The Ankle and Foot

By admin Last updated Jun 20, 2023

5 – The Ankle and Foot

Chapter 5

The Ankle and Foot

David W. Stoller

Richard D. Ferkel

Standard radiographic evaluation of the ankle joint requires anteroposterior, lateral, and mortise radiographs. In patients with foot trauma, an additional oblique view may be obtained. Less frequently, arthrography and tomography may be used, primarily in the evaluation of ligamentous tears and articular cartilage defects. In tarsal coalitions and sustentacular trauma, computed tomography (CT) scans have been used to delineate talocalcaneal, transverse tarsal, and tibiotalar joint anatomy.¹ CT is limited, however, to the specific plane of section (i.e., axial or angled coronal) and is dependent on reformatted images for visualization in the other orthogonal planes. Magnetic resonance (MR) imaging of the ankle and foot provides high tissue contrast and excellent spatial resolution, affording superior depiction of complex soft-tissue anatomy (e.g., muscles, ligaments, tendons, and fibrous coalitions).²–¹¹ In addition, marrow and cortical bone definition permit increased sensitivity in the detection of fractures, cysts, inflammatory and infectious conditions, and trauma.¹² The unique ability of MR imaging to directly display hyaline articular cartilage has made it valuable in assessing arthritis and osteochondral lesions, and in identifying intra-articular loose bodies.

Imaging Protocols for the Ankle and Foot

High-resolution anatomic images of the ankle and foot are obtained with a dedicated extremity surface coil (quadrature

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or phased-array design), using a 12- to 14-cm field of view (FOV) and a 512 × 256 or 256 × 256 acquisition matrix. Routine protocols for evaluation include:

T1- or proton density (PD)-weighted axial, sagittal, and coronal images
Fat-suppressed PD-weighted fast spin-echo sequences (FS PD FSE) in all three orthogonal planes (Fig. 5.1)
Thin (i.e., 2 to 3 mm) sections

FIGURE 5.1 ● Visualization of tibiotalar articular surfaces using a coronal FS PD FSE sequence. Separation of the tibial and talar chondral surfaces is important in characterizing osteochondral lesions.

Effective T2*-weighted contrast can be generated with gradient-echo (GRE) techniques using a partial flip angle of less than 90° (20° to 30°) and is used when FS is suboptimal or in the evaluation of the neuropathic foot.

To image the forefoot, the patient is placed in a prone position to orient the long axis of the foot with the orthogonal axial imaging plane or with the oblique image prescriptions parallel with the long axis of the metatarsals and cuneiform bones. Surface coils, which allow proper placement of the foot with the patient in the supine position, can also be used to evaluate the long axis of the forefoot without drop-off of signal intensity. STIR and fast STIR sequences are useful in identifying forefoot lesions in the coronal plane and stress fractures in the sagittal plane when FS PD FSE images are inhomogeneous with respect to fat suppression.

By placing both legs within the circular extremity or torso coil, comparison with the contralateral ankle and foot can be achieved. Alternatively, when smaller FOVs are needed, the extremities can be imaged one at a time by repositioning the surface coil. The foot is usually placed in a neutral position, although partial plantarflexion may be useful when comparing MR images to a CT ankle examination that was performed in 45° of tibiotalar angulation. A combination foot and ankle/knee coil provides adequate anatomic coverage for imaging the toes and distal metatarsals. Thin (3 mm or less) coronal T1-weighted and STIR images are most useful.

Intravenous contrast, in association with FS sequences, is useful for the evaluation of Morton's neuroma, inflammatory synovial processes, and certain tendon conditions (partial tears, the healing process, and infiltrative disorders). Intravenous and intra-articular contrast (MR arthrography) has been used on a limited basis in the study of osteochondral lesions and other intra-articular pathology. Articular cartilage is evaluated using a variety of techniques, including FD PD FSE, FSE STIR, and MR arthrography. FS PD FSE and STIR contrast are the more frequently used sequences in characterizing muscle injuries.

Related Muscles

The anterior muscles of the leg are the tibialis anterior (Fig. 5.2), the extensor hallucis longus (Fig. 5.3), the extensor digitorum longus (Fig. 5.4) and the peroneus tertius (Fig. 5.5).
The posterior muscles of the leg include a superficial group and deep group. The superficial group is represented by the gastrocnemius (Fig. 5.6), the soleus (Fig. 5.7), and plantaris (Fig. 5.8).
The deep group of posterior leg muscles comprises the popliteus (see discussion in Chapter 4 on the knee), the flexor hallucis longus (Fig. 5.9), the flexor digitorum longus (Fig. 5.10), and the tibialis posterior (Fig. 5.11).

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The lateral muscles of the leg are the peroneus longus (Fig. 5.12) and the peroneus brevis (Fig. 5.13).
The muscles of the foot are the extensor digitorum brevis (Fig. 5.14), the abductor hallucis (Fig. 5.15), the flexor digitorum brevis (Fig. 5.16), the abductor digiti minimi (Fig. 5.17), the quadratus plantae (Fig. 5.18), the lumbricals (Fig. 5.19), the flexor hallucis brevis (Fig. 5.20), the adductor hallucis (Fig. 5.21), the flexor digiti minimi brevis (Fig. 5.22), the dorsal interossei (Fig. 5.23), and the plantar interossei muscles (Fig. 5.24).

FIGURE 5.2 ● TIBIALIS ANTERIOR The tibialis anterior muscle functions eccentrically after the heel strike to control deceleration of the foot and concentrically after the toe-off in ankle dorsiflexion. In runners and hikers, paratenonitis is associated with the use of excessive eccentric contraction during midfoot and forefoot impact on downhill slopes. Paratenonitis is also associated with direct mechanical irritation from ski boots or hockey skates. The tibialis anterior dorsiflexes and inverts the foot.

FIGURE 5.3 ● EXTENSOR HALLUCIS LONGUS Extensor hallucis (and extensor digitorum) injuries are similar in origin to injuries of the tibialis anterior tendon. Extensor hallucis longus (EHL) paratenonitis is associated with pain and swelling localized to the ankle joint with painful resisted extension of the hallux. The EHL extends the great toe and dorsiflexes the foot.

FIGURE 5.4 ● EXTENSOR DIGITORUM LONGUS Extensor digitorum longus (EDL) paratenonitis is associated with pain and swelling over the ankle joint and lateral to the extensor hallucis longus. There is pain with resisted extension of the lesser toes in paratenonitis. The EDL extends the phalanges of the lateral four toes and dorsiflexes the foot.

FIGURE 5.5 ● PERONEUS TERTIUS The peroneus tertius represents a lateral slip of the extensor digitorum longus. Isolated ruptures of the peroneus tertius tendons do not occur. The peroneus tertius dorsiflexes and everts the foot.

FIGURE 5.6 ● GASTROCNEMIUS The gastrocnemius plantarflexes the foot and also flexes the knee joint, as its origin is on the femoral condyles. In contrast to the soleus muscle (which has a more postural function), the gastrocnemius generates the power for propulsion in walking, running, and jumping.

FIGURE 5.7 ● SOLEUS The gastrocnemius and the soleus muscles function in plantarflexion of the foot. The soleus consists primarily of type I or slow-twitch oxidative fibers and rapidly develops disuse atrophy in response to immobilization.

FIGURE 5.8 ● PLANTARIS The plantaris plantar flexes the foot and is visualized as a 2- to 3-mm hypointense dot-like structure on axial images anteromedial to the Achilles tendon. The plantaris tendon courses obliquely between the gastrocnemius and soleus muscles.

FIGURE 5.9 ● FLEXOR HALLUCIS LONGUS The flexor hallucis longus (FHL) flexes the great toe and plantarflexes the foot. The FHL is susceptible to injury during extremes of ankle plantarflexion and metatarsophalangeal dorsiflexion. The proximal sheath, 10 to 12 cm in length, has no mesotenon and may communicate with both the ankle joint and the sheaths of the flexor digitorum longus and tibialis posterior.

FIGURE 5.10 ● FLEXOR DIGITORUM LONGUS The flexor digitorum longus (FDL) flexes the phalanges of the lateral four toes and plantarflexes the foot. The FDL is superficial to the flexor hallucis in the sole of the foot. Paratenonitis of the FDL is more infrequent than involvement of the flexor hallucis longus.

FIGURE 5.11 ● TIBIALIS POSTERIOR The tibialis posterior plantarflexes and inverts the foot. The tibialis posterior tendon passes over (superficial to) the deltoid and changes from a tubular tendon to a flattened structure containing a fibrocartilaginous sesamoid (under the plantar calcaneonavicular ligament).

FIGURE 5.12 ● PERONEUS LONGUS The peroneus longus plantarflexes and everts the foot. The peroneus longus passes underneath the superior peroneal retinaculum, then runs superficial to the calcaneofibular ligament and passes deep to the inferior peroneal retinaculum. The third turn of the peroneus longus occurs as it enters the plantar tunnel between the cuboid and fifth metatarsal base. Ossification of the fibrocartilaginous sesamoid (which protects the tendon as it glides over the cuboid tuberosity) within the peroneus longus occurs in up to 20% of cases.

FIGURE 5.13 ● PERONEUS BREVIS The peroneus brevis plantarflexes and everts the foot. The peroneus brevis has a shorter and smaller muscle belly than the peroneus longus and becomes tendinous 2 to 3 cm proximal to the tip of the lateral malleolus.

FIGURE 5.14 ● EXTENSOR DIGITORUM BREVIS The extensor digitorum brevis extends the phalanges of the four medial toes. The extensor digitorum brevis and longus tendons contribute to the metatarsophalangeal extensor expansion.

FIGURE 5.15 ● ABDUCTOR HALLUCIS The abductor hallucis functions in abduction of the great toe. In tarsal tunnel syndrome the medial and lateral plantar nerves may be decompressed by releasing the fascia of the abductor hallucis muscle.

FIGURE 5.16 ● FLEXOR DIGITORUM BREVIS The flexor digitorum brevis (FDB) divides into two slips to allow the passage of the flexor digitorum longus tendon. The FDB flexes the middle phalanges (PIP joints) and is a weak plantarflexor of the MP joint (for the lateral four toes).

FIGURE 5.17 ● ABDUCTOR DIGITI MINIMI The abductor digiti minimi inserts into the plantar plate and the lateral plantar aspect of the proximal phalanx of the fifth toe. The abductor digiti minimi abducts the fifth toe and assists in flexion.

FIGURE 5.18 ● QUADRATUS PLANTAE The quadratus plantae originates from two heads from the medial and lateral aspect of the calcaneus and long plantar ligaments. The quadratus plantae flexes the terminal (distal) phalanges of the lateral four toes.

FIGURE 5.19 ● LUMBRICALS The lumbricals are plantarflexors of the metatarsophalangeal joint and extend the toes at the DIP and PIP joints. The lumbrical tendon inserts medially onto the extensor hood.

FIGURE 5.20 ● FLEXOR HALLUCIS BREVIS The flexor hallucis brevis functions in flexion of the great toe. Instability of the first metatarsophalangeal joint occurs with loss of flexor hallucis brevis function, as occurs with excision of both tibial and fibula sesamoids.

FIGURE 5.21 ● ADDUCTOR HALLUCIS The adductor hallucis has two heads and forms a conjoined tendon. The adductor hallucis adducts the great toe and assists in its flexion.

FIGURE 5.22 ● FLEXOR DIGITI MINIMI BREVIS The flexor digiti minimi brevis flexes the little toes.

FIGURE 5.23 ● DORSAL INTEROSSEI The four dorsal interosseous muscles stabilize the toes and abduct the second, third, and fourth toes laterally. They also assist in the flexion of the proximal phalanges and extension of the middle and distal phalanges.

FIGURE 5.24 ● PLANTAR INTEROSSEI There are four dorsal and three plantar interosseous muscles. The plantar interosseous muscles function in adduction of the third, fourth, and fifth toes medially toward the axis of the second toe. They also assist in flexion of the proximal phalanges and extension of the middle and distal phalanges.

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MR Atlas of the Ankle and Foot

Sagittal Images (Fig. 5.25)

The long axis of the tendons crossing the ankle joint is best seen on sagittal planar images.

Medial Sagittal Images

In the plane of the medial malleolus, the tibialis posterior and flexor digitorum longus tendons are directly posterior to the medial malleolus. The tibialis posterior tendon enters the foot by passing deep to the flexor retinaculum and superior to the sustentaculum tali to its insertion on the tuberosity of the navicular bone. The flexor digitorum longus tendon also enters the foot after passing posterior to the medial malleolus and deep to the flexor retinaculum. This tendon is divided into four segments after crossing the flexor hallucis longus tendon, which contributes slips to the medial two divisions. These segments insert onto the bases of the distal phalanges. The quadratus plantae muscle inserts at the division of the flexor hallucis into four tendons. Distally, each tendon is an origin for the lumbrical muscles.

The deltoid ligament, composed of the tibiocalcaneal, tibionavicular, and anterior and posterior tibiotalar ligaments, appears as a wide band of low signal intensity radiating from the distal tibia (i.e., medial malleolus) to the tuberosity of the navicular bone and the sustentaculum tali. The flexor hallucis longus tendon is located posterior to the tibialis posterior tendon and the flexor digitorum longus. It passes posterior to the medial malleolus, deep to the flexor retinaculum. The low-signal-intensity tendon hugs the posterior talar process and the inferior surface of the sustentaculum tali proximal to its insertion onto the base of the distal phalanx of the great toe.

The plantar flexor digitorum brevis (a first-layer muscle of the sole of the foot) and the quadratus plantae (a second-layer muscle of the sole of the foot) are displayed on medial sagittal images. The adductor hallucis (a first-layer muscle) inserts onto the medial proximal phalanx of the first toe and is seen between the first and second metatarsals on medial sagittal images. The tibialis anterior tendon crosses the dorsal surface of the talus before it inserts on the medial cuneiform bone and the bone of the first metatarsal.

Midplane Sagittal Images

The middle subtalar joint, the tarsal sinus, and the posterior subtalar joint are demonstrated on sagittal images medial to the midsagittal plane. The anterior subtalar joint is shown in the plane of the cuboid and calcaneocuboid joint. The peroneus longus, which extends anteriorly along the lateral inferior surface

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of the calcaneus and is inferior to the peroneal tubercle, enters the foot at the lateral inferior margin of the cuboid. The extensor hallucis longus tendon is identified along the dorsum of the foot and inserts onto the distal phalanx of the first toe. The interosseous talocalcaneal ligament, with its associated high-signal-intensity fat, is bordered anteriorly by the anterior process of the calcaneus and posteriorly by the lateral process of the talus. The pre-Achilles fat pad (high signal intensity on T1-weighted sequences) is located directly anterior to the Achilles tendon (low spin density).

FIGURE 5.25 ● Sagittal anatomy of the ankle and foot. (A) The origins of the anterior talofibular ligament and posterior talofibular ligament are identified arising from the anterior and posterior distal tip of the lateral malleolus. From the origin, the full course of these ligaments can be followed medially on successive sagittal images to their insertions on the anterior and posterior talus. (B) The vertical course of a long segment of the peroneus longus and brevis tendons is often visualized on a single sagittal image through the tendons. This image is useful to further characterize tendinosis and longitudinal tears or splits, and for measuring the gap between completely ruptured tendon fragments. (C) The anterior process of the calcaneus is a common location for fractures that are occult on plain film. They are optimally visualized in the sagittal plane on MR exams. (D) In addition to occurring at the tibiotalar joint, degenerative arthrosis is also commonly found at the posterior subtalar, calcaneocuboid, and talonavicular joints. The cartilage surfaces and subchondral bone at these articulations are optimally visualized in the sagittal plane. (E) The presence of an os trigonum posterior to the talus predisposes certain athletes with a predilection for plantarflexion to the os trigonum syndrome. This is diagnosed on sagittal MR images when edema is visualized within the os trigonum and extends across the synchondrosis into the posterior talus. (F) Abnormal signal in the sinus tarsi manifests as high signal on FS fluid-weighted sequences and low signal on non-FS sequences. This abnormal signal may suggest, but is not specific for, inflammation in the sinus tarsi. Other causes of abnormal signal in the sinus tarsi, which may be incidental and asymptomatic, include extension of joint fluid from the posterior and middle subtalar joints, extension of generalized edema throughout the soft tissues of the ankle from stasis or other causes, enlarged vessels, and ganglion cysts.(G) Two potential causes of an incidental “mass” palpated on physical examination about the Achilles tendon are a low-lying soleus muscle and an accessory soleus muscle, both of which are diagnosed by MR imaging. The normal soleus muscle extends to about the proximal one third or one half of the Achilles tendon. A low-lying soleus will extend to the distal third of the tendon. An accessory soleus is present when there is an extra muscle in the pre-Achilles fat, usually extending to the distal third of the tendon, often near the distal insertion. (H) In the setting of a complete Achilles tendon rupture, the location of the tear may be at the myotendinous junction, mid-tendon, distal tendon, or tendon insertion at the os calcis. In addition, the tear is characterized as transverse or oblique longitudinal. In the case of transverse tears, the distance between the tear and tendinous insertion at the calcaneus is measured. Also, the length of good-quality tendon stump at the calcaneal insertion is measured, since the surgeon often uses the distal stump in the surgical reconstruction or repair. (I) The anteromedial aspect of the tibiotalar joint is a common location for the formation of large osteophytes, which extend anteriorly from the anteromedial tibia and talus. These may cause pain, limit the range of motion, or break off and form loose bodies within the tibiotalar joint. This spectrum of findings is part of the anteromedial impingement syndrome. (J) Ancillary findings at the plantar aponeurosis visualized on sagittal images include bone marrow edema within the inferior calcaneus, inferior calcaneal enthesophyte with marrow edema, and high signal within the flexor digitorum brevis muscle and fat that surround the plantar aponeurosis. These findings suggest active inflammation in the tissues surrounding the plantar aponeurosis. (K) The deltoid ligament is found on sagittal images by finding its origin extending off the bilobed medial malleolus. The medial course of the deltoid ligament components is followed over the next two or three successive sagittal images. (L) The vertical course of the tibialis posterior tendon and the flexor digitorum longus tendon is often visualized on a single image. Triangulating on tendon pathology in both the sagittal and axial planes aids in further characterizing tendon abnormalities.

Lateral Sagittal Images

In the plane of the fibula, the peroneus brevis and longus tendons pass posterior to the lateral malleolus. The peroneus brevis tendon lies anterior to the peroneus longus and is in direct contact with the lateral malleolus. The peroneus brevis can be followed to its insertion on the base of the fifth metatarsal bone. The peroneus longus tendon disappears inferior and medial to the peroneus brevis tendon and enters the cuboid sulcus. Therefore, it appears shorter than the peroneus brevis tendon on lateral sagittal images.

Coronal Images (Fig. 5.26)

Coronal plane images demonstrate tibiotalar articular surfaces and are also used to assess medial, lateral, and posterior ligaments as well as the tendons.

Posterior Coronal Images

The thick, low-signal-intensity Achilles (calcaneal) tendon is clearly displayed on posterior coronal images. Its attachment to the calcaneal tuberosity can also be observed on these views. The soleus muscle, with its inverted-V-shaped origin from the soleal line of the tibia and posterior fibula, contributes to the calcaneal tendon, along with the gastrocnemius and plantaris. The peroneus brevis and flexor hallucis longus muscles are identified lateral to the soleus muscle, and the peroneal tendons are located inferior to the lateral malleolus. The flexor digitorum longus muscle and tendon cross superficially, in a medial-to-lateral direction, to the tibialis posterior in the distal calf. The tibialis posterior tendon is located medial to the posterior malleolus. The posterior talofibular and inferior tibiofibular ligaments are shown on coronal images at the level of the posterior malleolus and posterior process of the talus. The plantar aponeurosis is superficial to the flexor digitorum brevis muscle, whereas the quadratus plantae muscle lies deep to the flexor digitorum.

Midplane Coronal Images

The calcaneofibular ligament is best visualized at the level of the posterior subtalar joint and lateral malleolus. The lateral process of the talus can be seen in the same sections as the anterior lateral malleolus. The middle subtalar joint is formed by the sustentaculum tali and the inferior medial talar surface. This is the best plane for evaluating talocalcaneal coalitions. The peroneus brevis and longus tendons course laterally, superior and inferior, respectively, to the peroneal groove of the calcaneus. The separate chondral surfaces of the tibial plafond and the talar dome are demonstrated in this plane.

Anterior Coronal Images

The tibiotalar and tibiocalcaneal fibers of the deltoid ligament extend obliquely to the talus and vertically to the sustentaculum tali, respectively. The tibialis posterior tendon is medial to the deltoid ligament and superior to the sustentaculum tali and can be used as a landmark. The flexor digitorum longus tendon enters the foot, having crossed superficially in a medial-to-lateral direction to both the tibialis posterior and the flexor hallucis longus tendons, which are parallel. The flexor digitorum longus tendon is located medial to the sustentaculum tali. The anterior compartment tendons (the tibialis anterior, the extensor hallucis longus, and the extensor digitorum longus) are displayed medially and laterally on the anterior surface of the distal tibia. The anterior tibiotalar fibers of the deltoid ligament are also seen in the plane of the anterior tibia.

Axial Images (Fig. 5.27)

In the axial plane, the low-signal-intensity bands of the anterior and posterior inferior tibiofibular ligaments are demonstrated at the level of the tibial plafond. The inferior extensor retinaculum is identified anterior to and at its attachment to the medial malleolus, and represents the upper limb of this Y-shaped band of deep fascia. At the level of the tibiotalar joint, the tendons of the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius muscles occupy the anterior compartments in a medial-to-lateral direction. The peroneus brevis muscle and tendon and the more lateral peroneus longus tendon are located posterior to the lateral malleolus. The tendons of the tibialis posterior, flexor digitorum longus, and flexor hallucis longus can be identified posteriorly, running from a medial position posterior to the medial malleolus to a lateral position posterior to the tibial plafond and talar dome. Posterior and medial to the greater saphenous vein, the anterior tibionavicular fibers of the deltoid ligament blend with the low-signal cortex of the anterior surface of the medial malleolus.

The Achilles tendon is identified in cross-section as a thick structure of low signal intensity with a convex posterior sur-face and a flattened anterior surface. The posterior Achilles tendon is formed by the convergence of the gastrocnemius, plantaris, and soleus muscles. The soleus muscle group that is seen at the level of the distal tibia is not visible at the tibiotalar joint level. At the level of the distal lateral malleolus, both the anterior and posterior talofibular ligaments are demonstrated. Medially, the tibionavicular and tibiocalcaneal parts of the deltoid ligament are also shown at this level. The peroneal retinaculum can be seen coursing medial and posterior to the lateral malleolus. The interosseous talocalcaneal ligament is posterolateral

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to either the anterior talus or the talar head. The plantar calcaneonavicular ligament, or spring ligament, is located inferior to the lateral malleolus between the lateral talus and tibialis posterior tendon.

FIGURE 5.26 ● Coronal anatomy of the ankle and foot. (A) The calcaneofibular ligament (CFL) is identified by finding its origin at the inferior tip of the lateral malleolus. The posterior inferomedial course of the CFL is followed on three or four consecutive coronal images moving posteriorly through the ankle, to its insertion on the posterolateral calcaneus. Optimal evaluation of the CFL involves examining its full course on successive images in both the coronal and sagittal plane for tears, sprain, or scarring. (B) The medial cord of the plantar aponeurosis is normally slightly thicker than the lateral cord, and this mild asymmetry in thickness should not be misinterpreted as plantar aponeurosis scarring or plantar fasciitis. On successive coronal images, the course of the plantar aponeurosis should be followed back to its insertion on the inferior calcaneus and evaluated for the presence of thickening, decreased signal suggestive of scarring, increased signal indicative of plantar fasciitis, and tears. (C) Coronal images are optimal for viewing the lateral process of the talus, which is a frequent site of fractures that are occult on plain films. Fractures of the lateral process of the talus are most common in patients with snowboarding injuries. (D) The talar dome and tibial plafond are optimally visualized on coronal images. They are assessed for the presence of subchondral edema and cystic change with overlying chondral abnormalities. Close attention should be directed to the extreme anterior and posterior margins of the cartilage-bearing articular surfaces of the talar dome and tibial plafond to avoid overlooking osteochondral lesions at these locations. (E) The origin of the anterior talofibular ligament (ATFL) is found at the anterior distal tip of the lateral malleolus, and the ATFL is followed anteriorly on two or three successive coronal images to its insertion at the anterior lateral margin of the talus. (F) The deltoid ligament is optimally visualized in the coronal and axial planes. Tears of the deltoid manifest as loss of fiber striation or diffuse amorphous hyperintensity in the ligament on fluid-weighted sequences. Partial tears are more common than complete tears. (G) Focal fatty atrophy and denervation of the plantar flexor muscles of the foot (abductor digiti minimi, flexor digitorum brevis, and abductor hallucis) may indicate neuropathy involving the tibial nerve or its branches. (H) At the level of the anterior aspect of the talus and calcaneus, the peroneal tendons and flexor tendons turn from their cranial—caudal course to travel an anterior-to-posterior course along the plantar aspect of the foot. The distal portions of the tendons should be examined along the plantar aspect of the foot on successive coronal images for evidence of tendinosis and tears. (I) The base of the fifth metatarsal is a common location for fractures and is often visualized within the FOV on ankle MR exams. (J) At the level of the navicular, the flexor digitorum longus (FDL) and flexor hallucis longus (FHL) tendons run side by side, with the FDL medial to the FHL. Anterior to this level on successive coronal images, the two tendons cross, with the FHL medial to the FDL as the FHL courses to its insertion on the great toe. (K) Stress fractures of the navicular are commonly vertical in the midline of the navicular, an appearance that is well characterized on coronal images. (L) Contusions, stress-related edema, fractures, and degenerative arthritis of the midfoot bones and joints are common causes of midfoot pain and are often optimally identified on fluid-sensitive sequences.

FIGURE 5.27 ● Axial anatomy of the ankle and foot. (A) The flexor digitorum longus, flexor hallucis longus, peroneus brevis, soleus, and extensor digitorum muscles are examined at this level for strain, tears, or fatty atrophy that may suggest denervation. (B) The tibialis anterior, extensor hallucis longus, and extensor digitorum longus tendons are examined on every ankle MR examination. Extensor tendon pathology is frequently overlooked if these tendons are not included as part of the ankle checklist. (C) Tears and sprains of the anterior syndesmotic ligament are a frequent cause of persistent ankle pain following ankle sprain. The syndesmotic ligaments are thick, tough ligaments that are important ankle stabilizers, and delayed diagnosis of syndesmotic tears may result in significant degenerative arthrosis at the tibiotalar joint due to the resulting ankle instability. The syndesmotic ligaments course obliquely inferiorly from the tibia to the fibula and are not usually visualized in their entirety on a single axial image; rather, their course is followed on at least two or three successive axial images. (D) The peripheral margin of the peroneal tendons and tibialis posterior tendon should normally never extend beyond the peripheral margins of the lateral and medial malleoli, respectively. Tendon subluxation around the posterior corner of either malleolus is indicative of a tear of the overlying flexor retinaculum (medially) or peroneal retinaculum (laterally). When the retinacula are torn, the tendon is free to intermittently sublux or dislocate, leading to tendon degeneration, pain, and tendon dysfunction. (E) Suspected osteochondral lesions of the talar dome are visualized and further characterized on axial images through the top of the talar dome. (F) The peroneus brevis tendon may normally appear somewhat flattened. However, as the tendon degenerates, it becomes U-shaped and drapes around the anterior aspect of the peroneus longus and becomes impinged between the peroneus longus tendon and the lateral malleolus. With further degeneration, the peroneus brevis may split or completely rupture. (G) Evidence of anterior talofibular ligament injury is visualized on the majority of MR ankle examinations and appears as thickening, intermediate signal with ill-defined fibers, or attenuation of the ligament. This is commonly asymptomatic. (H) Because the flexor hallucis longus tendon sheath communicates with the tibiotalar joint, fluid may normally be present within the tendon sheath in proportion to the amount of fluid in the tibiotalar joint. If there is fluid within the tendon sheath out of proportion to that seen in the tibiotalar joint, tenosynovitis is most likely present. The finding of flexor hallucis longus tenosynovitis should prompt a search for an os trigonum, as impingement of the flexor hallucis longus tendon between an os trigonum and the posterior tibial plafond is a common cause for FHL tenosynovitis. (I) The calcaneofibular ligament (CFL) passes anterior and medial to the peroneal tendons. On the image at which the CFL passes directly medial to the peroneus brevis tendon, the appearance of the peroneus brevis and the CFL side by side is occasionally mistaken for a split peroneus brevis tendon. (J) Dilated posterior tibial veins within the tarsal tunnel occasionally compresses the tibial nerve. In the setting of clinical suspicion for tarsal tunnel syndrome or if there is evidence of muscle denervation on MR images, the size of the posterior tibial veins should be described. (K) The spring ligament is identified at this axial image location, extending from the anteromedial calcaneus to the posteromedial navicular. Tears of the spring ligament may result in medial instability and hindfoot valgus. (L) The posterior tibialis tendon (PTT) may normally become thickened and fan-like as it passes posterior to its navicular insertion (prior to also inserting on the cuneiforms and the base of the second through fourth metatarsals). In the absence of other findings, the thickening of the PTT at this level should not be mistaken for focal tendinosis. (M) On inferior images through the ankle, Lisfranc's ligament is occasionally included in the FOV. Lisfranc's ligament extends from the medial cuneiform to the base of the second metatarsal. If Lisfranc's ligament is included in the FOV, the status of the ligament should be described, as undiagnosed Lisfranc ligament tears can lead to debilitating midfoot arthrosis. (N) As the medial and lateral tendons turn from their vertical course to a horizontal course along the plantar aspect of the foot, the tendons may demonstrate a magic-angle artifact, causing the tendons to appear gray on short-TE images, mimicking tendinosis. Correlation with images using longer TE values is advised in such situations.

The calcaneofibular ligament is optimally seen with the foot in 40° of plantarflexion, and on neutral axial images it can be seen lateral to the posterior inferior talus and anterior and medial to the peroneus brevis tendon. The sural nerve, intermediate in signal intensity, is located posteromedial to the peroneus brevis muscle. The tibial nerve is medial to the flexor hallucis longus tendon and continues distally as the medial and lateral plantar nerves. The flexor retinaculum is superficial to the tendons of the deep muscles on the medial side of the ankle. In the foot, the tendons of the flexor hallucis brevis and longus muscles are seen posterior to the first metatarsal and cuneiform. The longitudinally oriented quadratus plantae and abductor hallucis muscles are medial to the calcaneus and cuboid. The peroneus longus tendon, a fourth-layer muscle of the sole of the foot, enters the foot by passing posterior to the lateral malleolus and can be seen obliquely crossing the foot to its insertion onto the base of the first metatarsal and medial cuneiform bone.

The anterior neurovascular bundle, composed of the anterior tibial artery and vein and the deep peroneal nerve, is located posterior to the extensor tendons, whereas the posterior neurovascular bundle, composed of the posterior tibial artery, vein, and tibial nerve, is located posterior to the flexor digitorum and flexor hallucis longus tendons.

Imaging Checklist for the Ankle

A simple way to organize a checklist for the ankle is to analyze the ankle by its constituents: bones and joints, ligaments, and tendons. To confirm and characterize pathology, most of the anatomic structures in the ankle are examined in all three planes.

Key articulations for examination include:

Tibiotalar joint
Posterior subtalar joint
Talocalcaneonavicular joint

All bones are examined for fractures, avascular necrosis (AVN), and edema. Fractures that may be occult on plain films but are well demonstrated on MR examination include:

Fractures occurring at the anterior process of the calcaneus
Fractures of the lateral process of the talus
Navicular fractures
Fractures of the metatarsals
Cuboid fractures (particularly stress fractures)

The ligaments are well displayed and are divided into the:

High tibiofibular ligaments (the anterior and posterior syndesmosis and the interosseous ligament)
Lateral ligaments (the anterior talofibular, calcaneofibular, and posterior talofibular ligaments)
Medial ligaments (the components of the deltoid ligament)
Sinus tarsi ligaments (the extensor roots, interosseous ligament, and cervical ligament)

The tendons are also evaluated. They can be divided into four groups:

The lateral tendons (the peroneus longus and brevis tendons)
The medial tendons (the posterior tibialis, the flexor digitorum longus, and the flexor hallucis longus tendons)
The anterior tendons (the tibialis anterior, the extensor hallucis longus, and the extensor digitorum longus tendons)
The posterior tendons (the Achilles and plantaris tendons)

In conjunction with evaluation of the tendons, the peroneal retinacula covering the peroneal tendons and the flexor retinaculum covering the medial tendons are also examined for tears, commonly diagnosed when the tendons are dislocated. Inferiorly, the plantar fascia should also be inspected.

Sagittal Plane Checklist

In the sagittal plane, all of the major articulations and bones of the ankle are demonstrated. In addition, certain ligamentous structures, including the anterior talofibular (ATFL), posterior talofibular, and transverse tibiofibular ligaments, are examined in the sagittal plane. The long axis of the Achilles tendon is well visualized and the medial, lateral, and anterior tendons are displayed in their long axes, although due to slice gaps, parts of the tendons may not be fully imaged. Triangulating on sagittal images of these tendons is useful for confirmation or further characterization of tendon abnormalities suspected in the axial or coronal plane.

(1) Bones and Articulations

Tibiotalar Joint (Figs. 5.28 and 5.29)

The cartilage surfaces covering the articular surfaces of the talar dome and tibial plafond are visualized on both sagittal and coronal images. Osteochondral lesions, classically described in the talar dome, also affect the tibial plafond. When an osteochondral lesion is identified, the condition of the overlying cartilage (e.g., full-thickness cartilage defect, deep fissuring), the state of the subjacent subchondral bone (including any subchondral cysts or edema), and the presence of any unstable chondral flaps or osteochondral fragments with fluid undermining are key elements in determining the stage and severity of the lesion. The joint is also examined for the presence of effusions, synovitis, and loose bodies.

FIGURE 5.28 Tibiotalar Joint.

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Impingement of the bony and capsular structures making up the tibiotalar joint can occur anywhere in the joint, and various impingement syndromes have been named according to where in the tibiotalar joint they occur. For example, anterior impingement occurs when large spurs of the anterior tibia and talus are present with anterior synovitis. Anterolateral impingement results from chronic anterior talofibular and calcaneofibular ligament injury (post-inversion injury) and is suggested when there is a synovial mass in the lateral gutter deep to a scarred or chronically torn ATFL and anterolateral capsule. Posterior impingement occurs when the posterior ligaments are impinged between the talus and tibia, and the related os trigonum syndrome occurs when the os trigonum is compressed during plantarflexion, with resulting edema within the os trigonum and across the synchondrosis between the os and the posterior talus.

Subtalar Joints (Fig. 5.30)

The two subtalar joints involve three subtalar facets on the superior surface of the calcaneus, all three of which are optimally visualized on sagittal images. The posterior subtalar facet is located at the posterior subtalar articulation between the talus and calcaneus. The middle and anterior facets make up part of the anterior subtalar joint (or talocalcaneonavicular joint), which is composed of the articulation of three bones: the talus, calcaneus, and navicular. These two joints are susceptible to the usual disorders associated with articular disease, including arthrosis, effusions, ganglion/synovial cysts, and even pigmented villonodular synovitis and other synovial inflammatory processes. The subtalar joints are examined on sagittal images for the presence of subchondral edema on one or both sides of the joint, subcortical cystic change, and cortical irregularity and bony hypertrophic change at the joint. Isolated degenerative joint disease (DJD) is a common underdiagnosed cause of foot pain. Also, subtalar joint DJD is not uncommonly associated with tarsal coalitions as a result of abnormal stresses across the joints. Careful evaluation of the ankle is necessary to identify coalitions in other joints when subtalar DJD is visualized. Coalitions may also involve the subtalar joints themselves.

FIGURE 5.29 Impingement.

Other Tarsal Joints (Fig. 5.31)

The calcaneocuboid joint, the talonavicular portion of the talocalcaneonavicular joint, and the cuneonavicular joints are also well visualized on sagittal images and should be examined for pathology. The joints are analyzed for the presence of subchondral edema and cystic change and hypertrophic spurring. The joints should also be inspected for fibrous or osseous coalitions, most commonly calcaneonavicular and talocalcaneal (less commonly talonavicular), and for associated arthrosis.

FIGURE 5.30 Subtalar Facets.

FIGURE 5.31 Tarsal Joints.

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Hindfoot Bones (Fig. 5.32)

The lateral-most sagittal image displays the lateral malleolus and lateral process of the talus, which should be examined for evidence of fracture or other posttraumatic changes. The talar dome is seen more centrally and should be inspected for evidence of osteonecrosis, osteochondral lesions, or subchondral fractures. The head, neck, and body of the talus are also reviewed for fractures and the tibial plafond for fractures, AVN, or osteochondral lesions. The anterior process of the calcaneus, a site of frequent fractures that are occult on plain films, is assessed for fractures, as is the medial malleolus. The superior and posterior aspects of the calcaneus are reviewed for fractures, AVN, or infection. In children and adolescents, patchy marrow edema is frequently found extending throughout hindfoot and forefoot. There is still debate as to whether this finding reflects a painful syndrome of chronic stress-related edema and bony remodeling or is simply an asymptomatic incidental finding. Less common causes of marrow edema include transient osteoporosis and reflex sympathetic dystrophy (which often is accompanied by soft-tissue edema).

Midfoot/Forefoot Bones (Fig. 5.33)

The navicular, cuneiforms, cuboid, and metatarsal bones are all displayed on sagittal images and should be examined for the presence of stress fractures/acute fractures, AVN, infection, or other bony abnormalities. When significant tarsal-metatarsal DJD is identified, it is imperative to examine Lisfranc's ligament, extending from the medial cuneiform to the base of the second metatarsal, to ensure the ligament demonstrates normal dark intact fibers. Tears of Lisfranc's ligament are debilitating injuries that often result in severe midfoot degenerative changes due to the associated tarsal-metatarsal instability caused by such injuries. Lisfranc's ligament is best evaluated in the axial and coronal planes.

FIGURE 5.32 Hindfoot.

(2) Ligaments

Lateral Ligaments (Fig. 5.34)

The origin and course of the lateral ligaments can be evaluated on sagittal images:

The ATFL is found on sagittal images one slice central to the lateral-most sagittal slice that includes the lateral malleolus. The origin of the ATFL is seen at the anterior inferior tip of the lateral malleolus. The anteromedial course of the ATFL can be followed on the next two images moving centrally, to where it inserts on the talus.
The posterior talofibular ligament (PTFL) is located in a similar fashion. The origin of the PTFL is at the inferior tip of the lateral malleolus, and the tendon can be followed medially to its insertion on the mid-posterior aspect of the talus. The PTFL is seen in cross-section on sagittal images and has a cord-like appearance. Posterior to the talus, this cord-like appearance should not be mistaken for a loose body in the posterior joint.
The calcaneofibular ligament (CFL) also originates from the inferior tip of the lateral malleolus, and courses inferomedially to its attachment on a tubercle on the lateral calcaneus. The course of the CFL is not always well visualized on sagittal images, however, because it may be obscured by overlying peroneal tendons.

FIGURE 5.33 Midfoot Forefoot.

FIGURE 5.34 Lateral Ligaments.

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The ATFL may be sprained or torn in isolation or together with the CFL, whereas the PTFL is uncommonly acutely injured.

Medial Ligaments (Fig. 5.35)

Although the deltoid ligament components are seen on sagittal images, abnormalities are probably better characterized on coronal and axial images. The deltoid ligament can be found on the medial-most slice of the medial malleolus, in which the medial malleolus appears as two contiguous inferiorly pointing bumps (known as the anterior and posterior colliculi). The origins of the superficial and deep fibers of the deltoid ligament complex are identified at the inferior margin of the medial malleolus, and the fibers can be followed as they course over the next one or two images centrally to their attachment sites.

Sinus Tarsi Ligaments (Fig. 5.36)

The sinus tarsi and canal are fat-filled structures located in the lateral aspect of the ankle between the anterior and posterior subtalar joints. The lateral, intermediate, and medial roots of the inferior extensor retinaculum are the first images seen on sagittal images in the lateral-most aspect of the sinus tarsi. The individual roots may be difficult to distinguish on MR images. On the next image medially, the cervical ligament can be seen originating from the neck of the talus and extending obliquely posteriorly to insert on the calcaneus. Medial to this is the interosseous ligament. Acute strain and high signal associated with these ligaments are seen after injuries. Ganglion cysts arising from these ligaments can also extend into the sinus tarsi fat and occasionally produce symptoms. Joint fluid from within the subtalar joints can also extend into the sinus tarsi, usually without symptoms. As opposed to acute ligamentous injury, the sinus tarsi syndrome represents a more chronic and indolent condition in which there is obliteration of the sinus tarsi fat and chronic scarring (manifested as dark signal on MR images) or synovitis (manifested as intermediate to bright signal on MR images) within the sinus tarsi. Sinus tarsi syndrome often occurs subsequent to ankle sprains or posterior tibialis tendon (PTT) injury. When sinus tarsi syndrome is diagnosed, the lateral ligaments and PTT should be closely examined for associated abnormalities.

FIGURE 5.35 Deltoid Ligament.

FIGURE 5.36 Sinus Tarsi Ligaments.

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(3) Tendons

Achilles Tendon (Fig. 5.37)

The full course of the Achilles tendon is imaged in the sagittal plane. The Achilles tendon should be homogeneously dark in signal and smooth, with a concave or flat anterior border. Midsubstance tendinosis (manifested by fusiform thickening) and insertional tendinitis (seen as distal thickening at the os calcis insertion) can be characterized, as can the location of longitudinal, partial, or complete tears, which are optimally measured in the sagittal plane. The distance from a tear to the os calcis insertion is measured, the location of the tear (at the myotendinous junction, midtendon, or distal tendon insertion) is specified, and the gap between tendon ends is measured. Tear morphology (transverse, oblique, interstitial, involving the medial and/or lateral aspect of the tendon, partial or full thickness) is assessed and specified. In addition, if there is a distal stump of reasonably high-quality tendon left at the distal os calcis insertion, this is measured and noted, as it may be possible to sew the torn tendon directly into an intact distal stump. The presence of associated abnormalities, such as retrocalcaneal bursitis and inflammation of the soft tissues surrounding the tendon (paratendinitis), should also be described.

FIGURE 5.37 Achilles Tendon.

FIGURE 5.38 Plantar Fascia.

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Plantar Aponeurosis (Fig. 5.38)

The plantar aponeurosis comprises three segments:

A medial segment inferior to the abductor hallucis muscle
A central segment, which originates from the medial process of the calcaneal tuberosity
A lateral segment, which originates along the lateral aspect of the calcaneal tuberosity

Pathology of the true medial segment is rare, whereas pathology of the true central segment is common. Therefore, the central segment is sometimes referred to as the medial segment or medial cord. The proximal portions of the central (or medial) and lateral segments are optimally visualized on sagittal images. When viewing the ankle on sequential sagittal images from medial to lateral, the central (or medial) cord is visualized first, with the lateral cord visualized subsequently, often with no gap seen between the two segments. The normal medial cord is usually somewhat thicker than the lateral cord. Most plantar aponeurosis pathology involves the medial cord first. Any doubt as to which segment is abnormal can be resolved by correlating findings with coronal images. Plantar fasciitis is suggested when there is thickening and increased signal in the proximal plantar aponeurosis. Associated findings such as inferior calcaneal spurs at the plantar aponeurosis origin, calcaneal tuberosity edema, and inflammation in the surrounding fat support the diagnosis. Also, the plantar aponeurosis may be involved by fibromatosis, which typically occurs near the midportion of the aponeurosis, as opposed to plantar fasciitis, which occurs at the calcaneal insertion.

FIGURE 5.39 Tendons.

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Other Tendons (Fig. 5.39)

The medial, lateral, and extensor tendons are not always optimally viewed in their entirety in the sagittal plane, as sagittal slices can gap over portions of the tendon. However, abnormalities of these tendons seen in the axial and coronal plane are confirmed or further characterized by triangulating on images of the tendon in the long axis on sagittal images. Sagittal images demonstrate the os peroneum, a normal-variant small ossicle within the peroneus longus tendon adjacent to the cuboid. Degeneration and tearing of the peroneus longus tendon around a fractured or otherwise inflamed os peroneum is known as the “painful os peroneum syndrome” and is diagnosed when high signal and tearing of the peroneus longus tendon are visualized about an edematous os peroneum.

Coronal Plane Checklist

The coronal plane is optimal for characterization of osteochondral lesions of the talar dome and tibial plafond. In addition, the deltoid ligament is best viewed in the coronal plane, and the superficial and deep components are readily distinguished. The ATFL, CFL, and PTFL are also visualized. The central and lateral segments of the plantar aponeurosis can be followed back to their individual posterior origins on the inferior calcaneus. The distal courses of the medial and lateral tendons are imaged in cross-section on coronal images. Osseous abnormalities can be further characterized in the coronal plane.

FIGURE 5.40 Tibiotalar Joint.

(1) Bones and Articulations

Tibiotalar Joint (Fig. 5.40)

The cartilage surfaces and subchondral regions are displayed on sequential anterior-to-posterior images through the tibiotalar joint and can be examined for abnormalities. Osteochondral lesions of the talar dome and tibial plafond can be localized and staged, and fractures of the medial and lateral malleolus, the tibial plafond, and the talus can be characterized.

Subtalar Joints and Other Articulations and Osseous Structures (Fig. 5.41)

Osseous structures and articulations in the hindfoot and forefoot, including the subtalar joints, the lateral process of the talus, the sustentaculum tali, the navicular, the cuneiforms, and the metatarsals, are also examined in the coronal plane for osseous abnormalities, fractures, arthrosis, or coalitions.

(2) Ligaments

Lateral Ligaments (Fig. 5.42)

In the coronal plane the lateral ligaments are found on the image that cuts through the middle of the lateral malleolus and displays the distal tip most prominently. On this image the PTFL is seen coursing medially from the distal tip of the lateral malleolus to insert on the mid-posterior tibia. The origin of the CFL may also be seen on

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this image (or possibly one image posterior). On the next one or two posterior images the course of the CFL can be followed from the distal lateral malleolus posteroinferiorly to its insertion on the lateral calcaneus. On the three or four images anterior to the slice through the middle of the lateral malleolus, the full course of the ATFL is seen as a dark bundle of fibers moving directly anteriorly to insert on the lateral aspect of the talus. The lateral ligaments are examined in the coronal plane, and any findings are correlated with those seen in other planes.

FIGURE 5.41 Subtalar Joint.

FIGURE 5.42 Lateral Ligaments.

FIGURE 5.43 High Ankle Ligaments.

High Ankle Ligaments (Fig. 5.43)

The anterior syndesmotic ligament (also known as the anterior inferior tibiofibular ligament [AITF]) and the posterior syndesmotic ligament (also known as the posterior inferior tibiofibular ligament [PITF]) are located superior to the ATFL and PTFL on the lateral aspect of the ankle. On coronal images they are visualized coursing obliquely upward from the lateral malleolus to the anterolateral and posterolateral tibia, respectively.

Although the anterior and posterior syndesmotic ligaments are most easily identified on axial images, the coronal and sagittal planes are useful for confirming and further characterizing tears and sprains. These ligaments are important stabilizers of the ankle and are not infrequent causes of persistent pain following inversion injuries. The anterior syndesmotic ligament is more frequently injured than the posterior syndesmotic ligament, and tears are often treated surgically. Undiagnosed tears can lead to significant degenerative arthritis.

Medial Ligaments (Fig. 5.44)

The coronal plane demonstrates both the deep and superficial fibers of the deltoid ligament complex. The deep fibers (posterior tibiotalar and anterior tibiotalar ligaments) form a thick triangular band of fibers that originate from the undersurface of the medial malleolus and attach along the medial aspect of the talus. There is normal high-signal fat interposed between individual fibers of the deep portion of the deltoid ligament, which should not be mistaken for a sprain. In general, the superficial fibers (the superficial posterior tibiotalar, tibiocalcaneal, tibiospring, and tibionavicular ligaments) are thinner than the deep fibers, run parallel with and medial to the deep fibers, and insert more distally (on the navicular, the talus, the spring ligament, and the calcaneus). The deltoid ligament can be acutely sprained or torn or may be scarred. Medial ligament injury commonly occurs in the presence of lateral-sided injury, and in the presence of deltoid ligament injury the lateral ligaments and osseous structures should be examined for concurrent injuries.

(3) Tendons and Muscles

Plantar Aponeurosis (Fig. 5.45)

The central (or medial) and lateral cords of the plantar aponeurosis are easily distinguished in the coronal plane, and abnormalities seen on sagittal plane images are confirmed in the coronal plane.

Inferior Flexor Muscles (Fig. 5.46)

The three most superficial muscles along the plantar aspect of the foot, from medial to lateral, are as follows:

Abductor hallucis
Flexor digitorum brevis
Abductor digiti minimi

These muscles, visualized in cross-section on coronal images, are evaluated for strain or tears and also for the presence of denervation. Chronic denervation is suspected when there is selective fatty atrophy of one or more of the muscles manifested as fatty T1 bright signal interdigitating throughout the muscle. Acute denervation is suggested when there is mild hazy ill-defined high signal on fluid-sensitive sequences throughout the muscle. Denervation suggests injury to one of the branches of the tibial nerve.

Other Tendons (Fig. 5.47)

The lateral, medial, Achilles, and extensor tendons are visualized in the coronal plane, and abnormalities seen on axial plane images are confirmed and further characterized in the coronal plane.

FIGURE 5.44 Deltoid Ligaments.

FIGURE 5.45 Plantar Aponeurosis.

FIGURE 5.46 Inferior Flexor Muscles.

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Axial Plane

The tendons and ligaments are visualized in cross-section on axial images, and the axial plane is optimal for evaluating pathology. Bones and articulations are also further analyzed in the axial plane.

(1) Osseous Structures

Hindfoot (Fig. 5.48)

The axial plane affords an additional opportunity to triangulate on and characterize abnormalities of the fibula, tibia, medial and lateral malleolus, talus, and calcaneus.

FIGURE 5.47 Coronal Tendons.

Midfoot/Forefoot (Fig. 5.49)

The navicular, cuboid, cuneiforms, and metatarsals are also evaluated on axial images. MR of the foot is commonly used to detect stress fractures of the metatarsals. Fractures at the base of the fifth metatarsal, which may be occult on plain films, are readily detected on MR images. Characterization of an accessory navicular as type 1, 2, or 3 is optimally performed on axial images. In addition, stress-related changes across a type 2 navicular synchondrosis, marrow edema in a type 3 cornuate navicular, and tendinosis or tears of the posterior tibialis tendon associated with an accessory navicular are evaluated in the axial plane. Lisfranc's ligament is often included in the FOV for standard ankle MR examination. Degenerative

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arthrosis at the tarsal-metatarsal joints in particular should prompt a careful search for Lisfranc fracture—dislocations in the axial plane.

FIGURE 5.48 ● Hindfoot.

(2) Tendons

Medial Tendons (Fig. 5.50)

Axial images are optimal for evaluating the three medial tendons in cross-section. The medial tendons are:

Posterior tibialis tendon (PTT), the most medial of the three tendons
Flexor digitorum longus (FDL), located just posterolateral to and in close apposition with PTT
Flexor hallucis longus (FHL), the most lateral and posterior of the three tendons

The tibial artery, veins, and nerve run between the FDL and the FHL. The course of the tendons can be followed on sequential images from superior to inferior as they run posteromedial to the tibia and medial malleolus. Inferior to the medial malleolus, the tendons turn and head anteroinferiorly beneath the medial hindfoot to run along the plantar aspect of the foot.

Axial images are particularly helpful in excluding mass lesions (including varices, ganglion cysts, or nerve sheath tumors) within the tarsal tunnel, which may compress the tibial nerve and its branches. Both axial and coronal images are useful for demonstrating denervation of the inferior flexor muscles (supplied by the tibial nerve and its branches). The medial tendons are covered by a flexor retinaculum, which is identified on axial MR images extending posteroinferiorly from the medial malleolus to insert on the calcaneus. The flexor retinaculum may tear from the medial malleolus, allowing subluxation of the medial tendons anterior and medial to the medial malleolus.

Lateral Tendons (Fig. 5.51)

The lateral tendons, the peroneus longus and brevis, are also optimally visualized in the axial plane. When sequential images through the ankle are viewed from superior to inferior, superior images demonstrate the peroneus longus and brevis located posterior to the distal fibula and the peroneus longus located lateral to the peroneus brevis. At this level, the brevis appears flatter and thinner than the longus. At and inferior to the lateral malleolus, the peroneus brevis swings anterior to the longus as the tendons course lateral to the calcaneus. Just inferior to the lateral malleolus, the CFL is visualized coursing anterior and then medial to the peroneus brevis tendon before attaching to the calcaneus. As part of the evaluation of the peroneal tendons, the superior peroneal retinaculum (SPR) at the level of the lateral malleolus is inspected. The SPR originates from the lateral posterior aspect of the lateral malleolus and wraps around the posterolateral aspect of the peroneal tendons before inserting on the calcaneus.

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The peroneal retinaculum prevents the peroneal tendons from subluxing laterally over the lateral malleolus. Tears or stripping of the peroneal retinaculum from the lateral malleolus is inferred when subluxation or dislocation of the peroneal tendons is seen lateral to the lateral malleolus.

FIGURE 5.49 Midfoot-Forefoot.

FIGURE 5.50 Medial Tendons.

FIGURE 5.51 Lateral Tendons.

FIGURE 5.52 Anterior Tendons.

As the peroneus brevis degenerates, it becomes C-shaped and wraps around the anterior aspect of the peroneus longus tendon. The peroneus brevis may also develop longitudinal tears and split into two subtendons. The peroneal tendons may be partially torn or completely ruptured. Partial tears can be subclassified as grade I (a thickened tendon) or grade II (a thinned attenuated tendon, representing more severe changes). Complete rupture, classified as grade III, is characterized by absence of the tendon on axial images located at the gap created by the rupture.

FIGURE 5.53 Posterior Tendons.

