pathophysiology of lateral ankle instability

364 Volume 37 Number 4 December 2002

Journal of Athletic Training 2002;37(4):364375q by the National Athletic Trainers Association, Incwww.journalofathletictraining.org

Functional Anatomy, Pathomechanics, andPathophysiology of Lateral Ankle InstabilityJay HertelPennsylvania State University, University Park, PA

Jay Hertel, PhD, ATC, provided conception and design and drafting, critical revision, and final approval of the article.Address correspondence to Jay Hertel, PhD, ATC, Pennsylvania State University, 269 Recreation Building, University Park, PA16802. Address e-mail to [email protected].

Objective: To describe the functional anatomy of the anklecomplex as it relates to lateral ankle instability and to describethe pathomechanics and pathophysiology of acute lateral anklesprains and chronic ankle instability.

Data Sources: I searched MEDLINE (19852001) andCINAHL (19822001) using the key words ankle sprain andankle instability.

Data Synthesis: Lateral ankle sprains are among the mostcommon injuries incurred during sports participation. The anklefunctions as a complex with contributions from the talocrural,subtalar, and inferior tibiofibular joints. Each of these joints mustbe considered in the pathomechanics and pathophysiology oflateral ankle sprains and chronic ankle instability. Lateral anklesprains typically occur when the rearfoot undergoes excessivesupination on an externally rotated lower leg. Recurrent anklesprain is extremely common; in fact, the most common predis-

position to suffering a sprain is the history of having suffered aprevious ankle sprain. Chronic ankle instability may be due tomechanical instability, functional instability, or most likely, acombination of these 2 phenomena. Mechanical instability maybe due to specific insufficiencies such as pathologic laxity, ar-throkinematic changes, synovial irritation, or degenerativechanges. Functional instability is caused by insufficiencies inproprioception and neuromuscular control.

Conclusions/Recommendations: Lateral ankle sprains areoften inadequately treated, resulting in frequent recurrence ofankle sprains. Appreciation of the complex anatomy and me-chanics of the ankle joint and the pathomechanics and patho-physiology related to acute and chronic ankle instability is in-tegral to the process of effectively evaluating and treating ankleinjuries.

Key Words: ankle sprain, talocrural joint, subtalar joint, me-chanical instability, functional instability

Injuries to the lateral ligaments of the ankle complex areamong the most common injuries incurred by athletes.1Lateral ankle sprains are thought to be suffered by menand women at approximately the same rates; however, onerecent report2 suggests that female interscholastic and inter-collegiate basketball players have a 25% greater risk of incur-ring grade I ankle sprains than their male counterparts. Morethan 23 000 ankle sprains have been estimated to occur perday in the United States, which equates to one sprain per10 000 people daily.3 The most common predisposition to suf-fering a lateral ankle sprain is the history of at least one pre-vious ankle sprain.48 In sports such as basketball, recurrencerates have been reported to exceed 70%.4,9 Repetitive sprainshave also been linked to increased risk of osteoarthritis andarticular degeneration at the ankle.10,11

Residual symptoms after lateral ankle sprain affect 55% to72% of patients at 6 weeks to 18 months.12,13 The frequencyof complications and breadth of longstanding symptoms afterankle sprain has led to the suggestion of a diagnosis of thesprained ankle syndrome14 and to the conclusion that thereis no such thing as a simple ankle sprain.15 It has also beenestimated that 55% of individuals suffering ankle sprains donot seek injury treatment from a health care professional.4,8Thus, the severity of ankle sprains may often be underesti-mated by athletes, and current treatment strategies for lateralankle sprains may not be effective in preventing recurrent in-juries or residual symptoms.

Lateral ankle sprains are also referred to as inversion anklesprains or occasionally as supination ankle sprains. Individualswho suffer numerous repetitive ankle sprains have been re-ported as having functional instability,1618 chronic instabili-ty,19 and residual instability.20 The multitude of terms used todescribe the phenomenon of repetitive ankle sprains has led toconfusion in terminology. For the purposes of this article, thefollowing definitions will apply: lateral ankle instability refersto the existence of an unstable ankle due to lateral ligamentousdamage caused by excessive supination or inversion of therearfoot. This term does not differentiate whether the instabil-ity is acute or chronic. Chronic ankle instability (CAI) denotesthe occurrence of repetitive bouts of lateral ankle instability,resulting in numerous ankle sprains.

Traditionally, CAI has been attributed to 2 potential causes:mechanical instability and functional instability. Tropp et al21discussed the notion of mechanical instability as a cause ofCAI due to pathologic laxity after ankle-ligament injury. Free-man et al16,17 first described functional instability in 1965when they attributed CAI to proprioceptive deficits after lig-ament injury. A more recent definition of functional instabilityis the occurrence of recurrent ankle instability and the sensa-tion of joint instability due to the contributions of propriocep-tive and neuromuscular deficits.22 While the dichotomy offunctional and mechanical instability helps explain 2 commonpotential causes of CAI, it does not adequately reflect the com-plete spectrum of pathologic conditions leading to CAI. Spe-

Journal of Athletic Training 365

Figure 1. The talocrural axis of rotation.

cific insufficiencies interact to create either mechanical insta-bility or functional instability. Functional instability may becaused by specific insufficiencies in proprioception, neuro-muscular control, postural control, or strength. Mechanical in-stability may be caused by factors that alter the mechanics ofone or more joints within the ankle complex. Potential me-chanical insufficiencies include pathologic laxity, impaired ar-throkinematics, synovial inflammation and impingement, anddegenerative changes. Chronic ankle instability may be causedby mechanical instability, functional instability, or a combi-nation of these entities.21,23

The purposes of this review article are to describe the func-tional anatomy of the ankle complex as it relates to lateralankle instability and to discuss the pathomechanics and path-ophysiology of acute lateral ankle sprain and CAI.

