Neuromuscular electrical stimulation has a global effect on corticospinal excitability for leg muscles and a focused effect for hand muscles.

The afferent volley generated during neuromuscular electrical stimulation (NMES) can increase the excitability of human corticospinal (CS) pathways to muscles of the leg and hand. Over time, such increases can strengthen CS pathways damaged by injury or disease and result in enduring improvements in function. There is some evidence that NMES affects CS excitability differently for muscles of the leg and hand, although a direct comparison has not been conducted. Thus, the present experiments were designed to compare the strength and specificity of NMES-induced changes in CS excitability for muscles of the leg and hand. Two hypotheses were tested: (1) For muscles innervated by the stimulated nerve (target muscles), CS excitability will increase more for the hand than for the leg. (2) For muscles not innervated by the stimulated nerve (non-target muscles), CS excitability will increase for muscles of the leg but not muscles of the hand. NMES was delivered over the common peroneal (CP) nerve in the leg or the median nerve at the wrist using a 1-ms pulse width in a 20 s on, 20 s off cycle for 40 min. The intensity was set to evoke an M-wave that was ~15% of the maximal M-wave in the target muscle: tibialis anterior (TA) in the leg and abductor pollicis brevis (APB) in the hand. Ten motor-evoked potentials (MEPs) were recorded from the target muscles and from 2 non-target muscles of each limb using transcranial magnetic stimulation delivered over the "hotspot" for each muscle before and after the NMES. MEP amplitude increased significantly for TA (by 45 ± 6%) and for APB (56 ± 8%), but the amplitude of these increases was not different. In non-target muscles, MEPs increased significantly for muscles of the leg (42 ± 4%), but not the hand. Although NMES increased CS excitability for target muscles to the same extent in the leg and hand, the differences in the effect on non-target muscles suggest that NMES has a "global" effect on CS excitability for the leg and a "focused" effect for the hand. These differences may reflect differences in the specificity of afferent projections to the cortex. Global increases in CS excitability for the leg could be advantageous for rehabilitation as NMES applied to one muscle could strengthen CS pathways and enhance function for multiple muscles.

Neuromuscular electrical stimulation: implications of the electrically evoked sensory volley.

Neuromuscular electrical stimulation (NMES) generates contractions by depolarising axons beneath the stimulating electrodes. The depolarisation of motor axons produces contractions by signals travelling from the stimulation location to the muscle (peripheral pathway), with no involvement of the central nervous system (CNS). The concomitant depolarisation of sensory axons sends a large volley into the CNS and this can contribute to contractions by signals travelling through the spinal cord (central pathway) which may have advantages when NMES is used to restore movement or reduce muscle atrophy. In addition, the electrically evoked sensory volley increases activity in CNS circuits that control movement and this can also enhance neuromuscular function after CNS damage. The first part of this review provides an overview of how peripheral and central pathways contribute to contractions evoked by NMES and describes how differences in NMES parameters affect the balance between transmission along these two pathways. The second part of this review describes how NMES location (i.e. over the nerve trunk or muscle belly) affects transmission along peripheral and central pathways and describes some implications for motor unit recruitment during NMES. The third part of this review summarises some of the effects that the electrically evoked sensory volley has on CNS circuits, and highlights the need to identify optimal stimulation parameters for eliciting plasticity in the CNS. A goal of this work is to identify the best way to utilize the electrically evoked sensory volley generated during NMES to exploit mechanisms inherent to the neuromuscular system and enhance neuromuscular function for rehabilitation.

Changes in corticospinal excitability evoked by common peroneal nerve stimulation depend on stimulation frequency.

