Passive Muscle Stiffness Research Articles

Ultrasound shear wave elastography in the assessment of passive biceps brachii muscle stiffness: influences of sex and elbow position

ObjectiveTo assess differences in biceps brachii muscle (BBM) stiffness as evaluated by ultrasound shear wave elastography (SWE). MethodsThe passive stiffness of the BBM was quantified with shear wave velocity (SWV) measurements obtained from 10 healthy volunteers (5 men and 5 women, mean age 50years, age range 42–63 years) with the elbow at full extension and 30° flexion in this IRB-approved study. Potential differences between two depths within the muscle, two elbow positions, the two arms, and sexes were assessed by using two-tailed t-test. The reproducibility of SWV measurements was tested by using intraclass correlation coefficient (ICC). ResultsSignificantly higher passive BBM stiffness was found at full elbow extension compared to 30° of flexion (p≤0.00006 for both arms). Significantly higher passive stiffness in women was seen for the right arm (p=0.04 for both elbow positions). Good correlation of shear wave velocity measured at the different depths. The ICC for interobserver and intraobserver variation was high. ConclusionsSWE is a reliable quantitative tool for assessing BBM stiffness, with differences in stiffness based on elbow position demonstrated and based on sex suggested.

Is the stiffness of human muscle and tendon structures related to muscle fiber composition in vivo?

The aim of the present study was to investigate the relationship between estimated muscle fiber composition (time-to-peak twitch torque; TPT) and muscle stiffness under passive and active conditions as well as stiffness of tendon structures in human plantar flexors. TPT was assessed using supramaximal electrical stimulation. Active muscle stiffness in the medial gastrocnemius muscle was calculated based on changes in estimated muscle force and fascicle length during fast stretching after 50% maximal isometric contractions. Passive muscle stiffness was also calculated from estimated passive muscle force and fascicle length during slow passive stretching. Stiffness of tendon structures was determined during isometric plantar flexion using ultrasonography. TPT did not correlate with passive muscle stiffness (r=0.039, P=0.790), active muscle stiffness (r=0.185, P=0.203), or stiffness of tendon structures (r=-0.178, P=0.477). These results suggested that the muscle fiber composition of the human medial gastrocnemius muscle was not related to the mechanical properties of muscles or tendon structures.

Resistance to radial expansion limits muscle strain and work.

The collagenous extracellular matrix (ECM) of skeletal muscle functions to transmit force, protect sensitive structures, and generate passive tension to resist stretch. The mechanical properties of the ECM change with age, atrophy, and neuromuscular pathologies, resulting in an increase in the relative amount of collagen and an increase in stiffness. Although numerous studies have focused on the effect of muscle fibrosis on passive muscle stiffness, few have examined how these structural changes may compromise contractile performance. Here we combine a mathematical model and experimental manipulations to examine how changes in the mechanical properties of the ECM constrain the ability of muscle fibers and fascicles to radially expand and how such a constraint may limit active muscle shortening. We model the mechanical interaction between a contracting muscle and the ECM using a constant volume, pressurized, fiber-wound cylinder. Our model shows that as the proportion of a muscle cross section made up of ECM increases, the muscle's ability to expand radially is compromised, which in turn restricts muscle shortening. In our experiments, we use a physical constraint placed around the muscle to restrict radial expansion during a contraction. Our experimental results are consistent with model predictions and show that muscles restricted from radial expansion undergo less shortening and generate less mechanical work under identical loads and stimulation conditions. This work highlights the intimate mechanical interaction between contractile and connective tissue structures within skeletal muscle and shows how a deviation from a healthy, well-tuned relationship can compromise performance.

Investigation of heat production deficiencies during cold stress and a nonshivering thermogenesis challenge in mice with a deletion in N2A titin