FUNCTIONAL ANATOMYThe ankle complex comprises 3 articulations: the talocrural

joint, the subtalar joint, and the distal tibiofibular syndesmosis.These 3 joints work in concert to allow coordinated movementof the rearfoot. Rearfoot motion is often defined as occurringin the cardinal planes as follows: sagittal-plane motion (plantarflexion-dorsiflexion), frontal-plane motion (inversion-ever-sion), and transverse-plane motion (internal rotation-externalrotation).24 Rearfoot motion, however, does not occur in iso-lation in the individual planes; rather, coordinated movementof the 3 joints allows the rearfoot to move as a unit about anaxis of rotation oblique to the long axis of the lower leg. Rear-foot motion does not occur strictly in the cardinal planes be-cause the talocrural and subtalar joints each have oblique axesof rotation. Coupled rearfoot motion is best described as pro-nation and supination. In the open kinetic chain, pronationconsists of dorsiflexion, eversion, and external rotation, whilesupination consists of plantar flexion, inversion, and internalrotation.25 In the closed kinetic chain, pronation consists ofplantar flexion, eversion, and external rotation, while supina-tion consists of dorsiflexion, inversion, and internal rotation.25

The 3 major contributors to stability of the ankle joints are(1) the congruity of the articular surfaces when the joints areloaded, (2) the static ligamentous restraints, and (3) the mus-culotendinous units, which allow for dynamic stabilization ofthe joints. The functional aspect of each of these as it relatesto lateral ankle instability will be discussed later.

Talocrural Joint AnatomyThe talocrural, or tibiotalar, joint is formed by the articu-

lation of the dome of the talus, the medial malleolus, the tibialplafond, and the lateral malleolus. The shape of the talocruraljoint allows torque to be transmitted from the lower leg (in-ternal and external rotation) to the foot (pronation and supi-nation) during weight bearing. This joint is sometimes calledthe mortise joint and, in isolation, may be thought of as ahinge joint that allows the motions of plantar flexion and dor-siflexion. The axis of rotation of the talocrural joint passesthrough the medial and lateral malleoli. It is slightly anteriorto the frontal plane as it passes through the tibia but slightlyposterior to the frontal plane as it passes through the fibula.Isolated movement of the talocrural joint is primarily in thesagittal plane, but small amounts of transverse- and frontal-plane motion also occur about the oblique axis of rotation.26

In an in vivo study of loaded ankles in the closed kinetic

chain, 308 of physiologic plantar flexion (actual motion) fromthe neutral position was composed of 288 sagittal-plane move-ment (plantar flexion), 18 transverse-plane movement (internalrotation), and 48 frontal-plane movement (inversion).26 Com-paratively, 308 of physiologic dorsiflexion (actual motion) inthe closed kinetic chain was composed of 238 sagittal-planemovement (dorsiflexion), 98 transverse-plane movement (ex-ternal rotation), and 28 frontal-plane movement (eversion).26Closed kinetic chain dorsiflexion occurs when the tibia movesanteriorly on the fixed talus during weight bearing. The con-cept of triplanar motion at the talocrural motion is importantin understanding the stability of the talocrural joint (Figure 1).

When the ankle complex is fully loaded, the articular sur-faces are the primary stabilizers against excessive talar rotationand translation27; however, the contribution of the ligamentsto talocrural joint stability is crucial. The talocrural joint re-ceives ligamentous support from a joint capsule and severalligaments, including the anterior talofibular ligament (ATFL),posterior talofibular ligament (PTFL), calcaneofibular ligament(CFL), and deltoid ligament. The ATFL, PTFL, and CFL sup-port the lateral aspect of the ankle, while the deltoid ligamentprovides medial support.

The ATFL lies on the dorsolateral aspect of the foot andcourses from the lateral malleolus anteriorly and medially to-ward the talus at an angle of approximately 458 from the fron-tal plane.28 The ATFL is an average of 7.2 mm wide and 24.8mm long.28 In vitro kinematic studies have shown that theATFL prevents anterior displacement of the talus from themortise and excessive inversion and internal rotation of thetalus on the tibia.27,2932 The strain in the ATFL increases asthe ankle moves from dorsiflexion into plantar flexion.29 TheATFL demonstrates lower maximal load and energy to failurevalues under tensile stress as compared with the PTFL, CFL,anterior inferior tibiofibular ligament, and deltoid ligament.33This may explain why the ATFL is the most frequently injuredof the lateral ligaments.34

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Figure 2. The subtalar axis of rotation allows the triplanar motions of pronation and supination. This picture illustrates these motionsin the open kinetic chain.

