This picture illustrates these motions in the open kinetic chain. The ligamentous support of the subtalar joint is extensive and not well understood.
Marked discrepancies exist in the literature regarding the terminology for the individual ligaments and the functions these ligaments serve. The intrinsic subtalar ligaments: 1 interosseous ligament, 2 cervical ligament, and 3 deep fibers of the extensor retinaculum. Talocrural and subtalar joint instability after lateral ankle sprain.
Med Sci Sports Exerc. The deep ligaments consist of the cervical and interosseous ligaments. Together these ligaments stabilize the subtalar joint and form a barrier between the anterior and posterior joint capsules. The cervical ligament lies within the sinus tarsi and provides support to both the anterior and posterior joints. The interosseous ligament lies just posterior to, and courses more medially than, the cervical ligament.
The interosseous ligament originates on the calcaneus just anterior to the posterior subtalar joint capsule and runs superiorly and medially to its insertion on the talar neck. Because of its diagonal orientation and oblique fiber arrangement across the joint, portions of the interosseous ligament are taut throughout pronation and supination.
Fibers of the inferior extensor retinacula IER have also been proposed to provide support to the lateral aspect of the subtalar joint. Only the lateral root of the IER has been shown to significantly affect subtalar joint stability 37 ; however, injury to any of the roots has been suggested in the cause of sinus tarsi syndrome. The CFL is integral in preventing excessive inversion and internal rotation of the calcaneus in relation to the talus.
It lies distinctly posterior to the CFL and assists in resisting excessive supination. The lateral ligaments of the ankle: 1 anterior talofibular ligament, 2 calcaneofibular ligament, 3 posterior talofibular ligament, 4 cervical ligament, and 5 lateral talocalcaneal ligament. The bifurcate ligament also deserves mention as a static supporter of the lateral ankle complex.
It consists of 2 branches: 1 dorsal calcaneocuboid, and 2 dorsal calcaneonavicular. This ligament resists supination of the midfoot and is often injured in conjuction with hypersupination mechanisms associated with lateral ankle sprain. The third joint of the ankle complex is the distal articulation between the tibia and fibula.
This joint is a syndesmosis that allows limited movement between the 2 bones; however, accessory gliding at this joint is crucial to normal mechanics throughout the entire ankle complex. The structural integrity of the sydesmosis is necessary to form the stable roof for the mortise of the talocrural joint.
The anterior inferior tibiofibular ligament is often injured in conjunction with eversion injuries, and damage results in the so-called high ankle sprain rather than the more common lateral ankle sprain. When contracted, musculotendinous units generate stiffness, which leads to dynamic protection of joints. The muscles that cross the ankle complex are often described based on their concentric actions; however, when considering their role in providing dynamic stability to joints, it may be helpful to think about eccentric functions.
The peroneal longus and brevis muscles are integral to the control of supination of the rearfoot and protection against lateral ankle sprains. In addition to the peroneals, the muscles of the anterior compartment of the lower leg anterior tibialis, extensor digitorum longus, extensor digitorum brevis, and peroneus tertius may also contribute to the dynamic stability of the lateral ankle complex by contracting eccentrically during forced supination of the rearfoot.
Specifically, these muscles may be able to slow the plantar-flexion component of supination and thus prevent injury to the lateral ligaments. The motor and sensory supplies to the ankle complex stem from the lumbar and sacral plexes. The motor supply to the muscles comes from the tibial, deep peroneal, and superficial peroneal nerves. The sensory supply comes from these 3 mixed nerves and 2 sensory nerves: the sural and saphenous nerves. The lateral ligaments and joint capsule of the talocrural and subtalar joints have been shown to be extensively innervated by mechanoreceptors that contribute to proprioception.
Lateral ankle sprains most commonly occur due to excessive supination of the rearfoot about an externally rotated lower leg soon after initial contact of the rearfoot during gait or landing from a jump. If the strain in any of the ligaments exceeds the tensile strength of the tissues, ligamentous damage occurs.
