Anomalies of motor unit amplitude and territory after botulinum toxin injection.

Objective. Botulinum toxin (BT) induced cholinergic denervation of hyperactive motor units (MUs) is a clinically accepted and extensively practiced way of managing focal spasticity after stroke. The denervation potentially initiates a temporary reorganization of the MU activation patterns and structures by inducing the emergence of a large number of newly innervated muscle fibers. In this study, we quantify the effect of the BT on MU action potential (MUAP) amplitudes and on the MU territory areas (MUTAs) as seen on the surface of the skin over the biceps brachii (BB) muscle.Approach. We have used a 128-channel high-density surface electromyography (HDsEMG) grid on the spastic and contralateral BB muscle and recorded the myoelectric activity along with the contraction force during isometric contraction of the elbow muscles. We have decomposed the recorded EMG signal into individual MU potentials and estimated the MUAP amplitudes and territory areas before and two weeks after a BT injection.Main result. There were significantly larger median (47 ± 9%) MUAP amplitudes as well as reduction of MUTA (20 ± 2%) two weeks after the injection compared to the respective pre-injection recording.Significance. The observed covariation of the amplitude and the territory area indicates that the large amplitude MUs that appeared after the BT injection have a relatively smaller territory area. These results provide a rare insight into the BT-induced changes of MU characteristics and have the potential to improve spasticity treatment. We discuss the potential contributing factors to these changes subsequent to the injection in the context of the investigated subject cohort.

Characteristic Variation of Electromechanical Delay After the Botulinum Toxin Injection in Spastic Biceps Brachii Muscles.

The objective of this study was to characterize the effects of intramuscular botulinum toxin (BT) injections on the electromechanical delay (EMD) in spastic human biceps muscles. The EMD is calculated as the time lag between the muscle activation onset, as recorded from the surface electromyogram (sEMG), and the onset of recorded force. In a cohort of chronic stroke survivors, we compared the computed EMD derived from the spastic (injected) biceps brachii with that from the contralateral muscle. Eight participants were tested before and up to 3 months after a BT injection. At each session, participants followed an isometric trapezoidal force trajectory at 50 and 30%, respectively, of the tested maximum voluntary contraction (MVC). Joint force and sEMG signals were recorded as well. The number of zero crossings (ZC) of the sEMG during the steady-state portion of the task was also computed. The EMD post-BT was found to increase by 64 ± 10% (at 50% MVC) and 93 ± 18% (at 30% MVC) when compared to pre-BT values, while the number of sEMG-ZC, the mean MVC values, and the force-EMD slope exhibited striking reductions. These parameters, calculated on the contralateral side, remained relatively constant across sessions, with the EMD significantly lower and the MVC values much higher. We discuss potential contributing factors to an increase in EMD values on the affected side, both pre- and post-BT. The observed co-variation across sessions of the increased EMD values with the decreased ZC estimates, a surrogate of motor outflow, and, potentially, more compliant muscle fascicles suggests that the altered motor unit (MU) behavior contributes, at least in part, to the delayed force production.

Performance Evaluation of a Wearable Tattoo Electrode Suitable for High-Resolution Surface Electromyogram Recording.

OBJECTIVE: High-density surface electromyography (HD-sEMG) has been utilized extensively in neuromuscular research. Despite its potential advantages, limitations in electrode design have largely prevented widespread acceptance of the technology. Commercial electrodes have limited spatial fidelity, because of a lack of sharpness of the signal, and variable signal stability. We demonstrate here a novel tattoo electrode that addresses these issues. Our dry HD electrode grid exhibits remarkable deformability which ensures superior conformity with the skin surface, while faithfully recording signals during different levels of muscle contraction. METHOD: We fabricated a 4 cm×3 cm tattoo HD electrode grid on a stretchable electronics membrane for sEMG applications. The grid was placed on the skin overlying the biceps brachii of healthy subjects, and was used to record signals for several hours while tracking different isometric contractions. RESULTS: The sEMG signals were recorded successfully from all 64 electrodes across the grid. These electrodes were able to faithfully record sEMG signals during repeated contractions while maintaining a stable baseline at rest. During voluntary contractions, broad EMG frequency content was preserved, with accurate reproduction of the EMG spectrum across the full signal bandwidth. CONCLUSION: The tattoo grid electrode can potentially be used for recording high-density sEMG from skin overlying major limb muscles. Layout programmability, good signal quality, excellent baseline stability, and easy wearability make this electrode a potentially valuable component of future HD electrode grid applications. SIGNIFICANCE: The tattoo electrode can facilitate high fidelity recording in clinical applications such as tracking the evolution and time-course of challenging neuromuscular degenerative disorders.

