Quantifying the Biomechanical and Neural Factors Contributing to Shoulder Instability

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PROJECT SUMMARY Multidirectional instability (MDI) is a common shoulder pathology in younger individuals impacting those in the military, employed in heavy lifting occupations, and participating in high demand activities. MDI is characterized by multidirectional atraumatic shoulder laxity with concurrent pain that limits participation in activities of daily living. Treatment for MDI begins with non-operative physiotherapy, but short-term and long-term outcomes are often ineffective. Subsequent surgical treatment is unpredictable, especially when compared to similar surgical treatment for unidirectional instability. In contrast to MDI, many individuals present clinically with multidirectional atraumatic shoulder laxity but report no pain (asymptomatic) with shoulder function. It is hypothesized that individuals with asymptomatic laxity, unlike patients with MDI, use neural activation of shoulder musculature to compensate for any deficits in passive shoulder structures. However, research has yet to investigate or quantify the inability to compensate with neural activation of shoulder musculature for passive deficits in MDI. This proposal will focus on identifying and quantifying differences in active and passive shoulder stability between individuals with MDI and asymptomatic laxity to isolate components of shoulder mechanics unique to shoulders with MDI. Aim 1 will quantify translational impedance (resistance to joint motion) of the shoulder in multiple directions and multiple arm postures during shoulder relaxation. Aim 2 will quantify translational impedance of the shoulder during constant isometric torque production in three rotational degrees-of-freedom. Passive and active translational impedance will be assessed in individuals with clinically- diagnosed MDI, asymptomatic shoulder laxity, and asymptomatic shoulders negative for clinical laxity. A custom-adapted linear motor will apply long slow (Aim 1) and small quick stochastic (Aim 1 and Aim 2) translational perturbations to the shoulder. The stiffness component of impedance will be quantified with computational analysis of shoulder displacement and forces following translational perturbations. The results of this work will provide the first comparison of passive and active translational shoulder impedance in individuals with MDI and asymptomatic laxity, informing future studies designed to predict individuals that progress from asymptomatic laxity to MDI and develop personalized MDI treatments to target individual biomechanical deficits.