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                                    Chapter 362femoris in collaboration with the iliotibial band can be responsible for counteracting the rotational forces, we hypothesise that even shortly after the injury a neuromuscular adaptation in patients with ACL-deficient knees may occur. Neuromuscular control is the result of a complex integration of vestibular, somatosensory and visual stimuli and is affected by situational awareness, arousal and attention.18 Muscular contraction is continuously fine-tuned on the anticipated demands of the knee to preserve joint equilibrium and stability. After ACL injury, it is suggested that the central nervous system relies more on visual feedback and spatial awareness, as the biomechanical feedback is disturbed.18 Accordingly, previous studies showed that muscle activation patterns of patients with an ACL-injured knee and after an ACLR are modified compared to healthy knees.5,16,24,39This ‘increased stiffening’ strategy as compensation for perceived instability has been proposed before; by altering jumping technique (less high and less far), and landing technique (less knee flexion), more stiffness is introduced in the knee joint.16 Altered landing techniques were also demonstrated by Keizer et al. in healthy subjects with intact ACLs but with higher knee laxity.20 In our study we also observed less maximum knee flexion in ACL-deficient knees compared to ACL-reconstructed knees, but there were no or only very small differences between the affected and the contralateral ACL-intact knees in terms of maximum knee flexion. When muscular compensation and, through this, altered landing kinematics indeed are a valid explanation for our observations, this mechanism would prevent symptomatic knee laxity in chronic ACL deficiency too. Yet, in the acute phase, shortly after a traumatic event, fear of re-injury may contribute to increased stiffening as well41, and as the fear diminishes over time this can cause the knee laxity to become clinically apparent. We therefore hypothesise that a combination of an altered landing strategy, altered muscular contraction patterns and fear of re-injury can lead to a smaller rTR in ACL-affected knees. Our results differ from other study results regarding rTR in ACL deficiency. Cadaveric studies and studies in passive situations have shown that rupture of the ACL allows more, passive, rotation of the tibia.44 An increased rTR in ACL deficiency compared to healthy knees has also been shown during functional yet low to moderate demand tasks.7,31,36,42,43 Results from these Mark Zee.indd 62 03-01-2024 08:56
                                
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