Spastic Co-contraction Research Articles

USO DA TERAPIA ESPELHO EM MEMBRO SUPERIOR EM PACIENTES COM SEQUELAS APÓS ACIDENTE VASCULAR ENCEFÁLICO: UMA REVISÃO INTEGRATIVA

Introduction: Stroke has become a public health problem worldwide, being the second leading cause of functional limitation, which results in motor dysfunctions in the upper limbs, affecting the notion of space and body senses. These alterations are related to touch, temperature, pain and proprioception, extensor/flexor spasms, increased tendon reflexes, spastic co-contraction, dystonia, fatigability or spasticity. Mirror therapy has been considered a very effective form of treatment for motor dysfunctions. Thus, the present study aims to evaluate the use of mirror therapy in the functional recovery of the upper limbs in patients with sequelae after stroke, in addition to its impact on the quality of life of the participants. Methodology: This study is an integrative literature review with searches in the following databases: PubMed, Medline, Cochrane and Pedro, with articles published between 2019 and 2024. Results and discussion: Thirteen studies were selected, which presented mirror therapy associated with other therapeutic approaches, demonstrating their results in relation to motor functionality, manual dexterity, motor control and grasping. Final Considerations: Based on the findings, it was possible to observe that mirror therapy can contribute significantly to the rehabilitation of upper limb motor function and quality of life of patients after stroke.

Broader Estimates of Gastrocnemius Activity Generated a More Representative Cocontraction Index: A Study in Pediatric Population.

The electromyography (EMG) cocontraction index (CCI) given by the antagonistic/agonistic Root Mean Square (RMS) amplitude ratio of the same muscle is a qualified biomarker used for spastic cocontraction quantification and management in cerebral palsy children. However, this normative EMG ratio is likely subject to a potential source of errors with biased estimates when measuring the gastrocnemius plantar flexors activity. Due to the uneven distribution of electrical activity within the muscle volume, cocontraction levels can be misestimated, if EMGs are obtained from the sole traditional bipolar sensor location recommended by SENIAM. This preliminary study, on 10 healthy children (mean age 10 yr), investigated whether surface EMG detected proximally and distally via two pairs of bipolar electrodes, within the medial gastrocnemius (MG), provides a significant difference in CCI estimates during non-dynamic (isometric dorsiflexion) and dynamic (swing phases of gait) conditions. Gait cycles were extracted from Inertial Measurement Unit sensors. Medial gastrocnemius activity was greater distally than proximally during plantar flexion when it acts as an agonist (~24±18%) and it was greater proximally during dorsiflexion (~23±9%) when it is acting as an antagonist. As a direct consequence, CCI estimates from the conventional sensor location were significantly different (~36%) from the CCIs computed by considering broader MG regions. This difference arose in all subjects during isometric efforts and in two of 10 healthy children during the swing phase of gait who presented cocontraction patterns (p<0.05). EMG bipolar sampling encompassing proximal and distal gastrocnemius muscle regions may reduce bias in CCI computation and provide a more representative and accurate cocontraction index that is especially important for comparisons to the diseased state.

Respective Contributions of Instrumented 3D Gait Analysis Data and Tibial Motor Nerve Block on Presurgical Spastic Equinus Foot Assessment: A Retrospective Study of 40 Adults.

Spastic equinus foot is a common deformity in neurologic patients who compromise walking ability. It is related to the imbalance between weak dorsiflexion and overactive plantar flexor muscles. To achieve the best functional results after surgical management, the challenge is to identify the relevant components involved in the deformity using several methods, namely, examination in the supine position, motor nerve blocks allowing transient anesthesia of suspected overactive muscles, and kinematic and electromyographic data collected during an instrumented 3D gait analysis. The procedure is not standardized; its use varies from one team to another. Access to gait analysis laboratories is limited, and some teams do not perform motor nerve blocks. When both examinations are available, instrumental data from the instrumented 3D gait analysis can be used to specify muscle targets for motor blocks, but data collected from both examinations are sometimes considered redundant.This retrospective cohort analysis compared examination in the supine position, temporary motor nerve blocks, and instrumented 3D gait analysis data in 40 adults after brain or spinal cord injuries. Clinical data collected before motor nerve block was not associated with instrumental data to assess calf muscle's overactivity and tibialis anterior function. Improvement of ankle dorsiflexion in the swing phase after tibial motor nerve block was associated with soleus spastic co-contraction during this phase corroborating its involvement in ankle dorsiflexion defects. This study showed the relevance of tibial motor nerve block to remove spastic calf dystonia and facilitate the assessment of calf contracture. It also underlined the need for complementary and specific analyses of the tibialis anterior abnormal activation pattern after motor nerve block to confirm or deny their pathological nature.

A modified surface EMG biomarker for gait assessment in spastic cerebral palsy.

