The mechanoreceptors located in anterior cruciate ligament (ACL) constitute an afferent source of information toward the central nervous system. It has been proposed that ACL deficiency causes a disturbance in neuromuscular control, affects central programs and consequently the motor response resulting in serious dysfunction of the injured limb.
The objective of this study was to investigate whether chronic anterior cruciate ligament injury causes plastic changes in brain activation patterns.
Case control study; Level of evidence, 3.
Seventeen right leg–dominant male participants with chronic anterior cruciate ligament deficiency and 18 matched healthy male participants with no special sport or habitual physical activity participated in this study. Patient selection criteria comprised a complete right unilateral anterior cruciate ligament rupture ≥6 months before testing. Brain activation was examined by using functional magnetic resonance imaging technique (1.5-T scanner).
Results show that patients with anterior cruciate ligament deficiency had diminished activation in several sensorimotor cortical areas and increased activation in 3 areas compared with controls: presupplementary motor area, posterior secondary somatosensory area, and posterior inferior temporal gyrus.
The current study reveals that anterior cruciate ligament deficiency can cause reorganization of the central nervous system, suggesting that such an injury might be regarded as a neurophysiologic dysfunction, not a simple peripheral musculoskeletal injury. This evidence could explain clinical symptoms that accompany this type of injury and lead to severe dysfunction. Understanding the pattern of brain activation after a peripheral joint injury such as anterior cruciate ligament injury lead to new standards in rehabilitation and motor control learning with a wide application in a number of clinical and research areas (eg, surgical procedures, patient re-education, athletic training, etc).