mri of sports-related injuries of the foot and ankle: part 2 · 2019. 12. 2. · mri of...

MRI of Sports-Related Injuries of the Foot andAnkle: Part 2

Jose A. Narvaez, MD,a Luıs Cerezal, MD,b and Javier Narvaez, MDc

Tendon LesionsThe ankle tendons can be divided into four anatomicand functional groups. Medially, the posterior tibial,flexor digitorum longus (FDL), and flexor hallucislongus (FHL) assist in inverting the foot as well asflexing the toes. Laterally, the peroneus brevis andperoneus longus act to evert the foot. Anteriorly, theanterior tibial, extensor hallucis longus, extensor digi-torum longus, and peroneus tertius are responsible fordorsiflexion of the foot and extension of the toes. TheAchilles tendon is the primary posterior tendon andacts to plantar flex the foot. On magnetic resonanceimaging (MRI), tendons demonstrate homogeneouslow-signal intensity regardless of pulse sequence. Toevaluate ankle and foot tendons, two imaging planeswith at least two pulse sequences are required. Ankletendons are best evaluated in oblique axial imagingperpendicular to the long axis of the tendon. Sagittalimaging allows a better depiction of the longitudinalextent of most tendon ankle injuries.

The spectrum of tendinous lesions includes teno-synovitis, stenosing tenosynovitis, tendinosis-tendini-tis, rupture, and dislocation. Tenosynovitis is an in-flammation of the tendon sheath, characterized by aconsiderable amount of synovial fluid that distends thetendon sheath. This condition demonstrates decreasedsignal intensity on T1-weighted MR images and in-creased signal intensity on T2-weighted images sur-

rounding low-signal intensity tendons. It is interestingto note that presence of small amounts of fluid inflexor tendon sheaths is considered a normal variant,especially in the FHL, which communicates with theankle joint in 20% of patients.10 Repetitive acutetenosynovitis can progress to a stenosing tenosynovi-tis, a chronic condition characterized by the formationof fibrous or scar tissue in the tendinous sheath thatinterferes with tendon gliding. These fibrous changesappear as an intermediate signal-intensity rind sur-rounding the tendon on both T1- and T2-weightedimages.

Tendinitis results from the inflammation within thetendon substance, whereas tendinosis is a structuraldegeneration of the tendon. These two terms are oftenused to designate an overuse tendon injury, which, ina chronic stage, is histologically characterized byminimal or absent inflammatory changes.11-13 Thus,the term tendinosis is preferred by most authors.Tendinosis is characterized by variable tendinousthickening and increased signal intensity on T1-weighted or proton-density-weighted MRI.1,6 Tendi-nous signal intensity is normal or only slightly in-creased on T2-weighted images. Partial ruptureappears as a tendon thickening with intratendinousareas of increased signal intensity on T1-weighted,proton-density, and T2-weighted images, similar tothat seen in chronic tendinosis.1,6 Complete rupture isdefined by the loss of continuity of the tendon fibers.

Achilles TendonThe Achilles tendon is the longest tendon of the

body. It is formed by the union of the tendons of thegastrocnemius and soleus muscles and inserts on theposterior aspect of the calcaneus. Distally, the tendonis separated from the calcaneus by the retrocalcanealbursa. It is not invested by a synovial sheath; instead itis surrounded by loose connective tissue referred to as

From the aDepartment of CT and MR imaging, I.D.I. Ciutat Sanitaria iUniversitaria de Bellvitge, Barcelona, Spain; bDepartment of Radiology,Instituto Cantabro de Radiologıa, Clınica Mompıa, Santander, Spain;cDepartment of Rheumatology, Clınica Delfos, Barcelona, Spain.Reprint requests: Dr. Jose Antonio Narvaez, Department of MR imaging.Institut de Diagnostic, Ciutat Sanitaria i Universitaria de Bellvitge, Hos-pital Duran i Reynals, Autovia de Castelldefels s/n, Hospitalet de Llobre-gat, 08907, Barcelona, Spain.Curr Probl Diagn Radiol 2003;32:177-193.© 2003 Mosby, Inc. All rights reserved.0363-0188/2003/$30.00 � 0doi:10.1016/S0363-0188(03)00044-6

Curr Probl Diagn Radiol, September/October 2003 177

the peritenon. The peritenon acts as an elastic sleevethat allows the tendon to move freely.

Achilles tendon injuries may be divided into inser-tional and noninsertional complaints.13 Insertional in-juries occur near or at the insertion of the tendon andinclude insertional tendinosis and retrocalcaneal bur-sitis, which often coexist (Figs 21 and 22). Insertionalinjuries may be associated with a Haglund deformity,which is a prominence of the posterosuperior aspect ofthe calcaneus (Fig 22).11,13 Noninsertional injuries areusually located 2-6 cm from the Achilles tendoninsertion in the calcaneus in an area characterized bydecreased vascularization.11,13 These injuries includeperitendinitis, tendinosis, and tendon rupture (Figs 23and 24).

Achilles tendon injuries are common in the courseof sports-related activities.11,13 Most of these sports-related injuries consist of peritendinitis, tendinosis andinsertional complaints caused by overuse.11,13 Theseinjuries are very common among runners and, lesscommonly, among dancers, tennis players, and basket-ball players.3,11,13 Clinical differentiation betweenachilleal tendinosis and peritendinitis is challenging,and both conditions may coexist in the same patient.12

The main symptom is pain associated with physicalactivity that improves with rest. Frequently, the pain isgreater when initiating the activity and improvesgradually with the exercise.

