In Upper Motor Neuron Lesion (UMNL) following stroke, patients can experience increased joint impedance, resisting joint rotation and hindering functional movement. This heightened impedance in UMNL is driven by both exaggerated reflexes and increased intrinsic muscle activation through co-contraction, hypertonus, or synergies. The simultaneous presence of these mechanisms complicates clinical distinction, especially given their theorised interplay, where increased intrinsic activation would further heighten reflex responses. Separate quantification of this intrinsic and reflexive impedance and their interaction, can aid in further investigation of the pathophysiology of post-stroke joint impairment and its treatment.

This work presents the investigation of an Open Loop System Identification (OL-SID) protocol, to perform this separate quantification of intrinsic and reflexive impedance for the elbow joint. Perturbation experiments were performed with 16 healthy subjects, using multisine positional perturbations and measuring the elbow torque response. An impedance model consisting of both intrinsic and reflexive parameters was fit to the estimated frequency response function (FRF), relating perturbation angle to joint torque. It was assessed how background muscle activation, as well as the frequency and velocity of the perturbation signal, influenced the modelled intrinsic stiffness, intrinsic damping, and reflex velocity-gain.

For this, three different biceps muscle activation levels were requested from the participants in different trials; 0%, 10%, and 30% of Maximum Voluntary Contraction (MVC), as confirmed by online EMG measurements. Participants were requested to not actively resist perturbations, but only to comply with the requested biceps activation level. Furthermore, three rotational multisine perturbations with a max. amplitude of 2 degrees were applied; Wide Bandwidth - High Velocity, Narrow Bandwidth - Low Velocity, and Wide Bandwidth - Low Velocity. Cross-combination of biceps activation levels and perturbation signal resulted in 9 impedance quantifications per participant.

Increased biceps activation resulted in a significant increase of intrinsic stiffness, intrinsic damping, and the reflex-gain. This confirmed the expected relationship between muscle activation and intrinsic impedance, as well as the theorised relation between intrinsic activation and the reflex response. Unexpectedly, differences in used perturbation bandwidth or velocity showed no clear influence on identified reflex gain. This contradicts findings of reflex suppression during high-bandwidth force perturbations in tasks that require resisting these perturbations, as well as during high-velocity binary or unidirectional joint stretches. This discrepancy shows that joint system identification results are highly dependent on perturbation type and subject task, emphasising the need to align the experimental design with the clinical question at hand.

Despite some shortcomings regarding low coherence of the estimated FRFs, and necessary further research on perturbation signal properties and their effect on the reflex response, the results of this study are promising. The observed trends in fitted parameters with increased activation levels in line with physiological expectations, indicate the ability of this technique to validly identify reflexive and intrinsic joint impedance. This distinction is highly valuable for advancing investigation of the pathophysiology and clinical presentation of UMNL post-stroke, in the pursuit of adequate treatment for different patients.