Functional instability is often a consequence of injury to the anterior cruciate ligament (ACL). Altered neuromuscular function secondary to ACL injuries has been identified as the key factor for functional instability of the affected knee joint. Effective treatment of ACL functional instability requires an understanding of the basic neurophysiology of proprioception, the function of the ACL, possible mechanisms through which the ACL contributes to neuromuscular control, the common consequences of ACL injuries and surgical reconstruction, and the importance of neuromuscular training.
Neuromuscular training may be key to improving function after an ACL injury.
Histologically, it has been demonstrated that the human anterior cruciate ligament (ACL) contains mechanoreceptors that can detect changes in tension, speed, acceleration, direction of movement, and the position of the knee joint.[1-3] Thus, altered neuromuscular function secondary to diminished somatosensory information (proprioception and kinesthesia) has been proposed as a key factor in functional instability after ACL injuries.[4,5]
Both proprioception and kinesthesia are specialized types of the sense of touch.[6,7] Both are involved in the control of movement and posture. Proprioception involves the unconscious sensation contributing to movement control. Kinesthesia, by contrast, involves conscious awareness. This awareness includes sensations of knee movement and position, sensations of force and heaviness, and sensations of the timing of muscular contractions.
Proprioception and kinesthesia arise from the discharge of sensory receptors in the skin, musculotendinous units, ligaments, and joint capsules from centrally generated motor commands, and from interactions between these afferent and efferent signals. The sensory receptors transduce mechanical deformation to a neural signal that is translated via cortical and reflex pathways through different nerve fibre types that are specific for each modality. An increased afferent discharge rate or an increased population of activated receptors indicate an increased stimulus of deformation.
Proprioception and kinesthesia are hypothesized to contribute to neuromuscular control. As neuromuscular control is essential for the functional stability of any joint, altered proprioception and kinesthesia have a direct effect on functional joint stability.
The major mechanical function of the ACL is to prevent excessive anterior tibial translation in various degrees of flexion. According to Butler and colleagues, the ACL provides 85% of the restraining force to anterior tibial displacement at 30 degrees and 90 degrees of knee flexion. In flexion, the anteromedial band of the ligament is the most important in preventing anterior tibial translation, whereas the posterolateral band contributes mostly to stability in extension. The ACL also prevents hyperextension of the knee, limits excessive tibial rotation (internal rotation more so than external rotation), and is a secondary restraint to both valgus and varus stresses. Finally, the ACL enhances the screw-home mechanism as the knee approaches terminal extension. Stability of the knee in terminal extension is of maximal importance, especially to athletes who participate in activities involving vigorous cutting (changing direction), jumping, and rapid deceleration.
A complete failure of the human ACL occurs at stress levels of about 1725 Newtons, while bone avulsions and ligamentous micro failures occur at lower stress levels. However, it has been demonstrated in vitro that during strenuous activities such as downhill skiing, the load on the knee joint and its ligaments may substantially exceed potential injury levels. Thus, the knee joint must rely on mechanisms other than the mechanical properties of its ligaments to maintain functional joint stability during strenuous physical activities. The lack of a strict relationship between the passive stability and the functional stability of the knee joint has been observed.[13,14]
It has been suggested that sensory information from the ACL assists in providing functional stability to the knee joint by contributing to neuromuscular control. Borsa proposed that the functional instability that occurs after an injury to the ACL is due to the combined effects of excessive tibial translation and a lack of coordinated muscle activity to stabilize the knee joint. The lack of coordinated muscle stabilization of the knee joint is thought to be due to diminished or absent sensory feedback from the ACL to the neuromuscular system. However, the relative importance of ACL sensory receptors to neuromuscular control, and ultimately to functional knee joint stability, is still undetermined.
As far back as 1944, researchers proposed that the ligaments supply input that makes neuromuscular control of the knee joint possible. However, the exact mechanism(s) by which muscular reflexes and the continuous regulation of muscle stiffness are initiated by receptors within ligaments is still a subject of debate. It is uncertain whether some impulses generated from the mechanoreceptors result directly in stimulation of alpha motor neurons or whether the effect is primarily on the gamma efferent muscle spindle system.
