MRI of the ankle.
Subject: Magnetic resonance imaging
Authors: Ali, Muhammad
Chen, Tim S.
Crues, John V., III
Pub Date: 08/01/2006
Publication: Name: Applied Radiology Publisher: Anderson Publishing Ltd. Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2006 Anderson Publishing Ltd. ISSN: 0160-9963
Issue: Date: August, 2006 Source Volume: 35 Source Issue: 8
Accession Number: 209239187
Full Text: Magnetic resonance imaging (MRI) is the modality of choice for the evaluation of joints, soft tissues, and most bone pathology. In addition to the commonly imaged knee and shoulder joints, MRI is increasingly being used for the evaluation of more peripheral joints such as the ankle, foot, wrist, and hand. This article will discuss clinically relevant issues in performing and interpreting MRI of the ankle. (A second article, which will be published at a later date, will address the issues related to performing and interpreting MRI of the foot.) The authors present technical aspects such as patient positioning, protocols for high and low field-strength extremity scanners, and artifacts that commonly occur in this region. Pathologic findings are described for the medial, lateral, anterior, and posterior regions of the ankle.

Technique High field-strength scanner

Positioning--The ankle is imaged in a neutral position. Plantar flexion of 20[degrees] to 30[degrees] has been advocated for reducing the "magic angle" artifact.

Protocol--All MRI sequences for the ankle are fast spin-echo (FSE) acquisitions unless specified otherwise, using a 12-cm field of view (FOV). Axial plane: By international anatomic convention, the axial plane is in cross section to the long axis of the tibia but is acquired along the long axis of the metatarsals. Short (T1-weighted or proton-density-weighted) and long echo time (TE) (T2-weighted) sequences for the evaluation of tendons and ligaments are acquired. T2-weighted images are particularly useful for detection of soft tissue edema or fluid and to increase specificity of abnormalities seen on the short TE sequences.

Sagittal plane: Short tau inversion recovery (STIR) images are very sensitive to marrow edema and plantar fasciitis. We do not recommend spectral fat suppression on most scanners, as failure of fat suppression is a common cause of interpretive error. Additional sagittal T1-weighted images are acquired to evaluate the sinus tarsi fat and also to get a "second look" at bone marrow signal.

Coronal plane: We also acquire coronal T1-weighted images, although many radiologists prefer coronal proton-density-weighted images with fat saturation for better evaluation of ankle mortise cartilage. Ligaments and tendons are well evaluated on the short TE sequences. The proton-density-weighted fat-saturated images are also sensitive to marrow pathology. The protocols can be tailored to personal preference; however, it is important to include a T2-weighted sequence without fat saturation, a STIR sequence in at least one plane (preferably the sagittal plane), a short TE sequence in the axial plane, and a T1-weighted sequence to evaluate the marrow.

Low field-strength extremity scanners

Positioning--Due to the smaller bore of the extremity magnets, the ankle is imaged in 20[degrees] to 30[degrees] of plantar flexion. Protocol--The protocol is the same as that of the high-field scanners. Spectral fat saturation cannot be performed on low-field scanners, and STIR is the preferred fluid-sensitive sequence for the evaluation of marrow. It is also essential to keep the FOV <14 cm for adequate spatial resolution.

Lateral pathology Peroneal tendons

Normal tendons are low in signal on all pulse sequences. The peroneus brevis tendon (PBT) is the most commonly torn lateral tendon,1 and split longitudinal tears are the most common type of tear. The tendon splits or acquires a "C"-shaped morphology at the level of the lateral malleolus, with the peroneus longus tendon (PLT) insinuating in the concavity of the "C" or between the 2 split components. The 2 splits usually rejoin before inserting at the base of the 5th metacarpal. Complete and partial tears of the PBT are less common (Figure 1). (2)

The peroneus longus tendon is prone to tear at 3 locations. (3,4) First, tears occur at the sharp angulation on the inferior aspect of the lateral malleolus because of the pulley action and friction. Secondly, tears occur at the peroneal tubercle (Figure 2). The tubercle acts as a second pulley for the tendon, and irregularity or hypertrophy of the tubercle can lead to PLT tears. The cuboidal tunnel is the third most common site for tears. Tears of the PLT may also be associated with PBT tears at the level of the lateral malleolus (Figure 3).