Muscle clinical metrics are crucial for spastic cocontraction management in children with Cerebral Palsy (CP). We investigated whether the ankle plantar flexors cocontraction index (CCI) normalized with respect to the bipedal heel rise (BHR) approach provides more robust spastic cocontraction estimates during gait than those obtained through the widely accepted standard maximal isometric plantar flexion (IPF). Ten control and 10 CP children with equinus gait pattern performed the BHR and IPF testing and walked barefoot 10-m distance. We compared agonist medial gastrocnemius EMG during both testing and CCIs obtained as the ratios of antagonist EMG during swing phase of gait and either BHR or IPF agonist EMG. Agonist EMG values from the BHR were: (i) internally reliable (Cronbach's α=0.993), (ii) ~50±0.4% larger than IPF, (iii) and positively correlated. Derived CCIs were significantly smaller (p<0.05) in both populations. The bipedal heel rise approach may be accurate enough to reveal greater agonist activity of plantar flexors than the maximal isometric plantar flexion and seems to be more appropriate to obtain cocontraction estimates during swing of gait. This modified biomarker may represent a step forward towards improved accuracy of spastic gait management in pediatric.

Spastic co-contraction is directly associated with altered cortical beta oscillations after stroke

ObjectiveSpastic co-contraction is a motor-disabling form of muscle overactivity occurring after a stroke, contributing to a limitation in active movement and a certain level of motor impairment. The cortical mechanisms underlying spastic co-contraction remain to be more fully elucidated, the present study aimed to investigate the role of the cortical beta oscillations in spastic co-contraction after a stroke. MethodWe recruited fifteen post-stroke participants and nine healthy controls. The participants were asked to perform active elbow extensions. In the study, multimodal analysis was performed to combine the evaluation of three-dimensional elbow kinematics, the elbow muscles electromyographic activations, and the cortical oscillatory activity. ResultsThe movement-related beta desynchronization was significantly decreased in post-stroke participants compared to healthy participants. We found a significant correlation between the movement-related beta desynchronization and the elbow flexors activation during the active elbow extension in post-stroke participants. When compared to healthy participants, post-stroke participants exhibited significant alterations in the elbow kinematics and greater muscle activation levels. ConclusionsCortical beta oscillation alterations may reflect an important neural mechanism underlying spastic co-contraction after a stroke. SignificanceMeasuring the cortical oscillatory activity could be useful to further characterize neuromuscular plasticity induced by recovery or therapeutic interventions.

Spastic co-contraction, rather that spasticity, is associated with impaired active function in adults with acquired brain injury: A pilot study.

To elucidate the adverse consequences of spasticity and spastic co-contraction of elbow flexors on motor impairment and upper limb functional limitation. A pilot case-controlled prospective observational study. Ten brain-injured adults, and 10 healthy controls. The co-contraction index was computed from electromyographic recordings of elbow flexors during sub-maximal (25% Maximal Voluntary Contraction) isometric elbow extension. Spasticity was assessed with the Tardieu scale, upper limb limitation using a goniometer during active elbow extension, motor selectivity with the Fugl-Meyer Assessment for the upper limb, and motor function with the Action Research Arm Test. Greater co-contraction occurred in patients with brain injury compared with controls. In contrast to spasticity, strong associations were found between the co-contraction index, the limitation of active elbow extension, the Fugl-Meyer Assessment, and the Action Research Arm Test. This pilot study suggests that spastic co-contraction rather than spasticity is an important factor in altered upper limb motricity in subjects with brain injury, leading to abnormal restricting arm movement patterns in subjects with more severe motor impairment. Practical applications directly concern the pre- and post-therapeutic evaluation of treatments aimed at improving motor skills in subjects with brain injury.

The neurophysiology of deforming spastic paresis: A revised taxonomy

This paper revisits the taxonomy of the neurophysiological consequences of a persistent impairment of motor command execution in the classic environment of sensorimotor restriction and muscle hypo-mobilization in short position. Around each joint, the syndrome involves 2 disorders, muscular and neurologic. The muscular disorder is promoted by muscle hypo-mobilization in short position in the context of paresis, in the hours and days after paresis onset: this genetically mediated, evolving myopathy, is called spastic myopathy. The clinician may suspect it by feeling extensibility loss in a resting muscle, although long after the actual onset of the disease. The neurologic disorder, promoted by sensorimotor restriction in the context of paresis and by the muscle disorder itself, comprises 4 main components, mostly affecting antagonists to desired movements: the first is spastic dystonia, an unwanted, involuntary muscle activation at rest, in the absence of stretch or voluntary effort; spastic dystonia superimposes on spastic myopathy to cause visible, gradually increasing body deformities; the second is spastic cocontraction, an unwanted, involuntary antagonist muscle activation during voluntary effort directed to the agonist, aggravated by antagonist stretch; it is primarily due to misdirection of the supraspinal descending drive and contributes to reducing movement amplitude; and the third is spasticity, one form of hyperreflexia, defined by an enhancement of the velocity-dependent responses to phasic stretch, detected and measured at rest (another form of hyperreflexia is "nociceptive spasms", following flexor reflex afferent stimulation, particularly after spinal cord lesions). The 3 main forms of overactivity, spastic dystonia, spastic cocontraction and spasticity, share the same motor neuron hyperexcitability as a contributing factor, all being predominant in the muscles that are more affected by spastic myopathy. The fourth component of the neurologic disorder affects the agonist: it is stretch-sensitive paresis, which is a decreased access of the central command to the agonist, aggravated by antagonist stretch. Improved understanding of the pathophysiology of deforming spastic paresis should help clinicians select meaningful assessments and refined treatments, including the utmost need to preserve muscle tissue integrity as soon as paresis sets in.