The afferent volley generated during neuromuscular electrical stimulation (NMES) can increase the excitability of the human corticospinal (CS) pathway. This study was designed to determine the effect of different frequencies of NMES applied over the common peroneal nerve on changes in CS excitability for the tibialis anterior (TA) muscle. We hypothesized that higher frequencies of stimulation would produce larger increases in CS excitability than lower frequencies. NMES was applied at 10, 50, 100, or 200 Hz during separate sessions held at least 48 h apart. The stimulation was delivered in a 20 s on, 20 s off cycle for 40 min using a 1 ms pulse width. The intensity of stimulation was set to evoke an M-wave in response to a single pulse that was 15% of the maximal M-wave. CS excitability was evaluated by the amplitude of motor-evoked potentials (MEPs) in TA evoked by transcranial magnetic stimulation. MEPs were recorded immediately before and after the 40 min of NMES and in each 20 s "off" period. For each subject, MEPs recorded during three successive "off" periods were averaged together (n = 9 MEPs), providing a temporal resolution of 2 min for assessing changes in CS excitability. When delivering NMES at 100 Hz, MEPs became significantly elevated from those evoked before the stimulation at the 24th min, and there was a twofold increase in MEP amplitude after 40 min. NMES delivered at 10, 50, and 200 Hz did not significantly alter MEP amplitude. The amplitude of MEPs evoked in soleus and vastus medialis followed similar patterns as those evoked simultaneously in TA, but these changes were mostly not of statistical significance. There were no changes in the ratio of maximal H-reflex to maximal M-wave in TA or soleus. These experiments demonstrate a frequency-dependent effect of NMES on CS excitability for TA and show that, under the conditions of the present study, 100-Hz stimulation was more effective than 10, 50, and 200 Hz. This effect of NMES on CS excitability was strongest in the stimulated muscle and may be mediated primarily at a supraspinal level. These results contribute to a growing body of knowledge about how the afferent volley generated during NMES influences the CNS and have implications for identifying optimal NMES parameters to augment CS excitability for rehabilitation of dorsiflexion after CNS injury.

Relationship between ventilatory constraint and muscle fatigue during exercise in COPD.

Dynamic hyperinflation and leg muscle fatigue are independently associated with exercise limitation in patients with chronic obstructive pulmonary disease (COPD). The aims of the present study were to examine 1) the relationship between these limitations and 2) the effect of delaying ventilatory limitation on exercise tolerance and leg muscle fatigue. In total, 11 patients with COPD (with a forced expiratory volume in one second of 52% predicted) completed two cycling bouts breathing either room air or heliox, and one bout breathing heliox but stopping at room air isotime. End-expiratory lung volume (EELV), leg muscle fatigue and exercise time were measured. On room air, end-exercise EELV was negatively correlated with leg fatigue. Heliox increased exercise time (from 346 to 530 s) and leg fatigue (by 15%). At isotime, there was no change in leg fatigue, despite a reduction in EELV compared with end-exercise, in both room air and heliox. The change in exercise time with heliox was best correlated with room air leg fatigue and end-inspiratory lung volume. Patients with chronic obstructive pulmonary disease who had greater levels of dynamic hyperinflation on room air had less muscle fatigue. These patients were more likely to increase exercise tolerance with heliox, which resulted in greater leg muscle fatigue.

Reflex pathways connect receptors in the human lower leg to the erector spinae muscles of the lower back.

Reflex pathways connect all four limbs in humans. Presently, we tested the hypothesis that reflexes also link sensory receptors in the lower leg with muscles of the lower back (erector spinae; ES). Taps were applied to the right Achilles' tendon and electromyographic activity was recorded from the right soleus and bilaterally from ES. Reflexes were compared between sitting and standing and between standing with the eyes open versus closed. Reflexes were evoked bilaterally in ES and consisted of an early latency excitation, a medium latency inhibition, and a longer latency excitation. During sitting but not standing, the early excitation was larger in the ES muscle ipsilateral to the stimulation (iES) than in the contralateral ES (cES). During standing but not sitting, the longer latency excitation in cES was larger than in iES. This response in cES was also larger during standing compared to sitting. Responses were not significantly different between the eyes open and eyes closed conditions. Taps applied to the lateral calcaneus (heel taps) evoked responses in ES that were not significantly different in amplitude or latency than those evoked by tendon taps, despite a 75-94% reduction in the amplitude of the soleus stretch reflex evoked by the heel taps. Electrical stimulation of the sural nerve, a purely cutaneous nerve at the ankle, evoked ES reflexes that were not significantly different in amplitude but had significantly longer latencies than those evoked by the tendon and heel taps. These results support the hypothesis that reflex pathways connect receptors in the lower leg with muscles of the lower back and show that that the amplitude of these reflexes is modulated by task. Responses evoked by stimulation of the sural nerve establish that reflex pathways connect the ES muscles with cutaneous receptors of the foot. In contrast, the large volley in muscle spindle afferents induced by the tendon taps compared to the heel taps did not alter the ES responses, suggesting that the reflex connection between triceps surae muscle spindles and the ES muscles may be relatively weak. These heteronymous reflexes may play a role in stabilizing the trunk for maintaining posture and balance.