Anterior Tendons (Fig. 5.52)

The anterior tendons are also optimally evaluated in the axial plane. The four anterior tendons that run from medial to lateral are:

Tibialis anterior (the most likely of the extensor tendons to tear)
Extensor hallucis longus
Extensor digitorum longus
Peroneus tertius

Posterior Tendons (Fig. 5.53)

The posterior tendons, the Achilles tendon and plantaris tendon, are also evaluated on axial plane images.

The Achilles tendon is seen in cross-section and appears convex posteriorly and concave or flat anteriorly. Tendinosis is

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associated with a convex appearance to the tendon anteriorly, as well as tendon thickening and often increased intrasubstance signal. Tears and tendinosis suspected in the sagittal plane are confirmed and further characterized in the axial plane.

FIGURE 5.54 High Lateral Ligaments.

The plantaris tendon is commonly identified on axial MR images as a small separate tendon inserting medial to the Achilles tendon on the os calcis. Not uncommonly, when the Achilles tendon completely ruptures, the plantaris tendon remains attached to the os calcis and the plantaris may be mistaken for small intact medial fibers of an otherwise torn Achilles tendon.

FIGURE 5.55 Lateral Ligaments.

(3) Ligaments

Lateral Ligaments (Figs. 5.54 and 5.55)

Both the anterior and posterior syndesmotic ligaments follow an oblique upward course from the anterior and posterior lateral malleolus to the tibia and are seen on sequential axial images from superior to inferior through the distal tibia—fibula articulation. The tibial attachments are first seen on superior images and can be followed to their fibular insertions over the next three or four inferior images. Syndesmotic tears (anterior more commonly than posterior), sprains, and chronic thickening and scarring from old injury can be characterized on MR images.

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Several images inferior to the syndesmoses, the ATFL is encountered coursing obliquely anteromedially from the anteroinferior lateral malleolus to the anterolateral talus. The ATFL fibers are taut and dark. The distal aspect of the PTFL is seen at the same level, and the course of the ligament to its posterior talar insertion can be followed on the next two or three images superiorly. The origin of the CFL from the lateral malleolus is located at the distal tip of the lateral malleolus and can be followed inferiorly for two or three images as it passes medial to the peroneal tendons and inserts on the calcaneus. A torn ATFL may appear as complete obliteration of fibers or as a fluid-filled discontinuity across the ruptured ligament with retraction of wavy and lax fibers. Subacute tears demonstrate amorphous intermediate-signal scarring, with less surrounding inflammation and fluid. Chronic tears may manifest as severe attenuation of fibers or as chronically thickened and scarred fibers. Also, following a short to moderate interval after ATFL sprain/tearing, lateral impingement of the lateral gutter synovium may occur due to the resulting lateral ankle instability. Lateral impingement is manifested on axial MR images as severe synovitis, often with a synovial impingement mass within the lateral gutter deep to the ATFL and anterolateral capsule. Surgical débridement of the impingement mass and other synovitis and scarring in the lateral gutter may alleviate symptoms associated with lateral gutter syndrome.

Medial Ligaments (Fig. 5.56)

The medial ligaments make up the deltoid ligament complex. On axial images the deltoid ligament is located by a superior-to-inferior review of images starting with the medial malleolus. The first image inferior to the distal tip of the medial malleolus displays the superior aspect of the deltoid ligament. The deltoid is composed of a superficial and a deep component. The deep component sweeps inferolaterally from the tip of the medial malleolus and is visualized on axial images as a striated band of fibers coursing laterally from the medial malleolus to insert onto the talus one or two slices inferior to the medial malleolus. The posterior tibialis tendon is visualized coursing directly posteromedial to the deltoid. The superficial deltoid is broader and is seen as a broad, thin band of fibers just superficial to the deep deltoid component. The superficial fibers fan out anterior and posterior to the deep fibers and extend inferiorly to insert on the calcaneus, the navicular, and the more inferior anterior and posterior talus. The spring ligament is seen more inferiorly extending from the sustentaculum talus to the posteromedial process of the navicular. Similar to other ligaments, the deltoid may be strained or torn, or thickened and scarred.

FIGURE 5.56 Medial Ligaments.

Sample MRI Report

Clinical Information: Old ankle sprain, inversion injury, continued pain

Technique: Sagittal proton density with fat saturation, sagittal T1, coronal proton density with fat saturation, coronal T1, axial proton density with fat saturation, axial proton density without fat saturation

Findings: There is an osteochondral lesion in the medial aspect of the talus (Fig. 5.57A, B). There is a 3 mm (medial to

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lateral) × 8 mm (anterior to posterior) fragment of bone within the osteochondral bed (Fig. 5.57C, D). There is bone marrow edema associated with the osteochondral lesion (Fig. 5.57E). The bone marrow edema is in a 1-cm area. There is interruption of the subchondral plate in the area of the osteochondral lesion (Fig. 5.57F).

FIGURE 5.57 Sample Case.

Degenerative change is seen in the anterior aspect of the tibiotalar joint with anterior spurring (Fig. 5.57G) and mild bone marrow edema in the anterior distal talus (Fig. 5.57H). This is consistent with anterior osseous impingement of the ankle.

The subtalar joints are intact. The Achilles tendon is intact. The plantar fascia is intact. The anterior talofibular ligament is mildly scarred but intact (Fig. 5.57I). The posterior talofibular ligament, the anterior and posterior syndesmotic ligaments, and the deltoid ligament are intact. The posterior tibialis, flexor digitorum and flexor hallucis longus, the peroneal tendons, and the extensor tendons are intact.

Coronal images confirm the osteochondral lesion in the talar dome. The area of involvement is 5 mm × 12 mm. The actual fragment within the osteochondral bed is appreciated with an anterior-to-posterior dimension of approximately 8 mm.

Impression:

Medial osteochondral talar dome lesion. There is a fragment of osseous tissue within the osteochondral bed that may be attached by synovium. The fragment measures 8 mm anterior to posterior and 3 mm medial to lateral. This correlates with a stage III osteochondral lesion. There is associated bone marrow edema of 10 mm and subchondral sclerosis. There is irregularity of the overlying subchondral plate. There are also mild cystic changes in the adjacent portion of the talus, although no fluid is directly undermining the osteochondral lesion itself.
Anterior osseous impingement of the ankle with spurring of the anterior aspect of the tibiotalar joint and bone marrow edema demonstrated in the anterior distal tibia
Chronic thickening of the anterior talofibular ligament without disruption

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Anatomy of the Ankle and Foot

Pearls and Pitfalls

Anatomy of Ankle and Foot

The syndesmotic ligaments consist of the anterior syndesmotic or anterior inferior tibiofibular ligament and the posterior syndesmotic or posterior inferior tibiofibular ligament, the interosseous membrane, and the transverse tibiofibular ligament.
The transverse tibiofibular ligament represents the posterior labrum of the ankle and projects inferior to the posterior tibial margin.
The deltoid ligament consists of superficial and deep layers.
The ATFL is taut in plantarflexion.
The tibial slip is the posterior intermalleolar ligament.
The tendons of the deep calf and the neurovascular structures of the posterior compartment pass deep to the flexor retinaculum.

Compartments of the Leg

Anterior and posterior intermuscular septa and the interosseous membrane define the major compartments of the lower leg (Fig. 5.58):

The anterior compartment of the leg consists of the tibialis anterior, the extensor hallucis longus, the extensor digitorum longus, and the peroneus tertius muscles. The neurovascular bundle contains the deep peroneal nerve and the anterior tibial artery.
The posterior compartment is divided into superficial and deep sections by deep transverse fascia. The superficial posterior compartment consists of the gastrocnemius, the plantaris, and the soleus muscles. The deep posterior compartment contains the popliteus, the FDL, the FHL, and the tibialis posterior muscles. The neurovascular supply is provided by the tibial nerve and posterior tibial artery.
The anterolateral compartment contains the peroneus longus and peroneus brevis muscles. The neurovascular supply is from the superficial peroneal nerve and branches of the peroneal artery.

Distal Tibiofibular Joint

The distal or inferior tibiofibular syndesmosis is a fibrous joint strongly connected by the interosseous ligament, which is continuous with the crural interosseous membrane. The tibiofibular joint is defined by the bony anatomy of the convex medial aspect of the distal fibula and the corresponding concavity on the lateral aspect of the distal tibia (Fig. 5.59).¹³^,¹⁴ The strong anterior and posterior inferior tibiofibular ligaments reinforce the joint anterior and posterior to the interosseous ligament. The transverse tibiofibular ligament represents the distal deep fibers of the posterior inferior tibiofibular ligament. Using ankle arthroscopy, we have identified four common variations of the arrangement of the posterior inferior tibiofibular ligament relative to the transverse tibiofibular ligament. The AITF extends obliquely from the anterior border of the lateral malleolus upward and medially to the anterolateral tibial tubercle more superiorly.¹³^,¹⁴ The flat band of fibers may be divided into two or three bands, or may present as a multifascicular structure. The PITF is smaller than the AITF and is quadrilateral in shape.¹³^,¹⁴ Fibers originate from the posterior border of the lateral malleolus and extend superomedially onto the posterolateral tibial tubercle. The transverse tibiofibular ligament (the deep component of the posterior inferior tibiofibular ligament) is a strong thick band that extends from the posterior fibular tubercle and upper digital fossa and inserts on the posterior aspect of the tibial articular surface, reaching to the medial malleolus. The transverse tibiofibular ligament forms a posterior labrum by projecting inferiorly to the posterior tibial margin, thus deepening the tibial articular surface of the tibiotalar joint. The transverse ligament is in contact with the posterolateral talar articular cartilage surface. Posterior impingement may be caused by hypertrophy of the transverse ligament and its synovial covering.

Ankle Joint

The ankle or tibiotalar joint is a synovial articulation formed by the distal tibia and fibula. Although it is often described as a hinge joint between the talus and the mortise (Fig. 5.60), the apex of rotation of the ankle joint is not fixed, as it would be in a simple hinge joint. In fact, the apex of rotation changes during extremes of plantarflexion and dorsiflexion. The articular surfaces of the tibiotalar joint are covered with hyaline cartilage (Fig. 5.61), and the fibrous capsule attaches to the articular margins of the tibia, fibula, and talus, with an anterior extension onto the talar neck. The capsule, which is thin anteriorly and posteriorly, is reinforced by strong collateral ligaments. The socket, framed by the distal tibia and medial and lateral malleoli, is wider anteriorly than posteriorly and is completed posteriorly by the transverse tibiofibular ligament (Fig. 5.62). The synovial membrane is attached to all articular margins and covers the intracapsular part of the talar neck.

Ankle Joint Ligaments

Deltoid Ligament

The medial or deltoid ligament is a strong band attached by its apex to the border of the medial malleolus and consists of superficial and deep fibers (Fig. 5.63). The triangular, superficial part of the deltoid is formed by the tibionavicular fibers anteriorly, the tibiocalcaneal fibers medially (the strongest component of the superficial deltoid), and the superficial posterior tibiotalar fibers posteriorly. Behind the navicular tuberosity, tibionavicular fibers blend with the medial margin of the plantar calcaneonavicular or spring ligament. A tibioligamentous

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fascicle inserts onto the superior border of the calcaneona vicular ligament. The deep part of the deltoid, which is rectangular, consists of a small anterior component (the anterior tibiotalar ligament) and a strong posterior component (the posterior tibiotalar ligament) (Fig. 5.64). The posterior tibiotalar ligament represents the strongest part of the entire medial ligament complex. The deep portion of the deltoid ligament, covered by synovium, is intra-articular.

FIGURE 5.58 ● transverse section through the midcalf shows the anterior and lateral compartments and their contents.

FIGURE 5.59 ● (A) The inferior tibiofibular joint is a fibrous joint. (B) Arthroscopic view of the right ankle demonstrates the syndesmotic ligament and the trifurcation. The trifurcation includes the fibula in the background with the tibia superior and the talus inferior. Approximately 20% of the ligament is intra-articular, and it runs at a 45° angle from the tibia to the fibula.

FIGURE 5.60 ● The bones of the ankle joint and their articular surfaces.

FIGURE 5.61 ● An anterior view of the ankle joint and its articular surfaces is revealed by removal of the capsule.

FIGURE 5.62 ● An oblique view of the wedge-shaped articular socket of the ankle joint.

FIGURE 5.63 ● (A) The medial collateral ligament of the ankle joint can be seen after removal of the capsule. (B) In the right ankle, the deep portion of the deltoid ligament runs from the medial malleolus on the right to the talus on the left.

Lateral Ligament

Three distinct bands make up the weaker lateral ligament of the ankle (Fig. 5.65): the ATFL, the CFL, and the PTFL. The posterior inferior tibiofibular ligament lies superior to the horizontally oriented PTFL. The inferior part of the posterior inferior tibiofibular ligament is also referred to as the transverse tibiofibular ligament (Fig. 5.66). In dorsiflexion, the posterior talofibular (Fig. 5.67) and posterior inferior tibiofibular ligaments diverge like the blades of a scissors, and in plantarflexion they lie edge to edge.

FIGURE 5.64 ● A coronal section through the ankle (tibiotalar joint) and talocalcaneal joints shows their articular surfaces.

The anterior talofibular ligament, which is a flat, relatively strong ligament (although the first to fail in lateral ligament injuries), may be divided into two bands. This ligament is taut in plantarflexion.¹³^,¹⁴ The CFL, the largest of the lateral collateral ligaments, is a strong, cord-like structure. It is deep to the peroneal tendons and their sheaths and extends from the distal anterior border of the lateral malleolus inferiorly and posteriorly to insert on the upper part of the lateral surface of the calcaneus. The PTFL, the strongest and deepest portion of the lateral ligament, is intracapsular but extrasynovial. The posterior intermalleolar ligament or tibial slip originates on the PTFL, which inserts on the posterior tibia and posterior surface of the medial malleolus and blends with the transverse tibiofibular ligament.

FIGURE 5.65 ● (A) The lateral collateral ligament of the ankle joint can be seen after removal of the capsule. (B) The anterior talofibular ligament is clearly demonstrated in this right ankle. The fibula is to the left, the talus to the right. It forms the floor of the lateral gutter of the ankle.

FIGURE 5.66 ● (A) A posterior view of the ankle joint shows the articular surface of the talus after removal of the capsule. (B) The posterior ankle ligaments in the right ankle. The thick structure to the left is the posterior inferior tibiofibular ligament. The structure to the right is the transverse tibiofibular ligament. In this picture, the tibia is on top and the talus is below.

FIGURE 5.67 ● Posterior coronal FS PD FSE image at the level of the posterior talofibular ligament (PTF) and posterior tibiotalar ligament (PTT). TP, tibialis posterior; FDL, flexor digitorum longus; PB, peroneus brevis tendon; PL, peroneus longus tendon.

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Tarsal Joints

Subtalar Joint

The subtalar or talocalcaneal joint is the posterior articulation between the talus and the calcaneus. Functionally, the subtalar joint includes the talocalcaneal part of the talocalcaneonavicular joint (Fig. 5.68). The strong t alocalcaneal or interosseous ligament attaches to the sulcus tali and sulcus calcanei. The capsule is strengthened by the medial and lateral talocalcaneal ligaments.

Talocalcaneonavicular Joint

The talocalcaneonavicular joint is a multiaxial articulation at the triple-faceted anterior-inferior talar surface with the talar head, the posterior concavity of the navicular bone, the middle and anterior talar facets of the calcaneus, and the fibrocartilaginous superior surface of the plantar calcaneonavicular (i.e., spring) ligament. The talonavicular, plantar calcaneonavicular, and calcaneonavicular parts of the bifurcated ligament support the osseous components of this joint.

Calcaneocuboid Joint

The calcaneocuboid joint is a separate joint with its own capsule between the anterior calcaneus and the posterior surface of the cuboid. The calcaneocuboid and the talonavicular part of the talocalcaneonavicular joint form the midtarsal joint (Fig. 5.69). Support is provided by the fibrous capsule, the calcaneocuboid part of the bifurcate ligament, and the long plantar and plantar calcaneocuboid (i.e., short plantar) ligaments. The bifurcate ligament is a strong, Y-shaped ligament on the dorsal surface of the joint, with attachments to the anterior dorsal calcaneal surface proximally and to the dorsomedial aspect of the cuboid and dorsolateral aspect of the navicular bone distally. The long plantar ligament, also a strong ligament, is located along the plantar surface. It is attached to the undersurface of the calcaneus, the cuboid, and the bases of the third, fourth, and fifth metatarsal bones. A tunnel for the peroneus longus is created as it bridges the tendon groove on the plantar surface of the cuboid. The plantar calcaneocuboid, or short plantar ligament, is a wide, short band attached to the anterior tubercle on the plantar aspect of the calcaneus and the adjacent surface of the cuboid.

Other Tarsal Joints

The cuneonavicular joint is a synovial joint formed by the navicular bone and the three cuneiform bones (see Fig. 5.69). The cuboideonavicular joint is a fibrous joint. The intercuneiform and cuneocuboid joints are synovial joints continuous with the cuneonavicular joint cavity.

Regional Anatomy of the Ankle

Retinacula

The extensor (Fig. 5.70) and flexor (Fig. 5.71) retinacula are formed by thickened deep fascia and maintain the position of the long tendons crossing the ankle. The superior extensor retinaculum attaches to the distal anterior fibula and tibia and invests the tibialis anterior tendon medially. The Y-shaped inferior extensor retinaculum attaches to the anterolateral part of the calcaneus (the stem) and extends to the medial malleolus (the upper limb) and the medial plantar fascia (the lower limb). The tibialis anterior, the extensor hallucis longus, the extensor digitorum longus, and the peroneus tertius tendons divide the upper limb of the retinaculum into superficial and deep layers. The flexor retinaculum extends inferiorly and posteriorly from the medial malleolus to the medial calcaneal surface. The tendons of the deep calf muscles (the FDL, the FHL, and the tibialis posterior) and the neurovascular structures in the posterior compartment pass underneath the flexor retinaculum before entering the foot.

The SPR extends inferiorly and posteriorly from the lateral malleolus to the lateral calcaneal surface, binding the peroneus longus and brevis tendons. The inferior peroneal retinaculum is attached to the peroneal trochlea and calcaneus above and below the peroneal tendons.

FIGURE 5.68 ● (A) In this gross photograph of the talocalcaneal and talonavicular joints, the talus has been disarticulated and turned over. (B) Arthroscopic picture of the interosseous ligament in the left ankle. The interosseous ligament is very thick and runs in an oblique vertical direction from the talus to the calcaneus. The talocalcaneal articulation is seen to the right of the ligament. (C) Talocal-caneal and talonavicular joints with the talus everted to demonstrate the talar and calcaneal articular surfaces.

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Anterior Structures

The saphenous nerve, the great saphenous vein, and the medial and lateral branches of the superficial peroneal nerve pass anterior to the extensor retinaculum in a medial-to-lateral direction. The tibialis anterior tendon, the extensor hallucis longus tendon, the anterior tibial artery with venae comitantes, the deep peroneal nerve, the extensor digitorum longus tendon, and the peroneus tertius pass deep to or through the extensor retinaculum in a medial-to-lateral direction (Figs. 5.72 and 5.73).

Posterior Structures

The tibialis posterior tendon (PTT), the FDL, the posterior tibial artery with venae comitantes, the tibial nerve, and the FHL flow in a medial-to-lateral direction and are located posterior to the medial malleolus and deep to the flexor retinaculum. The sural nerve and the small saphenous vein pass posterior to the lateral malleolus, superficial to the SPR. The peroneus longus and brevis tendons course posterior to the lateral malleolus deep to the SPR. The pre-Achilles fat pad and the Achilles tendon are located posterior to the ankle. The plantaris tendon is identified medial to the Achilles tendon and joins the anteromedial aspect of the Achilles tendon at the level of the subtalar joint.

Foot

Muscles of the Sole of the Foot

Deep to the plantar aponeurosis (Fig. 5.74), the muscles of the sole of the foot are divided into four layers from superficial to deep:

The first layer consists of the abductor hallucis, the flexor digitorum brevis, and the abductor digiti minimi (Fig. 5.75).
The second layer consists of the quadratus plantae, the lumbricals, the flexor digitorum longus tendons, and the flexor hallucis longus tendons (Fig. 5.76).
The third layer includes the flexor hallucis brevis, the adductor hallucis, and the flexor digiti minimi brevis (Fig. 5.77).
The fourth layer is made up of the interossei plantares (Fig. 5.78), the peroneus longus tendon, and the tibialis posterior tendon (Fig. 5.79).

Arches of the Foot

The arches of the foot, which provide support for bipedal motion and forward propulsion, are as follows:

The medial and lateral longitudinal arches are formed by the tarsal and metatarsal bones (Fig. 5.80). The higher medial arch, which forms the instep of the foot, consists of the calcaneus, the talus, the navicular, the three cuneiform bones, and the medial three metatarsals (see Fig. 5.80; Fig. 5.81). The plantar calcaneonavicular (i.e., spring) ligament helps support the head of the talus, which articulates with the navicular anteriorly and the sustentaculum tali posteriorly (Fig. 5.82). The lateral arch consists of the calcaneus, the cuboid, and the lateral two metatarsals.
The transverse arch of the foot consists of the five metatarsal bones and the adjacent cuboid and cuneiform bones.

FIGURE 5.69 ● (A) Vertical and horizontal sectioning of the foot and ankle reveals the interrelationships of the tarsal joints. (B) Tibiotalar, subtalar, talonavicular, and navicular cuneiform joints are shown on a FS PD FSE sagittal image. The posterior facet of the subtalar joint is identified (arrows). T, talus; C, calcaneus; N, navicular bone; Cun, cuneiform bone; Cub, cuboid.

FIGURE 5.70 ● (A) The lateral aspect of the ankle and foot shows the peroneal tendons and the retinacula. (B) Lateral view of the ankle tendons and tendon sheaths.

FIGURE 5.71 ● (A) The long tendons and the principal vessels and nerves from the posterior compartment of the leg pass deep to the flexor retinaculum to enter the sole of the foot. (B) A medial view of the ankle tendons and tendon sheaths.

FIGURE 5.72 ● The principal structures of the dorsum of the ankle and foot can be seen after removal of the extensor retinaculum.

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Body weight is transmitted through the anterior and posterior pillars of the arches. The posterior pillars of the medial and lateral arches are the tubercles on the inferior calcaneal surface. The anterior pillars of the medial and lateral arches are formed by their respective metatarsal heads.

Metatarsophalangeal and Interphalangeal Joints of the Foot

The metatarsophalangeal joints are ball-and-socket articulations between the metatarsal head and the base of the proximal phalanx and the fibrocartilaginous plantar plate (Figs. 5.83 and 5.84). The interphalangeal joints are hinge joints that permit flexion and extension (Fig. 5.85).

Anatomic Variants

A number of normal anatomic variants of the ankle are seen on MR images and may be misleading.¹⁵ These have been characterized in studies of asymptomatic patients and include the following:¹⁶

In the posterior tibiotalar joint, a low-signal-intensity cortical irregularity may mimic the appearance of osteonecrosis.
The posterior inferior tibiofibular ligament may be mistaken for a loose body in the posterior capsule on midsagittal images.
Occasionally, the intact PTFL appears as an attenuated structure with signal inhomogeneity.
Less frequently, fluid in the peroneal tendon sheath may be confused with a longitudinal tendon tear.
In one patient, axial planar images revealed marked asymmetry and hypertrophy of the peroneus brevis muscle and tendon as a normal anatomic variant.

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An accessory soleus muscle (Fig. 5.86) is an anatomic variant that may present as a mass in the distal calf or medial ankle.¹⁷^,¹⁸
The tensor fasciae suralis represents an anomalous muscle and tendon that contributes to the Achilles tendon and originates from the semitendinosus muscle.¹⁹ It may be mistaken for a posterior thigh, popliteal, calf, or Achilles tendon mass or lesion. MR imaging demonstrates imaging characteristics of either muscle or tendon.²⁰
The flexor digitorum accessorius is an anomalous muscle located posterior to the FHL and has been associated with tarsal tunnel syndrome, although it is usually asymptomatic (Fig. 5.87).
The peroneus quartus muscle is present in 13% to 22% of individuals (Fig. 5.88). This anatomic variant originates from the peroneus brevis muscle and inserts onto the peroneal tubercle of the calcaneus.²¹

FIGURE 5.73 ● (A) A transverse section through the ankle immediately above the joint cavity shows its anterior and posterior relations. (B) T1 axial MR arthrographic image at the level of the talar dome. Note the position of the distal plantaris tendon (p) medial to the Achilles tendon. MM, medial malleolus; tp, tibialis posterior; fdl, flexor digitorum longus tendon; pta, posterior tibial artery; arrow, tibial nerve; fhl, flexor hallucis longus tendon; pitf, posterior inferior tibiofibular ligament; p, plantaris tendon; A, Achilles tendon; pb, peroneus brevis tendon; pl, peroneus longus tendon; LM, lateral malleolus; T, talus; edl, extensor digitorum longus tendon; open arrow, deep peroneal nerve; white arrows, anterior tibial artery; ehl, extensor hallucis longus tendon; ta, tibialis anterior; gs, greater saphenous vein; tn, tibionavicular ligament. (C) The flexor hallucis longus tendon is an extra-articular structure that cannot usually be seen within the ankle. It normally runs in a sheath just posterior to the ankle capsule and medial to the transverse ligament.

In addition, the orientation of a tendon relative to the main magnetic field (B₀) affects its MR appearance. When the orientation approximates the “magic angle” of 55°, the collagen may demonstrate intermediate signal intensity with loss of the normal low spin-density characteristics (Fig. 5.89).²¹ The magic-angle effect is prominent on short-TE spin-echo or GRE images. T2-weighted images minimize the magic-angle signal intensity. On sagittal images, the peroneus longus and FHL tendons are commonly affected and often display intermediate signal intensity in their midportions. Changes in ankle position that alter the orientation relative to the main magnetic field can be used to confirm that the tendon is normal.

Most ankle ligaments, including the anterior talofibular, the calcaneofibular, and the superficial deltoid, show uniform low signal intensity on all pulse sequences. Mixed or striated signal intensity, however, can be seen in the posterior talofibular, posterior inferior tibiofibular, deep deltoid, and interosseous talocalcaneal ligaments.

Sesamoid bones within the peroneus longus (os peroneum) (Fig. 5.90) or the distal tibialis posterior normally demonstrate

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hyperintensity on T1-weighted images, secondary to fatty marrow. This finding should not be mistaken for tendon degeneration or a tear. Accessory bones, including the os tibiale externum (an accessory navicular bone medial to the navicular) and the os trigonum (located posterior to the talus and occurring approximately 10% of the time), represent commonly seen secondary ossification centers. These are normal variants that may be misinterpreted as a fracture or loose body.²¹

FIGURE 5.74 ● The plantar aponeurosis, deep fascia, and a cutaneous nerve are revealed by removing the skin of the sole of the foot.

FIGURE 5.75 ● (A) The superficial intrinsic muscles and plantar nerves are shown after removal of the deep fascia, part of the plantar aponeurosis, and the second fibrous tendon sheath. In this specimen, the flexor digitorum brevis has only three tendons. (B) The flexor digitorum brevis (FDB) muscle and the tendons of the first layer of plantar muscles are shown on a T1-weighted axial image.

FIGURE 5.76 ● (A) The tendons of the flexor digitorum longus, the flexor hallucis longus, the flexor accessorius, and the lumbricals can be seen after removal of the medial and lateral plantar nerves and the tendons of the flexor digitorum brevis. (B) All of the second layer of plantar muscles—the quadratus plantae muscle (QP), the lumbrical muscles (L), the tendons of the flexor digitorum longus (FDL), and the tendon of the flexor hallucis longus (FHL)—are shown on a T1-weighted axial image.

FIGURE 5.77 ● (A) The deep intrinsic muscles are revealed by removal of the long flexor tendon and abductors of the great and little toes. (B) The transverse head (th) and oblique head (oh) of the adductor hallucis muscle (AH) and the flexor hallucis brevis muscle (FHB) of the third layer of plantar muscles are shown on a T1-weighted axial image.

FIGURE 5.78 ● (A) The interosseous muscles and the plantar arterial arch are exposed by removal of the adductor hallucis. (B) The dorsal interosseous muscles (I) of the fourth layer of plantar muscles are shown on a T1-weighted axial image.

FIGURE 5.79 ● (A) The tendons of the peroneus longus and the tibialis posterior lie deep in the sole of the foot. The long plantar ligament has been preserved. (B) T1-weighted axial image showing the long plantar ligament (LPL) and the course of the peroneus longus (pl) tendon as it passes along the inferior surface of the cuboid within an osseous groove (arrow). An inferior extension of the LPL creates a tunnel for the passage of the pl tendon proximal to its insertion on the base of the first metatarsal and medial cuneiform. pb, peroneus brevis tendon; C, calcaneus. (C) T2* axial image displays the tibialis posterior (TP), the plantar calcaneonavicular ligament (Plantar cn), and the plantar calcaneocuboid ligament (Pcc). Cu, cuboid; C, calcaneus; N, navicular bone. (D) Ligaments and tendons of the plantar surface of the foot (superficial layer).

FIGURE 5.80 ● The dorsal aspect of the bones of the foot shows the medial and lateral longitudinal arches.

FIGURE 5.81 ● (A) The medial aspect of the bones of the foot shows the medial longitudinal arch (blue). (B) The transverse arch of the foot in coronal section at the level of the first metatarsal sesamoids.

FIGURE 5.82 ● A sagittal section of the foot shows the medial longitudinal arch.

FIGURE 5.83 ● (A) A sagittal section through the third toe shows the metatarsophalangeal and interphalangeal joints. (B) A T1-weighted sagittal image demonstrates the tendon of the flexor digitorum longus (FDL) and the plantar plate (PP).

FIGURE 5.84 ● The internal features of the first metatarsophalangeal joint are revealed when part of the capsule and the distal part of the metatarsal bone are removed.

Small fluid collections in the ankle joint, including the tibiotalar and subtalar joints as well as the ankle tendon sheath, are common in asymptomatic individuals.²² Relatively larger amounts of fluid, however, are usually associated with the FHL tendon. Fluid is not commonly seen in the extensor tendons. The amount of fluid in normal or asymptomatic and symptomatic patients may be similar in volume and distribution. Cystic change with hyperintensity in the anterolateral third of the calcaneus can be a normal finding (Fig. 5.91). Bone cysts, including intraosseous lipoma, however, may also occur in this area.

Pathology of the Ankle and Foot

Osteochondral Lesions

Pearls and Pitfalls

Osteochondral Lesions

Osteochondral lesion of the talus (OLT) is the accepted terminology and should be used in place of transchondral fracture, osteochondral fracture, or osteochondritis dissecans.
Osteochondral lesions may involve the posteromedial or anterolateral talus.
An equivalent tibial lesion is also referred to as an osteochondral lesion (osteochondral lesion of the tibia).
It is important not to overestimate the size of the lesion by including adjacent marrow edema in the dimensions of the lesion proper.

Osteochondral lesion of the talus (OLT) is the accepted term for a variety of disorders, including transchondral fracture, osteochondral fracture, osteochondritis dissecans, and talar dome fracture. Osteochondral lesions of the medial and lateral talar dome involve the articular cartilage and subchondral bone and have a high association with antecedent trauma (e.g., torsional impaction). They are responsible for 0.09% of all fractures, 1% of talar fractures, 4% of cases of osteochondritis, and 6.5% of sprained ankles. They occur more often in males (67%) than females (33%), usually approximately 25 years of age, although there is a second peak of occurrence in the fifth to sixth decades. They are not commonly seen in children.

Etiology, Pathology, and Clinical Features

Trauma remains the best-accepted theory for the etiology of OLT, which is thought to represent the chronic phase of a compressed or avulsed talar dome fracture.¹³ Anatomically relevant features include the wider anterior talus, the narrower posterior talus, and the ankle mortise (the medial and lateral malleolus). Direct trauma or repetitive microtrauma may contribute to the development of this lesion in individuals predisposed to talar dome ischemia. Subchondral fractures are susceptible to AVN, and an osteonecrotic process leads to subchondral fracture and collapse. Increased joint pressure forces synovial fluid into the fracture site, preventing healing. Torsional impaction may also be a contributing factor. Lesions are bilateral in 10% to 30% of cases.

The lateral and medial surfaces of the talus are involved in approximately 40% and 60% of osteochondral lesions of the talus, respectively. Lateral lesions (Fig. 5.92), which tend to be wafer-shaped and thin, are almost always (94%) caused by trauma. The most common mechanism is a strong inversion force with dorsiflexion of the foot and internal rotation of the tibia. The lateral talar margin is impacted or compressed against the medial fibula, causing shear end compression. Lateral lesions usually occur in the mid- to anterior aspect of the talar dome.

Medial lesions, which are usually cup-shaped and deeper than lateral lesions (see Fig. 5.92), are not as strongly associated with a history of antecedent trauma. The mechanism of injury is a strong inversion force with plantarflexion of the foot and lateral rotation of the tibia on the talus (external rotation). The posteromedial edge of the talar dome is impacted against the posteromedial tibia with shear stress injury (Fig. 5.93). Lesions are bilateral in 10% to 30% of cases.

If bone alone is affected by the shear stress, the result is a subchondral fracture with intact articular cartilage (Fig. 5.94). If the stress exceeds the ultimate strength of both bone and cartilage, the result is a complete displaced osteochondral lesion.²³

Classic pathologic findings include a soft, frayed cartilage, subchondral plate defects or cysts, loose bodies, joint effusion, and a stable or unstable fragment in the crater. Clinically, the patient presents with some or all of the following:

Pain: persistent ankle pain after an inversion injury or chronic ankle pain and sprains. If the collateral ligament fails to rupture because articular surfaces are in direct contact, pain may be minimal.
Stiffness, swelling, and reduced range of motion
Ecchymosis
Catching, clicking, locking, or giving way

Diagnosis and Staging

There are several staging systems for OLT. A surgical grading system, based on the articular cartilage, classifies lesions into six categories:

Grade A: The articular cartilage is smooth, intact, and soft.
Grade B: The articular cartilage has a rough surface.
Grade C: Fibrillations and fissures in the cartilage
Grade D: A flap and exposed bone
Grade E: A loose, undisplaced fragment
Grade F: The fragment is displaced.

FIGURE 5.85 ● A longitudinal section through the great toe shows its joints.

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Berndt and Harty²⁴ have developed a four-part staging system for characterizing OLT based on plain radiographs:

Stage I: A subchondral compression fracture of the talus with no ligamentous sprain. Radiograph results are negative, and lesions may be painless.
Stage II: A partially detached osteochondral fragment with a hinge or flap of articular cartilage. A T2- or T2*-weighted image may be necessary to identify the osteochondral fragment.
Stage III: A complete nondisplaced fracture remains within the bony crater.
Stage IV: Detachment with a loose osteochondral fragment

Although lesions in stages II to IV are themselves painless, they may be associated with a painful sprain or rupture of the collateral ankle ligaments.

To improve on the correlation between arthroscopic and conventional radiographic findings, another classification system, based on CT findings, was developed by Ferkel and Sgaglione.²⁵ CT is performed in the direct axial and coronal planes at 1.5 mm, in association with sagittal reformations. (CT scans are performed for a known diagnosis of OLT, whereas MR imaging is preferred in patients with ankle pain of unknown etiology.) The CT classification progresses from stage I to stage IV:

Stage I: A cystic lesion of the talar dome with an intact roof
Stage IIA: A cystic lesion with communication to the talar dome surface
Stage IIB: An open articular surface lesion with an overlying nondisplaced fragment
Stage III: A nondisplaced lesion with lucency
Stage IV: A displaced fragment

Both CT and MR imaging provide more information about the size and location of the lesion than does conventional radiography.

MR imaging can also be used to stage OLT, and it has the advantage of detecting radiographically occult lesions that in certain cases may not be evident on CT. In a direct comparison of CT with MR imaging, Anderson et al.²⁶ found that, compared with MR imaging, CT did not detect stage I lesions in 4 of 24 patients. The following proposed four-stage classification of OLT lesions is based on MR findings:

Stage I: Subchondral trabecular compression. Radiograph results are negative, bone scans are posi-tive, and marrow edema is seen on MR imaging (Fig. 5.95).
Stage IIA: A subchondral cyst (Fig. 5.96)
Stage IIB: Incomplete separation of the fragment (Fig. 5.97)
Stage III: Fluid around a nondetached, nondisplaced fragment (Figs. 5.98 and 5.99)
Stage IV: A displaced fragment (Fig. 5.100)

Two classification systems have been developed based on arthroscopic findings in OLT. In the system proposed by Pritsch et al.,²⁷ the appearance of the overlying cartilage is organized into three grades:

FIGURE 5.86 ● The accessory soleus muscle (A, sagittal image; B and C, axial images) originates from the anterior surface of the soleus or from the fibula and soleal line of the tibia. The variable insertion of the accessory soleus includes sites along the Achilles tendon, the superior surface of calcaneus, the muscle or fleshy insertion on the superior surface of the calcaneus, the muscular or fleshy insertion on the medial calcaneus, and the tendinous insertion on the medial calcaneus.

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Grade 1: The cartilage is intact, firm, and shiny.
Grade 2: The articular cartilage is intact but soft.
Grade 3: The cartilage is frayed.

Another arthroscopic staging system was developed by Cheng et al.²⁸ after reviewing 100 consecutive ankle arthroscopies.

MR Appearance

As mentioned, results of x-rays in the early stages of OLT may be negative, and the lesions may not be detected until a necrotic focus is observed.²⁶ Necrosis is characterized by increased bone density in the necrotic focus and surrounding demineralization secondary to increased vascularization. In addition, it is not possible to assess the integrity of hyaline articular cartilage surfaces in osteocartilaginous defects with conventional radiographs or CT scans. With MR imaging, however, tibiotalar anatomy can be displayed in the coronal, axial, or sagittal planes to identify the talar defect and the presence of an avulsed body fragment. Subchondral marrow and articular cartilage surfaces are uniquely demonstrated on MR images. The normal hyaline articular cartilage surface of the talar dome demonstrates intermediate signal intensity on T1- and T2-weighted images, low to intermediate signal intensity on FS PD FSE images, and high signal intensity on T2*-weighted images.

In OLT, the following MR findings are key:

A detached cortical fragment that remains low in signal intensity
Adherent hyaline articular cartilage, reparative fibrocartilage, and associated fibrous tissue

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A low- or intermediate-signal-intensity bony defect of the talus on T1-weighted images, depending on the degree of synovial fluid and fibrous tissue, respectively
Increased-signal-intensity synovial fluid contents on FS PD FSE images
Peripheral areas of low signal intensity within the subchondral bone on T1- and FS PD FSE images, which correlate with reactive bone sclerosis on plain radiographs
Abnormalities of the articular surface, including regions of cartilage thinning, bowing, nodularity, or disruption²⁹
Accumulation of joint fluid at or undermining the cartilage surface, indicating small fissures or breaks

FIGURE 5.87 ● The flexor digitorum accessorius longus muscle is located posterior to the flexor hallucis longus and courses through the tarsal tunnel with the posterior tibial neurovascular bundle.

FIGURE 5.88 ● The peroneus quartus (PQ) originates from the distal third of the lower leg, including the peroneal muscles, and inserts onto the calcaneus at and proximal to the lateral malleolus. The PQ is located medial or posterior to the peroneal tendons.

On STIR (including FSE STIR) and FS PD FSE sequences, there are large areas of adjacent subchondral talar marrow edema or hyperemia, which are hyperintense compared with the low signal intensity observed on T1-weighted images. These subchondral changes should not be misinterpreted and do not indicate that the overlying osteochondral lesion is more extensive or more aggressive than the focal and smaller superficially located lesion. In contrast to AVN of the talus, the marrow hyperemia associated with the osteochondral lesion is usually less extensive and directly radiates from the lesion. Early AVN of the talus may be seen in association with a more diffuse hyperemia or edema of the entire talar head and body.

On sagittal or coronal images, a focal, upward bowing of the hyaline cartilage overlying the bony defect may be demonstrated. The cartilage may be deformed or bowed without disruption (Fig. 5.101) (frequently showing softening at surgery), or both articular cartilage surface and bone may be involved in a complete lesion (when the shear stress surpasses the strength of both).²³ A postsurgical fibrocartilaginous scar can appear as an intermediate-intensity, focal area of thickening, bridging a cartilaginous defect. T2*-weighted images are useful for identification of small areas of cartilage disruption. However, FS PD FSE and STIR images are more sensitive.²³

MR imaging identifies both the presence of undermining fluid and fragment displacement. Fluid transgressing articular cartilage and subchondral bone edema can be identified routinely on FS PD FSE and STIR images with greater sensitivity than with corresponding FS PD FSE or T2*-weighted images. De Smet et al.³⁰ have correlated the stability of the osteochondral fragment with signal intensity on T2-weighted images. They found an irregular high-signal-intensity zone at the fragment—talar interface in partially attached fragments, whereas a complete ring of fluid signal intensity surrounded the lesion in unattached fragments. Granulation tissue may also produce a high-signal-intensity band at the fragment—subchondral bone interface, which should not be misinterpreted as articular cartilage violation.

Intravenous contrast administration may help to evaluate the congruity of the articular cartilage surface and to depict subchondral hyperemia and synovial tissue hypertrophy. Intra-articular contrast (MR arthrography) with FS is used to directly evaluate the flow of contrast over the articular cartilage surface of the talar dome. This is useful in identifying unstable and free fragments.

Osteochondral lesions may also involve the tibia. Coronal images that allow separation of tibial and talar chondral surfaces facilitate localization of the lesion to the tibial side of the ankle joint (Fig. 5.102).

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Value of MR Imaging

Since conventional radiographs are not sensitive to early lesions, immobilization and surgery may be delayed, resulting in arthritis in 50% of cases. MR imaging of the talar dome is more accurate than CT scanning and complements diagnostic arthroscopic examination of the tibiotalar joint in early diagnosis.

Although conventional radiographs are still the first choice for initial evaluation of patients with suspected osteochondral defects, MR imaging offers the ability to assess both the talar defect and the integrity of overlying cartilage surfaces. MR depiction of an intact articular surface, for example, may assist in the decision to use more conservative treatments, such as drilling, and obviate the need for surgical excision and curettage. Although the ultimate treatment decision in an osteochondral lesion is determined at surgery, preoperative MR imaging can help to determine whether the lesion is loose.

FIGURE 5.89 ● Increased signal intensity involving the peroneus longus tendon just proximal to the peroneal tubercle. This apparent signal intensity increase occurs when the orientation of the collagen fibers in the tendon approximates the magic angle of 55° with the main magnetic vector. T1, PD, and GRE sequences that use a short TE (typically <30 msec, often 10–20 msec) are susceptible to this effect. T2-weighted and FS PD FSE images with longer TE values minimize the magic-angle effect. The normal hypointense peroneus longus is seen at the level of the peroneal tubercle in B. (A, B) Axial T1-weighted images. (C) Sagittal T1-weighted image.

Treatment

Treatment protocols for osteochondral lesions of the talus vary depending on the stage of the lesion and whether it is acute or chronic. Without treatment there is usually progression to joint stiffness and ankle instability. Healing typically results in a stable fragment, although healing plus motion may result in the development of fibrous tissue at the fracture site plus sequestration. Degenerative arthritis is a not uncommon final outcome.

Conservative management is appropriate for stage I and II lesions and medial stage III lesions. For stage I lesions, reduced

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activity and limited ankle motion may be sufficient. For acute stage II lesions, casting is usually required.

FIGURE 5.90 ● Normal marrow fat signal intensity associated with an asymptomatic os peroneum. The os peroneum is an accessory ossicle within the substance of the distal peroneus longus tendon near the cuboid.

Stage III and IV lesions require surgery for healing. Approaches include:

Free fragment excision
Curettage
Drilling
Abrasion arthroplasty
Microfracture (Fig. 5.103).

A drilled or abraded base permits fibrocartilaginous ingrowth in lesions with a nonreplaceable fragment. Complications include locking of the joint, which occurs with larger bone fragments; degenerative arthritis, which is more likely to occur with lateral, often symptomatic, lesions; and nonunion of the fracture. These often lead to traumatic osteoarthritis.

Arthroscopic treatment of talar dome fractures has relatively low morbidity and complication rates.³¹ Cystic areas are bone-grafted if cartilage is intact; otherwise, the cyst is corrected with drilling or abrasion of the base. Arthroscopic treatment for acute osteochondral lesions of the talus is different from that for chronic lesions. Acute lesions may require the use of CT or MR imaging to identify the lesion and characterize the size, morphology, and stage. In displaced lesions, arthroscopy is performed with possible open pinning or removal of the osteochondral lesion. Acute lesions are palpated with a small joint probe. The chondral fragment is then assessed

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to determine whether there is enough bone to permit healing, if reattachment with absorbable pins, Kirschner wires, or screws is undertaken. Primary chondral lesions without attached bone are excised, with débridement and drilling or abrading of the base. Loose fragments are either fixed with absorbable pins, Kirschner wires, or screws or are excised with drilling of the base. Displaced lesions are excised, and the base is drilled or abraded if it cannot be reattached.

FIGURE 5.91 ● Anterior calcaneus cystic change. Prominent vascular remnants near the attachment of the cervical and interosseous ligaments are associated with hyperintensity on FS PD FSE images through the lateral aspect of the calcaneus.

FIGURE 5.92 ● Anterolateral and posteromedial locations of osteochondral lesions of the talus. The lateral lesions tend to be shallower and wafer-shaped, whereas the medial lesions are deeper and cup-shaped.

FIGURE 5.93 ● Medial cup-shaped osteochondral lesion (OLT). Medial OLTs are more common than lateral ones, but lateral lesions are associated with trauma in over 90% of cases. Medial lesions are ascribed to trauma in about 70% of cases. Coronal FS PD FSE image.

FIGURE 5.94 ● Lateral OLT with intact overlying chondral surface. Subchondral trabecular fracture and adjacent marrow edema are demonstrated on a coronal T1-weighted image (A). Mid-lateral talar dome location is shown with a cross-sectional area of reactive marrow edema. The edema associated with OLT should not be misinterpreted and result in overestimation of the area of trabecular bone involved. Coronal T1-weighted image. (B) Coronal FS PD FSE image. (C) Axial FS PD FSE image. (D) Color illustration with the capsule cut and the tibia and fibula reflected. Compression-type OLT corresponding with an area of subchondral trabecular compression in a stage I lesion.

FIGURE 5.95 ● Stage I OLT with subchondral bone marrow edema, which is hypointense on the coronal T1-weighted FSE image (A) and hyperintense on the coronal FS PD FSE image (B). The overlying talar articular cartilage is hyperintense on the FS PD FSE image (B).

FIGURE 5.96 ● Stage II (IIA) OLT of the medial talar dome with formation of a subchondral cyst and anterior communication with an injured chondral surface. (A) Coronal color graphic of medial OLT. (B) Coronal T1-weighted image. (C) Coronal FS PD FSE image. (D) Axial FS PD FSE image.

Injuries to the Tendons

A variety of studies have confirmed the usefulness of MR imaging in the evaluation of tendinous and ligamentous struc-tures about the ankle. Intact tendons and ligaments demonstrate low signal intensity on all pulse sequences. The thicker tendons of the ankle can be studied in multiple planes, although smaller ligamentous bands may be seen in only one orthogonal plane.

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Achilles Tendon Injuries

The Achilles tendon is subject to both midsubstance tendinosis (manifested by fusiform thickening) and insertional tendinitis (seen as distal thickening at the os calcis insertion) as well as longitudinal, partial, or complete tears, which are optimally evaluated in the sagittal plane. Associated abnormalities include retrocalcaneal bursitis and inflammation of the soft tissues surrounding the tendon (paratendinitis).

Achilles Tendinitis

Pearls and Pitfalls

Achilles Tendinitis

Tendinitis or tendinopathy represents intrasubstance tendon degeneration.
Achilles tendinitis is subdivided into non-insertional tendinosis and insertional tendinitis.
The Achilles tendon has no synovial sheath but is associated with a paratenon or connective tissue envelope.
MR identifies nodular or convex tendon thickening and intratendinous mucoid degeneration.
Haglund's deformity represents insertional tendinitis with a posterosuperior calcaneal bony prominence and retrocalcaneal tendo Achilles bursitis.

The Achilles tendon does not have a true tendon synovial sheath (Fig. 5.104). Instead, there is a connective tissue envelope surrounding the tendon, which is referred to as a paratenon (or peritenon) (Fig. 5.105). Achilles tendinopathy is classified into the following categories:

In tendinosis or tendinopathy, there is intrinsic or intrasubstance degeneration of the Achilles tendon.
Tendinitis represents the clinical symptoms that develop in association with the degenerative process of tendinosis.
In paratendinitis (also known as peritendinitis, since it refers to the peritendinous tissues), there is generalized inflammation of the tissues surrounding the Achilles tendon (pre-Achilles fat).³²
In paratendinitis (peritendinitis) (Fig. 5.106) with tendinosis, there is inflammation of the surrounding tissues with associated tendon degeneration.
The paratenon (also referred to as the peritenon) represents the connective tissue envelope surrounding the Achilles tendon.
Paratenonitis is an inflammation of the Achilles tendon connective tissue envelope (usually limited to the posterior paratenon on MR images).
An irregular pre-Achilles fat pad may be seen with paratendinitis (peritendinitis) with or without abnormal Achilles tendon morphology.

Etiology, Pathology, and Clinical Features

Achilles tendinitis is seen most often in adults 30 to 40 years of age. Young athletes and sedentary and older individuals may

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also be at risk. Although it may occur in both men and women, pronounced lesions are more often seen in males. It affects 11% of runners and 9% of dancers. Overuse of the calf muscles is a primary cause, and several mechanisms contribute to overuse injuries, including:

FIGURE 5.97 ● Stage II (IIB) OLT with a shallow and wafer-shaped fragment and incomplete separation from the lateral talar dome. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image. (C) Sagittal FS PD FSE image. (D) A nondisplaced partial fracture shown in a color graphic corresponding to either a communication with the talar dome or an open articular surface lesion with incomplete separation of the fragment. Subchondral cystic lesions are associated with extension of a fracture to the talar chondral surface.

FIGURE 5.98 ● Stage III OLT with fragment adherent to granulation tissue but separated from the overlying chondral surface, (A) Coronal section color graphic. (B) Coronal T1-weighted image. (C) Coronal FS PD FSE image.

Eccentric loading of a fatigued muscle—tendon unit, seen in overtraining. Runners are susceptible in both acceleration (sprinting) and deceleration (eccentric contraction).
Hyperpronation, in which the leg and foot generate opposing forces of rotation: the subtalar joint pronates, the calcaneus everts, and the knee extends.
Forefoot varus, particularly in cavus foot
Equinus deformity, including triceps surae contracture
Insertional changes, such as a calcaneus bony prominence
Hypertrophic spurring or enthesophytes
Systemic arthropathies, such as HLA-B27 antigen-associated arthritides or rheumatoid arthritis

Additional causes include direct trauma to the Achilles tendon, which may result in hematoma with associated inflammation and fibrosis with restricted tendon sliding. In stenosing tenosynovitis, there is chronic inflammation of the peritenon. Partial tearing, intrasubstance cysts from chronic partial tears,

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or nodules may also be identified. New collagen formation and associated fibrillation, nodularity, degeneration, and discoloration contribute to constriction of the peritenon.

FIGURE 5.99 ● Nondisplaced fragment in a stage III OLT with intermediate-signal-intensity granulation tissue at the fragment—talus interface. (A) Sagittal T1-weighted image. (B) Sagittal FS PD FSE image. (C) Color graphic with superior view of talus.

FIGURE 5.100 ● (A) Stage IV OLT with interruption of the subchondral plate, subchondral cystic change, and medially displaced chondral fragment on a coronal section color illustration. (B, C) Stage IV OLT with the displaced fragment located in the anterior tibiotalar joint capsule. The lateral OLT is the donor site. Arthroscopy is performed on all stage III and IV lesions and stage I and II lesions that fail conservative treatment. (B) Coronal T1-weighted image. (C) Axial FS PD FSE image. (D) Displaced fragment from a medial talar dome donor site in OLT on a color graphic superior view of the talus with the tibia and fibula resected.

FIGURE 5.101 ● Contour irregularity of the chondral and subchondral plate and fracture extension to the talar surface in a stage II lesion with incomplete separation of the involved fragment. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image.

Achilles tendinitis occurs in two locations: non-insertional and insertional. Non-insertional tendinosis (Fig. 5.107) is seen in the hypovascular watershed zone 2 to 6 cm proximal to the calcaneal insertion. The tendon is affected to varying degrees in both the longitudinal extent and anteroposterior thickening within the watershed region of decreased vascular perfusion. Insertional tendinitis (Fig. 5.108) affects the distal calcaneal tendon insertion.

Pathologically, inadequate healing is the key event, leading to adhesions, fibrotic changes and inflammation of the peritenon, loss of the normal tendon luster, nodular thickening, and calcification. Microscopically, chronic paratendinitis is characterized by the development of hypertrophic connective tissue, increased capillary infiltration, regional blood vessel degeneration, fibrinogen deposition and fibrinoid necrosis, a round cell infiltrate, an increase in glycosaminoglycans (chondroitin sulfate) (see Fig. 5.107), and mucoid degeneration. In addition, there is leakage of plasma proteins secondary to disruption of local blood flow. There may be absence of a tendon inflammatory response separate from inflammatory disease of the peritendinous tissues and peritenon.

The retrocalcaneal bursae between the Achilles insertion and calcaneus (Fig. 5.109) and the tendo-Achilles bursa located posterior to the Achilles tendon (Fig. 5.110) may also be involved.

Clinically, patients present with pain with weight-bearing. In non-insertional tendinosis (see Fig. 5.107) there is acute pain with altered biomechanics. Symptoms are most often proximal to the retrocalcaneal bursa, and there is tenderness with deep palpation and palpable tendon nodularity. Non-insertional tendinosis is more likely to occur in higher-level athletes and is found in 6.5% to 18% of runners. Insertional tendinitis tends to occur in older, less athletic, or sedentary individuals, and the tenderness is at the os calcis tendon insertion in Haglund's deformity.

