Abstract

The anterior cruciate ligament (ACL) is attached medially to the anterior inter-condylararea of the tibia partly blending with the anterior of the lateral meniscus; it ascends posterolaterally, twisting on itself and fanning out to attach to the posteromedial aspect of the lateral femoral condyle [1]. ACL is the main static stabilizer against anterior translation of the tibia on the femur. Because of oblique anatomy of ACL, it is efficient for limiting excessive anterior tibial translation as well as axial tibial and valgus with knee rotations [2]. Besides its mechanical function related to knee stabilization, there is also neuromuscular function of the ACL due to mechanoreseptors [3]. If there is an ACL deficiency, deafferentation zones can be seen. These zones alter spinal and supra-spinal motor control [4]. The changes in motor control strategy can reveal changes in proprioception, postural control, muscle strength, movement and recruitment patterns [3]. Therefore, an ACL injury is not only a musculoskeletal injury, both also neuro physiological dysfunction.