Abstract
Quantifying neural and non-neural contributions to the joint resistance in spasticity is essential for a better evaluation of different intervention strategies such as botulinum toxin A (BoTN-A). However, direct measurement of muscle mechanical properties and spasticity-related parameters in humans is extremely challenging. The aim of this study was to use a previously developed musculoskeletal model and optimization scheme to evaluate the changes of neural and non-neural related properties of the spastic wrist flexors during passive wrist extension after BoTN-A injection. Data of joint angle and resistant torque were collected from 21 chronic stroke patients before, and 4 and 12 weeks post BoTN-A injection using NeuroFlexor, which is a motorized force measurement device to passively stretch wrist flexors. The model was optimized by tuning the passive and stretch-related parameters to fit the measured torque in each participant. It was found that stroke survivors exhibited decreased neural components at 4 weeks post BoNT-A injection, which returned to baseline levels after 12 weeks. The decreased neural component was mainly due to the increased motoneuron pool threshold, which is interpreted as a net excitatory and inhibitory inputs to the motoneuron pool. Though the linear stiffness and viscosity properties of wrist flexors were similar before and after treatment, increased exponential stiffness was observed over time which may indicate a decreased range of motion of the wrist joint. Using a combination of modeling and experimental measurement, valuable insights into the treatment responses, i.e., transmission of motoneurons, are provided by investigating potential parameter changes along the stretch reflex pathway in persons with chronic stroke.
Highlights
Spasticity is a motor symptom commonly seen after a lesion of the upper motor neuron, e.g., after stroke, spinal cord injury, or cerebral palsy
Consistent findings were observed in all participants
The Variance Accounted For (VAF) values of three assessment occasions were similar for optimization, which validated the generalization properties of the model fitted to individual participants
Summary
Spasticity is a motor symptom commonly seen after a lesion of the upper motor neuron, e.g., after stroke, spinal cord injury, or cerebral palsy. Spasticity is defined as a velocitydependent increase in tonic stretch reflex with exaggerated tendon jerks as a component of upper motor neuron lesions (Lance, 1980). In current practice, it is commonly measured subjectively by rotating a joint and estimating the resistance according to an ordinal scale, such as the Modified Ashworth Score (MAS) (Ashworth, 1964). Lindberg et al (2011) have developed a mechanical device that functions as an instrumented version of the MAS test to quantify spasticity of wrist and finger flexors and the test is convenient for daily clinical practice. The NF-Method does not allow for identifying effects on detailed mechanical properties of the joint nor the transformation of the motoneuron pool and muscle spindles
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