MR Appearance

MR findings in Achilles tendinitis in-clude focal or fusiform thickening of the Achilles tendon and diffuse or linear low to intermediate signal intensity on T2-weighted, FS PD FSE, or STIR images.³³ Key findings include:

Increased cross-sectional diameter on axial images
Increased anteroposterior dimensions
Prominent anterior convexity with focal or diffuse thickening in the sagittal plane
Thickening and intermediate signal of peritendinous tissue dorsal, medial, and lateral to the Achilles tendon on T1- or PD-weighted images
Intermediate-signal-intensity effacement of peritendinous tissue anterior to the Achilles tendon on T1- or PD-weighted images
Hypointense to intermediate signal within an enlarged tendon in hypoxic fibromatosis (Fig. 5.111) on FS PD FSE images

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Inflammatory fluid anterior to the tendon and proximal extension of fluid in the retrocalcaneal bursa
Myxoid degeneration (Fig. 5.112) with increased signal on FS PD FSE or STIR images
Calcific (Fig. 5.113) or ossific degeneration with tendon thickening
Associated partial tears
Enthesopathic insertional tendinitis (Fig. 5.114)
Haglund's deformity (Figs. 5.115, 5.116, and 5.117) (insertional tendinitis with reactive calcaneal marrow edema [see Fig. 5.116], and the constellation of thickened tendon, retrocalcaneal/tendo Achilles bursitis, and a calcaneal bony prominence)
Effacement and edema of the pre-Achilles fat body with normal tendon morphology and/or signal

FIGURE 5.102 ● Coronal FS PD FSE images of an osteochondral lesion of the tibia (A). The subchondral plate fragment is defind on a 2-month follow-up study (B).

FIGURE 5.103 ● Microfracture treatment of a medial talar lesion. The microfracture awl is typically introduced through the contralateral arthroscopic portal. The awl is used to create subchondral holes in the bed of the lesion.

T2* sequences demonstrate increased hyperintensity (relative to other pulse sequences) in areas of tendon degeneration. FS PD FSE images are not as sensitive to intrasubstance signal intensity as are T2*-weighted or STIR techniques. After contrast administration there is soft-tissue inflammatory fluid enhancement in paratendinitis.

In chronic Achilles tendinitis there is focal or diffuse widening of the tendon diameter or contours, but intrasubstance increased signal intensity may not be evident in uncomplicated (not associated with partial tears) chronic lesions. Adhesions between the peritenon and Achilles tendon are associated with chronic peritendinitis. A healed Achilles tendon tear displays

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thickening without associated increased signal intensity. It may be difficult to distinguish areas of chronic tendinitis from intrasubstance tendon tears without visualizing either discontinuity in tendon fibers or discrete hyperintense signal intensity on T2-weighted or STIR images with partial tears.

FIGURE 5.104 ● Posterior view of the hindfoot demonstrating the relation of the Achilles tendon to the posterior neurovascular bundle. The musculotendinous junction of the triceps surae (the medial and lateral heads of the gastrocnemius and soleus muscles) marks the superior extent of the Achilles tendon.

In gout, deposition of tophaceous material (Fig. 5.118) may lead to spontaneous rupture of the Achilles tendon (see also the discussion below on Achilles tendon rupture). Tophi appear similar to nodular myxoid-like degeneration and demonstrate intermediate and increased signal inhomogeneity on T2-weighted, T2*-weighted, or STIR images. Xanthomas (Fig. 5.119) of the Achilles tendon have been shown to produce infiltrative lesions with diffuse tendon thickening and enlarged soft-tissue components (masses).³⁴–³⁴ Bilaterality of these lesions is common. Xanthomas enhance with intravenous gadolinium administration. The soft-tissue component displays hyperintense inhomogeneity on FS PD FSE images.

FIGURE 5.105 ● There is no true synovial sheath around the Achilles tendon. It is covered by the paratenon alone. The normal paratenon is not hyperintense on FS PD FSE images. Axial FS PD FSE image.

FIGURE 5.106 ● (A) Lateral color graphic of the normal anatomy of Kager's fat pad. Fat deposition deep to the Achilles tendon separates it from the deep compartment of the leg. Paratendinitis (also referred to as peritendinitis) demonstrates hypointensity and effacement of pre-Achilles fat on a sagittal T1-weighted image (B) and hyperintensity of the anterior soft tissue on a sagittal FS PD FSE image (C).

FIGURE 5.107 ● Non-insertional chronic Achilles tendinosis on sagittal T1-weighted (A) and FS PD FSE (B) images. Chemical inflammation is not involved in chronic Achilles tendinosis. Increased levels of the excitatory neurotransmitter glutamate and lactate, however, have been demonstrated in painful midportion tendinosis.

FIGURE 5.108 ● Insertional tendinitis with hyperintensity of the thickened distal Achilles tendon. Retrocalcaneal bursal inflammation and calcaneus marrow edema are shown. In contrast to non-insertional degenerative tendinosis, the process of insertional Achilles tendinitis demonstrates an inflammatory process histologically. Achilles enthesopathy is another term for insertional Achilles tendinitis. FS PD FSE (A) sagittal and (B) axial images.

FIGURE 5.109 ● (A) Disk-shaped retrocalcaneal bursa, posterior coronal perspective. (B) Distended retrocalcaneal bursa in rheumatoid arthritis. Sagittal FS PD FSE image.

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Treatment

Acute tendinitis may progress to chronic tendinopathy, which is characterized by perfusion insufficiency with vascular proliferation, abnormal tendon fiber morphology, and hypercellularity. Tendinopathy is symptomatic in 90% of cases, and partial tears are associated with regions of tendinosis. Tendinosis may be a precursor lesion to a final stage of partial or complete tendon tear.

Conservative treatment, used to alleviate the symptoms of tendinopathy, includes therapeutic rest, stretching exercises, cross-training or alternative exercise, anti-inflammatory medications, immobilization, orthoses to correct hyperpronation, and brisement to lift an adherent paratenon. If conservative treatment is not successful, surgical options include tendon release with or without stripping and excision of the thickened peritenon and granulation tissue, excision of the calcaneal prominence in insertional tendinopathy, repair of any associated partial tears, and débridement of mucoid degeneration.

FIGURE 5.110 ● (A) Anatomy of the retrocalcaneal and subcutaneous bursae. (B) Hyperintense retrocalcaneal bursa and more linear tendo-Achilles bursa on a sagittal FS PD FSE image.

FIGURE 5.111 ● Painful chronic tendinopathy of the midportion of the Achilles tendon with tendinosis. Tendinosis implies local degenerative changes in the Achilles tendon. (A) Sagittal PD FSE image. (B) Sagittal FS PD FSE image.

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Partial and Complete Tears of the Achilles Tendon

Partial Tears of the Achilles Tendon

Partial tendon tears can be defined on MR images in the sagittal and axial planes. Linear or focal regions of increased signal and thickening of fibers without a tendinous gap are characteristic.³⁷ Partial tears may involve either the anterior (Fig. 5.120) or posterior (Fig. 5.121) tendon surface. A decreased tendon diameter without loss of tendon continuity is seen in more extensive partial tears (Fig. 5.122). Incomplete tears may also present with partial continuity of a portion of the tendon fibers on at least one sagittal image. Longitudinal splits in chronic Achilles tendinitis that are low to intermediate in signal intensity on long-TR/TE images may be seen in association with a superimposed acute partial tear. The acute partial tear is hyperintense on long-TR/TE images.

Achilles Tendon Rupture

The Achilles tendon, formed by the confluence of the gastrocnemius and soleus muscle complexes, is the largest tendon in the body and is the third most frequently ruptured tendon. Injuries to this tendon are most commonly seen secondary to athletic activity in middle-aged (after 30 years of age and most frequently between 30 and 50) men.³⁸^,³⁹ Sports involving concentric loading (such as basketball, tennis, or racquetball) are frequently implicated. The male-to-female ratio is 5:1 to 6:1 for complete rupture secondary to indirect trauma. In younger individuals, the musculotendinous junction is more commonly injured. Disorders such as rheumatoid arthritis, systemic lupus erythematosus, diabetes mellitus, and gout may predispose to disruption of the Achilles tendon because of already weakened connective tissue and collagen fibers. The Achilles tendon is most susceptible to rupture 2 to 6 cm superior to the os calcis. Acute rupture is associated with forced dorsiflexion of the foot against a contracting force generated by the triceps surae group. Rupture of the contracted musculotendinous unit may occur secondary to direct trauma.

Etiology, Diagnosis, Pathology, and Clinical Features

In evaluating Achilles tendon rupture and healing, it is important to remember that the tendon has no true synovial sheath, the mesotendon provides the blood supply through the anterior mesentery, and there is a triangular fat pad anterior to the Achilles tendon called Kager's fat triangle (see Fig. 5.106).

The most common causes of Achilles tendon tears are:

Indirect trauma
Repetitive microtrauma
Overpronation of the foot or heel stress leading to microtears
Forced dorsiflexion of the foot against a contracting force (triceps surae group) or eccentric loading in a sudden stretch
Direct trauma, causing rupture at the myotendinous junction
Soleus muscle atrophy
Rheumatoid arthritis, systemic lupus, diabetes mellitus, and gout
Chronic tendinitis and partial tears are important predisposing causes in acute rupture.
Fluoroquinolone antibiotics (and statin drugs, retinoids, and calcium channel blockers) have been linked to Achilles tendon tears.

FIGURE 5.112 ● (A) Non-insertional tendinosis proximal to the os calcis insertion of the Achilles tendon. Intratendinosis degeneration (yellow) is shown on the cross-section through the affected tendon segment. Non-insertional Achilles tendinosis with intratendinous signal intensity is shown on sagittal T1-weighted (B), sagittal FS PD FSE (C), and axial FS PD FSE (D) images. Tendinosis is associated with alterations in the collagen fiber structure and arrangement. An increased amount of interfibrillar glycosaminoglycans (GAGs) occurs in affected areas of tendinosis.

FIGURE 5.113 ● Thickened calcific tendon degeneration in association with distal tendon rupture. Sagittal T1-weighted image.

FIGURE 5.114 ● (A) Achilles enthesopathy or insertional tendinitis with dystrophic changes at the enthesis. A plantar enthesophyte is also demonstrated on this sagittal T1-weighted image. (B) A prominent enthesophyte and os calcis insertion tendinosis. Sagittal T1-weighted image.

FIGURE 5.115 ● The retrocalcaneal bursa is located between the Achilles tendon and the posterosuperior calcaneal prominence. The adventitial bursa or tendo-Achilles bursa is located between the Achilles tendon and the skin. Lateral color graphic.

FIGURE 5.116 ● Haglund's deformity with distal Achilles tendinitis, osseous edema of the posterosuperior calcaneus, and visible fluid and/or thickening in the retrocalcaneal bursa and tendo-Achilles bursa. (A) Lateral color illustration. (B) Sagittal FS PD FSE image.

FIGURE 5.117 ● Excision of Haglund deformity. (A) Lateral color illustrations showing excision of the posterior superior os calcis before (top) and after (bottom) surgery. (B) Arthroscopic illustration showing image from the medial portal with lateral placement of a bur to remove the superior angle of the calcaneus.

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On pathologic examination a tear is found 2 to 3 cm proximal to the calcaneal insertion. Tears may be related to a reduction in the anterior mesenteric blood supply with increasing age. The posterior fibers rupture first (partial tearing may exist in anterior fibers, which are under less tension), and the plantaris usually remains intact because of its more anterior calcaneal insertion. Histologic examination reveals degeneration with decreased collagen cross-linking, resulting in increased stiffness and loss of viscoelasticity.

FIGURE 5.118 ● A soft-tissue sodium urate deposit (i.e., tophus) located posterior to the Achilles tendon (arrows) demonstrates (A) low signal intensity on a T1-weighted sagittal image and (B) high signal intensity on a STIR sagittal image.

The typical patient is a middle-aged man participating in athletic activity. Patients present with pain and soft tissue swelling, usually related to hemorrhage. With clinical examination alone, rupture of the Achilles tendon is missed in up

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to 25% of cases, perhaps because the other tendons of the posterior calf maintain plantarflexion and allow a tendinous gap to be missed on clinical examination. Clinical signs include the hyperdorsiflexion sign, O'Brien's needle test to detect proximal tendon motion as a sign of tendon continuity in acute ruptures, a palpable tendon defect, and Thompsen's sign. The Thompsen test is performed in the prone position and is positive if squeezing the calf does not produce the normal plantarflexion response.

FIGURE 5.119 ● Xanthomas of the Achilles tendon with a large soft-tissue component (curved arrow) and diffuse infiltration of the Achilles tendon (straight arrow) on (A) a sagittal T1-weighted image, (B) a sagittal color graphic, (C) an FS gadolinium-enhanced sagittal T1-weighted image, and (D) axial FS PD FSE image. Tendinous enhancement is demonstrated with intravenous gadolinium (C, D). The soft-tissue component posterior to the Achilles tendon is hyperintense on the FS PD FSE sequence (B) and demonstrates partial enhancement with intravenous contrast (C).

FIGURE 5.120 ● Anterior surface partial tear of the Achilles tendon on a lateral color graphic.

FIGURE 5.121 ● (A) Posterior surface partial tear of the Achilles tendon proximal to the os calcis. Lateral color lateral illustration. Sagittal (B) and coronal (C) FS PD FSE images of a partial tear of the Achilles tendon. The coronal plane image (C) is useful in demonstrating medial tendon fiber disruption.

FIGURE 5.122 ● Attenuated anterior-to-posterior tendon thickness in an extensive partial Achilles tendon tear without a tendinous gap. (A) Sagittal T1-weighted image. (B) Axial FS PD FSE image.

Lateral radiography and xerography have not been effective in identifying abnormalities in the Achilles tendon. Although tendon thickening in inflammation and discontinuities in tears have been observed with some success using real-time ultrasonography, this technique is limited in soft-tissue contrast discrimination and FOV, and by the inability to accurately evaluate both adjacent soft-tissue and bony structures.

Staging

A four-stage classification system has been developed to grade Achilles tendon ruptures:

Type 1: Partial ruptures affecting 50% or less of the tendon (Fig. 5.123)
Type 2: Complete ruptures with a tendinous gap of 3 cm or less (Fig. 5.124)
Type 3: Complete ruptures with a tendinous gap of 3 to 6 cm (Fig. 5.125)

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Type 4: Complete tendon ruptures with a defect greater than 6 cm (Fig. 5.126). Type 4 is associated with neglected ruptures.

FIGURE 5.123 ● Partial Achilles tendon tear with the “corkscrew” morphology of partially retracted fibers. Coronal FS PD FSE image.

FIGURE 5.124 ● Focal complete tear of the Achilles tendon with less than 3 cm of retraction. (A) Lateral color graphic. (B) Sagittal T1-weighted image. (C) Axial FS PD FSE image.

FIGURE 5.125 ● Type 3 or complete rupture of the Achilles tendon with a tendinous gap of 3 to 6 cm. (A) Lateral color graphic. (B) Sagittal PD FSE image.

MR Imaging Technique

The Achilles tendon can be demonstrated on sagittal, axial, and thin-section coronal MR images.⁴⁰ A routine examination of the tendon uses a 14- to 16-cm FOV and sections 3 to 4 mm thick. A T1-weighted sequence is performed in the sagittal plane through the Achilles tendon. T2*-weighted, FS PD FSE, or STIR images show associated hemorrhage or edema in the intratendinous or peritendinous soft-tissue structures. FS PD FSE or STIR axial sequences reveal fluid, hemorrhage, or inflammatory tendon changes and are useful in the evaluation of the integrity of other tendons and ligaments supporting the ankle. Thin-section (3 mm) coronal images display the width of the Achilles tendon and the condition of disrupted tendon fibers. In one study, preoperative MR imaging findings, including tendon morphology, orientation of torn fibers, and measurement of tendon diastases, all correlated with surgical findings during tendon repair.⁴¹

MR Appearance

The normal Achilles tendon demonstrates uniform low signal intensity. Axial images show the tendon in cross-section with a mildly flattened anterior surface and a convex posterior surface. In ruptures of the Achilles tendon, the relationship of the proximal and distal portions of the torn tendon can be seen on MR studies either before or after application of a plaster cast. Key MR findings include:

A fluid-filled gap with or without interposed fat at the tear site in complete tendinous disruptions with discontinuity
Fraying or corkscrewing (see Fig. 5.123) of the tendon edges associated with proximal tendon retraction
In the absence of overlapping tendon edges, no tendon fibers can be seen at the tear site on axial images.
Tendon disruption with discontinuity and a wavy retracted tendon
Associated hemorrhage or edema in intratendinous or peritendinous soft tissues on axial or sagittal images
Disruption of muscle fibers in a musculotendinous junction tear, although on gross examination the tendon appears intact
Effacement of Kager's triangle¹⁸
Intratendinous degeneration

In addition, there may be overlapping or nondisplaced proximal and distal tendon components (Fig. 5.127). Enlarged proximal and distal ends may be associated with an attenuated union bridging the tear site. Associated soleus muscle strain (Fig. 5.128) is also sometimes seen.

After surgery MR can also be used to follow healing. Intratendinous fluid may be seen for up to 6 months after treatment and tendon widening may be visible for up to 12 months. An increased size of the tendon associated with decreased tendinous signal intensity is secondary to scar tissue. Distal repairs are associated with distal tendon thickening and residual signal intensity (Fig. 5.129).

FIGURE 5.126 ● Complete Achilles rupture with greater than 6 cm of proximal tendon retraction. Fat fills the tendinous gap site proximally. (A) Lateral color graphic. (B) Sagittal PD FSE image. (C) Axial FS PD FSE image.

FIGURE 5.127 ● Partial overlap of torn Achilles tendon ends. (A) Lateral color illustration. (B) Sagittal FS PD FSE image.

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The main differential features between partial and complete tears include the following:

Partial tears demonstrate hyperintense signal with incomplete anterior-to-posterior or posterior-to-anterior extension on FS PD FSE images.
Complete tears demonstrate a hyperintense fluid-filled tendinous gap.
Tendon rupture usually occurs 2 to 6 cm superior to the os calcis.
The size of the rupture varies, based on the degree of tendon retraction.
Ruptures demonstrate diffuse convexity of the anterior margin and enlarged tendon ends at the tear site.

Treatment

MR imaging may be most useful in Achilles tendon rupture in the selection of patients best suited for conservative therapy, thereby improving the present statistics for rerupture.⁴²^,⁴³ Retear of a primary repaired tendon shows residual suture artifact.

Conservative or nonoperative measures may be recommended for acute ruptures, less than 48 hours old, and for steroid-induced ruptures.⁴⁴ Cast immobilization with an above-the-knee cast with equinus for 4 weeks, or a below-the-knee cast with decreased equines, is the main approach. Surgical repair is usually required. An end-to-end anastomosis is recommended for type 1 and 2 ruptures; an autogenous tendon graft flap is used for type 3 ruptures; and a free tendon graft or synthetic graft is needed for type 4 ruptures. Suture techniques include Bunnell, Kessler, Krackow (locking loop) with four sutures across the repair site, percutaneous repair, and use of synthetic graft materials. Alternative function bracing and plantaris reinforcement may also be part of surgical treatment.

In making a decision about surgery versus serial casting, MR is used to determine the degree of apposition of the disrupted proximal and distal tendon fragments. Retracted tendon sections are less likely to heal with conservative management, and MR evaluation allows early identification of these patients, who are candidates for surgical intervention. Fibrous bridging also appears to be more tenuous with increased tendon separation. A bulbous contour may be demonstrated in the proliferating ends of a torn Achilles tendon, and it increases with greater tendon diastases. Fibrous healing, with approximation of torn fibers, can be evaluated with MR imaging performed at monthly intervals. The healing of conservatively or surgically managed tendons may be associated with intratendinous fluid

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spaces, studied at 3 and 6 months by Dillon et al..⁴⁵ Over time, decreased signal intensity was found in the areas of successful healing. By 12 months, these areas demonstrated low signal intensity within a widened tendon. Caution must be exercised in interpreting MR images obtained in the first 2 months postoperatively; Achilles tendon pathology should not be overread as retear, poor healing, or failed surgical repair.⁴⁶

FIGURE 5.128 ● Grade 1 soleus muscle strain secondary to an Achilles rupture. Axial FS PD FSE image.

FIGURE 5.129 ● Residual post-surgical Achilles tendon thickening with an intratendinous scar. (A) Sagittal T1-weighted image. (B) Sagittal FS T1-weighted contrast enhanced image.

The Achilles tendon and overlying skin are relatively avascular and may become infected after surgery with implanted material or autogenous tendon. The incidence of complications with surgical repair is reported to be 20%. The incidence of rerupture of the Achilles tendon is significantly higher in patients who undergo nonsurgical treatment than in those who have had surgical repair. Surgery is the preferred treatment for any patient who has a rerupture of the Achilles tendon treated conservatively, and possibly should be the primary treatment choice for any patient who is active and athletic.⁴⁷ Chronic thickening of the Achilles tendon or residual inflammatory changes are demonstrated on axial and sagittal MR images. After repair with strands of a polymer of lactic acid (PLA), T1-weighted images show a thickened fusiform tendon with moderate-signal-intensity streaks.⁴⁸ Changes in signal intensity are attributed to the PLA implant and surrounding collagenogenic response.

Tibialis Posterior Injuries

Rupture of the tibialis posterior tendon (posterior tibial tendon [PTT]), which may occur spontaneously, is commonly associated with prior synovitis, steroid injection, or trauma.⁴⁹ Chronic PTT rupture usually occurs in middle-aged women in their fifth or sixth decades. Sixty percent of cases are associated with hypertension, diabetes, and obesity.

Etiology, Pathology, and Clinical Features

In assessing tibialis posterior injuries, it important to remember that the tibialis posterior is located superficial to the superomedial calcaneal navicular component of the spring ligament and that its relationship with the spring ligament is synergistic. The PTT inserts proximally on the navicular tuberosity, and there are also extensive plantar insertions. Functionally, the PTT supports the medial arch and stabilizes the foot. It is also responsible for supination of the foot and, with the medial malleolus, for pulley actions.

The most commonly seen indications of tibialis posterior injuries are a change in tendon size, morphology, and/or signal intensity. Most lesions are located at the midportion of the tendon at the level of and immediately distal to the medial malleolus, corresponding to the relative zone of tendon hypovascularity. The normal PTT is twice the size of the FDL. Tears presents as a spectrum of tendon hypertrophy, attenuation, or disruption. Morphologic characteristics include bulbous cross-sectional enlargement, attenuation in a curvilinear orientation, and a complete tendinous gap.

There are a number of causes of posterior tibialis failure, including:

Chronic degeneration
Trauma
Systemic disease
Tendon hypovascularity
Biomechanical disorders and abnormal insertions
Iatrogenic conditions

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Chronic degeneration is the most frequent etiology of tibialis posterior dysfunction. Acute trauma is less commonly involved, and although minor trauma, such as lacerations and puncture wounds, is sometimes implicated, rupture is usually associated with indirect trauma such as sprains and/or fractures. Rarely, traumatic dislocation of the PTT can be attributed to forced dorsiflexion with inversion.

Patients frequently have associated systemic disorders, such as chronic inflammatory disease, rheumatoid arthritis, seronegative spondyloarthropathies (including psoriasis, ankylosing spondylitis, Reiter's disease, and enteropathic arthritis), and infections (particularly gonococcal and tubercular). Tibialis posterior failure has also been found at sites of enthesopathy.

Tendon hypovascularity also contributes to failure. There is a zone of hypovascularity in the midportion of the tendon, at and distal to the medial malleolus, that is at particular risk for rupture. Diminished arterial perfusion (age-related) leads to tendon ischemia, and acute angulation of the tendon posterior to the medial malleolus compounds the problem. In addition, pronation of the hindfoot causes tendon compression.

Biomechanical causes include overuse, pes valgus, equinus deformity, and increased stress on the tendon with decreased medial longitudinal arch support. Abnormal insertions, such as an accessory navicular or a prominent medial navicular tubercle, are associated with tendon degeneration secondary to a change in leverage.

Iatrogenic tendon dysfunction is caused by medial ankle/tarsal tunnel surgery and sometimes by the use of corticosteroids.

On pathologic examination there is usually a longitudinal split with tendon laxity, fibrosis, and elongation. An irregular surface can be identified, and there are adhesions with the tendon sheath and flexor retinaculum. In addition, there is bone proliferation and atrophy of the sheath, and the scarred and frayed proximal and distal ends of the tendon rupture can be identified. Intrasubstance degeneration is noted on histologic examination.

The typical patient is a middle-aged woman who presents with unilateral, often left-sided flatfoot deformity accompanied by pain, swelling, and tenderness and no history of trauma.⁵⁰ There is flattening of the medial longitudinal arch with weakness of inversion, a severe pes planus deformity, heel valgus, talar plantarflexion, and forefoot abduction. There is intrinsic degeneration of the tendon, and the typical site of rupture is either at or within 6 cm proximal to its navicular insertion. It is the collapse of the medial longitudinal arch that creates the characteristic flatfoot deformity with associated heel valgus, talar plantarflexion, and forefoot abduction.⁵¹ Failure of calcaneal inversion with a valgus heel is observed on clinical examination when the patient stands on tiptoe. The clinical diagnosis is not straightforward, and in some cases several years may elapse between initial presentation and diagnosis.

Edema or soft-tissue thickening may be demonstrated inferior to the medial malleolus, although conventional radiographs do not demonstrate tendon pathology. Loss of a convex arch may be observed on weight-bearing views through the talonavicular or naviculocuneiform joint. Radiographs may also reveal a decreased calcaneal plantar angle, an increased lateral talometatarsal angle, an increased anterior talocalcaneal angle, and an increased lateral talocalcaneal angle.⁵¹ Forefoot abduction is associated with lateral subluxation of the navicular at the talonavicular joint, which is shown on axial images through the midfoot. The presence of an accessory navicular bone is associated with both pes planus and PTT dysfunction.

Tenosynovitis may also involve the tibialis posterior and peroneal tendons. Tibialis posterior tenosynovitis is associated with rheumatoid arthritis and planovalgus foot and usually occurs in older patients.

Classification

PTT tears have been divided into three classification types based on MR criteria. Types I and II are partial tears and type III is a complete tear. In comparison with CT scans, and using surgical exploration as the gold standard, MR imaging is superior in detecting the spectrum of early partial tendon ruptures, longitudinal tearing, and the presence of synovial fluid.⁵² Subtle areas of associated periostitis, however, are more readily delineated with CT.

Specific findings in the various tear types include the following:

Type 1: There is tendon hypertrophy with heterogeneous signal intensity in intrasubstance vertical splits (Fig. 5.130). Associated findings include increased signal intensity (intrasubstance striations) and girth at the distal tendon insertion to the navicular (a normal variant), osseous spurring with or without fatty marrow signal in the posteromedial aspect medial malleolus (see Fig. 5.130), and tendon dysfunction or dislocation with disruption of the flexor retinaculum (Fig. 5.131).
Type 2: There are thin or attenuated sections of the tendon at the level of the medial malleolus⁵³ with variable intratendinous signal change (Fig. 5.132). Subtendons may occur associated with mixed areas of atrophic and hypertrophic tendon segment (Fig. 5.133).
Type 3: There is complete tendinous discontinuity with a low- to intermediate-signal-intensity fluid-filled gap (Fig. 5.134). There may be subtendons associated with irregular tendon morphology of the retracted proximal or distal segments on either side of the tendinous gap. Digital avulsion (Fig. 5.135) in the foot at the insertion into the cuneiforms, cuboid, and medial metatarsal bases is uncommon.
Chronic dysfunction: In spring ligament laxity or rupture, the superomedial calcaneal navicular component is usually injured. The sinus tarsi syndrome may occur after progression from PTT dysfunction to spring ligament pathology. A more detailed discussion of spring ligament pathology can be found later in the chapter.

MR Appearance

In complete tears, MR imaging demonstrates disruption of the PTT with or without abnormal morphology

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of the ends of the tendon.³⁷ Partial or chronic tears or a retracted tendon may present with enlargement. FS PD FSE axial images that extend inferior to the medial malleolus should demonstrate the normal PTT anterolateral to the FDL tendon.

FIGURE 5.130 ● Type 1 tibialis posterior tendon tear associated with a medial malleolus osseous spur. The normal tibialis posterior tendon is approximately twice the cross-sectional diameter of the flexor digitorum longus. In a type 1 tear the PTT may demonstrate increased thickening, with a cross-sectional diameter up to 5 to 10 times larger than the adjacent flexor digitorum longus tendon. (A) Lateral graphic with an axial insert. (B) Axial FS PD FSE image.

The tendon hypertrophy seen in type I partial tears is best appreciated on axial images as an increased cross-sectional diameter. An increase in central intrasubstance signal intensity may also be seen on T1-weighted and often on FS PD FSE or STIR images. In a common pattern of presentation associated with prominent or long-segment longitudinal splits of the tibialis posterior in type I tears, three medial flexor tendons instead of two flexor tendons are seen at or proximal to the level of the medial malleolus. Proximal to the split, the PTT is enlarged and seen as a single tendon.

Longitudinal splitting of the PTT into two subtendons is seen in type II tears of the tibialis posterior. Type II partial tears, in which the PTT is attenuated or reduced in size, are usually identified at the level of the medial malleolus. A nonconcentric reduction in tendon width may give the tendon an elongated appearance, without any associated intrasubstance hyperintensity. In these type II tears, the two subtendons are usually located proximal to the medial malleolus, and a single attenuated PTT is identified at the level of the medial malleolus. A medial malleolus periostitis or spur may contribute to the spectrum of tendon degeneration preceding rupture. The native PTT is seen directly posterior to the medial malleolus, and the torn or split fragment is seen posterior to the tendon. The normal FHL tendon is the most posterior and laterally positioned of the three tendons. Normally, only two tendons (the PTT and FDL) should be visualized medially.

Complete (or type III) tears of the PTT demonstrate a discontinuity on axial, coronal, and sagittal images. Tendon retraction and a fluid-filled gap are present on FS PD FSE, T2*, or STIR images. Schweitzer et al.⁴⁶ reported the following additional, secondary, signs of rupture:

Prominence or hypertrophy of the medial tubercle of the navicular (sensitivity 89%, specificity 75%)
Abnormalities of talonavicular alignment (sensitivity 82%, specificity 100%)
Presence of an accessory navicular (sensitivity 20%, specificity 100%)

FIGURE 5.131 ● Chronically scarred flexor retinaculum. Dislocation of the tibialis posterior is associated with a torn flexor retinaculum. The retromalleolar groove may also be shallow. (A) Axial FS PD FSE image. (B) Coronal T1-weighted image.

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Normal talonavicular alignment can be determined by a line drawn through the long axis of the talus, which typically bisects the navicular bone. Schweitzer et al.⁵⁴ additionally found that there is an overlap in the range of normal and abnormal distal tibialis posterior tendon size. There is also overlap in the range of intratendinous signal intensity in normal and torn PTT. This overlap is primarily observed on T1-weighted images and is not observed on FS PD FSE. In clinical practice, tears of the PTT are usually evident proximal to the navicular and diagnosis can be made without reliance on characterizing the bulbous configuration of the distal attachment.

Intrinsic degenerations usually demonstrate varying degrees of increased internal signal intensity with fusiform enlargement. Fluid in the tendon sheath, which demonstrates increased signal intensity on conventional T2, FS PD FSE, and T2*-weighted images, may be observed in patients with tenosynovitis. Laxity or rupture of the plantar calcaneonavicular or spring ligament (see below) is associated with chronic dysfunction of the PTT⁵⁵ and may lead to a pes planovalgus deformity.

Treatment

The natural course of PTT injury includes a change in the shape of the foot, decreased exercise tolerance, plantar fasciitis, severe pes planus, tenderness of the sinus tarsi, and lateral ankle pain in advanced deformity.

Conservative treatment, which frequently fails, may be attempted if the tendon is intact and without significant degeneration. Approaches involve support of the medial longitudinal arch with orthoses such as a medial heel wedge, nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy.

Most patients require surgery, which may include osseous stabilization (i.e., osteotomies with double or triple arthrodesis) with hindfoot arthrodesis, primary repair, or replacement of the ruptured tendon. Excision of segmental defects with a side-to-side anastomosis to the FDL or transfer of the FDL with suturing of its distal stump to the FHL may also be attempted. Treatment of chronic dislocation, which occurs anterior to the ruptured flexor retinaculum and FDL tendon, involves reconstruction of the flexor retinaculum and deepening of the groove around the medial malleolus, as described by Healy et al.⁵⁶

Spring Ligament Complex and Pathology

The spring ligament complex comprises three distinct components: the lateral, intermediate, and superomedial oblique calcaneonavicular ligaments (Figs. 5.136 and 5.137). These

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structures are critical static stabilizers of the medial longitudinal arch of the foot, providing support for the head of the talus at the talocalcaneonavicular joint (or acetabulum pedis). The other major stabilizer of the medial longitudinal arch, the PTT, is a dynamic stabilizer. Pathology of the spring ligament complex rarely occurs in isolation and is almost always associated with PTT dysfunction. Attention to the components of the spring ligament on routine MR imaging of the foot is important, since there is often a cascade of failures that can lead to or be seen with acquired pes planus deformity.

FIGURE 5.132 ● (A) Type 2 tibialis posterior tear with the generation of two subtendons. Lateral color graphic with axial inset. (B, C) Attenuated tibialis posterior tendon at the level of the medial malleolus with hypertrophy of the more proximal tibialis posterior associated with tendinous fiber retraction. Axial FS PD FSE images.

In the literature, the nomenclature has not been consistent regarding the lateral and intermediate calcaneonavicular ligaments. The lateral calcaneonavicular ligament is also termed the inferoplantar longitudinal calcaneonavicular ligament ⁵⁷ and the inferior calcaneonavicular ligament.⁵⁸^,⁵⁹ The intermediate calcaneonavicular ligament is also termed the plantar medial oblique calcaneonavicular ligament ⁵⁸ and the “third ligament. ”⁵⁷ For purposes of clarity the ligaments will be referred to with respect to their relative navicular attachment sites.

FIGURE 5.133 ● (A) A T1-weighted axial image depicting a longitudinal rupture of the tibialis posterior tendon resulting in two subtendons of the tibialis posterior (TP) at the level of the medial malleolus and deltoid ligament. Note that this split creates the appearance of four separate medial tendons. The two anterior medial tendons represent the anterior and posterior half of the tibialis posterior. (B) A T2*-weighted sagittal image identifies the attenuated portion of the tibialis posterior at the longitudinal tear site (arrow). (C) The relationship of the tibialis posterior (TP) to the adjacent medial structures on a corresponding T1-weighted coronal image. fdl, flexor digitorum longus tendon; fhl, flexor hallucis longus tendon; N, navicular bone; tcl, tibiocalcaneal ligament; fr, flexor retinaculum.

FIGURE 5.134 ● (A) Type 3 tibialis posterior tendon tear with complete tendinous gap. Lateral color graphic. Sagittal (B) and axial (C) FS PD FSE images demonstrate the tendinous gap and frayed or split retracted tendon ends. (D) Normal arch. (E) Pes planus, with loss of the medial longitudinal arch and hindfoot valgus. From the posterior view, the “too many toes” sign can be seen secondary to a rupture of the posterior tibial tendon.

FIGURE 5.135 ● (A) Plantar view color illustration of the distal insertions of the tibialis posterior tendon to the tuberosity of the navicular plantar surface of all the cuneiform bones, the sustentaculum tali, and the cuboid (not shown). The posterior component of the tibialis posterior inserts on the anterior aspect of the spring ligament. (B) Sagittal FS PD FSE image showing the torn insertion of the anterior component of the tibialis posterior into the navicular tuberosity. (C) A coronal FS PD FSE image shows the avulsed middle component, which normally inserts to the cuneiforms, cuboid, and three metatarsal bones. The middle component has a ligamentous function and provides stability to the plantar arch.

FIGURE 5.136 ● Spring ligament complex anatomy. Lateral-plantar oblique (A), plantar (B), and superior (C) views.

FIGURE 5.137 ● Normal MR appearance of the spring ligament complex. (A) Axial PD image demonstrates the lateral and intermediate calcaneonavicular ligaments originating from the notch between the anterior and middle articular facets of the calcaneus. The lateral calcaneonavicular ligament inserts on the navicular beak. (B) Axial PD image a few slices superior demonstrates the superomedial calcaneonavicular ligament deep to the posterior tibial tendon as it passes along the lateral aspect of the talar head toward its attachment to the dorsal aspect of the navicular tubercle. (C) Coronal T1-weighted image at the level of the talar head demonstrates the superomedial calcaneonavicular ligament deep to the posterior tibial tendon along the lateral aspect of the talar head.

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The inferior (lateral and intermediate) calcaneonavicular ligaments originate adjacent to each other from the notch between the anterior and middle articular facets of the calcaneus. The lateral calcaneonavicular ligament is a short ligament that travels longitudinally to attach to the lateral and proximal aspect of the navicular bone (the “beak” of the navicular). This ligament is best visualized on sagittal and axial images on routine ankle MR examination. The intermediate calcaneonavicular ligament is a longer ligament that travels obliquely across the floor of the talocalcaneonavicular joint to attach on the lateral and plantar aspect of the tuberosity of the navicular bone. This ligament is best seen on axial and coronal images. Abnormalities in these components of the spring ligament complex are not commonly seen on MR imaging, and there are no current reports in the literature regarding surgical repair of these structures.

The superomedial calcaneonavicular ligament originates from the medial aspect of the sustentaculum tali. It then extends distally in an oblique orientation as it wraps around the tuberosity of the navicular to attach along the superomedial aspect of the navicular bone. The tibiospring ligament, part of the superficial fibers of the deltoid ligament, merges with the superficial and medial fibers of the superomedial calcaneonavicular ligament near its origin from the sustentaculum. The superomedial calcaneonavicular ligament is often difficult to visualize, and evaluation in all three imaging planes is required. It is often best seen on the coronal and axial images just deep to the PTT. Abnormalities in the superomedial calcaneonavicular ligament are commonly seen in cases where there is PTT pathology. Surgical repair of this ligament is now often being attempted along with repair of the PTT to improve the static support to the longitudinal arch of the foot.⁵⁹^,⁶⁰

Complete tears involving components of the spring ligament complex are typically clearly apparent on MR imaging as a fluid-filled gap in the ligament(s) and, depending on acuity, associated high intensity signal (edema) in the surrounding soft tissues. As mentioned, full-thickness tears of the spring ligament complex very rarely occur in isolation. Typically, there is associated pathology (tendinosis, strain, or tear) of the PTT.

Sprains and partial tears of the components of the spring ligament complex are a more difficult diagnostic dilemma on MR because there is significant overlap between normal and abnormal tendon morphologic characteristics. Findings include thickening, high signal, or heterogeneous signal within the spring ligament (Fig. 5.138A). Associated abnormalities in the PTT or reactive marrow edema in the talar head are useful in determining if the findings involving the spring ligament components indicate true pathology.

Degeneration of the spring ligament complex is more common than traumatic tears or stains. These degenerative changes are also typically seen in association with pes planus deformity and posterior tibial tendinopathy. In these instances the component ligaments demonstrate abnormal heterogeneous signal, attenuation, or thickening (Fig. 5.138B, C). Again, there is a great deal of overlap with surgically normal ligaments, and attention to associated abnormalities may help guide the diagnosis.

FIGURE 5.138 ● Pathologic appearances of the superomedial calcaneonavicular ligament. (A) Coronal FS PD image with fat saturation demonstrates a thickened and mildly edematous superomedial calcaneonavicular ligament in a patient who also had posterior tibial tendon strain. (B) Axial FS PD image with fat saturation demonstrates a thickened and edematous superomedial calcaneonavicular ligament in the setting of a partial posterior tibial tendon tear. (C) Axial PD image demonstrates a heterogeneous and irregular superomedial calcaneonavicular ligament in the setting of posterior tibial tendinosis and pes planus.

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Flexor Hallucis Longus Abnormalities

The FHL tendon is associated with a fibro-osseous tunnel and runs deep to the flexor retinaculum (between the medial and lateral tubercles of the posterior talar process) (Fig. 5.139). It passes underneath the sustentaculum tali to its plantar insertion at the base of the distal phalanx and great toe. The sheaths of the FHL and FDL cross at the master knot of Henry (see Fig. 5.139). The os trigonum is an ununited lateral tubercle in the posterior aspect of the talus found in 10% of individuals. FHL injuries at the level of the medial malleolus are seen in young athletes and dancers in conjunction with active plantarflexion mechanisms of injury. They are more common in female than male dancers. Hallux saltans refers to the development of a nodule or partial tear with triggering of the big toe.

Etiology, Pathology, and Clinical Features

The fibroosseous tunnel of the FHL runs between the medial and lateral posterior talar tubercles. Abnormalities are restricted to either the muscle or the tendon sheath.⁶¹ Muscle involvement may be focal or may involve the entire cross-sectional diameter. Tendon sheath involvement is variable. Muscle—tendon unit injuries are characterized by diffuse edema with or without focal muscle hemorrhage, and there may be accompanying tenosynovitis with a circular to elongated fluid collection.

Etiologic factors in FHL abnormalities include twisting injuries to the ankle and calcaneal fracture with involvement of the sustentaculum tali. Other causes include repetitive plantar-flexion and dorsiflexion that lead to tenosynovitis, a low-lying FHL muscle that is at risk for impingement, partial tearing or thickening with nodule development and hallux triggering (hallux saltans), and a fixed or locked FHL within the sheath (associated with severe tenosynovitis) (Fig. 5.140). The condition is exacerbated by hyper-plantarflexion.

In dancers, posterior impingement or talar compression syndrome results from full weight-bearing in maximum ankle plantarflexion in demi-pointe or full en pointe position.⁶² This is accentuated in the presence of an os trigonum, laxity of the lateral ligaments, and/or soft-tissue entrapment between the posterior lip of the talus and the os calcis. A fixed tethering of the FHL tendon proximal to the flexor retinaculum produces a check-rein deformity with a flexion contracture of the interphalangeal joint of the hallux and an extension contracture of the first metatarsophalangeal joint.⁶³ The FHL is sometimes called the Achilles tendon of the foot or “dancer's Achilles heel” (see Fig. 5.140; Fig. 5.141).

Paratendinitis (tenosynovitis) remains the most common abnormality (Figs. 5.136 and 5.137). With tendinosis and partial tears there is tendon thickening (Fig. 5.144), and with stenosing tenosynovitis there is fluid proximal to the talar fibro-osseous tunnel (Fig. 5.145). Complete tendon rupture in the talar fibro-osseous tunnel is uncommon (Figs. 5.136 and 5.137), and midfoot rupture at the distal insertion is more frequently seen. Paratenonitis occurs in three anatomic sites:

Fibro-osseous tunnel (first fibro-osseous tunnel) between the medial and lateral tubercles of the posterior talar process
Deep to the flexor retinaculum (see Fig. 5.143)
The level of the sesamoids within the distal hallux tunnel (third fibro-osseous tunnel) (see Fig. 5.146)

The clinical presentation is dominated by pain, swelling, and tenderness of the posterior ankle.

MR Appearance

Tearing of the FHL has been demonstrated on axial MR images at the level of the musculotendinous junction.³⁷^,⁶⁴ The FHL is a plantarflexor of the first toe and participates in plantarflexion and inversion of the foot. Rupture of this tendon may be difficult to identify on clinical examination without the assistance of MR localization. A distal rupture requires coronal images performed through the distal foot in addition to routine axial images through the tibiotalar joint.

MR imaging usually demonstrates communication of fluid between the FHL tendon sheath and the tibiotalar joint, commonly between the tibial plafond and the calcaneus. On FS PD FSE images the circular to elongated fluid collection generally demonstrates uniform hyperintensity with or without septations. The volume of fluid in the FHL tendon sheath is disproportionate relative to the tibiotalar joint (Fig. 5.148). Muscle strains are characterized by hyperintense edema or hemorrhage radiating from the trauma epicenter on FS PD FSE images. Foci of hemosiderin may also be found within the muscle.

In addition to tendinitis, ballet dancers may have muscle strains at or near the musculotendinous junction. FS PD FSE and STIR sequences are the most sensitive techniques in these injuries. In os trigonum syndrome (discussed in more detail below), there is hypertrophy of the os trigonum, resulting in a partial tethering of the FHL tendon.⁶³

Treatment

Repetitive stress may result in chronic muscle strain with or without hemorrhage, stenosing tenosynovitis, and partial or complete tendon tears. Conservative approaches to treatment include the use of anti-inflammatory agents, rest, modification of dance or related causative activities, and immobilization. When surgery is required, procedures include release of the constricting FHL tendon sheath and, if required, excision of an associated symptomatic os trigonum.

FIGURE 5.139 ● The flexor hallucis longus (FHL) is associated with three fibroosseous tunnels: a tunnel between the talar tubercles, a second tunnel deep to the sustentaculum tali, and a third tunnel between the hallucal sesamoids. (A) Lateral color illustration showing the course of the FHL and the knot of Henry where the flexor digitorum longus and flexor hallucis longus cross. The FHL is located between the medial and lateral talar tubercles on (B) a color illustration and (C) an axial T1-weighted MR arthrogram. (D) Arthroscopic image showing the FHL running in a sheath just posterior to the ankle capsule.

FIGURE 5.140 ● Flexor hallucis longus (FHL) tenosynovitis. Tendinitis of the FHL posterior to the medial malleolus is known as dancer's tendinitis. (A) Medial perspective lateral color illustration showing injury of the FHL as it passes through the fibro-osseous tunnel from the posterior aspect of the talus to the level of the sustentaculum tali; it acts like a rope through a pulley. Sagittal (B) and axial (C) FS PD FSE images demonstrating the extent of FHL tenosynovitis distal to the medial malleolus.

FIGURE 5.141 ● FHL injuries are associated with extreme plantarflexion and push-off maneuvers, as occur in football players and ballet dancers. There is chronic muscle strain of the FHL just proximal to the sustentaculum tali. (A) Axial FS PD FSE with FHL muscle chronic strain (hyperintense signal). (B) Sagittal T1-weighted image showing extreme plantarflexion in the en pointe position with proximity of the transverse ligament and posterior process.

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Tibialis Anterior Tendon Injuries

The tibialis anterior tendon inserts onto the medial cuneiform (Figs. 5.136 and 5.137) and functions in ankle dorsiflexion and inversion of the subtalar and metatarsal joints. It receives its blood supply exclusively from the anterior tibial artery, which puts it at risk for ischemia (Fig. 5.151). Rupture of the tibialis anterior tendon can occur between the extensor retinaculum and the insertion onto the medial first cuneiform and adjacent base of the first metatarsal. Weakness of dorsiflexion, localized tenderness, and drop foot gait are observed on clinical evaluation. The musculotendinous junction at the level of the middle to distal third of the tibia is a rare site of tendinosis.

Etiology, Pathology, and Clinical Features

Anterior tibialis tendon ruptures account for only 1% of muscle and tendon injuries. Spontaneous rupture is rare but may occur in association with diabetes, gout, or rheumatoid arthritis. It is usually seen in individuals over 45 years of age and more commonly in those over 60 years of age. Tibialis tendon ruptures may also occur in athletes, usually males, particularly

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runners, soccer players, and hikers. Steroid injections also predispose to tendon rupture. The usual mechanisms of injury are eccentric contraction during midfoot and forefoot forced plantarflexion⁶³ and repetitive dorsiflexion and plantarflexion, because plantarflexion places eccentric stress on the tibialis anterior. Rupture may also be related to abrasion from the inferior edge of the extensor retinaculum or from mechanical irritation, such as occurs from ski boots and hockey skates. Traumatic lacerations, related to the superficial and anterior location of this tendon, may also occur. Although the rupture usually occurs proximal to the insertion, no zone of hypovascularity has been documented.

FIGURE 5.142 ● Tenosynovitis of the FHL between the medial and lateral talar tuberosities.

FIGURE 5.143 ● Tenosynovitis of the FHL distal to the fibro-osseous tunnel between the medial and talar tubercles and underneath the sustentaculum tali. Tenosynovitis is associated with chronic friction and tendon wear between the talar tuberosities, deep to the flexor retinaculum inferior to the sustentaculum tali and distally between the hallucal sesamoids. (A) Sagittal FS PD FSE image. (B) Axial FS PD FSE image.

Morphologic and pathologic findings include:

A high-grade partial to complete tear (normal width 1 cm) with tendon retraction
A mass effect produced by protrusion of the tendon relative to the inferior extensor retinaculum
Secondary inflammation of adjacent tendon sheaths
Hemorrhage
An empty tendon sheath
Dorsal exostosis
Medial cuneiform morphology with ridge contour associated with distal tendon degeneration of a partial tear (Fig. 5.152)
Histologic evidence of peritenonitis
Inflammatory changes but no intrinsic tendon degeneration
Clinically, patients present with weakness with attempted dorsiflexion, local tenderness and foot drop, and a palpable mass and/or defect. Initial symptoms may be minimal.

MR Appearance

Tibialis anterior tendon injuries are best seen on oblique axial images oriented perpendicular to the tendon distal to the level of the medial malleolus.⁶⁵^,⁶⁶ In this location, partial tears are less likely to be overread as complete ruptures because the tibialis anterior tendon changes its course and orientation at the level of the midfoot (Fig. 5.153). The key finding on MR images is a fluid-filled tendinous gap with proximal tendon retraction located between the superior and inferior extensor retinaculum, 1.5 to 3 cm proximal to the insertion site. The size of the defect varies depending on the degree of retraction of the torn tendon deep to the superior slip of the inferior extensor retinaculum. Retraction is limited to the level of the ankle joint because of the inferior extensor retinaculum. Additional MR findings include:

Enlarged tendon and sheath
Fraying of the tendon ends

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Focal enlargement and partial tendon continuity with preserved tendon fibers in high-grade partial tears
Absence of the tendon at the tear site (empty sheath)
Associated dorsal osteophytes in ruptures at the medial tarsometatarsal joint
Inflammation of the synovial tendon sheath (may be associated with tendon rupture or rheumatoid disease, or may be idiopathic)
Fluid within the tendon sheath
Associated hemorrhage

FIGURE 5.144 ● (A) Sagittal FS PD FSE image showing a nodular partial tear (the partial tear binds in the fibro-osseous tunnel). (B) Hallux saltans may develop as the FHL binds as it passes through the second fibro-osseous tunnel on the medial side of the foot. A nodular partial tear of the FHL may cause triggering of the big toe.

FIGURE 5.145 ● Stenosing tenosynovitis resulting from chronic inflammation of the FHL peritenon occurs with entrapment of the FHL tendon in its sheath at the level of the ankle joint. A functional hallux rigidus or checkrein deformity (claw hallux) may subsequently develop. (A) Sagittal FS PD FSE image. (B) Axial FS PD FSE image.

FIGURE 5.146 ● Distal rupture of the FHL results from acute dorsiflexion or laceration. The fibrous slip connecting the FHL and flexor digitorum longus (FDL) at Henry's knot limits the retraction of FHL proximal to this point. FHL tears proximal to Henry's knot may be associated with tendon recoil into the calf. (A) Plantar view color illustration of FHL distal rupture. (B) Sagittal PD-weighted image with retracted FHL to the plantar aspect of the forefoot. (C) Coronal PD FSE image.

FIGURE 5.147 ● Distal rupture of the flexor hallucis longus (FHL) tendon with proximal retraction. FS PD FSE coronal (A) and axial (B) images. The retracted FHL tendon is enlarged in cross-sectional area relative to the normal adjacent flexor digitorum longus (FDL) tendon. Associated soft-tissue edema is hyperintense on FS PD FSE images. The FHL tendon normally inserts at the base of the distal phalanx of the first toe. C, cuboid.

FIGURE 5.148 ● Disproportionate fluid in FHL tendon sheath in a basketball player who had minimal tibiotalar joint fluid. Axial FS PD FSE image.

FIGURE 5.149 ● Distal insertion of the tibialis anterior to the medial cuneiform. The tibialis anterior also attaches to the base of the first metatarsal. Sagittal T1-weighted image.

FIGURE 5.150 ● At its insertion, the most lateral fibers of the tibialis anterior rotate anteriorly and insert on the cuneiform. The medial fibers rotate posteriorly and insert distally on the dorsolateral first metatarsal. Coronal T1-weighted image.

FIGURE 5.151 ● The tibialis anterior receives its neurovascular supply from the deep peroneal nerve and anterior tibial artery.

FIGURE 5.152 ● (A) Medial cuneiform morphology showing convex medial border (top), concave smooth border (middle), and a ridge associated with a concave border and tendon degeneration (bottom). (B) Coronal T1-weighted image showing normal tibialis anterior. However, there is ridge morphology along the medial cuneiform border.

Extensor tendon tenosynovitis may be observed involving the other anterior extensors (Fig. 5.154), including the extensor hallucis longus and extensor digitorum longus, although rupture in these locations is distinctly unusual.

Treatment

The diagnosis of tibialis anterior tendon tear is frequently delayed. The clinical history may include minor injury, or there may be an association with chronic rupture of the PTT. A history of steroid injections also suggests the diagnosis. There may also be an avulsion fracture of the medial cuneiform. Initially patients adapt their gait to compensate for the injured tendon and there is foot slapping, toe dragging, and an inability to heel walk. Active dorsiflexion produces eversion of the foot secondary to an engaged extensor hallucis longus and extensor digitorum longus. Eventually complications such as a progressive flat foot deformity in older patients and equinocavus deformity and Achilles tendon contracture in children develop.

Conservative treatment may be considered when the tendon displacement is less than 5 mm, with or without osseous fragments. Less active or older individuals may be treated with below-the-knee non—weight-bearing casting. Surgery is indicated for younger or more active patients within 3 to 4 months of injury. Procedures include end-to-end repair, a sliding tendon graft and extension hallucis transfer, and tendon grafts in the event of large tendon gaps. The extensor digitorum longus and free peroneus brevis grafts are used for tendon lengthening.