On MRI, Achilles peritendinitis shows a loss ofnormal signal intensity of peritendinous fat, withill-defined reticulated areas of decreased signalintensity on T1-weighted images and increasedsignal on short tau inversion recovery (STIR) andT2-weighted images that represent inflammatoryand edematous changes. Scarring of the preachillealfat, with low-signal intensity, is seen in cases ofchronic Achilles peritendinitis.1 Tendinosis is char-acterized by tendon thickening and loss of theanterior concave or flat surface on axial images (Fig23).12,14

Intratendinous areas of increased signal intensityare often seen on T1-weighted and proton density-weighted images. Increased signal intensity on STIRand T2-weighted images is less commonly seen and isrelated to a more severe derangement of tendon fiberstructure.12 Insertional tendinosis may be associatedwith calcaneal marrow edema and retrocalcaneal bur-sitis (Figs 21 and 22).3,12,14 On MRI, a bursal fluid

FIG 20. Sinus tarsi syndrome. Axial T1-weighted spin-echo (A) and coronal T2*-weighted (B) MRI show diffuse infiltration of the sinus tarsiconsistent with chronic cynovitis and nonspecific inflammatory changes. The interosseous ligament is poorly defined (arrow).

178 Curr Probl Diagn Radiol, September/October 2003

collection larger than 7 mm craniocaudally or 11 mmtransversely is considered diagnostic of bursitis (Figs21 and 22).4,15

Treatment consists of rest, avoidance of the aggra-vating athletic activity, shoe modification, heel eleva-tion to reduce tendon stretching during walking,nonsteroidal anti-inflammatory drugs, and physicaltherapy.

Achilles tendon ruptures, which are thought to bebecause of underlying tendinosis, are uncommon.11

Most Achilles tendon ruptures are related to sportsactivities. These injuries usually occur in sports thatrequire running, jumping, and quick turns.3,11 Partialruptures usually occur in well-trained athletes, pre-senting as chronic overuse injuries.11 Conversely,complete ruptures tend to occur in middle-aged,poorly conditioned men after abrupt calf muscle con-traction.11 In partial Achilles tendon rupture, activeplantar flexion of the ankle may be preserved butpainful. In those patients with complete Achillestendon rupture, it is still possible to actively plantar-flex the ankle with the adjacent intact flexor tendons.However, squeezing the calf muscles with the patientsitting or kneeling on a chair produces little or nopassive ankle plantar flexion (positive Thompson calfsqueeze test). Clinical differentiation between partialand complete rupture in cases of chronic tendinosis

might be complex. Moreover, clinical diagnosis ofcomplete ruptures of the Achilles tendon is missed inabout 25% of the cases.11

MRI is useful to differentiate between partial andcomplete ruptures, to plan the surgical treatment incomplete ruptures, and in the follow-up after surgi-cal intervention.16 On MRI, partial ruptures appearas a tendon thickening with intratendinous areas ofincreased signal intensity on T2-weighted images.In cases of acute partial rupture, edematous andhemorrhagic changes in the peritenon are oftenseen.1 Differential diagnosis with severe chronic

FIG 21. Insertional Achilles tendinitis and retrocalcaneal bursitis.Sagittal STIR MRI demonstrates thickening of the distal Achilles tendonwith increased intratendinous signal intensity (short arrows). Note alsodistention of the retrocalcaneal bursa by high-signal intensity fluid(long arrow), a finding that represents bursitis.

FIG 22. Haglund deformity. Sagittal T1-weighted (A) and STIR (B) MRIshow a prominent posterior superior calcaneal tuberosity (arrow),associated with marked Achilleal thickening and intratendinous in-creased signal intensity (arrowheads). Note also associated retrocal-caneal bursitis.


tendinosis only can be established on the basis of theclinical presentation of the patient.1 Acute completeruptures are seen in MRI as a complete disruption of thetendon fibers (Fig 24). The tendinous gap is filled byintermediate- to high-signal intensity on T1-weightedimages and high-signal intensity on T2-weighted imagesindicative of edema or hemorrhage.16 Fraying or retrac-tion of the tendon ends can be observed. In chroniccomplete rupture, the tendon gap may be occupied by

FIG 23. Achilles tendinitis. Axial proton-density-weighted (A) andT2-weighted (B) MRI show loss of the anterior concavity of the Achillestendon (arrow) without evidence of intrasubstance increased signalintensity.

FIG 24. Acute complete tear of the Achilles tendon. A, Sagittal T1-weighted depicts complete disruption and retraction of the torn ends of theAchilles tendon with a tendon gap. Note small hyperintense foci corre-sponding to hemorrhage (arrowheads). B, Sagital GD-enhanced T1-WIshows enhancement of the tendon ends, with better delineation of the tear(arrows). C, Axial T2-weighted shows the tendon gap filled with highsignal intensity fluid (arrows).


fat and/or scar tissue, and hemorrhagic and edematouschanges are absent.

The treatment of partial ruptures and, in some casesof complete ruptures, is conservative. Surgical treat-ment seems to be the treatment of choice for completeruptures in athletes and young people and in cases ofdelayed ruptures.

Peroneal TendonsThe lateral compartment of the leg is formed by the

muscles peroneus longus (PL) and peroneus brevis(PB). Their tendons pass behind the lateral malleoluswithin a fibro-osseous tunnel. The superior peronealretinaculum forms the posterolateral border of thisfibro-osseous tunnel. It extends inferiorly and posteri-orly from the lateral malleolus to the lateral calcanealsurface, binding the PL and PB tendons. Distal to thelateral malleolus, the PB tendon runs adjacent to thelateral wall of the calcaneus within a separate osteo-aponeurotic canal created by the inferior peronealretinaculum. The PB tendon inserts at the base of thefifth metatarsal. The PL tendon passes below theperoneal tubercle of the calcaneus and then it runsthrough a fibro-osseous tunnel formed by the longplantar ligament and the peroneal groove of the cuboiduntil it inserts onto the plantar face of the base of thefirst metatarsal and medial cuneiform.