Turning on the central contribution to contractions evoked by neuromuscular electrical stimulation.

Neuromuscular electrical stimulation can generate contractions through peripheral and central mechanisms. Direct activation of motor axons (peripheral mechanism) recruits motor units in an unnatural order, with fatigable muscle fibers often activated early in contractions. The activation of sensory axons can produce contractions through a central mechanism, providing excitatory synaptic input to spinal neurons that recruit motor units in the natural order. Presently, we quantified the effect of stimulation frequency (10-100 Hz), duration (0.25-2 s of high-frequency bursts, or 20 s of constant-frequency stimulation), and intensity [1-5% maximal voluntary contraction (MVC) torque generated by a brief 100-Hz train] on the torque generated centrally. Electrical stimulation (1-ms pulses) was delivered over the triceps surae in eight subjects, and plantar flexion torque was recorded. Stimulation frequency, duration, and intensity all influenced the magnitude of the central contribution to torque. Central torque did not develop at frequencies < or = 20 Hz, and it was maximal at frequencies > or = 80 Hz. Increasing the duration of high-frequency stimulation increased the central contribution to torque, as central torque developed over 11 s. Central torque was greatest at a relatively low contraction intensity. The largest amount of central torque was produced by a 20-s, 100-Hz train (10.7 +/- 5.5 %MVC) and by repeated 2-s bursts of 80- or 100-Hz stimulation (9.2 +/- 4.8 and 10.2 +/- 8.1% MVC, respectively). Therefore, central torque was maximized by applying high-frequency, long-duration stimulation while avoiding antidromic block by stimulating at a relatively low intensity. If, as hypothesized, the central mechanism primarily activates fatigue-resistant muscle fibers, generating muscle contractions through this pathway may improve rehabilitation applications.

Sensori-sensory afferent conditioning with leg movement: gain control in spinal reflex and ascending paths.

Studies are reviewed, predominantly involving healthy humans, on gain changes in spinal reflexes and supraspinal ascending paths during passive and active leg movement. The passive movement research shows that the pathways of H reflexes of the leg and foot are down-regulated as a consequence of movement-elicited discharge from somatosensory receptors, likely muscle spindle primary endings, both ipsi- and contralaterally. Discharge from the conditioning receptors in extensor muscles of the knee and hip appears to lead to presynaptic inhibition evoked over a spinal path, and to long-lasting attenuation when movement stops. The ipsilateral modulation is similar in phase to that seen with active movement. The contralateral conditioning does not phase modulate with passive movement and modulates to the phase of active ipsilateral movement. There are also centrifugal effects onto these pathways during movement. The pathways of the cutaneous reflexes of the human leg also are gain-modulated during active movement. The review summarizes the effects across muscles, across nociceptive and non-nociceptive stimuli and over time elapsed after the stimulus. Some of the gain changes in such reflexes have been associated with central pattern generators. However, the centripetal effect of movement-induced proprioceptive drive awaits exploration in these pathways. Scalp-recorded evoked potentials from rapidly conducting pathways that ascend to the human somatosensory cortex from stimulation sites in the leg also are gain-attenuated in relation to passive movement-elicited discharge of the extensor muscle spindle primary endings. Centrifugal influences due to a requirement for accurate active movement can partially lift the attenuation on the ascending path, both during and before movement. We suggest that a significant role for muscle spindle discharge is to control the gain in Ia pathways from the legs, consequent or prior to their movement. This control can reduce the strength of synaptic input onto target neurons from these kinesthetic receptors, which are powerfully activated by the movement, perhaps to retain the opportunity for target neuron modulation from other control sources.

Large involuntary forces consistent with plateau-like behavior of human motoneurons.

