Abstract
Gait alterations after ACL reconstruction have been reported in the literature. The current study examined a group of 14 patients who all had an ACL reconstruction with a patellar tendon autograft. Kinetic and kinematic data were obtained from the knee during walking. The flexion-extension deficit (FED) calculated from the angular difference between maximal flexion and maximal extension during the stance phase in the ACL-reconstructed and the normal knee was measured. We investigated whether these alterations in gait are related to quadriceps strength and residual laxity of the knee. It may be that patients modify their gait patterns to protect the knee from excessive anterior translation of the tibia by reducing the amount of extension during stance. On the other hand, persistent quadriceps weakness may also cause changes in gait patterns as the quadriceps is functioning as an important dynamic stabilizer of the knee during stance. Results showed that patients had a significantly higher FED value (4.9±4.0) than a healthy control group in a previous study (1.3±0.9). This is caused mainly by an extension deficit during midstance. External extension moments of the knee (TZMAX were significantly lower in the current patients group than in a healthy control group (TZMAX −0.27±0.19 Nm/kg in patients vs. −0.08±0.06 Nm/kg in controls). There were no significant correlations between quadriceps strength and gait analysis parameters. Furthermore no correlation was found between the amount of laxity of the knee and gait. The relevance of this study lies in the fact that apparently the measured gait alterations cannot be explained solely by often used biomechanical indicators such as laxity and strength. The measured gait alterations may be a result of the surgical procedure with subsequent modified motor programming.
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Gokeler, A., Schmalz, T., Knopf, E. et al. The relationship between isokinetic quadriceps strength and laxity on gait analysis parameters in anterior cruciate ligament reconstructed knees. Knee Surg Sports Traumatol Arthrosc 11, 372–378 (2003). https://doi.org/10.1007/s00167-003-0432-1
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DOI: https://doi.org/10.1007/s00167-003-0432-1