Pilot Project: The Effects of Aging and Ankle Injury on White Matter Integrity and Balance

Age-related declines in balance and postural control increase the likelihood of one of the most prominent health and safety concerns in older adults, falls. Falls are the leading cause of injuries that threaten quality of life and increase medical costs/services. Fall risk is inversely proportional to the ability to maintain upright posture, which is compromised following injury to the lower extremity. The most common musculoskeletal injury is the lateral ankle sprain, reported in up to 70% of the general population. Nearly three- fourths of individuals with a history of ankle sprain will experience re-injury and lifelong ankle disability, commonly referred to as chronic ankle instability (CAI). Disruption in sensory inputs to the central nervous system (CNS) following CAI likely contribute to chronic alterations in motor output from the corticospinal system and compensatory hip strategies observed in these patients, with associated declines in postural control. Our preliminary data show an additive effect of CAI on age-related declines in postural control, leading to our overall hypothesis that deleterious effects of CAI on the CNS compound age-related declines in balance. CAI is thus an important factor in the identification of individuals with increased risk of falls during aging. It is also important to determine the underlying mechanisms by which aging and the additive effect of CAI compromise postural control. Optimal balance at any age requires proper transfer of information to and from the cerebellum. In addition, efferent signaling from the motor cortex is a functional antecedent for proper muscle recruitment during postural control. This transfer of information is dependent on the underlying white matter (WM) tracts that receive, integrate, and distribute signals to output and modulatory centers of the CNS. Our published findings demonstrate that the aging process jeopardizes the fidelity of these signals via declines in WM microstructure. Further, our preliminary data suggest that individuals with a history of ankle sprain demonstrate greater age-related declines in cortical and cerebellar WM microstructure. These relationships form the basis of our hypothesis that CAI leads to changes in WM microstructure, which exacerbate age- related declines in postural control. Current research examining the effect of age on postural control and WM microstructure rarely considers the deleterious sensorimotor effects associated with a history of musculoskeletal injury and how this might amplify fall risk. Our preliminary findings support the hypothesis that altered sensorimotor control in CAI may amplify age-related declines in postural control and WM microstructure. The overall objective of this pilot study is to expand on our preliminary findings to determine definitively if there is an additive effect of CAI on age-related declines in postural control which are related to loss of WM microstructure.