In neurological diseases, muscles often become hyper-resistant to stretch due to hyperreflexia, an exaggerated stretch reflex response that is considered to primarily depend on the muscle's stretch velocity. However, there is still limited understanding of how different biomechanical triggers applied during clinical tests evoke these reflex responses. We examined the effect of imposing a rotation with increasing velocity vs. increasing acceleration on triceps surae muscle repsonse in children with spastic paresis (SP) and compared the responses to those measured in typically developing (TD) children. A motor-operated ankle manipulator was used to apply different bell-shaped movement profiles, with three levels of maximum velocity (70, 110, and 150°/s) and three levels of maximum acceleration (500, 750, and 1,000°/s2). For each profile and both groups, we evaluated the amount of evoked triceps surae muscle activation. In SP, we evaluated two additional characteristics: the intensity of the response (peak EMG burst) and the time from movement initiation to onset of the EMG burst. As expected, the amount of evoked muscle activation was larger in SP compared to TD (all muscles: p < 0.001) and only sensitive to biomechanical triggers in SP. Further investigation of the responses in SP showed that peak EMG bursts increased in profiles with higher peak velocity (lateral gastrocnemius: p = 0.04), which was emphasized by fair correlations with increased velocity at EMG burst onset (all muscles: r > 0.33–0.36, p ≤ 0.008), but showed no significant effect for acceleration. However, the EMG burst was evoked faster with higher peak acceleration (all muscles p < 0.001) whereas it was delayed in profiles with higher peak velocity (medial gastrocnemius and soleus: p < 0.006). We conclude that while exaggerated response intensity (peak EMG burst) seems linked to stretch velocity, higher accelerations seem to evoke faster responses (time to EMG burst onset) in triceps surae muscles in SP. Understanding and controlling for the distinct effects of different biological triggers, including velocity, acceleration but also length and force of the applied movement, will contribute to the development of more precise clinical measurement tools. This is especially important when aiming to understand the role of hyperreflexia during functional movements where the biomechanical inputs are multiple and changing.@en

Comprehensive instrumented muscle and joint assessments should be considered when prescribing Botulinum NeuroToxin-A (BoNT-A) treatment in spastic paresis. In a child with spastic paresis, comprehensive evaluation following treatment with BoNT-A, serial casting, and physiotherapy showed that short-term improvements in gait occurred without changes in muscle morphology. Rather, foot flexibility increased.@en

The developmental goal of 3D ultrasound imaging (3DUS) is to engineer a modality to perform 3D morphological ultrasound analysis of human muscles. 3DUS images are constructed from calibrated freehand 2D B-mode ultrasound images, which are positioned into a voxel array. Ultrasound (US) imaging allows quantification of muscle size, fascicle length, and angle of pennation. These morphological variables are important determinants of muscle force and length range of force exertion. The presented protocol describes an approach to determine volume and fascicle length of m. vastus lateralis and m. gastrocnemius medialis. 3DUS facilitates standardization using 3D anatomical references. This approach provides a fast and cost-effective approach for quantifying 3D morphology in skeletal muscles. In healthcare and sports, information on the morphometry of muscles is very valuable in diagnostics and/or follow-up evaluations after treatment or training.@en

Accurate assessment of the talo-crural (ankle) joint angle at physical examination is important for assessing extensibility of m. triceps surae (TS) in children with spastic cerebral paresis (SCP). The main aim of this study was to quantify foot flexibility during standardized measurements of TS muscle-tendon complex extensibility (i.e. based on foot-sole rotation) in SCP children, and typical developed (TD) ones. Additionally, we aim to define a method that minimizes the confounding effects of foot flexibility on estimates of talo-crural joint angles and TS extensibility. Children, aged 6–13 years, with SCP (GMFCS I-III, n = 13) and TD children (n = 14) participated in this study. Externally applied −1 Nm, 0 Nm, 1 Nm and 4 Nm dorsal flexion foot plate moments were imposed. Resulting TS origin-insertion lengths, foot sole (φFoSo) rotations, and changes in talo-crural joint angle (φTaCr) were measured. Foot flexibility was quantified as Δ(φTaCr -φFoSo) between the 0 Nm and 4 Nm dorsal flexion conditions. In both groups, φFoSo rotations of approximately 20° were observed between 0 Nm and 4 Nm dorsal flexion, of which about 6° (≈30%) was related to foot flexibility. Foot flexibility correlated to φFoSo (r = 0.69) but not to φTaCr (r = 0.11). For φFoSo no significant differences were found between groups at 4 Nm. However, for SCP children the mean estimate of φTaCr was 4.3° more towards plantar flexion compared to the TD group (p < 0.05). Normalized TS lengths show a higher coefficient of correlation with φTaCr (r2 = 0.82) than with φFoSo (r2 = 0.60), indicating that TS lengths are better estimated by talo-cural joint angles. In both SCP and TD children aged 6–13 year, estimates of TS length and extensibility based on foot sole assessments are confounded by foot flexibility. Assessments of TS extensibility at physical examination will be more accurate when based on measurements of talo-crural joint angles.@en