Quantifying the Peak Amplitude Distributions of Electromyogram in Bicep Brachii muscle after Stroke.

The objective of this study was to quantify the differences in surface electromyogram (EMG) signal characteristics between affected and contralateral arm muscles of hemispheric stroke survivors. EMG signals were recorded from the biceps brachii muscles using single differential electrodes. Four chronic stroke subjects performed isometric elbow flexions at sub-maximal voluntary contraction levels on both the affected and contralateral limbs. The force generated on the contralateral side was matched to the force generated on the affected side. We observed different types of EMG activation on the affected side compared to the contralateral side.Specifically, two subjects showed lower RMS EMG activity on the affected side whereas two subjects showed greater EMG activity on the affected side compared to the contralateral side. Analysis of the peak amplitudes of the EMG activity showed greater number of peaks in the EMG on affected side compared to the contralateral side in all subjects. The histogram of the peak amplitudes showed greater number of smaller peak amplitudes in subjects with lower EMG activity on the affected side suggesting a reliance on smaller motor units. Our combined EMG signal analysis techniques on one set of recorded signals provides insight regarding potential mechanisms of weakness.Clinical Relevance- Decoding neural information from surface EMG signals without decomposition into individual motor units could provide clinicians with quick insight about disease progress and potential treatment.

Characterization of Differences in the Time Course of Reflex and Voluntary Responses Following Botulinum Toxin Injections in Chronic Stroke Survivors.

Spasticity is a major impairment that can occur following a hemispheric stroke and is often treated with injections of botulinum toxin, a neurotoxin that impairs transmission at the neuromuscular junction. Hyperreflexia is a defining feature of spasticity. Our main objective here was to quantify the time course of changes in the deep tendon reflex (DTR) responses and voluntary activation capacity following BT injection as well as to track changes in a clinical assessment of spasticity. Four chronic stroke survivors, scheduled to receive BT in their Biceps Brachii(BB) as part of their clinical care plan, were recruited for repeated testing sessions over the course of 4 months post injection. Both surface BB EMG reflex response to bicipital tendon taps as well as signals of applied tendon tap forces were recorded before and up to 18 weeks post-BT. Voluntary force and biceps EMG signals were also recorded during maximum voluntary (isometric) contractions (MVC) at each testing session. Our results show major reductions (up to 75%) in voluntary sEMG and force arising between 11 to 35 days post-BT-injection. The stretch reflex gain declined two weeks after the maximal reductions in voluntary EMG and force. Paradoxically, there was a short-term increase in stretch reflex gain, in three out of four participants, approximately 11-35 days post BT. The time course of recovery of voluntary MVC and reflex responses varied considerably with a longer recovery time for the reflex responses.

In-Vivo Study of Passive Musculotendon Mechanics in Chronic Hemispheric Stroke Survivors.

We characterized the passive mechanical properties of the affected and contralateral musculotendon units in 9 chronic stroke survivors as well as in 6 neurologically-intact controls. Using a position-controlled motor, we precisely indented the distal tendon of the biceps brachii to a 20 mm depth from skin, recording both its sagittal motion using ultrasound movies and the compression force at the tip of the indenter. Length changes of 8 equally-spaced features along the aponeurosis axis were quantified using a pixel-tracking protocol. We report that, on the aggregate and with respect to contralateral and control, respectively, the affected side initiates feature motion at a shorter indentation distance by 61% and 50%, travels further by 15% and 9%, at a lower rate of 28% and 15%, and is stiffer by 40% and 57%. In an extended analysis including the spatial location of the 8 designated features, we report that in contrast to the contralateral and control muscles, the affected musculotendon unit does not strain measurably within the imaging window. These results confirm that chronic stroke-induced spasticity changes musculotendon unit passive mechanics, causing it to not strain under stretch. The mechanisms responsible for altered passive mechanics may lie within extracellular matrix fibrosis.

Stretch reflex excitability in contralateral limbs of stroke survivors is higher than in matched controls.