Other anatomical abnormalities that can predispose a patient to peroneal tendon tears include an abnormal superior peroneal retinaculum attachment (which can lead to recurrent subluxation or dislocation), a mass causing compression along the course of the tendons, and anomalous muscles (such as a peroneus quartus). (5) In partial tears, the tendons may be thickened with or without evidence of torn fibers. In complete tears, there is tendon retraction and discontinuity. Fluid in the tendon sheath without abnormal tendon morphology is consistent with tenosynovitis.







Ligaments are seen as smooth, low-signal broad bands or thin strands on all MRI pulse sequences. Some ligaments have a striated appearance with alternating low- and intermediate-signal strands. Trauma is the main etiology for ligament disruption in the ankle. The anterior talofibular ligament (ATFL), which extends between the anteroinferior aspect of the lateral malleolus (where the malleolus has a comma shape on axial sections) and the anterolateral talus, is the most commonly torn ankle ligament. (6) The sequence of lateral ankle ligament disruption is (in order) the ATFL, calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL). (7) It should be noted that the normal PTFL has a striated appearance (Figure 4).

Tears can be partial or complete and can be acute or chronic. In partial tears some intact fibers are seen, whereas in complete tears discontinuity of waviness of the ligament fibers is identified. In acute tears, there is edema and fluid in the region (Figure 4). In chronic tears, the ligament can have a thickened appearance due to scar tissue or a globular mass-like morphology from fibrous tissue formation (Figure 5). Chronic tears can also appear as an absence of the ligament without any appreciable scarring.

Associated fractures of the fibula should be specifically sought because they can be easily overlooked. It is also important to evaluate the integrity of the anterior inferior tibiofibular (ATF) and the posterior inferior tibiofibular (PTF) ligaments. Tears of these ligaments (Figure 6) are seen with high ankle sprains. (8-10) The presence of scar tissue along the anterolateral aspect of the ankle can cause impingement and chronic pain (anterolateral impingement). It can also be associated with lateral talar chondromalacia. (11,12) Absence of a joint effusion can make the visualization of scar tissue difficult. Arthrographic MR examination lends the greatest accuracy in making this diagnosis. Absence of a fluid-filled recess between the anterolateral fibula and the soft tissues is an ancillary finding in anterolateral soft tissue impingement. (13) Other masses, such as ganglion cysts and lipoma, can also cause anterolateral impingement syndrome.



Medial pathology


Among the medial tendons, the tibialis posterior (TP) tendon is the most commonly injured tendon. (14) Tears of the TP tendon are most prevalent in middle-aged and older women.14 Pathology includes tendinosis, partial or complete tears, and tenosynovitis. Tendinosis can manifest as increased signal and thickening of the tendon. Type I tears include split longitudinal tears or fusiform thickening of the TP tendon (Figure 7). A type II tear is a focal thinning of the tendon to less than the diameter of the adjacent normal flexor digitorum longus (FDL) or flexor hallucis longus (FHL) tendons. The normal TP tendon is roughly twice the diameter of the FDL or FHL tendons. Type III, or complete tears, manifest as disruption in the tendon continuity, with or without retraction (Figure 8). The tendon gap may be filled with fluid in acute cases, granulation tissue in subacute cases, and scar tissue in chronic cases (Figure 8). Presence of an os naviculare, which is an accessory ossicle at the base of the tarsal navicular, has been implicated as one of the predisposing factors for TP tendon tears (Figure 8).(15) Other anatomical risk factors include an enlarged or irregular medial navicular tubercle and the compression of the TP tendon in the tarsal tunnel. Tears of the TP tendon may result in the loss of the medial arch of the foot and, thus, can lead to a flatfoot deformity. (16)

A small amount of fluid is physiologic in the TP tendon sheath. However, fluid that completely surrounds the tendon or larger amounts of fluid in the tendon sheath are considered to be abnormal and are indicative of tenosynovitis (Figure 9).