When electrical stimulation is applied over human muscle, the evoked force is generally considered to be of peripheral origin. However, in relaxed humans, stimulation (1 msec pulses, 100 Hz) over the muscles that plantarflex the ankle produced more than five times more force than could be accounted for by peripheral properties. This additional force was superimposed on the direct response to motor axon stimulation, produced up to 40% of the force generated during a maximal voluntary contraction, and was abolished during anesthesia of the tibial nerve proximal to the stimulation site. It therefore must have resulted from the activation of motoneurons within the spinal cord. The additional force could be initiated by stimulation of low-threshold afferents, distorted the classical relationship between force and stimulus frequency, and often outlasted the stimulation. The mean firing rate of 27 soleus motor units recorded during the sustained involuntary activity after the stimulation was 5.8 +/- 0.2 Hz. The additional force increments were not attributable to voluntary intervention because they were present in three sleeping subjects and in two subjects with lesions of the thoracic spinal cord. The phenomenon is consistent with activation of plateau potentials within motoneurons and, if so, the present findings imply that plateau potentials can make a large contribution to forces produced by the human nervous system.

Modulation of human short latency reflexes between standing and walking.

Inhibition of the magnitude of soleus muscle homonymous (H) reflexes occurs in humans when walking, compared to standing. The current study asked, (1) was the task modulation of Ia reflexes limited to soleus muscle, (2) was there support for attributing a presynaptic source to the inhibition in humans and (3) did an oligosynaptic short latency reflex show similar task modulation? In 3 subjects, H reflexes were evoked in vastus medialis and soleus, at 4 levels of contraction in the target muscle, with constant stimulus intensity when walking and standing. The reflex magnitudes in both muscles were significantly inhibited during the contractions for walking, compared to standing. Such inhibition also occurred in H reflexes of tibialis anterior muscle. An excitatory oligosynaptic reflex was then evoked in vastus medialis, through low intensity stimulation of the common peroneal nerve during walking and standing. The mean amplitudes of this reflex were not significantly different (P less than 0.05) between the two conditions, at any contraction level. The depression of quadriceps H reflexes, compared to the oligosynaptic reflexes through the same quadriceps motoneuronal pool in the same task, strongly suggested that the inhibition of H reflexes arose at other sites besides the motoneuronal cell body and proximal dendrites. We conclude that Ia H reflexes of various leg muscles of humans are inhibited when walking but that this does not generalize to the oligosynaptic short latency reflex between the anterior shank and thigh.

Movement features and H-reflex modulation. I. Pedalling versus matched controls.

Modulation of soleus H-reflex magnitude over a cycle of leg movement and the adjustment of controls to account for it were explored. During pedalling, H-reflex magnitudes in all nine subjects were highest in the power producing phase and lowest in recovery. Stimulation intensity was standardized. Compared to sitting, these reflexes were significantly depressed (P less than 0.05). The sitting condition was modified in one experiment, so that the angles of the limb joints and the contraction level of soleus were matched to their values, measured at 13 equi-spaced points, around the pedal cycle. This matching resulted in some modulation of the H-reflex around the pedal cycle, when sitting. When the contraction of tibialis anterior was added to these changes to the seated control, this modulation came closer to that seen during movement. Movement-specific modulation of the reflex was now harder to identify. These data raise the question of whether the three features presently used for matching are causative in the movement modulation of the soleus H-reflex and whether they represent effects arising from centrally descending or peripheral sources.

Movement features and H-reflex modulation. II. Passive rotation, movement velocity and single leg movement.