BACKGROUND: Spasticity, characterized by hyperreflexia, is a motor impairment that can arise following a hemispheric stroke. While the neural mechanisms underlying spasticity in chronic stroke survivors are unknown, one probable cause of hyperreflexia is increased motoneuron (MN) excitability. Potential sources of increased spinal MN excitability after a stroke include increased vestibulospinal (VS) and/or reticulospinal (RS) drive. Spasticity, as clinically assessed in stroke survivors, is highly lateralized, thus RS contributions to stroke-induced spasticity are more difficult to reconcile, as RS nuclei routinely project bilaterally to the spinal cord. Yet studies in stroke survivors suggest that there may also be changes in neuromodulation at the spinal level, indicative of RS tract influence. We hypothesize that after hemispheric stroke, alterations in the excitability of the RS nuclei affect both sides of the spinal cord, and thereby contribute to increased MN excitability on both paretic/spastic and contralateral sides of stroke survivors, as compared to neurologically intact subjects. METHODS: We estimated stretch reflex thresholds of the biceps brachii (BB) muscle using a position-feedback controlled linear motor to progressively indent the BB distal tendon in both spastic and contralateral limbs of hemispheric stroke survivors and in age-matched intact subjects. RESULTS: Our previously reported results show a significant difference between reflex thresholds of spastic and contralateral limbs of stroke survivors recorded from BB-medial (p < 0.005) and BB-lateral (p < 0.001). For this study, we report that there is also a significant difference between the reflex thresholds in the contralateral limb of stroke subjects and the dominant arm of intact subjects, again measured from both BB-medial (p < 0.05) and BB-lateral (p < 0.05). CONCLUSION: The reduction in stretch reflex thresholds in the contralateral limb of stroke survivors, based here on comparisons with thresholds of intact subjects, suggests an increased MN excitability on contralateral sides of stroke survivors as compared to intact subjects. This in turn supports our contention that RS tract activation, which has bilateral descending influences, is at least partially responsible for increased stretch reflex excitability, post-stroke, as both contralateral and affected sides show increased MN excitability as compared to intact subjects. Still, spasticity, presently diagnosed only on the affected side, with increased MN excitability on the affected side as compared to the contralateral side (our previous study), may be due to a different strongly lateralized pathway, such as the VS tract, which has not been directly tested here. Currently available clinical methods of spasticity assessment, such as the Modified Ashworth Scale, lack the resolution to quantify this phenomenon of a bilateral increase in MN excitability.

Prolonged time course of population excitatory postsynaptic potentials in motoneurons of chronic stroke survivors.

Hyperexcitability of spinal motoneurons may contribute to muscular hypertonia after hemispheric stroke. The origins of this hyperexcitability are not clear, but we hypothesized that prolongation of the Ia excitatory postsynaptic potential (EPSP) in spastic motoneurons may be one potential mechanism, by enabling more effective temporal summation of Ia EPSPs, making action potential initiation easier. Thus, the purpose of this study is to quantify the time course of putative EPSPs in spinal motoneurons of chronic stroke survivors. To estimate the EPSP time course, a pair of low-intensity electrical stimuli was delivered sequentially to the median nerve in seven hemispheric stroke survivors and in six intact individuals, to induce an H-reflex response from the flexor carpi radialis muscle. H-reflex response probability was then used to quantify the time course of the underlying EPSPs in the motoneuron pool. A population EPSP estimate was then derived, based on the probability of evoking an H-reflex from the second test stimulus in the absence of a reflex response to the first conditioning stimulus. Our experimental results showed that in six of seven hemispheric stroke survivors, the apparent rate of decay of the population EPSP was markedly slower in spastic compared with contralateral (stroke) and intact motoneuron pools. There was no significant difference in EPSP time course between the contralateral side of stroke survivors and control subject muscles. We propose that one potential mechanism for hyperexcitability of spastic motoneurons in chronic stroke survivors may be associated with this prolongation of the Ia EPSP time course. Our subthreshold double-stimulation approach could provide a noninvasive tool for quantifying the time course of EPSPs in both healthy and pathological conditions. NEW & NOTEWORTHY Spastic motoneurons in stroke survivors showed a prolonged Ia excitatory postsynaptic potential (EPSP) time course compared with contralateral and intact motoneurons, suggesting that one potential mechanism for hyperexcitability of spastic motoneurons in chronic stroke survivors may be associated with this prolongation of the Ia EPSP time course.