The FDL and FHL tendons are rarely torn. They are more commonly affected by tenosynovitis (Figure 10). (17) Pathology of the FHL is seen commonly in patients whose activities require recurrent and extreme plantar flexion, such as ballet dancers or gymnasts. (18) The FHL tendon sheath can communicate with the subtalar joint in up to 15% of cases. Fluid in the tendon sheath in the absence of subtalar effusion or a disproportionately smaller volume of fluid in the subtalar joint is indicative of FHL tenosynovitis. (19) Stenosing tenosynovitis (tenosynovitis with compartmentalization of fluid due to adhesions and fibrosis) of the FHL can occur between the medial and lateral talar tubercles, in the tarsal tunnel, or at the "Henry knot" (the crossover of the FDL and the FHL tendons in the proximal plantar course underneath the base of the first metatarsal). More distally, it can occur between the hallux sesamoids. (19-21) Stenosing tenosynovitis can also be associated with an os trigonum. (22,23) Tears of the FHL and FDL tendons are rare and have the same pathology as tendons elsewhere.







The deltoid ligament (deep portion of the complex) is very strong, and a significant force is required to disrupt it. (24,25) Deltoid tears are associated with eversion injuries and with the later stages of other mechanisms of ankle fractures. In acute tears, there is edema and disruption in the ligament fibers (Figure 11). In chronic injuries, disorganized fibrous or scar tissue is seen in the region. Injuries to the tibiocalcaneal, tibionavicular, and superficial tibiotalar ligaments are rare. More commonly, a thickened ligament secondary to a chronic partial tear and scarring is seen. Tears of the spring ligament (plantar calcaneonavicular ligament) can lead to a flatfoot deformity and inferior subluxation of the talar head. (26) Focal capsular thickening and fibrous or scar tissue in the region of the tibiocalcaneal ligament and deep to the TP tendon can lead to anteromedial impingement and pain (Figure 12). (27,28) Posteromedial soft tissue impingement can occur with tears of the deep deltoid ligament. This leads to chronic instability, secondary thickening of the capsule, and proliferation of synovium. (29)

Neurovascular The posterior tibial nerve (between the FDL and FHL tendons) may become entrapped in the tarsal tunnel. Etiologies include soft tissue masses, such as ganglion cysts, tendon pathology with thickening and mass effect, thickening of the flexor retinaculum, or, less commonly, osseous abnormalities (Figure 13). Sensory symptoms are in the plantar aspect of the mid- and forefoot in the distribution of medial and lateral plantar nerves. (30)

Anterior pathology Tendons

Injuries to anterior tendons are quite rare, direct trauma being the most common etiology. Underlying diseases, such as collagen vascular disease or rheumatoid arthritis, can predispose a patient to tendon tears. Tears can be complete or partial. A complete tear of the tibialis anterior (TA) can lead to significant loss of foot dorsiflexion (Figure 14). Tenosynovitis is more common than tears in the anterior tendons, including the extensor digitorum longus (EDL) (Figure 15) and the extensor hallucis longus (EHL) tendons.

Anterior retinacular injuries are also a rare occurrence. Associated tendon subluxation or dislocation may be seen. Anterior impingement may be secondary to anterior tibiotalar spurs and synovial thickening. It can present as pain and limitation of dorsiflexion. Synovial thickening is low in signal on T1-weighted images and is of intermediate signal on T2 weighted images. Associated scar that is low on T1- and T2-weighted images may be seen. The clinical presentation includes pain and limitation of dorsiflexion. (31,32)





The deep peroneal nerve can become compressed in the fibro-osseous tunnel underneath the inferior extensor retinaculum. Here the EHL crosses over the nerve and predisposes a patient to nerve compression. Recurrent trauma in soccer players can lead to direct nerve damage or nerve compression from tendon pathology, such as tenosynovitis. Pain is on the dorsomedial aspect of the foot.

