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.

Context: Fear of reinjury after an anterior cruciate ligament (ACL) reconstruction (ACLR) may be associated with persistent deficits in knee function and subsequent injury. However, the effects of negative emotion on neuromuscular-control strategies after an ACL injury have remained unclear. Objective: To identify how negative emotional stimuli affect neural processing in the brain and muscle coordination in patients after anterior cruciate ligament reconstruction compared with healthy control participants. Design: Case-control study. Setting: Neuromechanics laboratory. Patients or Other Participants: Twenty patients after unilateral anterior cruciate ligament reconstruction and 20 healthy recruits. Main Outcome Measure(s): Electrocortical θ (4–8 Hz) activity (event-related synchronization, % increased power relative to a nonactive baseline) at selected electrodes placed at the frontal (F3, Fz, F4) and parietal (P3, Pz, P4) cortices using electroencephalography, neurophysiological cardiac changes (beats/min), and subjective fear perceptions were measured, along with joint stiffness (Nm/°/kg) with and without an acoustic stimulus in response to 3 types of emotionally evocative images (neutral, fearful, and knee-injury pictures). Results: Both groups had greater frontoparietal θ power with fearful pictures (Fz: 35.9% ± 29.4%; Pz: 81.4% ± 66.8%) than neutral pictures (Fz: 24.8% ± 29.7%, P = .002; Pz: 64.2 ± 54.7%, P = .024). The control group had greater heart-rate deceleration with fearful (−4.6 ± 1.4 beats/min) than neutral (−3.6 ± 1.3 beats/min, P < .001) pictures, whereas the ACLR group exhibited decreased heart rates with both the fearful (−4.6 ± 1.3 beats/min) and injury-related (−4.4 ± 1.5 beats/min) pictures compared with neutral pictures (−3.4 ± 1.4 beats/min, P < .001). Furthermore, during the acoustic startle condition, fearful pictures increased joint stiffness (Nm/°/kg) in the ACLR group at the midrange (0°–20°: 0.027 ± 0.02) and long range (0°–40°: 0.050 ± 0.02) compared with the neutral pictures (0°–20°: 0.017 ± 0.01, P = .024; 0°–40°: 0.043 ± 0.02, P = .014). Conclusions: Negative visual stimuli simultaneously altered neural processing in the frontoparietal cortices and joint-stiffness regulation strategies in response to a sudden perturbation. The adverse effects of fear on neuromuscular control may indicate that psychological interventions should be incorporated in neuromuscular-control exercise programs after ACL injury.

PURPOSE: Functional knee instability, which is defined as repetitive episodes of the knee "giving way" during physical activity, has received great attention to identify mechanisms due to serious pathological complications. Growing evidence suggests that insufficient neural adaptation in the central nervous system (CNS) may result in permanent functional deficits in patients with anterior cruciate ligament (ACL) injuries. The purpose of this review was to address neurophysiological mechanisms underlying functional joint instability following an anterior cruciate ligament rupture. METHODS: Previous studies conducted from PubMed with particular emphasis on mechanisms underlying joint instability and neuromuscular control deficits after an anterior cruciate ligament were reviewed. RESULTS: Inappropriate neuromuscular control, inconsistent correlations between joint laxity and functional outcomes, and altered neural activation in the brain during proprioceptive tasks may underscore the idea that persistent functional joint instability is an indication not only of the peripheral deafferentation input, but also neuromechanical decoupling between the injured ACL and CNS due to neuroplasticity. CONCLUSIONS: Persistent functional instability can develop following knee joint injury due to altered neural processing in the CNS. Therefore, it must be considered for improving patient outcomes, minimizing functional disability, and returning to one's chosen physical activity in ACL patients.

To identify, critically appraise, and synthesize the existing evidence regarding the effects of therapeutic interventions on arthrogenic muscle inhibition (AMI) in patients with chronic ankle insta... Therapeutic interventions on arthrogenic muscle inhibition (AMI) in patients with chronic ankle instability are scarce.Current studies incorporate mainly short-term therapeutic interventions.Focal ...