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.

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With the rise of biofeedback in gait training in cerebral palsy there is a need for real-time measurements of gait kinematics. The Human Body Model (HBM) is a recently developed model, optimized for the real-time computing of kinematics. This study evaluated differences between HBM and two commonly used models for clinical gait analysis: the Newington Model, also known as Plug-in-Gait (PiG), and the calibrated anatomical system technique (CAST). Twenty-five children with cerebral palsy participated. 3D instrumented gait analyses were performed in three laboratories across Europe, using a comprehensive retroreflective marker set comprising three models: HBM, PiG and CAST. Gait kinematics from the three models were compared using statistical parametric mapping, and RMSE values were used to quantify differences. The minimal clinically significant difference was set at 5°. Sagittal plane differences were mostly less than 5°. For frontal and transverse planes, differences between all three models for almost all segment and joint angles exceeded the value of minimal clinical significance. Which model holds the most accurate information remains undecided since none of the three models represents a ground truth. Meanwhile, it can be concluded that all three models are equivalent in representing sagittal plane gait kinematics in clinical gait analysis.

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Spasticity is an important, but not the only, component contributing to the increased joint resistance experienced by children with spastic cerebral palsy. Conventional clinical spasticity scales, based on physical examination of the passive muscle, are easy to apply in pediatric populations. Unfortunately, these have low reliability and are unable to differentiate between the different components of joint hyper-resistance. To correctly differentiate spasticity from other neural and non-neural contributions, instrumented assessments that integrate electrophysiological and biomechanical measures are required. In the last 15 years, great advancements in clinically applicable, instrumented assessments were made. However, the translation from research to clinical setting is lagging behind. Simple, yet accurate, instrumented assessments are expected to greatly advance clinical practice in terms of treatment planning based on etiological classification and subsequent outcome evaluation. In addition, the transfer of the research findings to functional outcome would require to extend our research agenda to include assessments of hyperreflexia in the active muscle. Altogether these instrumented methods are not only needed to classify different aspects of joint hyper-resistance but will also provide further insight into its pathophysiology enabling the development of future treatment options for children with spastic cerebral palsy.@en

Background and purpose: To support clinical decision-making in central neurological disorders, a physical examination is used to assess responses to passive muscle stretch. However, what exactly is being assessed is expressed and interpreted in different ways. A clear diagnostic framework is lacking. Therefore, the aim was to arrive at unambiguous terminology about the concepts and measurement around pathophysiological neuromuscular response to passive muscle stretch. Methods: During two consensus meetings, 37 experts from 12 European countries filled online questionnaires based on a Delphi approach, followed by plenary discussion after rounds. Consensus was reached for agreement ≥75%. Results: The term hyper-resistance should be used to describe the phenomenon of impaired neuromuscular response during passive stretch, instead of for example ‘spasticity’ or ‘hypertonia’. From there, it is essential to distinguish non-neural (tissue-related) from neural (central nervous system related) contributions to hyper-resistance. Tissue contributions are elasticity, viscosity and muscle shortening. Neural contributions are velocity dependent stretch hyperreflexia and non-velocity dependent involuntary background activation. The term ‘spasticity’ should only be used next to stretch hyperreflexia, and ‘stiffness’ next to passive tissue contributions. When joint angle, moment and electromyography are recorded, components of hyper-resistance within the framework can be quantitatively assessed. Conclusions: A conceptual framework of pathophysiological responses to passive muscle stretch is defined. This framework can be used in clinical assessment of hyper-resistance and will improve communication between clinicians. Components within the framework are defined by objective parameters from instrumented assessment. These parameters need experimental validation in order to develop treatment algorithms based on the aetiology of the clinical phenomena.

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