Peroneal Tendon Abnormalities

The peroneal brevis and longus tendons are lateral stabilizers of the ankle joint. They share a common synovial sheath posterior to the lateral malleolus (Fig. 5.155). The peroneal brevis is anterior to the peroneus longus tendon within the retromalleolar

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sulcus of the distal fibula.⁶³ The peroneal tendons may rupture secondary to trauma or laceration of the lateral aspect of the ankle. MR imaging defines the position of the peroneal tendons as well as the fibular and retinacular anatomy.⁵² Absence of the low-signal-intensity tendon within the peroneal tendon sheath may be observed on sagittal or axial images. The peroneal tendons are also involved in partial or complete dislocations.

FIGURE 5.153 ● (A) Partial tear of the tibialis anterior on a lateral color illustration. The tibialis anterior tendon has a relatively straight course deep to the superior extensor retinaculum. There is a potential site of compression and paratenonitis as the tibialis anterior courses between the deep and superficial superior subdivisions of the superomedial band of the inferior extensor retinaculum. The distal tibialis anterior courses deep to the inferior subdivision of the superomedial band of the inferior extensor retinaculum and inferomedial band of the inferior extensor retinaculum. Partial tear of the tibialis anterior tendon (arrow) is shown on (B) fast STIR sagittal and (C) gadolinium-enhanced FS T1-weighted axial oblique images. The axial oblique prescriptions designated from the STIR sagittal image ensure that the axial images are acquired perpendicular to the long axis of the tendon. The gadolinium contrast enhances the partial tear pattern within the tibialis anterior tendon (C, cross-section). (D) Complete discontinuity of the tibialis anterior in younger individuals is usually secondary to tendon laceration. Tendinosis of the tibialis anterior is rare, although paratenonitis may be indirectly caused by eccentric contraction in runners and hikers on downhill surfaces.

FIGURE 5.154 ● Tenosynovitis (paratenonitis) of the extensor hallucis longus (EHL) (A) and extensor digitorum longus (EDL) (B) tendons is shown on axial FS PD FSE images. The EHL tendon enlarges distally at its insertion on the dorsal aspect of the distal hallucal phalanx. The EDL bifurcates below the superior extensor retinaculum, and each branch then divides into two tendons under the stem of the inferior extensor retinaculum.

FIGURE 5.155 ● Normal relationship of the peroneal tendons to the distal fibula and common synovial sheath of the peroneal tendons posterior to the lateral malleolus. The peroneus brevis makes two turns in its course, one at the fibular groove and the other at the peroneal tubercle. The peroneus longus makes three turns, at the fibular groove, the peroneal tubercle, and the cuboid notch (os peroneum).

Peroneus Brevis Tendon Tear

The peroneus brevis tendon is anterior to the peroneus longus in a retrofibular groove. It can be seen distal to the lateral malleolus and superior to the peroneal trochlea in an osteoaponeurotic canal contributed to by the inferior peroneal retinaculum. The SPR restrains tendon subluxation or dislocation and inserts into medial and lateral ridges of the tendon sulcus. There is a close relationship of the common peroneal tendon sheath and adjacent, more medially located, CFL. This intimate relationship is appreciated on axial MR images through the ankle joint. The peroneus brevis functions in ankle eversion.

Etiology, Pathology, and Clinical Features

Partial or complete tearing of the peroneal tendons usually occurs in association with an acute injury, although it may occur spontaneously.⁶³ Spontaneous rupture is more common in young adults, as are ruptures associated with sports-related (especially soccer) trauma. Partial tears are more common than complete rupture.

Degenerative tendon splits are more usually seen in older adults. In a cascade of events, overuse and repetitive trauma cause chronic injury, subsequent mechanical friction and shearing injury induce degeneration, and degenerative changes precede the longitudinal splits. An autopsy study by Sobel et al.⁶⁷ showed that 11% of specimens had varying degrees of attritional changes in the peroneus brevis tendon. The existence of preexisting tendon degeneration, prior to tendon rupture, is also suggested by McMaster's work,⁶⁸ which shows that intratendinous rupture is less common than failure of the musculotendinous unit at the insertion to bone, within the muscle or at the musculotendinous junction.⁶⁸

Peroneal brevis tears may also be dynamic injuries associated with CFL sprains, a shallow fibular groove, and SPR laxity. Lateral ligament tears and SPR laxity lead to splits and tendon subluxation. Tendon dislocation may also be associated with stripping of the loosely attached SPR.

Anatomic factors contributing to peroneus brevis injury include a hypertrophic fibular ridge, an associated peroneus quartus, an accessory or anomalous peroneal tendon, and calcaneal friction associated with entrapment or tearing. An absent or convex peroneal canal in the distal fibula may also be a contributing factor.

Pathologic changes include peroneal tenosynovitis (Fig. 5.156), which is associated with spastic flat feet and is characterized by tendon and synovial thickening (Fig. 5.157). Synovial proliferation, degenerative changes, longitudinal splits, and frayed tendon edges can also be seen. Tears have been classified as either grade I, with less than 50% of the cross-sectional tendon area involved, or grade II, with more than 50% of the cross-sectional tendon area affected.

Patients present with the insidious onset of chronic ankle pain, edema within the peroneal sheath, popping and clicking with active foot eversion, subclinical subluxation, and crepitus. The peroneal compression test (compression of the peroneus longus against the peroneus brevis) produces pain.

MR Appearance

MR imaging demonstrates the split of the peroneus brevis tendon into two subtendons. The defect is centered at the retrofibular groove near the distal tip of the lateral malleolus and extends distally or proximally or in both directions. Longitudinal tears are usually 2.5 to 5 cm in length and have a C-shaped configuration relative to the peroneus longus.

Key MR findings include the following:

Longitudinal splits/clefts and fluid are seen within partial tears of the peroneus brevis tendon (Fig. 5.158).
There is anteroposterior separation of the split components of the tendon.
Subtendons are hypointense on T1- or PD-weighted images with hyperintense fluid between the split subtendons on FS PD FSE images. The peroneus longus tendon may interpose between the two subtendons of the brevis.
Partial tears or longitudinal splits occur at the level of the lateral malleolus (Fig. 5.159), and may be associated with a sprain and SPR or lateral ligament complex injury. Identification of peroneus brevis involvement is important in case the peroneus brevis is to be used in a lateral ligament reconstruction.
Abrasion of the peroneus brevis from the calcaneofibular ligament or lateral cartilaginous ridge of the fibula is thought to be an initiating factor in the development of longitudinal tears.⁶⁹ Lateral ligament tears with associated SPR laxity may lead to peroneus brevis tendon splits and anterolateral subluxation of both peroneal tendons.
Complete rupture (Fig. 5.160) of a peroneal tendon should be confirmed on images obtained in more than one imaging plane.
Reactive lateral calcaneal marrow edema at the attachment site of the inferior peroneal retinaculum (the peroneal tubercle) is associated with acute rupture of the peroneus brevis tendon.
Degeneration and intrasubstance longitudinal splits of the peroneus longus tendon may also be seen in association

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with tears of the peroneus brevis tendon (Fig. 5.161). A complete tendon rupture of the peroneus longus is unusual (see discussion below).
Peroneal tendon entrapment or impingement is associated with a fracture of the calcaneus in which lateral fragment displacement narrows the fibulocalcaneal space.⁶³
In partial tears the tendon is attenuated and decreased in cross-sectional diameter with an irregular contour.
Degenerative changes are intermediate in signal on T1- and PD-weighted images, and fluid associated with tenosynovitis is hyperintense on FS PD FSE images.
A split brevis tendon may wrap around the longus tendon (Fig. 5.162).

FIGURE 5.156 ● Tenosynovitis (paratenonitis) of the peroneal tendons on sagittal FS PD FSE (A) and axial FS PD FSE (B) images. Tenosynovitis is associated with overuse injuries. Tendon morphology is intact.

FIGURE 5.157 ● In chronic peroneal tenosynovitis, thickened low-signal-intensity synovium (arrows) encases the peroneus brevis and longus tendons. There is no increased signal intensity within synovial tissue on (A) intermediate-weighted or (B) T2-weighted axial images.

FIGURE 5.158 ● (A) Color illustration of a peroneus brevis partial tear. Tenosynovitis (paratenonitis) with tendinosis including longitudinal tears and tendinosis of the peroneus brevis usually occurs at the level of the fibular groove at the distal lateral malleolus. Longitudinal tendon tear is shown on sagittal FS PD FSE (B) and axial FS PD FSE (C, D) images. The resultant two subtendons distal to the lateral malleolus are shown in (D).

FIGURE 5.159 ● (A) Intermediate-weighted axial image displaying anterolateral dislocation of the peroneus longus tendon (PL) and split of the peroneus brevis tendon (PB; black arrows), both associated with a torn superior peroneal retinaculum (white arrows). LM, lateral malleolus. (B, C) In a separate case there is anterolateral subluxation of the split (small arrows) peroneus brevis tendon (PB) associated with a torn superior peroneal retinaculum (curved arrow) and partial lateral subluxation of the peroneus longus tendon (PL). (B) FS PD FSE axial image. (C) FS PD FSE sagittal image. (D) Corresponding color illustration of the peroneus brevis split at the level of the lateral malleolus.

FIGURE 5.160 ● Acute rupture of both the peroneus brevis and longus tendons. Complete rupture of the peroneus brevis is associated with mechanical trauma and tendon irritation from direct abrasion against the fibular groove in cases of superior peroneal retinacular laxity of the peroneus longus. Tears of the peroneus longus may be associated with peroneus brevis tendon tears at the level of the malleolus. Up to one third of peroneus brevis ruptures are associated with peroneus longus tears. (A) Sagittal T1-weighted image. (B) Axial FS PD FSE image.

Peroneus Longus Tendon Tear

The peroneus longus tendon is located along the lateral surface of the calcaneus, inferior to the peroneus brevis tendon and peroneal trochlea and superior to the calcaneal tubercle, which is the point of insertion of the calcaneofibular ligament.⁷⁰ The peroneus longus tendon courses deep to the inferior peroneal retinaculum and occupies a groove and tunnel (created by the long plantar ligament) along the plantar surface of the cuboid (Fig. 5.163).

Peroneus longus tendon ruptures (Fig. 5.164) are associated with peroneus brevis tendon tears at the level of the malleolus. Isolated peroneus longus tears are more commonly seen at the midfoot (Fig. 5.165). Attritional tears of the peroneus longus may be associated with an os peroneum and occur within the cuboid peroneus tendon groove.⁷¹ In the painful os peroneum syndrome (POPS) there may be an associated avulsion fracture through the os peroneum (Fig. 5.166) that occurs with inversion or forced eversion of a supinated foot. POPS may exist without a fracture of the os perineum, however, and midfoot tears of the peroneus longus may occur without an os peroneum. A prominent or hypertrophied peroneal tubercle that serves as the attachment site for the inferior peroneal retinaculum is related to chronic tears of the peroneus longus. The peroneus longus is also susceptible to injury as it curves around the cuboid bone.

Superior Peroneal Retinacular Tears

FIGURE 5.161 ● Rupture of the peroneus brevis tendon on (A) T2*-weighted and (B) FS PD FSE axial images. Note the hypointense torn fibers of the peroneus brevis tendon, which are seen more clearly on the FS PD FSE sequence (B) compared with the T2*-weighted sequence (A), which generates greater hyperintensity at the tear site. (C) Rupture of the peroneus brevis tendon is associated with avulsion of the inferior peroneal retinacular attachment (small black arrows) to the peroneal tubercle of the calcaneus. Adjacent hyperintense subchondral marrow edema is seen in the characteristic location within the peroneal tubercle (large white arrows). PL, peroneus longus tendon.

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The superior peroneal retinaculum (SPR) (Fig. 5.167) contributes to the posterolateral border of the peroneal tunnel and helps keep the peroneal tendons within the retromalleolar groove.⁷² Acute or chronic dislocation of the peroneal tendons may be associated with congenital absence or traumatic laxity or tear of the SPR.⁷⁰ SPR trauma is associated with a dorsiflexion injury compounded by inversion or eversion of the foot. Detachment of the SPR occurs with potential lateral subluxation or dislocation of the peroneal tendons. Inversion injuries that stress the SPR result in the common association of SPR injuries with lateral collateral ligament tears. Chronic ankle instability associated with SPR laxity predisposes to an increased risk of chronic peroneal dislocation.

SPR injuries are classified surgically into three grades:

Grade I: Elevation of the retinaculum and periosteum from the lateral malleolus with pouch formation
Grade II: Elevation of the fibrocartilaginous ridge, the retinaculum, and the periosteum
Grade III: Osseous avulsion associated with the fibrocartilaginous lip, retinaculum, and periosteum

In another system, Oden classifies injuries into four types (Fig. 5.168):⁷³

Type I: A stripped SPR (Figs. 5.136 and 5.137)
Type II: A retinacular tear at the distal fibula (Fig. 5.171)
Type III: Osseous avulsion of the SPR
Type IV: An SPR tear posterior to the distal fibular attachment (Fig. 5.172)

Treatment of Peroneal Tendon Injuries

Peroneal tendon instability with SPR disruption will progress to tendon fissuring and eventually frank tendon rupture. Frequently there is concomitant involvement of the peroneus brevis and longus and stenosing tenosynovitis. Conservative approaches to treatment include limited immobilization, anti-inflammatory medications, physical therapy, and orthotics. If these measures fail, surgery is necessary, and procedures include primary anastomosis, tendon débridement, and excision of tenosynovial inflammation. A reconstruction of the SPR is combined with repair or débridement of the involved peroneal tendons.

FIGURE 5.162 ● Peroneus brevis tendon split associated with a peroneus quartus muscle, which may contribute to mechanical crowding in the retromalleolar groove of the distal fibula. Axial PD FSE (A) and FS PD FSE (B) images.

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Ligamentous Injuries

Pathogenesis

Injuries to the ligaments about the ankle usually result from inversion and internal rotation of the foot combined with ankle plantarflexion.⁷⁴^,⁷⁵ Normally, when the foot is positioned in neutral or plantarflexion, the orientation of the anterior talofibular ligament is 45° to the horizontal, and it functions as a restraint to internal rotation.⁷⁴ The vertically oriented CFL primarily protects against varus force and offers little resistance to internal rotation. The ATFL is the weakest and is usually the first ligament to rupture with forced inversion and plantarflexion.⁷⁶ Even when inversion and plantarflexion forces cause rupture of the CFL, the PTFL may remain uninjured, except in severe ankle trauma with dislocation.⁷⁶

When all three ligaments are ruptured, the ankle is unstable. With complete disruption of the ATFL, there is forward displacement of the talus in the ankle mortise. With sequential rupture of the ATFL and CFL, there is medial tilting of the talus with progressive widening of the lateral joint space. The strong deltoid or medial collateral ligament, which consists of the tibionavicular, anterior tibiotalar, tibiocalcaneal, and posterior tibiotalar ligaments, rarely ruptures. Avulsion fracture of the medial malleolus and disruption of the AITF are associated with abduction and laterally directed forces.⁷⁶

Diagnosis

Ankle sprains are classified into three clinical grades:⁷⁴

Grade I: Stretching or partial tearing of ATFL fibers
Grade II: A moderate sprain associated with significant edema in which there is partial tearing of the ATFL with stretching of the CFL
Grade III: Tearing of the ATFL and CFL, causing ankle instability

MR Appearance

The normal ligamentous anatomy (see Fig. 5.167) of the ankle is clearly demonstrated on MR images.⁷⁵ Indications for the use of MR imaging in the evaluation of patients with ligament sprains or ruptures, however, have not yet been established. Clinical assessment of ligament injury is frequently difficult because of concomitant soft-tissue swelling and joint effusion. MR imaging provides direct visualization of the ankle ligaments, which is not possible with conventional radiographs, arthrography, or CT. Results of stress positioning with conventional radiographs may be variable, and the patient may require anesthesia to limit pain and guarding. Comparison views with the opposite ankle are also necessary. MR imaging is particularly

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useful in assessing the tibial plafond and talar dome. Subchondral and articular damage to the superior talar dome may occur with subluxation of the ankle (i.e., talar displacement in plantarflexion) secondary to ATFL interruption.

FIGURE 5.163 ● (A) Normal anatomy of the peroneus longus tendon below the peroneal tubercle and within the cuboid groove. In the plantar aspect (sole) of the foot the peroneus longus receives a second synovial sheath from the groove of the cuboid to its insertion on the base of the first metatarsal and medial cuneiform. Plantar course of the peroneus longus is shown on an axial PD FSE image (B) and a plantar perspective color illustration (C).

FIGURE 5.164 ● Longitudinal split of the peroneus longus tendon is visualized adjacent to a prominent peroneal tubercle on a sagittal T1-weighted image (A) and an axial FS PD FSE image (B). Two subtendons are demonstrated at the level of the calcaneus (B). (C) Axial PD FSE image in a separate case with a prominent peroneal tubercle separating the peroneus brevis and longus tendons. Chronic tears of the peroneus longus tendon may occur at the last two turns of the tendon at the level of the peroneal tubercle (seen with a hypertrophied peroneal tubercle) or around the cuboid bone (also associated with an os peroneum).

FIGURE 5.165 ● Acute midfoot tear of the peroneus longus visualized on sagittal FS PD FSE (A) and axial FS PD FSE (B) images. Acute tears of the peroneus longus occur in sports-related injuries or trauma. The midfoot is a common location for tears in older patients secondary to preexisting attritional and mechanical wear.

FIGURE 5.166 ● Sagittal FS PD FSE image of a partial tear of the peroneus longus tendon associated with a fractured os peroneum. Peroneus longus tears are associated with an avulsion fracture in the painful os peroneum syndrome (POPS). In a bipartite os peroneum, separation greater than 6 mm is associated with a fracture and complete tear of the peroneus longus. In a non-bipartite os peroneum, proximal displacement greater than 10 mm is associated with a peroneus longus rupture.

FIGURE 5.167 ● Normal superior peroneal retinaculum blending with hypointense fibrous ridge along the posterolateral aspect of the lateral malleolus. Axial T1-weighted MR arthrogram.

FIGURE 5.168 ● Spectrum of superior peroneal retinaculum (SPR) injuries based on Oden's surgical classification. In the normal SPR the retinaculum originates from the distal fibula and a small fibrous ridge is identified. A type I injury represents stripping of the SPR from the distal fibula and formation of a potential pouch lateral to the distal fibula. This pouch is associated with subluxation or dislocation of the peroneal tendons. In a type II injury the SPR is avulsed from its fibular insertion. In a type III injury there is an osseous avulsion from the distal fibula. Type IV injuries are associated with SPR disruption at its posterior attachment.

FIGURE 5.169 ● Dislocation of the peroneal tendons in a type I SPR injury with the peroneus longus and brevis tendons contained within the lateral pouch created by the stripped-off periosteum. The SPR is thickened and is associated with a remnant of the peroneus longus tendon. (A) Sagittal FS PD FSE image. (B) Axial FS PD FSE image.

FIGURE 5.170 ● Longitudinal split of the peroneus longus tendon into two subtendons associated with dislocation of the torn peroneus longus in a type I SPR injury. Axial PD FSE image.

Lateral Ligament Complex Injuries

The lateral collateral ligament complex includes the ATFL, CFL, and PTFL (Fig. 5.173). The lateral gutter (Fig. 5.174) is formed by the ATFL and PTFL.

Anterior Talofibular Ligament Tear

The anterior talofibular ligament (ATFL), which is separated into two distinct bands, is the weakest of the lateral collateral ligaments. It is taut in plantarflexion and therefore more susceptible to injury than the CFL, which is taut in the neutral position. ATFL tears are frequently associated with a capsular rupture and extravasation of joint fluid into the anterolateral soft tissues.⁷⁷ They most commonly occur in individuals 15 to

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35 years of age, and males predominate in this age group. After 40 years of age there is a higher incidence in females. Eighty-five percent of ankle sprains occur laterally, representing 12% of emergency room trauma. A significant number (25% to 50%) of lateral sprains are associated with running and jumping sports.

FIGURE 5.171 ● (A) A rim fracture of the lateral aspect of the lateral malleolus is associated with recurrent subluxation and dislocation of the peroneal tendons, as shown on lateral and superior view illustrations. (B, C) Type III superior peroneal retinacular injury with lateral malleolus fracture or rim sign. Sagittal (B) and axial (C) FS PD FSE images demonstrate hyperintense edema in the lateral malleolus associated with subtle osseous avulsion of the SPR attachment.

FIGURE 5.172 ● A superior retinacular tear posterior to the fibular attachment is seen posterior to the peroneal tendons, which are located in a normal position.

Etiology, Pathology, and Clinical Features

The most common mechanism of injury is inversion and internal rotation with plantarflexion, as occurs with loading the ball of the foot on landing from a jump or fall. In plantarflexion the talus moves anteriorly and is unlocked from mortise. Inversion mechanisms are confirmed by the observation of a medial talar bone contusion in association with an acute tear of the ATFL.

Tears commonly occur along the long course of the ligament, from the anterior border at the lateral malleolus to the talar insertion anterior to the lateral articular facet, and are characterized by loss of the normal ligament morphology and partial or complete ligament interruption. Injuries range from ligament laxity, to midsubstance rupture with interstitial involvement and hemorrhage, to avulsion, to complete ligamentous disruption of both larger upper and smaller lower bands. An avulsed ATFL may be associated with a distal fibular avulsion fracture. When combined with CFL injury, there is widening of the lateral joint space and the talus is tilted medially.

Acute injuries are characterized by a hyperplastic synovial reaction and accumulation of hemosiderin. Chronically torn talofibular ligament fibers have been infrequently reported to form a meniscoid lesion, with tissue interposed between the talus and the fibula. Chronic or healed ligamentous disruptions show generalized thickening of the ligament.

Clinically, patients present with ATFL tenderness. In acute grade III lesions (see below) patients report a pop followed by pain and swelling. In acute grade II and III lesions there is difficulty bearing weight on the affected ankle. Patients also report a sense of giving way, which indicates functional joint instability. The anterior drawer test (Fig. 5.175) and the inversion stress test (Fig. 5.176) are used to make the diagnosis clinically.

Classification

Lateral ankle sprains are classified into three grades:

Grade 1: ATFL stretching
Grade II: Partial tear of the ATFL, with stretching of the CFL (Fig. 5.177)
Grade III: Complete tears of both the ATFL and CFL (Fig. 5.178)

MR Appearance

The normal anatomy and pathologic changes affecting the ATFL are best displayed on axial or axial oblique planar images with FS PD FSE, or 3DFT T2*-weighted contrast and MR arthrography.⁷⁸^,⁷⁹ MR arthrography is more accurate and sensitive in diagnosing ATFL tears than noncontrast MR imaging or stress radiography.⁸⁰

3DFT axial images with thin (1 to 2 mm) sections eliminate the need to dorsiflex the foot (to optimize visualization of the tibiofibular and talofibular ligaments) or to plantarflex the foot (to optimize visualization of the calcaneofibular ligament in the axial plane). At the level of the distal lateral malleolus,

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the ATFL is seen as a prominent, low-signal-intensity, 2- to 3-mm band, oriented anteromedially and extending to its talar attachment. Axial oblique images perpendicular to the talonavicular joint may be used to demonstrate ATFL fibers more parallel with the plane of section.

FIGURE 5.173 ● (A) Anterior and dorsal view of the medial and lateral ligaments of the ankle. (B) Lateral ligaments of the ankle in a lateral view color illustration. (C) Anterior and posterior talofibular ligaments are visualized in the sagittal plane on a sagittal T1-weighted MR arthrogram.

FIGURE 5.174 ● (A) Axial T1-weighted MR arthrogram showing the lateral gutter between the anterior and posterior talofibular ligaments. The posterior talofibular ligament is the strongest and most deeply seated of the lateral ligaments. It is intracapsular but extrasynovial. On MR axial images, the posterior talofibular ligament fans out at its fibular origin from the depression at the medial and posterior aspect of the lateral malleolus and converges at its insertion onto a prominent tubercle on the posterior surface of the talus. The anterior talofibular ligament may be separated into two distinct bands. (B) The medial and lateral boundaries of the lateral gutter consist of the talus medially and the fibula laterally. (C) Differentiating pain in the lateral gutter from subtalar pain is done by careful palpation. Selective injections can also be helpful in distinguishing the area of maximum pain.

FIGURE 5.175 ● Anterior drawer test. With the tibia secured, the heel is pulled forward and internally rotated. Note the subluxation of the talus anteriorly on the distal tibia (inset). A double ligament tear leads to increased anterior excursion of the talus on the tibia.

FIGURE 5.176 ● Inversion stress test. A single ligament tear allows increased talar tilt (inset). A double ligament tear leads to significant talar tilt with inversion stress.

FIGURE 5.177 ● (A) Grade 2 ATFL sprain with thickened ligament and poorly defined margins on an axial T2-weighted FSE image. (B) Associated lateral malleolus edema and calcaneofibular sprain are demonstrated on a coronal FS PD FSE image.

Acute tears are associated with partial or complete ligamentous disruption, ligament laxity, or partial or complete absence of the ligament. Additional MR findings include:

A change from hypointense to intermediate signal intensity on T1- or PD-weighted images (Fig. 5.179) and hyperintensity on FS PD FSE images along the course of the tendon at a 45° angle from the lateral malleolus to the talus
Localized high-signal-intensity fluid or hemorrhage on FS PD FSE or T2*-weighted images⁷⁹
Extension of hyperintense fluid anterolaterally into soft tissues
Blurring of the anterior and posterior ligament margins
Thickening (Fig. 5.180) or absence of the ligament in acute injury
Subacute to chronic residual thickening in a healed and scarred ligament (Fig. 5.181)
Chronic instability associated with attenuated or hypoplastic ligament with sharper, more defined ligament margins
Ligament hyperplasia secondary to reinjury with continued stress
Avulsed ligament with or without distal fibula avulsion fracture
Associated capsular rupture
Synovial inflammation
Inhomogeneity and hemosiderin associated with hemorrhage
Soft-tissue edema adjacent to anterolateral gutter
Bone marrow edema at the distal fibular or talar insertion
Fluid in tibiotalar effusion and adjacent tendon sheaths (peronea l tendons)

ATFL injuries may occur at the talus insertion (Fig. 5.182) or lateral malleolus attachment (Fig. 5.183). Osseous avulsions often demonstrate the ATFL fibers attached to the avulsed fragment in the lateral gutter (Fig. 5.184). In addition to associated CFL injuries, ATFL pathology is frequently associated with injuries to the deltoid ligament (Fig. 5.185) or syndesmotic ligaments (see Fig. 5.182).

Calcaneofibular Ligament Sprain

FIGURE 5.178 ● Grade 3 ATFL tear (A) distally associated with CF ligament disruption (B) on FS PD FSE axial images. Associ-ated medial malleolus edema (C) may occur with a contusion of the anteromedial talus (D) in a combined lateral ligament injury with inversion and dorsiflexion. A posteromedial talar contusion may also be seen in a combined inversion and plantarflexion injury. (C) Coronal FS PD FSE image. (D) Sagittal FS PD FSE image.

FIGURE 5.179 ● (A) Normal hypointense anterior talofibular ligament. The anterior talofibular ligament is closely related to the capsule of the talofibular joint and becomes taut in plantarflexion as it braces the body of the talus. Grade 2-3 ATFL sprain with the ATFL is intermediate in signal on the PD-weighted axial image (B) and abnormally thickened and lax on the FS PD FSE image (C).

FIGURE 5.180 ● Thickened ATFL ligament resulting from a grade 2 sprain. Lateral view color illustration.

FIGURE 5.181 ● Chronically thickened ATFL as a sequela of a previous ligament tear.

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The calcaneofibular ligament (CFL) is crossed superficially by the peroneal tendons and their sheaths (Fig. 5.186). It is an extracapsular cord-like structure, usually 2 cm in length and 4 to 6 mm in diameter, that stabilizes both the tibiotalar and subtalar joints. The normal angle of the CFL to the ATFL is between 70° and 140° and the alignment of the CFL (parallel to the tibia in neutral dorsiflexion) places it at risk for sprain. CFL sprains are most commonly caused by twisting injuries involving both dorsiflexion and internal rotation. The CFL is the second most frequently injured ankle ligament; injury occurs most commonly in males from 15 to 35 years of age.

The defect may be located anywhere along the course of the ligament from the distal lateral malleolus to the lateral surface of the calcaneus. Injuries frequently involve a midsubstance rupture complex of the CFL, the ATFL, and the intervening capsule. Morphologically there is partial or complete ligament interruption, ligament laxity, an irregular ligament contour, and attenuation of ligament fibers. Ligament fiber disruption and hemorrhage are also seen. When combined with ATFL ligament injury, there is widening of the lateral joint space and varus tilting of the talus. Peroneal retinacular thickening and tenosynovitis are commonly seen with CFL injuries.

As described above, lateral ankle injuries are classified into three grades: grade I lesions are characterized by ATFL stretching; in grade II lesions there is a partial tear of the ATFL with stretching of the CFL (see Fig. 5.177); and in grade III there are complete tears of both the ATFL and CFL (see Fig. 5.178).

FIGURE 5.182 ● (A) Acute disruption of the ATFL from its talar insertion. Normally the ATFL inserts anterior to the lateral articular facet of the talus. Axial FS PD FSE images showing a complete distal ATFL tear with wavy ligament morphology associated with a high ankle ligament sprain and CF ligament tear (B) and anterior syndesmotic ligament injury (C).

FIGURE 5.183 ● Acute ATFL disruption from the anterior border of the lateral malleolus. The torn proximal end of the ATFL is wavy and frayed. Fluid is interposed between the ligament and lateral malleolus. (A) Color lateral illustration. (B) Axial PD FSE image. (C) Axial FS PD FSE image.

FIGURE 5.184 ● Chronic osseous avulsion from the lateral malleolus with the ATFL fibers and deep fibers of the PTFL attached to the displaced fragment. These avulsions would be interpreted as a loose body in the lateral gutter on conventional radiography.

FIGURE 5.185 ● Association of deltoid ligament sprain with an ATFL tear. Axial FS PD FSE image.

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The clinical picture is dominated by a painful and swollen lateral ankle. There is tenderness at both the ATFL and the CFL, with increased varus tilt of the talar dome. The ankle is unstable in acute grade III injuries, which are associated with a pop followed by severe pain and swelling. Hemorrhage may cause ecchymosis. In severe lateral ankle sprains patients cannot continue physical activity.

MR Appearance

CFL tears, when associated with ATFL injuries, are best seen on coronal or axial plane images distal to and through the plane of the lateral malleolus.⁷⁶ Posterior oblique (i.e., anterior-superior to posterior-inferior) axial images, or axial images performed with the foot in plantarflexion, also display the CFL fibers.⁸¹ Axial images show the CFL between the peroneal tendons and the lateral aspect of the calcaneus (anteromedial to the peroneal tendons). The normal calcaneofibular ligament is 2 to 3 mm thick and is visualized as a linear or cord-like low-signal-intensity structure.⁷⁷ MR arthrography is very sensitive for the detection of ATFL and CFL tears—100% and 90%, respectively.⁸⁰ Tearing of the CFL may result in communication between the ankle joint and the peroneal tendon sheaths.⁷⁴

CFL tears are associated with the following MR findings:

Localized edema
Peroneal retinacular thickening
Tenosynovitis
Tendon subluxation
Segmental interruption or absence of the ligament

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Edema surrounding disrupted or irregular ligament morphology between the calcaneus and peroneal tendons (Fig. 5.187)
Blurring of the medial and lateral margins of the ligament
Tenosynovitis
An associated tear of the peroneal tendon sheath
Attenuation of the ligament with adjacent edema or hemorrhage

FIGURE 5.186 ● (A) The calcaneofibular (CF) ligament is a strong cord-like ligament originating from the lower segment of the anterior border of the lateral malleolus and coursing inferiorly and slightly posteriorly to its insertion on the upper part of the lateral surface of the calcaneus. Coronal FS PD FSE image. (B) The CF ligament is crossed superficially by the peroneal tendons and their sheaths, which may leave an imprint on the ligament. Axial FS PD FSE image.

Treatment of Lateral Ligament Complex Injuries

Lateral ligament complex injuries lead to scarring of the ligament and chronic instability associated with persistent laxity and anterolateral impingement. There is often a history of frequent ankle sprains, subtalar injury with associated sinus tarsi ligament injury, and osteochondral lesions as well as peroneal tendon instability. Conservative approaches include early functional rehabilitation, the RICE protocol (rest, ice, compression, and elevation), range-of-motion exercises, protected weight-bearing, and casting for immobilization. Some patients use a functional CAM (controlled ankle motion) walker for stability. Once stability has improved, early mobilization is recommended.

Surgery is necessary for acute grade III sprains or chronic instability. In lateral ligament (ATFL and CFL) reconstruction, the recommended surgical procedures attempt to either rebuild the lateral ligaments with a primary repair (Fig. 5.188) or use a peroneus brevis tendon tenodesis.⁸²^,⁸³ The mobilized peroneus brevis tendon, rerouted through the fibula, can be seen in patients with a Watson-Jones reconstruction of the lateral (i.e., ATFL and CFL) ligaments or in an Evans reconstruction of the CFL (see below for descriptions of the procedures). In the Watson-Jones reconstruction, MR imaging identifies the reconstructed lateral ligaments and assesses the course of the peroneus brevis tendon through the tunnel in the neck of the talus. The status of the ATFL is also seen in other lateral ligament reconstructions.

The following reconstructive procedures are commonly used:

Evans reconstruction (Fig. 5.189): Transposition of the entire peroneus brevis through the distal fibula
Watson-Jones reconstruction (Fig. 5.190): Peroneus brevis tenodesis replaces the ATFL without anatomic replacement of the CFL.

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Modified Watson-Jones reconstruction: A split peroneus longus or brevis tenodesis, a plantaris tenodesis or graft, and a split Achilles tenodesis
Elmslie-fascia lata graft: Used to replace or augment the ATFL and the CFL (more anatomic than modified Watson-Jones)
Chrisman and Snook repair (Fig. 5.191): A split peroneus brevis tendon is used instead of fascia lata to replace the ATFL and CFL (more anatomic than modified Watson-Jones).
Modified Bröstrom procedure: The modified Bröstrom direct repair with imbrication technique repairs and reinforces the ATFL without sacrificing another musculotendinous unit. Tendon augmentation is achieved using the extensor retinaculum. This technique is particularly useful in athletes and dancers.

FIGURE 5.187 ● Calcaneofibular (CF) ligament disruption on a lateral color illustration (A) and coronal (B) and axial (C) FS PD FSE images. CF injuries may be associated with fluid distending the peroneal tendon sheath as a secondary sign. Rupture of the CF ligament does not occur as an isolated finding, and the CF is the second ligament injured in association with the ATFL.

FIGURE 5.188 ● Primary surgical repair of acutely torn ligaments is usually reserved for high-performance athletes.

Medial Ligament Complex Injuries/Deltoid Ligament Sprain

The medial or deltoid ligament complex (Fig. 5.192) is a strong band attached by its apex to the border of the medial malleolus and comprises the tibiocalcaneal, tibionavicular, and anterior and posterior tibiotalar ligaments. The triangular, superficial part of the deltoid (Fig. 5.193) is formed by the tibio-navicular, tibiocalcaneal, tibioligamentous (tibiospring), and superficial posterior tibiotalar fibers. The deep part of the deltoid (Fig. 5.194), which is rectangular, consists of a small anterior component (the anterior tibiotalar/talotibial ligament) and a strong posterior component (the conical posterior tibiotalar/talotibial ligament). The posterior tibiotalar ligament represents the strongest part of the entire medial ligament complex. The deep portion of the deltoid ligament, covered by synovium, is intra-articular. The superficial deltoid is longer, with the tibiocalcaneal ligament measuring approximately 2 cm in length and 1 cm in width at its insertion. The deep component is shorter, approximately 1.5 cm in length, 1.5 cm in width, and 1.0 cm thick at its origin.

Etiology, Pathology, Classification, and Clinical Features

Medial ligament complex injuries and deltoid ligament sprains usually occur in individuals 15 to 35 years of age. In this age group males predominate. After 40 years of age the incidence is higher in females. Injuries are usually related to increased load and significant ankle trauma. Although they are less common than lateral ankle injury, they account for 10% to 15% of all ankle sprains. The deep deltoid ligament is the last to fail. Injuries are often associated with ankle fractures, abduction (deep deltoid injury), external rotation (anterior deltoid injury), or eversion and may represent the end stage of a supination and external rotation injury. In 10% of cases there is an associated syndesmosis injury. Isolated medial ligament complex injuries are rare.

In order of strength, the weakest to the strongest components of the deltoid are (Fig. 5.195) the tibiocalcaneal, the tibionavicular, the tibiospring, and the posterior tibiotalar ligaments. Disruption of the tibiocalcaneal fibers of the superficial layer results in increased talocrural contact pressure and a decreased contact area. Tears of the posterior deep tibiotalar

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(talotibial) ligament are seen with medial malleolus fractures. Partial tears are more common than complete disruption of fiber morphology with an absent ligament. Hemorrhage frequently accompanies the injury, and there is increased valgus talar tilt. Acute injuries are characterized by a hyperplastic synovial reaction and hemosiderin. Chronic injuries are recognized by fibrous ingrowth or scarring (Fig. 5.196).

FIGURE 5.189 ● In the Evans procedure the peroneus brevis tendon is rerouted through a fibular tunnel with proximal reattachment. In a separate case, the Evans technique is used to reconstruct only the calcaneofibular ligament, shown on T1-weighted (B) and FS PD FSE (C) sagittal images. The peroneus brevis tendon is divided, mobilized, and placed in a fibular tunnel. Erosion of the bony tunnel, fluid (straight arrow), and a longitudinal tear of the peroneus brevis tendon within the tunnel (curved arrow) are demonstrated in this symptomatic patient.

FIGURE 5.190 ● Watson-Jones procedure with rerouting of the peroneus brevis tendon through fibular and talar tunnels. Reattachment is shown distally (distal to the lateral malleolus).

Medial ligament complex injuries are classified into three grades:

Grade I: Stretch injuries (Fig. 5.197)
Grade II: Partial tearing (Fig. 5.198)
Grade III: Complete ligamentous disruption (Fig. 5.199)

FIGURE 5.191 ● (A) Lateral color illustration of the Chrisman-Snook procedure with the split peroneus brevis tendon coursing through a fibular tunnel and secured to the talus and calcaneus with the use of periosteal flaps. (B) Corresponding sagittal PD-weighted image demonstrates the mobilized peroneus brevis at the level of the fibular tunnel.

Clinically, patients present with swelling and tenderness over deltoid ligaments and the surrounding soft tissue. Pain is usually anteromedial or medial, and there is blister formation, gross deformity, and ecchymosis. Medial sprains are usually more painful than lateral sprains, with tenderness over the distal tip of the medial malleolus as well as the deltoid. Mechanical instability is characteristic of medial ligament injuries.

MR Appearance

Both superficial and deep portions of the deltoid ligament can be identified on axial images. On these images, deltoid ligament injuries usually demonstrate inflammatory or edematous changes without complete ligament disruptions.⁸⁴ Axial FS PD FSE images are used to assess associated tendon and neurovascular structures. On coronal plane images it is often possible to identify associated avulsions of the medial malleolus and to separate tibiotalar from tibiocalcaneal fibers. Focal areas of increased signal intensity on T2-, FS PD FSE, or T2*-weighted images are more commonly seen than complete absence of the ligament. On medial sagittal images through the superficial layer there is some loss of detail in the individual ligamentous components.

In its normal configuration, the tibiotalar ligament demonstrates separated fibers with interposed fatty tissue. This finding should not be mistaken for ligament disruption on T1-weighted images. Most injuries to the deltoid ligament are ligamentous sprains that appear as an amorphous increase in signal intensity on FS PD FSE, T2*-weighted, or STIR images. Isolated deltoid ligament injuries are rare, and most deltoid injuries have associated lateral ligamentous pathology, a fibular fracture, and/or syndesmotic injuries.⁸⁵ Kinematic and

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stress positioning of the ankle may be effective in showing rupture, thinning, and lengthening of the ligament.

FIGURE 5.192 ● Medial ligaments of the hindfoot. The fibers of the deltoid ligament provide stability to the medial aspect of the ankle.

FIGURE 5.193 ● Superficial deltoid ligament with the tibioligamentous and tibiocalcaneal components identified. The posterior talotibial component of the deep deltoid is also shown. The thick deltoid or medial collateral ligament consists of two sets of fibers, superficial and deep. The superficial fibers are broad and triangular and fan out as an extra-articular sheet from the medial malleolus to the navicular, talus, spring ligament, and calcaneus. Sagittal T1-weighted MR arthrogram.

The key MR findings are:

Interstitial intermediate signal intensity on T1- or PD-weighted images and diffuse amorphous hyperintensity on FS PD FSE images
Associated medial malleolus fractures
Medial malleolus subchondral edema
Marrow containing ligament ossification
Lateral or posterolateral talar displacement
Osseous degenerative change in the medial malleolar talar articulation
Indistinct margins and loss of fiber striation, especially of talotibial (tibiotalar) fibers of deep layer
A mass-like morphology in disruption with associated edema, hemorrhage, and granulation tissue
A fluid-filled gap in complete disruption (Fig. 5.200)

Treatment

Since medial collateral ligament injuries usually involve associated lateral ligamentous injury, fibular fracture, and/or syndesmosis injuries, treatment considerations must include the following:

Fullness in the region of the retromalleolar tendons is secondary to chronic irritation and inflammation.
A widened ankle mortise is more common with deltoid injuries with preexisting lateral complex injuries.
There may be alignment and translation deformities.

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Chronic medial ankle pain and instability are usual findings.
The tendon tends to heal in the lengthened position.
Deltoid ossification is not uncommon.

FIGURE 5.194 ● The posterior talotibial portion of the deep deltoid is shown on a coronal T1-weighted image (A) and an axial T1-weighted MR arthrogram (B). The deep layer of the deltoid ligament consists of a small anterior component, the anterior talotibial ligament, and a strong posterior talotibial ligament.

FIGURE 5.195 ● (A) Superficial (cut) and deep portions of the deltoid as displayed on central arthroscopic examination of the ankle. (9) medial dome talus; (10) central portion of the tibia; (11) articulation of the lateral dome with the distal tibia and fibula and the syndesmotic articulation; (12) posterior inferior tibiofibular ligament; (13) transverse tibiofibular ligament; (14) capsular reflection of the flexor hallucis longus tendon medial to the transverse ligament. (B) Sprain of the deep posterior talotibial deltoid and superficial tibiotalar and tibiocalcaneal fibers on a sagittal FS T1-weighted image. The posterior talotibial ligament is conical, with its base superior and apex posteroinferior. The deep portion of the deltoid ligament is intra-articular and covered only by synovium. (C) Corresponding color illustration of a superficial layer sprain.

FIGURE 5.196 ● Chronic deltoid ligament sprain with ossification within the ligamentous fibers. Medial ligament injuries are associated with eversion stress injuries. The weaker tibionavicular and tibiocalcaneal ligaments are injured before the stronger tibioligamentous (tibiospring) and the posterior talotibial ligaments are torn. Avulsion fractures of the medial malleolus are seen in over 50% of eversion injuries. (A) Coronal FS PD FSE image. (B) Axial T1-weighted FSE image.

FIGURE 5.197 ● Deltoid ligament sprain without loss of ligamentous continuity or fiber striations on a coronal FS PD FSE image. The medial talar edema is a secondary sign of acute ligamentous injury.

FIGURE 5.198 ● (A) Posterior view color illustration of a partial tear of the superficial and deep fibers of the deltoid ligament. The deep layer posterior talotibial ligament runs obliquely inferiorly and posteriorly to insert on the medial surface of the talus. Posterior talotibial ligament sprain is usually associated with severe lateral collateral ligament sprain. Coronal (B) and axial (C) FS PD FSE images with contusions indicating combined inversion and ankle eversion. Deltoid ligament injuries are also associated with syndesmotic injuries.

FIGURE 5.199 ● Complete tear of the deep fibers of the deltoid in a football player sustaining a high ankle sprain with associated syndesmotic and lateral ligamentous injury. (A) Coronal FS PD FSE image. (B) Axial FS PD FSE image.

Conservative approaches to management include the RICE protocol, range-of-motion exercises, protected weight-bearing, and, in grade III injuries, complete immobilization with a short-leg cast.

Surgery is infrequently used, but procedures include débridement of a symptomatic anterior deltoid ossicle, imbrication, delayed primary repair, and ligament reconstruction with a tendon transfer or graft.

FIGURE 5.200 ● Fluid-filled gap in a tear of the deep deltoid posterior talotibial fibers. Associated lateral tibiotalar contusions are the result of an eversion mechanism. Coronal FS PD FSE image.

Syndesmosis Sprains

Pearls and Pitfalls

Syndesmosis Sprains

Syndesmotic sprains or high ankle sprains may involve the anterior inferior tibiofibular (anterior syndesmotic) ligament, the posterior inferior tibiofibular (posterior syndesmotic) ligament, the transverse tibiofibular ligament, and interosseous membrane.
Tearing is associated with bi- and tri-malleolar and fibular subluxation and fractures.
Severe syndesmosis injuries are seen with superior dislocation of the talus and an increased intermalleolar distance.
Axial images at the level of the distal tibial plafond are used to evaluate the anterior and posterior syndesmotic ligaments.

The three key ligaments connecting the tibia and fibula are the anterior syndesmotic ligament, also known as the anterior inferior tibiofibular ligament (AITF); the posterior syndesmotic ligament, also known as the posterior inferior tibiofibular ligament (PITF); and the interosseous ligaments.⁸⁶^,⁸⁷ The lower fibers of the interosseous membrane also contribute to the stability of the distal ankle syndesmosis.

The AITF (Fig. 5.201) is a flat band of fibers that may be divided into two or three bands or may present as a multifascicular structure. Twenty percent is intra-articular. The PITF (Fig. 5.202) is a thick band of fibers with a quadrilateral

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shape. The transverse tibiofibular ligament represents its deep and inferior component and is a true posterior labrum. The PITF also has an interosseous membrane and short fibrous bands.

FIGURE 5.201 ● (A) Lateral color illustration of the anterior inferior tibiofibular ligament (AITF/anterior syndesmotic ligament). The AITF is a flat band of fibers that may be divided into two or three bands or may be multifascicular. It extends obliquely from the anterior inferior border of the lateral malleolus upward and medially to the anterolateral tubercle of the tibia. (B) The AITF is hypointense on this axial T1-weighted image at the level of the tibial plafond.

Etiology, Pathology, and Clinical Features

Syndesmotic injuries are the second most common ankle injury after lateral ligament injury and represent 10% to 20% of ankle sprains. Although they are frequently seen as a complication of fractures, sprain of the syndesmosis ligaments can occur without a tibial or fibular fracture or diastasis.⁴⁸^,⁸⁸ Abduction, external rotation, and dorsiflexion of the ankle/lower leg are thought to represent the primary mechanisms of syndesmosis sprain. External rotation forces can result in disruption of the AITF, the interosseous ligament, and the interosseous membrane. Hyperdorsiflexion has also been implicated as a mechanism of injury. Sports-related injuries are particularly likely to occur in football, soccer, basketball, and downhill skiing. They are most commonly seen in young males who participate in contact sports.

General pathologic features of the components of the syndesmosis include the following:

The oblique fibers of the AITF run from the anterior inferior lateral malleolus to the anterolateral tubercle tibia and contact the lateral ridge of the trochlear surface of the talus in plantarflexion (Fig. 5.203).
The PITF (Fig. 5.204) runs from the posterior lateral malleolus to the posterolateral tibial tubercle.
The transverse tibiofibular ligament is deep and inferior to the PITF and runs from the fibular tubercle and digital fossa to the posterior tibial articular surface and the medial border of the medial malleolus. It is a true posterior labrum, projecting below the posterior tibial margin (Fig. 5.205).
The tibial slip (Fig. 5.206) extends from the PTFL to the posterior tibia and transverse tibiofibular ligament.
The interosseous membrane extends from the medial distal fibular shaft to the lateral distal tibia and forms a vault over the tibiofibular synovial recess.
The 1-cm-high synovial recess contains a reddish synovial fringe that descends into the ankle joint between the fibula and the lateral talar surface as the ankle is brought into plantarflexion (Fig. 5.207).

On gross pathologic and surgical examination there is substantial tearing of the AITF, PITF, and interosseous membrane, accompanied by hemorrhage and usually associated with bi- and tri-malleolar fractures. There is also fibular subluxation, plastic deformation, and posterior rotation. The talus may be dislocated superiorly. Histologic examination shows hemorrhagic cellular elements, soft-tissue hyperplasia, and heterotopic calcification.

The clinical presentation is dominated by severe pain with external rotation. Patients report pain at the anterolateral leg, and

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there is palpable tenderness over the syndesmosis and pain on the squeeze test of the fibula and tibia (Fig. 5.208). There may also be mild pain over the ATFL and CFL. The leg is swollen, the ankle is unstable, and the patient cannot bear weight. Muscular splinting and reflex spasms may also be seen.

FIGURE 5.202 ● (A) The posterior ankle ligaments that make up the syndesmosis are the anterior and posterior inferior tibiofibular ligaments, the transverse tibiofibular ligament, and the interosseous ligament. (B) The posterior inferior tibiofibular ligament (PITF/posterior syndesmotic ligament) is quadrilateral in shape and smaller than its anterior counterpart. Axial T1-weighted MR arthrogram. (C) The PITF originates from the posterior border of the lateral malleolus and extends upward and medially onto the posterolateral tibial tubercle. Coronal T1-weighted image.

FIGURE 5.203 ● The anterior inferior tibiofibular ligament fibers increase in length from above downward. During plantarflexion they contact the lateral ridge of the trochlear surface of the talus. Approximately 20% of the ligament is seen intra-articularly via the arthroscope.

FIGURE 5.204 ● (A) The transverse tibiofibular ligament lies deep and inferior to the posterior tibiofibular ligament and is sometimes called the deep component of the posterior inferior tibiofibular ligament. It constitutes a true posterior labrum, deepening the tibial articulating surface of the talus. Posterior perspective color illustration. (B) The transverse ligament on a posterior T1-weighted coronal image. The transverse ligament fills the posterior aspect of the medial surface of the lateral malleolus and comes in contact with the articular cartilage of the posterolateral talar surface.

FIGURE 5.205 ● The transverse tibiofibular ligament or posterior labrum of the ankle demonstrates hypertrophy and degenerative tearing in a ballet dancer. Sagittal FS PD FSE image.

Classification

One classification system based on clinical findings groups injuries into three types:

Grade I: Stretching of the ligament
Grade II: Partial tear
Grade III: Complete rupture (Fig. 5.209)

Radiographs can be used to determine frank diastasis, which is identified on unstressed radiographs, or latent diastasis, which is identified on stress radiographs.

MR Appearance

The clinical diagnosis of AITF injuries may be difficult because acute swelling is uncommon in this setting of distal anterior tibiofibular syndesmotic pain. Therefore, identification of an intact or disrupted ligament on MR scans may be particularly useful in diagnosing and treating an ankle injury.

Tears of the AITF and PITF are characterized by ligament thickening, irregularity (e.g., a lobulated contour), or frank discontinuity. Ligament thickening results in an increased anteroposterior dimension, usually seen in association with areas of increased signal intensity within the ligaments. Posterior inferior tibialis ligament rupture is uncommon. The normal appearance of the anterior inferior tibialis ligament is variable, and it may be visualized as a thick substantial ligament or a thin attenuated structure even in the absence of pathology. Interosseous membrane injuries are seen as a linear hyperintensity at the level of the distal tibia and fibula on heavily weighted T2, FS PD FSE, or STIR images. Low-signal-intensity foci in the interosseous membrane represent hemosiderin, fibrosis, or calcification.

Additional characteristic findings on MR include:

Blurring of the syndesmotic ligaments
Lateral fibular subluxation
Fibular shortening
A tibiofibular diastasis
Thickening and contour irregularity of syndesmotic ligaments (AITF or PITF) (see Fig. 5.209)
Frank discontinuity (Fig. 5.210)
Fluid hyperintensity and diastasis of AITF and PITF on FS PD FSE images
Linear interosseous membrane hyperintensity (Fig. 5.211)
Interosseous membrane hemosiderin, fibrosis, or calcification (Fig. 5.212).

Treatment

Syndesmosis injuries eventually lead to tibiofibular joint snapping and chronic instability of the distal tibiofibular syndesmosis. Reduction of the syndesmosis is necessary to minimize dysfunction and the eventual development of arthritis. Signs of syndesmotic impingement (see discussion below) include an inflamed synovium, AITF scarring, talar chondromalacia, and osteophytes. Open reduction and internal fixation (ORIF) is usually required. The AITF is repaired using the plantaris or peroneal tendons, and arthrodesis is used for severe pain and degenerative changes.

Impingement Syndromes

Chronic pain after an ankle sprain is commonly caused by soft-tissue impingement. Impingement syndromes include anterolateral, syndesmotic, and posterior impingement¹⁴^,⁸⁹ as well as anteromedial and posteromedial impingement syndromes.⁹⁰

Anterolateral Impingement

Anterolateral impingement is the most common of the soft-tissue impingements because of its relationship to the inversion mechanism of most ankle sprains.⁹⁰–⁹² It usually occurs in a subset of inversion injuries (20% to 40% of cases occur after ankle sprain), and in this setting it may be a cause of chronic ankle pain.

FIGURE 5.206 ● (A) The tibial slip extends from the superior border of the posterior talofibular ligament and courses medially and superiorly. It inserts on the posterior tibial margin, blending with fibers of the transverse tibiofibular ligament. During plantarflexion, the transverse tibiofibular ligament is tightly squeezed between the posterior tibial margin and the posterior talofibular ligament. During dorsiflexion, however, a synovium-lined cul-de-sac and the tibial slip become apparent. FS PD FSE image. (B) Sagittal illustration showing the relationship of the posterior ligaments. The tibial slip is not illustrated on this section. (C) The tibial slip on a posterior coronal FS PD FSE image. The insertion of the tibial slip may reach to the posterior surface of the medial malleolus and is also referred to as the posterior intermalleolar ligament. (D) The tibial slip (marker) runs from the posterior talofibular ligament and inserts on the posterior tibial margin, blending with the fibers of the transverse tibiofibular ligament.

FIGURE 5.207 ● (A) Synovial fringe seen in the recess between the tibia and fibula. The tissue is usually located posteriorly, adjacent to the posterior inferior tibiofibular ligament. (B) Intermediate-signal-intensity synovial fringe on an axial T1-weighted MR arthrogram.

