Quantifying neural and non-neural contributions to increased joint resistance in spasticity is essential for a better understanding of its pathophysiological mechanisms and evaluating different intervention strategies. However, direct measurement of spasticity-related manifestations, e.g., motoneuron and biophysical properties in humans, is extremely challenging. In this vein, we developed a forward neuromusculoskeletal model that accounts for dynamics of muscle spindles, motoneuron pools, muscle activation and musculotendon of wrist flexors and relies on the joint angle and resistant torque as the only input measurement variables. By modeling the stretch reflex pathway, neural and non-neural related properties of the spastic wrist flexors were estimated during the wrist extension test. Joint angle and resistant torque were collected from 17 persons with chronic stroke and healthy controls using NeuroFlexor, a motorized force measurement device during the passive wrist extension test. The model was optimized by tuning the passive and stretch reflex-related parameters to fit the measured torque in each participant. We found that persons with moderate and severe spasticity had significantly higher stiffness than controls. Among subgroups of stroke survivors, the increased neural component was mainly due to a lower muscle spindle rate at 50% of the motoneuron recruitment. The motoneuron pool threshold was highly correlated to the motoneuron pool gain in all subgroups. The model can describe the overall resistant behavior of the wrist joint during the test. Compared to controls, increased resistance was predominantly due to higher elasticity and neural components. We concluded that in combination with the NeuroFlexor measurement, the proposed neuromusculoskeletal model and optimization scheme served as suitable tools for investigating potential parameter changes along the stretch-reflex pathway in persons with spasticity.
Keywords: Constant angular velocity; NeuroFlexor; Optimization; Stretch reflex; Stroke.
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