The CFL courses from the lateral malleolus posteriorly andinferiorly to the lateral aspect of the calcaneus at a mean angleof 1338 from the long axis of the fibula.28 The CFL restrictsexcessive supination of both the talocrural and subtalar joints.In vitro experiments have demonstrated that the CFL restrictsexcessive inversion and internal rotation of the rearfoot and ismost taut when the ankle is dorsiflexed.27,32,35 The CFL is thesecond most-often injured of the lateral talocrural ligaments.19

The PTFL runs from the lateral malleolus posteriorly to theposterolateral aspect of the talus. The PTFL has broad inser-tions on both the talus and fibula28 and provides restraint toboth inversion and internal rotation of the loaded talocruraljoint.27 It is the least commonly sprained of the lateral ankleligaments.19

Subtalar Joint AnatomyThe subtalar joint is formed by the articulations between the

talus and the calcaneus and, like the talucrural joint, it convertstorque between the lower leg (internal and external rotation)and the foot (pronation and supination). The subtalar joint al-lows the motions of pronation and supination and consists ofan intricate structure with 2 separate joint cavities. The pos-terior subtalar joint is formed between the inferior posteriorfacet of the talus and the superior posterior facet of the cal-caneus.25 The anterior subtalar, or talocalcaneonavicular, jointis formed from the head of the talus, the anterior-superior fac-ets, the sustentaculum tali of the calcaneus, and the concaveproximal surface of the tarsal navicular. This articulation issimilar to a ball-and-socket joint, with the talar head being theball and the anterior calcaneal and proximal navicular surfacesforming the socket in conjunction with the spring ligament.36Viladot et al37 reported great individual variation in the archi-tecture of the anterior subtalar joint.

The anterior and posterior subtalar joints have separate lig-amentous joint capsules and are separated from each other bythe sinus tarsi and canalis tarsi.37 The anterior joint lies farthermedial and has a higher center of rotation than the posteriorjoint, but the 2 joints share a common axis of rotation.36,37

This discrepancy results in an oblique axis of rotation of thesubtalar joint, which averages a 428 upward tilt and a 238 me-dial angulation from the perpendicular axes of the foot (Figure2).38 Great variations have been identified in the position ofthe axis of rotation across individuals.38

The ligamentous support of the subtalar joint is extensiveand not well understood. Marked discrepancies exist in theliterature regarding the terminology for the individual liga-ments and the functions these ligaments serve.37,39 Essentially,the lateral ligaments may be divided into 3 groups: (1) deepligaments, (2) peripheral ligaments, and (3) retinacula (Figure3).37,40

The deep ligaments consist of the cervical and interosseousligaments. Together these ligaments stabilize the subtalar jointand form a barrier between the anterior and posterior jointcapsules. These ligaments, which cross obliquely through thecanalis tarsi, have been described as the cruciate ligamentsof the subtalar joint.37 The cervical ligament lies anterior andlateral to the interosseous ligament and runs from the cervicaltubercle of the calcaneus anteriorly and medially to the talarneck. The cervical ligament lies within the sinus tarsi and pro-vides support to both the anterior and posterior joints.42 It isthe strongest of the subtalar ligaments and has been shown toresist supination during in vitro kinematic experiments.30,37,39

The interosseous ligament lies just posterior to, and coursesmore medially than, the cervical ligament. The interosseousligament originates on the calcaneus just anterior to the pos-terior subtalar joint capsule and runs superiorly and mediallyto its insertion on the talar neck. Because of its diagonal ori-entation and oblique fiber arrangement across the joint, por-tions of the interosseous ligament are taut throughout prona-tion and supination.30,37,39 This ligament is sometimes calledthe ligament of the canalis tarsi.30

Fibers of the inferior extensor retinacula (IER) have alsobeen proposed to provide support to the lateral aspect of thesubtalar joint.40 Three roots of the IER have been identifiedwithin the sinus tarsi: lateral, intermediate, and medial. Onlythe lateral root of the IER has been shown to significantlyaffect subtalar joint stability37; however, injury to any of the

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Figure 3. The intrinsic subtalar ligaments: (1) interosseous liga-ment, (2) cervical ligament, and (3) deep fibers of the extensor ret-inaculum. Reprinted with permission of Hertel J, Denegar CR, Mon-roe MM, Stokes WL. Talocrural and subtalar joint instability afterlateral ankle sprain. Med Sci Sports Exerc. 1999;31:15011508; Lip-pincott Williams & Wilkins.41

Figure 4. The lateral ligaments of the ankle: (1) anterior talofibularligament, (2) calcaneofibular ligament, (3) posterior talofibular lig-ament, (4) cervical ligament, and (5) lateral talocalcaneal ligament.Reprinted with permission of Hertel J, Denegar CR, Monroe MM,Stokes WL. Talocrural and subtalar joint instability after lateral an-kle sprain. Med Sci Sports Exerc. 1999;31:15011508; LippincottWilliams & Wilkins.41

roots has been suggested in the cause of sinus tarsi syn-drome.43

The peripheral ligaments of the subtalar joint include theCFL and lateral talocalcaneal (LTCL) and fibulotalocalcaneal(FTCL) ligaments. The CFL is integral in preventing excessiveinversion and internal rotation of the calcaneus in relation tothe talus.30,31,34,35 While the CFL does not normally connectthe calcaneus to the talus, various attachments of the anterioraspect of the CFL to the talus have been reported.40