Gait of children with spastic paresis (SP) is frequently characterized by a reduced ankle range of motion, presumably due to reduced extensibility of the triceps surae (TS) muscle. Little is known about how morphological muscle characteristics in SP children are affected. The aim of this study was to compare gastrocnemius medialis (GM) muscle geometry and extensibility in children with SP with those of typically developing (TD) children and assess how GM morphology is related to its extensibility. Thirteen children with SP, of which 10 with a diagnosis of spastic cerebral palsy and three with SP of unknown etiology (mean age 9.7 ± 2.1 years; GMFCS: I–III), and 14 TD children (mean age 9.3 ± 1.7 years) took part in this study. GM geometry was assessed using 3D ultrasound imaging at 0 and 4 Nm externally imposed dorsal flexion ankle moments. GM extensibility was defined as its absolute length change between the externally applied 0 and 4 Nm moments. Anthropometric variables and GM extensibility did not differ between the SP and TD groups. While in both groups, GM muscle volume correlated with body mass, the slope of the regression line in TD was substantially higher than that in SP (TD = 3.3 ml/kg; SP = 1.3 ml/kg, p < 0.01). In TD, GM fascicle length increased with age, lower leg length and body mass, whereas in SP children, fascicle length did not correlate with any of these variables. However, the increase in GM physiological cross-sectional area as a function of body mass did not differ between SP and TD children. Increases in lengths of tendinous structures in children with SP exceeded those observed in TD children (TD = 0.85 cm/cm; SP = 1.16 cm/cm, p < 0.01) and even exceeded lower-leg length increases. In addition, only for children with SP, body mass (r = −0.61), height (r = −0.66), muscle volume (r = − 0.66), physiological cross-sectional area (r = − 0.59), and tendon length (r = −0.68) showed a negative association with GM extensibility. Such negative associations were not found for TD children. In conclusion, physiological cross-sectional area and length of the tendinous structures are positively associated with age and negatively associated with extensibility in children with SP.@en

Typically, Spastic Paresis (SCP) causes morphological changes of m. gastrocnemius medialis (GM) that may change its mechanical characteristics. An enhanced resistance to dorsal flexion may in part be explained by such changes.@en

Spasticity as part of a central neurological disorder is characterized by a ‘velocity dependent hyperactive stretch-reflex’ [1]. Secondary, morphological adaptations of the muscle-tendon complex reduce the passive joint angle-moment relationship (i.e. passive ROM) [2]. Potentially, joint hyper-resistance, as a result of either the neurological disorder, muscle morphology or both, can be clinically assessed [3]. Botulinum Toxin-A (BoNT-A), in combination with casting and physiotherapy are regularly used as conservative treatment in children with a spastic paresis to improve gait. While in some studies improvements resulting from this approach are reported, large treatment response variability persists [4]. Heterogeneity in treatment effectiveness may be due to a clinical focus at the joint impairment level rather than on the contributing mechanisms of joint hyper-resistance. In recent years great advances have been made in standardized, objective assessments of stretch reflexed induced joint hyper resistance [5]. 3D ultrasound (3DUS), allows morphometry of the muscle-tendon complex in children with spastic paresis [6]. The combination of instrumented assessments of neurological, muscle morphology and gait characteristics following treatment has not been carried out.@en

Spasticity as part of a central neurological disorder is characterized by a ‘velocity dependent hyperactive stretch-reflex’ [1]. Secondary, morphological adaptations of the muscle-tendon complex reduce the passive joint angle-moment relationship (i.e. passive ROM) [2]. Potentially, joint hyper-resistance, as a result of either the neurological disorder, muscle morphology or both, can be clinically assessed [3]. Botulinum Toxin-A (BoNT-A), in combination with casting and physiotherapy are regularly used as conservative treatment in children with a spastic paresis to improve gait. While in some studies improvements resulting from this approach are reported, large treatment response variability persists [4]. Heterogeneity in treatment effectiveness may be due to a clinical focus at the joint impairment level rather than on the contributing mechanisms of joint hyper-resistance. In recent years great advances have been made in standardized, objective assessments of stretch reflexed induced joint hyper resistance [5]. 3D ultrasound (3DUS), allows morphometry of the muscle-tendon complex in children with spastic paresis [6]. The combination of instrumented assessments of neurological, muscle morphology and gait characteristics following treatment has not been carried out.@en

Spasticity as part of a central neurological disorder is characterized by a ‘velocity dependent hyperactive stretch-reflex’ [1]. Secondary, morphological adaptations of the muscle-tendon complex reduce the passive joint angle-moment relationship (i.e. passive ROM) [2]. Potentially, joint hyper-resistance, as a result of either the neurological disorder, muscle morphology or both, can be clinically assessed [3]. Botulinum Toxin-A (BoNT-A), in combination with casting and physiotherapy are regularly used as conservative treatment in children with a spastic paresis to improve gait. While in some studies improvements resulting from this approach are reported, large treatment response variability persists [4]. Heterogeneity in treatment effectiveness may be due to a clinical focus at the joint impairment level rather than on the contributing mechanisms of joint hyper-resistance. In recent years great advances have been made in standardized, objective assessments of stretch reflexed induced joint hyper resistance [5]. 3D ultrasound (3DUS), allows morphometry of the muscle-tendon complex in children with spastic paresis [6]. The combination of instrumented assessments of neurological, muscle morphology and gait characteristics following treatment has not been carried out.@en