Homeothermic animals strive to maintain core body temperature across varying ambient temperatures. Studies have demonstrated that mice with the muscular dystrophy with myositis (mdm) mutation shiver at a lower than expected frequency, are heterothermic, and have reduced active muscle stiffness in vivo compared to wildtype mice. Mdm mice are characterized by a deletion in the N2A region of titin that results in a lower body mass, stiffer gait, and reduced lifespan. The underlying defect that leads to a lower shivering frequency is not known but could be caused by muscle properties. The titin protein is known to behave like a spring and contribute to passive muscle stiffness. Recent studies have shown that titin contributes to active muscle stiffness as well. Shivering thermogenesis can be modeled as simple harmonic motion, where the spring constant k represents muscle stiffness. This impairment in heat production could be due to the N2A deletion in the titin protein, leading to a more compliant spring and a lower shivering frequency as explained by simple harmonic motion. An alternative hypothesis is that the ability of mdm mice to use nonshivering thermogenesis and/or uncoupling protein 1 (UCP1), found in brown adipose tissue (BAT) to generate heat during cold stress is impaired. The purpose of this study was to evaluate potential causes for the inability of mdm mice to maintain homeothermy during cold stress. We hypothesize that the inability of mdm mice to thermoregulate properly is due primarily to an impairment in heat production (e.g. shivering thermogenesis and nonshivering thermogenesis). Mice underwent a 4‐day cold stress experiment during which they lived in a mouse cage that used a continuous system for indirect calorimetry. The cages were placed in an incubator so that ambient temperature could be controlled. During each experiment, temperature was controlled to either 34°C, 29°C, 25°C, 19°C. Upon conclusion of the cold stress experiment, a nonshivering thermogenesis challenge was employed by administering 1.5 mg/kg of norepinephrine. As expected, wildtype mice increased their metabolic rate during cold stress and during the nonshivering thermogenesis challenge. RQ values reached 0.7, representing pure fat oxidation and utilization of uncoupling protein 1, present in BAT. Core body temperature for an mdm mouse decreased with decreasing ambient temperature within a range of 28C to 37C. During the nonshivering thermogenesis challenge, both wildtype and mdm mice increased their oxygen consumption. Both mdm and wildtype mice increased their oxygen consumption by 37% during the nonshivering thermogenesis challenge. These results suggest that the failure to maintain homeothermy is due to reduced shivering frequency and not a reduced capacity for nonshivering thermogenesis, pending additional experiments.Support or Funding InformationOur funding sources include NSF IOS‐0742483, NSF IOS‐1025806, NSF IOS‐1456868, and the W.M. Keck Foundation.

Influence of subjects' characteristics and technical variables on muscle stiffness measured by shear wave elastosonography.

The aim of this study is to quantitatively assess lower limbs muscle elasticity in a court of healthy subjects and to evaluate the influence of technical variables (e.g., diameter of the ROI-region of interest) and examined subjects' characteristics (e.g., sex, levels of physical activity, side evaluated) on muscle stiffness. 54 healthy subjects (48 men, 6 women) were evaluated for a total of 108 lower limbs. Shear wave elastography was performed with a multifrequency linear probe (15-4MHz). Two radiologists performed the evaluation of lower limbs from left to right side (first calf and then thigh). The measures were taken on gastrocnemius and on femoral biceps muscle belly. We chose to place for this study two ROIs of 4 and 2mm of diameter. The mean muscle stiffness was 1.98±0.48 (range between 1.89±0.36 and 2.15±0.57m/s). The difference in muscle stiffness between left and right side of the body and between different levels of physical activity never became statistically significant (p value between 0.314 and 0.915). Only in one test out of eight the difference of muscle stiffness between male and female resulted statistically significant (p value 0.020). When comparing the measurement obtained with a 2 and 4mm diameter ROIs the values were statistically different only for the left thigh (p value 0.028). Our study, despite its limitations (low sample and low female population), seems to give some clear advice: physiological or technical factors do not determine statistically significant differences on passive muscle stiffness.

Acute effect of static stretching on passive stiffness of the human gastrocnemius fascicle measured by ultrasound shear wave elastography.

Passive muscle stiffness and muscle architecture at a given joint angle, as well as slack angle of the muscle have been shown to change after an acute bout of stretching. However, it remains unclear whether passive muscle stiffness at a given fascicle length is reduced after stretching. We aimed to elucidate the acute effect of static stretching on the passive fascicle stiffness using ultrasound shear wave elastography. Shear modulus, fascicle length, and slack angle of the medial gastrocnemius (MG) as well as passive plantar flexion torque during passive dorsiflexion were measured before and after a 5-min static stretching in 14 healthy males. After stretching, passive torques were significantly reduced at >50% of range of motion (ROM). Shear modulus at a given fascicle length was significantly reduced at >80% of the change in fascicle length during passive dorsiflexion. Slack angle of MG was observed at the middle part of ROM and significantly shifted toward more dorsiflexed position after stretching. The present study showed the significant effectiveness of static stretching on the passive fascicle stiffness. Furthermore, the present results suggest that both the shift in slack angle and the reduction in passive fascicle stiffness contribute to produce the change in passive torque-joint angle relationship during passive dorsiflexion. Notably, the contribution of the reduced passive fascicle stiffness to the decrease in passive torque is substantial over the latter part of ROM.