Increase in Muscle Activation during Physiotherapy with Electromyography Biofeedback for Patients with Acute Cervical Spinal Cord Injuries.

Surface electromyography (sEMG) can be used as a biofeedback (BFB) parameter to provide information to participants regarding muscle activation in a variety of settings. The objective of our study is to assess whether an sEMG BFB display during physical therapy sessions for acute spinal cord injured inpatients would assist in increasing muscle use and patient engagement during therapy. In addition, we sought to assess whether the therapist and patients would find the sEMG BFB relevant and useful. To achieve this objective, we examined the effect of visual sEMG BFB system in improving muscle activation and therapeutic outcomes during experimental sessions that mimicked conventional slings therapy sessions with a research therapist providing the therapy. We recruited two inpatients with recent spinal cord injuries (SCI) that had been prescribed (clinical) slings therapy as part of their clinical standard of care at our acute rehabilitation hospital. During each experimental session there were two portions. One was the control period which required the participants to repeat elbow flexion 10 times under conventional clinical slings therapy protocols. The other was the BFB period, where the therapist guided the participant in the same movement but both therapist and the participant were provided with visual feedback of real-time sEMG signals recorded from participant's biceps brachii muscles. Our preliminary results show that both participants demonstrated statistically significant improvement of muscle activation level with the sEMG BFB system compared with conventional clinical slings therapy protocols.

A Tendon Indentation Method to Quantify Velocity-Dependent Reflex Responses after Hemispheric Stroke.

Stretch reflex responses in passive muscle can be utilized to assess spasticity in chronic stroke survivors. In this study, we present a different method of eliciting the reflex response by imposing tendon indentation using a linear motor. Specifically, we test a "Ramp-and-hold" protocol, utilizing a linear motor controlled by a position-controlled feedback loop (Linmot, Inc), to indent the biceps brachii distal tendon at different velocities. The protocol was tested on the affected arm of three stroke subjects. We also utilized a tendon indentation combined with tendon-tapping method to quantify the reflex threshold. Our results indicate that the reflex response was elicited at velocities equal to or above 50 mm/s in 2/3 subjects. No reflex response was detected in one subject. All subjects showed a distinct reflex threshold using the indentation/tapping method. Furthermore, the presence of a reflex response during tendon-tapping was not necessarily accompanied by the elicitation of a reflex response during the ramp-and-hold. However, our data suggests that the indentation threshold during tapping is correlated to the presence of a reflex response at the velocities tested during the ramp-and-hold. Though more time consuming, tendon indentation using ramp-and-hold could provide greater resolution of the reflex response to quantify spasticity than the current clinically employed ballistic tapping method using a reflex hammer.

Effect of Botulinum Toxin on the Spatial Distribution of Biceps Brachii EMG Activity Using a Grid of Surface Electrodes: A Case Study.

Botulinum toxin (BT) is widely prescribed by physicians for managing spasticity post stroke. In an ongoing study, we examine the spatial pattern of muscle activity in biceps brachii of stroke survivors before and after receiving BT, examined over the course of 11 weeks (2 weeks before - 9 weeks after). We hypothesize that BT alters muscle electrophysiology by disrupting fiber neuromuscular transmission in an inhomogeneous manner and we seek to detect these changes using grid surface electromyography (sEMG). Also, we obtained B-mode ultrasound images to have an accurate interpretation of sEMG data by looking at the fiber angle and subcutaneous fat thickness distribution across muscle. Here, we are reporting a single case where a chronic stroke survivor received BT injection in the biceps brachii (BB). A 16x8 sEMG electrode grid was used to capture the muscle activity distribution of BB during sustained non-fatiguing isometric contraction at 40% of maximal voluntary (MVC) elbow flexion. We obtained the root mean squared (RMS) maps of the signal recorded at each of the $16 \times 8$ electrodes. We observed substantial changes in the RMS pattern of BB muscle after receiving BT. More than 80% decrease in sEMG amplitude (RMS) was observed for the channels around the BT injection site as well as about 74% elbow flexion force reduction at the time point of 3-4 weeks post-injection. We also found significant differences between the spatial voluntary activation pattern of pre and post BT RMS maps. We further observed a non-uniform effect and recovery caused by the BT on the distribution of muscle activity. In conclusion, we observed evidence of alteration of the amplitude and pattern of muscle activity after botulinum toxin injection and can document the capability of grid recordings to detect these pattern changes. Our major goals target further investigation to provide an indepth understanding of the effect of botulinum toxin injection at motor unit level.