Peroneal tenosynovitis is an overuse injury rela-tively common in athletic individuals.17,18 Displacedfractures of the calcaneus, enlarged peroneal tubercleof the calcaneus, and alterations of the mechanics ofthe foot (ie, flat foot, tarsal coalition) are consideredpredisposing factors.1,19 Clinical findings are pain andswelling in the inferolateral malleolar region, whichcan radiate to the external face of the leg. On physicalexamination, flexion and pronation of the foot arepainful. Although a small amount of fluid in theperoneal tendon sheath is physiological,10,18 MR iden-tification of a large volume of fluid indicates tenosyn-ovitis (Fig 25). However, after an ankle sprain, thedetection of a large amount of fluid in the peronealtendon synovial sheath indicates the rupture of thecalcaneofibular ligament.8,19

Peroneal tendinosis represents a more advancedoveruse injury that depelops over a period of severalweeks or months.19 MRI demonstrates tendon thick-ening and intratendinous signal abnormalities.16 Inacute peroneal tendinosis, intratendinous signal abnor-malities are less extensive than in chronic forms.18

Longitudinal ruptures of the peroneal tendons havebeen described more frequently in recent years.17-22

These injuries may occur as a result of overuse indancers, runners, and competitive walkers.1,22 Longi-tudinal rupture or split lesion of the PB tendon occursat the level of the lateral malleolus and can progressproximally or distally.21,22 It takes place as a result ofthe repeated compression of the PB tendon betweenthe lateral malleolus and the PL tendon17-22 and isoften associated with lateral ligamentous injuries,

FIG 25. Peroneal tenosynovitis. Sagittal T1-weighted (A) and STIR (B)MRI show a fluid distending the sinovial sheath of the peroneal tendons(arrows). Note mild intrasubstance increased signal signal in the PLtendon on STIR image.


insufficiency of the superior peroneal retinaculum, andrepetitive peroneal tendon subluxation.1,19,24 A flat-tened or convex retromalleolar groove, a low-lyingmuscle belly of the PB tendon, and the existence of anaccessory muscle, the peroneus quartus, are predispos-ing factors for longitudinal tearing of the peroneusbrevis tendon.1,19,21,23 Clinically, it presents withlong-standing retromalleolar pain and swelling, and ahistory of recurrent inversion injuries is often noted.Longitudinal ruptures of the PB tendon are oftenconfused with chronic ankle instability syndrome and,indeed, both are frequently associated.19,21,23 Theselesions can be difficult to diagnose, and MRI is anuseful technique for demonstrating tendon tears aswell as showing associated or predisposing abnormal-ities.18-22

MRI findings include morphologic and signal in-tensity abnormalities of the PB tendon as well asmarked peroneal tenosynovitis. The torn PB oftenwraps itself against the PL tendon, assuming a C-shaped configuration (Figs. 26 and 27).18,19,21,22 Someauthors describe this morphologic abnormality as thechevron sign.20 In advanced stages, the PB tendonmay be completely divided in two portions (Fig27).18-22 Intrasubstance areas of high-signal intensityon T2-weighted images in the PB tendon are com-monly seen.22,24 About one third of PB tendon longi-tudinal ruptures are associated with PL tendon tears(Fig 27).19 When the PB tendon is bisected, the PLtendon comes into direct contact with the hard surfaceof the retromalleolar groove and becomes exposed tosimilar mechanical attrition, which causes a PB tendontear.29 On MRI, thickening and increased signal PLtendon are seen (Fig 27).

Ruptures of the PL tendon in the midfoot candevelop as a result of sports-related trauma.17,25 Thesetears are typically located at the level of the calcane-ocuboid joint, distal to the os peroneum.18,26 Thelesional mechanism is an acute inversion or forcedeversion of a supinated foot, causing forced contrac-tion of the PL tendon.26 Hypertrophied peroneal tu-bercle of the calcaneus and calcaneal and cuboid bonefractures are predisposing factors for PL tear.19 Clin-ical diagnosis is difficult, and MRI is often required toconfirm the diagnosis.19,26 These injuries are betteridentified on oblique coronal MRI. MRI findingsinclude an empty PL tendon sheath with retractedproximal and distal segments of the tendon in com-plete tears, and tendon thickening and increased signalintensity in partial tears.26 Other associated MR find-

ings are increased tenosynovial fluid, enlarged pero-neal tubercle, and bone marrow edema in the peronealtubercle as well as along the lateral wall of thecalcaneus.26 Treatment of peroneal tendon tears inathletes is surgical in most cases.

Subluxation and dislocation of the peroneal tendonsare common in skiers and to a lesser extent in iceskaters and basketball and soccer players.18,19 Thelesional mechanism is traumatic detachment of supe-

FIG 26. Longitudinal rupture of the PB tendon. A, B, Consecutiveoblique axial proton-density-weighted images. At the level of theretromalleolar groove, the PB tendon presents a C-shaped configura-tion (arrows), wrapping against the adjacent the PL tendon. Distally tothe lateral malleolus, the PB tendon is completely divided in twoportions (arrows).


rior peroneal retinaculum produced by a sudden dor-siflexion injury, with either inversion or eversion ofthe foot. Chronic ankle instability associated withsuperior peroneal retinaculum is considered a predis-posing factor for chronic peroneal dislocation. Con-genital absence of the superior peroneal retinaculum,low-lying PB muscle belly, peroneus quartus muscle,and flattened or convex retromalleolar grooves are alsoconsidered predisposing factors.18,19 Acute dislocationof the peroneal tendons may be clinically confusedwith lateral ankle ligament sprain. Physical examina-tion demonstrates tenderness around the retromalleolartunnel. Tendon luxation is elicited with foot plantarflexion and eversion. MRI reveals the peroneal ten-dons located anteriorly and laterally to the distal fibula(Fig 28). The tendon dislocation is best demonstratedon axial images that are also useful in identifying thetorn or stripped-off superior peroneal retinaculum.18,19

Associated MR findings are tenosynovitis and longi-tudinal ruptures of the peroneal tendons.1,19 Treatmentof peroneal dislocation in athletes with lateral anklepain and instability is surgical.

