The most important findings of this study are that we found two distinct kinematic deviations on ACL-ruptured knee associated with the peak and amplitude of KEM, respectively. At IDS phase of the gait cycle, kinematic strategy to extend the knee contributed to the reduction of peak KEM, showing consistency with the quadriceps avoidance strategy. At SLS to TDS phase, kinematic strategy to flex the knee leads to reduced KEM amplitude, reflecting the stiffening strategy. Our findings suggest that kinematic control of knee joint is an important gait deviation mechanism in patients with ACL rupture.

. To our knowledge, this is the first study to describe two distinctive kinematic controls associated with kinetics in patients with ACL rupture. 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 “quadriceps avoidance gait” [6]. However, subsequent 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 [3,4,5,6,7,8,9,10,11,12,13]. 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 noticed that the studies that did not observe the reduction of KEM used different patient selection criteria and/or different gait examination timing. For example, Georgoulis and colleagues performed the gait examinations 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 acute or chronic ACL rupture to minimize these possible confounding effects. As described above, gait features differ according to sex [17,18,19,20]. An 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 are very important. Further studies analyzed the kinetic patterns of quadriceps avoidance gait by examining muscle strength and electromyography (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.

To understand the gait deviation of patients with ACL rupture, one must examine the mechanism involved when the internal KEM decreases. The most common interpretation is direct inhibition of the quadriceps femoris [5, 16]. The internal KEM is generated by eccentric contraction of the quadriceps with a moment opposite to the external knee flexion moment (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; thus, the quadriceps is unconsciously suppressed in the patients with ACL rupture [5, 6, 16]. In support of this hypothesis, studies using EMG have shown that quadriceps muscle activity is suppressed in patients with ACL rupture [15, 16]. In addition, increased hamstring activity is associated with this suppression. This increase in muscle activity is referred to as muscle coactivation; both phenomena are considered major neuromuscular adaptations in patients with ACL rupture [5, 14,15,16, 25].

Unlike the study by Berchuck et al. that described the quadriceps avoidance pattern at the mid-stance phase, our study, as well as previous studies, reported knee extensions at the IDS phase [8, 10, 14, 15]. 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). The results showed that 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 kinetic control may be associated with the gait of patients with ACL rupture. In the uninjured leg, knee flexion occurs with quadriceps eccentric contraction to reduce GRF during the IDS phase. However, an ACL-ruptured leg creates knee extension at the IDS phase to minimize the use of the quadriceps, and consequently reduces KEM. When the knee is further extended, the transverse vector decreases, reducing the force applied to the anteroposterior direction of the tibia [6] (Fig. 3). However, this reduction is expected to increase the GRF distribution in the axial direction (while decreasing the transverse vector). This increased GRF distribution may increase the impact on the tibiofemoral (TF) joint and may also contribute to the development of TF arthritis or subsequent meniscus injury after ACL rupture [10, 11]. In conclusion, this study is meaningful in interpreting the quadriceps avoidance gait at the IDS phase from the viewpoint of kinematic control. This phenomenon likely corresponds to a centrally controlled mechanism of the knee joint [26]. A study in a rat model showed that the central nervous system (CNS) regulates muscle activation to reduce the load within the joint [27]. We think that similar regulation occurs centrally in ACL-injured knees in terms of kinematic control of the joint. 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 stiffening strategy described by Hurd et al [5, 6, 8, 15]. However, the knee stiffening strategy in the SLS to 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 adjusted 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. The correlation has been observed by others [5].

This study has some limitations. First, participants were restricted to non-coping men. This selection limits the degree to which the results of this study can be applied to other groups. Women are known to have greater rotational laxity than men; therefore, the results may be different in women [17,18,19,20]. However, since men and women have different gait patterns and skeletal alignments, analyzing men and women together without controls could make the results harder to interpret [17,18,19,20]. Future research should focus on women. Second, only non-copers were tested. Nonetheless, analysis of the gait pattern of copers is not as important as that of non-copers at present. Moreover, analysis that fails to discriminate non-copers from copers could lead to inadequate conclusions. Third, the gait and clinical tests were performed between 3 and 8 months after the injury, meaning that pain and stiffness may have affected the gait. As a retrospective study, the patients arrived at the institution at different timepoints following the injury. The result was that the conservative treatment at other hospitals prior to the first visit varied. 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]. This study does not have healthy subjects as a control; instead, contralateral uninjured limb was used. ACL rupture can affect the gait pattern of the opposite limb as well. Having a control group of healthy individuals will enhance our understanding of the gait deviation in patients with ACL injury. In the future, we hope to expand the studies with healthy subjects included. Lastly, quadriceps atrophy may be present in patients with ACL injury. No subject had severe observable quadriceps atrophy, especially because the time between the injury and the gait study was short. Nevertheless, quantitative assessment of quadriceps atrophy would allow the assessment of possible confounding effects that the atrophy may have on the gait analysis.

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