Organization of the motor-unit pool for different directions of isometric contraction of the first dorsal interosseous muscle.

INTRODUCTION: Muscle force generation involves recruitment and firing rate modulation of motor units (MUs). The control of MUs in producing multidirectional forces remains unclear. METHODS: We studied MU recruitment and firing properties, recorded from the first dorsal interosseous muscle, for 3 different directions of contraction: abduction; abduction/flexion combination; and flexion. RESULTS: MUs were recruited systematically at higher threshold force during flexion. Larger MUs were recruited and firing rates of MUs were lower during abduction. There was an orderly recruitment of MUs according to MU size regardless of contraction direction, obeying the "size principle." Firing rates of earlier-recruited MUs were consistently higher than later-recruited MUs, affirming the "onion-skin" property. DISCUSSION: Our findings suggest that the size principle and onion-skin organization together provide a general description of MU recruitment patterns and firing properties. The directional alternations of MU control properties likely reflect changes in neural drive to the muscle. Muscle Nerve 57: E85-E93, 2018.

Relative contribution of different altered motor unit control to muscle weakness in stroke: a simulation study.

OBJECTIVE: Chronic muscle weakness impacts the majority of individuals after a stroke. The origins of this hemiparesis is multifaceted, and an altered spinal control of the motor unit (MU) pool can lead to muscle weakness. However, the relative contribution of different MU recruitment and discharge organization is not well understood. In this study, we sought to examine these different effects by utilizing a MU simulation with variations set to mimic the changes of MU control in stroke. APPROACH: Using a well-established model of the MU pool, this study quantified the changes in force output caused by changes in MU recruitment range and recruitment order, as well as MU firing rate organization at the population level. We additionally expanded the original model to include a fatigue component, which variably decreased the output force with increasing length of contraction. Differences in the force output at both the peak and fatigued time points across different excitation levels were quantified and compared across different sets of MU parameters. MAIN RESULTS: Across the different simulation parameters, we found that the main driving factor of the reduced force output was due to the compressed range of MU recruitment. Recruitment compression caused a decrease in total force across all excitation levels. Additionally, a compression of the range of MU firing rates also demonstrated a decrease in the force output mainly at the higher excitation levels. Lastly, changes to the recruitment order of MUs appeared to minimally impact the force output. SIGNIFICANCE: We found that altered control of MUs alone, as simulated in this study, can lead to a substantial reduction in muscle force generation in stroke survivors. These findings may provide valuable insight for both clinicians and researchers in prescribing and developing different types of therapies for the rehabilitation and restoration of lost strength after stroke.

Motor Unit Activity during Fatiguing Isometric Muscle Contraction in Hemispheric Stroke Survivors.

Enhanced muscle weakness is commonly experienced following stroke and may be accompanied by increased susceptibility to fatigue. To examine the contributions of central and peripheral factors to isometric muscle fatigue in stroke survivors, this study investigates changes in motor unit (MU) mean firing rate, and action potential duration during, and directly following, a sustained submaximal fatiguing contraction at 30% maximum voluntary contraction (MVC). A series of short contractions of the first dorsal interosseous muscle were performed pre- and post-fatigue at 20% MVC, and again following a 10-min recovery period, by 12 chronic stroke survivors. Individual MU firing times were extracted using surface EMG decomposition and used to obtain the spike-triggered average MU action potential waveforms. During the sustained fatiguing contraction, the mean rate of change in firing rate across all detected MUs was greater on the affected side (-0.02 ± 0.03 Hz/s) than on the less-affected side (-0.004 ± 0.003 Hz/s, p = 0.045). The change in firing rate immediately post-fatigue was also greater on the affected side than less-affected side (-13.5 ± 20 and 0.1 ± 19%, p = 0.04). Mean MU firing rates increased following the recovery period on the less-affected side when compared to the affected side (19.3 ± 17 and 0.5 ± 20%, respectively, p = 0.03). MU action potential duration increased post-fatigue on both sides (10.3 ± 1.2 to 11.2 ± 1.3 ms on the affected side and 9.9 ± 1.7 to 11.2 ± 1.9 ms on the less-affected side, p = 0.001 and p = 0.02, respectively), and changes in action potential duration tended to be smaller in subjects with greater impairment (p = 0.04). This study presents evidence of both central and peripheral fatigue at the MU level during isometric fatiguing contraction for the first time in stroke survivors. Together, these preliminary observations indicate that the response to an isometric fatiguing contraction differs between the affected and less-affected side post-stroke, and may suggest that central mechanisms observed here as changes in firing rate are the dominant processes leading to task failure on the affected side.