Increased plantar flexion at initial contact appears to increase the likelihood of suffering a lateral ankle sprain. Martin et al 55 demonstrated significantly greater strain in the cervical ligament after complete disruption to the CFL.
A pathomechanical model described by Fuller 58 suggested that the cause of lateral ankle sprain is an increased supination moment at the subtalar joint. The increased supination moment is caused by the position and magnitude of the vertically projected ground-reaction force at initial foot contact.
Fuller hypothesized that a foot with its center of pressure COP medial to the subtalar-joint axis has a greater supination moment from the vertical ground-reaction force than a foot with a more lateral relationship between the COP and the joint axis.
Individuals with a rigid supinated foot would be expected to have a more laterally deviated subtalar axis of rotation and a calcaneal varus inverted rearfoot malalignment, which could predispose those with a rigid supinated foot to lateral ankle sprains.
Inman 38 described great variation in the alignment of the subtalar-joint axis across individuals, and it is possible that those with a more laterally deviated subtalar-joint axis may be predisposed to recurrent ankle sprains. A foot with a laterally deviated subtalar-joint axis would have a greater area on the medial side of the joint axis.
Thus, during initial foot contact, the likelihood is greater that COP would be medial to the subtalar-joint axis and the ground-reaction force would cause a supination moment at the subtalar joint. Additionally, the further medial the COP is in relation to the subtalar-joint axis, the longer the supination moment arm is. If the magnitude of this supination moment exceeds the magnitude of a compensatory pronation moment produced by the peroneal muscles and the lateral ligaments , excessive inversion and internal rotation of the rearfoot occur, likely causing injury to the lateral ligaments.
Some have questioned whether the peroneal muscles are able to respond quickly enough to protect the lateral ligaments from being injured once the ankle begins rapid inversion. Konradsen et al 60 reported that a dynamic protective reaction from the peroneal muscles would take at least milliseconds to occur after sudden, unexpected inversion perturbation of the ankle.
This includes 54 milliseconds for reaction time of initial electromyographic activity after the onset of inversion perturbation and 72 milliseconds of electromechanical delay needed to generate force in the muscle after electromyographic activity has been initiated. In fact, the peroneal muscles are active before initial foot contact during stair descent 61 and landing after a jump. Relatively few research reports in the literature have described predispositions to first-time ankle sprains.
Structural predispositions included increased tibial varum 64 and nonpathologic talar tilt, 64 whereas functional predispositions included poor postural-control performance, 65 , 66 impaired proprioception, 67 and higher eversion-to-inversion and plantar flexion-to-dorsiflexion strength ratios.
After acute injury, the ankle typically becomes swollen, tender, and painful with movement and full weight bearing. Depending on the severity of the injury, function usually returns over the course of a few days to a few months. What remains elusive to clinicians and researchers is why most individuals who suffer an initial ankle sprain are prone to recurrent sprains.
The mechanism of recurrent ankle injury is not thought to be different than that of initial acute ankle sprains; however, adverse changes that occur after primary injury are believed to predispose individuals to recurrent sprains.
These 2 terms, however, do not adequately describe the full spectrum of abnormal conditions related to CAI. By further clarifying the potential insufficiencies leading to each type of instability, we can better describe the full complement of potential causes of CAI. Paradigm of mechanical and functional insufficiencies that contribute to chronic ankle instability. Mechanical instability of the ankle complex occurs as a result of anatomic changes after initial ankle sprain, which lead to insufficiencies that predispose the ankle to further episodes of instability.
These changes include pathologic laxity, impaired arthrokinematics, synovial changes, and the development of degenerative joint disease, which may occur in combination or isolation. Pathologic Laxity. Ligamentous damage often results in pathologic laxity of injured joints, thus causing these joints to be mechanically unstable. The extent of pathologic laxity of the ankle depends on the amount of ligamentous damage to the lateral ligaments. Pathologic laxity can result in joint instability when the ankle is put in vulnerable positions during functional activities, resulting in subsequent injury to joint structures.