Botulinum toxin injection causes hyper-reflexia and increased muscle stiffness of the triceps surae muscle in the rat.

Botulinum toxin is used with the intention of diminishing spasticity and reducing the risk of development of contractures. Here, we investigated changes in muscle stiffness caused by reflex activity or elastic muscle properties following botulinum toxin injection in the triceps surae muscle in rats. Forty-four rats received injection of botulinum toxin in the left triceps surae muscle. Control measurements were performed on the noninjected contralateral side in all rats. Acute experiments were performed, 1, 2, 4, and 8 wk following injection. The triceps surae muscle was dissected free, and the Achilles tendon was cut and attached to a muscle puller. The resistance of the muscle to stretches of different amplitudes and velocities was systematically investigated. Reflex-mediated torque was normalized to the maximal muscle force evoked by supramaximal stimulation of the tibial nerve. Botulinum toxin injection caused severe atrophy of the triceps surae muscle at all time points. The force generated by stretch reflex activity was also strongly diminished but not to the same extent as the maximal muscle force at 2 and 4 wk, signifying a relative reflex hyperexcitability. Passive muscle stiffness was unaltered at 1 wk but increased at 2, 4, and 8 wk (P < 0.01). These data demonstrate that botulinum toxin causes a relative increase in reflex stiffness, which is likely caused by compensatory neuroplastic changes. The stiffness of elastic elements in the muscles also increased. The data are not consistent with the ideas that botulinum toxin is an efficient antispastic medication or that it may prevent development of contractures.

Altered viscoelastic properties of stroke-affected muscles estimated using ultrasound shear waves - Preliminary data.

As a result of a brain injury such as stroke, the skeletal muscles may undergo numerous structural and functional alterations. These abnormal changes are linked to muscle weakness, joint contracture, and abnormal muscle tone and eventually, result in motor impairment. A subset of these alterations affects passive muscle stiffness, i.e., viscoelastic properties. However, in vivo estimation of changes in viscoelastic properties is a challenging task. Here, we used the shear wave velocity, estimated through ultrasound SuperSonic imaging (SSI), as a surrogate for viscoelastic properties. We estimated shear wave group and phase velocities (dispersion), and thus, quantified both elasticity and viscosity of the muscle tissue, respectively in muscles of hemiplegic stroke survivors. In these individuals, we found significantly higher group and phase velocities in the stroke-affected muscles (p<; 05) compared to those of the contralateral non-affected side. We hypothesize that in addition to changes in neural and contractile properties, there are also, changes in elastic and tissue dispersive properties through local mechanisms. An enhanced understanding of post-stroke changes in skeletal muscles will lead to better and targeted interventions for rehabilitation.

Neuro-musculoskeletal simulation of instrumented contracture and spasticity assessment in children with cerebral palsy.

BackgroundIncreased resistance in muscles and joints is an important phenomenon in patients with cerebral palsy (CP), and is caused by a combination of neural (e.g. spasticity) and non-neural (e.g. contracture) components. The aim of this study was to simulate instrumented, clinical assessment of the hamstring muscles in CP using a conceptual model of contracture and spasticity, and to determine to what extent contracture can be explained by altered passive muscle stiffness, and spasticity by (purely) velocity-dependent stretch reflex.MethodsInstrumented hamstrings spasticity assessment was performed on 11 children with CP and 9 typically developing children. In this test, the knee was passively stretched at slow and fast speed, and knee angle, applied forces and EMG were measured. A dedicated OpenSim model was created with motion and muscles around the knee only. Contracture was modeled by optimizing the passive muscle stiffness parameters of vasti and hamstrings, based on slow stretch data. Spasticity was modeled using a velocity-dependent feedback controller, with threshold values derived from experimental data and gain values optimized for individual subjects. Forward dynamic simulations were performed to predict muscle behavior during slow and fast passive stretches.ResultsBoth slow and fast stretch data could be successfully simulated by including subject-specific levels of contracture and, for CP fast stretches, spasticity. The RMS errors of predicted knee motion in CP were 1.1 ± 0.9° for slow and 5.9 ± 2.1° for fast stretches. CP hamstrings were found to be stiffer compared with TD, and both hamstrings and vasti were more compliant than the original generic model, except for the CP hamstrings. The purely velocity-dependent spasticity model could predict response during fast passive stretch in terms of predicted knee angle, muscle activity, and fiber length and velocity. Only sustained muscle activity, independent of velocity, was not predicted by our model.ConclusionThe presented individually tunable, conceptual model for contracture and spasticity could explain most of the hamstring muscle behavior during slow and fast passive stretch. Future research should attempt to apply the model to study the effects of spasticity and contracture during dynamic tasks such as gait.Electronic supplementary materialThe online version of this article (doi:10.1186/s12984-016-0170-5) contains supplementary material, which is available to authorized users.

