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It is well defined that functional joint stability protects a joint through simultaneous dynamic control of muscles surrounding the joint [1], while structural (mechanical) stability is provided by anatomical limits of the joint properties, such as ligaments in the knee [2,3]. The maintenance of functional joint stability is essential not only for activities of daily living and the prevention of recurrent injury, but also for the recovery and clearance to return to pre-injury level of physical performance following a ligamentous injury [3-5]. For these reasons, functional joint instability, which is defined as repetitive episodes of a joint “giving way” or “buckling” during physical activity, has received great attention in anterior cruciate ligament (ACL) ruptures and other peripheral joint pathologies, such as ankle sprains and shoulder subluxations [6-10]. This increased interest is due to serious pathological complications following these injuries, including recurrent ligamentous injuries, early development of posttraumatic osteoarthritis and disability. In fact, almost 30% of ACL patients have a second ACL rupture within 10 years [11]. Moreover, approximately 50% of ACL patients develop early knee osteoarthritis and experience a diminished health-related quality of life [9]. Therefore, many researchers have attempted to examine the possible mechanisms contributing to functional joint instability in this population. It has been suggested that factors leading to a failure in neuromuscular control, such as excessive joint laxity (mechanical instability) [12], and its consequential proprioception deficits [2,4,13] and inappropriate muscle stiffness strategies [2,4,13], may put individuals at risk of having unREVIEW ARTICLE

Neurophysiological Mechanisms Underlying Functional Knee Instability Following an Anterior Cruciate Ligament Injury