The number of studies on skeletomotor effects caused by natural stimulation of sensory endings in the knee joint is limited and the results are discordant. While there is some evidence to suggest that the activity in the hamstring muscle might be altered by increased tension in the ACL,[17,18] studies have also indicated that stretching the ACL at moderate loads (i.e., less than 130 Newtons) does not exert much influence directly on the skeletomotor system.[19,20]
In 1967, Freeman and Wyke theorized that Type I and II joint mechanoreceptors could impose an effect on the primary muscle spindle afferent through the gamma motor neurons. Johansson and colleagues provide the most convincing evidence for this theory to date. After conducting several thorough investigations, Johansson concluded that modest stretching of the cruciate and collateral ligaments (at loads of 5 to 40 Newtons) elicits activity in the low-threshold mechanoreceptors.[22-25] Activity in these ligamentous afferents was found to primarily influence the gamma efferent muscle spindle system, rather than causing direct reflex effects on the alpha motor neurons. Johansson found the effects of the ligamentous receptors on the gamma efferent muscle spindle system to be potent and frequent, and to induce major changes in the responses of the primary muscle spindle afferents. As the activity in the primary muscle spindle afferents modifies muscle stiffness through the reflex-mediated component, the ACL mechanoreceptors may participate in the coordination and continuous preparatory adjustment of muscular stiffness around the knee joint during dynamic conditions through the gamma efferent muscle spindle system.
Once the ACL is ruptured or plastically elongated, the knee becomes vulnerable to degenerative changes secondary to unguided femoral motion. A significant injury to the ACL often results in anterolateral instability of the knee, especially if the lateral collateral ligament and the posterolateral complex of the capsule are also damaged. Thus, decreased stability of the knee associated with functional disability is common after ACL injuries.
Altered kinesthesia is another common consequence of ACL injuries. Corrigan and colleagues measured both the ability to reproduce passive positioning and to detect passive motion of the knee joint in individuals with torn ACLs and age-matched controls. When compared with the controls, those with ACL deficient (ACLD) knees exhibited significantly diminished ability to reproduce passive positioning and to detect passive motion. Barrett studied static awareness of knee joint position in three groups: those with ACL intact (ACLI) knees, those with ACLD knees, and those with ACL reconstructed (ACLR) knees. In the study, those with ACLD knees had significantly poorer knee position sense than age-matched counterparts with ACLI and ACLR knees. Those with ACLI knees had the most accurate static joint position sense. More importantly, clinical assessments of ACL laxity and subjective knee scoring systems correlated poorly with an individual’s satisfaction and the functional capability of the knee. In contrast, static awareness of joint position was found to correlate closely with satisfaction and functional capability.
Altered muscle activity or coordination is also a consequence of ACL injuries and thought to be an essential adaptation to secure joint stability. For example, higher hamstring moments secondary to altered muscle coordination have been observed in those with ACL insufficiency during functional testing.[28,29] The hamstring muscle is synergistic in action with the ACL.
One question remains: what are the effects of surgical reconstruction on the neuromuscular function of the affected knee? Current research findings on the effects of ACL reconstruction on knee proprioception and kinesthesia provide no consensus. The discrepancy between studies may be due to the different measures of proprioception and kinesthesia used, time from injury to surgery, time after surgery, age of the subjects, and different surgical techniques. Some studies have demonstrated that ACL reconstruction restores proprioception and kinesthesia equivalent to those with ACL intact knees.[30,31] Others have found that kinesthesia are better in ACLR knees than in ACLD knees, but are still diminished when compared with the knees of uninjured controls. Evidence suggests that surgical ACL reconstructions may enhance proprioception and kinesthesia by preserving afferents and regenerating mechanoreceptors.
According to Safran and colleagues, surgeries around the knee joint should be done in a way that preserves the integrity of the knee’s mechanoreceptors and the afferent nerves of its surrounding structures such as the capsule, the collateral ligaments, the fat pad, the synovium, and the perimeniscal tissue. The primary goal during surgery should be to save as much sensory function as possible. With the preservation or restoration of the sensory function of disrupted ligament, symptoms such as functional instability and muscle weakness may be avoided.
Denti and colleague examined the fate of mechanoreceptors in the following three groups:
• Group 1—20 humans with untreated complete ACL tears.
• Group 2—12 sheep with three types of ACL reconstruction: bone-patellar-bone graft; bone-patellar-bone with ligament augmentation device (LAD); Leeds-Keio artificial ligament.
• Group 3—2 humans with failed ACL (semitendinous) reconstruction.