FHL and FDL TendonsThe FDL and the FHL tendons course through the

posteromedial ankle. The FDL tendon lies just pos-terolaterally to the posterior tibial tendon, running

posteriorly to the talus. The FHL tendon coursesposterolaterally to the posterior tibial tendon and theFDL tendon, running through a shallow groove in theposteromedial aspect of the talus between the lateraland medial processes; it then continues distally underthe sustentaculum tali. On the plantar aspect of theheel, the FHL tendon crosses deep to the FDL tendon,and both course along the plantar aspect of the sole.The FHL tendon inserts on the big toe. The FDLtendon inserts on the bases of the second through thefifth distal phalanges.

FHL tenosynovitis is common in athletes whoperform extreme plantar flexion and push-off maneu-vers from the forefoot, such as ballet dancers andsoccer players.1-3,27 Repetitive full plantar flexioncompresses the tendon within the talar tunnel.2,3 Re-petitive episodes of acute tenosynovitis may progressto stenosing tenosynovitis, leading to fibrosis, tendonentrapment, and tendinosis.27 Clinically, FHL teno-synovitis can mimic posterior impingement, and bothoften may coexist.27

In acute tenosynovitis, synovial fluid surroundingthe FHL tendon can be seen on MRI. Because synovialsheaths of the FHL and FDL tendons communicatewith the ankle joint in 20% of individuals,10 thediagnosis of FHL tenosynovitis requires a dispropor-tionate amount of fluid within the sheath.1,4,10 Fibroticchanges of stenosing tenosynovitis appear as an inter-

FIG 27. Longitudinal tear of the PB and PL. Axial T2-weighted showsa C-shaped split PB tendon (short arrow) partially enveloping the PLtendon that is thickened and presents a high signal intratendinousfocus (long arrows). Synovial tendinous sheath is filled with high-signalintensity fluid.

FIG 28. Dislocation of PB tendon. Consecutive axial proton density-weighted MRI shows the PB tendon (arrow) lateral to the peronealmalleolus. Note peroneous longus tendon normally located behind themalleolus.


mediate-signal-intensity rind surrounding the tendonon both T1- and T2-weighted images.4 Other MRfindings of FHL stenosing tenosynovitis are a FDLaccesorious muscle, distal FHL muscle edema, and ostrigonum edema.27

Treatment is conservative and includes rest, nonste-roidal anti-inflammatory drug therapy, and physicaltherapy. Surgical release of the FHL tendon is per-formed if conservative treatment fails.27

Tenosynovitis may also affect the FHL tendonbetween the sesamoid bones of the first metatarsal,where it is subject to repetitive impact, and under thebase of the first metatarsal bone in the region ofHenry’s knot, where the FDL crosses under the FHLtendon.1 Rupture of the distal FHL tendon is a veryuncommon injury that occurs as a result of acute orrepetitive dorsiflexion injuries.

Posterior Tibial TendonThe posterior tibial muscle forms part of the deep

posterior compartment of the calf. It originates fromthe proximal third of the tibia and interosseous mem-brane and sends a tendon than runs directly behind themedial malleolus. The tendon then curves sharplytoward its main insertion on the navicular tuberosity.The posterior tibial tendon is the most powerfulinvertor of the foot. It participates in maintaining themedial longitudinal arch and is one of the mainstabilizers of the hindfoot against valgus deformity.

Posterior tibial tendon injuries in athletes are un-common.28 Acute tenosynovitis represents almost allof these sports-related injuries13,29 and has been de-scribed as an overuse injury in young athletes engagedin running and in sports that require rapid changes indirection, including ice hockey, soccer, basketball, andtennis.28,29 Clinically, tenosynovitis is characterizedby medial ankle pain and swelling. On MRI, tenosy-novial changes are seen along the course of the tendonbehind or distally to the medial malleolus.

Tendon rupture of the posterior tibial tendon israrely seen in athletes. Usually, these tendon tearsoccur in middle-aged athletes, but cases in youngpatients have been described.29 The most common siteof rupture is at the level of the medial malleolus.Surgical and MRI classification of posterior tibialtendon ruptures divides these injuries into three types.Partial tears are classified as hypertrophic (type I) oratrophic (type II). Type III consists of complete tears.Tendon rupture results in a progressive flatfoot defor-mity, with hindfoot valgus and forefoot abduction.

Clinical diagnosis of posterior tibial tendon ruptures inathletes is often missed. Early diagnosis and treatmentare important to avoid irreversible deformities andprolonged disabilities. In this setting, MRI is a usefuldiagnostic tool and helps to plan treatment.30,31 MRIcan distinguish between partial and complete tears ofthe posterior tibial tendon.28–31 In hypertrophic tears,the tendon is increased in size and loses its oval shape,appearing with a more rounded configuration (Fig 29).The signal intensity is often markedly increased, moreso on proton density and T1-weighted than on T2-weighted images. In atrophic tears, the tendon showsthinning and an increased signal. Complete tears aredelineated by a tendinous gap filled with fluid orgranulation tissue, depending on the chronicity of theinjury.

Most patients with tenosynovitis or type I tendonrupture respond to conservative treatment with anti-inflammatory medication, protected mobilization, andphysical therapy.29 Surgical treatment is reserved forcases in which conservative therapy fails, completetendon rupture, or progressive deformity.

FIG 29. Posterior tibial tendon hypertrophic partial tear (type I).Oblique axial T2-weighted MRI. Note markedly enlarged tendon girth(arrow) and mild intrasubstance signal heterogeneity. There is alsotenosynovial fluid surrounding the tendon.