Quantifying passive muscle stiffness in children with and without cerebral palsy using ultrasound shear wave elastography.

The aim of this study was to compare passive muscle stiffness in children with cerebral palsy (CP) and children with typical development using a novel ultrasound technique: ultrasound shear wave elastography (SWE). We conducted a prospective study of 13 children with CP (six females and seven males, median age 5y 1mo [interquartile range 4y 4mo-7y 8mo]) and 13 children with typical development (six females and seven males, median age 5y 3mo [interquartile range 4y 4mo-9y 4mo]). Demographic information and physical exam measurements were obtained in addition to shear modulus measurements (passive muscle stiffness) of the lateral gastrocnemius muscle at 20° plantar flexion, 10° plantar flexion, and 0° plantar flexion using SWE. Children with CP had significantly greater shear modulus measurements at all three foot positions (p<0.050). When the shear modulus values were normalized to the baseline value for each child, there was no significant difference between the two groups. Passive muscle stiffness, measured without the influence of spasticity, is greater in children with CP than in children with typical development when a muscle is at slack and at stretch. When shear modulus was normalized, the results indicate that muscle in children in both groups responds similarly to passive stretch. Further work includes evaluating effect of botulinum toxin on passive muscle properties.

Stretching of Active Muscle Elicits Chronic Changes in Multiple Strain Risk Factors.

The muscle stretch intensity imposed during "flexibility" training influences the magnitude of joint range of motion (ROM) adaptation. Thus, stretching while the muscle is voluntarily activated was hypothesized to provide a greater stimulus than passive stretching. The effect of a 6-wk program of stretch imposed on an isometrically contracting muscle (i.e., qualitatively similar to isokinetic eccentric training) on muscle-tendon mechanics was therefore studied in 13 healthy human volunteers. Before and after the training program, dorsiflexion ROM, passive joint moment, and maximal isometric plantarflexor moment were recorded on an isokinetic dynamometer. Simultaneous real-time motion analysis and ultrasound imaging recorded gastrocnemius medialis muscle and Achilles tendon elongation. Training was performed twice weekly and consisted of five sets of 12 maximal isokinetic eccentric contractions at 10°·s. Significant increases (P < 0.01) in ROM (92.7% [14.7°]), peak passive moment (i.e., stretch tolerance; 136.2%), area under the passive moment curve (i.e., energy storage; 302.6%), and maximal isometric plantarflexor moment (51.3%) were observed after training. Although no change in the slope of the passive moment curve (muscle-tendon stiffness) was detected (-1.5%, P > 0.05), a significant increase in tendon stiffness (31.2%, P < 0.01) and a decrease in passive muscle stiffness (-14.6%, P < 0.05) were observed. The substantial positive adaptation in multiple functional and physiological variables that are cited within the primary etiology of muscle strain injury, including strength, ROM, muscle stiffness, and maximal energy storage, indicate that the stretching of active muscle might influence injury risk in addition to muscle function. The lack of change in muscle-tendon stiffness simultaneous with significant increases in tendon stiffness and decreases in passive muscle stiffness indicates that tissue-specific effects were elicited.

Quantitative Evaluation of Passive Muscle Stiffness in Chronic Stroke

The aim of this study was to evaluate the potential for shear wave elastography (SWE) to measure passive biceps brachii individual muscle stiffness as a musculoskeletal manifestation of chronic stroke. This was a cross-sectional study. Nine subjects with stroke were evaluated using the Fugl-Meyer and Modified Ashworth scales. Electromyography, joint torque, and SWE of the biceps brachii were obtained during passive elbow extension in subjects with stroke and four controls. Torque values at the time points corresponding to each SWE measurement during all trials were selected for direct comparison with the respective SWE stiffness using regression analysis. Intraclass correlation coefficients (ICC(1,1)) were used to evaluate the reliability of expressing alterations in material properties. Torque and passive stiffness increased with elbow extension-minimally for the controls and most pronounced in the contralateral limb of those with stroke. In the stroke group, several patterns of shear moduli and torque responses to passive elbow extension were identified, with a subset of several subjects displaying a very strong torque response coupled with minimal stiffness responses (y = 2.712x + 6.676; R = 0.181; P = 0.0310). Values of ICC(1,1) indicate consistent muscle stiffness throughout testing for the dominant side of controls, but largely inconsistent stiffness for other study conditions. SWE shows promise for enhancing evaluation of skeletal muscle after stroke. The wide variability between subjects with stroke highlights the need for precise, individualized measures.