Lateral Ankle LigamentsThe LTCL runs parallel and anterior to the CFL but only

crosses the posterior subtalar joint (Figure 4). While the LTCLis smaller and weaker than the CFL, it helps prevent excessivesupination of the subtalar joint.28,30,37 Various shapes of theLTCL have been reported, and occasionally its fibers are con-tinuous with those of the CFL.28,40 The FTCL, or ligament ofRouviere, runs from the posterior surface of the lateral mal-leolus to the posterolateral surface of the talus and then to theposterolateral calcaneus. It lies distinctly posterior to the CFLand assists in resisting excessive supination.37

The bifurcate ligament also deserves mention as a staticsupporter of the lateral ankle complex. It consists of 2 branch-es: (1) dorsal calcaneocuboid, and (2) dorsal calcaneonavicu-lar. This ligament resists supination of the midfoot and is ofteninjured in conjuction with hypersupination mechanisms asso-ciated with lateral ankle sprain.34

Distal Tibiofibular Joint AnatomyThe third joint of the ankle complex is the distal articulation

between the tibia and fibula. This joint is a syndesmosis thatallows limited movement between the 2 bones; however, ac-cessory gliding at this joint is crucial to normal mechanics

throughout the entire ankle complex.44 The joint is stabilizedby a thick interosseous membrane and the anterior and pos-terior inferior tibiofibular ligaments. The structural integrity ofthe sydesmosis is necessary to form the stable roof for themortise of the talocrural joint. The anterior inferior tibiofibularligament is often injured in conjunction with eversion injuries,and damage results in the so-called high ankle sprain ratherthan the more common lateral ankle sprain.45

Muscles and TendonsWhen contracted, musculotendinous units generate stiffness,

which leads to dynamic protection of joints. The muscles thatcross the ankle complex are often described based on theirconcentric actions; however, when considering their role inproviding dynamic stability to joints, it may be helpful to thinkabout eccentric functions. The peroneal longus and brevismuscles are integral to the control of supination of the rearfootand protection against lateral ankle sprains.46

In addition to the peroneals, the muscles of the anteriorcompartment of the lower leg (anterior tibialis, extensor digi-torum longus, extensor digitorum brevis, and peroneus tertius)may also contribute to the dynamic stability of the lateral anklecomplex by contracting eccentrically during forced supinationof the rearfoot. Specifically, these muscles may be able to slowthe plantar-flexion component of supination and thus preventinjury to the lateral ligaments.47

InnervationThe motor and sensory supplies to the ankle complex stem

from the lumbar and sacral plexes. The motor supply to themuscles comes from the tibial, deep peroneal, and superficialperoneal nerves. The sensory supply comes from these 3mixed nerves and 2 sensory nerves: the sural and saphenousnerves. The lateral ligaments and joint capsule of the talocrural

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and subtalar joints have been shown to be extensively inner-vated by mechanoreceptors that contribute to propriocep-tion.37,48,49 The major importance of muscle spindles, espe-cially of those in the peroneal muscles, to proprioception aboutthe ankle complex has been described.50

PATHOMECHANICS OF ACUTE LATERAL ANKLESPRAIN

Lateral ankle sprains most commonly occur due to exces-sive supination of the rearfoot about an externally rotated low-er leg soon after initial contact of the rearfoot during gait orlanding from a jump.5,7 Excessive inversion and internal ro-tation of the rearfoot, coupled with external rotation of thelower leg, results in strain to the lateral ankle ligaments. If thestrain in any of the ligaments exceeds the tensile strength ofthe tissues, ligamentous damage occurs. Increased plantar flex-ion at initial contact appears to increase the likelihood of suf-fering a lateral ankle sprain.51

The ATFL is the first ligament to be damaged during alateral ankle sprain, followed most often by the CFL.52,53 Ca-daveric-sectioning studies have demonstrated that after theATFL is ruptured, the amount of transverse-plane motion (in-ternal rotation) of the rearfoot increases substantially, thus fur-ther stressing the remaining intact ligaments.39 This phenom-enon has been described as rotational instability of the ankleand is often overlooked when considering laxity patterns inthe sprained ankle.54 Concurrent damage to the talocrural jointcapsule and the ligamentous stabilizers of the subtalar joint isalso common with lateral ankle sprains. Martin et al55 dem-onstrated significantly greater strain in the cervical ligamentafter complete disruption to the CFL. The incidence of subtalarjoint injury has been reported to be as high as 80% amongpatients suffering acute lateral ankle sprains.56 Injury to thePTFL is typical only in severe ankle sprains and is often ac-companied by fractures or dislocations or both.57

A pathomechanical model described by Fuller58 suggestedthat the cause of lateral ankle sprain is an increased supinationmoment at the subtalar joint. The increased supination momentis caused by the position and magnitude of the vertically pro-jected ground-reaction force at initial foot contact. Fuller hy-pothesized that a foot with its center of pressure (COP) medialto the subtalar-joint axis has a greater supination moment fromthe vertical ground-reaction force than a foot with a more lat-eral relationship between the COP and the joint axis.58 Thisincreased supination moment could thus cause excessive in-version and internal rotation of the rearfoot in the closed ki-netic chain and potentially lead to injury of the lateral liga-ments. Individuals with a rigid supinated foot would beexpected to have a more laterally deviated subtalar axis ofrotation and a calcaneal varus (inverted rearfoot) malalign-ment, which could predispose those with a rigid supinated footto lateral ankle sprains.