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Etiology, Pathology, and Clinical Features

Impinge-ment can occur at the AITF, the lateral gutter, and the ATFL (Fig. 5.213) with resultant synovitis, fibrosis, and chondromalacia. The appearance of thickened adhesive bands and synovium, osteophytes, and loose bodies indicates impingement. Wolin et al.⁹³ have described the “meniscoid” lesion as massive hyalinized connective tissue extending into the joint from the anterior inferior portion of the talofibular ligament. Although the meniscoid lesion is often discussed, the lesion itself is rarely seen.

There are a number of causes of anterolateral impingement, but posttraumatic change with plantarflexion inversion is the most common. Other contributing factors include synovial and capsular irritation (Fig. 5.214), infection, rheumatologic disorders, and degenerative disorders. When associated with lateral ligament injury, anterolateral impingement occurs in the same younger population. In sports-related injuries there is a male predominance.

Pathologic changes include a partial or complete tear of the AITF or ATFL, intra-articular hemorrhage, synovial hyperplasia and compression, and possibly entrapment of the synovial membrane. Hyalinized scarring after lateral sprains or a meniscoid lesion (Fig. 5.215) may be found, characterized by a synovial impingement lesion, attachment to the anteroinferior talofibular joint capsule, extension into the lateral gutter, and a fibrocartilaginous consistency. The lesion is usually seen anterior to the fibula, between the lateral talus and the distal medial fibula. It may be approximately 5 mm in width, with morphology similar to hypertrophic synovitis (see Fig. 5.215). Chondral erosion of the lateral talar dome may also be a feature.

Histologic findings include synovial hyperplasia, subsynovial capillary proliferation, hyaline cartilage degenerative change and fibrosis, a chronic inflammatory process, and absence of ligamentous tissue.

Radiographic findings include calcification or heterotopic bone in the interosseous space (distal tibiofibular syndesmosis injury), ossicles distal to the lateral malleolus, and lateral talar dome (ATFL) injuries. Arthroscopic findings indicate pathology usually limited to the syndesmosis and lateral gutter. Synovitis usually affects the AITF and ATFL. There is often lateral gutter fibrosis and associated chondromalacia of the talus and fibula.⁹⁴ Less commonly, a meniscoid lesion is seen extending from the anterolateral aspect of the distal tibia toward the lateral gutter. Ferkel et al. attribute soft-tissue impingement primarily to chronic hypertrophy of the synovium without a mass of ligamentous tissue as the meniscoid lesion.⁹⁵ The meniscoid lesion is thus thought to represent an advanced form of anterolateral soft-tissue impingement.

Clinically, patients present with vague anterolateral ankle pain that is absent at rest and most noticeable with activity requiring cutting or pivoting movements. There is also tenderness along the syndesmosis and anterior gutter, although tenderness at the posterior subtalar joint and sinus tarsi is variable.

MR Appearance

In 30% to 40% of cases, it is possible to identify lateral gutter lesions on MR images. Some impingement lesions may require kinematic or dynamic imaging techniques.

Key MR imaging findings include:

Signal-intensity changes in the anterolateral gutter
Associated AITF and ATFL injury and effacement of fat signal anterior to the AITF

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Fluid- to intermediate-signal synovium deep to the AITF and in the anterolateral gutter (Fig. 5.216)
Ossicles and/or loose body in soft tissues at the tip of the fibula
Hyalinized mass
Fibrosis and scarring
Talar chondromalacia, indicated by a denuded chondral surface

FIGURE 5.208 ● Tear of the anterior inferior tibiofibular (AITF/anterior syndesmotic) ligament on a coronal color illustration (A), a coronal FS PD FSE image (B), and in a separate case on an axial FS PD FSE image (C). Syndesmosis injuries are associated with an external rotation mechanism, although hyperdorsiflexion may also lead to tears of the syndesmosis.

FIGURE 5.209 ● (A) The “squeeze test” is used clinically to diagnose syndesmosis injuries. By palpating directly over the syndesmosis and more proximally along the interosseous membrane, the fibula is compressed against the tibia above the midpoint of the calf. The test is positive when proximal compression produces distal pain in the area of the torn interosseous membrane and syndesmotic ligament. Anterolateral view illustration. (B) The “external rotation stress test” is also used in diagnosing syndesmotic ankle sprains. It is performed by applying external rotation stress to the foot and ankle with the knee bent in 90° of flexion and the ankle in a neutral position. The test is positive if pain is produced over the anterior or posterior inferior tibiofibular ligaments.

FIGURE 5.210 ● Tears of both the anterior inferior and posterior inferior tibiofibular ligaments on a lateral color illustration (A) and an axial FS PD FSE image (B). Injuries to the syndesmosis are underestimated and occur in as many as 10% of all ankle injuries.

Treatment

The natural course of the injury includes development of heterotrophic bone in the interosseous space, ossicles at the tip of the fibula and the talar dome, and inflammatory tissue in the lateral gutter and the syndesmosis between the tibia and fibula. Chronic lateral ankle pain is typical. Conservative treatment consists of physical therapy and NSAIDs. If conservative measures fail, however, surgery to relieve the impingement is necessary. Treatment approaches include arthroscopy with shavers, burs, graspers, and baskets and débridement. The inflamed synovium, thickened adhesive bands, osteophytes, and loose bodies are removed (Fig. 5.217) and the involved tissue is excised down to the underlying cartilage. The ATFL remnant is not excised. After surgery, splinting and a CAM walker may be required.

Syndesmotic Impingement

As discussed earlier, syndesmotic injuries involve the AITF, the PITF (including its distal and deep component, the transverse ligament), and the interosseous membrane. They are frequently underestimated clinically. Syndesmotic sprains represent approximately 10% of ankle injuries and syndesmotic impingement represents approximately 3%.

Etiology, Pathology, and Clinical Features

Impingement usually occurs as a result of soft-tissue changes associated with sprains and fractures and is frequently seen in military cadets and in young high-performance male athletes engaging in collision sports such as hockey, football, and soccer. Arthroscopic findings include an inflamed synovium (and synovial nodules) and scarring that envelop the AITF and the inferior articulation of the tibia and fibula. Synovitis of the anterior and posterior aspects of the syndesmotic ligament (AITF) may also be seen. Loose bodies, chondromalacia, and osteophytes are associated findings. A separate fascicle of the AITF that rubs over the talar dome is known as Bassett's ligament (Fig. 5.218) and may cause impingement by abrading against the lateral dome of the talus, particularly in an unstable ankle. Size varies depending on the degree of involvement of the anterior, central, or posterior syndesmosis.

The mechanism of injury is external rotation or hyperdorsiflexion. In tibiofibular joint mechanics, the posterior trochlear surface of the talus is smaller than the anterior surface,

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and the lateral malleolus is pulled superiorly when the fibula is rotated medially (Fig. 5.219).

FIGURE 5.211 ● Interosseous membrane tears as part of a high ankle sprain complex and associated fibular diaphyseal fracture. The interosseous membrane fibers form a vault over the underlying tibiofibular synovial recess. On MR images this recess is approximately 1 cm high. Hyperintense fluid seen in the coronal plane extending above this recess is associated with interosseous membrane injuries in high ankle sprains. (A) Illustration of the relationship of the interosseous membrane to the posterior inferior tibiofibular ligament and other posterior ankle ligaments. (B) Coronal FS PD FSE image. (C, D) Axial FS PD FSE images.

FIGURE 5.212 ● Chronic interosseous membrane tear (as a complication of a syndesmotic sprain) with ossification. Syndesmotic sprains occur in collision sports such as ice hockey, football, and soccer. (A) Coronal reformatted CT image. (B) Axial FSE PD FSE image.

Impingement can occur in the anterior, central, or posterior syndesmosis (Fig. 5.220). Pathologic findings include an inflamed synovium, AITF involvement with fraying, inferior articulation of the tibia and fibula, synovial nodules, chondromalacia of the talus, and osteophytes involving the syndesmosis. Microscopic features include synovial hyperplasia, capillary proliferation, and chondral degeneration.

Clinically, there is tenderness along the syndesmosis and interosseous membrane, and palpation of the syndesmosis elicits symptoms. The squeeze test, in which the fibula is compressed against the tibia proximal to the mid-calf (see Fig. 5.208), is positive for pain, as is the external rotation test (pain with external rotation of the foot with the knee in 90° flexion). The passive dorsiflexion test is also helpful in making the diagnosis, as is an anterior popping sensation.

MR Appearance

MR is useful in evaluating ankle sprains because of its ability to depict tendons, ligaments, bony structures, and capsular thickening associated with ligamentous injuries. Key findings include:

Synovial inflammation
Synovial nodules
Possibly a torn AITF
Loose bodies
Osteophytes
Fluid in the syndesmosis (Fig. 5.221)
Chondromalacia of the talar dome with focal fissuring
Soft-tissue thickening directly involving or anterior to the AITF (Fig. 5.222)
Intermediate signal intensity within the distal fascicle of the AITF on FS PD FSE images
Scarring within the inferior articulation of the tibia and fibula (Fig. 5.223)

Treatment

Without treatment there is laxity of the lateral ankle, causing the talar dome to extrude anteriorly with dorsiflexion. Tibiofibular synostosis, pain with push-off, restricted dorsiflexion, ossification between the distal tibia and fibula, and talar surface degeneration are all part of the progression of the lesion.

Conservative treatment includes physical therapy and nonsteroidal anti-inflammatory drugs, but surgery may be necessary to stabilize the ankle. Arthroscopic procedures include dé-bridement of the AITF and hypertrophic synovium, partial ligament excision (Fig. 5.224), and removal of synovial nodules from the tibiofibular interspace.

Posterior Impingement

Pearls and Pitfalls

Posterior Impingement

Posterior impingement can occur alone or in combination with anterolateral and syndesmosis impingement.
Generalized posterolateral impingement occurs with fibrosis, capsulitis, and synovial swelling involving any or a combination of the posterior ankle ligaments, including the posterior syndesmotic (inferior tibiofibular) ligament, the transverse tibiofibular ligament, the tibial slip, and the PTFL.
Normal variations exist in the size of the tibial slip and transverse ligament. These structures should be evaluated for hypertrophy and tears.

Posterior impingement usually occurs along the lateral side of the posterior ankle from the posterior syndesmosis

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proximally to the PTFL distally. Although the PITF and the transverse tibiofibular ligament are primarily involved, any of the posterior ligaments may be affected, including the tibial slip and the PTFL (Fig. 5.225).⁹⁰ It is seen most often in younger patients who participate in activities involving plantarflexion: female ballet dancers and gymnasts and male football players.

FIGURE 5.213 ● (A) Dissection with anterolateral exposure of the anterior inferior tibiofibular ligament (anterior syndesmotic ligament), the anterior talofibular ligament, and the lateral gutter. (B) The potential soft-tissue impingement sites. The accessory fascicle of the anterior inferior tibiofibular ligament can impinge across the lateral talar dome. (C) Plane of cross-section through the lateral gutter. (D) Cross-sectional illustration of the lateral gutter. The boundaries of the lateral gutter are the talus medially, the fibula laterally, and the anterior and posterior talofibular ligaments.

FIGURE 5.214 ● Soft-tissue impingement. (A) Arthroscopic view through the anteromedial portal shows anterolateral soft-tissue impingement with synovitis and fibrosis and chondromalacia in the anterolateral gutter. (B) Arthroscopic view of the anterolateral impingement lesion. Note the hemosiderin staining of the lateral gutter and associated scar bands and synovitis.

FIGURE 5.215 ● Anterolateral impingement with hypointense soft-tissue thickening in the anterolateral gutter on an axial FS PD FSE image. Anterolateral impingement of the ankle is the most common type of soft-tissue impingement because of the mechanism of most ankle sprains in inversion. The meniscoid lesion as originally described represented a massive hyalinized connective tissue extending into the joint.

Etiology, Pathology, and Clinical Features

Impingement is caused by hypertrophy or tear of the posterior inferior or transverse tibiofibular ligaments, by a bucket-handle tear or tibial slip, or by a pathologic labrum (transverse ligament) on the posterior ankle joint.¹⁴ Posterior impingement may coexist with anterolateral and syndesmosis impingement.

The mechanism of injury is thought to be plantarflexion with trauma and repetitive stress. Athletes, particularly gymnasts and football players, are susceptible to plantarflexion and inversion injuries. Ballet dancers are predisposed to impingement as a result of forced turn-out and foot plant (Fig. 5.226). A prominent posterior labrum or tibial slip also predisposes to impingement, and a pseudomeniscus lesion on the tibial slip with or without displacement into the joint may become symptomatic.

Pathologic changes include fibrosis, capsulitis, and synovial swelling and hypertrophy of the transverse tibiofibular ligament or the tibial slip. There may also be a pseudomeniscus of the tibial slip, synovial nodules and/or hyperplasia, subsynovial capillary proliferation, chronic inflammation, and fibrous ingrowth.

The most common signs and symptoms are pain and tenderness in the posterior ankle. The pain can be reproduced with passive plantarflexion of the ankle and is accompanied by posterior soft-tissue fullness.

MR Appearance

The most obvious diagnostic clue is edema and fluid associated with the PTFL, the transverse tibiofibular ligament, or the tibial slip. Size varies depending on the degree of synovitis, presence of ganglion formation, and the combination of ligaments involved. Key findings are:

FIGURE 5.216 ● Soft-tissue anterolateral impingement on a coronal color illustration (A) and an axial FS PD FSE image (B). Pathology is usually limited to the anterior syndesmosis and the lateral gutter. Synovitis may surround the anterior inferior tibiofibular ligament (both anteriorly and posteriorly) and involve the anterior talofibular ligament as well. Fibrosis of the lateral gutter and chondromalacia of the talus and fibula may also be demonstrated.

FIGURE 5.217 ● Débridement of the lateral gutter. (A) Débridement is performed with a small-joint shaver and includes removing inflamed synovium, thickened adhesive bands, osteophytes, and loose bodies. (B) Arthroscopic view through the anteromedial portal. A full-radius shaver is débriding the lateral gutter while avoiding injury to the anterior talofibular ligament.

FIGURE 5.218 ● Syndesmotic impingement may occur from a separate distal fascicle (Bassett's ligament) of the anterior inferior tibiofibular ligament. A tear of the anterior talofibular ligament contributes to laxity in the lateral ankle, and the anterolateral talar dome extrudes anteriorly with dorsiflexion. Bassett's ligament then impinges against the talus. (A) Coronal color illustration. (B) Coronal FS PD FSE image. (C) Lateral view color illustration.

FIGURE 5.219 ● Tibiofibular joint mechanics. (A) The width of the trochlear surface of the talus is smaller posteriorly than anteriorly. (B) During plantarflexion of the ankle, the malleoli are approximated actively as the lateral malleolus is pulled inferiorly and rotated medially. (C) With dorsiflexion of the ankle, the lateral malleolus moves always from the medial malleolus and is pulled slightly superiorly as the fibula is medially rotated.

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Inhomogeneous fluid and synovium surrounding the posterior ligaments (Fig. 5.227)
Capsular thickening
Fibrosis
Periostitis
Ganglion cysts protruding between posterior ligaments
Interstitial signal in the posterior ligaments (Fig. 5.228)
Gross enlargement of tibial slip or labrum (transverse ligament) (Fig. 5.229)
Synovial nodules

Treatment

Although impingement usually improves with rest and conservative treatment (NSAIDs, corticosteroid injections, and an alteration of foot plantarflexion mechanics), chronic ankle pain may result from continued plantarflexion associated with fibrosis, a thickened synovium, and development of a ganglion. In these cases arthroscopic débridement of the synovium and fibrosis may provide pain relief.

Anteromedial and Posteromedial Impingement

Anteromedial impingement is associated with partial tearing of the anterior fibers of the deltoid ligament (Fig. 5.230).⁹⁰ Although the exact mechanism is not fully understood, eversion injuries usually represent the antecedent trauma. MR findings may include:

Capsular thickening
Thickening of the anterior component of the superficial deltoid

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Anteromedial tibiotalar sclerosis and osteophytes (Fig. 5.231)
Associated lateral ligament sprains and osteochondral lesions of the talus

FIGURE 5.220 ● Syndesmotic impingement. (A) Plane of cross-section through the syndesmosis. (B) Cross-sectional view through the syndesmosis demonstrates that impingement can occur anteriorly, centrally, or posteriorly. (C) Corresponding axial FS PD FSE image shows potential syndesmotic impingement sites.

FIGURE 5.221 ● Syndesmotic impingement with scarred anterior and posterior tibiofibular (syndesmotic) ligaments as a result of a chronic inversion injury with associated ATFL rupture. There is fluid in the tibiofibular synovial recess. Axial FS PD FSE image.

FIGURE 5.222 ● Nodular thickening in the region of the anterior syndesmotic ligament on an axial FS PD FSE image.

FIGURE 5.223 ● Syndesmosis scarring in a basketball player with chronic thickening of the anterior and posterior inferior tibiofibular ligaments. Coronal FS PD FSE image.

Posteromedial impingement (PoMI)⁹⁰ (Fig. 5.232) is the consequence of severe ankle inversion injuries with tearing of the deep fibers of the deltoid ligament. These deep fibers are crushed between the medial wall of the talus and the medial malleolus. Thickened and fibrotic tissue (Fig. 5.233) causes impingement between the talus and the posterior margin of the medial malleolus. PoMI lesions frequently coexist with lateral ligament injuries, including an osteochondral lesion of the talus.

Anterior Impingement

Anterior impingement is recognized by the presence of a distal anterior tibial osteophyte⁹² that is triangular (with the

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tibial side spur narrower than the talar spur) and, in grade 3 and 4 lesions, greater than 1 cm. Impingement occurs between the anterior surface of the tibia and the superior aspect of the neck of the talus (Fig. 5.234). Typically, the talar sulcus is seen in the superior aspect of the talar neck and the normal tibial—dorsal talar neck angle is at least 60° (Fig. 5.235). Osteophytes on the distal tibia and talar neck, however, decrease the tibiotalar angle to less than 60°.

FIGURE 5.224 ● Excision of torn syndesmotic ligament. (A) Visualization is performed from the anteromedial portal, and a suction punch or small basket is brought into the joint through the anterolateral portal to remove the torn fascicle. (B) Arthroscopic view of excision of the torn syndesmotic ligament using a suction basket.

FIGURE 5.225 ● Posterior impingement sites. Note that the tibial slip can also be an area of soft-tissue impingement.

FIGURE 5.226 ● Posterior impingement in a ballet dancer with synovitis involving the posterior ligaments on color illustration with posterior perspective (A) and a sagittal FS PD FSE image (B). A thickened posterior labrum represents pathology of the transverse ligament. A pseudomeniscus of a hypertrophied tibial slip may also become symptomatic in ballet dancers.

FIGURE 5.227 ● Generalized posterolateral impingement with fibrosis, capsulitis, and synovial swelling along the posterior aspect of the ankle. Synovial thickening is intermediate on this sagittal FS PD FSE image.

FIGURE 5.228 ● Hyperintensity of the posterior ligaments as potential sites of soft-tissue impingement on this coronal FS PD FSE image.

FIGURE 5.229 ● Enlarged bifid appearance of the tibial slip. The presence of a prominent transverse tibiofibular ligament and large tibial slip may predispose to an increased risk of posterior impingement. Sagittal FS PD FSE image.

FIGURE 5.230 ● Anteromedial impingement with soft-tissue thickening associated with a capsular component and a torn anterior component of the deltoid ligament. (A) Axial color illustration. (B) Sagittal FS PD FSE image.

FIGURE 5.231 ● Osseous sequelae of anteromedial impingement with hypointense tibiotalar sclerosis and osteophyte. Coronal T1-weighted image.

Etiology, Pathology, and Clinical Findings

Hyperdorsiflexion has been implicated in the development of anterior impingement as a result of direct repetitive and forceful tibiotalar microtrauma. Younger individuals (under 40 years of age), both male and female, who participate in sports or activities such as running, soccer, football, the high jump, rock climbing, gymnastics, and dancing, are at particular risk.

Repetitive trauma results in spur formation at the anterior inferior tibial plafond and at the neck of the talus (the capsular attachment site), resulting in synovial impingement, an osteochondral reaction, and exostosis formation. The exostosis and secondary dorsal talar spurs may or may not be associated with fragmentation of the secondary osteophytes. Anterior impingement is not secondary to a single episode of acute trauma but is more likely to be found with disorders that contribute to degeneration, such as pantalocrural arthritic destruction, lateral ankle ligament laxity, and equinus foot deformity.

On pathologic examination the talar osteophytes are seen to project dorsally and the tibial osteophytes project anteriorly. Exuberant bone formation may be focal or bridging, and there may be a “door jam” effect between the osteophytes. Fracture or fragmentation of the osteophytes may occur, as well as full-thickness talar chondral defects. Histologically, there is an inflammatory cellular response, synovial hyperplasia, and fibrous ingrowth.

Clinically, patients present with generalized anterior ankle pain that is aggravated by dorsiflexion (which is restricted) and is most noticeable at the end of the range of motion. In soccer players there is a divot in the anterior talar neck secondary to tibial spur abutment and “tram track” lesions caused by contact of the prominent tibial osteophyte with talar dome articular cartilage.

Classification

Anterior impingement has been classified into four grades, based on the spur development in the anterior distal tibia and the dorsum of the talar neck:

Grade 1: Abnormal osseous contour of the anteroinferior tibia (Fig. 5.236)
Grade 2: A sharp interface between tibial hypertrophic bone and the tibial exostosis (Fig. 5.237). Spurs are greater than 3 mm, but no talar spur is seen.
Grade 3: Tibial exostosis with secondary spur formation on the dorsum of the talus (Fig. 5.238)
Grade 4: Pantalocrural osteoarthritic destruction (Fig. 5.239)

MR Appearance

MR imaging is superior for the identification of talar longitudinal chondral defects. Typical findings include:

Osteophytes
Fluid and synovium adjacent to the anterior talar neck, between the tibial osteophyte and the talus at the capsular attachment
Subchondral sclerosis
Tibiotalar effusion
Talar and anterior distal tibial subchondral edema
Discrete cartilaginous defects or a trough in the talus (“tram track” lesion)
Fibrous overgrowth

Treatment

Over a period of time anterior impingement produces pronounced ankle restriction and progressive development of hypertrophic bone. There is inflammation, spur fragmentation, and synovitis. Conservative approaches to treatment are activity modification, immobilization, anti-inflammatory agents, and steroids. Arthroscopic surgery (see Fig. 5.239) is used for decompression and resection of the hypertrophic synovitis. Open surgical resection of large exostoses may be necessary.

FIGURE 5.232 ● Posteromedial impingement secondary to disruption of the deep fibers of the deltoid ligament (posterior talotibial component) with associated thickened synovial response deep to the tibialis posterior tendon. (A) Coronal color illustration. (B) Coronal FS PD FSE image. (C) Axial T1-weighted image.

FIGURE 5.233 ● Gross fibrotic thickening posteromedially deep to the tibialis posterior tendon associated with chronic deltoid tearing. Anteromedial soft tissue fibrosis is also demonstrated. Axial T2-weighted FSE image.

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Sinus Tarsi Syndrome

Pearls and Pitfalls

Sinus Tarsi Syndrome

Sinus tarsi syndrome is associated with sinus tarsi and lateral hindfoot pain and instability with injury to the contents of the tarsal canal and sinus.
T1- or PD-weighted sagittal or coronal images demonstrate effacement of sinus tarsi fat.
Synovitis, fibrosis, or ligament disruption is identified on FS PD FSE images.
Tibialis posterior tendon dysfunction and spring ligament pathology may be associated with sinus tarsi syndrome.
The three layers of lateral ligamentous support of the joint are the superficial or peripheral layer (e.g., the calcaneofibular ligament), the intermediate layer (e.g., the cervical ligament), and the deep layer (e.g., the interosseous talocalcaneal ligament).

The sinus tarsi syndrome is a clinical disorder characterized by pain and tenderness on the lateral side of the hindfoot at the sinus tarsi. It is thought to represent a minor subtalar instability⁸⁵ caused by hemorrhage or inflammation with or without tears of the sinus tarsi ligaments. It frequently occurs after ankle sprains, most commonly in young males (as a function of chronic ankle sprain history) 20 to 40 years of age.

Anatomy of the Tarsal Sinus and Canal

The tarsal canal and cone- or funnel-shaped tarsal sinus are found between the posterior lateral subtalar joint and the anteriorly located talocalcaneonavicular or anterior subtalar joint (Fig. 5.240).⁹⁶ The tarsal sinus and canal are visualized from posteromedial to anterolateral. The tarsal canal narrows and extends medially, posterior to the sustentaculum tali. The contents of the tarsal canal and sinus include fat, proprioceptive nerve endings, arterial anastomoses with the posterior tibial and peroneal artery branches, and ligaments (Fig. 5.241). The five distinct ligaments of the tarsal canal and sinus are the medial, intermediate, and lateral roots of the inferior extensor retinaculum, the cervical ligament, and the interosseous talocalcaneal ligament (Fig. 5.242). The sinus tarsi is the larger lateral opening of the tarsal canal, and its long axis forms a 45° angle with the lateral aspect of the calcaneus (Fig. 5.243). The ligaments are divided into three layers (Table 5.1): the superficial (peripheral) layer (Fig. 5.244) and the intermediate and deep layers (Fig. 5.245). The sinus tarsi and tarsal canal separate the subtalar joint into anterior and posterior articulations. The sinus canal is 10 to 15 mm high, 3 to 5 mm wide, and 15 to 20 mm long.

Etiology, Pathology, Diagnosis, and Clinical Features

The initiating event in sinus tarsi syndrome is usually a traumatic injury associated with decreased venous outflow and resulting in fibrosis with vascular engorgement or nerve irritation. Approximately 70% of cases occur after trauma, and the mechanism is frequently an inversion injury of the ankle or hindfoot. The sequence of ligament injuries is usually:

Calcaneofibular ligament
Lateral talocalcaneal ligament
Interosseous ligament
Subtalar joint sprain

The pathologic changes described include scarring and degenerative changes to the soft-tissue structures of the sinus tarsi, specifically interosseous ligament tears, osteoarthrosis, arthrofibrosis, partial tears of the calcaneofibular ligament, synovial hypertrophy and hyperplasia, chronic synovitis, and hemosiderin deposition. On clinical examination, there is swelling and edema in the acute setting and lateral ankle pain and tenderness over the sinus tarsi. The pain is described as a deep aching or throbbing. Symptoms are exacerbated with weight-bearing and relieved by local anesthetic injection. There may be associated PTT disruption and subtalar instability.

MR Appearance

Conventional radiographs and stress views yield negative results, and MR is an excellent tool for the evaluation of nonlocalized symptoms, persistent pain, failed conservative treatment, or associated injuries. Sagittal T1- or PD-weighted images and FS PD FSE images are recommended. Contrast enhancement is useful for the identification of hypertrophied synovium. Subtalar arthrography may show the absence of normal subtalar joint microrecesses in the area of the interosseous and cervical ligaments, with cutoff of contrast at the interosseous ligament. This finding,

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however, has not been validated on MR scans of the tarsal sinus and canal, on which the absence of anterior microrecesses of the posterior subtalar joint may be a normal finding.⁹⁶ Klein and Spreitzer reported that 60% of patients with an abnormal tarsal sinus and canal were clinically diagnosed as having sinus tarsi syndrome.⁹⁶

FIGURE 5.234 ● (A) Lateral color illustration showing potential sites for anterior tibiotalar spurs.(B) Sagittal T1-weighted image with opposing talar and anterior tibial plafond osteophytes. (C) Lateral color illustration demonstrates complications of anterior osseous impingement with anterior osteophytes, synovitis, and a loose body.

FIGURE 5.235 ● (A) The normal angle between the distal tibia and the talar neck should be 60° or greater. (B) The presence of osteophytes on the distal tibia or talus can narrow the angle to less than 60°.

FIGURE 5.236 ● Anterior impingement with an anterior tibial spur up to 3 mm on a lateral color illustration (A) and a sagittal T1-weighted image (B). Osteophytes may develop as a consequence of degenerative joint disease or be associated with posttraumatic conditions.

FIGURE 5.237 ● (A) Osteochondral exostosis with a prominent tibial osteophyte greater than 3 mm. There is no talar spur in a grade 2 ankle spur. Anterior spurs may result from direct trauma following forced dorsiflexion injuries or from forced plantarflexion trauma with capsular avulsion. Osteophytes are seen in anterior impingement associated with athletic trauma, as might occur in football and basketball players and dancers. (B) Prominent anterior tibial spur associated with tibiotalar synovitis and effusion. Sagittal FS PD FSE image.

MR findings in the sinus tarsi syndrome include abnormalities of the sinus tarsi, including tears of the tarsal sinus and tarsal canal ligaments, and associated lateral collateral ligament tears. Key findings include:

Poorly defined margins of interosseous and cervical ligaments (Fig. 5.246)
Diffuse infiltration with synovitis and fibrosis (Fig. 5.247)
Multiple synovial cystic fluid collections
Associated posterior tibial tendon tears⁹⁷
Secondary sclerosis and subchondral cystic change in roof of sinus tarsi and calcaneus
Osseous flattening and subchondral sclerosis of the posterior facet of the subtalar joint
Subchondral erosions within the critical angle of Gissane
Increased signal in the intermediate and medial roots of the inferior extensor retinaculum on FS PD FSE images
Synovitis of the anterior capsule of the posterior talocalcaneal joint
Lateral ankle ligament sprain (anterior talofibular, calcaneofibular)
Subtalar joint dislocation (complete rupture of the interosseous talocalcaneal and cervical ligaments)

Treatment

Almost half of patients respond to conservative treatment including physical therapy, NSAIDs, steroid injections into the sinus tarsi, orthotics, and casting or aircast splints. When conservative therapy fails, surgical measures such as sinus tarsi evacuation, subtalar arthroscopy and débridement of the posterior subtalar joint and sinus tarsi, removal of the hypertrophic synovium and scarred ligamentous tissue, and arthrodesis for posterior facet arthrosis of the subtalar joint may be necessary.

Os Trigonum Syndrome

Pearls and Pitfalls

OS Trigonum Syndrome

Os trigonum syndrome pain may be associated with disruption of the cartilaginous synchondrosis between the os trigonum and the lateral tubercle of the posterior process.
Stieda's process is a prominent posterior extension of the lateral tubercle.
Compression of the os trigonum between the FHL and posterior talofibular ligaments occurs in extreme ankle flexion. Compression of the os trigonum between the calcaneus and talus occurs in the end range of plantarflexion.

FIGURE 5.238 ● Opposing tibiotalar spurs on a lateral color illustration (A), a sagittal PD-weighted image (B), and a sagittal FS PD FSE image (C). Osteophytes involving both the tibia and talus can impinge on each other in dorsiflexion and potentially limit motion. Pain, catching, and joint swelling may occur. Osteophytes may be intra-articular, intracapsular, or extra-articular in location.

FIGURE 5.239 ● (A) Lateral color illustration showing superimposed tibial arthrosis with fragmentation. (B –D) Arthroscopic osteophyte removal using the posterolateral portal. (B) Using the posterolateral portal for visualization, the extent of the anterior distal tibial spur can be seen. Posterior view. (C) The osteophyte is removed using a motorized bur. View from the posterolateral portal. (D) The arthroscope is switched to the anterior portals to confirm complete removal of the distal tibial osteophyte. Lateral view.

FIGURE 5.240 ● Anterior subtalar joint with the talus opened away from the calcaneus.

FIGURE 5.241 ● Ligaments of the subtalar joint. (A) Superficial lateral view of the subtalar joint with bones and ligaments. From this position, the interosseous ligament cannot be seen. (B) Superior view of the insertion sites on the calcaneus with the talus removed.

FIGURE 5.242 ● Tarsal canal and sinus tarsi anatomy on an axial superior view color graphic (A), a color coronal section (B), and a corresponding T1-weighted MR arthrogram (C).

FIGURE 5.243 ● (A) Lateral view of the sinus tarsi. The sinus tarsi and tarsal canal separate the anterior and posterior articulations of the subtalar joint. The sagittal plane of section helps to demonstrate the anatomy more clearly. (B) After sectioning, the tarsal canal and subtalar articulations are more clearly seen. (C) Axial view of the tarsal canal. Note the location of the interosseous talocalcaneal and cervical ligaments. There is a 45° angle of orientation of the long axis of the sinus tarsi to the lateral aspect of the calcaneus. The interosseous talocalcaneal ligament (part of the deep layer of the subtalar ligaments) is demonstrated on T1-weighted coronal (D) and sagittal (E) images.

FIGURE 5.244 ● Superficial or peripheral ligaments. (A) Lateral view of the right ankle demonstrates the peripheral ligaments. (B) Axial view of the ankle shows the peripheral ligaments. The lateral talocalcaneal and calcaneofibular ligaments can be seen arthroscopically. (C) Corresponding axial MR image shows components of the superficial, intermediate, and deep layers of the lateral ligamentous support of the subtalar joint.

FIGURE 5.245 ● Intermediate and deep ligaments. (A) Axial view of the subtalar joint demonstrates the deep ligaments. (B) Coronal section of the subtalar joint shows the course of the interosseous talocalcaneal ligament in relation to the cervical ligament and surrounding roots. (C) Corresponding T1-weighted sagittal image of the cervical and intermediate root of the inferior extensor retinaculum (intermediate layer of subtalar ligaments).

FIGURE 5.246 ● (A) Sinus tarsi syndrome with synovitis of the synovial recesses and inflammation of the fat contained within the sinus tarsi. Subchondral erosions and synovitis of the sinus tarsi root with hyperintense synovial cysts are shown on sagittal T1-weighted (B) and FS PD FSE (C) images. The majority of cases of sinus tarsi syndrome involve trauma, usually related to a significant inversion sprain. Scarring and degenerative changes to the soft-tissue structures of the sinus tarsi are associated with pain.

FIGURE 5.247 ● Poorly defined cervical (A) and interosseous talocalcaneal (B) ligaments associated with synovitis and fibrosis in a patient with lateral foot pain and clinical hindfoot instability. Tibialis posterior tendon dysfunction, spring ligament pathology, and sinus tarsi syndrome may represent a continuum of progressive and related pathologies. Loss of proprioceptive function of the nerve endings in the ligaments in the sinus and tarsal canal secondary to injury may be another causative factor in the progression of sinus tarsi syndrome.

TABLE 5.1 Lateral Ligamentous Support for the Subtalar Joint

Superficial Layer

Lateral root of the inferior extensor retinaculum

Lateral talocalcaneal ligament

Calcaneofibular ligament

Posterior talocalcaneal ligament

Medial talocalcaneal ligament

Intermediate Layer

Intermediate root of the inferior extensor retinaculum

Cervical ligament

Deep Layer

Medial root of the inferior extensor retinaculum

Interosseous talocalcaneal ligament

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The os trigonum is a lateral tubercle in the posterior aspect of the talus found in 10% of individuals. When present it occurs bilaterally in 50% of cases. It varies in size from complete absence to a grossly enlarged structure. Bipartite morphology is rare. It usually appears as a triangular ossicle posterior to the lateral tubercle of the posterior talar process and articulates with the posterolateral process of the talus and the superior aspect of the calcaneus (Fig. 5.248). The ossicle is united to the posterior process by cartilaginous, fibrous, or fibrocartilaginous tissue. In 7% to 14% of patients, it remains unfused as a separate ossicle. There are four anatomic variations of the posterolateral talus:

Type I: Normal tubercle (Fig. 5.249)
Type II: Stieda's process (enlarged posterior extension of the lateral tubercle of the talus (Fig. 5.250)
Type III: An accessory bone or os trigonum (Fig. 5.251)
Type IV: The os trigonum is fused with the talus via the synchondrosis or the syndesmosis (Fig. 5.252).

Etiology, Pathology, and Clinical Features

As discussed earlier in the chapter, posterior bony impingement or talar compression is a condition seen with injuries in dancers. This syndrome may be associated with an os trigonum or posterior trigonal process.⁶² The os trigonum syndrome is characterized by symptoms caused by pathology of the lateral tubercle of the posterior talar process⁹⁸ and includes various descriptions including posterior ankle impingement, talar compression syndrome, and posterior tibiotalar impingement syndrome. It accounts for 0.2% of ankle sprains and is seen more frequently in females because of its association with ballet.

Pain is associated with disruption of the cartilaginous synchondrosis between the os trigonum and the lateral tubercle secondary to repetitive microtrauma and chronic inflammation. Activities involving extreme plantarflexion may result in compression and entrapment of synovial and capsular tissue against the posterior tibia, causing soft-tissue thickening, fibrosis, and sometimes the development of associated FHL tenosynovitis. It is frequently seen in ballet dancers (and other athletes, including soccer and football players and downhill runners), in whom extreme ankle dorsiflexion causes compression of the ossicle between the FHL and the PTFL. At the end-range of plantarflexion there is compression of the ossicle between the calcaneus and the tibia. In the high-arched or supinated foot, the PTFL applies traction force on the posterolateral talar process. In the pronated foot, the traction force is applied by the posterior talocalcaneal ligament. In calcaneal eversion there is impingement between the superior surface of the calcaneus or ossicle and the tibia. Combined plantarflexion and dorsiflexion produce irritation of the FHL at the level of the posterior talar process.⁹⁹ Trigonal process fracture, FHL tenosynovitis, posterior tibiotalar bony impingement, and intra-articular loose bodies are considered additional etiologies.

FIGURE 5.248 ● Lateral perspective color illustrations of the os trigonum and related anatomic structures in the differential diagnosis of posterior impingement.

FIGURE 5.249 ● Superior view color illustration of the normal medial and lateral tubercles of the posterior process.

FIGURE 5.250 ● Lateral color illustration of a prominent lateral talar tubercle of the posterior process (referred to as Stieda's process or a trigonal process).

FIGURE 5.251 ● Os trigonum represents a nonunited secondary ossification center. Less commonly, the ossicle may be attributed to a chronic fracture through the lateral talar tubercle. Superior view color illustration.

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Pathologic processes include FHL tendon sheath thickening, synchondrosis fissuring, arthritic changes between the talar projection and the calcaneus, and degenerative changes across the synchondrosis. Enlargement of the os trigonum is not required for the diagnosis.

Clinically there is chronic pain, stiffness, tenderness, and soft-tissue swelling in the posterior ankle. The pain, described as deep and aching, is exaggerated by plantarflexion and weight-bearing activities. The subtalar range of motion is decreased and peroneal spasm is common. In ballet dancers, pain is seen with demi-pointe, full pointe, tendu, frappe, relevé, and jumping (weight-bearing in plantarflexion) (Fig. 5.253). The onset is frequently associated with chronic ankle sprain. Clinical confirmation of the diagnosis is often provided by relief of symptoms following the injection of a local anesthetic.¹⁰⁰

FIGURE 5.252 ● Intact synchondrosis of os trigonum. Young athletes engaged in sports that involve forced plantarflexion (including ballet dancers, javelin throwers, and soccer players) are prone to os trigonum syndrome. (A) Sagittal T1-weighted image. (B) Sagittal FS PD-weighted image.

FIGURE 5.253 ● Nutcracker phenomenon of posterior ankle impingement with the os trigonum situated between the posterior tibial margin and the calcaneus. Acute or chronic disruption of the cartilaginous synchondrosis between the os trigonum and lateral talar tubercle may subsequently develop.

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MR Appearance

MR imaging or CT may not be able to distinguish between a chronic un-united fracture of the lateral tubercle (Shepherd's fracture) and the unfused os trigonum. The FHL tendon is medial to the os trigonum in the sulcus between the smaller medial tubercle and the larger lateral tubercle. This relationship is seen on axial MR images. Isolated tenosynovitis of the FHL tendon sheath may not be associated with a corresponding effusion in the tibiotalar joint. The best MR diagnostic clue is hyperintensity across the synchondrosis on FS PD FSE images produced by disruption of the cartilaginous synchondrosis between the os trigonum and the lateral talar process.

Key MR findings include:¹⁰¹

An enlarged marrow fat-containing os trigonum (Fig. 5.254)
Degenerative sclerosis or cystic change between the os trigonum and the talus
Sclerosis and edema of the trigonal process
Fluid and effacement of surrounding soft tissues
Os trigonum or trigonal process hyperintensity on FS PD FSE or STIR images (Fig. 5.255)
Hyperintensity in the synchondrosis or posterior talus on FS PD FSE images (Fig. 5.256)
Edema and synovitis posterior to the talus and superior to the os trigonum
Edema and synovitis posterior to the os trigonum on sagittal images
Fracture of the lateral tubercle of the posterior process (Stieda's process) with hyperintense marrow and adjacent hyperintense synovitis on FS PD FSE images (Fig. 5.257)
Isolated tenosynovitis of the FHL tendon sheath (partial tethering FHL tendon) (see Fig. 5.254)
Possible associated intra-articular loose bodies

Treatment

Symptoms are frequently relieved with rest and other conservative measures such as splinting, anti-inflammatory agents, steroid injections, and casting. Sometimes, however, there is progression to recalcitrant pain, fracture, or stenosing tenosynovitis of the FHL, in which case surgery may be necessary. Surgical procedures include resection of the os trigonum (Fig. 5.258), recontouring of the prominences in the superior calcaneus and posterolateral talus, resection of hypertrophic or fibrotic tissue, and resection of the hypertrophic or scarred FHL sheath. Arthroscopic techniques are available. Complications include arthritis and impingement of soft tissue.

Accessory Navicular

An accessory navicular ¹⁰¹ is caused by the congenital development of a navicular tuberosity from a secondary center of ossification with a synchondrosis to the medial part of the navicular body. It is usually seen as an accessory bone or sesamoid of the PTTI in the plantar portion at the level of the inferior calcaneonavicular ligament. There is a 2% to 20% incidence of accessory ossicles, and os tibiale externum is the second most common accessory bone of the foot.

Accessory navicular has been classified into three types, although some represent a combination:

Type I: A type I accessory navicular is a 4- to 6-mm ossicle. It is a true sesamoid within the PTT and represents 30% of cases.
Type II: A type II accessory navicular is triangular or heart-shaped and has a nonossified zone of 1 to 3 mm. There are two subtypes. Type IIa represents more superior placement of the accessory bone, which is subject to avulsion and tension forces. In type IIb, placement of the accessory bone is more inferior and it is subject to shearing forces.
Type III: Type III represents a cornuate or enlarged navicular tuberosity.

Symptoms associated with an accessory navicular may vary depending on the type. A type I accessory navicular may be associated with tibialis posterior tendinosis with or without associated pes valgo planus. Type II may produce symptoms of chronic stress, such as navicular pain and shoe irritation. Type III is associated with irritation of the navicular prominence, causing complaints of shoe irritation and superficial pain. Since the os tibiale externum ossifies between 9 and 11 years of age, symptoms usually appear after 5 years of age and are most common during adolescence. They occur more frequently in females than in males. On pathologic examination the synchondrosis may be fibrous, cartilaginous, fibrocartilaginous, or partially osseous.

MR Appearance

The appearance of accessory navicular varies depending on the type. Type I (Fig. 5.259) is characterized by:

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A small (4 to 6 mm), usually marrow fat-containing ossicle proximal to the navicular tuberosity
Hypointense to intermediate signal intensity within the distal PTT on T1- or PD-weighted images
A 5- to 7-mm separation from the navicular
Fat signal in the ossicle suppressed on FS PD FSE images
The ossicle may be difficult to differentiate from surrounding hypointense tibialis posterior on FS PD FSE images.

FIGURE 5.254 ● Edema across the synchondrosis of the os trigonum. Edema associated with degenerative change is hypointense on T1-weighted images and hyperintense on FS PD FSE images. Flexor hallucis longus tenosynovitis is an associated finding. Edema is associated with chronic shearing stress and bone remodeling across the synchondrosis. The os trigonum is also at risk for fragmentation with secondary osteonecrosis. Marrow fat signal is present in the os trigonum on the axial T1-weighted image (C). (A) Axial color illustration, superior view of talus. (B) Sagittal FS PD FSE image. (C) Axial T1-weighted image. (D) Axial FS PD FSE image.

FIGURE 5.255 ● Degenerative change with edema in a Stieda's process of the talus. There is associated reactive change in the posterior aspect of the posterior facet of the calcaneus. (A) Sagittal T1-weighted image. (B) Sagittal FS PD FSE image.

FIGURE 5.256 ● (A) Hyperintensity within the synchondrosis on a sagittal FS PD FSE image. The synchondrosis interface is irregular. Fluid is seen in the flexor hallucis longus tendon sheath. (B) Associated degeneration of the posterior talofibular ligament and transverse tibiofibular ligament are identified lateral to the os trigonum. Sagittal FS PD FSE image.

FIGURE 5.257 ● (A) Normal posterior structures with the foot in demi-pointe position without posterior impingement. Lateral color illustration. (B) Sagittal T1-weighted image showing the proximity of the lateral tubercle of the posterior process and the transverse tibiofibular ligament or posterior labrum of the ankle in demi-pointe position. (C, D) Posterior impingement in a world-class ballet dancer with a fractured lateral talar tubercle representing a pseudoarthrosis. Associated inflammation of the posterior recess of the tibiotalar and subtalar joints is identified. (C) Sagittal T1-weighted image. (D) Sagittal FS PD FSE image.

FIGURE 5.258 ● (A) Excision of an os trigonum. A nonunion of the os trigonum shows significant motion at its fibrous attachment to the talus and irregularity and chondromalacia and fibrosis at its insertion. (B, C) Arthroscopic excision of an os trigonum. (B) Visualization of fibrous attachment of the os trigonum with subtalar arthroscopy. (C) As the os trigonum is removed from the subtalar joint, the flexor hallucis longus is seen.

FIGURE 5.259 ● Type I accessory navicular is seen as a small (marrow fat-containing) ossicle imbedded within the distal tibialis posterior (posterior tibial tendon) on a T1-weighted axial image.

A type II (Fig. 5.260) navicular demonstrates:

Marrow fat-containing triangular or heart-shaped ossicle with direct connection to the medial navicular through a synchondrosis
Nonossified synchondrosis of low to intermediate signal intensity on T1- or PD-weighted images and hyperintense on FS PD FSE images
Associated degenerative sclerosis with or without subchondral cystic degeneration (hypointensity across the synchondrosis on T1- or PD-weighted images)
Bursitis
Distal thickening in the tibialis posterior tendinosis and tenosynovitis with or without partial to complete PTT tear
In asymptomatic patients, there is normal fat-suppressed marrow signal intensity on FS PD FSE images.
In symptomatic patients there is usually marrow edema and degenerative hyperemia of the subchondral bone.
Osseous edema, which may involve the accessory navicular, the accessory and navicular tuberosity, or the tuberosity alone

Typical findings in a type III navicular (Fig. 5.261) are:

Enlarged os cornuate marrow fat signal intensity extension of the medial navicular proximally
No synchondrosis
Normal marrow fat characteristics on all pulse sequences

Treatment

Symptoms may first occur or be exacerbated after local trauma to the foot and ankle. Eventually chronic irritation leads to bursa development over the bony protuberance, degenerative changes (progressive at the synchondrosis), and possible loss of height of the medial longitudinal arch. The range of motion at the ankle and the subtalar and transverse tarsal joints remains intact. Conservative treatment, consisting of orthotics, shielding, and shoe modifications, can be tried for all three types of accessory navicular. If conservative approaches fail, surgery (the Kidner operation) is necessary to remove the accessory navicular prominence and to reinsert the tibialis posterior. In type I lesions surgery is performed to remove the ossicle from the PTT in symptomatic tibialis posterior tendinosis. In type II lesions resection of the entire nonossified synchondrosis or bone grafting and arthrodesis are necessary. In type III lesions surgical approaches include remodeling and reconstructive procedures for pes valgo planus. Complications include the development of weakness of the tibialis posterior muscle after excision of the navicular prominences.

Turf Toe

Pearls and Pitfalls

Turf Toe

The key ligaments of the capsuloligamentous complex of the first MTP joint are the metatarsosesamoid and sesamoid-phalangeal ligaments.
The plantar plate is less substantial in the hallux relative to the lesser metatarsals. It can be visualized between the sesamoid-phalangeal ligaments extending from the sesamoids to the proximal aspect of the proximal phalanx.
Turf toe evaluation must include assessment of tearing of the sesamoid-phalangeal ligament, plantar plate, and displacement or fracture of the sesamoids.

The first metatarsophalangeal (MTP) joint is a chondroloid joint that is a source of frequent pathology. Turf toe, a hallux MTP joint injury with disruption of the plantar joint capsule and plantar plate, is one of the most important of the MTP injuries.

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Other sesamoid and plantar plate injuries are covered in subsequent discussions.

FIGURE 5.260 ● (A) Type II accessory navicular on a superior view color illustration. (B, C) Symptomatic type II accessory navicular in a professional basketball player with prominent marrow edema on either side of the synchondrosis. The connection of the accessory ossification is through a fibrous or cartilaginous bridge. Repetitive contraction of the tibialis posterior tendon insertion onto the accessory navicular can generate painful shearing forces across the synchondrosis at the level of the medial aspect of the midfoot. (B) Axial T1-weighted image. (C) Axial FS PD FSE image.

FIGURE 5.261 ● Type III or cornuate navicular on an axial T1-weighted image. Both the type II and type III navicular are associated with tibialis posterior tendon degeneration and tear and a painful os naviculare syndrome. Degenerative sclerosis may be observed without hyperintensity on FS PD FSE images but may coexist with reactive edema. Edema in the type II and cornuate navicular is associated with more acute clinical symptoms.

Anatomy and Biomechanics of the MTP Joint

An understanding of the structure and function of the first MTP joint is helpful in understanding the etiology and pathology of these injuries. The MTP joint of the great toe is composed of the metatarsal head and neck, the proximal phalanx, and the medial and lateral sesamoids. The sesamoid complex consists of two sesamoid bones, eight ligaments, and seven muscles (Figs. 5.262, Figs. 5.263, Figs. 5.264 and 5.265). Most of these structures are concentrated on the plantar surface of the joint. The dorsal surface of the MTP joint is dominated by the extensor hallucis longus tendon, which lies in the dorsal midline. The extensor hallucis brevis tendon is just plantar and lateral to the extensor hallucis longus. The sagittal hood spreads out from the tendon sheath, encasing the ligaments to form a confluence of thickened capsular tissue extending in a plantar direction toward to the collateral ligaments in the midline both medially and laterally. These fan-like, capsuloligamentous structures align at the equator of the joint and extend from the upper condylar region of the first metatarsal head to the base of the proximal phalanx.

A small bony ridge or crista separates the two sesamoid bones as they lie in their respective grooves (see Figs. 5.262, Figs. 5.263 and 5.264). A dense plantar plate anchors the sesamoids to the proximal phalanx. The plantar plate is located midline to the sesamoid-phalangeal and metatarsosesamoid ligaments. The medial sesamoid is usually slightly more distal than the lateral one. This allows visualization more easily via the arthroscope. The sesamoids are encased by two heads of the flexor hallucis brevis tendons (see Figs. 5.262 and 5.264A).

The capsuloligamentous complex of the MTP joint is the key factor contributing to its stability. The relevant ligaments of the first MTP joint are:

Medial and lateral metatarsosesamoid ligaments
Medial and lateral sesamoid-phalangeal ligaments
Intersesamoid ligament
Medial and lateral collateral MTP ligaments

Minimal stability is offered by the bony architecture of the joint and long flexor and extensor tendons. The adductor and abductor hallucis tendons provide some support to the lateral and medial capsule, respectively; the short flexor and extensor tendons blend into the capsule and give strong stabilizing elements. The medial and lateral collateral ligaments provide strong support and have two components, the MTP and the metatarsosesamoid ligaments. The origins of these ligaments are on the medial or lateral border of the metatarsal head and fan out onto the proximal phalanx and plantar plate.

The importance of the MTP joint of the great toe to weight-bearing and gait is obvious. The great toe supports more than twice the load of the lesser toes, with the maximum force reaching 40% to 60% of body weight in normal walking. During running and jumping, these forces are increased proportionately. The instant center of motion for the first MTP joint falls within the first metatarsal head. With range of motion of the MTP joint, a gliding motion occurs at the joint surface.

Etiology, Pathology, and Clinical Features

Traumatic hyperextension of the hallux MTP as well as other biomechanical variations, including hyperflexion and valgus- and varus-type injuries, may affect the capsular-ligamentous-sesamoid complex. The risk for turf toe injury is connected with extreme dorsiflexion and valgus or varus strain of the MTP. It is associated with artificial sports surfaces that affect the shoe—surface interface. Flexible turf shoes without a stiff sole make athletes more prone to injury. This injury may occur in a variety of sports, including football, baseball, basketball, and soccer.

Tears of the MTP joint capsule usually occur at the metatarsal neck, which is the weakest point of attachment, rather than the proximal phalanx.¹⁰² Capsular tearing leads to

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unrestricted motion of the proximal phalanx and compression of the dorsal articular surface of the metatarsal head. The plantar aspect of the ligamentous complex tears with associated detachment of the plantar plate distal to the sesamoids (Fig. 5.265). An abductor injury may be associated with a turf toe injury (Fig. 5.266). Fracture of the sesamoids or separation of a bipartite sesamoid may result (Fig. 5.267). Other mechanisms of injury may occur with turf toe variants, including:

FIGURE 5.262 ● (A) Superolateral view of the bone-ligament-capsular anatomy of the MTP joint. (B) Axial PD FSE image demonstrating the anatomy of the MTP joint anatomy at the level of the sesamoids. The medial sesamoid is embedded in the tendons of the abductor hallucis and medial head of the flexor hallucis brevis. (C) Coronal PD-weighted image showing the lateral sesamoid embedded in the tendons of the lateral head of the flexor hallucis brevis and transverse and oblique heads of the adductor hallucis.

FIGURE 5.263 ● Sesamoid position. (A) Plane of cross-section to study the sesamoids. (B) Cross-sectional anatomy of the metatarsal head with the medial and lateral sesamoids separated by a small bony ridge, or crista. (C) Coronal T1-weighted image demonstrates the crista of the first metatarsal head and the relationship to the intersesamoid ligament deep to the flexor hallucis longus tendon. (D) Sagittal FS PD FSE and (E) axial PD FSE images of a torn inter-sesmoid ligament visualized in a turf toe with dislocation of the first MTP.