In Group 1, the results indicated that while morphologically normal mechanoreceptors remained in the torn ligament for 3 months postinjury, their number gradually decreased after this time, and that in lesions that were 1 year old there was a total absence of corpuscles and free nerve endings.
In Group 2, mechanoreceptors were present in ACL reconstructions with both of the autologous bone-patellar-bone grafts. Mechanoreceptors were identified at 3 months and continued to be evident up to 9 months after the procedure. No mechanoreceptors, however, were found when the ACL reconstruction was done with a Leeds-Keio artificial ligament.
In Group 3, the two human participants with ACL reconstructions using the semitendinous tendon demonstrated a significant number of Ruffini and pacinian corpuscles, especially near the tibial insertion. Of special note, these two participants demonstrated significant laxity during clinical and instrumental testing but did not report episodes of giving way or instability. Furthermore, during arthroscopy, their semitendinous grafts were slack and degenerated. Denti hypothesized that the absence of functional instability in Group 3 was secondary to the mechanoreceptors, which were supplying useful proprioceptive information even in a mechanically nonfunctional graft. Although a repopulation of mechanoreceptors after ACL autologousgraft reconstruction was demonstrated in this study, whether these sensory receptors recovered their physiological roles was not determined.
Despite intensive research in this area, the source and the importance of the new population of mechanoreceptors within ACL surgical grafts are currently undetermined. It is possible the receptors supply the ACL graft by either regrowth, regeneration, growth from the surrounding tissues, dedifferentiation of other cells, or some other mechanism. Also, it has not yet been demonstrated that these mechanoreceptors actually function. Thus, the enhanced proprioception and kinesthesia after ACL reconstructions may simply be due to enhanced functioning of other sensory receptors secondary to the restoration of knee joint osteokinematics.
There is strong evidence in the literature that neuromuscular training, such as training on wobble boards, agility training, and perturbation training has a beneficial effect on the functional ability of those with ACL injuries.[14,33-36] Furthermore, evidence suggests that neuromuscular training can significantly reduce the incidence of ACL injuries.[37,38] However, the exact mechanisms responsible for these observed improvements are not well defined.
Unfortunately, despite the strong evidence for the benefit of neuromuscular training after ACL injuries, clear guidelines for training content and progression are not well defined in the literature. Currently, the best-described neuromuscular training program in the literature is that of Fitzgerald and colleagues. This program consists of 10 treatment sessions administered at a frequency of two to three times per week and is intended for those with a unilateral ACL rupture. Individuals are classified as candidates for this neuromuscular training program if they have no concomitant ligament or mensical damage associated with the ACL injury, have a unilateral ACL injury, and meet all of the following criteria:
• Timed hop test score of 80% or more for the uninjured limb.
• Knee Outcome Survey Activities of Daily Living Scale score of 80% or more.
• Global rating of knee function of 60% or more.
• No more than one episode of giving way from the time the injury occurred to the time of testing. Individuals meeting the criteria of a rehabilitation candidate undergo an intensive rehabilitation program before returning to high-level activity.
The rehabilitation program consists of lower extremity strength training, cardiovascular endurance training, and a neuromuscular training program that includes agility training, sport-specific skill training, and perturbation training. For the perturbation training component, five variables of the applied perturbations are manipulated: predictability, direction, speed, amplitude, and force. The agility training incorporates drills such as cariocas (also known as the grapevine drill), shuttle running, cutting, and changing directions on command. The intensity of the drills begins at 50% effort and progresses to 100% effort. Sport-specific skill training only occurs once an individual exhibits proficiency and no adverse response with both the perturbation and agility training. Examples of sport-specific skill training are:
• Soccer—passing the ball while the stance leg is on a wobble board.
• Squash—lunging forward onto a wobble board while swinging the racquet.
• Basketball—dribbling the ball while performing cutting drills.
Although the exact neurocircuitry is not currently mapped out, there is convincing evidence that the ACL contributes to functional stability of the knee joint by providing sensory feedback to the neuromuscular system. Therefore, functional instability after ACL injuries is likely secondary to both the loss of an important mechanical restraint and a source of proprioception and kinesthesia. Because evidence strongly suggests that neuromuscular training can improve function, a rehabilitation program that includes perturbation training, agility training, and sport-specific skill training is essential after ACL injuries.
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T. Liu-Ambrose, MSc, PT, PhD (C)
Ms Liu-Ambrose is a PhD candidate at the School of Human Kinetics, University of British Columbia.
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