Inman38 described great variation in the alignment of thesubtalar-joint axis across individuals, and it is possible thatthose with a more laterally deviated subtalar-joint axis may bepredisposed to recurrent ankle sprains. A foot with a laterallydeviated subtalar-joint axis would have a greater area on themedial side of the joint axis. Thus, during initial foot contact,the likelihood is greater that COP would be medial to thesubtalar-joint axis and the ground-reaction force would causea supination moment at the subtalar joint. Additionally, thefurther medial the COP is in relation to the subtalar-joint axis,

the longer the supination moment arm is. If the magnitude ofthis supination moment exceeds the magnitude of a compen-satory pronation moment (produced by the peroneal musclesand the lateral ligaments), excessive inversion and internal ro-tation of the rearfoot occur, likely causing injury to the lateralligaments.58

Some have questioned whether the peroneal muscles areable to respond quickly enough to protect the lateral ligamentsfrom being injured once the ankle begins rapid inversion.59,60Ashton-Miller et al46 estimated that the span of the inversionmotion upon landing may be as short as 40 milliseconds. Kon-radsen et al60 reported that a dynamic protective reaction fromthe peroneal muscles would take at least 126 milliseconds tooccur after sudden, unexpected inversion perturbation of theankle. This includes 54 milliseconds for reaction time of initialelectromyographic activity after the onset of inversion pertur-bation and 72 milliseconds of electromechanical delay neededto generate force in the muscle after electromyographic activ-ity has been initiated.60 This value assumes no preparatoryelectromyographic activity in the peroneal muscles before ini-tial contact of the heel with the ground. In fact, the peronealmuscles are active before initial foot contact during stair de-scent61 and landing after a jump.62 This preparatory activity,along with similar activity in the other muscle groups thatcross the ankle, is likely to create stiffness in tendons beforeinitial foot contact with the ground.47,63 If the peroneal mus-cles are to protect against unexpected inversion of the rearfoot,preparatory muscle activation before foot contact with theground is necessary.47,60

Relatively few research reports in the literature have de-scribed predispositions to first-time ankle sprains. Structuralpredispositions included increased tibial varum64 and nonpath-ologic talar tilt,64 whereas functional predispositions includedpoor postural-control performance,65,66 impaired propriocep-tion,67 and higher eversion-to-inversion and plantar flexion-to-dorsiflexion strength ratios.68 Further research into preventionprograms based on these predisposing factors is clearly war-ranted.

After acute injury, the ankle typically becomes swollen, ten-der, and painful with movement and full weight bearing. De-pending on the severity of the injury, function usually returnsover the course of a few days to a few months. What remainselusive to clinicians and researchers is why most individualswho suffer an initial ankle sprain are prone to recurrentsprains.

PATHOMECHANICS OF CHRONIC INSTABILITY

The mechanism of recurrent ankle injury is not thought tobe different than that of initial acute ankle sprains; however,adverse changes that occur after primary injury are believedto predispose individuals to recurrent sprains.54 Two theoriesof the cause of CAI have traditionally been postulated: me-chanical instability and functional instability. These 2 terms,however, do not adequately describe the full spectrum of ab-normal conditions related to CAI. By further clarifying thepotential insufficiencies leading to each type of instability, wecan better describe the full complement of potential causes ofCAI. Mechanical instability and functional instability are prob-ably not mutually exclusive entities but more likely form acontinuum of pathologic contributions to CAI (Figure 5).

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Figure 5. Paradigm of mechanical and functional insufficienciesthat contribute to chronic ankle instability.

Figure 6. The medial subtalar glide test is performed by translatingthe calcaneus medially in the transverse plane. Reprinted with per-mission of Hertel J, Denegar CR, Monroe MM, Stokes WL. Talocru-ral and subtalar joint instability after lateral ankle sprain. Med SciSports Exerc. 1999;31:15011508; Lippincott Williams & Wilkins.41

Mechanical InstabilityMechanical instability of the ankle complex occurs as a re-

sult of anatomic changes after initial ankle sprain, which leadto insufficiencies that predispose the ankle to further episodesof instability. These changes include pathologic laxity, im-paired arthrokinematics, synovial changes, and the develop-ment of degenerative joint disease, which may occur in com-bination or isolation.

Pathologic Laxity. Ligamentous damage often results inpathologic laxity of injured joints, thus causing these joints tobe mechanically unstable. The extent of pathologic laxity ofthe ankle depends on the amount of ligamentous damage tothe lateral ligaments. Pathologic laxity can result in joint in-stability when the ankle is put in vulnerable positions duringfunctional activities, resulting in subsequent injury to jointstructures. Pathologic laxity may be assessed clinically withphysical examination, stress radiography,69,70 or instrumentedarthrometry.71,72 After lateral ankle sprain, pathologic laxitymost often occurs in the talocrural and subtalar joints.69

