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Published on: August 9, 2024
Interaction between muscle tone, short-range stiffness and increased sensory feedback gains explains key kinematic
Friedl De Groote1, Kyle P Blum2, Brian C Horslen2
1Department of Movement Sciences, KU Leuven, Leuven, Belgium.
Insights
A new pendulum test model reveals spasticity in children with cerebral palsy is linked to increased muscle tone and force-based reflexes, not just velocity. This explains key limb motion outcomes and offers insights into spasticity mechanisms.
Area of Science:
- Biomechanics
- Neuroscience
- Rehabilitation Engineering
Background:
- The pendulum test assesses spasticity by measuring lower leg motion after a drop.
- Key kinematic features (excursion, oscillations, resting angle) correlate with spasticity severity in cerebral palsy.
- Existing models based on velocity-dependent resistance do not fully explain observed pendulum test outcomes.
Purpose of the Study:
- To investigate the role of muscle tone and short-range stiffness in explaining pendulum test kinematics.
- To determine if force-based or velocity-based hyperreflexia better explains reduced limb oscillations.
- To develop a computational model simulating spasticity during the pendulum test.
Main Methods:
- Simulated the lower leg as a torque-driven single-link pendulum.
- Modeled muscle tone, short-range stiffness (dependent on tone), and delayed sensory feedback (velocity or force-based).
- Varied baseline muscle torque and reflex gain to match observed pendulum test kinematics.
Main Results:
- Muscle tone and short-range stiffness were essential to simulate decreased initial swing excursion and non-vertical resting limb angle.
- Force-based feedback reflex activity best reproduced the reduction in limb oscillations.
- The model successfully simulated a range of pendulum test kinematics by adjusting muscle torque and reflex gain.
Conclusions:
- Increased muscle tone and short-range stiffness contribute to specific pendulum test outcomes in spasticity.
- Force-based hyperreflexia, not velocity-based, is crucial for reducing oscillations.
- The model provides insights into the variable physiological mechanisms underlying spasticity in neurological disorders.
Abstract:
The pendulum test is a sensitive clinical assessment of spasticity where the lower leg is dropped from the horizontal position and features of limb motion are recorded. Three key kinematic features are associated with the degree of severity of spasticity in children with cerebral palsy: decreased initial limb excursion, reduced number of limb oscillations, and a non-vertical resting limb angle. While spasticity is attributed to increased velocity-dependent resistance to motion, prior models simulating increased sensorimotor feedback of muscle velocity fail to explain the key pendulum test kinematic outcomes in spastic individuals. Here we hypothesized that increased muscle tone, causing a transient increase in muscle force, i.e. short-range stiffness, could account for reduced first swing excursion and non-vertical resting limb angle. We further hypothesized that hyperreflexia modeled based on muscle fiber force, and not velocity, feedback would be necessary to reduce the number of oscillations because of its interaction with transiently increased muscle force due to short-range stiffness. We simulated the lower leg as a torque-driven single-link pendulum. Muscle tone was modeled as a constant baseline joint torque, short-range stiffness torque was dependent on the level of muscle tone, and delayed sensory feedback torque to simulate reflex activity was based on either muscle velocity or force. Muscle tone and transient short-range stiffness were necessary to simulate decreased initial swing excursion and non-vertical resting leg angle. Moreover, the reduction in the number of oscillations was best reproduced by simulating stretch reflex activity in terms of force, and not velocity, feedback. Varying only baseline muscle torque and reflex gain, we simulated a range of pendulum test kinematics observed across different levels of spasticity. Our model lends insight into physiological mechanisms of spasticity whose contributions can vary on an individual-specific basis, and potentially across different neurological disorders that manifest spasticity as a symptom.
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