraction (RMSMVC ) with surface motor unit potentials (S-MUPs) of ∼145 μV and 236 μV, respectively. Older participants had a MUNE of ∼23 and ∼16 at 30% and 50% RMSMVC with S-MUPs of 168 μV and 232 μV, respectively. In this muscle, an age limit to successful remodeling through collateral reinnervation, to compensate for the presumed ongoing losses of MUs, may have been surpassed. Muscle Nerve 57: 659-663, 2018.

Pilot study: quantification of motor unit stability, or “jiggle”, in amyotrophic lateral sclerosis (731.11)

Loss of motor units (MUs) have been found in aging, neuropathies, and motor neuron diseases. With MU loss, subsequent collateral reinnervation results in unstable motor unit potentials (MUPs) with variability in firing times and generation of muscle fiber action potentials. Jiggle is a measure of MUP stability, which can be calculated using Decomposition‐based Quantitative Electromyography (DQEMG). Two previous studies have attempted to measure jiggle, but both studies were limited by the EMG decomposition algorithms used. The purpose of this study is to measure jiggle in the upper trapezius muscle of 11 amyotrophic lateral sclerosis (ALS) patients compared to age‐matched healthy controls. Jiggle will be calculated using the normalized value of the median consecutive amplitude difference (CAD). Jiggle will also be compared to other MUP parameters including motor unit number estimation (MUNE), mean surface MUP (S‐MUP) size, MUP amplitude, and near fiber count. As a result of denervation and incomplete reinnervation, we expect to see significantly higher jiggle values in patients with ALS relative to controls. We also expect jiggle to be negatively correlated with MUNE, and positively correlated with mean S‐MUP size, MUP amplitude, and near fiber count. If successful, jiggle may be a valuable diagnostic parameter or outcome measure in age‐related sarcopenia, neuropathies, or motor neuron diseases such as ALS.

Effects of muscle fibre shortening on the characteristics of surface motor unit potentials

Traditionally, studies dealing with muscle shortening have concentrated on assessing its impact on conduction velocity, and to this end, electrodes have been located between the end-plate and tendon regions. Possible morphologic changes in surface motor unit potentials (MUPs) as a result of muscle shortening have not, as yet, been evaluated or characterized. Using a convolutional MUP model, we investigated the effects of muscle shortening on the shape, amplitude, and duration characteristics of MUPs for different electrode positions relative to the fibre-tendon junction and for different depths of the MU in the muscle (MU-to-electrode distance). It was found that the effects of muscle shortening on MUP morphology depended not only on whether the electrodes were between the end-plate and the tendon junction or beyond the tendon junction, but also on the specific distance to this junction. When the electrodes lie between the end-plate and tendon junction, it was found that (1) the muscle shortening effect is not important for superficial MUs, (2) the sensitivity of MUP amplitude to muscle shortening increases with MU-to-electrode distance, and (3) the amplitude of the MUP negative phase is not affected by muscle shortening. This study provides a basis for the interpretation of the changes in MUP characteristics in experiments where both physiological and geometrical aspects of the muscle are varied.

Length dependent loss of motor axons and altered motor unit properties in human diabetic polyneuropathy

ObjectiveTo assess the number and properties of motor units in an upper and lower limb muscle (tibialis anterior [TA] and first dorsal interosseous [FDI]) in human diabetic polyneuropathy (DPN) using decomposition-based quantitative electromyography (DQEMG). MethodsDQEMG protocols were performed in the TA and FDI of 12 patients with confirmed diabetes mellitus and associated DPN, as well as 12 age-matched control participants. Maximal dorsiflexion strength was also assessed using a dynamometer. ResultsIn both muscles, patients with DPN had significantly reduced motor unit number estimates (MUNEs) (ΔTA ∼45%; ΔFDI ∼30%), compound muscle action potentials (CMAPs) (ΔTA ∼30%; ΔFDI ∼20%), and mean firing rates were reduced (ΔTA ∼15%; ΔFDI ∼15%) compared to controls (p<0.05). For the TA, patients with DPN had larger mean surface motor unit potentials (SMUPs) (ΔTA ∼40%; p<0.05), whereas in the FDI no differences were found (p>0.05). ConclusionsDPN may result in motor unit loss, remodeling, and altered firing rate patterns. The magnitude of changes in the neuromuscular properties of DPN patients are muscle dependent and reflect a length-dependent disease progression. SignificanceDQEMG may be a clinically useful technique in identifying the presence and severity of neuromuscular pathophysiology and tracking disease progression in DPN.

Peculiarities of extracellular potentials produced by deep muscles. Part 2: motor unit potentials

The potential fields generated by single fibres far from the sources are non-propagating. This suggests that there should be differences in the features of surface motor unit (MU) potentials (MUPs) detected from deep and superficial muscles. We explored the features using a simulation approach. We have shown that the non-propagating character and similar shapes among surface MUPs recorded over a wide area above deep muscles with monopolar or longitudinal single differential (LSD) electrodes are natural. Contrary to close distances, at large radial distances single differentiation did not emphasize MUP main phase relative weight. The position of the end plate area could be estimated with LSD detections only for MUs with long (123mm) almost symmetric fibres. With short fibres, the LSD main phase was masked by the outlined terminal phases. This could be misleading in MUP analysis since the terminal phases reflect standing sources. The highly asymmetric fibres could yield peculiar MUP shapes resembling MUPs of two distinct MUs. We have shown that the relative weight of terminal phases at large fibre-electrode distance decreases under abnormal peripheral conditions. However, the changes in membrane depolarization due to fatigue or pathology could be assessed non-invasively also from deep muscles.