Talocrural instability is caused primarily by injury to theATFL and CFL.73 Injury to the ATFL is often assessed bydetermining the amount of anterior displacement of the talusfrom the tibiofibular mortise using an anterior drawer test. In-tegrity of the ATFL may also be assessed by inverting the taluswith the talocrural joint in a plantar-flexed position and deter-mining the amount of talar tilt present. Calcaneofibular liga-ment integrity is best assessed by determining the amount oftalar tilt present when inverting the rearfoot with the talocruraljoint in a dorsiflexed position. The amount of inversion talartilt assessed with stress radiography increases dramaticallywith combined lesions of the ATFL and CFL.32 Whereas path-ologic laxity is often present in those with CAI, 11% ofhealthy individuals also have asymmetric ankle laxity as as-sessed by the anterior drawer and talar tilt tests.74

Mechanical instability of the talocrural joint is traditionallyexplained in single planes, although this disregards the normaltriplanar movement allowed at this joint. An excessive anteriordrawer represents laxity in the transverse plane, while in-creased talar tilt indicates laxity in the frontal plane. These

simplifications disregard the fact that the talocrural joint nor-mally moves about a triplanar axis and ignore the issue of rotaryinstability of the talocrural joint. Specifically, in the absence ofan intact ATFL, the talus is able to excessively supinate, witha large internal-rotation component in relation to the tibia.75Comprehensive assessment of the unstable talocrural jointshould focus on uniplanar and triplanar instability patterns.

Injury to the CFL also causes pathologic laxity of the sub-talar and talocrural joints. On arthrography, many injuries tothe CFL are accompanied by injury to the subtalar-joint cap-sule, cervical ligament, and other lateral ligaments.56,76 Rup-ture of the LTCL has also been implicated in chronic insta-bility of the lateral subtalar joint.42 Stress radiography hasbeen used to quantify the amount of subtalar tilt77,78 and an-terior displacement of the calcaneus from the talus,79 althoughthe validity of the most common method used for these as-sessments, the modified Broden view, has been challenged.80Hertel et al41 described the medial subtalar glide test, whichassesses the amount of medial translation of the calcaneus onthe talus in the transverse plane (Figure 6). The results of themedial subtalar glide test compared favorably with the resultsof stress radiography.41

Arthrokinematic Impairments. Another potential insuffi-ciency contributing to mechanical instability of the ankle isimpaired arthrokinematics at any of the 3 joints of the anklecomplex. One arthrokinematic restriction related to repetitiveankle sprains involves a positional fault at the inferior tibio-fibular joint. Mulligan44 suggested that individuals with CAImay have an anteriorly and inferiorly displaced distal fibula.If the lateral malleolus is indeed stuck in this displaced posi-tion, the ATFL may be more slack in its resting position. Thus,when the rearfoot begins to supinate, the talus can go througha greater range of motion before the ATFL becomes taut. Thispositional fault of the fibula may result in episodes of recurrentinstability, leading to repetitive ankle sprains. The findings of2 case studies81,82 and one pilot study83 present preliminaryevidence for restriction of posterior fibular glide after lateralankle sprain, suggesting that the lateral malleolus may be sub-luxated in an anteriorly displaced position.

Hypomobility, or diminished range of motion, may also bethought of as a mechanical insufficiency. Restricted dorsiflex-

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Figure 7. Paradigm of proprioception and neuromuscular control.CNS indicates central nervous system.

ion range of motion is thought to be a predisposition to lateralankle sprain.84 If the talocrural joint is not able to fully dor-siflex, the joint will not reach its closed-pack position duringstance and, therefore, will be able to invert and internally ro-tate more easily. Limited dorsiflexion in the closed kineticchain is also typically compensated for by increased subtalarpronation. Some evidence demonstrates dorsiflexion restric-tions in athletes with repetitive ankle sprains.85,86 Greene etal87 recently demonstrated that altered arthrokinematics maylimit dorsiflexion after acute ankle sprain. Patients with acuteankle sprains who were treated with posterior mobilization ofthe talus on the tibia recovered their dorsiflexion range of mo-tion more quickly than those not treated with joint mobiliza-tion. Denegar et al88 found restricted posterior talar glide inathletes 12 weeks after acute ankle sprain. Interestingly, theseathletes did not have significantly decreased dorsiflexion rangeof motion as assessed through standard clinical measures. Thissuggests that dorsiflexion may be returned to normal rangesin the absence of normal arthrokinematics due to extensivestretching of the triceps surae. Further research is needed toelucidate the clinical implications of altered arthrokinematicsafter ankle sprain.

Synovial and Degenerative Changes. Mechanical instabil-ity of the ankle complex may also occur due to insufficienciescaused by synovial hypertrophy and impingement or the de-velopment of degenerative joint lesions. Synovial inflamma-tion has been shown in the talocrural and posterior subtalar-joint capsules. Patients with synovial inflammation oftenreport frequent episodes of pain and recurrent ankle instability,which are due to impingement of hypertrophied synovial tissuebetween the respective bones of the ankle complex. Di-Giovanni et al89 identified anterolateral impingement syn-drome of the talocrural joint in 67% and talocrural synovitisin 49% of patients requiring surgery for lateral instability. Si-nus tarsi syndrome, or synovitis of the lateral aspect of theposterior subtalar joint, often occurs as a sequela to repetitivebouts of ankle instability.43,90

Repetitive bouts of ankle instability have also been relatedto degenerative changes in the ankle complex.10 Individualsundergoing surgery for ankle-ligament repair were 3.37 timesmore likely to have osteophytes, or loose bodies, than thosewith asymptomatic ankles.74 Similarly, Gross and Marti11demonstrated more osteophytes and subchondral sclerosis involleyball players with a history of repetitive ankle sprainscompared with a group of healthy controls. Greater varus an-gulation of the tibial plafond has also been identified in sub-jects with CAI when compared with those suffering initialacute sprains.91 It is unclear whether this is a developmentalchange in response to numerous bouts of ankle instability ora structural predisposition to recurrent ankle sprains.