Weakness of the extensor digitorum brevis can occur from motor branch compression. On fluid-weighted sequences, increased signal in this muscle can be an indirect sign of neuritis. (33)

Posterior pathology Tendons

Achilles tendon injury is common in basketball players or in players of other sports that involve extreme and recurrent plantar flexion. Achilles tendon pathology is divided into insertional and noninsertional categories. The Achilles tendon, like the triceps tendon, does not have a tendon sheath and is surrounded by fibrofatty tissue called the peritenon. Tendinosis can occur at the insertional site and presents as increased signal, thickening of the tendon, and focal pain at the insertion site. It can be associated with the Haglund deformity, which is an irregularity and humplike morphology of the posterior superior calcaneus (Figure 16). Other associated findings include retrocalcaneal or tendo-Achilles bursitis and edema in the Kager's fat pad, ie, peritenonitis. The Haglund deformity is more common in women who wear high heels or ill-fitting shoes. (34,35)




Insertional tears present with signal abnormalities in the distal-most aspect of the tendon at the posterior calcaneus. Therefore, they may not be associated with edema in the Kager's fat (Figure 17). Noninsertional Achilles tendon abnormalities have been classified by Weinstabi et al. (36) Type I tears represent inflammatory reactions or peritenonitis; type II, degenerative changes; type III, partial ruptures; and type IV, complete ruptures. Increased signal with a convexity of the anterior margin of the tendon is consistent with tendinosis. Differentiating partial tears from chronic tendinosis or degenerative changes with severe thickening of the tendon is sometimes difficult to determine by imaging findings, and clinical history is more useful. The presence of hemorrhage and edema in the Kager's fat is more suggestive of an acute partial tear than of chronic tendinosis (Figure 18). Partial disruption of the Achilles tendon fibers and longitudinal split morphology can also be seen in cases of partial tears, making the diagnosis easier. In complete tears, there is discontinuity of the tendon with or without retraction. The usual site is the relatively avascular zone, approximately 2 to 6 cm above the calcaneal insertion. The gap is usually filled with fluid and hemorrhage (Figure 19).



MRI is useful in differentiating complete from partial tears and in preoperative evaluation of the tendon gap. In most patients, complete tears are treated conservatively. In younger patients and athletes with a >1-cm gap, a surgical approach may be taken. Postoperatively, MRI can be useful in the evaluation of re-tears and the degree of tendon union. High signal and biconvex morphology that mimics a chronic partial tear or tendinosis may persist indefinitely. (35)

Peritenonitis is seen as edema and fluid in Kager's fat without associated tendon abnormalities.


Tears of the posterior inferior tibiofibular ligament are rare. Significant force is required to tear this strong ligament. Pronation-dorsiflexion injuries are the usual mechanism of this injury. (37) Posterior tibiotalar impingement syndrome (PTTIS) can occur in the presence of an os trigonum (Figure 20), a prominent stieda process, or hypertrophy of the transverse ligament (the inferior portion of the PTFL). Posterior tibiotalar impingement syndrome is seen more commonly in ballet dancers or in those whose activities involve recurrent plantar flexion of the foot. (38-40)


The sural nerve runs lateral to the Achilles tendon and then inferior to the peroneal tendon sheath and continues in its plantar course laterally to divide into medial and lateral branches at the level of the 5th metatarsal base. It can be damaged in displaced fractures of the fibula, during ankle surgery with posterolateral approach and more distally with 5th metatarsal base or cuboid fractures.41,42 Sural neuropathy presents as pain and paresthesia along the lateral border of the ankle and foot.


MRI can provide a comprehensive evaluation of the ankle, including soft tissue and bone pathology. The soft tissue contrast resolution of MRI is superior to that of CT, and MRI is as good as or better than CT for most bone pathology. MRI is more sensitive than CT in the detection of trabecular bone injury and stress fractures. CT is still the preferred imaging modality to evaluate the complex calcaneal fractures for surgical planning. CT also offers better detection of small bony avulsion fragments or cortical bone evaluation. Evaluating the thin cartilage of the ankle mortise for early cartilage loss is still a challenge, and more work needs to be done to overcome this limitation.

Osseous pathology involving the ankle will be reviewed in a future article on MRI of the foot.


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Dr. Ali and Dr. Chen are MRI Fellows, Radnet Management, Inc., Los Angeles, CA; Dr. Crues is the Fellowship and Medical Director, Radnet Management, Inc., and a Volunteer Clinical Professor, University of California, San Diego School of Medicine, San Diego, CA.

Muhammad Ali, MBBS; Tim S. Chen, MD; John V. Crues, III, MD
Gale Copyright: Copyright 2006 Gale, Cengage Learning. All rights reserved.