Is spasticity or spastic cocontraction of the elbow flexors associated with the limitation of voluntary elbow extension in adults with acquired hemiparesis?

Muscle overactivity, including spasticity and spastic cocontraction, is an involuntary motor unit recruitment participating in the spastic paresis syndrome after cerebral injury. Spasticity is defined as velocity-dependent increase in tonic stretch reflexes. Spastic cocontraction refers to increased antagonist muscles recruitment triggered by the volitional command of agonist muscles. This study aimed to clarify the association between spasticity and spastic cocontraction of elbow flexors and to study their contribution to the limitation of active elbow extension in hemiparetic adults. Ten adults with acquired hemiparesis and ten healthy participants were included. Surface EMG recorded from elbow muscles during elbow isometric extension contractions was used to compute the index of cocontraction (ICC) for each participant, while spasticity, limitation of active elbow extension, and upper extremity Fugl-Meyer Assessment (FMA-UE) score were obtained in hemiparetic participants. Non-parametric Spearman correlations were performed to investigate the relationship between ICC and (i) limitation of active elbow extension, (ii) elbow flexors spasticity and (iii) FMA-UE. Our results showed significant ICC in three hemiparetic participants compared with healthy participants, and significant associations between cocontraction and (i) active elbow extension limitation ( r s = 0.81, P < 0.001) and iii) Fugl-Meyer Assessment score ( r s = −0.53, P = 0.017) in hemiparetic participants. No significant correlation was found between spasticity and active elbow extension limitation. Our results are the first to show that spastic cocontraction directly contributes to elbow extension deficit in adults with acquired hemiparesis, and further confirm that spasticity and spastic cocontraction have different functional repercussions with regards to impaired motor function. Our findings support the conclusion that spastic cocontraction, rather than spasticity, has significant functional repercussions on impaired active motor function in hemiparetic adults. Therapeutic innovations should be directed toward reduction of spastic cocontraction to improve motor function in acquired hemiparesis.

Correlation between coefficients of impairment at various muscles and active function in the paretic upper limb

In hemiparesis, motor function may be hindered to various degrees by soft tissue contracture, spasticity, spastic co-contraction and agonist paresis. This retrospective study explores correlations between neuromuscular impairments at shoulder, elbow, wrist and fingers and overall function in the paretic upper limb. Fifty-one patients with chronic hemiparesis [25 W, 48(±15) years (mean[±SD]), time since lesion, 7.7(±5.5) years] were assessed using the Five Step Assessment, at least three months after any botulinum toxin injection. The first step assessed motor function of the upper limb by the Modified Frenchay scale (MFS; score between 0 and 10). The 2nd, 3rd and 4th steps assessed coefficients of impairment in four key muscles: shoulder extensors, elbow flexors, wrist flexors and fingers flexors. These coefficients were calculated as: coefficient of shortening [C SH = (X N − X V1 )/X N ; X N , normally expected amplitude; X V1 , angle of arrest upon slow stretch], coefficient of spasticity [C SP = (X V1 − X V3 )/X V1 ; X V3 , angle of catch upon fast stretch], coefficient of weakness [C W = (X V1 − X A )/X V1 ; X A , maximal active range of motion]. For each impairment factor, a mean coefficient across the four muscles was calculated (C SHmean , C SPmean , C Wmean ). For each muscle group and for the mean, multivariable correlations were explored between C SH , C SP , C W and MFS. The MFS correlated with C SH-shoulder ( r = −0.28, P = 0.03) and C W-shoulder ( r = −0.46, P = 0.001); C W-elbow ( r = −0.45, P = 0.002); C W-wrist ( r = −0.33, P = 0.003); C W-Fingers ( r = −0.63, P < 0.0001); C Wmean ( r = −0.78, P < 0.0001). The main factors impeding motor function in chronic spastic paresis are the combination of paresis in agonist and spastic co-contraction in antagonist (limiting active motion) for shoulder extensors and for elbow, wrist and finger flexors. Soft tissue contracture for shoulder extensors also contributed to hinder motor function. Spasticity was not correlated with the mean score of MFS, whichever the muscle considered.