Pathologic laxity may be assessed clinically with physical examination, stress radiography, 69 , 70 or instrumented arthrometry. Integrity of the ATFL may also be assessed by inverting the talus with the talocrural joint in a plantar-flexed position and determining the amount of talar tilt present.
Calcaneofibular ligament integrity is best assessed by determining the amount of talar tilt present when inverting the rearfoot with the talocrural joint in a dorsiflexed position. Mechanical instability of the talocrural joint is traditionally explained in single planes, although this disregards the normal triplanar movement allowed at this joint. An excessive anterior drawer represents laxity in the transverse plane, while increased talar tilt indicates laxity in the frontal plane.
These simplifications disregard the fact that the talocrural joint normally moves about a triplanar axis and ignore the issue of rotary instability of the talocrural joint.
Specifically, in the absence of an intact ATFL, the talus is able to excessively supinate, with a large internal-rotation component in relation to the tibia. Injury to the CFL also causes pathologic laxity of the subtalar and talocrural joints. On arthrography, many injuries to the CFL are accompanied by injury to the subtalar-joint capsule, cervical ligament, and other lateral ligaments.
The results of the medial subtalar glide test compared favorably with the results of stress radiography. The medial subtalar glide test is performed by translating the calcaneus medially in the transverse plane. Arthrokinematic Impairments. Another potential insufficiency contributing to mechanical instability of the ankle is impaired arthrokinematics at any of the 3 joints of the ankle complex.
One arthrokinematic restriction related to repetitive ankle sprains involves a positional fault at the inferior tibiofibular joint. Mulligan 44 suggested that individuals with CAI may have an anteriorly and inferiorly displaced distal fibula.
If the lateral malleolus is indeed stuck in this displaced position, the ATFL may be more slack in its resting position. Thus, when the rearfoot begins to supinate, the talus can go through a greater range of motion before the ATFL becomes taut. This positional fault of the fibula may result in episodes of recurrent instability, leading to repetitive ankle sprains. The findings of 2 case studies 81 , 82 and one pilot study 83 present preliminary evidence for restriction of posterior fibular glide after lateral ankle sprain, suggesting that the lateral malleolus may be subluxated in an anteriorly displaced position.
Hypomobility, or diminished range of motion, may also be thought of as a mechanical insufficiency. Restricted dorsiflexion range of motion is thought to be a predisposition to lateral ankle sprain. Limited dorsiflexion in the closed kinetic chain is also typically compensated for by increased subtalar pronation.
Some evidence demonstrates dorsiflexion restrictions in athletes with repetitive ankle sprains. Patients with acute ankle sprains who were treated with posterior mobilization of the talus on the tibia recovered their dorsiflexion range of motion more quickly than those not treated with joint mobilization.
Denegar et al 88 found restricted posterior talar glide in athletes 12 weeks after acute ankle sprain. Interestingly, these athletes did not have significantly decreased dorsiflexion range of motion as assessed through standard clinical measures. This suggests that dorsiflexion may be returned to normal ranges in the absence of normal arthrokinematics due to extensive stretching of the triceps surae. Further research is needed to elucidate the clinical implications of altered arthrokinematics after ankle sprain.
Synovial and Degenerative Changes. Mechanical instability of the ankle complex may also occur due to insufficiencies caused by synovial hypertrophy and impingement or the development of degenerative joint lesions. Synovial inflammation has been shown in the talocrural and posterior subtalar-joint capsules. Patients with synovial inflammation often report frequent episodes of pain and recurrent ankle instability, which are due to impingement of hypertrophied synovial tissue between the respective bones of the ankle complex.
Sinus tarsi syndrome, or synovitis of the lateral aspect of the posterior subtalar joint, often occurs as a sequela to repetitive bouts of ankle instability.