Functional InstabilityInjury to the lateral ligaments of the ankle results in adverse

changes to the neuromuscular system that provides dynamicsupport to the ankle. Freeman et al16,17 first described the con-cept of functional instability in 1965. They attributed impairedbalance in individuals with lateral ankle sprains to damagedarticular mechanoreceptors in the lateral ankle ligaments,which resulted in proprioceptive deficits. The contribution ofimpaired proprioception, while important, does not fully ex-plain why ankle-ligament injury predisposes athletes to func-tional ankle instability. The pathoetiologic model is not com-

plete without including impaired neuromuscular control, thusresulting in inadequacies of the dynamic defense mechanismprotecting against hypersupination of the rearfoot.92 Figure 7illustrates the links between proprioception and neuromuscularcontrol of joint stability. Over the past 2 decades, functionalinsufficiencies among individuals with either acute anklesprains or CAI have been demonstrated by quantifying deficitsin ankle proprioception, cutaneous sensation, nerve-conduc-tion velocity, neuromuscular response times, postural control,and strength.

Impaired Proprioception and Sensation. Proprioceptionat the ankle is impaired in individuals prone to repetitive anklesprains on measures of kinesthesia9395 and active replicationof joint angles.9698 While Gross99 did not find significant dif-ferences in active and passive replication of joint angles insubjects with unilateral CAI, most studies assessing proprio-ception in subjects with CAI demonstrate impairments. Recentevidence suggests that alteration in muscle-spindle activity inthe peroneal muscles may be more important than altered ar-ticular mechanoreceptor activity in the manifestation of pro-prioceptive deficits at the ankle.50 The clinical relevance ofproprioceptive deficits is not fully understood at this time, andwhether proprioception is improved through rehabilitation ex-ercises has not yet been conclusively demonstrated.100

Impaired cutaneous sensation101104 and slowed nerve-con-duction velocity102,105 have been reported as indicators ofcommon peroneal nerve palsy after acute lateral ankle sprain,but no evidence exists that such impairments are present inpatients with CAI. Further research in this area is warranted.

Impaired Neuromuscular-Firing Patterns. Impaired neu-romuscular-recruitment patterns have been demonstrated in in-dividuals with a history of repetitive lateral anklesprain.104,106111 This has been most commonly shown by as-sessing the reflexive response times of the peroneal musclesto inversion or supination perturbations. Conflicting results inthe literature may be due to methodologic differences amonginvestigators.59,112116 If peroneal response is impaired inthose with CAI, it may be due to impaired proprioception,slowed nerve-conduction velocity, or central impairments inneuromuscular-recruitment strategies. Evidence of the latterwas presented by Bullock-Saxton et al,111 who found bilateraldeficits of gluteus medius recruitment in subjects with a his-

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tory of severe unilateral ankle sprain. This finding suggeststhat neuromuscular impairments are not only present in struc-tures that cross the affected ankle but also exist along otherneuromuscular pathways in both limbs, thus indicating centralneural adaptations to peripheral joint conditions.

Impaired Postural Control. Impaired postural control dur-ing single-leg stance has been demonstrated frequently in in-dividuals after acute ankle sprain1617,104,117126 and in thosewith a history of repetitive ankle sprains.21,93,127132 Nonin-strumented assessment of the modified Romberg test has beenperformed by having subjects stand as motionless as possibleon one leg for a period usually ranging from 10 to 30 seconds.This task is performed while standing on the involved limband then the uninvolved limb, first with eyes open and thenwith eyes closed. Both the subject and the examiner make asubjective judgment as to which limb either feels or appearsto cause greater postural instability. Subjective assessment ofpostural control has consistently identified functional insuffi-ciencies in those with chronically unstable ankles.16,17,93,129,132

Instrumented assessment of postural control has also beenused to discriminate between functionally stable and unstableankles. Piezoelectric force plates allow for assessment of theCOP during single-leg standing. Two very common dependentmeasures of postural control include the overall length of thepath of COP and the velocity of COP excursions during theduration of an entire trial of single-leg standing. Shorter lengthof COP displacement and slower velocity of COP excursionsare associated with better postural control. Dozens of dependentmeasures of postural control have been reported related to bal-ance deficits and ankle instability. Despite varying methods,postural-control deficits have consistently been demonstratedbetween stable and unstable ankles when using instrumentedassessment, although conflicting findings exist.65,133136

Postural-control deficits are likely due to a combination ofimpaired proprioception and neuromuscular control. Whenbalancing in single-leg stance, the foot pronates and supinatesin an effort to keep the bodys center of gravity above the baseof support. This is referred to as the ankle strategy of pos-tural control. Individuals with CAI have been shown to usemore of a hip strategy to maintain unilateral stance thanuninjured individuals.137 The hip strategy is less efficient thanthe ankle strategy in maintaining unilateral stance. This alter-ation in postural-control strategy is likely due to changes incentral neural control that occur in the presence of ankle-jointdysfunction. Further evidence of central changes in neuro-muscular control were presented by Friden et al,117 who foundbilateral impairment of postural control in subjects with acuteankle sprains.