Effect of functional electrical stimulation of the peroneal nerve on antagonist resistances measured during swing phase of gait in spastic paresis. A randomized, controlled study

In hemiparesis, functional electrical stimulation (FES) of the peroneal nerve aims to compensate for ankle dorsiflexor paresis in swing phase. The present prospective study compared the effects of gait training with FES vs. conventional therapy on plantar flexor overactivity. Twenty subjects with chronic hemiparesis (6 ± 4years post-lesion; mean ± SD) were randomized into two groups: FES (45 min/day of gait self-training using FES) and Control (CON, 3 × 45 min/week of conventional physiotherapy) for 10 weeks. Outcomes at Day 1 and Week 10 included comfortable speed barefoot gait analysis with gastrocnemius medialis (GM) and soleus (SO) electromyography, yielding:, walking speed; and, at the paretic ankle: maximal passive dorsiflexion during stance, maximal active dorsiflexion during swing, velocity of active dorsiflexion over early swing, coefficient of spastic cocontraction in GM and SO over the three thirds of swing (CSC, calculated by the ratio of the RMS of the electromyogram in the period of interest over the RMS of the electromyogram of the same muscle over 100 ms around its maximal voluntary contraction). Intra- and inter-group comparison used rank-ANOVAs. No difference was observed in walking speed changes (both groups pooled; D1, 0.73 ± 0.25 m/s, W10, 0.80 ± 0.30 m/s, ns) and in passive and active dorsiflexion amplitudes (ns). However, the velocity of active dorsiflexion increased in FES while it decreased in Controls (D1 vs. W10, FES, +5 ± 2°/s, P = 0.02; CON, −4 ± 1°/s, P = 0.04). In parallel, CSC GM in early swing tended to improve in FES only (FES, −41 ± 23%, P = 0.09; CON, −24 ± 89%, ns; between group difference ns). In chronic hemiparesis, FES, which focuses on agonist dorsiflexor stimulation during gait improves active dorsiflexion velocity in swing and may also be associated with reduction of plantar flexor spastic cocontraction. Further studies are required to confirm these findings and evaluate whether reciprocal inhibition toward plantar flexors may be restored by FES.

Relationships between coefficients of impairments at lower limb muscles in chronic spastic paresis–Could the muscle disease impact on the neurological disease?

At the onset of hemiparesis, muscle tissue is normal and spastic overactivity is nil. Later, motor function becomes gradually hindered by: spastic myopathy (part of soft tissue contracture) and co-contraction, in addition to paresis. Relationships between these remain unclear. This retrospective study explores correlations between muscle shortening on one hand, and, spastic co-contraction and agonist paresis on the other hand. Eighty participants with chronic hemiparesis (29 W, 51 (± 13) years (mean (± SD)), time since lesion, 6.4 (± 3.2) years)) were assessed through the Five Step Assessment, at least three months after any botulinum toxin injection, in six key lower limb antagonists: soleus (SO), gastrocnemius (GN), gluteus maximus (GM), hamstrings (HS), vastus (VA), rectus femoris (RF). Coefficients of impairment were calculated as: coefficient of shortening (C SH = (X N − X V1 )/X N ; X N , normally expected amplitude; X V1 , angle of arrest upon slow stretch), coefficient of weakness (C W = (X V1 − X A )/X V1 ; X A , maximal active range of motion). For each muscle and for the mean of the six muscles, bivariate correlations between C SH and C W were explored, using Pearson's coefficients. The mean C SH are as follows: C SH-SO , 0.15 ± 0.05; C SH-GN , 0.17 ± 0.04; C SH-GM , 0.14 ± 0.08; C SH-HS , 0.06 ± 0.05; C SH-VA , 0.09 ± 0.05; C SH-RF , 0.13 ± 0.07. C W strongly correlated with C SH across the six muscles ( r = 0.30, P = 0.006). This correlation was also found individually for GN ( r = 0.43, P < 0.0001), GM ( r = 0.22, P = 0.04) and HS ( r = 0.21, P = 0.052). While causality is not explored in this study, one may speculate that spastic myopathy (assessed through coefficient of shortening) may play a role in neurologic impairments, potentially by chronic modifications of afferent volleys to the spinal cord.

Gait improvement with decreased tibialis anterior recruitment after botulinum toxin injections into peroneus longus in very young children with hemiparetic cerebral palsy