Altered Motor Unit Discharge Coherence in Paretic Muscles of Stroke Survivors.

After a cerebral stroke, a series of changes at the supraspinal and spinal nervous system can alter the control of muscle activation, leading to persistent motor impairment. However, the relative contribution of these different levels of the nervous system to impaired muscle activation is not well understood. The coherence of motor unit (MU) spike trains is considered to partly reflect activities of higher level control, with different frequency band representing different levels of control. Accordingly, the objective of this study was to quantify the different sources of contribution to altered muscle activation. We examined the coherence of MU spike trains decomposed from surface electromyogram (sEMG) of the first dorsal interosseous muscle on both paretic and contralateral sides of 14 hemispheric stroke survivors. sEMG was obtained over a range of force contraction levels at 40, 50, and 60% of maximum voluntary contraction. Our results showed that MU coherence increased significantly in delta (1-4 Hz), alpha (8-12 Hz), and beta (15-30 Hz) bands on the affected side compared with the contralateral side, but was maintained at the same level in the gamma (30-60 Hz) band. In addition, no significant alteration was observed across medium-high force levels (40-60%). These results indicated that the common synaptic input to motor neurons increased on the paretic side, and the increased common input can originate from changes at multiple levels, including spinal and supraspinal levels following a stroke. All these changes can contribute to impaired activation of affected muscles in stroke survivors. Our findings also provide evidence regarding the different origins of impaired muscle activation poststroke.

Spatial Analysis of Multichannel Surface EMG in Hemiplegic Stroke.

We investigated spatial activation patterns of upper extremity muscles during isometric force generation in both intact persons and in hemispheric stroke survivors. We used a 128-channel surface electromyogram (EMG) grid to record the electrical activity of biceps brachii muscles during these contractions. EMG data were processed to develop 2-D root mean square (RMS) maps of muscle activity. Our objective was to determine whether motor impairments following stroke were associated with changes in the muscle activity maps and in the spatial distribution of muscular activation. We found that, for a given subject, spatial patterns in muscle activity maps were consistent across all measured contraction levels differing only the RMS EMG. However, the maps from opposite arms (stroke-affected versus non-affected) of stroke survivors were significantly different from each other, especially when compared with the differences observed intact participants. Our analyses revealed that chronic stroke altered the size and location of the active region in these maps. The former is potentially related to disruption of fiber and tissue structure, possibly linked to factors such as extracellular fat accumulation, connective tissue infiltration, muscle fiber atrophy, fiber shortening, and fiber loss. Changes in spatial patterns in muscle activity maps may also be linked to a shift in the location of the innervation zone or the endplate region of muscles. Furthermore, the textural analysis of EMG activity maps showed a larger pixel-to-pixel variability in stroke-affected muscles. Alterations in the muscle activity maps were also related to functional impairment (estimated using Fugl-Meyer score) and to the degree of spasticity (estimated using the modified Ashworth scale). Overall, our investigation revealed that the muscle architecture and morphology were significantly altered in the chronic stroke.

Altered motor unit discharge patterns in paretic muscles of stroke survivors assessed using surface electromyography.

OBJECTIVE: Hemispheric stroke survivors often show impairments in voluntary muscle activation. One potential source of these impairments could come from altered control of muscle, via disrupted motor unit (MU) firing patterns. In this study, we sought to determine whether MU firing patterns are modified on the affected side of stroke survivors, as compared with the analogous contralateral muscle. APPROACH: Using a novel surface electromyogram (EMG) sensor array, coupled with advanced template recognition software (dEMG) we recorded surface EMG signals over the first dorsal interosseous (FDI) muscle on both paretic and contralateral sides. Recordings were made as stroke survivors produced isometric index finger abductions over a large force range (20%-60% of maximum). Utilizing the dEMG algorithm, MU firing rates, recruitment thresholds, and action potential amplitudes were estimated for concurrently active MUs in each trial. MAIN RESULTS: Our results reveal significant changes in the firing rate patterns in paretic FDI muscle, in that the discharge rates, characterized in relation to recruitment force threshold and to MU size, were less clearly correlated with recruitment force than in contralateral FDI muscles. Firing rates in the affected muscle also did not modulate systematically with the level of voluntary muscle contraction, as would be expected in intact muscles. These disturbances in firing properties also correlated closely with the impairment of muscle force generation. SIGNIFICANCE: Our results provide strong evidence of disruptions in MU firing behavior in paretic muscles after a hemispheric stroke, suggesting that modified control of the spinal motoneuron pool could be a contributing factor to muscular weakness in stroke survivors.

