The anterior cruciate ligament deficiency as a model of brain plasticity.

This paper describes a plausible mechanism for the development of brain plastic changes due to a peripheral joint injury, such as anterior cruciate ligament (ACL) rupture. Evidence for the hypothesis is based on mainly three indications derived from the literature review: (a) the existence of two different categories of ACL patients, the copers and non-copers, presenting different features of functional deficiencies, (b) the demand of a sufficient post-traumatic time (more than 6 months) for the dysfunction development and (c) the fact that the dysfunction is not limited to the injured limb but also concerns the non-injured one. Considering the fact that ACL contains mechanoreceptors, which inform the central nervous system (CNS) about joint sense position and kinaesthesia, it can be suggested that this kind of injury might be regarded as a neurophysiological dysfunction, not being a simple musculoskeletal injury. The rupture of the ACL could lead to the cessation/depletion or differentiation of the ascending afferent pathway from the injured joint towards CNS, inducing to the joint de-afferentation and consequently CNS reorganization and joint de-efferentation. In case of presumable evidence of the proposed hypothesis, its clinical application could concern several aspects of the intervention procedures. For example, a number of clinical findings, such as the functional differences presented between two separate clinical groups of patients (copers and non-copers) could be justified or the rehabilitation strategies might have to be revised, provided that certain therapeutic components have influence on facilitating brain plastic changes that induce to beneficial functional outcomes.