Effect of suspension training on neuromuscular function, postural control, and knee kinematics in anterior cruciate ligament reconstruction patients

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.

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Longitudinal Effects of Anterior Cruciate Ligament Injury and Patellar Tendon Autograft Reconstruction on Neuromuscular Performance

The American Journal of Sports Medicine ◽

10.1177/03635465000280030901 ◽

2000 ◽

Vol 28 (3) ◽

pp. 336-344 ◽

Cited By ~ 88

Author(s):

Edward M. Wojtys ◽

Laura J. Huston

Keyword(s):

Anterior Cruciate Ligament ◽

Muscle Strength ◽

Anterior Cruciate Ligament Reconstruction ◽

Anterior Cruciate Ligament Injury ◽

Ligament Reconstruction ◽

Cruciate Ligament ◽

Neuromuscular Function ◽

Ligament Injury ◽

Cruciate Ligament Reconstruction ◽

Anterior Cruciate

We examined persons after anterior cruciate ligament injury and for 1.5 years after anterior cruciate ligament reconstruction to analyze changes in anterior knee laxity, lower extremity muscle strength, endurance, and several parameters of neuromuscular function. Sixteen men and nine women (average age, 23.8 years) were evaluated preoperatively, then underwent intraarticular autogenous patellar tendon anterior cruciate ligament reconstruction by the same surgeon and were evaluated at 6, 12, and 18 months postoperatively. Muscle strength was measured isokinetically and neuromuscular function was quantified with simultaneous anterior tibial translation and surface electromyography tests. Forty subjects (26 men and 14 women; average age, 23.5 years) with no known knee abnormalities served as the control group. Subjective questionnaire results showed that by 18 months postoperatively, 20 subjects (80%) believed they had regained their preoperative levels of function. Unfortunately, muscle function in most subjects had not returned to normal. At 12 to 18 months postoperatively, when knee rehabilitation was terminated, significant deficiencies in muscle performance persisted in most patients. Interestingly, in this group of stable knees, quadriceps and hamstring muscle reaction times appeared to be the best objective indicators of subjective knee function.

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