The presence of an accessory navicular bone is apredisposing factor for posterior tibial tendon tears.9

This ossicle, which is present in up to 14% of thepopulation, is an anatomic variant that increases stresson the distal posterior tibial tendon, which predisposesit to rupture. Moreover, the accessory navicular boneitself may become symptomatic.32 This clinical con-dition has been termed painful accessory navicularbone.32 There are three types of accessory navicular:type I is a large sesamoid bone that is located in theposterior tibial tendon and is usually asymptomatic.Type II is a triangular or heart-shaped ossicle con-nected to the tarsal navicular by a cartilaginous orfibrocartilaginous bridge. Type III accessory navicularcorresponds to a prominent navicular tuberosity.

Most cases presenting a painful accessory navicularbone have a type II variant. The lesional mechanismmay be either acute or chronic repetitive trauma thatdamages the synchondrosis. Clinical symptoms in-clude recurrent pain on the medial ankle that isaggravated by prolonged exercise. In cases of painfulaccessory navicular bone, MRI may show bone mar-row edema changes in the ossicle and in the adjacentmedial aspect of the navicular bone and surroundingincreased signal intensity on STIR images reflectinginflammatory and edematous changes.32

Anterior Tibial TendonThe anterior tibial tendon is a dorsiflexor of the foot

that originates on the anterior surface of the tibia. Atthe ankle joint, it passes under the superior and inferiorextensor retinacula and inserts on the medial cunei-form bone and base of the first metatarsal bone.

Injuries of the tendons on the anterior aspect of theankle are uncommon.1 The anterior tibial tendon maybe injured in athletes engaged in downhill running orhiking.16 Tenosynovitis and tendinitis are more com-mon than tendon rupture. Rupture of the anterior tibialtendon is a very rare injury in athletes. The tendonrupture is caused by a forced plantarflexion and mostcases occur in middle-aged or elderly patients, whopresent with degenerative changes of the tendon. Mainsymptoms are inability or weakness of foot dorsiflex-ion, pain, and a palpable gap. Delayed diagnosis iscommon, and MRI can help to establish the diagnosis.The usual site for tendon rupture is 0.5 to 3 cmproximal to its bony insertion, where the tendon passesunder the inferior extensor retinaculum.33 Completediscontinuity and retraction of the proximal tendonsegment are seen on MRI as indicative of complete

anterior tibial tendon rupture (Fig 30).33 Treatment ofanterior tibial tendon rupture is surgical.

Ankle Impingement SyndromesAnkle impingement syndromes are painful entitiescaused by the friction of joint tissues, which is both thecause and the effect of altered joint biomechanics. Theleading causes of impingement lesions are posttrau-matic ankle injuries, usually ankle sprains, leading tochronic ankle pain.34,35

From the anatomical and clinical viewpoints, thesesyndromes are classified as anterolateral, anterior,anteromedial, posteromedial, and posterior.34 Carefulanalysis of patient history and features at physicalexamination can suggest a specific diagnosis in mostcases. MRI and magnetic resonance arthrography(MRA) are the most useful imaging methods fordetecting the osseous and soft-tissue abnormalitiespresent in these syndromes and to rule out otherpotential causes of chronic ankle pain.34

Anterolateral Impingement Syndrome (ALI)ALI is a syndrome produced by entrapment of

abnormal soft tissue in the anterolateral gutter of theankle.34-39 ALI is a relatively uncommon cause ofchronic lateral ankle pain and is frequently seen aftersingle or multiple ankle inversion injuries. It is esti-mated that 3% of ankle sprains may lead to ALI.34

ALI is thought to occur subsequent to relatively minor

FIG 30. Acute complete tear of the tibialis anterior tendon in an oldertennis player. Note the absence of left tendon with high signal fluid atthe tear site (arrow) and surrounding edema changes on axialT2-weighted images. The right tibialis anterior tendon (ta) has normalsize and intensity signal.


trauma involving forced ankle plantar flexion andsupination. The traumatic insult is usually sportsrelated and is found most frequently in soccer, basket-ball, and football players. Such trauma may result intearing of the anterolateral soft tissues and ligamentswithout substantial associated mechanical instability.Repeated microtrauma and soft-tissue hemorrhage canresult in synovial scarring, inflammation, and hyper-trophy in the anterolateral gutter of the ankle, withsubsequent soft-tissue impingement.34-39 Other con-tributing factors are thought to include hypertrophy ofthe inferior portion of the anterior inferior tibiofibular(AITF) ligament and osseous spurs. First described byBassett, a separate distal fascicle of the AITF ligamentis a common variant.20 It becomes pathologic when atear of the anterior talofibular ligament results inanterolateral joint laxity. With increasing joint laxity,the talus extrudes anteriorly in dorsiflexion and comesinto contact with the fascicle. Constant rubbing of thefascicle against the talus thickens the fascicle, whichthen develops into an impinging lesion in the antero-lateral gutter.40

The clinical diagnosis of ALI can be establishedbased on the combined presence of the following signsand symptoms: chronic ankle pain after an anklesprain, anterolateral ankle joint tenderness, recurrentjoint swelling, anterolateral pain with forced ankledorsiflexion and eversion, pain during the single-legsquat, and lack of lateral ankle stability.34-39 However,the clinical diagnosis of ALI is one of exclusion.Lesions producing similar symptoms have to be ex-cluded before invasive treatment is instituted, becausesimilar symptoms can be attributed to peroneal tendontears or subluxations, sinus tarsi syndrome, stressfractures, loose bodies, osteochondral lesions, bonyimpingement, and degenerative joint disease.34,38

When the diagnosis is straightforward, no supplemen-tary imaging examination is necessary. In complicatedcases, CT arthrography, MRI, and MRA have beenused to aid the diagnosis.34-39

The MR findings of an abnormal soft-tissue mass orfibrous band in the anterolateral ankle gutter, distinctfrom the anterior talofibular ligament, suggest thediagnosis of ALI.34-39 The mass has low signal onTI-weighted and low or intermediate signal no T2-weighted images. Care should be taken not to confusethe frayed margins of the torn ATF ligament with themeniscoid lesion.34-39

