Functional implications of stroke and Botulinum Neurotoxin on ankle stiffness and viscosity during gait

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PROJECT SUMMARY Gait impairments are ubiquitous after stroke, leading to persistent mobility deficits in most stroke survivors. Assessment of these impairments guides patient care and the use of clinical interventions, yet obtaining a complete picture of the factors that underlie these deficits remains an ongoing challenge. Clinicians currently assess patients post-stroke with coarse, qualitative metrics obtained at rest, combined with functional evaluations and visual inspection of walking. However, these tools only enable assessment of the external changes that underlie patient symptoms and cannot provide insight into internal changes that may cause these symptoms. These internal properties—including how joint stiffness and viscosity vary throughout locomotion— are fundamental mechanical descriptions that govern the movement of the body. Joint stiffness is a key factor in energy storage and forward movement, while joint viscosity describes resistance during gait, and yet these concepts are currently unaccounted for or misjudged in clinical decision making. For example, ankle joint stiffness and viscosity, which clinicians believe to be increased post-stroke, were surprisingly found to be reduced or unchanged when compared to the less-affected side. Additionally, Botulinum Neurotoxin (BoNT) injections—a commonly-used medication for lowering joint stiffness—may cause further reduction in these properties, which could be detrimental to mobility. These initial results highlight the need for treatment that accounts for how joint stiffness and viscosity are affected after stroke and injection therapy. In the proposed work, we go beyond traditional descriptions of gait using quick displacements of the ankle while measuring its mechanical response. We use these data to measure how joint stiffness and viscosity vary during walking. In previous work, we pioneered this approach to quantify joint stiffness and viscosity during motion. In this project, we will extend our approach to determine how stroke and BoNT injection treatment affect these properties. In this project, three aims lay the foundation to transform treatment post-stroke by both investigating new assessments techniques for ankle stiffness and viscosity, and also quantifying how anti-spastic treatment (i.e. BoNT therapy) affects these properties. In our first Aim, we extend the results from our R21 to assess how ankle stiffness and viscosity change post-stroke. In our second Aim, we quantify the effect of Botulinum Neurotoxin to understand how this treatment affects ankle stiffness and viscosity, gait biomechanics, and functional outcomes. This aim is also supported by our preliminary data that demonstrates BoNT reduces joint stiffness. Finally, in our third Aim, we investigate a simpler, surrogate measure for joint stiffness, namely the slope of the joint's torque-angle curve, which could improve the clinical feasibility of our approach. While this research builds upon our previous work, the proposed studies will provide a clear picture of the internal changes that drive gait deficits which can be used to guide treatment, such as injections and orthoses.