In very young cerebral palsy (CP) children, peroneus longus (PL) overactivity by spastic co-contraction is a major contributor to dynamic equinovalgus during swing phase (SW) and at initial contact (IC). This study assessed the effects of abobotulinum toxin A injections into PL. Eleven male children with hemiparesis (7 right; age 3.1 ± 0.6 yo) were injected once in PL, without GastroSoleusComplex (GSC) injection. GSC was assessed for functional length (X V1 ) and spasticity (X V3 ). Gait analysis videos were evaluated using the Edinburgh visual gait score (EVGS-validated in CP): pre- vs. post-injection values were compared using paired t-tests. EMG monitored tibialis anterior (TA), gastrocnemius medialis (GM) and PL during gait. Swing phase was divided into three periods (SW1, SW2, SW3) to measured, using EMG: GM and PL co-contractions and TA recruitment during SW (SW, SW1, SW2, SW3), during standing on tiptoes (EMGmaxPL, EMGmaxGM), standing on heels (EMGmaxTA). For each measured EMG variable, efficacy indices was assessed using the ratio (EMG VARIABLE-X_POST − EMG VARIABLE-X_PRE )/(EMG VARIABLE-X_POST + EMG VARIABLE-X_PRE ) and compared with an inefficacy theoretical index of 0. Comparison involved 1937 pre-toxin strides (mean per child 176 ± 114) vs. 1231 post-toxin strides (mean 112 ± 79). There were no difference in X V1-GSC (X V1-GSC-pre 103°[6]; X V1-GSC-post 103°[6] or in X V3-GSC (X V3-GSC-pre 89°[8]; X V3-GSC-post 96°[4.5]). EVGS-global-score was improved ( P = 0.007) with better clearance in SW ( P = 0.07), increased knee re-extension in terminal SW ( P = 0.04) and decreased hindfoot valgus at IC ( P = 0.02). The normalised-EMGmax was unchanged for PL (−0.06 [0.16]) but increased for GM (0.18 [0.20], P = 0.007) and TA (0.28 [0.19], P < 0.001). There were reductions of co-contraction in PL ( P < 0.0001; SW, −0.26 [0.14]; SW1, −0.22 [0.14]; SW2, −0.27 [0.14]; SW3, −0.26 [0.18]) and in GM (SW, −0.26 [0.14]), P = 0.06; SW1,−0.21(0.18), P < 0.001; SW2, −0.25 [0.20], P < 0.01; SW3, −0.21 [0.25], P = 0.06). TA recruitment was decreased: SW, −0.08 (0.18), P = 0.06; SW1, −0.11 (0.20), P < 0.001; SW2, −0.07 (0.17) NS; SW3, −0.07 (0.24), NS. In this retrospective study, PL injections in very young CP children improved foot clearance and decreased hindfoot valgus, which was associated with reductions of PL and GM co-contractions and of TA recruitment. This constitutes an argument supporting that increased TA recruitment in children with hemiparesis may be an attempt by the nervous system to compensate for plantar flexor co-contraction rather than the opposite (increased co-contraction due to increased TA recruitment). We can discuss a central action of abobotulinum toxin A.

Muscle Shortening and Spastic Cocontraction in Gastrocnemius Medialis and Peroneus Longus in Very Young Hemiparetic Children.

Objectives Muscle shortening and spastic cocontraction in ankle plantar flexors may alter gait since early childhood in cerebral palsy (CP). We evaluated gastrosoleus complex (GSC) length, and gastrocnemius medialis (GM) and peroneus longus (PL) activity during swing phase, in very young hemiparetic children with equinovalgus. Methods This was an observational, retrospective, and monocentric outpatient study in a pediatric hospital. Ten very young hemiparetic children (age 3 ± 1 yrs) were enrolled. These CP children were assessed for muscle extensibility (Tardieu scale XV1) in GSC (angle of arrest during slow-speed passive ankle dorsiflexion with the knee extended) and monitored for GM and PL electromyography (EMG) during the swing phase of gait. The swing phase was divided into three periods (T1, T2, and T3), in which we measured a cocontraction index (CCI), ratio of the Root Mean Square EMG (RMS-EMG) from each muscle during that period to the peak 500 ms RMS-EMG obtained from voluntary plantar flexion during standing on tiptoes (from several 5-second series, the highest RMS value was computed over 500 ms around the peak). Results On the paretic side: (i) the mean XV1-GSC was 100° (8°) (median (SD)) versus 106° (3°) on the nonparetic side (p = 0.032, Mann–Whitney); (ii) XV1-GSC diminished with age between ages of 2 and 5 (Spearman, ρ = 0.019); (iii) CCIGM and CCIPL during swing phase were higher than on the nonparetic side (CCIGM, 0.32 (0.20) versus 0.15 (0.09), p < 0.01; CCIPL, 0.52 (0.30) versus 0.24 (0.17), p < 0.01), with an early difference significant for PL from T1 (p = 0.03). Conclusions In very young hemiparetic children, the paretic GSC may rapidly shorten in the first years of life. GM and PL cocontraction during swing phase are excessive, which contributes to dynamic equinovalgus. Muscle extensibility (XV1) may have to be monitored and preserved in the first years of life in children with CP. Additional measurements of cocontraction may further help target treatments with botulinum toxin, especially in peroneus longus.

Localised sampling of myoelectric activity may provide biased estimates of cocontraction for gastrocnemius though not for soleus and tibialis anterior muscles

Proper muscle activity quantification is highly relevant to monitor and treat spastic cocontraction. As activity may distribute unevenly within muscle volumes, particularly for pennate calf muscles, surface electromyograms (EMGs) detected by traditional bipolar montage may provide biased estimations of muscle activity. We compared cocontraction estimates obtained using bipolar vs grids of electrodes (high-density EMG, HD-EMG). EMGs were collected from medial gastrocnemius, soleus and tibialis anterior during isometric plantar and dorsi-flexion efforts at three levels (30%, 70% and 100% MVC), knee flexed and extended. Cocontraction index (CCI) was estimated separately for each electrode pair in the grid. While soleus and tibialis anterior CCI estimates did not depend on the detection system considered, for gastrocnemius bipolar electrodes provided larger cocontraction estimates than HD-EMG at highest effort levels, at both knee angles (ANOVA; P < .001). Interestingly, HD-EMG detected greater gastrocnemius EMGs distally during plantar flexions, and greater CCI values proximally during dorsiflexions. These results suggest that bipolar electrodes: (i) provide reliable estimates of soleus and tibialis anterior cocontraction; (ii) may under-or overestimate gastrocnemius cocontraction, depending on their distal or proximal position.