Controversies exist concerning the accuracy of theMRI in the diagnosis of ALI. Most authors believe that

the assessment of the anterolateral recess with conven-tional MRI is accurate only when a substantial jointeffusion is present.39 MRA has been proven to be anaccurate technique for assessing the presence of soft-tissue scarring in the anterolateral recess of the ankleand elucidating its extent in patients with ALI beforearthroscopy.38 Another MRA finding of ALI is theabsence of a recess of arthrographic fluid between theanterolateral soft tissues and the anterior surface of thefibula. This absence may be a result of the presenceof adhesions and scar tissue that prevent fluidentering the normal recess between the fibula andjoint capsule.38 Anterolateral scarring and/or syno-vitis at MRA can be noted in patients withoutclinical features consistent with those of ALI (Fig31). Nevertheless, the identification of abnormalsoft tissue itself does not imply the presence ofclinical ALI. Therefore, image confirmation of an-terolateral soft-tissue abnormalities must be consid-ered with the clinical findings.38

Most patients with ALI respond to conservativetherapy, including nonsteroidal anti-inflammatorydrugs, rehabilitative physiotherapy, or local injectionof steroids. If nonoperative treatment fails after 6months, significant relief has been shown to be pro-vided by arthroscopic debridement of hypertrophicsynovial tissue in the lateral gutter.34-39

Anterior Impingement SyndromeAnterior impingement is a relatively common cause

of chronic pain in the ankle, especially in athletessubjected to repeated stress in ankle dorsiflexion, thatis typical in soccer players.34 This condition involvesa beak-like prominence at the anterior rim of the thetibial plafond, usually associated with a correspondingarea over the apposed margin of talus proximal to thetalar neck, well within the anterior ankle joint capsule.These osteophytes can impinge on each other, espe-cially with ankle dorsiflexion, trapping soft tissues,and may actually limit motion.34,41 The cause andorigin of anterior impingement are uncertain and manyfactors are probably involved. It has been suggestedthat forced dorsiflexion results in repeated microtrau-mas on the tibia and talus, leading to microfractures oftrabecular bone or periosteal hemorrhage, which thenheal with the formation of new bone. Another mech-anism suggested in the etiology of these lesions isforced plantarflexion trauma, which causes capsularavulsion injury.34,41


Plain radiographs most often demonstrate ante-rior osteophytes, and lateral stress radiographs takenin maximum dorsiflexion may demonstrate physicalimpingement of the osteophytes. Scranton et aldeveloped a classification for anterior ankle osteo-phytes, categorizing ankle spurs on the basis of thesize of the spur and the presence of associatedarthritis.41

MRI is useful in assessing the degree of cartilagedamage and in detecting bone marrow edema and syno-vitis in the anterior capsular recess (Fig 32).34 Conser-vative treatment consisting of heel lifts, rest, modificationof activities, and physical therapy may be tried first. Ifthere is persistent pain despite conservative treatmentarthroscopic or open resection of the spurs may beconsidered.42

FIG 31. Anterolateral impingement. A, Axial T1-weighted spin-echoMRA shows focal nodular soft tissue thickening in the anterolateralgutter (arrow). B, Arthroscopic image demonstrates a thickened bandof scarring and synovitis in the anterolateral gutter (meniscoid lesion)(asterisk).

FIG 32. Anterior impingement. A, Sagittal T1-weighted spin-echo MRIshows anterior osteophytes in the tibia and talus (arrows). B, Sagittalfat-suppressed T1-weighted MRI after intravenous administration ofgadolinium reveals bone marrow edema in the talar osteophyte(arrow) and synovial enhancement (asterisk).


Anteromedial Impingement SyndromeAnteromedial impingement is a very uncommon

cause of chronic ankle pain. It can be caused by ameniscoid lesion, represented by a mass of hyalinizedconnective tissue arising from a partially torn deepdeltoid ligament or by a thickened anterior tibiotalarligament.34,43-45 This thickened ligament or a menis-coid lesion, along with hypertrophic synovium, im-pinges on the anteromedial corner of the talus duringdorsiflexion of the ankle. Anteromedial impingementis rarely an isolated condition but is most commonlyassociated with an inversion mechanism of injury withlateral as well as medial ligamentous injury.34,45

Conventional MRI has not yet been proven usefulin detecting the medial impingement syndromes. MRIcan depict a partially torn deep deltoid ligament but isinsensitive for other findings. MRA is the imagingmethod of choice, clearly defining the medial menis-coid lesion, the thickened anterior tibiotalar ligament,and chondral- or osteochondral-associated lesions.45 Ifconservative treatment fails, debridement of the im-pinging lesion by arthroscopic methods yields goodclinical results.

Posteromedial Impingement SyndromePosteromedial impingement is a very uncommon

etiology of posteromedial ankle pain occurring after asevere ankle-inversion injury in which the deep pos-terior fibers of the medial deltoid ligament becomecrushed between the medial wall of the talus and themedial malleolus.46 Initially, posteromedial symptomsdo not predominate, compared with the symptoms ofthe lateral ligament disruption, and they usually re-solve without specific treatment. However, inadequatehealing of the contused deep posterior deltoid ligamentfibers may lead to chronic inflammation and hypertro-phic fibrosis and metaplasia. In such cases, this disor-ganized fibrotic scar tissue may impinge between themedial wall of the talus and the posterior margin of themedial malleolus.46

MRI has been found to demonstrate the lesion,showing the thickened soft tissues and evidence ofsubchondral bruising of both the medial talus andmedial malleolus. However, MRA is more sensitiveand accurate than conventional MRI in the evaluationof this entity.46

This posteromedial lesion usually resolves sponta-neously or with nonoperative treatment. This lesioncannot generally be fully appreciated arthroscopically

via anterior portals in a stable ankle and requires ahigh index of suspicion and careful examination forthe diagnosis to be made clinically. Arthroscopicsurgery, via posterior portal, or limited open surgicalexcision of the lesion is successful in resolving thepain.46