Modulation of soleus H-reflex magnitudes during pedalling, and their approximation when seated with appropriate joint positions and contractile activity was demonstrated in the previous paper. The present study investigated the modulation of H-reflexes during (A) pedalling movement in the absence of contractile activity, (B) different movement velocities and (C) movement of a single limb. Using a customized tandem cycle ergometer, seated subjects with trunk supported relaxed their leg muscles and allowed their legs to be rotated. Their feet were supported on the pedals with the ankle braced. Reflexes were collected at four phases in the movement cycle (with some at 13 phases) and with speeds of 5-60 revolutions per min (cycle times from 12 to 1 s). The results showed that (i) reflex magnitude substantially decreased with limb rotation (P less than 0.05). The degree of inhibition was dependent on the phase position. (ii) Increasing speed of passive rotation increased the inhibition at all positions, but was most pronounced near the fullest flexion of hip and knee. When subjects actively pedalled, the relationship between speed and inhibition remained. (iii) When the contralateral leg was moved and the target leg was stationary, crossed projection of reflex inhibition was clear. (iv) The reflex gain measured during active pedalling of one leg was similar to that observed during two legged pedalling. Again, a crossed effect from the contralateral leg could be observed. We conclude that the net influence of discharge from movement-elicited afference is inhibitory on this reflex path and that the reflex modulation during pedalling arises from overlaid sources.(ABSTRACT TRUNCATED AT 250 WORDS)

Contralateral inhibition of soleus H reflexes with different velocities of passive movement of the opposite leg.

The research question was, do events arising from rhythmic passive movement of the human leg lead to inhibition of the H reflex pathway in the stationary leg contralateral to that movement? Further, as the angular velocity of the passive movement increases, does the contralateral reflex inhibition also increase? Stable stimulation of the tibial nerve elicited H reflexes in the EMG of soleus. Trials involved the stimulated or the contralateral leg being rotated passively in a pedalling motion, at various velocities. The controls were made with the subjects seated and relaxed. The results showed that reflex magnitudes were significantly depressed when the test limb was passively rotated at 60 rpm. in comparison to the seated control trials. Rotation of the opposite limb depressed reflex magnitudes in the test limb, which was stationary. This contralateral inhibition increased, (mean reflex magnitudes of 62.68%, 41.04%, 16.65% and 9.58% of peak-to-peak Mmax), as the velocity of rotation of the opposite limb increased (10, 30, 60, 90 rpm, respectively) (P < 0.01). The effect of movement velocity was interpreted as the result of altered sensory receptor discharge arising from the passive movement. It is concluded that contralateral sensory activity contributes to the movement-elicited afferent discharge which tunes the spinal somatosensory-motor mechanisms for human locomotion.

Mechanisms within the human spinal cord suppress fast reflexes to control the movement of the legs.

Passive locomotor-like movement induces depression of the gain of a fast conducting spinal sensorimotor path in humans. It was hypothesized that this gain control is mediated through a spinal circuit. In the first experiment, passive pedalling motion was rapidly initiated in eight able bodied subjects. Soleus H-reflexes (used to reveal the gain of the short latency stretch reflex) were recorded over the first 250 ms after the movement started. Significant depression in H-reflex magnitude was observed by 50 ms after the onset of movement. On the basis of the timing, this gain attenuation was likely mediated through a spinal circuit. In a second experiment we tested chronic quadriplegics with clinically complete lesions of the spinal cord. Of five subjects tested, three expressed the reflex and all three showed significant inhibition with passive pedalling movement (mean depression was to 39% of controls). Both the rapid onset of the gain change (Expt. 1) and the presence of movement-induced inhibition in individuals with spinal lesions (Expt. 2) provide evidence that this component of human locomotor control is located in the spinal cord. The initiating source is probably somatosensory receptor discharge due to the movement.

Depression and recovery of reflex amplitude during electrical stimulation after spinal cord injury.