Valgus injury plus dorsiflexion with injury to the medial ligamentous structures and medial sesamoid
Varus injury with lateral capsular tear (Fig. 5.268) and rupture of the adductor hallus tendon
Hyperflexion injury secondary to MTP forced plantarflexion (also referred to as sand toe). Hyperflexion occurs in beach volleyball players, football players, dancers, and skimboarders,¹⁰³ who may develop sprain or tear of the dorsal capsule secondary to exaggerated hyperflexion (Fig. 5.269). Associated injury to the lesser MTP joint may also occur.

Clinically, patients with turf toe present with pain on dorsiflexion and weight-bearing.

Classification

Dorsiflexion and hyperflexion injuries of the capsular-ligamentous complex have been classified into three grades:

Grade 1: Stretch injury or minor tearing of first MTP joint capsular-ligamentous complex
Grade 2: Partial tear of first MTP capsular-ligamentous complex with an intact articular surface
Grade 3: Disruption of the capsular-ligamentous complex with a plantar plate tear from its metatarsal head/neck origin. There is associated impaction of the proximal phalanx into the dorsal aspect of the metatarsal head as well as articular cartilage damage, subchondral marrow edema, and sesamoid fracture or diastasis.

MR Appearance

Key MR findings include:

Disruption with edema or discontinuity of the sesamoid-phalangeal ligament on sagittal images
Tear of the intersesamoid ligament as assessed on axial or coronal images
Absence or irregularity of the plantar plate between the sesamoid-phalangeal ligaments (direct visualization of the plantar plate is more difficult in the first MTP compared to the lesser metatarsal MTP joints because of the presence of the sesamoids in the first MTP)
Proximal retraction of the sesamoid on sagittal images
Edema and/or tearing of the flexor hallucis brevis, abductor, or adductor hallucis tendons
Metatarsal head edema

Treatment

Turf toe may improve, although recurrent sprains are not uncommon, or there may be continued pain with rupture of the sesamoid complex. If conservative treatment (below-the-knee casting) fails, arthroscopy or surgical therapy is necessary. The diagnostic indications for arthroscopy of the MTP joint of the

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great toe include persistent pain, swelling, stiffness, locking, or grinding. The therapeutic options include treatment of chondromalacia, synovitis, osteochondral lesions, osteophytes, loose bodies, and arthrofibrosis. Arthrodesis may eventually be necessary. The contraindications include the presence of infection, advanced DJD, severe edema, or poor vascular status. Surgical treatment options include ORIF for diastasis of a bipartite sesamoid, a sesamoidectomy, and reattachment of the plantar plate with suture anchor technique.

FIGURE 5.264 ● (A) Hallux MTP capsular-ligamentous-sesamoid complex demonstrates the relationship of the plantar plate distal to the sesamoids and between the sesamoid phalangeal ligaments. The plantar plate is a strong fibrous structure that has a firm attachment to the proximal phalanx and a less substantial attachment to the metatarsal neck. The medial and lateral collateral ligaments consist of an MTP and a metatarsosesamoid ligament. The medial and lateral sesamoid-phalangeal ligaments are directly adjacent to the plantar plate and also bridge and stabilize the sesamoids to the proximal phalanx. (B) Axial PD-weighted image at the level of the plantar plate and sesamoid-phalangeal ligament. (C) Sagittal FS PD FSE image through the plantar plate adjacent to the medial sesamoid and lateral to the sesamoid-phalangeal ligament. (D) Sagittal T1-weighted image of the sesamoid-phalangeal ligament located medial to the plantar plate at the level of the medial sesamoid.

FIGURE 5.265 ● Turf toe with disruption of the sesamoid-phalangeal ligament and plantar plate of the first (hallux) MTP joint. (A) Lateral color illustration of a retracted sesamoid and disruption of the plantar plate complex. (B) Sagittal PD-weighted image of a retracted medial sesamoid and complete discontinuity of the medial sesamoid-phalangeal ligament and plantar plate. (C) Sagittal FS PD FSE image of the disrupted plantar plate directly lateral to the torn medial sesamoid-phalangeal ligament. (D) Coronal PD-weighted image immediately distal to the sesamoids demonstrates disruption of the plantar plate complex.

FIGURE 5.266 ● (A) Turf toe variation with disruption of the abductor hallucis tendon attachment to the medial sesamoid in a professional baseball player. Coronal FS PD FSE image. (B) Normal abductor hallucis tendon attachment shown for comparison in a separate individual. Coronal PD FSE image.

FIGURE 5.267 ● Turf toe with traumatic separation of a bipartite sesamoid. The sesamoid-phalangeal ligament and plantar plate were intact. (A) Lateral color illustration. (B) Sagittal FS PD FSE image.

FIGURE 5.268 ● Lateral collateral ligament disruption at the level of the first metatarsal head. Axial FS PD FSE image.

FIGURE 5.269 ● (A) Color illustration of skimboarder's toe secondary to a hyperdorsiflexion injury with disruption of the dorsal portion of the extensor expansion. (B) Separate case with a dorsal capsular sprain and osseous contusions involving the first metatarsal head and dorsal aspect of the proximal phalanx secondary to a forced plantarflexion injury. Sagittal FS PD FSE image.

Complications of turf toe include sesamoid fracture, separation of a bipartite sesamoid, proximal migration of the sesamoids, instability, hallux rigidus, and an MTP joint cartilage flap or loose body.

Sesamoid Dysfunction

Abnormalities of the plantar plate of the foot (extending from the distal metatarsal neck to the plantar aspect of the proximal phalangeal base) and metatarsal sesamoids can be detected and characterized on MR studies.¹⁰⁴^,¹⁰⁵ The two plantar sesamoids (Fig. 5.270) articulate with the first metatarsal head¹⁰⁶ within the double tendon of the flexor hallucis brevis. The medial sesamoid

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is slightly larger than the lateral sesamoid. They are ovoid in shape, separated by an intersesamoidal ridge or crista, and the dorsal surface is cartilaginous and articulates with the concave facets of the first metatarsal head. The sesamoids and the collateral ligaments together stabilize the first MTP joint. Sesamoid disorders include bipartite sesamoids, fractures, turf toe (discussed above), osteochondritis and AVN, sesamoiditis, and arthritis. Ossification of the hallucal sesamoids occurs from 7 to 10 years of age (earlier in females than in males).

FIGURE 5.270 ● Coronal color section through the sesamoids. The sesamoids vary in morphology from semiovoid to circular to bean-shaped. The medial sesamoid is usually larger and can be bi-, tri-, or quadripartite.

Etiology and Pathology

Bipartite sesamoid bone morphology is caused by irregular ossification and is more common than a complete sesamoid bone fracture. The bipartite cleft is transverse, smooth, and round, with sclerotic cortical edges without callus. Almost all bipartite sesamoids are bilateral, and up to 90% involve the tibial or medial sesamoids. Tibial sesamoids may be divided into two or three fragments. Asymmetrical division is not uncommon, and there may be associated MTP joint swelling.

Sesamoid fractures are usually transverse and involve the tibial sesamoid. The fracture site is irregular and may displacement and be associated with soft-tissue swelling. Sudden loading or repetitive stress, an increase in medial weight-bearing function, and dorsiflexion or hyperflexion have all been implicated.

Osteochondritis and AVN are associated with fragmentation and stress fractures, and sesamoiditis (sesamoid chondromalacia) is associated with trauma, MTP joint swelling, and inflammation of the plantar sesamoid complex. Sesamoiditis is often seen in young athletes.

Arthritis may or may not result from a progression of sesamoiditis, chondromalacia, or trauma and is characterized by erosion of articular cartilage and osteophytes.

FIGURE 5.271 ● Stress fracture of the lateral sesamoid in a long-distance runner. (A) Plantar view color graphic of the sesamoids. Sesamoid marrow is hypointense on coronal PD-weighted image (B) and hyperintense on coronal FS PD FSE image (C).

Clinical Features

Patients with sesamoid dysfunction present with pain over the plantar aspect of the sesamoids. Fractures are characterized by nonspecific swelling of the first MTP joint and discomfort on passive range of motion. In osteochondritis there is tenderness on palpation, and in sesamoiditis there is pain on weight-bearing or athletic activity (e.g., running), localized tenderness, and MTP joint swelling. Arthritis is recognized by the presence of warmth and swelling as well as a restricted range of motion and pain on palpation. Hallux valgus and hallux rigidus (stiff big toe) should be considered in the differential diagnosis of pain referred to the first MTP joint.

MR Appearance

The MR appearance on sesamoid studies varies depending on the specific pathology:

Bipartite sesamoids, which more frequently involve the medial sesamoid, are characterized by the following:
- Identical rather than asymmetric division with marrow fat signal intensity on T1- or PD-weighted images
- The lateral sesamoid is rarely separated into more than two fragments.
- Smooth margins (rounded edges)
- No increase in signal intensity on FS PD FSE images
- Normal surrounding soft tissue and capsular structures
Typical findings in sesamoid fractures (Fig. 5.271) are:
- Sharp or discrete linear morphology
- Replacement of marrow fat with edema
- Adjacent capsular and soft-tissue edema
- Visualization of linear transverse fracture with or without displacement of the fragment
- Serrated and irregular edges
- Variable subchondral edema in one or both fragments
In osteochondritis and AVN (Fig. 5.272) typical MR findings include:
- Fragmentation of the involved sesamoid
- Greater involvement of the lateral sesamoid
- An acute/subacute phase with variable increased signal intensity and a chronic phase with hypointensity on FS PD FSE images
Sesamoiditis is characterized by:
- Effusion and synovitis of the first MTP joint
- Mild subchondral sclerosis between the first metatarsal facets and the dorsal articular surface sesamoids
- Dorsal sesamoid chondral degeneration with narrowing relative to the metatarsal concave articular facets
Arthritis signs include:
- Maintenance of the marrow fat signal by osteophytes
- Subchondral sclerosis at the articulation with the first metatarsal head
- Osteophytic spurring
- MTP joint fluid and effusion
- Associated hallux valgus (Fig. 5.273) and hallux rigidus (Fig. 5.274)

Treatment

In the natural course of sesamoid dysfunction, sesamoid fractures may heal by bony consolidation or fibrous union; osteochondritis is associated with fragmentation and sesamoiditis

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by reduced ability for weight-bearing. Conservative methods are usually successful and include:

FIGURE 5.272 ● Bipartite fibular sesamoid with osteochondritis. The bipartite sesamoid is enlarged with smooth edges (curved arrow). Osteochondritis demonstrates hypointensity on both T1-weighted (A) and FS PD FSE (B) axial images.

FIGURE 5.273 ● (A) Hallux valgus deformity on superior view color illustration. There is subluxation of the first MTP base. Axial (B) and sagittal (C) T1-weighted images demonstrate the prominence of the medial eminence of the metatarsal head. With subluxation of the tibial sesamoid there is erosion of the crista of the metatarsal head. The crista normally helps maintain alignment and prevents lateral subluxation of the tibial sesamoid. The first metatarsal may deviate both medially and dorsally. Metatarsus primus varus (medial inclination of the first metatarsal) with dorsal splaying of both the first and fifth metatarsal heads occurs in hallux valgus.

FIGURE 5.274 ● (A) Hallux rigidus with pain elicited by the axial grind test (axial compression and dorsiflexion). Lateral color illustration. (B) Sagittal T1-weighted image with degenerative first metatarsal osteophytes and joint changes. Hallux rigidus or stiff big toe may be secondary to trauma or increased stress on the joint.

A below-the-knee walking cast for fractures
A shoe with an insert or pad and NSAIDs for osteochondritis and AVN
Activity modification and reduced weight-bearing for sesamoiditis
Orthotics, a shoe with a stiff insole and padding, and NSAIDs for arthritis

For failed conservative treatment or a chronically painful sesamoid, excision of the dorsal osteophyte (Fig. 5.275) may be necessary.

Plantar Plate Injuries of the Lesser Metatarsophalangeal Joints

Pearls and Pitfalls

Plantar Plate Injuries of the Lesser Metatarsophalangeal Joints

Pitfalls in the MR interpretation of the lesser MTP joints include the normal plantar plate recess, the capsular plantar plate attachment, and the distal phalangeal bare area.
Intermediate-signal-intensity hyaline articular cartilage may undercut the plantar plate on sagittal images.
Plantar plate tears occur most frequently at their distal attachment.
MTP joint instability is associated with plantar plate degeneration and rupture.

Plantar plate degeneration and rupture may be associated with metatarsalgia, MTP instability, and toe deformities including hammertoe, claw toe, and crossover toe. In evaluating these disorders it is helpful to understand the relevant anatomy of the lesser MTP joints. In the first MTP joint, the hallucal sesamoids disperse the forces at the metatarsal head and protect the intersesamoidal course of the FHL tendon.¹⁰⁷ In contrast to the great toe, the lesser metatarsals lack sesamoids and articulate directly with the plantar plate (Fig. 5.276). The lesser MTP joints are stabilized by the plantar plate, the joint capsule, and the collateral ligaments. Compressive loads of weight-bearing and tensile forces of ambulation are greatest at the second metatarsal head.

In the sagittal plane the following attachments onto the plantar plate are displayed:¹⁰⁸

The collateral ligaments, represented by the accessory collateral ligament (ACL) and the phalangeal collateral ligament (PCL) (the PCL is also known as the proper collateral ligament and the main collateral ligament)
The flexor tendons, including the flexor digitorum brevis (FDB) and the FDL tendon
The extensor head, which, along with the extensor sling, represents the fibroaponeurotic expansion from the extensor digitorum longus (EDL) tendon sheath

In the coronal plane the following structures associated with the plantar plate are demonstrated (Fig. 5.277):¹⁰⁸

ACL
Extensor tendon and hood
Deep transverse intermetatarsal ligament, which blends with the medial and lateral margins of the plantar plate
Flexor tendon sheath located centrally within a groove at the undersurface of the plantar plate

Metatarsalgia, which is a painful condition in the region of the metatarsal heads commonly affecting the second MTP joint, may be caused by plantar plate rupture (Fig. 5.278) and MTP joint instability and joint synovitis. Plantar plate rupture is the result of capsular distention from chronic MTP synovitis. Plantar plate degeneration and rupture usually occur at the distal insertion onto the base of the proximal phalanx. Tears can occur medially, paracentrally, or laterally along the plantar plate but are more common at the distal lateral insertion and are often found in association with a PCL rupture. MTP joint instability usually occurs secondary to plantar degeneration and rupture (Fig. 5.279). MTP joint synovitis may progress to

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MTP joint instability. Capsular distention results in degeneration and weakening of the plantar plate and collateral ligaments. Metatarsalgia may also be associated with stress fractures, Freiberg's infraction, Morton's neuroma, arthritis, and synovial cyst formation.

FIGURE 5.275 ● Excision of a dorsal osteophyte. (A) Visualization from the dorsomedial portal (viewed proximally from within the MTP joint). (B) A small-joint abrader is used to remove enough osteophyte to permit adequate MTP joint dorsiflexion. (C) Arthroscopic view of osteophyte removal with a motorized bur.

FIGURE 5.276 ● MTP joint plantar plate anatomy. The hypointense plantar plate is directly deep to the superior border of the flexor tendons. There is a normal undercutting of the plantar plate at the base of the proximal phalanx at the interface with hyaline articular cartilage. (A) Lateral view color illustration of the third MTP joint plantar plate. (B) Sagittal PD FSE image.

FIGURE 5.277 ● Coronal plane anatomy of the second MTP joint identifies the plantar plate, the collateral ligaments, the flexor tendons, and the extensor hood. (A) Coronal PD FSE image. (B) Coronal FS PD FSE image.

FIGURE 5.278 ● Distal plantar plate rupture associated with chronic second MTP joint synovitis. Sagittal T1-weighted image.

FIGURE 5.279 ● Third MTP joint instability after aggressive Morton's neuroma resection. There is secondary disruption to the plantar plate complex with associated medial subluxation of the flexor tendons. Sagittal T1-weighted image.

Toe deformities associated with progressive plantar plate degeneration and rupture include hammertoe deformity, flexion deformity of the proximal interphalangeal joint, dorsiflexion of the MTP joint, and neutral to hyperextension of the distal interphalangeal joint. A claw toe deformity (Fig. 5.280) is similar to hammertoe but includes a flexion deformity of the distal interphalangeal joint. Crossover toe may be seen withmedial crossover and deviation of the second toe and widening of the second webspace. Associated hallux valgus deformity, lateral collateral ligament rupture, and medial displacement of both the plantar plate flexor tendons may occur.

Fractures

Ankle Fractures

In an ankle fracture, there is complete cortical fracture of one or more of the bones that make up the ankle (the malleolus, the distal tibia, and the fibula) (Fig. 5.281). Fracture size varies based on the location (the malleoli, tibia, or fibula) and the pathomechanics of the injury. Fractures may occur as the result of a high-energy injury (e.g., motorcycle accident) or may be related to a low-energy mechanism, as is seen in medial malleolar injuries.

Fracture types and locations include:

FIGURE 5.280 ● A claw-toe deformity represents a hammertoe deformity (flexion deformity at the PIP joint with MP dorsiflexion and the DIP in neutral or hyperextension) with the addition of a hyperextension deformity at the MP joint. Both hammertoe and claw toe are examples of sagittal plane deformities. Lateral color illustration.

Medial malleolus (Fig. 5.282)
Lateral and posterior malleoli (Fig. 5.283)
A pilon fracture of the distal tibia/load-bearing surface with intra-articular extension
A Tillaux fracture of the lateral margin of the distal tibia to the distal articular surface (Fig. 5.284)
A juvenile Tillaux fracture of the distal tibial growth plate (Salter-Harris type III) (see Fig. 5.284)
A triplane fracture of the lateral distal tibial epiphysis with sagittal, axial, and coronal plane components (a juvenile Tillaux/Salter-Harris type III and Salter-Harris type II combination) (Fig. 5.285)
A Pott's fracture of the distal third of the fibula (Fig. 5.286)
Le Fort (Wagstaffe-Le Fort) fracture, an avulsion fracture of the anterior syndesmotic ligament from the medial aspect of the distal fibula¹⁰⁹
A Dupuytren fracture of the fibula, 2 to 7 cm proximal to the distal tibiofibular syndesmosis (Fig. 5.287)
A Maisonneuve fracture of the proximal fibula at the proximal to middle third of the diaphysis (Fig. 5.288)

Fracture morphology varies based on the location or type of fracture. Malleolar fractures are transverse to oblique to vertical (posterior malleolus), pilon fractures display comminution of the distal tibia and extension through the tibial plafond. Tillaux fractures have a horizontal physeal component with vertical extension to the articular surface of the distal tibia. A triplane fracture is vertical in the sagittal plane, horizontal in the axial plane, and oblique in the coronal plane. Fibular fractures are horizontal to oblique.

Classification, Etiology, Pathology, and Clinical Features

The classification of ankle fractures by the Lauge-Hansen system is based on the position of the foot and the direction of the injuring force at the time of loading.¹¹⁰ Four categories of fracture are recognized:¹¹¹

Supination-external rotation injuries
Supination-adduction injuries
Pronation-external rotation injuries
Pronation-abduction injuries

Another system classifies ankle fractures into three categories, which correspond to the Lauge-Hansen system as follows:

FIGURE 5.281 ● Distal tibial fracture with hypointense fracture line and extension to cortex. Adjacent edema is hyperintense on FS PD FSE image (B). (A) Sagittal T1-weighted image. (B) Sagittal FS PD FSE image.

FIGURE 5.282 ● Medial malleolus fracture on coronal color illustration (A) and coronal FS PD FSE image (B). Isolated malleolar involvement represents a unimalleolar fracture and occurs in eversion injuries. MR is used to evaluate associated ligamentous injury.

FIGURE 5.283 ● Posterior malleolus fracture on a lateral color illustration (A) and a sagittal FS PD FSE image (B). Posterior malleolus fractures are associated with trimalleolar fractures also involving the medial and lateral malleoli.

FIGURE 5.284 ● (A) Coronal color illustration of a Tillaux fracture with avulsion of the lateral margin of the distal tibia. The fracture extends from the distal tibial articular surface (plafond) obliquely and vertically to the lateral tibial cortex. (B) Coronal FS PD FSE image showing a juvenile Tillaux fracture, a Salter-Harris type III injury of the distal tibial physis. The lateral tibial physis is weaker than the medial side of the growth plate since the physis fuses from medial to lateral.

FIGURE 5.285 ● Triplane fracture with a vertical fracture component of the epiphysis, a horizontal component involving the physis, and a posterior coronal component of the metaphysis. The triplane fracture represents a combination of a juvenile Tillaux fracture and a Salter-Harris type II fracture. (A) Coronal color illustration. (B) Sagittal FS PD FSE image.

FIGURE 5.286 ● Coronal T1-weighted image of a large distal fibular fracture associated with a deltoid ligament sprain. The classic Pott's fracture is more proximal at the level of the interosseous membrane. The term “Pott's fracture” usually indicates a distal fibular fracture superior to the tibiofibular syndesmosis. Frequently there is an associated rupture of the deltoid ligament with lateral subluxation of the talus.

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Danis-Weber type A fractures are caused by Lauge-Hansen supination-adduction mechanisms.
Danis-Weber type B fractures are caused by Lauge-Hansen supination external rotation or pronation-abduction mechanisms.
Danis-Weber type C fractures are caused by Lauge-Hansen pronation-external rotation mechanisms.

Eversion fractures include the Pott, Maisonneuve, Dupuytren, and Tillaux types. Eccentric vertical loading causes asymmetric compression and torsional loading causes helical fracture patterns. Combined loading forces (medial, lateral, torsional, and axial) are most common.

The most common mechanism of injury, seen in 40% to 75% of all malleolar fractures, is the supination-external rotation mechanism, in which the injury progresses through four stages:

Stage 1: ATFL rupture
Stage 2: Oblique spiral fracture of the lateral malleolus from the plafond extending proximally
Stage 3: PITF tear and posterior lip or margin fracture of the tibia
Stage 4: Avulsion fracture of the medial malleolus or deltoid ligament rupture.

Supination-adduction injuries are considered to have two stages:

FIGURE 5.287 ● Dupuytren fracture involving fracture of the fibula 2 to 7 cm superior to the torn tibiofibular syndesmosis. There is associated disruption of the deltoid ligament. (A) Coronal view color illustration. (B, C) Coronal FS PD FSE images.

FIGURE 5.288 ● Maisonneuve eversion fracture involving the proximal fibula with associated disruption of the tibiofibular syndesmosis including the interosseous membrane. A fracture of the medial malleolus is also demonstrated. The more proximal location of the fibular fracture indicates a more extensive injury of the interosseous membrane.

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Stage 1: Lateral ligamentous failure and lateral malleolus avulsion (a transverse fracture at the level of the plafond)
Stage 2: A vertical, medially displaced fracture of the medial malleolus

The pronation-external rotation injury starts with fracture of the medial malleolus and progresses clockwise through injuries similar to those outlined for supination-external rotation fractures above. In supination-external rotation injuries, fracture of the fibula usually occurs within 2.5 cm of the ankle mortise. In pronation-external rotation injuries, the fracture is usually 8 to 9 cm proximal to the tip of the lateral malleolus (more than 2.5 cm from the ankle joint). Adduction forces usually result in horizontal transverse fractures of the lateral malleolus and vertical oblique fracture of the medial malleolus, whereas abduction forces produce a horizontal fracture of the medial malleolus and an oblique distal fibular fracture.⁷⁴^,¹¹¹

Pronation-abduction injuries (tibial pilon/pylon fractures) occur in three stages:

Stage 1: Transverse avulsion fracture of the medial malleolus or deltoid ligament rupture
Stage 2: Rupture of the anterior and posterior inferior tibiofibular syndesmotic ligaments
Stage 3: Horizontal, oblique fibular fracture above the joint (plafond)

Fractures of the distal tibia include the pilon (pylon) fracture, the Tillaux fracture, and the triplane fracture.

Tibial pilon (pylon) fractures usually occur secondary to vertical loading. There is cancellous bone compression above the tibial plafond¹¹² and a stable comminuted fracture of the distal tibia, which may be associated with a fracture of the fibula. The pilon fracture extends into the tibiotalar joint, and incongruity of the joint surfaces may result in the late complication of posttraumatic arthritis. Pilon fractures are subdivided into three types:

Type I: Undisplaced fissure fracture
Type II: Displaced fracture and articular incongruity
Type III: A compression fracture and displacement of weight-bearing segments (crushing subchondral cancellous bone)

In Tillaux fractures there is a fracture line from the distal tibial articular surface proximally and toward the lateral cortex. Triplane fractures are vertical, horizontal, and oblique, and Maisonneuve fractures are spiral fractures of the proximal fibula and an unstable ankle injury.

Clinically, patients present with localized pain and tenderness over the malleoli, distal tibia, or fibula. Deformity usually indicates dislocation. Swelling and ecchymosis usually accompany the injury. The fibular compression test is positive.

MR Appearance

MR imaging complements conventional radiographic and CT evaluation of these injuries, allowing more specific demonstration of trabecular and soft-tissue ligamentous lesions. For example, conventional radiographs rely on the positive predictive value of an ankle joint effusion to suggest the presence of an occult fracture (effusions greater than 13 mm have a positive predictive value of 82%). With MR imaging, however, the fracture can be visualized directly.⁷⁶

Key findings include:

Malleolar fractures: fracture line, diffuse marrow edema to localized edema adjacent to the fracture site
Pilon fractures: separate comminuted distal tibial fragment, fracture extension to the tibial plafond, may or may not be displaced
Tillaux fractures: vertical fracture line perpendicular to the epiphysis and a thick lateral physis with lateral fracture extension
Triplanar fractures: separate fractures oriented anteroposteriorly in the axial plane, proximal to distal in the coronal plane, and oblique in the sagittal plane
Fibular fractures: transverse to oblique fracture line
Distal tibial fractures: localized edema adjacent to the fracture site, variable proximal extension of signal, interruption of the distal chondral surface with fluid signal

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Treatment

Ankle fractures are associated with degenerative changes in 85% of cases if they are not anatomically reduced. Many proceed to arthritis, depending on the severity of the injury. A conservative approach using closed reduction may be successful, but if not, ORIF is necessary.

Epiphyseal Fractures

Normal MR Appearance

The normal MR pattern of distal tibial and fibular epiphyseal ossification and physeal closure has been described by Chung and Jaramillo.¹¹³ It is important to understand these normal patterns in order to appreciate physeal and epiphyseal injuries. For example, prior to closure the normal tibial physis shows an anteromedial undulation (Kump hump), which may be mistaken for premature physeal closure. In addition, since the cartilaginous epiphysis has a lower signal intensity than the physis on T2-weighted images, they are particularly useful for differentiating the epiphysis from the physeal articular cartilage before complete ossification of the epiphysis. The ossific nucleus is most conspicuous on T2*-weighted images and is seen as a low-signal-intensity area surrounded by a relatively hyperintense articular cartilage. The physis is best visualized on GRE and FS PD FSE images, especially when ossification of the epiphysis is almost complete. Distal epiphyseal ossification and physeal closure begin anteromedially and occur earlier than in the fibula.

FIGURE 5.289 ● Salter-Harris type I fracture through the physis. (A) Coronal section color illustration. (B) Sagittal FS PD FSE image.

Specific Patterns of Epiphyseal Injuries

The Salter-Harris classification describes injuries to the physis (growth plate) and classifies them into five types:

Type I: The most common epiphyseal injury is a lateral malleolus Salter-Harris type I fracture (Fig. 5.289), which is through the growth plate.¹¹² A Salter-Harris type I fracture may be complicated by the interposition of periosteum in the growth plate (Fig. 5.290).
Type II: Salter-Harris type II fractures (Fig. 5.291) extend through the physis and metaphysis, and displaced type II fractures of the tibial epiphysis are usually associated with a greenstick fracture of the fibula, which occurs with eversion and external rotation injuries.
Type III: Salter-Harris type III fractures (Fig. 5.292) extend through the physis and into the epiphysis.
Type IV: Salter-Harris type IV fractures (Fig. 5.293) involve the physis, metaphysis, and epiphysis.
Type V: In Salter-Harris type V injuries, there is compression across the physis.

FIGURE 5.290 ● Enfolded or trapped periosteum in the lateral aspect of a distal tibial Salter-Harris type I physeal fracture. The periosteum typically tears on the tension or distraction side of the fracture site. Entrapped periosteum may result in an irreducible fracture.

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Fractures of the Calcaneus

Fractures of the calcaneus are the most common (60%) of tarsal bone fractures and represent 2% of all fractures. They are bilateral in 5% to 9% of cases and are usually associated with falls from a height of 3 to 50 feet. They are seen most often in males (a 5:1 male-to-female ratio) between the ages of 30 and 50 years. Associated thoracic/lumbar (T12-L2) compression injuries are seen in 10% of cases and lower extremity injuries in 25% to 70%.

In evaluating calcaneal fractures, it is important to understand the normal anatomy. The middle third of the calcaneus supports the posterior facet, and the posterior facet is separated from the anterior and middle facets by the tarsal canal and the sinus tarsi. The cortical bone supporting the posterior facet is the thalamic bone and the thick cortex of the anterior lateral tarsal canal is the angle of Gissane. The calcaneocuboid joint is located between the anterior calcaneus and the posterior surface of the cuboid.

Calcaneal fractures are divided into intra-articular and extra-articular types according to the involvement or extension of the fracture into the subtalar joint.¹¹¹^,¹¹⁴^,¹¹⁵ Extra-articular fractures that do not involve the subtalar joint include fractures of the tuberosity, the anterior process, the sustentaculum tali, or the body and represent 15% to 25% of fractures.¹¹¹ In intra-articular fractures, which are more common (75% in adults and 25% in children), there is a vertical fracture line from Gissane's crucial angle (the anterior lateral aspect of the tarsal canal) to the calcaneal plantar surface. Fracture involvement varies from localized tuberosity, sustentaculum, process, avulsion, and depression to comminution. Morphologically, intra-articular fractures are Y-shaped on a lateral perspective.

Etiology, Pathology, and Clinical Features

The principal mechanism of injury is axial loading of the hindfoot and a downward talar force, as occurs in falls from a height (75% of cases). The primary fracture line shears the calcaneus obliquely (the anteromedial and posterolateral portions) and the secondary fracture line divides the calcaneus transversely. The posterior facet is forced into the body and rotated anteriorly and the lateral wall is blown out. Although injury is most commonly associated with direct trauma, stress or overuse in athletes has been known to be a causative factor.

Clinically patients present with ankle pain, swelling, and tenderness and ecchymosis of the heel and arch. They cannot walk.

Classification

There are several classification schemes for these fractures. Intra-articular fractures are classified by Essex-Lopresti into two categories based on the secondary fracture pattern seen in association with the primary or oblique fracture segment (Fig. 5.294):¹¹¹

Essex-Lopresti type A or tongue-type fractures: The tongue-type fracture is transverse and extends posterior to the posterior facets and the dorsal calcaneal tuberosity.
Essex-Lopresti type B or joint depression-type fractures: The depression-type fracture has a secondary fracture line that runs from the body of the calcaneus directly posterior to the fractured articular surface posterior facet.

In the Rowe system fractures are classified into five types:¹¹⁶

Type I: Fractures of the tuberosity, the sustentaculum tali, and the anterior process; 21% of cases
Type II: Beak fractures of the calcaneus and avulsion fractures of the Achilles tendon insertion; 3.8% of cases
Type III: Oblique fractures without subtalar involvement; 19.5% of cases
Type IV: Involvement of the subtalar joint; 24.7% of cases
Type V: Central depression with or without comminution; 31% of cases

FIGURE 5.291 ● Salter-Harris type II fracture through the phy-sis and metaphysis of the distal tibia. There is no epiphyseal extension. (A) Lateral color illustration. (B) Sagittal T1-weighted image. (C) Axial FS PD FSE image.

FIGURE 5.292 ● Salter-Harris type III fracture extending through the physis and epiphysis. (A) Coronal section color illustration. (B) Coronal T1-weighted FSE image.

FIGURE 5.293 ● Salter-Harris type IV with fracture extension through the physis, metaphysis, and epiphysis. Coronal section color illustration.

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The Sanders classification is based on number of fragments in the posterior facet (the sustentaculum and the medial, central, and lateral columns) as seen on coronal CT images.

MR Appearance

Both MR imaging and CT are useful in demonstrating joint alignment, fragment displacement, and involvement of the subtalar joint. MR imaging is sensitive to the hyperemia, morphology, and location of calcaneal stress fractures. STIR and FS PD FSE sequences are used to identify areas of hyperintensity. T1-weighted images may be unremarkable.

Findings vary depending on the type of fracture:

For anterior process (Rowe type I) fractures (Fig. 5.295), key characteristics include:
- Avulsion at the origin of the bifurcate ligament, edema, or chronic hypointense sclerosis
- Edema on lateral sagittal images
- Compression fracture with or without avulsion of the navicular tuberosity, edema, and extension to the calcaneocuboid joint
- Involvement of the extensor digitorum brevis muscle and calcaneocuboid ligament
For fractures of the sustentaculum tali (Rowe type I), findings include:
- Possible medial displacement
- Edema, fluid, or hemorrhage on axial and coronal images

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For beak and avulsion (Rowe type II) fractures, findings are:
- Edema in the beak or avulsed tuberosity
- Achilles tendon attached to superior tuberosity
- A smaller beak fracture and a larger avulsion secondary to sudden contraction of the Achilles tendon
- Fracture line posterior to the superior calcaneus
Calcaneal body (Rowe type III) fractures are evaluated on sagittal images to exclude posterior facet involvement and demonstrate:
- No subtalar joint communication
- Fracture line posterior to the posterior facet or comminution
Intra-articular fractures are evaluated on coronal images to display widening of the calcaneus and sagittal images to separate a central depression from a tongue-like fracture. Characteristic findings include:
- Edema in the joint
- Depression or tongue-type fracture
- Chondral extension
- Free fragments, displayed as hypointense bodies outlined by hyperintense fluid on FS PD FSE images
Stress fractures (Fig. 5.296) are characterized by:
- Linear pattern of signal intensity in the posterior calcaneus perpendicular to the long axis
- More diffuse posterior calcaneus trabecular microfracture edema

FIGURE 5.294 ● Essex-Lopresti calcaneal fracture with central depression and subtalar extension. Up to 75% of calcaneal fractures extend into the subtalar joint. Subtalar fracture types are further subdivided into either joint-depression or tongue-type fractures. In the Rowe classification there is subtalar joint involvement in stage IV and stage V (central depression) injuries. (A) Lateral color illustration. (B) Sagittal PD FSE image. (C) Sagittal FS PD FSE image.

FIGURE 5.295 ● (A) Fracture of the anterior process of the calcaneus on a lateral perspective color illustration. (B) Calcaneal origin of the bifurcate ligament with an intact anterior process. Sagittal T1-weighted image. (C) Fractured anterior process with extensive reactive anterolateral calcaneal edema. Sagittal FS PD FSE image. (D) Anterior process fracture with osseous avulsion injury of the calcaneonavicular and calcaneocuboid parts of the bifurcate ligament. Inversion and plantarflexion injuries may result in an avulsion injury at the origin of the bifurcate ligament. Associated distal avulsion is less common. Sagittal FS PD FSE image.

FIGURE 5.296 ● Posterior calcaneus stress fractures with hypointense fracture segments and adjacent hyperintense marrow edema. (A) Sagittal T1-weighted image. (B) Sagittal FS PD FSE image. A common location for a calcaneal stress fracture is the upper posterior margin, anterior to the apophyseal plate, perpendicular to the trabecular pattern of the calcaneus.

Treatment

Prognosis is better for extra-articular fractures that do not involve the subtalar joint.¹¹⁴ Sequelae include a widened heel (blown-out lateral wall) and/or a shortened heel (anterior process split) as well as limitation of ankle motion (a flattened calcaneus and talar dorsiflexion). Conservative approaches are often sufficient for nondisplaced or minimally displaced intra-articular fractures and include early range of motion without reduction and closed reduction with or without fixation. Surgery is required for displaced intra-articular fractures and includes open reduction and internal fixation and arthrodesis for comminuted fractures. Complications include the compartment syndrome.

Fractures of the Talus

The talus is the second most commonly fractured bone of the foot, and talar fractures account for 0.5% of all fractures.

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The talus may be injured at the neck, the body, the head, and the posterior and lateral processes. Since the ankle mortise protects the talus from direct injury, talar fractures usually result from transmitted forces.¹¹¹ Neck fractures are the most common (50% of cases) and usually occur in males (male-to-female ratio is 3:1) between 30 and 38 years of age. Fractures of the lateral process of the talus are a recently recognized complication of snowboarding, associated with dorsiflexion and inversion injuries.¹¹⁷ Fractures may be nondisplaced, displaced, or open. Open fractures account for 15% of cases. Associated injuries include calcaneus, medial malleolus, and spine fractures.

Etiology, Pathology, and Clinical Features

Morphologic features vary depending on the location of the fracture. Fractures of the head of the talus may be avulsion, peripheral, or compression injuries. Lateral process fractures are usually comminuted or are noncomminuted with a large fragment. Posterior process fractures as vertical fractures at the synchondrosis may involve the os trigonum. Talar neck fractures are vertical and talar body fractures may be coronal, sagittal, or horizontal.

FIGURE 5.297 ● Snowboarder's or lateral process fracture of the talus. The mechanism of injury is related to eversion of an axial-loaded and dorsiflexed ankle. A lateral process fracture may be further classified as a simple comminuted fracture or as a chip fracture. (A) Superior view color illustration. (B) Coronal FSE PD FSE image. (C) Sagittal FS PD FSE image.

Talar fractures are usually associated with high-energy trauma such as occurs in falls and motor vehicle accidents. The mechanism of injury in talar head fractures is forcible dorsiflexion of the plantarflexed foot, causing axial loading and shearing force. Lateral process injuries (Fig. 5.297) are most often caused by inversion and dorsiflexion, causing compressive force. This is seen most often in motor-vehicle accidents or in snowboarders, in whom the combination of flexible boots and increased subtalar motion contributes to the injury. Posterior process fractures are caused by forced plantarflexion and compression. Talar neck fractures (Fig. 5.298) are caused by forced dorsiflexion resulting in contact between the anterior lip of the tibia and the dorsal talar neck sulcus. Talar body fractures (Fig. 5.299) are caused by axial compression and a plantarflexed talus.

FIGURE 5.298 ● Talar neck fracture on lateral color illustration (A) and sagittal T1-weighted image (B). The talar fracture line (straight arrow) and calcaneal trabecular trauma (curved arrow) are hypointense on the T1-weighted sequence. Talar neck fractures may be associated with medial malleolus, sustentaculum tali, or metatarsal head fractures.

FIGURE 5.299 ● Talar body fracture on a lateral color illustration (A) and a coronal FS PD FSE image (B). The mechanism of injury is axial loading or a shear force. Associated injuries include fractures of the calcaneus, tibia, or talar neck.

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Pathologic features also depend on the location of the fracture. Fractures of the head of the talus most commonly involve the periphery of the head (medially), subtalar dislocation, and comminution versus compression. Lateral process injuries are more likely to be comminuted fractures with minimal displacement or a larger fragment with or without displacement. Posterior process fractures are recognized by irregular separation from the talus. In talar neck fractures the head and neck are separated from the talar body and there may or may not be failure of the interosseous talocalcaneal ligament. There is often disruption of the vascular supply and talar dislocation from the mortise. Talar body injuries are simple comminuted fractures without dislocations, and less comminuted fractures are associated with dislocations of the ankle and subtalar joint.

Clinically, patients present with ankle and foot pain, swelling, and ecchymosis.

Classification

Hawkins has proposed a four-type classification system for talar neck injuries:¹¹⁸^,¹¹⁹

Type I: No talar displacement
Type II: Subluxation and/or dislocation of the talus with respect to the subtalar joint (dislocation of the posterior facet). Type II injuries are the most common type.
Type III: Displacement of the talar body (ankle and subtalar dislocation). Type III injuries are also common.
Type IV: A rare injury in which there is additional dislocation of the talonavicular joint

MR Appearance

AVN is a known complication of talar neck fractures, and with MR imaging it is possible to assess adjacent bone marrow for signs of this process and to demonstrate nondisplaced fracture morphology.¹¹⁷ The articular cartilage surfaces also can be directly evaluated on MR studies. MR imaging has also been used to identify talar insufficiency fractures.¹²⁰ In addition to demonstrating talar stress fractures in the classic location (paralleling the talonavicular articulation at the level of the talar neck), MR imaging depicts other fracture locations. These fractures involve vertically and horizontally oriented insufficiency fractures of the medial aspect of the posteroinferior talus, and transverse or horizontal fractures of the talar body parallel to the tibiotalar joint.

Characteristic MR findings depend on the location of the fracture:

Fractures of the head of the talus show:
- Avulsion, usually medially
- Intra-articular displacement or dislocation of the talonavicular joint
- Single versus multiple hypointense fracture lines
- Associated diffuse hypointensity on T1- and PD-weighted images
- Hyperintense talar head on FS PD FSE images
- Edema, which may obscure the fracture line
- Chondral extension to the talonavicular joint
Lateral process fractures show:
- Edema in comminuted fracture on coronal and sagittal images
- Oblique/vertical single fracture and intra-articular displacement
- Increased subtalar fluid and chondral interruption
Posterior process fractures, which may be difficult to differentiate from a painful os trigonum on TI-weighted images, display:
- Irregular separation on sagittal images, which represents the talus and a fragment
- A complete vertical fluid gap between the talus and the posterior process
- Adjacent marrow edema
- Soft-tissue fluid and edema
- Fluid in the FHL tendon sheath
Talar neck fractures display:
- A posterior to transverse sulcus
- A vertical nondisplaced segment (type I)
- Subluxation or dislocation of the talus in the subtalar joint (type II)
- Displacement of the talar body (type III)
- Fluid and hemorrhage with separation between the head and the neck and body
- Adjacent marrow fragment
- Extrusion of the talus from the subtalar joint (Hawkins type III injury) seen on sagittal plane images
Talar body injuries show:
- Comminuted fracture
- Primary fracture in any of the three orthogonal planes
- Edema across the fracture plane (coronal, sagittal, or axial)
- Soft-tissue edema and hemorrhage.

Treatment

Treatment outcomes are related to fracture type. Malunion is common in comminuted fractures and arthritis develops in 40% to 90% of cases. The most serious complication is AVN. Conservative treatment is a short cast, but ORIF is needed for displaced fractures of the talar body or lateral process and for type III talar neck fractures.

Navicular Fractures

Navicular fractures are characterized by ligamentous capsular avulsions and fractures of the tuberosity and body¹¹¹ with

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a fracture line perpendicular to the long axis of the navicular. They represent 62% of midfoot fractures and 37% of all foot fractures.

Four types have been recognized:

Avulsion fracture s: Avulsion fractures usually affect the dorsal lip at the insertion of the dorsal tibionavicular ligament (the tibialis posterior insertion). Cortical avulsion fractures involve part of the dorsal cortex, and there may be an elongated cortical fragment. They represent 47% of navicular fractures.
Tuberosity fractures: Tuberosity fractures vary in size with the size of the tuberosity but are usually minimally displaced. The fracture edges may be sharp and/or jagged. They represent 24% of navicular fractures.
Body fractures: Body fractures are most commonly horizontal and nondisplaced, and may be associated with crush injuries. They account for 29% of navicular fractures.
Stress fractures: Stress fractures usually affect the central third of the navicular (in the sagittal plane), which is avascular and therefore at risk for stress fracture and nonunion. They also involve the anteroposterior or short axis length of the navicular. They may be complete or incomplete, but most stress fractures are characterized as partial (96%) and linear. In nonunion, persistence of a fracture gap can be seen. Medullary cysts and cortical notching may persist even after fracture healing.

Etiology, Pathology, and Clinical Features

The usual mechanism of injury in avulsion fractures is plantar displacement of the foot and inversion or eversion. These mechanisms cause the taut dorsal tibionavicular ligament to avulse at the dorsal cortex insertion. In tuberosity fractures the usual mechanism is avulsion of the tibialis posterior caused by forceful eversion and contraction. Body fractures may be caused by direct or indirect mechanisms such as a fall with the foot in plantarflexion or plantarflexion and abduction of the meta-tarsal joint. Body fractures are associated with falls from a great height or motor vehicle accidents. Stress fractures are associated with running and excessive pronation and are often seen in sprinters, hurdlers, and jumpers.

Pathologic changes vary depending on the type of fracture. In avulsion injuries the fragment may contain a segment of articular cartilage. In tuberosity fractures, which are usually nondisplaced, there may be associated injury of the calcaneocuboid joint. In body fractures, which are also usually nondisplaced, the navicular may be compressed between the talar head and the cuneiform. Stress fractures may be complete, with or without dislocation, but 96% are incomplete.

Patients usually present with midfoot pain. In avulsion injuries there is tenderness and edema at the fracture site. In tuberosity fractures the tenderness may be located at the medial navicular. In body fractures there is pain at the mid-medial arch and local swelling and tenderness, and in stress fractures there is poorly localized pain at the dorsum and the medial longitudinal arch with minimal swelling.

Classification

Body fractures have been classified into three types:

Type 1: Transverse with a dorsal fragment (affecting over 50% of the body)
Type 2: A transverse fracture from dorsolateral to plantar medial across the body. The major fragment is dorsomedial; the smaller comminuted fracture is plantar lateral.
Type 3: Central or lateral comminution. The major fragment is medial.

MR Appearance

Sagittal plane MR images are particularly useful for identification of fractures involving one or both cortices. Axial images, however, may be required to display fracture lines that are parallel with the sagittal plane. When present, diffuse edema demonstrates hyperintensity on STIR or FS PD FSE sequences.

Although AVN is not common, MR imaging is also helpful in demonstrating subchondral sclerosis prior to the appearance of increased radiographic density. A navicular stress fracture should be differentiated from a symptomatic accessory tarsal navicular bone.¹²¹ In the latter, the normal variant of the medially located accessory tarsal navicular bone may develop a bone marrow edema pattern on FS PD-weighted images in symptomatic patients with focal pain in the adjacent navicular tuberosity. This hyperemia or edema pattern is associated with chronic stress or osteonecrosis and can be seen adjacent to the synchondrosis with a diffuse nonlinear hyperintensity. The pattern of bone marrow edema just described is not seen in asymptomatic patients. Cuneiform fractures are less common and are associated with direct trauma.

Typical MR findings vary depending on the type of fracture:

Avulsion fractures are characterized by:
- Elongated dorsal cortical fragment
- Adjacent dorsal soft-tissue and navicular edema
- Cortical-based fragment that remains hypointense on FS PD FSE images
Tuberosity fractures (Fig. 5.300) show:
- Subchondral edema across the fracture
- Irregular edges at the fracture site
- Fluid and/or hemorrhage at the fracture site
- Fluid involving the PTT
Body fractures display:
- Vertical or horizontal fracture line and edema
- Subchondral edema
- Hyperintensity on FS PD FSE images: epicentered in coronal plane, from dorsolateral to plantar medial within navicular or comminution in sagittal plane
Stress fractures (Fig. 5.301) are characterized by:
- Fracture line on direct coronal or axial images
- Marrow edema, sometimes with a visualized fracture on sagittal images

FIGURE 5.300 ● Navicular tuberosity fracture on axial T1-weighted (A) and FS PD FSE (B) images. A navicular tuberosity fracture involving the tibialis posterior tendon insertion may require operative repair if the proximal displacement is 1 cm or greater.

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Treatment

The course and treatment of navicular fractures also vary depending on the type of fracture. In displaced avulsion fractures closed reduction is usually unstable. Approximately 50% of tuberosity fractures are associated with calcaneocuboid joint injury and persistent pain, although edema decreases after 72 hours. Fractures of the body of the navicular remain nondisplaced and heal without sequelae. Stress fractures, which are characterized by increased symptoms with activity, are underdiagnosed. Failure to treat leads to delayed healing or nonunion.

Most patients are placed in a non—weight-bearing short-leg cast. Unstable fractures may require surgery. Avulsion fractures are treated with ORIF if more than 20% of the articular cartilage is involved. Tuberosity fractures are treated with reattachment for displacement and resection. Displaced body fractures may require ORIF or closed reduction. Displaced stress fractures, nonunion, comminution, and cyst formation require grafting, excision, or ORIF. Nonunion and the development of degenerative arthritis are the main complications of navicular fractures.

Tarsometatarsal or Lisfranc Fractures

Pearls and Pitfalls

Tarsometatarsal or Lisfranc Fractures

Lisfranc fractures may be homolateral or divergent tarsometatarsal fracture dislocations.
Lisfranc's ligament extends from the medial cuneiform to the medial aspect of the second metatarsal base.
Axial MR images are used to evaluate Lisfranc's ligament and to assess the lateral effect of the first metatarsal base relative to the medial cuneiform and the medial second metatarsal base relative to the intermediate cuneiform in the homolateral type of injury.
Fractures are associated with sports-related injuries in athletes and Charcot arthropathy in diabetic patients.
Direct coronal images are used to appreciate dorsal/plantar displacement.

A Lisfranc tarsometatarsal fracture-dislocation usually occurs at the midfoot. It is a relatively uncommon injury, occurring in only 1 in 55,000 people per year and representing 0.2% of all fractures and less than 1% of dislocations. The majority, 67%, are high-energy or crush injuries, usually related to motor vehicle accidents. Lisfranc fractures are also seen in conjunction with Charcot arthropathy in an older diabetic population. Sports-related injuries occur in a younger population (predominantly college-aged males) who participate in basketball, running, gymnastics, or football. Motorcycle accidents are also more common in this age group.

These injuries can be subtle, and an understanding of the normal anatomic relationships is essential in accurate evaluation. Relevant anatomic features include the following:

The base of the second metatarsal, a frequent site of injury, is recessed.
The metatarsals are bound by the transverse dorsal and the stronger plantar ligaments.
There is no ligament that directly attaches the first metatarsal base to the base of the lesser (second to fifth) metatarsals.
The dorsal medial ligament originates from the medial cuneiform and attaches to the first metatarsal.

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Lisfranc's ligament originates from the medial cuneiform and attaches to the second metatarsal base (the medial aspect).

FIGURE 5.301 ● Navicular stress fracture involving the central to medial aspect of the dorsum of the navicular. Edema is often prominent in the sagittal plane, whereas fracture morphology is visualized in the axial plane. Delayed union and nonunion are potential risks secondary to the relative avascularity and increased shear forces that occur in this region. (A) Lateral color graphic. (B) Sagittal FS PD FSE image. (C) Axial FS PD FSE image.

Etiology, Pathology, and Clinical Features

Fractures occur most frequently at the bases of the second and third metatarsals and may involve dislocation of the metatarsocuneiform joint and lateral shift of the second to fifth metatarsals. In homolateral fractures the first to fifth metatarsals are dislocated laterally (Fig. 5.302), and in divergent fractures the first metatarsal is dislocated medially and the second to fifth metatarsals laterally (Fig. 5.303). The pathognomonic flock fracture involves the proximal medial second metatarsal.

The mechanism of injury is usually forced plantarflexion of the forefoot on the rearfoot; Lisfranc fractures are most commonly caused by motor vehicle and industrial injuries. Other causes, such as falling while stepping off a curb, have also been seen. Plantarflexion and longitudinal force, as occurs in an equestrian injury caused by a fall from a horse with the foot caught in the stirrup, may also cause these fractures; in fact, this was the original injury described by Lisfranc. Direct trauma, a blow, or a crush injury (as occurs when the foot is run over by a motor vehicle) may also cause a Lisfranc fracture.

Pathologic examination reveals osseous avulsion or disruption of Lisfranc's ligament. In the homolateral type of Lisfranc injury (see Fig. 5.302), there is lateral displacement of all rays. In divergent injuries (see Fig. 5.303), the first ray is displaced medially and the second to fifth rays are displaced laterally. The intermetatarsal space between the first and second metatarsals is widened, and there is metatarsal and cuneiform malalignment. There may be associated fractures (cortical, subchondral, or trabecular), hemorrhagic elements, soft-tissue edema, and chondrolysis. Ligament injuries range from microtears to complete collagen fiber disruption. Arterial spasms may affect the branch between the dorsalis pedis and the plantar arterial arch.

Patients present with pain at the tarsometatarsal joint and midfoot and cannot bear weight on the affected foot. There is popping or snapping, midfoot edema, shortening of the foot, forefoot abduction or adduction, and plantar ecchymosis. Palpation reveals dorsal or plantar displacement of the second metatarsal. Dislocation may be associated with an excessive range of motion or hypermobility.

Classification

One of the classification schemes for Lisfranc fractures divides them into three types:

Type A: Total incongruity and lateral or dorsoplantar displacement of the first to fifth metatarsals.
Type B: Partial incongruity with medial dislocation of the first metatarsal and lateral dislocation of the second to fifth metatarsals
Type C: Divergent, with partial or total displacement of the first metatarsal medially and the lesser metatarsals laterally

FIGURE 5.302 ● Homolateral Lisfranc fracture-dislocation with lateral dislocation of the first to fifth metatarsals. Both the homolateral and divergent types of injuries are associated with a fracture of the base of the second metatarsal. Superior view color graphic.

Imaging Findings and MR Appearance

The best diagnostic clue is lateral offset of the lateral aspect of the first metatarsal relative to the medial cuneiform and of the medial aspect of the second metatarsal relative to the medial aspect of the intermediate cuneiform. Lisfranc fractures are best evaluated by standard radiographs or coronal reformatted 1.5-mm CT scans. The medial border of the middle or intermediate cuneiform and the lateral border of the medial cuneiform should be in line with or directly congruent with their respective metatarsals. MR imaging is sensitive to nondisplaced fractures with marrow edema and soft-tissue and capsular structure changes and is useful when radiographic

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or CT examination results are negative. MR imaging has proved to be more sensitive than CT in identifying the extent of posttraumatic marrow hyperemia and the number of bones of the tarsus affected, but thin-section (1.5 mm) CT scans in both the coronal and axial planes are more accurate in identifying small osseous corner or chip fragments in the cuneiforms and base of the metatarsals.