Muscle fatigue increases beta-band coherence between the firing times of simultaneously active motor units in the first dorsal interosseous muscle.

Synchronization between the firing times of simultaneously active motor units (MUs) is generally assumed to increase during fatiguing contractions. To date, however, estimates of MU synchronization have relied on indirect measures, derived from surface electromyographic (EMG) interference signals. This study used intramuscular coherence to investigate the correlation between MU discharges in the first dorsal interosseous muscle during and immediately following a submaximal fatiguing contraction, and after rest. Coherence between composite MU spike trains, derived from decomposed surface EMG, were examined in the delta (1-4 Hz), alpha (8-12 Hz), beta (15-30 Hz), and gamma (30-60 Hz) frequency band ranges. A significant increase in MU coherence was observed in the delta, alpha, and beta frequency bands postfatigue. In addition, wavelet coherence revealed a tendency for delta-, alpha-, and beta-band coherence to increase during the fatiguing contraction, with subjects exhibiting low initial coherence values displaying the greatest relative increase. This was accompanied by an increase in MU short-term synchronization and a decline in mean firing rate of the majority of MUs detected during the sustained contraction. A model of the motoneuron pool and surface EMG was used to investigate factors influencing the coherence estimate. Simulation results indicated that changes in motoneuron inhibition and firing rates alone could not directly account for increased beta-band coherence postfatigue. The observed increase is, therefore, more likely to arise from an increase in the strength of correlated inputs to MUs as the muscle fatigues.

Quantification of a single score (1+) in the Modified Ashworth Scale (MAS), a clinical assessment of spasticity.

The Modified Ashworth Scale (MAS) is an assessment that is often used by clinicians to grade spasticity in the affected limbs of stroke survivors. The MAS is a function of the angle at which the clinician perceives a resistance to stretch and/or a `catch' during a passive joint rotation. The qualitative nature of the assessment in combination with the low resolution of the scale could result in varied grouping of spastic patients, even for a single score. The objective of this pilot study was to develop a method for the quantification of the MAS, which could provide greater resolution and could eventually guide better informed therapeutic interventions. The MAS assessment at the elbow joint for four stroke survivors with the same clinical MAS score of 1+ was performed by a clinician and quantified using signals from surface electromyography (EMG) and an electrogoniometer. The subjects were tested on both the affected and contralateral upper limbs. The findings from this study show a varied set of signal outputs across four stroke survivors, all graded at 1+. The quantification provides insight as to the mechanisms underlying the passive resistance.

Using surface electromyography to detect changes in innervation zones pattern after human cervical spinal cord injury.

Human spinal cord injuries (SCI) disrupt the pathways between brain and spinal cord, resulting in substantial impairment and loss of function. Currently, we do not have the ability to precisely quantify the "functional" level of motor injury. The aim of this study is to determine if high-density surface electromyography imaging (SEI) can be used to characterize the location and extent of the spinal lesion. SEI is a safe and non-invasive technique, which uses several electrodes to provide a map of muscle activity. We applied the SEI technique to characterize muscle activity in individuals with chronic incomplete cervical SCI. Surface electromyogram signals (sEMG) from Biceps Brachii (BB) were recorded at submaximal levels (20%, 40%, and 60%) of maximum voluntary contractions (MVC) during isometric elbow flexion, shoulder flexion, and elbow abduction in two individuals with SCI. Through time-domain analysis of the collected data, we detected signs of de-innervation and re-innervations by analyzing the innervation zones (IZ) on the left and right BB muscles. We found that the distribution of IZs was different between the two sides. In addition, analysis of sEMG data collected at rest (no voluntary contraction) showed evidence of superficial active motor units that were active during rest (in the absence of spasms). These findings highlight the potential of SEI technique as a potential clinical tool to quantitatively describe the extent of the damage to motor spinal circuitry, and provide added precision to the clinical examinations and radiological findings.