Repetitive bouts of ankle instability have also been related to degenerative changes in the ankle complex. Greater varus angulation of the tibial plafond has also been identified in subjects with CAI when compared with those suffering initial acute sprains. Injury to the lateral ligaments of the ankle results in adverse changes to the neuromuscular system that provides dynamic support to the ankle.
Freeman et al 16 , 17 first described the concept of functional instability in They attributed impaired balance in individuals with lateral ankle sprains to damaged articular mechanoreceptors in the lateral ankle ligaments, which resulted in proprioceptive deficits. The contribution of impaired proprioception, while important, does not fully explain why ankle-ligament injury predisposes athletes to functional ankle instability.
The pathoetiologic model is not complete without including impaired neuromuscular control, thus resulting in inadequacies of the dynamic defense mechanism protecting against hypersupination of the rearfoot. Moreover, it has been suggested that loss of proprioception following ACL rupture is not due only to loss of input from the Table 3 The values of absolute angular error of reconstructed knee in nerve endings in the ACL, but also to altered kinematics caused patients and the dominant knee in healthy subjects by disruption of the ligament.
AAE, absolute angular error. Furthermore, our study showed no significant difference Test Uninjured Dominant knee, between the operated and uninjured knee of the patients.
These position knee, patients healthy subjects p Value results are inconsistent with the results of some researches, thus, further studies are needed to detect the exact mechanism A 4. Competing interests: None. Lamoreux LW. Coping with soft tissue movement in human motion analysis In: 1. Human motion analysis: Current applications and future functional importance.
Am J Sports Med ;— Neural anatomy of the human anterior Proprioceptive sensibility in women with normal cruciate ligament. J Bone Joint Surg Am ;—7. Clin Rheumatol ;—5. Anterior cruciate ligament Marks R. The reliability of knee position sense measurements in healthy women. Clin Orthop ;— Physiother Can ;— Mechanoreceptors in human cruciate Functional measurement of knee joint ligaments: A histological study.
J Bone Joint Surg ;66A—6. Arch Phys Med Rehabil 5. The sensorimotor system. Part II: The role of proprioception ;— J Athl Train ;—4. The regeneration of sensory neurones in the 6. The science of reconstruction of the anterior cruciate reconstruction of the anterior cruciate ligament. J Bone Joint Surg Br ;—6. Ann Rheum Dis. W Rauschning.
Copyright and License information Disclaimer. Copyright notice. This article has been cited by other articles in PMC. Abstract The anatomy and function of the opening between the knee joint cavity and gastrocnemio-semimembranosus bursa was studied in necropsy specimens of knee joints both by conventional knife dissection and by a newly modified technique of serial cryosectioning of undecalcified joints frozen at various angles of flexion. Images in this article Image on p. Image on p.
Valvular mechanisms in juxta-articular cysts. All capsule-reinforcing muscular tendons were removed in order to demonstrate the main ligaments in relation to the menisci. Note the large distance between the lateral meniscus and the fibular collateral ligament, which runs outside of the fibrous capsule.
Note the course of the infrapatellar plica IPP , extending to the anterior of the intercondylar fossa and covering the anterior cruciate ligament. The quadriceps tendon can be seen forming the anterior wall of the suprapatellar bursa SPB , which extends far proximally on the anterior aspect of the femur. The articularis genus muscle, formed by deep distal fibers of the vastus medialis muscle, is inserted into the suprapatellar plica preventing impingement of that synovial fold during knee extension.
With increasing extension, the proximal components of the patella meet the suprapatellar plica SPP , which forms a gliding surface for the patella on the anterior surface of the femur proximal to the patellar surface PaS.
The lateral and central components of the patella P glide exclusively on the patellar surface PaS , while the smaller medial articular surface of the femur is augmented by the ipsilateral alar folds AF. Note both lateral alar folds AF and the central infrapatellar plica IPP extending on the anterior surface of the anterior cruciate ligament.
Fibula Figs.
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