FIGURE 5.303 ● Divergent Lisfranc fracture-dislocation with medial dislocation of the first metatarsal and lateral dislocation of the second to fifth metatarsals. Superior view color graphic.

MR findings include the following:⁷⁵

Axial images show lateral displacement of the first to fifth metatarsals in homolateral fractures (Fig. 5.304), medial dislocation of the first metatarsal and lateral dislocation of the second through fifth metatarsals in divergent fractures, and widening of the first-second metatarsal interspace.
Fractures may be seen at the base of the second or third metatarsal, the medial/intermediate cuneiform, or the navicular.
There may be lateral column shortening caused by an impaction injury of the cuboid with an abduction deformity of the forefoot.
Direct coronal images show disruption of the dorsal arch (the second metatarsal is normally found at the apex of the arch).
Discontinuity of Lisfranc's ligament may be seen at the medial cuneiform to the medial proximal second metatarsal.
Edema is seen at the Lisfranc ligament avulsion fracture, at the proximal medial aspect of the second metatarsal.
Subchondral marrow edema of tarsometatarsal joints indicates a chip or trabecular fracture (Fig. 5.305).
There may be fraying or tearing of the oblique (Lisfranc) ligament with or without synovitis (Fig. 5.306).
Cuboid marrow hyperintensity with trabecular impaction injury (Fig. 5.307)
Diabetes-related Lisfranc injuries are chronic and associated with midfoot neuropathic changes, as seen in Charcot arthropathy (Fig. 5.308). On FS PD FSE images superimposed neuropathic hyperintensity can be seen throughout the midfoot and the Lisfranc fracture-dislocation.
On direct coronal plane FS PD FSE images, intramedullary hyperintensity in the displaced metatarsals is seen in cross-section.
Associated arterial injury is shown on coronal images.

Treatment

Almost 20% of Lisfranc fractures are missed on initial evaluation. Delayed or failed treatment may lead to chronic instability, compartment syndrome, or posttraumatic arthritis, and the long-term morbidity is high. Anatomic reduction improves the outcome.

Conservative treatment may be appropriate for injuries that are anatomically stable and includes the RICE protocol (rest, ice, compression, and elevation), non—weight-bearing, a cast boot (for stretching or partial tears of the capsule and ligament), physical therapy, and orthotics. Surgery is necessary for fracture-dislocations and instability. Nondisplaced unstable injuries are treated with percutaneous wire fixation. Displaced or angled fractures require ORIF with cannulated screws (Fig. 5.309).

Metatarsal Fractures

FIGURE 5.304 ● Ruptured Lisfranc ligament. Lisfranc's ligament is normally composed of a weaker dorsal component and a stronger plantar component. (A) Axial T1-weighted image. (B) Coronal T1-weighted image.

Metatarsal fractures are among the most common fractures in the foot. The injury may be acute, caused by trauma, or due to stress or insufficiency fracture. Stress fractures are most common in young runners, dancers, and marchers. Females, because of thinner cortices, are more susceptible to metatarsal fractures, except in the military population. The level of fitness is the most important determinant in stress fractures.

The metatarsal bones have a base, diaphysis, neck, and head, and injury may occur at any of these locations. The base of the metatarsal is broad and cancellous with strong plantar ligaments. The diaphysis is the origin of intrinsic foot muscles, the neck has strong intermetatarsal ligaments, and the metatarsal heads are responsible for weight-bearing. The apophysis and the os vesalianum may mimic a fracture (Fig. 5.310).

Etiology, Pathology, and Clinical Features

The size and morphologic features of metatarsal fractures vary depending on the kind of fracture. Stress fractures usually occur in the proximal third of the bone, but fractures of the head, neck, shaft, base, or central metatarsals may also occur. Stress fractures are perpendicular to long axis (transverse) and may or may not show angulation and periosteal reaction or exuberant callus. Fractures of the metatarsal head may be seen with or without angulation, rotation, or shortening in impaction injuries. Neck fractures may show plantar and lateral displacement and multisegment involvement. Midshaft fractures may show oblique, transverse, spiral, or comminuted patterns. A fracture of the base of the metatarsal may be associated with a Lisfranc fracture-dislocation, but there is usually minimal displacement and alignment is maintained. A fracture of the first metatarsal may be either direct, with or without comminution, or indirect, with or without avulsion. When the central metatarsals (second through fourth) are affected, displacement is in the same direction, fractures are usually transverse, and the parallel relationship of fractured segments is maintained. Fractures of the fifth metatarsal are avulsion or transverse Jones fractures. Gross involvement of the fifth metatarsal is most common, followed by the third, second, first, and fourth.

Causes of metatarsal fractures include direct force (such as crushing, blunt trauma, or penetrating injuries), indirect force (such as occurs with axial loading), and stress (such as occurs with overuse associated with activities like running or dancing or with decreased bone density, as occurs in amenorrhea). Causes of specific types of injury include:

Fractures of the head are usually caused by direct trauma.
Neck fractures are caused by shearing force or direct trauma.

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Midshaft fractures are caused by direct, blunt, or torsional forces.
Fractures of the base are caused by direct trauma, frequently sustained in motor vehicle accidents or a fall from a height.
First metatarsal fractures are often caused by crush or twisting injuries.
Fractures of the central metatarsals are caused by direct impact or crushing.
Fifth metatarsal fractures are caused by plantarflexion and inversion or direct impact.

FIGURE 5.305 ● Homolateral type Lisfranc fracture-dislocation with lateral displacement (large black arrows) shown in metatarsal bases on direct axial CT scan (A), T1-weighted axial image (B), axial STIR image (C), and transverse (superior view) color illustration (D). Although the fracture fragment (open arrow) can be identified between the base of the first and second metatarsals on the CT scan, MR imaging is more sensitive to the extent of traumatic marrow edema (small closed arrows) involving the cuneiforms and metatarsal bases. Associated fractures in a Lisfranc tarsometatarsal dislocation occur at the base of the second or third metatarsals, medial or intermediate cuneiforms, or the navicular bone.

FIGURE 5.306 ● Complete tear of the obliquely oriented Lisfranc's ligament. Lisfranc's ligament normally connects the lateral aspect of the medial cuneiform to the medial aspect of the second metatarsal base. Complex ligament tears are associated with displacement of the second metatarsal and medial cuneiform on weight-bearing. Axial FS PD FSE image.

FIGURE 5.307 ● Cuboid fractures may be associated with Lisfranc injuries. Partial tears of Lisfranc's ligament usually involve the weaker dorsal band. Diastasis of the bases of the first and second metatarsal should always be assessed on MR relative to the medial and intermediate cuneiforms. Axial FS PD FSE image.

FIGURE 5.308 ● Lisfranc fracture-dislocation as a complication of diabetes. Associated hyperintense neuropathic changes are present in the midfoot. Axial FS PD FSE image.

Patients present with pain at the fracture site. In stress fractures (most commonly of the diaphysis or neck) there is focal tenderness and pain with activity. First metatarsal fractures cause altered gait.

Classification

The Stewart classification divides fifth metatarsal base fractures into five types (Fig. 5.311):¹²²

Type I: Jones fracture (Fig. 5.312)
Type II: Intra-articular fracture
Type III: Avulsion fracture (Fig. 5.313)
Type IV: Comminuted intra-articular fracture
Type V: Involvement of the apophysis

MR Appearance

Bone marrow edema and a fracture line are classic imaging findings. Findings specific to fractures types include:

Stress fractures (Fig. 5.314) show the following characteristics:

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- Subchondral hypointensity on T1- and PD-weighted images
- Asymmetric thickening of the cortex
- Single or multiple fracture lines
- Location is usually perpendicular to the metatarsal long axis
- Medullary edema
- Soft-tissue hyperintensity on FS PD FSE images
- Edema without visualization of a fracture line in the acute stage
Fractures of the metatarsal head show:
- Displacement
- Edema of the metatarsal head
- May or may not show dislocation
- Angulation or rotation of articular surface on sagittal images
- Chondral fracture with interruption of articular cartilage
Fractures of the metatarsal neck (Fig. 5.315) are characterized by:
- Oblique or transverse fracture and edema
- May or may not be plantar displacement
- Edema, marrow, and sometimes soft tissue
- Tendinous interposition
- Muscle hyperintensity on FS PD FSE images
Midshaft fractures (Fig. 5.316) show:
- Oblique or transverse marrow edema
- Possible shortening, angulation, or displacement
- Variable proximal-to-distal diaphysis edema
Fractures of the base of the metatarsal (see Fig. 5.314), including stress fractures of the base of the second metatarsal in ballet dancers (Fig. 5.317), show:
- Marrow edema
- Multiple areas of metatarsal involvement
- Hyperintense base on FS PD FSE images, sometimes with visualization of a fracture fragment in Lisfranc injuries
- Chip fractures
Fractures of the first metatarsal show:
- Soft-tissue effacement with edema/hemorrhage
- Comminution in direct injuries
- Avulsion fragment
- Possible associated Lisfranc injuries
- Marrow hyperintensity on FS PD FSE images
Fractures of the central metatarsals show:
- Displacement as a unit
- Multiple metatarsal involvement (second, third, and fourth)
- Displacement with extensive soft tissue and muscle edema
Fractures of the fifth metatarsal show:
- Hypointensity of base on T1- or PD-weighted images
- Extension into the proximal diaphysis
- Increased fracture gap in nonunion
- Fibrous tissue or sclerosis.

FIGURE 5.309 ● Surgical fixation options for Lisfranc joint injuries. Lisfranc injuries have been classified as stage I (Lisfranc ligament sprain), stage II (ruptured Lisfranc ligament with a 2- to 5-mm diaphysis between the first and second metatarsals), and stage III (rupture of Lisfranc's ligament with >5 mm of diastasis and loss of longitudinal arch height). ORIF is used for stage III injuries. Athletes may require early ORIF for all grade 2 and 3 sprains. Screws are placed across the tarsometatarsal joint to create stiffness and support the arch and form a rigid lever.

FIGURE 5.310 ● Comparison of the morphology of a proximal fifth metatarsal fracture (A), nonunion of the metatarsal apophysis (B), and an os vesalianum (C). Note the irregular margins of a fracture site and the more proximal location of the os vesalianum.

FIGURE 5.311 ● Lateral color illustration of the three zones of proximal fifth metatarsal fractures: (1) tuberosity avulsion fractures, (2) Jones fractures at the junction of the metaphysis and diaphysis, (3) diaphyseal stress fractures. Avulsion fractures of the tuberosity are the most common type. Contraction of the peroneus brevis tendon secondary to an inversion injury may result in this fracture. The Jones fracture and more distal diaphyseal stress fractures are susceptible to nonunion.

FIGURE 5.312 ● Open reduction and internal fixation of a Jones fracture. Displaced fractures often require open reduction and internal fixation. Screw fixation and bone grafting are also treatment options.

FIGURE 5.313 ● Simple avulsion fracture of the proximal fifth tuberosity. Contraction of the lateral band of the plantar aponeurosis as well as peroneus brevis tendon pulls may be a causative factor in this injury. Sagittal FS PD FSE image.

FIGURE 5.314 ● Stress fractures of the first, third, or fourth metatarsals and the distal aspect of the second metatarsal can be treated conservatively. Stress fracture of the proximal (base) first (A) and distal second (B) metatarsals are shown on these sagittal FS PD FSE images.

Treatment

Management decisions depend on the type of fracture (stress or acute) and degree of displacement. Injuries that have a bridging callus have a good prognosis, but postfracture malalignment leads to displacement, shortening, or angulation. Stress fractures may be treated conservatively with decreased or altered activity and sometimes immobilization. Closed treatment may also be successful with fractures of the metatarsal head if there is an intact nondisplaced articular surface. Nondisplaced fractures of the neck, base, central rays, and fifth metatarsal may also be treated with immobilization and casting. Displaced fractures, regardless of location, are treated

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surgically, usually with ORIF. Complications include nonunion, malunion, and unresolving pain.

FIGURE 5.315 ● Distal second metatarsal stress fracture with diffuse trabecular marrow edema on sagittal T1-weighted (A) and FS PD FSE (B) images.

Compartment Syndrome

Compartment syndrome occurs when the pressure inside a closed fascial compartment increases to the point where it compromises the blood supply to the structures. A cascade of injuries follows, including impairment of myoneural function and necrosis of soft tissues. There are four anatomic compartments in the leg: the anterior, posterior, deep posterior (medial), and anterolateral. The anterior compartment muscles (Fig. 5.318) include the tibialis anterior, the extensor hallucis longus, the extensor digitorum longus, and the peroneus tertius. The anterior compartment neurovascular bundle consists of the deep peroneal nerve (see Fig. 5.318) and the anterior tibial artery. The posterior compartment is divided by deep transverse fascia into superficial and deep sections. The superficial posterior compartment muscles include the gastrocnemius, the plantaris, and the soleus. The deep posterior compartment muscles include the popliteus, the FDL, the FHL, and the tibialis posterior. The neurovascular supply to the posterior compartment is provided by the tibial nerve and the posterior tibial artery. The muscles of the anterolateral compartment include the peroneus longus and the peroneus brevis. The neurovascular supply to the anterolateral compartment is provided by the superficial peroneal nerve and the branches of the peroneal artery.

FIGURE 5.316 ● Persistent diaphyseal marrow edema in a healing third metatarsal stress fracture. Coronal FS PD FSE image.

Etiology, Pathology, and Clinical Features

Compartment syndrome may be either acute or chronic. Acute compartment syndrome is related to fracture or severe trauma and is associated with resting intracompartmental pressures greater than 30 mm Hg (by Wick catheter measurement).

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Tibial fractures, especially open fractures involving the proximal and middle thirds, are the most common fractures leading to compartment syndrome. Twenty percent of tibial fractures are associated with this complication. Muscle ruptures, crush injuries, and burns may also precede the development of compartment syndrome.

FIGURE 5.317 ● (A) Second metatarsal base stress fractures are frequently seen in ballet dancers. Cessation of training for up to 6 weeks or until pain with weight-bearing subsides is necessary for healing. MR findings may persist after clinical healing. Lateral color illustration. (B) Second metatarsal base stress fracture in a ballet dancer is shown with hypointense linear stress fracture (straight white arrow) on T1-weighted image. (C) STIR sagittal image displays associated hyperintense bone marrow edema (curved arrows).

FIGURE 5.318 ● (A) The lower leg contains four major compartments (A, L, SP, DP): the anterior compartment, the lateral compartment, the superficial posterior compartment, and the deep posterior compartment. The tibialis posterior is sometimes classified as its own separate compartment and not grouped with the deep posterior compartment. (B) Anterior color illustration showing the relationship of the deep peroneal nerve to the anterior compartment. Weakness of dorsiflexion or toe extension, paresthesias of the dorsum of the foot, first web space numbness, and foot drop may be seen in anterior compartment syndrome. The superficial peroneal nerve is contained within the lateral compartment. The sural nerve is within the superficial posterior compartment. The posterior tibial nerve is contained within the deep posterior compartment. (C, D) Benign peripheral nerve sheath tumor (schwannoma) involving the deep peroneal nerve of the anterior compartment. There are no associated findings of compartment syndrome. (C) Axial PD FSE image. (D) Sagittal STIR image.

Chronic compartment syndrome is the result of elevated compartment pressures and the development of muscle and nerve ischemia.⁸⁵ Wick catheter measurements show that pre-exercise (resting) compartment pressures are 10 mm Hg or more, and at 15 minutes after exercise pressures are 15 mm Hg or more. Noncompliant fascial compartments, increased muscle bulk (secondary to contraction, and intracellular and extracellular fluid accumulation), and muscle microtears contribute to increased pressures and associated venous and lymphatic compromise. Chronic compartment syndrome is seen most frequently in runners with symptoms of pain during exercise with or without neurologic symptoms. Bilateral and asymmetric involvement is common. The anterior and deep posterior compartments are more commonly involved than the lateral and superficial posterior compartments. The tibialis posterior may be classified as its own compartment.⁸⁶ There may be a history of a recent stress fracture. Muscle herniations through fascial defects may be identified following exercise in 40% of cases, although herniations can also cause chronic leg pain in the absence of compartment syndrome.

Acute compartment syndrome of the foot, with elevation of tissue fluid pressure within a closed space, has also been reported following trauma. The medial, central, lateral, and interosseous and calcaneal compartments may be involved. It is usually associated with calcaneal fracture (5%)⁹⁶ but may also follow crush injuries, even in the absence of severe fracture.¹²³ MR imaging can be used to confirm clinical findings and identify a compartment hematoma, but appropriate treatment with fasciotomy should not be postponed to obtain such studies.

The severity of compartment syndromes varies depending on the affected muscle group or groups within a given compartment. Combined foot and leg compartment syndromes may occur.

There are several theories as to the causes of the increased pressure in compartment syndrome. The arteriovenous gradient theory holds that compromised blood flow (arterial, capillary, or venous) results in hypotension, increased vascular resistance (caused by shock or arterial spasm), and increased tissue pressure from extravasated blood. In the ischemia-reperfusion theory compromised blood flow leads to ischemia, impaired cellular metabolism, interstitial edema, and increased compartmental pressure. Reperfusion is thought to worsen the preexisting cellular damage when cellular activity is restored.

Pathologic findings include a fracture, which may or may not be open, hemorrhage, inflammation, decreased compartment size (e.g., from the use of pressure dressings), venous obstruction, and venous obstruction. Histologic studies show cellular damage (muscle and nerve ischemia), increased neutrophils and leukocytes with reestablished flow, interstitial edema, and local vasodilation.

Patients often present with pain that is disproportionate to the injury. There is palpable swelling (possibly with tense skin), pallor, paralysis, and paresthesias. The distal pedal pulses are usually intact. In crush injuries to the foot there is massive swelling and associated fractures or dislocations.

MR Appearance

MR techniques using axial STIR or FS PD FSE sequences are sensitive to early changes of muscle compartment edema, which is seen as an infiltrative or feather-like pattern of hyperintensity. Bulging and hyperintensity may also be seen in the adjacent fascia. Other MR findings include:

Loss of normal muscle striations
Subacute hemorrhage
Foci of hemosiderin deposition
Enlargement and peripheral convex bowing of affected muscle group
Calcification (in chronic compartment syndrome)
Fat and muscle atrophy (in chronic compartment syndrome)
Chronic fibrous replacement
Calcific myonecrosis (liquefied necrotic muscle and with a calcific shell)
T1 images may be normal in exertional compartment syndrome.
Diffuse hyperintensity within the cross-sectional anatomic boundaries of affected muscle and proximal/ distal extension on FS PD FSE images (Fig. 5.319)
Fluid, hemorrhage, and edema between muscles in the fascial planes
Edema, rhabdomyolysis, and fascial convexity (see Fig. 5.319)
Subcutaneous tissue edema
Intermediate to increased muscle signal on FS PD FSE or STIR images in exertional compartment syndrome
Muscle herniation

Treatment

In treating a fracture, bivalving a cast results in an 85% reduction in intracompartmental pressure and may help to avoid the development of compartment syndrome. Untreated, compartment syndrome leads to nerve and muscle ischemia, and after 12 hours there is usually permanent injury, including muscle necrosis and Volkmann's contracture (fibrous contracture and neurologic damage). Conservative treatment is not an option. Surgical decompression is required, and fasciotomy procedures include fibulectomy, perifibular fasciotomy, or

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double-incision fasciotomy. Reperfusion injury is a potential complication.

FIGURE 5.319 ● Anterior compartment syndrome involving the tibialis anterior, extensor digitorum longus, and extensor hallucis longus muscles. The inelastic fascial sheath and increased volume of the involved muscles are associated with edema and relative muscle hypertrophy. Myofiber damage and an increase in osmotic pressure contribute to decreased blood flow. The anterior compartment is the most common of the four compartments involved, followed by the deep posterior compartment, the lateral compartment, and the superficial posterior compartment. (A) Axial color illustration. (B) Axial FS PD FSE image. (C) Sagittal FS PD FSE image.

Medial Tibial Stress Syndrome

The medial tibial stress syndrome (also known as shin splints) is characterized by leg pain and discomfort, primarily in the middle and distal third of the leg 4 cm proximal to the medial malleolus with or without up to 12 cm of proximal extension. It is secondary to repetitive overuse, usually in runners (13% of cases) and hikers. It has been ascribed by some to stress fractures and deep posterior compartment syndrome⁸⁵^,⁸⁶ and is thought to be caused by a stress reaction of the fascia, periosteum, and/or bone along the posteromedial tibia. It is uncommon in children under 15 years of age and is seen more frequently in females who are at risk because of their smaller bone size and amenorrhea in competitive runners. The risk for stress fracture is 12 times greater in female runners than in their male counterparts.

Beck and Osternig,¹²⁴ performing cadaveric dissections, studied the structures that attach to the tibia at the site of symptoms of medial

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tibial stress syndrome. They found that the soleus, the FDL, and the deep crural fascia attached more frequently at the site corresponding to the symptoms of the medial tibial stress syndrome. The tibialis posterior was not found to attach in this area.

Etiology, Pathology, and Clinical Features

Medial tibial stress syndrome is no longer thought to be related to tibialis posterior overload. Instead, the soleus, through its posteromedial tibial aponeurotic insertion, is considered to be the major contributor. The soleus muscle is thought to cause muscle traction-induced periostitis of the distal half to third of the medial border of the tibia. Surgical findings in shin splints include avulsion of the tibial periosteum by the soleus.¹²⁵ The mechanism of injury is related to the velocity of pronation, which affects the stress and strain of the supporting musculature and the soleus bridge. Hyperpronation of the foot increases stress on the medial soleus. Other contributing factors are varus hindfoot, genu valgum, excessive femoral anteversion, external tibial torsion, and decreased heel cord flexibility. A change in activity level or intensity of training is frequently the inciting cause.

Pathologic changes include hypertrophy of the posteromedial tibial cortex, surface scalloping of the anterior or medial tibia, and periostitis/inflammatory response. As mentioned, there may also be avulsion of the periosteum. Histologic findings include an increase in erythrocytes resulting in vascular congestion and thrombosis within the bone, osteoclastic resorption, a periosteal reaction resulting in an increase in osteoblasts, osseous remodeling, formation of a periosteal callus, and cortical hypertrophy. Continued repetitive stress eventually causes increased bone mineralization.

Clinically, pain and tenderness are present along the medial aspect of the mid- to distal tibia, and symptoms are exacerbated by exercise and decreased by rest. Pain, which is characterized as a dull ache, is elicited with active resistance plantarflexion and toe raises. There is associated muscle soreness and mild swelling. Compared to a complete stress fracture, the tenderness in medial tibial stress syndrome is more diffuse.

FIGURE 5.320 ● (A) Hyperintense periosteal edema adjacent to the anteromedial tibial cortex in grade I medial tibial stress syndrome. (B) Grade 1 extensor hallucis longus muscle strain in a long-distance runner with grade 1 medial tibial stress syndrome. Axial FS PD FSE images.

Classification

The early changes of medial tibial stress syndrome are not appreciated on conventional radiography and require bone scans or MR imaging for detection.¹²⁶ Fredericson et al.¹²⁷ have proposed an MR rating system to ensure accuracy when correlating MR findings with clinical symptoms and scintigraphy. There are four grades in this system:

Grade I: Periosteal edema (Fig. 5.320), which demonstrates mild to moderate increased signal intensity on T2-weighted images, and normal marrow on T1- and T2-weighted images
Grade II: Moderate to severe periosteal edema and associated marrow edema, both hyperintense on T2-weighted images
Grade III: Marrow edema demonstrated on both T1-weighted and FS PD FSE images (Fig. 5.321)
Grade IV: A fracture line is visualized (Fig. 5.322).

Periostitis or shin splints corresponds to a grade I stress injury. The bone marrow edema in grades II and III represents a more severe injury along a spectrum that could lead to a defined fracture. Fat-suppressed MR imaging is helpful in the identification of these early changes, similar to our experience in using STIR or FS PD FSE sequences to identify early periosteal edema and muscle reaction. It is interesting to note that Fredericson's work shows periosteal edema at the origin of the

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tibialis posterior, the FDL, and the soleus muscles, without the predominant involvement of any one particular muscle group.

FIGURE 5.321 ● (A) Axial color cross-section showing marrow and periosteal edema. Grade III medial tibial stress syndrome with marrow and periosteal edema appears hypointense on T1-weighted images (B) and hyperintense on FS PD FSE images (C, D). (B) Axial T1-weighted image. (C) Axial FS PD FSE-weighted image. (D) Coronal FS PD FSE image.

FIGURE 5.322 ● Grade IV medial tibial stress fracture with a linear hyperintense fracture line within the anteromedial cortex. Axial FS PD FSE image.

MR Appearance

The best indication of the medial tibial stress syndrome is hyperintense edema or fluid signal at the medial tibial border on FS PD FSE images. Imaging changes are seen in the posteromedial to anteromedial tibia and the medial periosteum. Other key MR findings include:

Intermediate signal within deep subcutaneous tissue overlying the medial tibial cortex on T1- or PD-weighted images
Intermediate signal within the normally hypointense cortex on T1- or PD-weighted images
Eccentric marrow in the medullary bone of the diaphysis
Anteromedial to posteromedial extension
Extension of edema or fluid to the origin of the soleus posteromedially (soleus bridge)

It is important to correlate the extent of a fracture seen on coronal images with sagittal or axial plane images in order not to overestimate the involvement of bone stock (Fig. 5.323). In older patients, insufficiency fractures of the tibia (Fig. 5.324) may also demonstrate the same pattern as that observed in stress fractures of the tibia in younger patients. Stress fractures of the fibula may be seen in association with the medial tibial stress syndrome or as isolated injuries (Fig. 5.325).

Treatment

Rest, for a minimum of 7 to 10 days before a return to low-impact activity, is the key to treatment of the medial tibial stress syndrome. A premature return to training will most likely result in recurrent pain. The development of a complete fracture line indicates a tibial stress fracture (the end stage of the medial tibial stress syndrome), and stress fractures may take up to 12 weeks to heal completely. In addition to rest, anti-inflammatory medications, heel cord stretching, casting, a heel cup for hindfoot valgus, orthotics for excessive foot pronation, and cushioned insoles to decrease the velocity of foot pronation on heel strike (which decreases eccentric muscle stress) may be part of a conservative treatment regimen. In determining the correct approach to management, it is important to evaluate gait mechanics and lower limb alignment. Surgery may be necessary for resistant medial tibial stress syndrome and involves release of the soleus investing fascia and cauterization of the posteromedial periosteum.

Gastrocnemius—Soleus Strain

Pearls and Pitfalls

Gastrocnemius—Soleus Strain

Represents a strain or tear of the medial head of the gastrocnemius muscle
There is diffuse hyperintense signal intensity within the medial head on FS PD FSE or STIR images.
Soleus muscle strains should be evaluated in association with medial head gastrocnemius strains.
Deep venous thrombosis with prominent venous collaterals should not be mistaken for a muscle strain.
Axial images are useful in the identification of fascial tearing.

Strain or rupture of the gastrocnemius—soleus muscle complex (sometimes known as tennis leg, a term that has also been used to refer to plantaris rupture) is a common sports injury seen in racquet sports, basketball, running, or skiing.⁸⁵ There is a tear of the medial head of the gastrocnemius at the muscle—tendon junction, usually associated with soleus muscle rupture. The medial head of the gastrocnemius is larger than the lateral head and originates on the medial condyle and adjacent femur and capsule of the knee joint. It inserts on the calcaneus with the Achilles tendon. The gastrocnemius, composed of fast-twitch fibers, crosses both the knee and the ankle joints. The soleus muscle is composed of slow-twitch fibers.

The size of the tear varies from a portion of the gastrocnemius to entire cross-sectional areas. There may be a feathery or diffuse edema pattern (Fig. 5.326) and irregularity of the intermuscular fascia. Localized muscle hemorrhage is usually found in grade 2 tears, and there is muscle discontinuity in grade 3 disruption. There may also be an associated plantaris muscle rupture at the myotendinous junction.¹²⁸ Because of the paucity of reported cases in the surgical literature, the association between the rupture of the plantaris muscle and the clinical presentation of tennis leg has not been fully appreciated.

Etiology, Pathology, and Clinical Features

The mechanism of injury is overstretching, caused by forced dorsiflexion and extension of the knee. In eccentric actions, there is increased force during muscle fiber lengthening. In jumping injury, plyometric muscle activity is a factor.

FIGURE 5.323 ● Intact anterior tibial diaphyseal bone stock with stress fracture restricted to posterior cortex. On coronal plane images (A) it is possible to overestimate the extent of a posterior tibial diaphyseal stress fracture. Stress fractures must always be evaluated in more than one orthogonal plane (B, C). (A) Coronal T1-weighted image. (B) Sagittal T1-weighted image. (C) Sagittal FS PD FSE image.

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These are common injuries: muscle strains represent 30% of sports-related injuries and are commonly seen in runners. The gastrocnemius, rectus femoris, hamstring, and adductor longus are the most susceptible to injury. Gastrocnemius—soleus strains can also be caused by passive stretch if it is too aggressive.

Changes seen on pathologic examination include:

Tearing of the medial head of the gastrocnemius at the muscle—tendon junction (the “weak link”)
Hemorrhage between the medial head and the soleus without plantaris tearing
A partial tear of fascia between the medial head of the gastrocnemius and the soleus
A partial tear of the transverse intermuscular septum at the border of the superficial posterior and deep posterior compartments

Microscopic features include muscle strain in the fast-twitch type II fibers of the medial head of the gastrocnemius and acute or chronic strain in the soleus muscle group (Fig. 5.327). An inflammatory cell infiltrate can be found, as well as separation of muscle fibers from the tendon or fascia (Fig. 5.328).

Patients present with a sharp sudden calf pain, frequently followed by swelling and ecchymosis. They are most often young to middle-aged recreational athletes with a history of running or activities that require sudden stops or changes in direction. Calf swelling and pain usually develop in the first 24 hours. There may be localized tenderness to the medial head of the gastrocnemius and soleus. There is difficulty in walking, and activity results in stress in preexisting muscle—tendon unit injury. This injury occurs during knee extension with the ankle dorsiflexed while in the crouched position. There is impaired gait locomotion and difficulty with the toe-off portion of the

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stance phase. The calf hemorrhage can be associated with aching and cramping pain for several weeks.

FIGURE 5.324 ● Insufficiency fracture in a 65-year-old presenting with imaging characteristics similar to those found in medial tibial stress syndrome, which occurs in athletes. Axial FS PD FSE image.

FIGURE 5.325 ● Fibular stress fracture in a basketball player shows periosteal thickening and periostitis with hyperintense signal adjacent to fibular diaphyseal cortex. Axial FS PD FSE image.

FIGURE 5.326 ● Hyperintensity in a grade 1 strain of the medial head of the gastrocnemius muscle.

Classification

Strains are classified into three grades:

Grade 1: There is no myofascial disruption, but edema and swelling are evident (Fig. 5.329).
Grade 2: There is weakness caused by variable separation of muscle from the tendon or fascia (Fig. 5.330).
Grade 3: The myofascial separation is complete and there is loss of muscle function.

MR Appearance

Diffuse hyperintensity within the medial head of the gastrocnemius with or without involvement of the soleus muscle is the key imaging finding. Additional MR characteristics include:

Edema of the medial head
Subacute hemorrhage
Laxity of the intermuscular septum between the gastrocnemius and soleus
Fluid deep to subcutaneous tissue and between the gastrocnemius and soleus (Fig. 5.331)
Fascial discontinuity
Fluid-filled gap in myofascial separation
Foci of hemosiderin deposition, especially on T2* GRE images.

FIGURE 5.327 ● Delayed-onset muscle soreness in a ballet dancer with hyperintense diffuse edema from soleus muscle strain. Axial FS PD FSE image.

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Treatment

Although there may be a palpable knot or defect on physical examination, surgical treatment is not indicated in a simple gastrocnemius—soleus strain. Conservative management with a brace or crutches is used in the acute stages, and there is usually improvement with non—weight-bearing and rest. The greatest pain and swelling occur during the first 24 hours; however, reinjury is common if there is a premature return to activity. Additional conservative measures include supportive wraps, ice, anti-inflammatory medications, and a CAM (controlled ankle motion) walker to assist ambulation without crutches to avoid activation of the injured muscle—tendon unit. Early ankle motion and stretching exercises as pain decreases, followed by strengthening exercises, usually produce successful results. The criteria for a return to activity are pain-free motion and a 90% return of gastrocnemius muscle strength. Complications include compartment syndrome, either acute posterior (deep or superficial), anterior, or lateral. If compartment syndrome develops, surgery (fasciotomy) is required.

FIGURE 5.328 ● Grade 2 tear of the medial head of the gastrocnemius with disruption of the fascial layer between the soleus and gastrocnemius and discontinuity of the crural fascia medially. Axial FS PD FSE image.

Plantaris Rupture

FIGURE 5.329 ● Feathery edema pattern of a grade 1 soleus muscle strain on an axial FS PD FSE image.

FIGURE 5.330 ● Grade 2 muscle strain characterized by a partial muscle tear of the medial head of the gastrocnemius muscle with hemorrhage and fascial tearing of the muscle—tendon unit. Intramuscular edema and extramuscular fluid are identified. The epimysium of the connective tissue sheath surrounding the muscle is disrupted. Hypointense fascia and hemorrhage with hemosiderin may be mistaken for a retracted plantaris tendon.

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Although the term tennis leg is used to describe plantaris rupture, it is now thought to result more frequently from rupture of the medial head of the gastrocnemius (see discussion above). The plantaris is found anterior to the lateral head of the gastrocnemius at the level of the knee joint. It extends obliquely, from lateral to medial, and is medial to the Achilles tendon in its distal course. It originates at the distal lateral supracondylar line of the femur, and its myotendinous junction is at the level of the origin of the soleus from the tibia. The plantaris plane is between the medial head of the gastrocnemius and the soleus. Since the plantaris tendon is absent in 7% to 10% of the population, it does not require repair when torn; in fact, the plantaris tendon is frequently used as an autograft for ligament reconstructions.

FIGURE 5.331 ● Hemorrhagic fluid collection between the soleus and the medial head of the gastrocnemius in tennis leg. The plantaris tendon is not disrupted. Axial FS PD FSE image.

Etiology, Pathology, and Clinical Features

Ruptures of the plantaris are less common than gastrocnemius injuries and usually occur at the myotendinous junction (Fig. 5.332), although distal tendon avulsion does occur. Myotendinous proximal tears are usually associated with distal retraction. Plantar muscle strains at the level of the knee joint have been associated with anterior cruciate ligament and posterolateral corner injuries. The size of the tear varies, and the tendon and hemorrhage may extend up to 50% of the anteroposterior length of the fascial division between the soleus and the medial head. The hemorrhagic fluid collection may assume a tubular morphology, and the tendon mass and hemorrhage are often seen with convex medial and lateral margins.

The mechanism of injury is usually forceful muscle contraction caused by overstretching (i.e., forced dorsiflexion with an extended knee), eccentric loading, plyometric muscle action (as seen in jumping), or running on uneven terrain. Plantaris ruptures are seen most commonly in young to middle-aged recreational athletes.

Patients present with acute-onset calf pain, often with a history of a sudden pop followed by calf swelling and tenderness. They have difficulty walking and impaired weight-bearing on the affected leg. When plantaris rupture is seen in association with myotendinous and posterolateral complex injuries, the symptoms are localized more proximally. Tenderness may be medial to the Achilles tendon in cases of distal rupture.

MR Appearance

FS PD FSE and STIR images are the most sensitive sequences for detection of hemorrhage and associated intramuscular strain and should be performed from the level of the proximal tibia to the ankle joint distally. The keys to diagnosis in myotendinous junction rupture of the plantaris muscle include hemorrhage (intermuscular hematoma) between the medial head of the gastrocnemius muscle and the soleus muscle and mass effect. The hematoma is greatest in acute injury. The retracted tendon of the plantaris and associated hemorrhage may produce a condensed mass of intermediate-signal-intensity

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blood and tissue within the plane of the hematoma. Characteristic MR findings include:

A curvilinear fluid collection in the expected location of the plantaris tendon contribution to the medial aspect of the Achilles tendon on distal axial images at the level of the ankle joint
Hemorrhage with or without a hemosiderin ring between the medial head of the gastrocnemius and the soleus and inhomogeneity in the retracted tendon (Fig. 5.333)
Mass effect from retracted tendon
Associated injuries, including partial tear of the gastrocnemius or popliteus muscles, anterior cruciate ligament injuries (with or without anterior translation of the tibia relative to the femur), tibialis posterior strain, and posterolateral corner sprains
Identification of the proximal retracted muscle between the popliteus tendon and the lateral head of the gastrocnemius muscle at the level of the knee
A distal tear with absence of the distal course of the plantaris (less common)
Edema within a portion of or of a complete cross-sectional area at a specified level
Edema of the soleus and less commonly of the lateral head of the gastrocnemius
Hemorrhagic fluid tracking medially deep to the subcutaneous tissue
Possible anterolateral and posteromedial fluid extension between the subcutaneous tissue and the medial head/soleus plane
Possible fluid extension anteromedial to the tibia
Disruption of the fascia separating the medial head of the gastrocnemius and soleus
Curvilinear “comet sign” of fluid extending along the distal course of the plantaris adjacent to the Achilles tendon
Absence of the plantaris muscle in proximal tears in the sagittal plane through the knee joint

FIGURE 5.332 ● Plantaris myotendinous rupture with the path of hemorrhage corresponding to the course of the retracted plantaris tendon. (A) Posterior view coronal color graphic. (B) Coronal FS PD FSE image.

Treatment

Plantaris tears usually improve with non—weight-bearing and rest, although recovery is affected by associated injuries of the posterolateral corner, anterior cruciate ligament, popliteus muscle, or lateral head of the gastrocnemius. The greatest pain and swelling occur during the first 24 hours. Conservative measures include supportive wraps, ice, anti-inflammatory medications, a CAM (controlled ankle motion) walker, and stretching and strengthening exercises for the gastrocnemius—soleus complex after the acute phase. Although surgery is not required to repair the plantaris tendon, it may be necessary if a posterior compartment syndrome results from the swelling and hematoma associated

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with complete rupture of the plantaris or tear of the gastrocnemius—soleus muscle complex.

FIGURE 5.333 ● Acute rupture of the plantaris with intermuscular hemorrhage (solid curved arrow) identified in the plane between the soleus (S) and medial head of the gastrocnemius muscle (M) groups. (A) Hemorrhage is isointense to hyperintense on an FS PD FSE axial image. (B) On a T2*-weighted axial image the hemorrhage demonstrates hypointensity (magnetic susceptibility effect). Edema of the medial head of the gastrocnemius muscle (open curved arrow) is best demonstrated on the FS PD FSE sequence (A).

Tarsal Coalition

Pearls and Pitfalls

Tarsal Coalition

Coalitions can be osseous, cartilaginous, or a fibrous union of two or more bones involving the hindfoot or midfoot.
A synostosis is a complete coalition, a synchondrosis is cartilaginous, and a syndesmosis is fibrous.
An osseous bar is extra-articular, whereas a bridge is intra-articular.
Talocalcaneal coalitions are best visualized on coronal images; calcaneonavicular coalitions require sagittal images.

A tarsal coalition is a congenital or acquired fibrous, cartilaginous, or bony fusion of the tarsal bones.¹²⁹ Calcaneonav-icular coalition ¹³⁰ is the most common type, reported in 53% of cases, and talocalcaneal coalition ¹³¹ represents 37%.¹⁰⁰ Talonavicular and calcaneocuboid (cubonavicular) types are infrequent. Tarsal coalition may affect the subtalar articulation through anterior, middle, and posterior facets and the transverse tarsal joint (calcaneocuboid and talonavicular joints). The normal functions of the joints include subtalar motion, rotation, and gliding. Tarsal coalition may also be associated with a painful pes planus or flatfoot in a child or adolescent.¹³² Forefoot abduction and hindfoot valgus can result in tension in the peroneal muscles and tendons (i.e., peroneal spastic flatfoot).

The morphology of tarsal coalitions varies and includes:

Synostosis (a complete coalition)
Synchondrosis (cartilaginous coalition)
Syndesmosis (fibrous coalition)
Extra-articular bars (e.g., calcaneonavicular)
Intra-articular bridges (e.g., talocalcaneal)

Etiology, Pathology, and Clinical Features

Congenital tarsal coalition results from a failure of differentiation and segmentation of the primitive mesenchyme. Coalitions may be associated with an autosomal genetic mutation and inherited as autosomal dominant disorders, and there is a slight male predominance. Although present at birth, radiographic detection is difficult in infants or children because ossification of the fibrous or cartilaginous connection does not occur until the second decade, when most tarsal coalitions are diagnosed.¹²⁹ Acquired tarsal coalition is associated with arthritis, infection, trauma, and neoplasia.

The overall incidence of talocalcaneal coalitions is 1%, and 90% of tarsal coalitions are either talocalcaneal or calcaneonavicular. Talocalcaneal coalitions (Fig. 5.334) are slightly more common than calcaneonavicular (Fig. 5.335). Talonavicular coalitions are the third most common type. About one quarter to two thirds of talocalcaneal coalitions are bilateral, and half to two thirds of calcaneonavicular coalitions are bilateral. Coalitions between the navicular first cuneiform articulations (Fig. 5.336) and calcaneocuboid and cubonavicular coalitions are uncommon.

As mentioned, coalitions may be osseous (see Fig. 5.334), cartilaginous (Fig. 5.337), or fibrous (Fig. 5.338). Although

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there are no neural elements in nonosseous coalitions, microfractures and osseous remodeling act as pain generators. Histologic examination also reveals vascular proliferation, osteoblastic and osteoclastic activity, fibrous connective tissue, and cellular components.

FIGURE 5.334 ● Talocalcaneal coalition. (A) Coronal color section of a solid osseous talocalcaneal coalition. (B) T1-weighted coronal image with continuity (arrow) of marrow fat from the tali (T) through the sustentaculum tali (ST). (C) T1-weighted sagittal images show secondary signs of talocalcaneal coalition with talar beaking. N, navicular; T, talus.

FIGURE 5.335 ● Solid calcaneonavicular coalition visualized laterally on a T1-weighted sagittal image.

The clinical presentation is characterized by limitation of subtalar and midtarsal joint motion, including peroneal muscle spasm, and pain, although some coalitions are asymptomatic. Talocalcaneal coalition tends to produce rearfoot pain with localization to the sustentaculum medially and the sinus tarsi laterally. Tarsal coalition is the most common cause of peroneal spastic flatfoot.

MR Appearance

Although tarsal coalition can usually be identified on plain radiographs, MR imaging allows more precise determination of articular involvement and is especially useful in the detection of nonosseous fibrous and cartilaginous coalitions. MR findings differ based on the kind of coalition.

FIGURE 5.336 ● Fibrous coalition between the navicular first cuneiform articulations on a sagittal T1-weighted image.

Calcaneonavicular coalition is best evaluated on sagittal plane images for accurate visualization of morphology (osseous, cartilaginous, or fibrous). MR signs include:

Hypoplasia of the head of the talus
Abnormal close approximation of the navicular bone and the calcaneus, with irregularity of opposing cortical surfaces
Subchondral sclerosis at a synchondrosis or syndesmosis
A linear hyperintense (on FS PD FSE images) calcaneonavicular interface in nonosseous coalitions
Reactive subchondral marrow edema
Solid marrow continuity between the calcaneus and navicular on lateral sagittal images

Talocalcaneal coalitions usually occur through the sustentaculum tali in the middle facet and are best evaluated on coronal plane images. In symptomatic patients, adjacent subchondral hyperemia may be seen on FS PD FSE or STIR sequences in selected cases of fibrous coalitions across the sustentaculum tali. Direct sagittal MR images have also demonstrated contour irregularities in the middle facet in patients with fibrous coalitions.

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Wechsler et al.¹³³ have also demonstrated subchondral hyperintensity, thought to be secondary to altered biomechanics, in calcaneonavicular coalitions. A potential pitfall of MR imaging is mistaking proliferative low-signal-intensity synovitis for fibrous coalition.

FIGURE 5.337 ● (A) Sagittal T1-weighted image showing a symptomatic talocalcaneal cartilaginous coalition. (B) The adjacent marrow edema can be appreciated on this sagittal FS PD FSE image.

FIGURE 5.338 ● Fibrous calcaneonavicular coalition (arrows) displayed on a T2*-weighted sagittal image (A) and a corresponding 2D reformatted CT sagittal image (B). The MR image demonstrates the lack of complete solid bony continuity between the calcaneus and navicular bone more accurately than the CT scan. N, navicular bone; C, calcaneus.

Secondary signs of a talocalcaneal coalition are:¹²⁹

Talar beaking adjacent to the talonavicular articulation (not to be confused with the normal talar ridge)
Degenerative dorsal changes in the calcaneocuboid joint on lateral sagittal images
A broadening lateral talar process
A ball-and-socket ankle joint
An osseous connection with fat signal bone marrow continuity between the talus and the calcaneus
Narrowing with an irregular articular interface and sclerosis across the middle facet in cartilaginous, fibrous, or fibrocartilaginous unions
Possible hypoplastic sustentaculum tali
Talar neck concavity on sagittal views
Intermediate-signal fibrocartilaginous interface on FS PD FSE images
Low to intermediate signal in fibrous tissue syndesmosis on FS PD FSE images

Treatment

Coalitions are initially cartilaginous, eventually progressing to ossification. The decreased rearfoot motion results in increased laxity of ankle ligaments, making patients susceptible to sprains. There is also progressively decreased subtalar and midtarsal joint motion.

Conservative treatment includes shoe modifications, orthotics, and sometimes casting. If necessary, surgery consists of resection of the coalition and fusion of the involved joint.

Tarsal Tunnel Syndrome

Tarsal tunnel syndrome is an entrapment or compression neuropathy of the posterior tibial nerve as it passes through the fibro-osseous tunnel deep to the flexor retinaculum and posterior and inferior to the medial malleolus.⁷⁶ Located in the distal deep posterior compartment of the leg (Fig. 5.339), the tarsal tunnel is formed by the medial talar wall, the sustentaculum tali, and the medial calcaneal wall. The flexor retinaculum (the lacinate ligament) forms the roof of the tarsal tunnel. The contents of the tunnel include the tibialis posterior, the FDL and FHL tendons, and the neurovascular bundle. The neurovascular bundle is located between the compartments containing the FDL and FHL tendons. Within 1 cm of the medial malleolus, the posterior tibial nerve bifurcates into the medial and lateral plantar nerves (Fig. 5.340).¹³² A third branch of the posterior tibial nerve, the medial calcaneal nerve, may arise from the lateral plantar nerve. Potential sites of entrapment of the tibial nerve are shown in Fig. 5.341.

Etiology, Pathology, and Clinical Features

In up to half of cases, the tarsal tunnel syndrome is idiopathic. The typical patient is a middle-aged (average age is 47 years) female (56% predilection). When a cause can be identified, the following are potential factors:¹³²^,¹³⁴

Trauma (a fractured sustentaculum tali or medial tu-bercle posterior talar process), identified in 17% of cases
Varicosities (Fig. 5.342), identified in 13% of cases (Perthes' tourniquet test for varicosities tests the deep venous system and the posterior tibial venae comitantes by occluding the superficial venous system)
Ganglia (Fig. 5.343)
Lipomas (see Fig. 5.342)
Neurilemomas
A thickened flexor retinaculum
Accessory muscle (FDL)
Synovitis (inflammatory arthropathies)
Tarsal coalition
Diabetes or other systemic disease, identified in 34.4% of cases
Valgus heel and forefoot pronation, identified in 8% of cases
Fibrosis, identified in 9% of cases

Many of these conditions are evident on gross pathologic examination. Additionally, histologic examination shows inflammation of the posterior tibial nerve, axonal compression, vascular changes, and atrophy of the muscles innervated by the posterior tibial nerve or one of its branches. Common surgical findings are entrapment of the flexor retinaculum or the fibrous origin of the abductor hallucis muscle, tenosynovitis, and posttraumatic (i.e., post-fracture) fibrosis.¹³⁵^,¹³⁶

Patients present with a variety of signs and symptoms referable to nerve compression, the most common of which are pain and sensory deficits in the plantar aspect of the foot and intrinsic muscle weakness. Pain is localized to the posterior tibial nerve or one of its three terminal branches and is aggravated by activity and prolonged standing. There is tenderness to palpation. The clinical profile also includes burning, tingling, nocturnal paresthesias, and a sensation of numbness. Valleix's phenomenon, radiation of paresthesias proximally to the calf and leg, is another sign of tarsal tunnel syndrome, and Tinel's sign (percussion of the tibial nerve over the tarsal tunnel producing sensory impediment) is positive. Motor symptoms are less common.

FIGURE 5.339 ● (A) Course of the tibial nerve in the lower leg. (B) The posterior tibial nerve lies between the flexor digitorum longus and flexor hallucis longus, divides into the medial and lateral plantar nerves, and gives off calcaneal branches. (C) Axial T1-weighted image of the distal tibia at the level of the tarsal tunnel. The tibial nerve can be seen proximal to its division into the medial and lateral plantar nerves. The tarsal tunnel is bordered by the flexor retinaculum (medially), the calcaneus, and the talus (laterally). The longitudinal course of the tarsal tunnel extends from about the medial malleolus to the level of the abductor hallucis muscle distally.

FIGURE 5.340 ● The tibial nerve divides into its two terminal branches (the lateral and medial plantar nerves) as it passes through the tarsal tunnel. These terminal branches supply the muscles on the plantar aspect of the foot. (A) Axial plantar view of the plantar nerves. (B) Axial T1-weighted image with branching of the medial and lateral plantar nerves at the level of the sustentaculum tali.

FIGURE 5.341 ● (A) Potential sites of entrapment of the tibial nerve. Compression of the tibial nerve or its lateral and medial plantar nerve branches may result in tarsal tunnel syndrome. Pain or sensory disturbances of the sole of the foot and palsies of the intrinsic foot muscles may result. (B) The course of the tibial nerve as it passes deep to the flexor retinaculum and posterior to the flexor digitorum longus tendon. Sagittal T1-weighted image.

FIGURE 5.342 ● (A) Tarsal tunnel syndrome with fatty atrophy of the abductor hallucis, flexor digitorum brevis, and abductor digiti minimi. Coronal T1-weighted image. (B) Prominent veins in association with denervation hyperintensity of the abductor hallucis and flexor digitorum brevis. Coronal FS PD FSE image. (C) In comparison, an example of a lipoma as a true space-occupying lesion resulting in atrophy of the abductor digiti minimi muscle. Axial FS PD FSE image.

FIGURE 5.343 ● (A) Intermediate-weighted and (B) T2-weighted axial images display the tarsal tunnel syndrome secondary to neurovascular compression by a septated ganglion (open arrows) at the level of the medial (straight arrow) and lateral plantar (curved arrow) nerves. The ganglion is hyperintense on the T2-weighted image (B). fhl, flexor hallucis longus tendon.

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MR Appearance

MR findings in the tarsal tunnel syndrome, including a ganglion cyst originating from the FHL tendon sheath, posttraumatic fibrosis, and neuroma, have been documented with surgical correlation.¹³⁷ The anatomy of the tarsal tunnel is effectively displayed on MR images, including the posterior tibial nerve and its branches.¹³⁸

Specific MR findings include:

Fractures (usually of the sustentaculum tali or medial tubercle posterior process of the talus)
Serpiginous venous signal varicosities, intermediate signal on T1- or PD-weighted images and hyperintense on FS PD FSE images
Ganglia, hypointense to intermediate on T1- or PD-weighted images and hyperintense on FS PD FSE images
Lipomas, hyperintense on T1- or PD-weighted images and hypointense on FS PD FSE or STIR images
Neurilemomas, intermediate signal on T1- or PD-weighted images and hyperintense on FS PD FSE images
Thickened flexor retinaculum (lacinate ligament), hypointense on T1- or PD-weighted images
Muscle signal in the presence of accessory muscle
Proliferative synovitis, intermediate signal on T1- or PD-weighted images and intermediate to hyperintense on FS PD FSE images
Fat marrow signal in bony coalition or low to intermediate signal in a fibrous coalition on T1- or PD-weighted images
Fat marrow signal in talar exostosis
Diffuse muscle edema in muscle groups supplied by the posterior tibial nerve and its branches (e.g., the abductor hallucis by the medial plantar nerve and the abductor digiti quinti by the lateral plantar nerve)
Tenosynovitis with hyperintense fluid in the flexor hallucis sheath on FS PD FSE images

Treatment

The natural course and management of tarsal tunnel syndrome vary with its etiology. Synovitis responds to rest and anti-inflammatory medications, whereas space-occupying lesions usually require surgery. In addition to rest and NSAIDs to decrease posterior tibial nerve inflammation, conservative approaches to management include corticosteroid injections, orthotics, physical therapy, compressive stockings, and immobilization.

If conservative treatment is not successful, surgical decompression is performed, with division of the retinaculum and mobilization of the medial and lateral plantar nerves and the fibrous origin of the abductor hallucis.¹³⁵ Space-occupying lesions are excised.

Clinical results of tarsal tunnel decompression reported by Pfeiffer and Cracchiolo,¹³⁹ however, suggest that unless a specific

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lesion is identified near or within the tarsal tunnel preoperatively, subsequent surgical decompression of the posterior tibial nerve may not be successful. They found that surgical decompression in patients with a history of previous surgical treatment for pain in the foot, plantar fasciitis, or systemic inflammatory disease did not show favorable results compared with patients with space-occupying lesions and coalitions.¹³⁹ Complications include recurrent tarsal tunnel syndrome.

Morton's Neuroma

Morton's neuroma is a metatarsalgia that involves localized enlargement of the interdigital nerve. There is a fusiform teardrop-shaped enlargement with bulbous plantar extension: the nerve may reach 5 mm or greater in diameter versus the normal diameter of 2 mm. The enlargement begins between the third and fourth metatarsal heads (Fig. 5.344),¹⁴⁰ and the lateral (common digital) branch of the medial plantar nerve to the third interspace is usually involved. The second and fourth interspaces are also occasionally involved (Fig. 5.345).¹⁴¹ The communicating branch of the lateral plantar nerve may contribute to the third common digital nerve and also supplies the third interspace. In this location the plantar nerve is superficial to the deep transverse intermetatarsal ligament, as are the third plantar metatarsal artery and veins and the tendon of the third lumbrical muscle. There is also a fat pad of subcutaneous tissue superficial to the plantar nerve with Pacinian corpuscles.