Spastic cocontraction of triceps surae increases with the tension applied during swing phase of gait in chronic hemiparesis

The present study aimed to quantify the impact of the tension applied on triceps surae during the swing phase of gait on its cocontraction in chronic hemiparesis. Forty-one subjects with chronic hemiparesis (50 ± 15 years; time since lesion, 7 ± 7 years; mean ± SD) completed a kinematic gait analysis, barefoot at comfortable speed (10 opto-electronic cameras, 6 dynamometric force plates, 27 ± 13 cycles analyzed/subject), with electromyography of soleus (so) and gastrocnemius medialis (gm) on the paretic side. The Coefficients of Spastic Cocontraction, CSCso and CSCgm, were calculated over 3 periods of swing phase (T1, [0–33] %; T2, [34–66] %; T3, [67–100] %), by the ratio of the RMS of the electromyogram in the period of interest over the RMS of the electromyogram of the same muscle over 100 ms around the maximal agonist isometric activity (measured on standing position by a maximal effort against resistance). In addition, a coefficient of lengthening of triceps surae, CLts, was computed over each period in the sagittal plane, from the ankle/knee displacements recorded during the period of interest divided by the total range of ankle/knee movements measured across all gait cycles. CSCso, CSCgm and CLts were compared between the 3 periods (ANOVA, significant effect P < 0.05). Exploration of individual correlations were performed with all gait cycles of each patient, using univariate regression analysis with CLts as predictor and coefficients of spastic cocontraction (CSCso and CSCgm) as dependent variables. Between T2 et T3, CSCso increased by 233 ± 54% (mean ± SEM, P < 1E-5) and CSCgm by 67 ± 10% ( P = 0.0017). CLts increased by 23 ± 7% in T2 ( P = 0.009) and 52 ± 12% in T3 ( P < 1E-5). CLts was positively correlated with CSCso in 63% of cases ( n = 25, r = 0.63 ± 0.04, P < 0.1) and with CSCgm in 53% of cases ( n = 21, r = 0.60 ± 0.04, P < 0.1). In chronic hemiparesis, tension (lengthening) applied on triceps surae is associated with the increase of its spastic cocontraction during swing phase of gait at comfortable speed.

Spastic cocontraction of plantar flexors during swing phase of gait in chronic hemiparesis

In spastic hemiparesis, quantify agonist recruitment of tibialis anterior and triceps surae spastic cocontraction during swing phase of gait. Thirty-seven subjects with chronic hemiparesis (49 ± 14 years, mean ± SD; time since lesion, 8 ± 7 years) performed a 3D gait analysis, barefoot at comfortable speed (10 optoelectronic cameras, 6 dynamometric force plates, analysis of 9 cycles), with bilateral electromyography of tibialis anterior (TA), soleus (SO) and gastrocnemius medialis (GM). Speed, step length and maximal active dorsiflexion during swing were measured. Indices of agonist recruitment, IRATA, and spastic cocontraction, ICCSO and ICCGM, were calculated over 3 periods of swing phase (T1, [0–33%]; T2, [34–66%]; T3, [67–100%]), by the ratio of the RMS of the electromyogram in the period of interest over the RMS of the electromyogram of the same muscle over 100 ms around the maximal agonist isometric activity (measured on standing position by a maximal effort against resistance). IRA and ICC were compared between the 3 periods and between paretic and non paretic sides using repeated measures MANOVA (significant effect, P < 0.05). Speed, 0.68 ± 0.26 m/s; paretic step length, 0.48 ± 0.12 m, non paretic, 0.43 ± 0.15 m; paretic maximal active dorsiflexion, −3 ± 8°, non paretic, 6 ± 4°. On the paretic side: IRATA decreased between T1 and T2 (T1, 0.69 ± 0.59; T2, 0.48 ± 0.39, P = 2E-4) and then remained unchanged at T3 (0.47 ± 0.45; vs T1, P = 1E-4; vs T2, ns), while ICCSO and ICCGM increased at T3 only (ICCSO, T2, 0.25 ± 0.21; T3, 0.57 ± 0.50; P = 5E-8; ICCGM, T2, 0.39 ± 0.40; T3, 0.59 ± 0.50; P = 2E-4). On the non-paretic side, IRATA, ICCSO and ICCGM remained unchanged (IRATA, T1, 0.32 ± 0.20; T2, 0.23 ± 0.13; T3, 0.25 ± 0.10, ns; ICCSO, T1, 0.12 ± 0.12; T2, 0.13 ± 0.12; T3, 0.25 ± 0.18 ns; ICCGM, T1, 0.17 ± 0.31; T2, 0.19 ± 0.27; T3, 0.26 ± 0.25 ns). Side xperiod effect, P = 0.04. During comfortable gait in chronic hemiparesis, there is a decrease in tibialis anterior recruitment from mid-swing phase on and an increase in soleus and gastrocnemius spastic cocontraction at late swing were found.

