The most important findings of this study are that we found two distinct kinematic deviations on ACL-ruptured knee, and it was associated with the peak and amplitude of KEM. It suggests that kinematic control of knee joint is important gait deviation mechanisms of patients with ACL rupture.
\Gait deviations of ACL-rupture patients have been reported in the literature. In 1990, Berchuck and colleagues described the quadriceps avoidance gait 6. This study became a benchmark for studying the gait characteristics of patients with ACL rupture 6. However, the presence of quadriceps avoidance gait has been debated. Further studies analyzed the existence of quadriceps avoidance gait by examining muscle strength and EMG 5,16. However, kinematic control has not been widely studied, even though this type of control is one of the main means of neuromuscular control in patients with ACL rupture.
In this study, we confirmed the decreases in KEM amplitude and peak. In addition, we described the kinematic control of gait and showed that it is associated with kinetics. To our knowledge, this is the first study to describe two distinctive kinematic controls associated with kinetics in patients with ACL rupture. As described previously, Berchuck et al. found that the KEM was decreased and sometimes even reversed in the mid-stance walking phase of patients with ACL rupture, terming this phenomenon “quad avoidance gait” 6. However, future studies did not yield consistent results. Studies by Georgoulis et al. (and others) found no difference in sagittal-plane kinematics, while studies by Hurd et al. (and others) found significant KEM reduction 3−13. More recent reports with delicate study designs found that patients with ACL rupture had a reduced KEM, although the KEM was still greater than zero and was not reversed, as in the original article 5,8,13. We found that studies that did not find reduction of KEM used different patient selection criteria and/or different gait exam timing. For example, Georgoulis and colleagues performed the gait exams on average at 7.6 ± 4.3 weeks after ACL rupture and did not classify patients as copers or non-copers 12. Furthermore, Berchuck et al. found normal biphasic patterns in 25% of the analyzed patients, suggesting that pattern results may vary according to patient selection criteria 6. In the present work, we excluded females, copers, and final acute/chronic ACL rupture to minimize these possible confounding effects. As described above, gait features differ according to sex 17−20. Acute ACL rupture can result in antalgic gait, whereas chronic ACL rupture can result in arthritic gait features 3,12. Proper control and selection of the patient group is very important. Based on our findings, we conclude that KEM is decreased in patients with ACL rupture.
Another important question is the mechanism by which the KEM decreases. The most common interpretation is direct inhibition of the quadriceps femoris 5,16. The KEM is generated by eccentric contraction of the quadriceps with a moment opposite to the KFM, which acts as an external flexion force in the loading phase. The KEM has the same size as the KFM, but the opposite mechanical balance. During gait, the KEM can act as an anterior translation force for the proximal tibia, thereby unconsciously suppressing the quadriceps in the ACL rupture 5,6,16. In support of this hypothesis, studies using EMG have shown that quadriceps muscle activity is suppressed 15,16. In addition, increased hamstring activity is associated with this suppression. This increase in muscle activity is referred to as muscle co-activation; both of these phenomena are considered major neuromuscular adaptations in patients with ACL rupture 5,14−16,25. However, quadriceps avoidance cannot fully explain the phenomenon of ‘knee extension in the IDS phase’. The hamstrings and quads are antagonistic to each other; therefore, if quadriceps avoidance occurs throughout the gait cycle, the knee should always be more flexed compared to the opposite side. Although this explanation is consistent with the knee flexion phenomenon from the SLS to the TDS phase 8,15. it is inconsistent with previous studies that reported knee extensions at the IDS phase and with our results 8,10,14,15. Based on this inconsistency, we infer that another mechanism exists at the IDS phase. We investigated the relationship between peak KEM and peak knee flexion angle in the IDS phase and found a strong linear relationship (Pearson r = 0.694, p < 0.001). Therefore, knee extension in the IDS phase reduces the KEM. Extension of the knee in the IDS phase has been observed in previous studies, but was not previously interpreted mathematically as in the present study 3,5,10. These results suggest that both kinematic control and muscular control may be associated with the gait of patients with ACL rupture. Patients with ACL rupture extend their knee in order to reduce the KEM at the IDS phase. When the knee is further extended, the transverse vector decreases, reducing the force applied to the anteroposterior direction of the tibia 6. However, this reduction is expected to increase the GRF distribution in the axial direction (instead of reducing the transverse vector). This increased GRF distribution may increase the impact on the TF joint and may also contribute to the development of TF arthritis or subsequent meniscus injury after ACL rupture 10,11. We conclude that at the early part of the IDS phase, kinematic control of knee extension is more important than the quadriceps avoidance strategy. This phenomenon likely corresponds to a feed-forward (central control) mechanism of knee joint neuromuscular control 26. This strategy could be a coordinated way to reduce peak KEM in the early stages through feed-forward signaling at the IDS phase (by kinematic control).
After the IDS phase, the walking strategy from the SLS to the TDS phase was similar to the later quadriceps avoidance pattern and stiffening strategy described by Hurd et al 5,6,8,15. The quadriceps avoidance mechanism or stiffening strategy (based on increased muscle co-activation) is likely to work here. However, the knee stiffening strategy in the SLS-TDS phases seems to affect the amplitude rather than the KEM peak value. When the two walking strategies were modeled by regression analysis (Table 2), the adj R2 values were 0.475 and 0.497. These correlations could account for significant portions of the KEM peak and amplitude. The rest of the KEM peak and amplitude are likely to be due to direct inhibition or muscle coactivation, which were not included in this study but which have been observed by others 5.
This study has some limitations. First, participants were restricted to noncoping men, which limits the degree to which the results of this study can be applied to other groups. In this regard, women are known to have greater rotational laxity than men; therefore, the results may be different in women 17−20. However, since men and women have different gait patterns and skeletal differences, analyzing men and women together without controls could make the results harder to interpret 17−20. Future research should focus on women. Also, only non-copers were tested. However, analysis of the gait pattern of copers is not as important as that of non-copers at present. Moreover, analyses that fail to discriminate non-copers from copers could lead to incorrect conclusions being drawn. Secondly, the gait and clinical tests were performed between 3 and 8 months after the injury, meaning that pain and stiffness may have affected gait. However, before gait measurements, each participant was verified to have minimal knee effusion, no knee extension deficits, minimal pain in the injured limb with walking, and no visually identifiable gait impairments. These criteria were applied to minimize the effects of pain and stiffness. The average pain numeric rating was 1.2 ± 0.8 and the average range of motion (ROM) prior to gait analysis in the laboratory was 138.7 ± 15.8°. However, the gait patterns of patients with acute or chronic ACL ligament rupture may be different; therefore, further studies are needed 3,12.