Interestingly, side-to-side differences in postural control of-ten return to insignificant levels in the weeks and months afterinitial injury, whether structured rehabilitation programs areadhered to or not.118,126,138 Holme et al126 reported that 4months after acute ankle sprain, both subjects who did andthose who did not perform a comprehensive rehabilitation pro-gram emphasizing balance and coordination exercises showedno significant postural-control deficits. However, subjects whodid not undergo rehabilitation were more than twice as likelyto suffer recurrent sprains than those who did rehabilitate theirankles. Thus, while quantification of postural control may notbe able to predict those at risk of recurrent sprain in all in-stances, retraining of postural control after ankle sprain isnonetheless advantageous.

Strength Deficits. Strength deficits have been reported

among individuals with CAI.20,139142 Diminished strength hasbeen reported for both eversion20,139,141,142 and inver-sion,140,142 although reports of no strength deficits also ex-ist.95,132,134,143 Assuming that strength deficits do exist insome patients with CAI, the reason for such impairments isunclear. Is this weakness due to muscle damage or atrophy?Or could deficits be due to impaired neuromuscular recruit-ment in the presence of ankle-joint abnormality and, therefore,be causing functional insufficiency in the dynamic defensemechanism? Further research is needed to elucidate the roleof strength deficits in CAI.

Relationships Between Functional InsufficienciesThe individual symptoms of functional ankle instability do

not occur in isolation but are likely all components of a com-plex pathoetiologic paradigm. Joint injury results in proprio-ceptive decrements, which also lead to impairments in neu-romuscular control. These changes limit the dynamic defensesystem of the ankle and predispose the ankle to recurrent ep-isodes of instability. Altered muscle-spindle activity, as me-diated through the g-motoneuron system, may be the keystoneto these interrelated symptoms.50 Figure 7 illustrates the feed-back loop among the somatosensory system, the central ner-vous system, and the a- and g-motoneuron systems. The keyto treating functional insufficiency may lie in restoration ofnormal g-motoneuron activity.

Relationships Between Mechanical and FunctionalInsufficiencies

The interactions between mechanical insufficiency andfunctional insufficiency and the relationships between the spe-cific insufficiencies have not been clearly elucidated. Researchis needed to examine the relationships between mechanical andfunctional insufficiencies and the effects of common treatmentstrategies on both types of insufficiency. While this new modelof functional and mechanical insufficiency helps to explain thecausative spectrum related to CAI, further developments areneeded to improve the clinical outcomes of athletes who sufferfrom lateral ankle instability.

An example of an assessment technique that evaluates mul-tiple insufficiencies is the Star Excursion Balance Tests. Thesetests are a series of dynamic postural-control tasks that requirestabilization on one lower limb and a functional reach withthe contralateral lower limb in different directions. In order tooptimally execute these tasks, adequate postural control,strength, and range of motion must be present. Olmsted et al144demonstrated impairment in performance on the Star Excur-sion Balance Tests among a group of athletes with CAI. Fur-ther research is needed to identify which specific mechanicaland functional insufficiencies are related to such impaired per-formance on these tests of dynamic balance. The developmentof more evaluation tools will allow the assessment of multipleinsufficiencies simultaneously during functional activities.

Prevention of Chronic InstabilityThe natural progression of acute ankle sprains is for subjects

to report gradual improvement as the initial symptoms of pain,swelling, and loss of function subside in the weeks after in-jury.136 The conundrum facing clinicians is how to convincepatients with an ankle sprain that is improving that they need

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to continue rehabilitation for several weeks or months aftertheir initial symptoms have subsided. Comprehensive rehabil-itation programs that emphasize proprioceptive, neuromuscu-lar control, and balance training significantly reduce the riskof recurrent ankle sprains.126,145,146 While ankle taping andbracing also appear to be effective in preventing repetitiveankle sprains,145,147,148 it is unlikely that ankle taping or brac-ing alone is as effective as completion of a comprehensiverehabilitation program in combination with taping or bracing.Preventive measures to reduce the incidence of recurrentsprains must address pathologic laxity, arthrokinematic chang-es, and other mechanical insufficiencies related to mechanicalinstability and the proprioceptive and neuromuscular deficitsseen with functional instability.

CONCLUSIONSLateral ankle sprains are among the most common injury

seen in physically active populations, yet the treatment strat-egies being used by clinicians appear to be inadequate in pre-venting recurrence of these injuries. Appreciating the anatomyand mechanics of the rearfoot complex aids in understandingthe pathomechanics of lateral ankle sprains and CAI. Mechan-ical instability of the ankle may be due to the specific insuf-ficiencies of pathologic laxity, arthrokinematic restrictions, sy-novial irritation, or degenerative changes to the joints of theankle complex. Functional instability is driven by insufficien-cies in proprioception, neuromuscular control, postural control,and strength. The clinical management of patients with unsta-ble ankles should include identifying symptoms of both me-chanical and functional instabilities. Once specific insufficien-cies have been identified, treatment efforts should focus onaddressing these impairments and emphasis should be placedon reducing the risk of recurrent ankle sprains.

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