OBJECTIVE: The aim of this study was to quantify, for the first time, H-reflexes evoked during prolonged trains of wide-pulse neuromuscular electrical stimulation (WP-NMES) in individuals with chronic spinal cord injury (SCI). We hypothesised that after the first H-reflex, reflex amplitudes would be depressed (due to post-activation depression), but would recover and this recovery would be enhanced after a "burst" of 100 Hz WP-NMES. METHODS: Soleus M-waves and H-reflexes evoked during WP-NMES (1 ms pulse width) of the tibial nerve were quantified in nine individuals with SCI. WP-NMES was delivered in two patterns: "constant-frequency" (15 or 20 Hz for 12 s) and "burst-like" (15-100-15 Hz or 20-100-20 Hz; 4 s each phase) at an intensity that evoked an M-wave between 10% and 15% of the maximal M-wave (M(max)). RESULTS: During constant frequency stimulation, after the initial depression from the first to the second H-reflex (1st: 57% M(max); 2nd: 25% M(max)), H-reflexes did not recover significantly and were 37% M(max) at the end of the stimulus train. During the burst-like pattern, after the initial depression (1st: 62% M(max); 2nd: 30%), reflexes recovered completely by the end of the stimulation (to 55% M(max)) as they were not significantly different from the first H-reflex. M-waves were initially depressed (1st: 12% M(max); 2nd: 7% M(max)) then did not change throughout the stimulation and were not significantly different between stimulation patterns. An analysis of covariance indicated that the depression in M-wave amplitude did not account for the depression in H-reflex amplitude. CONCLUSIONS: Relatively large H-reflexes were recorded during both patterns of NMES. The brief burst of 100 Hz stimulation restored H-reflexes to their initial amplitudes, effectively reversing the effects of post-activation depression. SIGNIFICANCE: For individuals with chronic SCI, generating contractions through central pathways may help reduce muscle atrophy and produce contractions that are more fatigue-resistant for rehabilitation, exercise programs, or to perform activities of daily living.

Motor unit recruitment when neuromuscular electrical stimulation is applied over a nerve trunk compared with a muscle belly: quadriceps femoris.

Neuromuscular electrical stimulation (NMES) can be delivered over a nerve trunk or muscle belly and both can generate contractions through peripheral and central pathways. Generating contractions through peripheral pathways is associated with a nonphysiological motor unit recruitment order, which may limit the efficacy of NMES rehabilitation. Presently, we compared recruitment through peripheral and central pathways for contractions of the knee extensors evoked by NMES applied over the femoral nerve vs. the quadriceps muscle. NMES was delivered to evoke 10 and 20% of maximum voluntary isometric contraction torque 2-3 s into the NMES (time(1)) in two patterns: 1) constant frequency (15 Hz for 8 s); and 2) step frequency (15-100-15 Hz and 25-100-25 Hz for 3-2-3 s, respectively). Torque and electromyographic activity recorded from vastus lateralis and medialis were quantified at the beginning (time(1)) and end (time(2); 6-7 s into the NMES) of each pattern. M-waves (peripheral pathway), H-reflexes, and asynchronous activity (central pathways) during NMES were quantified. Torque did not differ regardless of NMES location, pattern, or time. For both muscles, M-waves were ∼7-10 times smaller and H-reflexes ∼8-9 times larger during NMES over the nerve compared with over the muscle. However, unlike muscles studied previously, neither torque nor activity through central pathways were augmented following 100 Hz NMES, nor was any asynchronous activity evoked during NMES at either location. The coefficient of variation was also quantified at time(2) to determine the consistency of each dependent measure between three consecutive contractions. Torque, M-waves, and H-reflexes were most variable during NMES over the nerve. In summary, NMES over the nerve produced contractions with the greatest recruitment through central pathways; however, considering some of the limitations of NMES over the femoral nerve, it may be considered a good complement to, as opposed to a replacement for, NMES over the quadriceps muscle for maintaining muscle quality and reducing contraction fatigue during NMES rehabilitation.

Loss of short-latency afferent inhibition and emergence of afferent facilitation following neuromuscular electrical stimulation.

Neuromuscular electrical stimulation (NMES) increases the excitability of corticospinal (CS) pathways by altering circuits in motor cortex (M1). How NMES affects circuits interposed between the ascending afferent volley and descending CS pathways is not known. Presently, we hypothesized that short-latency afferent inhibition (SAI) would be reduced and afferent facilitation (AF) enhanced when NMES increased CS excitability. NMES was delivered for 40 min over the ulnar nerve. To assess CS excitability, motor evoked potentials (MEPs) were evoked using transcranial magnetic stimulation (TMS) delivered at 120% resting threshold for first dorsal interosseus muscle. These MEPs increased by ∼1.7-fold following NMES, demonstrating enhanced CS excitability. SAI and AF were tested by delivering a "conditioning" electrical stimulus to the ulnar nerve 18-25 ms and 28-35 ms before a "test" TMS pulse, respectively. Conditioned MEPs were compared to unconditioned MEPs evoked in the same trials. TMS was adjusted so unconditioned MEPs were not different before and after NMES. At the SAI interval, conditioned MEPs were 25% smaller than unconditioned MEPs before NMES but conditioned and unconditioned MEPs were not different following NMES. At the AF interval, conditioned MEPs were not different from unconditioned MEPs before NMES, but were facilitated by 33% following NMES. Thus, when NMES increases CS excitability there are concurrent changes in the effect of afferent input on M1 excitability, resulting in a net increase in the excitatory effect of the ascending afferent volley on CS circuits. Maximising this excitatory effect on M1 circuits may help strengthen CS pathways and improve functional outcomes of NMES-based rehabilitation programs.

