Neuromechanical links between cognition, fear and joint instability
Date
2016
Authors
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Journal ISSN
Volume Title
Publisher
University of Delaware
Abstract
Functional joint instability following an anterior cruciate ligament (ACL) sprain can lead to a secondary ipsilateral or contralateral ACL rupture and untimely knee osteoarthritis, despite surgical repair. Previous research has examined neuromuscular control (NMC) interventions to address functional joint stability; however, clinical outcomes have varied. Recent neuroimaging studies suggest an ACL injury not only damages static restraints and peripheral mechanoreceptors, but also alters neural networks in the brain (neuroplasticity). These neural adaptations are responsible for perceiving and integrating sensory input, as well as executing the appropriate motor responses necessary for dynamic restraint. Additionally, ACL patients who have higher fear of re-injury/movement seem to have diminished knee function compared to those with relatively less fear perception. Emotion regulatory neural circuits in the brain demand greater cognitive processing to manage increased attentional resources, which suggests that greater fear interrupts executive functions related to neuromuscular control. This coordination is necessary for maintaining functional joint stability by optimizing muscle stiffness surrounding the knee. However, minimal data exists on how the brain perceives sensory information emanating from the knee, how fear may disrupt NMC, or how enhanced executive-function skills can improve fear-regulation and muscle stiffening strategies following ACL rupture. The results of this study demonstrate that: 1) the brain increases cortical activation in response to joint loading following an ACL injury; 2) general and specific situation-related fearful stimuli result in greater alterations in heart rate and neural processing in the brain, as well as joint stiffness regulation strategies; 3) a cognitive-based online training intervention improves executive-function skills, neurophysiological emotional responses, and joint stiffness regulation strategies in ACL patients. These findings suggest that measure of electrocortical signals can detect instantaneous neuromechanical coupling between joint load and brain activity and that ACL injured patients have altered somatosensory networks following ACL injury. This altered neural circuits in ACL patients may be insufficient to regulate feed-forward and feedback dynamic restraint mechanisms, when unanticipated negative events occur during high velocity physical activity. However, we can enhance executive functioning skills and emotional regulation which may help with functional joint stability. These findings offer that we can better assess instantaneous neuromechanical coupling and test individualized brain plasticity among various patient population to determine neurocognitive intervention strategies that may enhance patient outcomes.