Superficial warming and cooling of the leg affects walking speed and neuromuscular impairments in people with spastic paraparesis

BackgroundPeople with hereditary and spontaneous spastic paraparesis (HSSP) report that their legs are stiffer and walking is slower when their legs are cold. ObjectivesThis study explored the effects of prolonged superficial cooling and warming of the lower leg on walking speed and local measures of neuromuscular impairments. MethodsThis was a randomised pre- and post-intervention study of 22 HSSP participants and 19 matched healthy controls. On 2 separate occasions, one lower leg was cooled or warmed. Measurements included walking speed and measures of lower limb impairment: ankle movement, passive muscle stiffness, spasticity (stretch reflex size), amplitude and rate of force generation in dorsi- and plantarflexors and central and peripheral nerve conduction time/velocity. ResultsFor both participants and controls, cooling decreased walking speed, especially for HSSP participants. For both groups, cooling decreased the dorsiflexor rate and amplitude of force generation and peripheral nerve conduction velocity and increased spasticity. Warming increased dorsiflexor rate of force generation and nerve conduction velocity and decreased spasticity. ConclusionsSuperficial cooling significantly reduced walking speed for people with HSSP. Temperature changes were associated with changes in neuromuscular impairments for both people with spastic paraparesis and controls. This study does not support the use of localised cooling in rehabilitation for people with spastic paraparesis as reported in other neurological conditions. Rehabilitation interventions that help prevent heat loss (insulation) or improve limb temperature via passive or active means, particularly when the legs and/or environment are cool, may benefit people with spastic paraparesis.

Tension-referenced measures of gastrocnemius slack length and stiffness in Parkinson's disease.

It is not known how passive muscle length and stiffness contribute to rigidity in Parkinson's disease. The objective of this study was to compare passive gastrocnemius muscle-tendon slack length and stiffness at known tension in Parkinson's disease subjects with ankle rigidity and in able-bodied people. Passive ankle torque-angle curves were obtained from 15 Parkinson's disease subjects with rigidity and 15 control subjects. Torque-angle data were used to derive passive gastrocnemius length-tension data and calculate slack length and stiffness of the gastrocnemius muscle. Between-group comparisons were made with linear models. Gastrocnemius muscle-tendon slack lengths (adjusted between-group difference, 0.01 m; 95% CI, -0.02 to 0.04 m; P = 0.37) and stiffness (adjusted between-group difference, 15.7 m-1 ; 95% CI, -8.5 to 39.9 m-1 ; P = 0.19) were not significantly different between groups. Parkinson's disease subjects with ankle rigidity did not have significantly shorter or stiffer gastrocnemius muscles compared with control subjects. © 2016 International Parkinson and Movement Disorder Society.

Muscle-specific acute changes in passive stiffness of human triceps surae after stretching.

It remains unclear whether the acute effect of stretching on passive muscle stiffness differs among the synergists. We examined the muscle stiffness responses of the medial (MG) and lateral gastrocnemii (LG), and soleus (Sol) during passive dorsiflexion before and after a static stretching by using ultrasound shear wave elastography. Before and after a 5-min static stretching by passive dorsiflexion, shear modulus of the triceps surae and the Achilles tendon (AT) during passive dorsiflexion in the knee extended position were measured in 12 healthy subjects. Before the static stretching, shear modulus was the greatest in MG and smallest in Sol. The stretching induced significant reductions in shear modulus of MG, but not in shear modulus of LG and Sol. The slack angle was observed at more plantar flexed position in the following order: AT, MG, LG, and Sol. After the stretching, the slack angles of each muscle and AT were significantly shifted to more dorsiflexed positions with a similar extent. When considering the shift in slack angle, the change in MG shear modulus became smaller. The present study indicates that passive muscle stiffness differs among the triceps surae, and that the acute effect of a static stretching is observed only in the stiff muscle. However, a large part of the reduction of passive muscle stiffness at a given joint angle could be due to an increase in the slack length.

