Background: As hyperactive muscle stretch reflexes hinder movement in patients with central nervous system disorders, they are a common target of treatment. To improve treatment evaluation, hyperactive reflexes should be assessed during activities as walking rather than passively. This study systematically explores the feasibility, reliability and validity of sudden treadmill perturbations to evoke and quantify calf muscle stretch reflexes during walking in children with neurological disorders. Methods: We performed an observational cross-sectional study including 24 children with cerebral palsy (CP; 6–16 years) and 14 typically developing children (TD; 6–15 years). Short belt accelerations were applied at three different intensities while children walked at comfortable speed. Lower leg kinematics, musculo-tendon lengthening and velocity, muscle activity and spatiotemporal parameters were measured to analyze perturbation responses. Results: We first demonstrated protocol feasibility: the protocol was completed by all but three children who ceased participation due to fatigue. All remaining children were able to maintain their gait pattern during perturbation trials without anticipatory adaptations in ankle kinematics, spatiotemporal parameters and muscle activity. Second, we showed the protocol’s reliability: there was no systematic change in muscle response over time (P = 0.21–0.54) and a bootstrapping procedure indicated sufficient number of perturbations, as the last perturbation repetition only reduced variability by ~ 2%. Third, we evaluated construct validity by showing that responses comply with neurophysiological criteria for stretch reflexes: perturbations superimposed calf muscle lengthening (P < 0.001 for both CP and TD) in all but one participant. This elicited increased calf muscle activity (359 ± 190% for CP and 231 ± 68% for TD, both P < 0.001) in the gastrocnemius medialis muscle, which increased with perturbation intensity (P < 0.001), according to the velocity-dependent nature of stretch reflexes. Finally, construct validity was shown from a clinical perspective: stretch reflexes were 1.7 times higher for CP than TD for the gastrocnemius medialis muscle (P = 0.017). Conclusions: The feasibility and reliability of the protocol, as well as the construct validity—shown by the exaggerated velocity-dependent nature of the measured responses—strongly support the use of treadmill perturbations to quantify stretch hyperreflexia during gait. We therefore provided a framework which can be used to inform clinical decision making and treatment evaluation.

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.