Far-field potentials in hypothenar motor unit number estimation

Contamination by far-field potentials (FFPs) may interfere with motor unit number estimation (MUNE) in the ulnar nerve. Surface motor unit potentials (SMUPs) from 29 spinal and bulbar muscular atrophy (SBMA) patients and 27 control subjects were classified into SMUPs from the abductor digiti minimi muscle (ADM SMUPs) or non-ADM SMUPs, based on the waveform patterns from 3-channel recordings. The mean areas of the ADM SMUPs and non-ADM SMUPs in control subjects were 219.0 ± 131.3 and 63.7 ± 48.5 μVms, respectively. In SBMA patients they were 1988.9 ± 999.4 and 222.7 ± 125.7 μVms, respectively. The percentages of non-ADM SMUPs were 68 ± 22% in controls and 84 ± 15% in SBMA patients. Non-ADM SMUPs generated mainly by FFPs often had a negative onset in the routine lead and were indistinguishable from ADM SMUPs. More frequent exclusion of smaller non-ADM SMUPs in controls by size criteria would reduce the diagnostic yield of MUNE.

Effect of small motor unit potentials on the motor unit number estimate

Small surface motor unit potentials (S-MUPs) may have a negative influence on the variability of the motor unit number estimate (MUNE). According to published consensus criteria S-MUPs with a negative peak amplitude smaller than 10 muV should be omitted. The effect of omitting small S-MUPs on the MUNE was evaluated using a simulation model. The model incorporated a healthy and amyotrophic lateral sclerosis (ALS) distribution formed with real S-MUPs. Using a random drawing process the MUNE was calculated with and without small S-MUPs. In the healthy population 27% of all S-MUPs were small. MUNE determined without these S-MUPs was marginally less variable. However, MUNE values dropped about 24% at a sample size of 20. In ALS, only 12% of the total population of 130 S-MUPs were small. MUNE dropped about 12% without the small S-MUPs. By omitting small S-MUPs the differences between the healthy and ALS distributions become smaller. Therefore, incorporating small S-MUPs in the estimate is suggested.

Assessment of axonal loss in Charcot–Marie–Tooth neuropathies

Sensory loss and weakness in Charcot–Marie–Tooth (CMT) neuropathy is due to axonal loss. However, the pattern and degree of axonal loss cannot be accurately determined from routine electrodiagnostic or strength testing due to collateral reinnervation. We sought to quantify axonal loss in two upper extremity muscles in CMT1A and CMT2 subjects using the electrophysiologic endpoint measure of motor unit number estimation (MUNE). Hypothenar and biceps–brachialis muscle groups were studied in 9 CMT1A, 9 CMT2, and 10 control subjects. The spike-triggered averaging (STA) technique was used to collect surface motor unit potentials for MUNE calculations, and a needle electrode was used to collect corresponding intramuscular data. Maximal voluntary hypothenar and handgrip strength was measured quantitatively, while biceps–brachialis strength was measured qualitatively. Compared to normal subjects, CMT1A and CMT2 subjects had significantly lower MUNE values in hypothenar muscles. Biceps–brachialis MUNE values were reduced in CMT2 but not in CMT1A subjects. In support of proximal axonal loss in CMT2 subjects, surface motor unit and intramuscular potential amplitudes were higher in biceps–brachialis muscles compared to controls. Correlations between quantitative strength and MUNE were significant for hypothenar but not for grip muscle groups. Axonal loss is demonstrated in distal muscles in CMT1A and CMT2 supporting a length-dependent axonopathy. Despite clinical findings of normal or near-normal strength and small reductions in compound muscle action potential (CMAP) amplitude, MUNE values were significantly lower in CMT2 subjects in proximal muscles, consistent with more diffuse denervation. These data indicate that subclinical axonal loss is present that cannot be appreciated using clinical examination or routine electrodiagnostic techniques.

What do we learn from motor unit action potentials in surface electromyography?

This article gives an overview of what multichannel surface electromyography can teach us about a motor unit. Background information is given about the generation of surface electromyography in general and surface motor unit potentials in particular. Furthermore, we describe how surface motor unit potentials are related to several motor unit characteristics, such as size, location, neuromuscular junction position, fiber length, fiber type, and metabolic fiber properties. In addition, we show how the spatial characteristics of multichannel surface electromyography can be used to obtain single-surface motor unit potentials. The possibilities, challenges, and problems are discussed. Finally, several examples of surface motor unit potential analyses are given.

Motor unit estimation: Reproducibility of the spike‐triggered averaging technique in normal and ALS subjects

Reproducibility of the spike-triggered averaging technique of motor unit estimation (MUE) was assessed in biceps-brachialis muscle in 10 normal subjects and 15 subjects with amyotrophic lateral sclerosis (ALS). MUE was calculated by dividing the compound muscle action potential by the mean amplitude of 15 surface motor unit potentials (S-MUPs) of low recruitment threshold. Averaged MUE values in normal subjects were higher than in ALS subjects, with few values overlapping. Differences between test and retest MUE values were not significant for either subject group. The relative differences between test-retest values were 45.3% for normal subjects and 32.6% for ALS subjects. Correlation coefficients between test and retest values were low (r = 0.07) for normal subjects when influential outlying points were removed, and higher (r = 0.65) for ALS subjects when individuals with MUE values within the normal range were removed. The higher correlation of test-retest MUE values in ALS subjects compared to normal subjects may be due to a greater probability of resampling among the smaller number of motor units in ALS subjects. In summary, the reproducibility and technical aspects of the spike-triggered averaging technique are similar to those reported for other MUE techniques.