Intensive gait training in toddlers with cerebral palsy: A pilot study

Background: Reduced muscle growth may be involved in the development of contractures in children with cerebral palsy (CP). Here, we report data from a pilot study of intensive gait training in CP toddlers. Methods: Five children with CP aged 8-30 months performed activity-based gait training for one hour/day, five days/week for three consecutive months. Included children were diagnosed with spastic CP, had a Gross Motor Function Classification System (GMFCS) score of I–II, and were not epileptic. All children wore pedometers during training. Before and after the training period, kinematic and qualitative gait analysis, clinical and objective evaluation of spasticity, Gross Motor Function Measure-66 (GMFM-66), and ultrasound of the affected medial gastrocnemius (MG) muscle were performed. Two children were also tested before and after three months of receiving only standard care (SC). Results: On average 1410 steps/session were logged during 63 days of training. More steps were achieved at home than at a central facility. During training, MG muscle volume increased significantly, while it decreased for SC children. Gait improved qualitatively in all children, and GMFM-66 score improved in four of the five children. Similar improvements were seen among the SC children. Two children had pathologically increased muscle stiffness prior to training, which was reduced during training. Reflex stiffness was unchanged in all five children. Conclusions: This pilot study suggests that intensive gait training may increase muscle volume, improve walking skills and reduce passive muscle stiffness in toddlers with CP.

Effects of hamstring stretching on passive muscle stiffness vary between hip flexion and knee extension maneuvers

The purpose of this study was to examine whether the effects of hamstring stretching on the passive stiffness of each of the long head of the biceps femoris (BFl), semitendinosus (ST), and semimembranosus (SM) vary between passive knee extension and hip flexion stretching maneuvers. In 12 male subjects, before and after five sets of 90s static stretching, passive lengthening measurements where knee or hip joint was passively rotated to the maximal range of motion (ROM) were performed. During the passive lengthening, shear modulus of each muscle was measured by ultrasound shear wave elastography. Both stretching maneuvers significantly increased maximal ROM and decreased passive torque at a given joint angle. Passive knee extension stretching maneuver significantly reduced shear modulus at a given knee joint angle in all of BFl, ST, and SM. In contrast, the stretching effect by passive hip flexion maneuver was significant only in ST and SM. The present findings indicate that the effects of hamstring stretching on individual passive muscles' stiffness vary between passive knee extension and hip flexion stretching maneuvers. In terms of reducing the muscle stiffness of BFl, stretching of the hamstring should be performed by passive knee extension rather than hip flexion.

Muscle structure and stiffness assessment after botulinum toxin type A injection. A systematic review

BackgroundBotulinum toxin type A manages spasticity disorders in neurological central diseases. Some studies have reported that it might induce muscle changes. MethodsWe present a literature review abiding by the PRISMA statement guidelines. The purpose was to explore the structural and passive biomechanical muscle properties after botulinum toxin type A injections in healthy and spastic limb muscles, on animals and humans, as well as methods for evaluating these properties. We searched the PubMed and Cochrane Library databases using the following keywords: “Botulinum toxin” AND (“muscle structure” OR “muscle atrophy”) and, “Botulinum toxin” AND “muscle elasticity”. ResultsFrom the 228 initially identified articles, 21 articles were included. Histological analyses were performed, especially on animals. A neurogenic atrophy systematically occurred. In humans, one year after a single injection, the histological recovery remained incomplete. Furthermore, 2D ultrasound analyses showed a reduction of the gastrocnemius thickness and pennation angle. MRI volumetric analysis evidenced muscular atrophy six months or one year after a single injection. Passive muscle stiffness depends on these structural changes. On the short term, the biomechanical analysis showed an elastic modulus increase in animals whereas no change was recorded in humans. On the short term, ultrasound elastography imaging showed a decreased elastic modulus. DiscussionTo date, few data are available, but all show a structural and mechanical muscle impact post injections, specifically muscle atrophy which can linger over time. Further studies are necessary to validate this element, and the possibility of change must be taken into account particularly with repeated injections. Thus, in clinical practice, 2D ultrasound and ultrasound elastography are two non-invasive techniques that will help physicians to develop an efficient long term monitoring.

Structural and Genetic factors responsible for the development of contractures and the effect of botox treatment on reflex activity and passive muscle stiffness

Structural and Genetic factors responsible for the development of contractures and the effect of botox treatment on reflex activity and passive muscle stiffness

Calf muscle passive stiffness and function during gait in children with cerebral palsy

Calf muscle passive stiffness and function during gait in children with cerebral palsy