Anterior Cruciate Ligament Reconstructed Patients Who Recovered Normal Postural Control Have Dissimilar Brain Activation Patterns Compared to Healthy Controls

초록

Simple Summary We report that patients with anterior cruciate ligament reconstruction have similar postural control but different cortical activation patterns in several regions of the brain when compared to healthy controls. This is significant because dissimilar cortical activation patterns indicate that neural adaptation in the brain is responsible for motor coordination, possibly due to altered proprioception, despite having a surgical reconstruction after an anterior cruciate ligament injury. Such neuroplasticity in ACLR patients may imply compensatory neural protective mechanisms in order to sustain postural control, which is a fundamental functional skill in daily activities. We believe that our findings will elucidate other researchers and clinicians about the effects of a peripheral joint injury on the brain's function during postural control. Postural control, which is a fundamental functional skill, reflects integration and coordination of sensory information. Damaged anterior cruciate ligament (ACL) may alter neural activation patterns in the brain, despite patients' surgical reconstruction (ACLR). However, it is unknown whether ACLR patients with normal postural control have persistent neural adaptation in the brain. Therefore, we explored theta (4-8 Hz) and alpha-2 (10-12 Hz) oscillation bands at the prefrontal, premotor/supplementary motor, primary motor, somatosensory, and primary visual cortices, in which electrocortical activation is highly associated with goal-directed decision-making, preparation of movement, motor output, sensory input, and visual processing, respectively, during first 3 s of a single-leg stance at two different task complexities (stable/unstable) between ACLR patients and healthy controls. We observed that ACLR patients showed similar postural control ability to healthy controls, but dissimilar neural activation patterns in the brain. To conclude, we demonstrated that ACLR patients may rely on more neural sources on movement preparation in conjunction with sensory feedback during the early single-leg stance period relative to healthy controls to maintain postural control. This may be a compensatory protective mechanism to accommodate for the altered sensory inputs from the reconstructed knee and task complexity. Our study elucidates the strategically different brain activity utilized by ACLR patients to sustain postural control.

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