Spastic co-contraction of gastrocnemius medialis and peroneus longus during swing phase of gait in hemiplegic children

Spastic cocontraction [1] is a form of muscle overactivity [1] , [2] that may alter gait in infant hemiparesis. We quantified EMG activity in Gastrocnemius Medialis (GM) and Peroneus Longus (PL) during the swing phase (SW) of gait in very young hemiparetic children with an equino-valgus pattern [3] , comparing the paretic and non-paretic side. Ten hemiparetic children (age 3 ± 1, mean ± SD) were monitored for GM and PL EMG during gait. The SW was divided into three thirds (initial-T1, middle-T2 and end-T3). In each period, a Cocontraction Index (CCI) [4], ratio of the Root Mean Square (RMS) EMG from each muscle during that period to the peak 500-ms RMS obtained from voluntary plantar flexion during a selected submaximal state (standing on tiptoes) was measured. GM and PL CCIs during SW were higher on the paretic than on the non-paretic side (Wilcoxon:CCI GM , P < 0.01;CCI PL , P < 0.01). When subdividing the SW, there was a CCI increase on the paretic side during mid and late SW for GM (Wilcoxon: CCI GMT2 , P < 0.01;CCI GMT3 , P < 0.001), and during early, mid and late SW for PL (Wilcoxon: CCI PLT1 , P = 0.03;CCI PLT2 , P = 0.014 and CCI PLT3 , P < 0.001). GM and PL cocontraction increases may contribute to the equinus on the paretic side. Specifically, PL cocontraction increase might cause the hind-foot valgus at late swing, moving the first metatarsal downwards and pronating the forefoot. Quantification of cocontraction could provide a better understanding of the adverse muscle actions and contribute to better target the therapeutic actions, especially botulinum toxin injection in PL, to improve gait in very young hemiparetic children before orthopaedic deformation.

Impact of stretched position of a shortened muscle on active command in spastic paresis

In spastic paresis, factors limiting active movement include antagonist contracture, agonist paresis, and spastic cocontraction. We studied agonist and antagonist muscle activation around the elbow to determine the role of the degree of muscle stretch in modifying paresis and cocontraction. Eighteen healthy (age 47 ± 10) and 15 hemiparetic (age 42 ± 16) subjects performed maximal isometric elbow flexion and extension 5-second efforts, with elbow flexed and extended. Using biceps and triceps brachii surface electromyography, we determined for each muscle: (i) the Mean Rectified Voltage (MRV) during the 500 ms peak voluntary agonist recruitment elbow flexed (MRV ago500F ) and elbow extended (MRV ago500E ); (ii) the coefficient of stretch-sensitivity (CSS) of agonist recruitment, calculated as (MRV ago500F -MRV ago500E )/MRV ago500F ; (iii) the cocontraction index (CCI) in each elbow position, ratio of the MRV from each muscle during an opposite movement, MRV antago5 to MRV ago500 . We compared the dominant arm in healthy subjects with the non-paretic and paretic arms in hemiparetic subjects. X V1 was 175 ± 11° in the elbow flexors (maximal passive elbow extension; coefficient of shortening, 2.7%) and 163 ± 7° in the elbow extensors (no shortening) . CSS was not significantly different from 0 in the healthy and non-paretic arm; however, CSS in the paretic arm was −21 ± 10% in the paretic elbow extensors vs −4 ± 7% in the non-paretic arm ( P vs extended, P = 0.013). Triceps brachii CCI with the elbow flexed was 0.10 ± 0.05 [95%CI, 0.03–0.17], 0.15 ± 0.10 [0.07–0.23] and 0.26 ± 0.24 [0.18–0.34], in the healthy, non-paretic and paretic arm respectively (between-group difference P = 0.011), and 0.12 ± 0.06 [95%CI, 0.03–0.21], 0.15 ± 0.08 [0.06–0.25], and 0.38 ± 0.32 [0.28–0.48] with the elbow extended (between-group difference P vs extended, NS). In hemiparesis, elbow extended position deteriorates active command at both agonist and antagonist levels: decreasing voluntary recruitment of agonist MNs–a phenomenon defined as stretch-sensitive paresis–and increasing antagonist co-contraction. This may occur through physiological effects of high-threshold afferent fiber recruitment in contractured elbow flexors.

