Abstract
Neuromuscular adaptations are well-reported in stroke survivors. The death of motor neurons and the reinnervation of residual muscle fibers by surviving motor neurons, for example, seem to explain the increased density of muscle units after stroke. It is, however, unknown whether reinnervation takes place locally or extensively within the muscle. Here we combine intramuscular and surface electromyograms (EMGs) to address this issue for medial gastrocnemius (MG); a key postural muscle. While seven stroke survivors stood upright, two intramuscular and 15 surface EMGs were recorded from the paretic and non-paretic gastrocnemius. Surface EMGs were triggered with the firing instants of motor units identified through the decomposition of both intramuscular and surface EMGs. The standard deviation of Gaussian curves fitting the root mean square amplitude distribution of surface potentials was considered to assess differences in the spatial distribution of motor unit action potentials and, thus, in the distribution of muscle units between limbs. The median number of motor units identified per subject in the paretic and non-paretic sides was, respectively, 2 (range: 1–3) and 3 (1–4). Action potentials in the paretic gastrocnemius were represented at a 33% wider skin region when compared to the non-paretic muscle (Mann-Whitney; P = 0.014). Side differences in the representation of motor unit were not associated with differences in subcutaneous thickness (skipped-Spearman r = −0.53; confidence interval for r: −1.00 to 0.63). Current results suggest stroke may lead to the enlargement of the gastrocnemius muscle units recruited during standing. The enlargement of muscle units, as assessed from the skin surface, may constitute a new marker of neuromuscular plasticity following stroke.
Highlights
Motor impairment is a widely recognized consequence of stroke [1]
Thirty-four motor units (13 in the paretic medial gastrocnemius (MG)) were identified from EMGs collected from both limbs for the seven participants analyzed
Our results show action potentials of individual, postural muscle units were represented in relatively larger skin regions in the paretic than non-paretic MG (Figures 4, 5)
Summary
Motor impairment is a widely recognized consequence of stroke [1]. Structural changes in the spinal motor neuron and its muscle fibers have been advocated a contributing factor for the loss of motor control in stroke survivors [2, 3]. Loss of motor neurons, muscle atrophy and fiber-type grouping have been reported within 2–5 months after stroke [2,3,4,5]. Muscle fibers belonging to dead motor neurons seem to be re-innervated by surviving ones This structural change is substantiated by increases in the size of motor unit action potentials and, more directly, by collateral sprouting and greater fiber density at chronic, stroke stages [6,7,8]. In virtue of the increased number of fibers per motor unit, it seems reasonable to ask whether these fibers span a larger region within the paretic muscle
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