The present study represents a novel investigation into the relationship between CNS connectivity and history of LAS. Specifically, we aimed to determine the relationship between SMN-FC and measures of static postural control in injured and non-injured limbs of individuals with a history of LAS. The results indicated a negative relationship between contralateral SMN-FC and COPV in the non-injured limb of older adults with history of LAS. Further, no relationship was observed between contralateral SMN-FC and COPV in the injured limb of older adults with history of LAS. These findings support our hypothesis and suggest an altered signal fidelity in afferent portions of the SMN related to static postural control in the injured limb. The details and implications of these findings are discussed below.
We observed a potential dissociation between SMN-FC and static postural control in the injured, but not the non-injured, limb of older adults with a history of LAS. Altered CNS sensorimotor communication has been observed in both the injured and non-injured limbs following musculoskeletal injury.20,24,25 Both findings suggest a reorganization of cortical communication following peripheral injury. Our findings demonstrate an unspecified loss of signal fidelity, or aberrant neurologic communication, at some point along the afferent pathway. This potential loss of signal fidelity may help to further explain why individuals with functionally unstable ankles are unable to discriminate afferent input related to load when compared to healthy controls.26 Taken together, peripheral musculoskeletal injury may lead to maladaptive neuroplastic changes in the CNS.27,28
Neuroplastic changes are common following peripheral injury.27 Greater variability in supplementary motor cortex activation has been observed during a single limb balance task in individuals with a history of LAS.29 What remains a mystery is whether this finding is a downstream effect of altered afferent signal fidelity. Interestingly, individuals with history of LAS exhibit peripheral alterations in plantar cutaneous somatosensation15, lateral ligament deafferentation30, and diminished kinesthesia and joint position sense.31–33 Further, articular deafferentation following a LAS may alter proprioceptive feedback to the CNS, creating a loss of signal fidelty.30,34 Our findings provide additional support for a potential change in the communication of afferent signal, as the level of functional connectivity is proposed to reflect the amount of signaling exchange between network nodes.35
While our findings demonstrate altered SMN communication, the underlying mechanisms remain unknown. Altered SMN connectivity could be the cause or the result of musculoskeletal injury. For example, athletes who go on to experience an ACL injury exhibited differences in pre-injury FC compared to those who did not experience an ACL injury during their sport season. Such findings suggest that pre-existing levels of CNS communication may predispose individuals to musculoskeletal injury. Our findings provide additional insight into the existence of different levels of connectivity within SMN nodes that govern injured and non-injured limbs. Taken together, it appears that altered SMN-FC is related to peripheral musculoskeletal injury at multiple lower extremity joints.
Importantly, any predisposition to musculoskeletal injury may be enhanced by age-related declines in postural control and/or FC. Older adults show declines in postural control in conjunction with naturally occurring age-related alterations in FC. 36,37 For example, older adults typically demonstrate a larger degree of excursion and greater variability of COP, resulting in less stable balance.38 Neurophysiological evidence has found increased sway in the ML direction to be indicative of fall risk and age-related disease in older adults. 39,40 Additionally, age-related decreases in SMN-FC are present in otherwise healthy older adults.41 Taken together, the additive effect of age-related declines in postural control and FC may place older adults at an increased risk of falls. Although we did not examine fall risk specifically, reduced afferent processing is ubiquitous in this population42 and has been correlated with an increased risk of falling.43
The present study has several caveats that warrant further investigation. First, the cross-sectional nature of our study limits the ability to draw causal conclusions. Future studies should incorporate longitudinal designs to determine the degree to which SMN-FC interacts with LAS across the life span. Second, it is difficult to generalize findings since time of initial ankle sprain, severity of ankle sprain, and previous history of rehabilitation following initial LAS are unknown. Third, we utilized a self-reported questionnaire and interview to identify individuals with history of LAS, which may have provided limited information to the overall impact of their LAS. Future studies should include multiple questionnaires and clinical tests to minimize recall bias. Future studies should also explore measures of structural and functional connectivity, as well as potential associations between postural control and white matter microstructure within sensory pathways. White matter microstructure, or anatomical connectivity, contributes to FC and is related to static postural control.44,45 Finally, we recognize our relatively healthy sample prevents us from generalizing findings to all older adults with history of LAS.
In conclusion, our findings demonstrate a significant relationship between contralateral SMN-FC and COPV in both the AP and ML direction in the non-injured, but not the injured, limb of older adults with history of LAS. This provides preliminary evidence for future studies to determine if LAS leads to alterations in SMN-FC that may have a negative impact on postural control. Additionally, future research should aim to unearth the mechanisms explaining these relationships and to track longitudinal changes in postural control and SMN-FC to enhance our understanding of mechanisms that contribute to age- and injury-related declines in postural control.