Abstract

Whereas initial findings have already identified cortical patterns accompanying proprioceptive deficiencies in patients after anterior cruciate ligament reconstruction (ACLR), little is known about compensatory sensorimotor mechanisms for re-establishing postural control. Therefore, the aim of the present study was to explore leg dependent patterns of cortical contributions to postural control in patients 6 weeks following ACLR. A total of 12 patients after ACLR (25.1 ± 3.2 years, 178.1 ± 9.7 cm, 77.5 ± 14.4 kg) and another 12 gender, age, and activity matched healthy controls participated in this study. All subjects performed 10 × 30 s. single leg stances on each leg, equipped with 64-channel mobile electroencephalography (EEG). Postural stability was quantified by area of sway and sway velocity. Estimations of the weighted phase lag index were conducted as a cortical measure of functional connectivity. The findings showed significant group × leg interactions for increased functional connectivity in the anterior cruciate ligament (ACL) injured leg, predominantly including fronto−parietal [F(1, 22) = 8.41, p ≤ 0.008, η2 = 0.28], fronto−occipital [F(1, 22) = 4.43, p ≤ 0.047, η2 = 0.17], parieto−motor [F(1, 22) = 10.30, p ≤ 0.004, η2 = 0.32], occipito−motor [F(1, 22) = 5.21, p ≤ 0.032, η2 = 0.19], and occipito−parietal [F(1, 22) = 4.60, p ≤ 0.043, η2 = 0.17] intra−hemispherical connections in the contralateral hemisphere and occipito−motor [F(1, 22) = 7.33, p ≤ 0.013, η2 = 0.25] on the ipsilateral hemisphere to the injured leg. Higher functional connectivity in patients after ACLR, attained by increased emphasis of functional connections incorporating the somatosensory and visual areas, may serve as a compensatory mechanism to control postural stability of the injured leg in the early phase of rehabilitation. These preliminary results may help to develop new neurophysiological assessments for detecting functional deficiencies after ACLR in the future.

Highlights

  • Injuries to the anterior cruciate ligament (ACL) substantially affect knee joint laxity and cause long-term consequences for injured athletes

  • No statistically significant differences between patients after anterior cruciate ligament reconstruction (ACLR) and controls were found for age, height, weight, sport experience, or activity

  • Overall knee function (IKDC) prior to the ACL injury showed no significant difference to the matched controls

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Summary

Introduction

Injuries to the anterior cruciate ligament (ACL) substantially affect knee joint laxity and cause long-term consequences for injured athletes. ACL injuries have repeatedly been shown to cause deficits in knee function even after surgical anterior cruciate ligament reconstruction (ACLR), knowledge about associated mechanisms of the sensorimotor system for compensating these functional impairments is still lacking (Ageberg, 2002). As a consequence of increased motor thresholds of the injured limb and decreased responsiveness of motor areas, greater cortico-cortical stimulation is required to evoke efferent neural signaling in the motor cortex for properly controlling motion and stability of the knee joint (Lepley et al, 2020). Patients with ACL injury have been shown to recruit motor areas to a larger extent than healthy individuals, indicating that cortical adaptations may facilitate the restoration of lower limb motor functions by driving compensatory synergistic muscle patterns (Courtney et al, 2005). Whereas initial findings have identified compensatory cortical patterns in patients after ACLR during proprioceptive tasks (Baumeister et al, 2008, 2011), little is known about the cortical mechanisms behind the postural deficiencies in this population

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