Length of the gastrosoleus complex and dynamic EMG of peroneus longus and gastrocnemius medialis in hemiplegic children with equinovarus: The hypothesis of the spastic cocontraction

Chronic pain affects about 100 million U.S. adults, with chronic low back pain (CLBP) cited as the most prevalent type. Although there is evidence that non-pharmacological therapies seem to be effective for treating low back pain, there is limited evidence of the effectiveness of EMG biofeedback with non-specific chronic low back pain (NCLBP). The purpose of this study is, therefore, to determine the efficacy of a portable EMG biofeedback device on pain in individuals with CLBP.This study is a prospective, single-center, assessor-blind, two-arm, parallel randomized controlled trial to be conducted at Brigham and Women's Hospital, Boston, MA. Eighty patients with CLBP will be randomized in a 2:1 ratio to receive sEMG-BF (surface EMG biofeedback) or continued care (no intervention). All participants will receive treatment virtually weekly for 8 weeks. The primary outcome will be pain intensity (Brief Pain Inventory). The secondary outcomes will include pain interference (Brief Pain Inventory), disability (The Oswestry Disability Index (ODI)), anxiety and depression (Hospital Anxiety and Depression Scale). All outcomes will be assessed at baseline, immediately post-intervention, and 3 months follow-up.To our knowledge, this study will be the first powered randomized controlled trial to compare the effectiveness of a virtual sEMG-BF protocol specifically designed for CLBP. The outcome of the study may provide evidence for the effectiveness of biofeedback using digital therapeutics to relieve pain in individuals with CLBP.Trial registration: Clinical Trials Registry (http://ClinicalTrials.gov Identifier: NCT04607460). Registered on October 29, 2020.

Safety and efficacy of abobotulinumtoxinA for hemiparesis in adults with upper limb spasticity after stroke or traumatic brain injury: a double-blind randomised controlled trial

Resistance from antagonistic muscle groups might be a crucial factor reducing function in chronic hemiparesis. The resistance due to spastic co-contraction might be reduced by botulinum toxin injections. We assessed the effects of abobotulinumtoxinA injection in the upper limb muscles on muscle tone, spasticity, active movement, and function. In this randomised, placebo-controlled, double-blind study, we enrolled adults (aged 18-80 years) at least 6 months after stroke or brain trauma from 34 neurology or rehabilitation clinics in Europe and the USA. Eligible participants were randomly allocated in a 1:1:1 ratio with a computer-generated list to receive a single injection session of abobotulinumtoxinA 500 U or 1000 U or placebo into the most hypertonic muscle group among the elbow, wrist, or finger flexors (primary target muscle group [PTMG]), and into at least two additional muscle groups from the elbow, wrist, or finger flexors or shoulder extensors. Patients and investigators were masked to treatment allocation. The primary endpoint was the change in muscle tone (Modified Ashworth Scale [MAS]) in the PTMG from baseline to 4 weeks. Secondary endpoints were Physician Global Assessment (PGA) at week 4 and change from baseline to 4 weeks in the perceived function (Disability Assessment Scale [DAS]) in the principal target of treatment, selected by the patient together with physician from four functional domains (dressing, hygiene, limb position, and pain). Analysis was by intention to treat. This study is registered with ClinicalTrials.gov, number NCT01313299. 243 patients were randomly allocated to placebo (n=81), abobotulinumtoxinA 500 U (n=81), or abobotulinumtoxinA 1000 U (n=81). Mean change in MAS score from baseline at week 4 in the PTMG was -0·3 (SD 0·6) in the placebo group (n=79), -1·2 (1·0) in the abobotulinumtoxinA 500 U group (n=80; difference -0·9, 95% CI -1·2 to -0·6; p<0·0001 vs placebo), and -1·4 (1·1) in the abobotulinumtoxinA 1000 U group (n=79; -1·1, -1·4 to -0·8; p<0·0001 vs placebo). Mean PGA score at week 4 was 0·6 (SD 1·0) in the placebo group (n=78), 1·4 (1·1) in the abobotulinumtoxinA 500 U group (n=80; p=0·0003 vs placebo), and 1·8 (1·1) in the abobotulinumtoxinA 1000 U group (n=78; p<0·0001 vs placebo). Mean change from baseline at week 4 in DAS score for the principal target of treatment was -0·5 (0·7) in the placebo group (n=79), -0·7 (0·8) in the abobotulinumtoxinA 500 U group (n=80; p=0·2560 vs placebo), and -0·7 (0·7) in the abobotulinumtoxinA 1000 U group (n=78; p=0·0772 vs placebo). Three serious adverse events occurred in each group and none were treatment related; two resulted in death (from pulmonary oedema in the placebo group and a pre-existing unspecified cardiovascular disorder in the abobotulinumtoxinA 500 U group). Adverse events that were thought to be treatment related occurred in two (2%), six (7%), and seven (9%) patients in the placebo, abobotulinumtoxinA 500 U, and abobotulinumtoxinA 1000 U groups, respectively. The most common treatment-related adverse event was mild muscle weakness. All adverse events were mild or moderate. AbobotulinumtoxinA at doses of 500 U or 1000 U injected into upper limb muscles provided tone reduction and clinical benefit in hemiparesis. Future research into the treatment of spastic paresis with botulinum toxin should use active movement and function as primary outcome measures. Ipsen.