The effects of wide pulse neuromuscular electrical stimulation on elbow flexion torque in individuals with chronic hemiparetic stroke.

OBJECTIVE: Neuromuscular electrical stimulation that incorporates wide pulse widths (1ms) and high frequencies (100Hz; wide pulse-NMES (WP-NMES)) augments contractions through an increased reflexive recruitment of motoneurons in individuals without neurological impairments and those with spinal cord injury. The current study was designed to investigate whether WP-NMES also augments contractions after stroke. We hypothesized that WP-NMES would generate larger contractions in the paretic arm compared to the non-paretic arm due to increased reflex excitability for paretic muscles after stroke. METHODS: The biceps brachii muscles were stimulated bilaterally in 10 individuals with chronic hemiparetic stroke. Four stimulation patterns were delivered to explore the effects of pulse width and frequency on contraction amplitude: 20-100-20Hz (4s each phase, 1ms pulse width); 20-100-20Hz (4s each phase, 0.1ms); 20Hz for 12s (1ms); and 100Hz for 12s (1ms). Elbow flexion torque and electromyography were recorded. RESULTS: Stimulation that incorporated 1ms pulses evoked more torque in the paretic arm than the non-paretic arm. When 0.1ms pulses were used there was no difference in torque between arms. For both arms, torque declined significantly during the constant frequency 100Hz stimulation and did not change during the constant frequency 20Hz stimulation. CONCLUSIONS: The larger contractions generated by WP-NMES are likely due to increased reflexive recruitment of motoneurons, resulting from increased reflex excitability on the paretic side. SIGNIFICANCE: NMES that elicits larger contractions may allow for development of more effective stroke rehabilitation paradigms and functional neural prostheses.

Motor unit recruitment when neuromuscular electrical stimulation is applied over a nerve trunk compared with a muscle belly: triceps surae.

Neuromuscular electrical stimulation (NMES) can be delivered over a nerve trunk or muscle belly and can generate contractions by activating motor (peripheral pathway) and sensory (central pathway) axons. In the present experiments, we compared the peripheral and central contributions to plantar flexion contractions evoked by stimulation over the tibial nerve vs. the triceps surae muscles. Generating contractions through central pathways follows Henneman's size principle, whereby low-threshold motor units are activated first, and this may have advantages for rehabilitation. Statistical analyses were performed on data from trials in which NMES was delivered to evoke 10-30% maximum voluntary torque 2-3 s into the stimulation (Time(1)). Two patterns of stimulation were delivered: 1) 20 Hz for 8 s; and 2) 20-100-20 Hz for 3-2-3 s. Torque and soleus electromyography were quantified at the beginning (Time(1)) and end (Time(2); 6-7 s into the stimulation) of each stimulation train. H reflexes (central pathway) and M waves (peripheral pathway) were quantified. Motor unit activity that was not time-locked to each stimulation pulse as an M wave or H reflex ("asynchronous" activity) was also quantified as a second measure of central recruitment. Torque was not different for stimulation over the nerve or the muscle. In contrast, M waves were approximately five to six times smaller, and H reflexes were approximately two to three times larger during NMES over the nerve vs. the muscle. Asynchronous activity increased by 50% over time, regardless of the stimulation location or pattern, and was largest during NMES over the muscle belly. Compared with NMES over the triceps surae muscles, NMES over the tibial nerve produced contractions with a relatively greater central contribution, and this may help reduce muscle atrophy and fatigue when NMES is used for rehabilitation.