Posterior Ankle Impingement (PAI)Syndrome

PAI syndrome refers to a group of pathologicentities that result from repetitive or acute forcedplantar flexion of the foot.47-49 Different names havebeen given to PAI syndrome, including os trigonumsyndrome, talar compression syndrome, and posteriorblock of the ankle.47-49 The mechanisms of injuryhave been likened to a nut in a nutcracker because theposterior talus and surrounding soft tissues are com-pressed between the tibia and the calcaneus duringplantar flexion of the foot. This syndrome has beenextensively described in classical ballet dancers, but italso has been recognized in individuals who are activein sports, including soccer, basketball, running, andvolleyball.47 The anatomy of the posterior aspect ofthe ankle is a key factor in the occurrence of PAIsyndrome. The more common causes are osseous innature, such as the os trigonum (an accessory ossicleof the lateral tubercle that may persist unfused intoadulthood in 7% of individuals), an elongated lateraltubercle termed a Stieda process, a downward slopingposterior lip of the tibia, the prominent posteriorprocess of the calcaneus, and loose bodies.47-49 Softtissue causes of impingement encompass synovitis ofthe flexor hallucis longus tendon sheath, the posteriorsynovial recess of the subtalar and tibiotalar joints, andthe posterior intermalleolar ligament (IML).47-50 PAIsyndrome may manifest as an inflammation of theposterior ankle soft tissues, as an osseous injury, or asa combination of both. The osseous injuries includefracture, fragmentation, and pseudoarthrosis of the ostrigonum or lateral talar tubercle. As such, posteriorankle and subtalar synovitis as well as FHL tenosyn-ovitis are soft-tissue changes associated with PAIsyndrome.47 The diagnosis of PAI syndrome is basedprimarily on the patient’s clinical history and physicalexamination results and is supported by findings atradiography, scintigraphy, CT, and MRI.47

MRI is useful in establishing the diagnosis of PAIsyndrome, showing abnormal signal intensity in thelateral talar tubercle and/or os trigonum, consistentwith bone marrow edema that is believed to be the


result of bone impaction, and thus represents bonecontusions or occult fractures (Fig 33).47,49

MRI also depicts inflammatory changes in theposterior ankle soft tissues (the posterior synovialrecess of the subtalar and tibiotalar joints and the FHLtendon sheath). The combined presence of marrowedema and posterior ankle synovitis may suggest thediagnosis of PAI.47 Diagnosis of an abnormal IML onMRI requires a thickened IML, which can readily beseparated from the surrounding posterior talofibularligament and the transverse inferior tibiofibular liga-ment.50,51 It is equally important that MRI can specif-ically identify the wide range of pathology that maycontribute to posterior ankle pain that might be clini-cally confused with PAI, including Achilles tendon-itis/tear, retrocalcaneal bursitis, FHL tenosynovitis,

Haglund’s deformity, ankle or subtalar arthritis, osteo-chondral lesion, tarsal tunnel syndrome, post-trau-matic instability, sprain, or peroneal tendon subluxa-tion.47 The treatment of PAI syndrome is initiallyconservative. If conservative treatment fails, then sur-gical excision of the osseous fragments, with potentialrelease of the FHL tendon, may be indicated.7

Plantar Fascial InjuriesThe plantar fascia has been defined as the investingfibrous layer of the foot’s plantar aspect, locatedsubcutaneously and originating from the calcaneus toinsert into the deep sof tissues of the forefoot, theproximal phalages and the skin via superficial exten-sion.

The plantar fascia comprises three variably devel-oped components: central, lateral, and medial cords.52

The term plantar fascia usually refers to the largecentral component. It originates from the medial cal-caneal tuberosity and extends anteriorly, adhering tothe underlying flexor digitorum brevis muscle. Atabout the midsole, it splits into five bands, one for eachtoe, that insert on the proximal phalanges. The lateraland medial components of the plantar fascia actmainly as covering layers peripheral to the centralcomponent. The lateral component serves as the fas-cial covering of the abductor digiti minimi. It arisesfrom the lateral margin of the medial calcaneal tuber-osity and extends to the cuboid and base of the fifthmetatarsal bone. The medial component is very thinand forms the investing fascia of the abductor hallucismuscle. The plantar fascia acts as a strong mechanicaltie for the longitudinal arches by joining the three mainweight-bearing points of the foot: the calcaneus, thefirst metatarsal head (including the two sesamoids),and the fifth metatarsal head.52

On MRI, the normal fascia appears as a thin bandwith low-signal intensity with all pulse sequences; thethickness of the plantar fascia in normal individualsranges between 2 to 4 mm.4,14,53-55 The plantar fasciais best examined by MRI in both sagittal and coronalplanes.4,55 The coronal plane represents the true axialplane perpendicular to the plantar fascia. It allowssimultaneous visualization of the three components ofthe plantar fascia and is optimal to assess the size,shape, and internal signal characteristics of thesestructures. The medial component appears as either asemilunar or fusiform-shaped sharply delineated band.Sagittal imaging allows optimal evaluation of the

FIG 33. Posterior impingement. A, Sagittal fat-suppressed protondensity image demonstrates abnormal high-signal intensity in theposterior aspect of the talus and in the os trigonum (arrow). Jointeffusion in the posterior synovial recess of the tibiotalar and subtalarjoints is noted (asterisk). B, Arthroscopic image showing the ostrigonum and a normal flexor hallucis longus tendon.


plantar fascia along its length. On sagittal images, thenormal fascia has a uniform thickness from its calca-neal origin through its proximal half, whereas moredistally, progressively thins until it reaches its meta-tarsal insertions.4,55

Plantar FasciitisPlantar fasciitis is a common overuse injury found

in athletes engaged in sports that require running orjumping.3 Plantar fasciitis accounts for 7% to 9% ofall running injuries. Repetitive microtrauma leads tomicrotears in the plantar fascia near its attachment atthe inferior aspect of the calcaneus, and elicit a localinflammatory reaction.56,57 In cases of persistent over-use there will appear chronic changes with collagennecrosis, angiofibroblastic hyperplasia, and matrix cal-cification. Commonly cited predisposing factors ofplantar fasciitis are excessive pronation, a flat or cavusfoot, and a tight Achilles tendon. The type of trainingshoes worn and errors in training routines are predis-posing factors in runners.

Pain on the undersurface of the heel on weightbearing is the principal complaint. The pain is oftenworse when weight is borne after a period of rest (eg,in the morning) and eases with walking. Localizedtenderness without swelling is present over the antero-medial portion of the plantar surface of the calcaneus.Passive dorsiflexion of the toes often exacerbates thediscomfort. Plantar fasciitis is essentially a clinicaldiagnosis. Radiological evaluation is reserved for am-biguous or clinically equivocal cases or for cases thatare refractory to treatment. Radiographs, ultrasonog-raphy, and MRI have been used in the evaluation ofplantar fascia injuries. Radiographs are mainly usefulin evaluation of osseous structures to exclude unrec-ognized traumatic injuries. Also, radiographs mayreveal a plantar calcaneal spur, although this entitymay also be observed in asymptomatic adults.56,57 Theetiologic significance of this spur remains controver-sial, but most authors believe that it is not the primarycause of pain.3,56,57

Both ultrasonography and MRI have been recog-nized as useful tools in the assessment of the plantarfascia.4,5,14,53-55,58,59 MRI has an advantage over ul-trasound imaging in that it allows an effective assess-ment of both soft-tissue and osseous structures. OnMRI, plantar fasciitis is characterized by perifascialedema, fascial thickening, and increased signal inten-sity. Perifascial edema involves the adjacent fat padand underlying soft tissues and has been described as

the most common MR finding in patients with plantarfasciitis (Fig 34).55,58

Fascial thickening is often fusiform and typicallyinvolves the proximal portion and extends to thecalcaneal insertion. Increased signal intensity of theplantar fascia reflects edematous and inflammatorychanges as well as intrasubstance microtears. STIRsequences are often the most sensitive in the detectionof both fascial and perifascial edema, which appear aspoorly marginated areas of high-signal intensity (Fig34).4 Limited marrow edema changes within the me-dial calcaneal tuberosity are a less common MRIfinding.4,54,55 Successful outcome of plantar fasciitisis directly related to early diagnosis and treatment.56

Therefore, in equivocal cases, especially in elite ath-letes, MRI can allow an early diagnosis of plantarfasciitis, and thus, improve the prognosis in thesepatients.

Treatment is conservative. Surgical treatment ofplantar fasciitis is reserved to cases in which conser-vative treatment fails, especially in athletes engaged inhigh-level competition.3,56,57

Plantar Fascial RuptureRupture of the plantar fascia is typically a sports-

related injury. It occurs in athletes engaged in sportsthat require running and jumping, such as distancerunning, basketball, football, and tennis.60-62 Mostplantar fascial tears in athletes are acute.61,62 How-ever, it can also be associated with local steroidinjection in patients with plantar fasciitis.63 Suddenplantar heel pain typically indicates a traumatic tear.The individual usually hears a clicking or snappingsound when the traumatic event occurs,60 and apalpable, tender mass is detected at the site of injury.Clinical manifestations in patients with tears related tocorticosteroid injection are more insidious.63 Mostcases involve the proximal portion of the plantar fascianear its calcaneal insertion, although more anteriortears have also been described.5,14,52 In a previousstudy, half of cases presented as ruptures located in themiddle plantar fascia.55

MRI is advocated as the modality of choice toconfirm the diagnosis and to plan the treatment strat-egy in both clinical and radiological series.4,55,58,60,62

MRI findings of tears of the plantar fascia are similarto those seen in tendinous ruptures. Acute tears of theplantar fascia are characterized by partial or completeinterruption of the normally low-signal intensity fasciaby large areas of prominent increased signal-intensity


on T2-weighted and STIR images, presumably repre-senting edema and hemorrhage (Figs 35 and36).4,5,14,60 Perifascial fluid accumulations are com-monly seen on T2-weighted and STIR images (Fig36).4,55 In addition, acute tears of the plantar fascia

commonly involve the underlying flexor digitorumbrevis muscle.14 Acute and subacute muscle tears arecharacterized by high-signal intensity with a featheryappearance on both T1- and T2-weighted imagesrepresenting muscle bleeding and edema (Fig 36).Less commonly, strains of other plantar muscles, suchas abductor hallucis or quadratus plantae, are associ-ated with plantar fascia rupture.14 Chronic tears of theplantar fascia are characterized by focal fascial thick-ening and intrafascial scar tissue, which show low-signal intensity on all pulse sequences.55 Perifascialedema is usually absent in these chronic tears.55

Conservative treatment consisting of rest, arch sup-ports and orthotics, and physical therapy is sufficientin most cases.60,63

FIG 34. Plantar fasciitis. A, Sagittal T1-weighted MR shows markedthickening of the proximal plantar fascia (black arrow) with increasedintrasubstance signal intensity (white arrow). Note also the perifascialedema, which has low signal intensity in A and high-signal intensity inB (arrowheads). B, Sagittal STIR MRI better demonstrates fascialthickening (arrows), intrasubstance increased signal as well as peri-fascial edema (arrowheads). Note also calcaneal bone marrowedema (small arrowhead).

FIG 35. Partial plantar fascia rupture. A, Coronal proton-density-weighted MRI shows thickening of the central component of the leftplantar fascia with abnormal intermediate signal intensity (arrow-head). B, Sagittal proton-density-weighted MRI demostrates the fascialrupture at distance of the calcaneal insertion (arrows). Note fusiformfascial thickening and loss of its low-signal intensity.


Surgical treatment, including plantar fasciotomyand excision of scar tissue, is advocated in youngactive athletes.62

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