FIGURE 5.344 ● Morton's neuroma with localized fusiform enlargement of the common digital nerve between the third and fourth metatarsal heads.

Morton's neuroma occurs more frequently in women 40 to 60 years of age and is less common in teenagers. It accounts for over 90% of patients with foot pain, occurs in the third intermetatarsal space in well over half of cases, and only occasionally involves two intermetatarsal spaces. It is bilateral in approximately 10% of cases.

Etiology, Pathology, and Clinical Features

Entrapment neuropathy secondary to compressive forces against the deep transverse intermetatarsal ligament is the most common etiology. The localized enlargement of the third common digital branch of the medial plantar nerve is a fibrotic response, not a true tumor. There may also be tethering of the interdigital nerve by an anastomotic or communicating branch between the medial and lateral plantar nerves. Traction on the third interspace nerve by hindfoot valgus, intermetatarsal bursitis, or extreme dorsiflexion of the toes (as is seen in patients who wear high-heeled shoes) is another common cause of Morton's neuroma.

Pathologic examination reveals a benign fusiform enlargement of the third common digital nerve, often associated with a perineural fibroma. The lesion has a shiny and glistening white to yellowish surface, bifurcating digital branches, and fusiform enlargement in resected specimens. The nodule may or may not be attached to the intermetatarsal bursa, which is inflamed.

FIGURE 5.345 ● Teardrop-shaped Morton's neuroma involving the second intermetatarsal space. There is both dorsal and plantar extension with direct adherence of the perineural fibroma to the intermetatarsal bursa. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image.

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Histologic findings of deposition of eosinophilic material and degeneration of nerve fibers are attributed to the entrapment neuropathy.¹⁴¹ There is neural proliferation, dense fibrosis of axons and the sheath (Schwann cells), endoneural and neural edema (early in the course), and perineural and epineural fibrosis and hypertrophy (in the late stages). Endoneural blood vessel wall hyalinization, perivascular fibrosis, vascular occlusion, endoneural and perineural mucinous change, demyelination, and axonal loss can also be demonstrated. Renaut's bodies (hyaline granules) are found in endoneural tissue in response to compressive nerve trauma. There is Wallerian or fatty degeneration and axon regeneration.

Most patients have plantar foot pain and tenderness in the involved interspace. The pain may be sharp, dull, or throbbing, or there may be a paroxysmal burning sensation. There is neurologic pain localized to the toe and sometimes the interdigital space. A tingling toe or forefoot is also common. Pain is increased with walking and may also occur at night. There may also be numbness of the third and fourth toes. Discomfort is exacerbated by shoes and activity and relieved by rest. A positive Mulder's sign is found with palpation of the plantar interspace distal to the metatarsal heads.

MR Appearance

Frequently, no palpable mass is clinically apparent, and MR coronal or sagittal T1- and T2-weighted images have been used to identify these lesions.¹⁴² Forefoot imaging can be performed using smaller FOVs (8 to 10 cm) to provide for increased spatial resolution defining musculotendinous and neurovascular structures.¹⁴³ Fat-suppressed contrast-enhanced MR imaging is the most sensitive technique, providing high-contrast images for depicting Morton's neuroma.¹⁴⁴ This technique displays lesion hyperintensity in cases where conventional T2-weighted images either fail to demonstrate the lesion or show the lesion with decreased conspicuity. Key findings include:

A teardrop-shaped mass arising between the plantar aspects of the involved metatarsal heads, hypointense to intermediate on T1- and PD-weighted images and intermediate to hyperintense on FS PD FSE and STIR images (Fig. 5.346)
Fibrosis of the epineurium and perineurium modifying the degree of signal inhomogeneity
Increased signal intensity on T2*-weighted, STIR, and FS PD FSE images (in contrast to a conventional neuroma or neurofibroma, which displays hyperintensity on both FS PD FSE and T2*-weighted images)
Fat signal in the plantar subcutaneous tissue superficial to the mass
Thickened and inflamed intermetatarsal bursa
Effacement of the plantar subcutaneous fat by the convex border of the mass
Intermetatarsal bursal fluid (Fig. 5.347)
Intermediate to hyperintense mass on T2* GRE images
Diffuse enhancement after contrast administration (Fig. 5.348)
Enhanced lining of the inflamed intermetatarsal bursa

Treatment

Without treatment there is continued tenderness with applied pressure to MTP joints and eventually a palpable dorsal or plantar mass. Associated inflammation of the intermetatarsal bursa usually accompanies progression. Conservative treatment is successful in somewhat less than 60% of cases and includes avoidance of high-heeled shoes, use of wider shoes with an arch support, metatarsal pads, and corticosteroid injections. Surgical treatment involves excision of the neuroma or swelling proximal to the site of digital nerve bifurcations¹⁴¹ and possibly epineural neurolysis or decompression. Endoscopic methods, percutaneous electrocoagulation, and carbon dioxide laser techniques are all available. Possible complications include hematoma, vascular ischemia, development of hammertoe related to the division

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of the deep transverse intermetatarsal ligament, a painful stump neuroma, and continued pain. Steroid injections may cause subcutaneous fat pad atrophy.

FIGURE 5.346 ● Morton's neuroma (straight arrow), located between the third and fourth metatarsal heads, is isointense with adjacent inflammation on a T1-weighted coronal image (A) and is mildly hyperintense on a STIR coronal image (B). Inflammatory soft-tissue edema demonstrates greater hyperintensity (curved arrow) than reactive connective-tissue proliferation and associated nerve degeneration. STIR protocols are more sensitive for Morton's neuroma than either T1- or T2-weighted images.

FIGURE 5.347 ● Intermetatarsal bursa sites for potential inflammation in association with Morton's neuroma. Axial (A) and coronal (B) color illustrations.

FIGURE 5.348 ● Recurrence of a Morton's neuroma (straight arrow) identified on an intravenous gadolinium-enhanced FS T1-weighted coronal image. Irregularly marginated hyperintensity can be identified between the plantar aspects of the third and fourth metatarsals. Reactive inflammatory soft-tissue changes also demonstrate hyperintensity on gadolinium-enhanced image (curved arrow).

Plantar Fibromatosis

Plantar fibromatosis is characterized by the development of fibrous nodules in the plantar aponeurosis similar to Dupuytren's contracture of the palmar aponeurosis.⁷⁶^,¹⁴⁵ The plantar fascia runs from the calcaneus to the metatarsal heads distally, with central, lateral, and medial segments or cords. The central section may be formed from contributions from the plantaris and Achilles tendon. The lateral plantar aponeurosis extends from the plantar to the abductor digiti minimi muscle, and the medial plantar aponeurosis from the plantar to the abductor hallucis muscle.

Etiology, Pathology, and Clinical Features

Plantar fibromatosis is one of the superficial collagenous fibromatoses. There may be an association with Dupuytren's contracture (palmar fibromatosis) as well as Peyronie's disease (penile fibromatosis). Single (Fig. 5.349) or multiple (Fig. 5.350) unilateral or bilateral nodules, usually less than 1 cm in diameter, are found in thickened plantar fascia and subcutaneous tissue usually in the non—weight-bearing surfaces of the foot, with lesions frequently identified in the longitudinal arch.¹⁴¹ A genetic link has been proposed based on the simultaneous occurrence of plantar and palmar fibromatosis in some individuals, although plantar fibromatosis is less common. Fibromatosis, especially palmar fibromatosis, usually occurs in individuals 65 years of age or older, and there is a slight predilection for men.

On pathologic examination the nodules are firm, with a thin poorly defined capsule and a gray-white or gray-yellow cut surface. Histologic findings include proliferating fibro-blasts and a dense, acellular collagenous stroma,⁷⁶ myofibro-blasts, and infiltration of surrounding structures without malignant transformation. Mitotic figures are uncommon.

Patients usually present with mild plantar pain and discomfort with walking or prolonged standing, although they may be asymptomatic. The nodules are firm and fixed to the plantar aponeurosis and there may be associated palmar nodules (Dupuytren's contracture). Three separate phases have been described:

A proliferative phase, in which there is fibroblastic activity and cellular proliferation
An involutional phase, which is an active phase with nodule formation
A residual phase, in which there is reduced fibroblastic activity and collagen maturation

MR Findings

The nodules are hypointense on sagittal or coronal T1- and FS PD FSE images, and the increased collagen content of the

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plantar fibromas may explain their relative hypointensity on FS PD FSE sequences. Adjacent inflammatory edema is usually not present. The differential diagnosis includes a ganglion, neurofibroma, or fibrosarcoma and in most cases can be made by the presence of increased signal intensity on FS PD FSE images. Characteristic MR findings include:

Hypointense nodule (see Fig. 5.349)
A central region of low to intermediate signal intensity
Effacement of plantar subcutaneous tissue
The long axis of the nodule is seen along the long axis of the plantar fascia.
Adjacent plantar fascia is unaffected and of normal thickness.
Mild hyperintensity of the plantar subcutaneous tissue on FS PD FSE images
Convex dorsal (deep) and plantar (superficial) margins (see Fig. 5.350)
Infiltrative upper margins and lesions deep to the plantar aponeurosis¹⁴⁶
The plantar margin is better defined than the infiltrative upper margin.
Inhomogeneous signal intensity in lesions consisting of multiple nodules
Inhomogeneous enhancement after contrast administration
Central areas of intermediate to increased signal intensity on FS PD FSE, T2* GRE, or STIR images¹⁴⁶

FIGURE 5.349 ● Single, less than 1 cm, nodular lesion of plantar fibromatosis distal to the os calcis attachment of the plantar fascia. Note the well-defined plantar margin and mild central hyperintensity on the FS PD FSE sequence. (A) Sagittal T1-weighted image. (B) Sagittal FS PD FSE image.

Treatment

Without intervention there is usually gradual enlargement of the nodules, increasing numbers of nodules, and a more extensive distribution. Contractures of the toes do not usually develop. Management begins with conservative measures such as orthotics and anti-inflammatory agents if needed. Surgical excision of the nodules is definitive, but there may be local recurrence.

Plantar Fasciitis

Pearls and Pitfalls

Plantar Fasciitis

Plantar fasciitis is also known as heel pain syndrome or subcalcaneal pain syndrome.
The origin of the plantar fascia from the calcaneal tuberosity is most commonly affected.
Microtrauma of the plantar fascia or repetitive tensile overload may lead to an inflammatory response.
There may be plantar fascial tearing, or involvement may be localized to the medial, central, or lateral portions of the aponeurosis.
Effacement of subcutaneous fat by fibrosis and edema seen in the sagittal plane may assist in early diagnosis.

Plantar fasciitis (subcalcaneal pain syndrome) is caused by inflammation of the plantar aponeurosis and may be associated

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with a calcaneal spur, inflammatory changes, or thickening of the plantar aponeurosis adjacent to the calcaneus. Subcutaneous edema may be seen both superficial and deep to the plantar fascia. A heel spur (a plantar calcaneal enthesophyte, actually located in the short toe flexor origins and not the aponeurosis) is identified in 50% of cases of adult plantar heel pain. It usually occurs in middle-aged (average 45 years of age) females (twice as common in women as in men).

FIGURE 5.350 ● Large lesion of plantar fibromatosis with capsular margins demonstrates heterogeneous areas of hyperintensity on the FS PD FSE sequence and enhancement with intravenous contrast. The long axis is parallel to the plantar aponeurosis in the sagittal plane. (A) Axial plantar view color illustration. (B) Coronal FS PD FSE image. (C) Sagittal FS T1-weighted contrast-enhanced image.

The plantar aponeurosis originates at the os calcis. The plantar fascia is a multilayered fibrous aponeurosis with three segments or cords (Fig. 5.351) and distal superficial tracts. The central segment is the largest and extends from the plantar posteromedial calcaneal tuberosity to the proximal phalanges and the skin of the ball of foot. The lateral cord runs from the lateral process of the os calcis tuberosity to the base of the fifth metatarsal. The medial cord is thin and covers the plantar aspect of the abductor hallucis. The medial calcaneal nerve is located in the subcutaneous tissue between the plantar fascia and the skin. The nerve to the abductor digiti quinti (from the lateral plantar nerve) passes between the long plantar ligament and the calcaneal plantar enthesophyte.

Etiology, Pathology, and Clinical Features

The pain of plantar fasciitis is related to microtrauma of the plantar fascia adjacent to its attachment, leading to attempted repair and chronic inflammation.¹⁴⁷ Nerve entrapment and irritation of the medial calcaneal nerve and/or of the lateral plantar nerve to the abductor digiti quinti off the lateral plantar nerve have also been proposed as causes of pain (Fig. 5.352). Additional causes of plantar fasciitis include:

Repetitive tensile overload affecting the central band
A reparative inflammatory response to traumatic overload
Heel cord contractures
Pes planus or cavus
A calcaneal spur within the flexor brevis origin

On pathologic examination there is inflammation and thickening of the proximal plantar fascia from a normal thickness of 3 mm to over twice its normal size. Calcaneal enthesophytes and fatigue fractures and periostitis of the medial calcaneal tuberosity are also seen. Histologic examination reveals angiofibroblastic hyperplasia, collagen, degenerative and necrosis, chondroid metaplasia, and matrix calcification. Acute plantar fascia rupture, with a palpable defect distal to the medial calcaneal tuberosity, is less common than chronic proximal plantar fasciitis.

Pain in the area of the medial tuberosity of the calcaneus is the most common manifestation.¹⁴⁸ The onset of pain is slow and gradual. Pain is worse in the morning and is exacerbated by activity such as dorsiflexion of the toes, and may or may not be associated with a twisting injury to the foot. There is severe inflammation and the patient cannot bear weight on the affected heel. There may be an associated medial tuberosity enthesophyte and sometimes a history of seronegative spondyloarthritis (HLA-B27 antigen positive) or of increased stress on the foot, either standing- or activity-related.

MR Appearance

On MR studies¹⁴⁹^,¹⁵⁰ plantar fasciitis frequently demonstrates hyperintense signal intensity changes on T2-weighted, T2*-weighted, STIR, and FS PD FSE images. T1-weighted sagittal images display the low-signal-intensity fascia in contrast to high-signal-intensity superficial fat. Typical findings include:

Initial prefascial thickening and effacement of subcutaneous tissue superficial (plantar) to the os calcis attachment (Fig. 5.353 and 5.354)
Enthesophyte, with or without marrow fat signal (Fig. 5.355)
Partial detachment of the medial or lateral cord (Fig. 5.356)
Adjacent calcaneal erosions (tuberosity of the calcaneus)
Thickening of the proximal plantar fascia (Fig. 5.357)
Subcutaneous tissue edema deep to the plantar fascia (see Fig. 5.357)
Reactive calcaneal marrow edema
Fluid-filled gap in fascial rupture (Fig. 5.358)

Treatment

Even without treatment, the pain partially resolves during the day, although it is exacerbated by prolonged standing or athletic activity. Up to 90% of patients improve with conservative treatment, including nonsteroidal anti-inflammatory medications, rest, orthotics, physical therapy with stretching, and immobilization with a cast. The use of steroid injections is controversial, since they have been associated with rupture of the plantar fascia and fat pad atrophy. If conservative therapy fails, surgical options include plantar fasciotomy, excision of the calcaneal spur when present, and release of the nerve to the abductor digiti quinti. Endoscopic procedures for plantar fascia release are available, but complications include stress fractures, pseudoaneurysm, and recurrence of pain.

Avascular Necrosis of the Talus

FIGURE 5.351 ● (A) The plantar fascia consists of a central aponeurosis and medial and lateral components. Plantar view axial plane color illustration. (B) On MR studies the plantar aponeurosis is usually described in terms of a medial and lateral cord or component. Axial T1-weighted image. (C) Normal position of plantar aponeurosis. (D) Dorsiflexion with the toes increases the tension on the plantar aponeurosis, which causes the longitudinal arch to rise (windlass mechanism). Failure of the longitudinal arch to rise is associated with pes planus and abnormal stretching and elongation of the plantar aponeurosis.

FIGURE 5.352 ● Plantar fasciitis. (A) Palpation of the plantar fascia at the medial calcaneal tuberosity often elicits pain. (B) There are numerous causes for plantar heel pain, including entrapment of the medial or lateral plantar nerves.

FIGURE 5.353 ● (A) Structures associated with the presence of heel pain. Lateral color illustration. (B) Plantar fasciitis with partial tearing of the central to medial component of the plantar aponeurosis. Perifascial soft-tissue edema is hyperintense. Sagittal FS PD FSE image.

FIGURE 5.354 ● (A) The subcutaneous tissue is up to 2 cm thick at the sole of the foot. It has a pressure chamber system that functions as a shock absorber and stabilizer for the sole of the foot. (B) Signal-intensity changes of fibrosis and edema frequently precede plantar aponeurosis inflammatory changes and thickening.

FIGURE 5.355 ● Plantar calcaneal enthesophyte associated with a thickened plantar fascia. A spur or enthesophyte on the leading edge of the inferior calcaneal surface is not pathognomonic of plantar fasciitis and may be seen in as few as 10% of symptomatic patients. Sagittal T1-weighted image.

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AVN of the body of the talus most commonly occurs with talar neck fractures associated with subtalar joint disruption,¹⁵¹^,¹⁵² although it may also be associated with atraumatic etiologies. AVN may appear as a localized, well-demarcated linear to ovoid area of central subchondral talar dome ischemia with bone marrow edema, or it may have a more diffuse pattern involving the entire body of the talus, resembling a bone infarct. In its long axis the lesion is directed from anterior to posterior. In either case the lesion is surrounded by a sclerotic, serpiginous border. AVN usually occurs in middle-aged (peak incidence during the fourth decade) adults.

FIGURE 5.356 ● Thickened segment of the medial cord in plantar fasciitis on a sagittal FS PD FSE image. Plantar fasciitis may have a traumatic, vascular, neurologic, arthritic, infectious, autoimmune, or mechanical cause. Plantar fasciitis is the result of chronic overload of the plantar fascia with inadequate healing, chronic inflammation, and fatigue failure.

The major talar blood supply is from the tarsal canal artery, a branch of the posterior tibial artery, which extends through the medial aspect of the tarsal canal. There are anastomoses between the tarsal canal artery and branches of the dorsal pedis and peroneal arteries, which enter the lateral aspect of the tarsal canal at the base of the tarsal sinus to form a rich vascular arcade to supply the body of the talus. The posterolateral corner of the talus has the poorest blood supply.

Etiology, Pathology, and Clinical Features

Posttraumatic AVN occurs after talar neck fracture¹⁵³ with talar dislocation. The neck of the talus is susceptible to fracture, and 40% to 50% of cases of AVN of the talus are associated with talar neck fracture and subtalar dislocation. Complete talar dislocation and subtalar dislocation results in AVN 90% of the time, and all cases of comminuted fracture of the body of the talus result in AVN. During reduction, operative preservation of a small deltoid branch of the tarsal canal artery proximal to where it enters the tarsal canal can reduce the risk of AVN.

Atraumatic AVN is associated with vasculitis or fat or arterial embolism. It may occur in patients receiving corticosteroids or in those with systemic disease such as diabetes mellitus, systemic lupus erythematosus (vasculitis), or sickle cell anemia. It is not seen as frequently as AVN of the femoral head, Kienböck's disease, or scaphoid fracture necrosis and Freiberg's infraction. There is bilateral involvement in 30% to 70% of cases.

Pathologic examination reveals talar neck fracture, subtalar or talar dislocation, disruption of the tarsal canal artery (a posterior tibial artery branch) (Fig. 5.359), and subchondral collapse with a necrotic focus. There may be focal involvement, or the entire body of the talus may be affected. Histologic features include arterial and/or venous insufficiency, intraluminal capillary obstruction and compression, ischemic marrow edema, increased intraosseous pressure, necrosis (from vascular insufficiency), and trabecular insufficiency and subchondral plate fractures.

Pain with weight-bearing is the most common clinical complaint. The patient cannot walk, has a limited range of motion, and demonstrates a compensatory weight shift. There may be a joint effusion. Bilateral lesions occur with asynchrony.

Classification

AVN has been classified into four stages:

Stage 0: Ischemia
Stage I: A necrotic focus with edema
Stage II: A large well-defined necrotic area
Stage III: A subchondral fracture (analogous to Ficat III lesion in the hip)
Stage IV: Subchondral collapse and secondary osteoarthrosis

MR Appearance

On MR images, AVN of the talus may appear as a localized, well-demarcated area of subchondral talar dome ischemia with

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bone marrow edema, or it may demonstrate a diffuse pattern of involvement, similar in morphology to bone infarcts seen in other locations. Nontraumatic AVN of the talus is similar in appearance to AVN of the distal femoral condyle of the knee. Early in the disease, there is a small hypointense focus that corresponds to the necrotic lesion seen in the superior talar dome. This, however, is frequently overshadowed by an extreme pattern of diffuse bone marrow edema throughout the entire talus. This hyperemia or bone marrow edema is hypointense on T1-weighted images and hyperintense on FS PD FSE or STIR images. Caution should be taken not to mistake this pattern of bone marrow edema for infection, tumor, or reflex sympathetic dystrophy. Bone biopsy is not required. Within 12 months, the bone marrow edema shows partial resolution, leaving behind a persistent, well-defined focus of osteonecrosis. In contrast to the bone marrow edema pattern in the hip, which may precede the development of AVN, it is less common to see diffuse marrow talar edema without an associated focus of AVN. The morphology of this early AVN, however, may be less well demarcated and smaller prior to the resolution of associated marrow edema. Bilaterality and asynchrony of involvement is not uncommon in the talus with AVN. Follow-up MR examination within 12 months can be used to document resolution of bone marrow edema.

FIGURE 5.357 ● Inflammation of the lateral cord of the plantar fascia with perifascial edema deep and plantar to the aponeurosis. There is reactive calcaneal marrow hyperintensity adjacent to the insertion of the plantar fascia. Sagittal FS PD FSE image.

FIGURE 5.358 ● Complete rupture of the medial cord of the plantar fascia. Steroid injections may be associated with delayed rupture of the plantar fascia. Surgical plantar fasciectomy has fewer associated complications (longitudinal arch strain, lateral plantar nerve dysfunction, stress fracture) than are seen in patients who sustain plantar fascia rupture after steroid injection. (A) Sagittal FS PD FSE image. (B) Coronal FS PD FSE image.

FIGURE 5.359 ● Talar arterial blood supply. The main artery to the body of the talus is supplied by the artery of the tarsal canal. Lateral color graphic.

MR features include:

A small hypointense necrotic focus in the superior talar dome (Fig. 5.360)
A sclerotic line directly adjacent to the subchondral plate
A sclerotic line marginating the central marrow fat signal
Diffuse osteonecrosis with a serpiginous bone infarct pattern (Fig. 5.361)
Associated talar neck fracture
Disproportionate diffuse marrow edema
Marrow edema adjacent to an ischemic focus
A central signal void secondary to necrosis with a hyperintense rim (on FS sequences)
Resolution of bone marrow edema in chronic cases with persistence of a well-demarcated focus of osteonecrosis
Double line sign (a hypointense outer line caused by sclerosis and fibrosis and a hyperintense inner line caused by granulation tissue) on FS PD FSE images

It is important to exclude a subchondral fracture or regional migratory osteoporosis if edema is limited to the talar head and neck (Fig. 5.362).

Treatment

The onset of AVN is frequently delayed 3 months or more after trauma, and revascularization of the avascular fragment may take up to 24 months. Acute symptoms with ankle pain are frequently significantly relieved with the resolution of marrow edema. The risk of osseous collapse is dependent on vertical load, and partial or decreased weight-bearing is usually recommended at the onset of symptoms. Collapse and repair are indicated by a change in talar morphology. Degenerative osteoarthritis, joint space narrowing, and ankylosis may all complicate the course. A distal tibial infarct may clinically mimic talar osteonecrosis (Fig. 5.363).

Conservative treatment includes protection from weight-bearing during the revascularization phase, bracing, NSAIDs, and orthotic support. Surgical procedures include external fixation, anatomic reduction of a talar fracture with screw fixation, decompression (core) of necrosis, débridement and autogenous grafting, and ankle and subtalar arthrodesis.

Freiberg's Infraction

Freiberg's infraction is osteochondrosis of the metatarsal head, usually prior to closure of the epiphyseal plate. It most commonly occurs during the second decade of life, with a peak incidence from 11 to 17 years of age. In adults it may be associated with degenerative arthrosis. There is a female predominance.

Etiology, Pathology, and Clinical Features

The primary event is usually trauma, either a single event or repeated microtrauma and biomechanical stress (e.g., from high-heeled shoes) with microfracture at the metaphyseal—physeal junction.⁷⁶ Resultant vascular damage and compression produce vascular occlusion, subchondral trabecular fracture, secondary

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compression of the chondral surface, cortical thickening, and necrosis of the trabecular marrow. Deformity of the metatarsal head, shaft hypertrophy, and secondary osteoarthritis of the MTP joint result from repeated weight-bearing trauma.

FIGURE 5.360 ● Focal subchondral talar ischemic focus characteristic of AVN (osteonecrosis) of the talus. The ischemic zone is well demarcated. The associated talar edema may extend diffusely in the acute stages of ischemia. (A) Lateral color illustration. (B) Sagittal T1-weighted image. (C) Sagittal FS PD FSE-weighted image.

FIGURE 5.361 ● Diffuse form of talar ischemia with an infarction pattern involving the entire talar body. (A) Lateral color illustration. (B) Sagittal T1-weighted image. (C) Lateral reformatted CT image.

FIGURE 5.362 ● Talar head subchondral fracture, which may be mistaken for regional migratory osteoporosis or ischemia. Sagittal FS PD FSE image.

The second metatarsal head (Fig. 5.364) is the most frequently involved (85% of cases), possibly because the long second metatarsal is susceptible to increased stresses and the epiphysis has a unique vascular pattern of penetrating radial arteries to the periosteal shaft network. The third (Fig. 5.365) and fourth metatarsal heads, and rarely the first, may also be affected. Characteristically the lesion is unilateral, although bilateral involvement and changes in two or more metatarsal heads are possible.

FIGURE 5.363 ● Serpiginous distal tibial infarct pattern with the ischemic zone demonstrating marrow fat signal on a sagittal T1-weighted image (A) and hypointensity on FS PD FSE image (B).

Initially, osteochondrosis is restricted to the distal dorsocentral subchondral bone and is seen as a focal area of sclerosis. Advanced changes, with more extensive involvement of the distal metatarsal, are associated with central collapse and articular cartilage separation. There is flattening and enlargement of the metatarsal head with cystic lesions and periostitis.

Patients usually present with localized pain (metatarsalgia) and swelling. The forefoot pain is vague and increases with weight-bearing, activity, and extreme range of motion. Most patients report a decreased range of motion at the MTP joint. Some patients are asymptomatic initially but eventually experience metatarsalgia. Disease progression is associated with periarticular edema, soft-tissue thickening, localized warmth, and synovitis. Many patients have an antalgic gait to compensate for the metatarsalgia. Later findings include an enlarged metatarsal head, dorsal osteophytes, loose bodies, and proliferative changes in the proximal aspect of the adjacent proximal phalanx.

Classification

In the Bragard classification there are three stages of disease:

Stage I: Decreased subchondral density plus metatarsal head flattening
Stage II: Sclerotic and radiolucent areas leading to fragmentation, metatarsal head deformity and enlargement, cortical thickening, and physeal fusion
Stage III: Degenerative osteoarthritis

MR Appearance

In a patient with a normal or widened joint space, MR imaging allows early identification of Freiberg's infraction by demonstrating the hypointense signal of subchondral sclerosis that occurs prior to radiographic signs of increased density and fragmentation of the epiphysis. An undiagnosed stress fracture can also be excluded using T1-weighted and STIR

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images. The increased signal intensity of the articular cartilage surface is best shown on FS PD FSE images. Other changes include:

Subchondral marrow hyperemia on STIR and FS PD FSE sequences
Irregularity and flattening of the epiphysis with spurring (in more advanced disease)
Loss of joint space and metatarsal shaft hypertrophy (in more advanced disease)
Sclerosis (see Figs. 5.364 and 5.365)
Fragmentation and flattening of the subchondral plate on sagittal images
Variable degenerative subchondral marrow changes and edema (see Figs. 5.364 and 5.365)
Joint effusion
Loose bodies

FIGURE 5.364 ● (A) Lateral color illustration of Freiberg's infraction, which represents an osteochondrosis most commonly involving the second metatarsal head. Freiberg's infraction (curved arrow) with osteonecrosis of the second metatarsal head is hypointense on a T1-weighted sagittal image (B) and hyperintense on STIR coronal image (C). Early flattening of the metatarsal head is appreciated on the T1-weighted sagittal image (small arrows).

FIGURE 5.365 ● Less common third metatarsal head involvement in Freiberg's infraction. Degenerative arthritis and synovitis with distal metatarsal head fragmentation of articular cartilage and subchondral bone may occur as complications. (A) Axial T1-weighted image. (B) Axial FS PD FSE image.

Treatment

Initial nonoperative management includes cast immobilization, non—weight-bearing, and corticosteroids. With protection of the metatarsal head during remodeling, most patients experience decreased symptoms. If conservative measures fail, surgery may be necessary, including débridement of the second metatarsal head with synovectomy, metatarsal head excision or reshaping, cheilectomy of osteophytes, dorsiflexion osteotomy, or even joint replacement. Complications are related to fragmentation of cartilage and subchondral bone.

Neuropathic Foot in Diabetes Mellitus

Pearls and Pitfalls

Neuropathic Foot

Osteomyelitis is associated with pressure point ulcers and marrow changes that are hypointense on T1-weighted images and hyperintense on FS PD FSE or STIR images.
Neuropathic joint involvement is usually independent of the presence of soft-tissue ulcers and typically involves multiple joints.
Neuropathic marrow changes are not hyperintense on T2* GRE images. Hyperintense marrow on T2* contrast indicates increased free water and thus has a high association with osteomyelitis.

The overall incidence of diabetes mellitus is approximately 5%, and foot problems account for 20% to 25% of hospital admissions in the diabetic population. Of diabetic patients, 2% to 4% develop foot ulcers or deep infections. The elderly population is most at risk.

A Charcot or neuropathic joint may develop secondary to underlying neuropathic processes, commonly diabetes-associated, with repetitive microtrauma. The end result is articular cartilage and bone fragmentation, disintegration and dislocation of the involved joint, and new bone formation.¹⁵⁴ The ankle and midfoot, including the MTP and midtarsal joints, are frequently

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involved in diabetic neuropathy without overlying ulcers. Common sites for pressure lesions and infection include the metatarsal heads, the calcaneal tuberosity, the tendo-Achilles bursa, the soft tissue medial to the first metatarsal head, the malleoli, the distal toes, and the tarsometatarsal joints. Ulcers often are found at the curve of the first and fifth metatarsal heads. Approximately one third of diabetic foot ulcers are neuropathic, one third are ischemic, and one third are mixed. Neuropathic ulcers are more likely to be under the metatarsal head with thick hyperkeratosis, whereas ischemic ulcers have a fibrotic base without hyperkeratosis. “Charcot foot” is a term indicating foot collapse, with flattening of the arch, osseous destruction, bone formation, and subluxation/ dislocation. Osteomyelitis is an important consequence of foot ulcers and skin or soft-tissue infection. A tract from ulcer to bone is sometimes found.

Clinically, differential diagnosis includes superimposed or associated infection. When there is extensive involvement of all midtarsal joints and pathologic fractures, the cause is likely to be neuropathic involvement.¹⁴¹ Soft-tissue changes in diabetes mellitus include subaponeurotic edema, cellulitis, abscess, sinus tracts, ulcers, and tenosynovitis (acute and chronic). When there is central compartment fluid in the foot, it may be associated with infections affecting the second through fourth metatarsal heads. Medial or lateral dissections may also be associated with the central compartment and corresponding medial or lateral compartment fluid collections, respectively.¹⁵⁵

Etiology, Pathology, and Clinical Features

It is important to remember that foot ulcers can have a multifactorial etiology, including neuropathy (sensory and autonomic), peripheral arterial occlusive disease, structural deformities, and joint mobility limitations. Sensory neuropathy, possibly attributable to sorbitol accumulation and glycosylation of proteins, is responsible for many diabetic foot complications. Motor neuropathy may cause intrinsic muscle atrophy, weakness, and foot deformity. Charcot neuroarthropathy is a combined motor and autonomic process. Arteriosclerotic disease, a major complication in diabetes, causes lower extremity ischemia, and biomechanical disorders cause a decreased range of motion and tightness of the gastrocnemius—soleus complex.

FIGURE 5.366 ● Osteomyelitis of the distal phalanx of the hallus in a diabetic. There is involvement of the periosteum, cortex, marrow, and cancellous bone. (A) Axial T1-weighted image. (B) Axial FS PD FSE image.

Diabetic foot ulcers (Fig. 5.366) may affect the plantar surface of the forefoot or the midfoot, and midfoot ulcers may be associated with claw toes and Charcot's neuropathy. Posterior heel ulcers are often related to heel pressure, and ulcers affecting the sides and dorsum of the foot are often related to footwear. Charcot joint (Fig. 5.367) is characterized by fracture, subluxation, dislocation, resorption, and new bone formation.

Microscopic findings in ulcers include the presence of platelets, cytokines, neutrophils, granulocytes, and lymphocytes. There may be associated chemotactic fractures, fibro-blastic and endothelial cell migration, and failure of wound remodeling. Microscopic features of Charcot neuroarthropathy include osseous resorption and new bone formation in neuropathic joints and detritic synovitis with cartilaginous and osseous debris.

The typical presentation in diabetic foot ulcer is a nonhealed plantar ulcer with sinus tracts, abscess, and bone or joint involvement. In Charcot joint there is painless swelling and erythema of the foot and ankle and fragmentation or dislocation.

FIGURE 5.367 ● (A) Acute neuropathic osteoarthropathy with edema of multiple regional joints without contiguous soft-tissue signal intensity changes. Lateral color illustration. Sagittal T1-weighted (B) and FS PD FSE (C) images show chronic neuropathic disease with deformity and fragmentation of the navicular and advanced talonavicular arthritis. The hyperintense changes of the talus and navicular are not associated with infection.

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Classification

Diabetic foot ulcers are classified according to their depth and the degree of ischemia. Charcot joint is classified according to the stage of development:

Stage I: An acute inflammatory process
Stage II: A reparative process
Stage III: Consolidation stage of healing

MR Appearance

Morrison et al.¹⁵⁶ reported that MR studies were useful and cost-effective in the evaluation of osteomyelitis in the feet of diabetics. Sensitivity and specificity for the diagnosis of osteomyelitis were 82% and 80%, respectively, in nondiabetics and 89% and 94%, respectively, in diabetics. MR imaging also improved delineation of the extent of infection, allowing limited surgical resection. MR accuracy increases with FS intravenous contrast-enhanced studies. Since intravenous MR contrast may demonstrate enhancement in both osteomyelitis and neuropathic joints, it is important to identify other findings associated with osteomyelitis, including cortical interruption, a rim-enhancing abscess within the marrow cavity, a sequestrum, an osseous to skin sinus tract extension, or cellulitis adjacent to an osseous erosion or abnormality. Osteomyelitis-related bone changes may be in direct communication with an open ulcer, decreasing the likelihood of a focal neuropathic process. In reflex sympathetic dystrophy, the marrow signal alteration is more periarticular. STIR contrast is required to demonstrate any significant marrow hyperintensity.¹⁵⁷

Yuh et al.¹⁵⁸ studied osteomyelitis in diabetic patients and reported a higher sensitivity and specificity with MR imaging than with 99mTC-MDP bone scans. Wang et al.¹⁵⁹ compared MR findings using T1-weighted and STIR images with histologic reports and found MR imaging to have a sensitivity rate of 99%, a specificity rate of 81%, and an accuracy rate of 94%. Chemical-shift imaging may be used to assess the water content of the sural nerve, a technique that may help to identify patients with acute neuropathic changes.¹⁶⁰

MR imaging is also sensitive to underlying marrow hyperemia in the ankle, subtalar, midtarsal, and MTP joints. Areas that demonstrate diffuse or patchy low signal intensity on T1-weighted images show increased signal intensity on T2-weighted, T2*-weighted, FS PD FSE, and STIR images. Early destructive changes, such as periarticular fractures and associated soft-tissue reactions, are frequently detected with MR imaging.¹⁶¹

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Collapse of the midmetatarsus along the weight-bearing axis of the foot is commonly seen as a deformity associated with neuroarthropathy. A more localized region or focus of increased subchondral or medullary signal intensity may be associated with osteomyelitis.

Characteristic MR features include:

Hypointense to intermediate-signal pressure lesion or ulcer
The ulcer may have a necrotic cystic center.
Effacement of the subcutaneous fat or fat plane
Replacement of fat marrow in neuropathic arthropathy
Neuropathic changes in the MTP, tarsometatarsal, and intertarsal joints
A periosteal reaction and cortical destruction in osteomyelitis or neuropathic foot
Muscle atrophy with fat signal intensity in neuropathic foot
Cellulitis
Thick-walled abscess with central necrosis
Neuropathic and osteomyelitis changes are hyperintense on FS PD FSE or STIR images.
Osteomyelitis superimposed over neuropathic change produces a focal area of greatest hyperintensity.
Soft-tissue tract from skin ulcer to bone and osseous erosion and marrow edema in osteomyelitis (Fig. 5.368)
Joint abnormalities including fragmentation and resorption associated with neuropathic changes
Reactive marrow edema in area adjacent to soft-tissue inflammation
Associated diabetic muscle infarction (Fig. 5.369)
Hyperintensity on T2* GRE images in osteomyelitis versus neuropathic marrow, which is not hyperintense
Abscess enhances along peripheral wall after contrast administration.
Enhancement may be present in both neuropathy and osteomyelitis.
A larger area of diffuse enhancement in cellulitis

FIGURE 5.368 ● Osteomyelitis of the navicular is hypointense on axial T1-weighted image (A) and hyperintense on FS PD FSE image (B). The osteomyelitis coexists with adjacent neuropathic changes. A draining ulcer is located adjacent to the navicular. The navicular marrow demonstrates greater hyperintensity than surrounding neuropathic change.

Treatment

Without treatment diabetic foot ulcers are at risk for infection (leading to spontaneous drainage, erythema, cellulitis, lymphadenitis, and osteomyelitis) and Charcot neuroarthropathy will become a fixed deformity. Conservative measures in the management of ulcers are bed rest, orthotics, casting, cast boots, crutches, and a walker or wheelchair. For Charcot neuroarthropathy initial measures are non—weight-bearing, casting, and an orthotic walker (total contact cast). Surgical management of ulcers includes débridement and off-loading. Surgery for Charcot neuroarthropathy includes exostosectomy, arthrodesis, ORIF, reconstruction, and fusion.

Because of decreased vascular supply, the treatment of diabetic foot problems is challenging and complications are not uncommon. Ulcers and osteomyelitis may result in a polymicrobial infection that leads to amputation, and surgery for Charcot joint is associated with prolonged healing times.

FIGURE 5.369 ● Diabetic muscle infarction with hyperintensity of the medial head of the gastrocnemius muscle on axial FS PD FSE image.

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Infection/Osteomyelitis

Early detection and treatment of osteomyelitis and joint sepsis are critical in preserving joint function before cartilage breakdown and local or hematogenous spread occur.¹⁶²^,¹⁶³ Changes on conventional radiographs are frequently nonspecific, with effusion (i.e., capsular distention) or disruption of soft-tissue planes as the only findings. Often there is no evidence of cortical destruction until marrow involvement is extensive, possibly up to 10 to 14 days after initial infection.

MR imaging is helpful in the early detection of musculoskeletal infections. The ability to detect skip lesions, to obtain high soft-tissue contrast in a multiplanar format, and to evaluate marrow, cartilage, and cortex separately is useful in detecting and monitoring infection targeting the foot and ankle.

Infection causes an alteration in the ratio of free water to bound water that prolongs T1 and T2 tissue relaxation times. As a result, infected areas demonstrate low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. Although this provides the basis for diagnostic sensitivity, neoplastic tissues undergo similar TI and T2 relaxation changes. Therefore, secondary characteristics such as the location, distribution, extent, and morphology of signal intensity assume an important role in improving diagnostic specificity.

Osteomyelitis has been studied in the calcaneus (Fig. 5.370), the cuboid, the metatarsals, and the distal tibia and fibula.¹⁶⁴ Infectious soft-tissue and osseous involvement is successfully identified using a combination of T1-, T2- (FS PD FSE), T2*-weighted, and STIR protocols.¹⁶⁵ FS contrast-enhanced MR imaging is significantly more sensitive than scintigraphy and more specific than nonenhanced MR imaging in the diagnosis of osteomyelitis.¹⁶⁶ Osteomyelitis of the talus is frequently in the differential diagnosis of limping in children.¹⁶⁷

The following features are characteristically seen:

Early osteomyelitis (see also the discussion on the neuropathic foot in diabetes) is hypointense on T1-weighted images and hyperintense on T2, FS PD FSE, or STIR images.
On FS PD FSE sequences in the acute or subacute phase, a diffuse or patchy increase of signal intensity in the medullary bone indicates marrow involvement.
Primary signs of osteomyelitis include osseous erosion with a soft-tissue mass (Fig. 5.371) and a sinus tract or adjacent abscess.
A soft-tissue hemangioma may mimic soft-tissue infection; however, adjacent osseous marrow fat signal is preserved.
A peripheral rim of low signal intensity, representing reactive bone, may demarcate the focus over time.
Alterations in signal intensity may also be seen at sites of cortical transgression, periosteal reaction, soft-tissue masses, and sequestra.
Staphylococcal osteomyelitis of the distal tibial metaphysis may present with a stellate pattern of signal change that mimics the MR appearance of a stress fracture. On FS PD FSE images, infected material in serpiginous tracts is seen as linear segments of high signal intensity.
MR imaging defines the metaphyseal-equivalent locations of the talus at risk for infection both proximally and distally (Fig. 5.372). FS PD FSE or STIR techniques are required to increase sensitivity for areas that are adjacent to cartilage and that border the physeal plates, areas commonly involved in hematogenous osteomyelitis.

Reflex Sympathetic Dystrophy

Pearls and Pitfalls

Reflex Sympathetic Dystrophy

New terminology is complex regional pain syndrome (CRPS).
Type I CRPS replaces the term sympathic dystrophy (pain related to a noxious event or immobilization).
Type II CRPS replaces the term causalgia (pain related to nerve injury, but not necessarily limited to the distribution of the injured nerve).
Osteoporosis and CRPS may demonstrate similar patchy marrow patterns of hypointensity on T1-weighted images and hyperintensity on FS PD FSE images.

Reflex sympathetic dystrophy (RSD) is an incompletely understood response of the body to an external stimulus, resulting in pain that usually is nonanatomic and disproportionate to

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the inciting event or expected healing response. The incidence of RSD following trauma is difficult to estimate.

FIGURE 5.370 ● Calcaneal osteomyelitis with an interosseous abscess, cortical erosion, and direct communication with a sinus tract communicating to the skin. (A) Axial T1-weighted image. (B) Axial FS PD FSE image.

The term complex regional pain syndrome (CRPS) has been introduced to encompass a variety of chronic pain syndromes. All sympathetically maintained pain syndromes, however, may not be RSD, and officially RSD is now known as CRPS, which is divided into two types. Type 1 is diagnosed when there are symptoms but no identifiable nerve injury. Type 2 can be traced to an identifiable nerve injury.

Symptomatically, RSD is a condition of the extremities, known and most easily identified when it affects the upper extremity, predominantly in a regional distribution involving the distal forearm, wrist, and hand, and occasionally the arm and shoulder. No pathophysiologic mechanism has been established, although several, including overactivity of the efferent sympathetic nervous system and/or abnormal activity involving spinal internuncial neurons, peripheral nociceptors, and/or mechanoreceptors, have been postulated.

The key feature is pain, which is often the initial presenting symptom. In most cases recovery is spontaneous, but the mainstay of treatment is pain relief and physiotherapy. Various clinical classification schemes have been proposed that relate stages of disease to signs and symptoms and the time elapsed since the inciting event. One example of staging by Rosenthal and Wortmann is as follows:¹⁶⁸

Stage 1: Stage 1 has a duration of weeks to months. The limb has nonfocal pain, swelling with associated joint stiffness and decreased range of motion, and increased skin temperature.
Stage 2: Stage 2 has a duration of 3 to 6 months. Pain continues but decreases over time. Swelling evolves into thickening of the dermis and fascia. Early signs of atrophy and osteoporosis become evident, and the extremity becomes cooler.
Stage 3: Stage 3 is the atrophic stage. Pain continues and atrophy is exacerbated by continued decreased range of motion and increased joint stiffness. The extremity is cooler, with decreased vascularity.

MR Appearance

MR imaging using FS PD-weighted sequences, FS contrast-enhanced sequences, and STIR images have increased the sensitivity for detecting soft-tissue and osseous (Fig. 5.373) abnormalities in RSD. Schweitzer et al.¹⁶⁹ have demonstrated the following changes:

Skin thickening and the presence of soft-tissue edema in stage I RSD
Skin thickening and thinning without soft-tissue edema in stage II RSD
Muscle atrophy in stage III RSD

We have used STIR and FS PD FSE sequences as primary techniques for identification of subchondral hyperemia in either a subarticular distribution or in a more atypical diffuse punctate pattern of hyperintensity. This corresponds to CT changes of osteopenia and focal lucencies. T1-weighted and conventional T2- and T2*-weighted techniques may not be sensitive to the bone marrow edema of RSD.

FIGURE 5.371 ● (A) Metatarsal osteomyelitis with medullary and soft-tissue extension in a diabetic foot. Lateral color illustration. (B –D) Fourth metatarsal osteomyelitis with plantar surface forefoot ulcer. Soft-tissue hyperintense hemangioma with associated marrow signal changes may be mistaken for infection. (B) Sagittal T1-weighted image. (C) Axial FS PD FSE image. (D) Coronal FS PD FSE image.

FIGURE 5.372 ● (A) Osteomyelitis with hematogenous spread to the talus. Lateral color illustration. (B, C) Osteomyelitis of the left talus with involved metaphyseal-equivalent locations (arrows) of the talus. There is hypointense signal intensity on T1-weighted sagittal images (B) and hyperintense signal intensity on STIR sagittal images (C).

FIGURE 5.373 ● Complex regional pain syndrome (reflex sympathetic dystrophy) with patchy marrow hypointensity in subarticular areas on T1-weighted image (A) and patchy hyperintensity on FS PD FSE image (B). Disuse osteopenia (osteoporosis) may mimic MR findings of complex regional pain syndrome. Diffuse hyperemia is also common in the pediatric age group. Follow-up MR studies are helpful in documenting the return of normal marrow homogeneity. (C) Coronal FS PD FSE image. (D) Coronal CT image.

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Arthritis

MR imaging of ankle arthritis is primarily used in the evaluation of osteoarthritis (Fig. 5.374) (including posttraumatic arthritis), rheumatoid arthritis (Fig. 5.375),¹⁷⁰ and infectious and hemophiliac arthropathies.¹⁷¹

Osteoarthritis

In osteoarthritis, including cases of posttraumatic etiology, thinning of the tibiotalar and subtalar hyaline cartilage surfaces can be appreciated on coronal and sagittal T1-weighted images. Identification of loose bodies may require FS PD FSE imaging to create contrast with the surrounding synovial fluid, which demonstrates high signal intensity on FS PD FSE sequences. Osteophytic spurs with marrow contents are seen as areas of bright signal intensity, isointense with fat, with a cortical rim of low signal intensity (i.e., anterior tibial border). Cortical and subchondral irregularities can be seen in association with denuded articular cartilage. A calcaneal enthesophyte and adjacent subchondral marrow edema may be seen in the seronegative arthritides (Fig. 5.376).

FIGURE 5.374 ● Anterior tibiotalar joint loose bodies on sagittal FS PD FSE image.

FIGURE 5.375 ● Talonavicular hyperemia with diffuse joint space narrowing in midfoot involvement of rheumatoid arthritis. Sagittal FS PD FSE image.

The presence of an acute or chronic joint effusion of low signal intensity on T1-weighted images can also be determined with MR scans. Subchondral or juxta-articular cysts, which possess gelatinous synovial fluid, demonstrate increased signal intensity with progressive T2-weighting. MR imaging is particularly useful in assessing subtalar joint arthrosis (Fig. 5.377), displaying the anterior, middle, and posterior facets separately. Subchondral and metaphyseal infarcts may coexist with joint space narrowing and arthrosis. STIR images are more sensitive than T2*-weighted images in documenting subchondral fluid through fissured articular cartilage. We have not routinely used MR imaging to document uncomplicated osteoarthritis or hallux valgus.

Degenerative arthritis of the tibiotalar joint is usually secondary to a fracture or trauma to the ankle joint. Joint space narrowing with chondral loss, subchondral sclerosis, and loose bodies may be identified on MR examination. End-stage ankle arthritis is treated with arthrodesis.

Degenerative hindfoot changes include arthrosis of the subtalar joints, the talonavicular joint, and the calcaneocuboid joint. Primary, or more commonly secondary (related to trauma), osteoarthritis can affect these articulations in association with or independently of tibiotalar joint disease. Loss of subtalar joint motion and lateral impingement against the fibula may develop. The posterior facet of the subtalar joint is a common location for both subchondral sclerosis and cystic change.

Midfoot arthrosis of the tarsometatarsal articulation is either primary or secondary to a Lisfranc fracture-dislocation.

Hemophilic arthropathy is indicated by low-signal-intensity synovial hypertrophy with paramagnetic hemosiderin deposits. On GRE images, hyaline cartilage demonstrates high signal intensity, permitting identification of subtle cartilage irregularities.¹⁷¹

FIGURE 5.376 ● Seronegative arthritis with a painful heel correlated with a calcaneal enthesophyte (straight arrow). The band-like region of marrow edema (curved arrow) is hypointense on the T1-weighted sagittal image (A) and hyperintense on the FS PD FSE sagittal image (B).

FIGURE 5.377 ● Degenerative subchondral cyst involving the anterior aspect of the posterior facet of the subtalar joint on (A) T1-weighted sagittal image and (B) FS PD FSE sagittal image. The cyst and adjacent marrow are hyperintense on the FS PD FSE (B). Patient also has a tibiotalar joint effusion with capsular distention and synovitis.

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Rheumatoid Arthritis

The forefoot is more frequently involved than the hindfoot in rheumatoid arthritis. The typical progression of rheumatoid involvement of the ankle shows forefoot involvement first, followed by the midtarsal joints and the hindfoot last. The talo-navicular joint is affected most frequently and demonstrates joint space narrowing with subchondral hyperintensity on FS PD FSE images. The subtalar joint is affected with the greatest severity, and patients may develop a valgus deformity related to soft-tissue laxity.

Miscellaneous Arthropathies (Sarcoid and Sickle Cell)

Sarcoidosis-related joint disease (Fig. 5.378) may demonstrate areas of synovial inflammation, tenosynovitis, tendinosis, and bursal inflammatory change. There is intermediate to hyperintense signal on FS PD FSE images, with a granulomatous or lobulated morphology. Osseous lesions and/or cystic erosions (adjacent to areas of soft-tissue involvement) may be demonstrated. Soft-tissue involvement may be extensive or limited to a single joint.

In sickle cell disease (Fig. 5.379), marrow is visualized with hypointensity on T1- or PD-weighted images and prominent red marrow (red marrow reconversion) signal in the diaphysis and metaphysis of the tibia and posterior calcaneus. Bone infarcts or acute hematogenous osteomyelitis may produce acute bone pain in patients with sickle cell disease. The red marrow prominence in sickle cell disease should not be mistaken for the marrow edema seen in inflammatory arthritis.

FIGURE 5.378 ● Distal metatarsal erosion and hypointense soft-tissue mass in sarcoid arthropathy of the second MTP joint. Axial FS PD FSE image.

Ganglia of the Foot and Ankle

Ganglia, small swellings that may appear near any joint or tendon, are most commonly seen in women and are rare over the age of 50 years. Each ganglion cyst is surrounded by a fibrous capsule attached to the deep tissues. The microscopic appearance is conspicuous for the absence of inflammatory cells, lack of mitotic activity, and lack of a synovial or epithelial lining of the single or multiloculated cysts. These cyst walls are composed of compressed collagen fibers and occasional flattened cells. The wall of the synovial cyst is formed by fibrous tissue and contains amorphous, often myxoid, material.

Ganglia may appear either gradually or suddenly, and they occasionally develop after an injury. A change in size is common. They are thought to arise because of a tiny hole in the lining of joints or the sheaths that surround tendons. Sometimes this is caused by an injury. The tissue inside the joint or sheath pokes through this hole to form the ganglion. A number of cysts may develop through a single hole. Once the ganglion has formed, the channel between the joint and the ganglion usually disappears.

The most common sites of involvement are the dorsolateral aspect of the foot, where ganglia may cause sinus tarsi syndrome, and at the distal interphalangeal joints in association with arthritis. They may also be found in the tarsal tunnel, where they are a cause of tarsal tunnel syndrome, and a few are related to the great toe. They have also been known to compress the common peroneal nerve, leading to foot drop.

MR imaging is an excellent tool for evaluating suspected ganglia about the foot and ankle, which appear as cystic defects in bone. Ganglion cysts arise from tendon sheaths, the tibiotalar joint, or the subtalar joints (Fig. 5.380). They may or may not be septated, and they demonstrate uniform low signal intensity on T1-weighted images and high signal intensity on FS PD FSE, T2*, and STIR images. Posterior subtalar joint ganglions may be mistaken for effusion with capsular distention.

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Giant cell tumor of the tendon sheath about the ankle appears as a heterogeneous mass on GRE images, with low-signal-intensity hemosiderin deposits. The intense vascularity of these lesions may demonstrate enhancement on dynamic perfusion imaging with a MR paramagnetic contrast agent.¹⁷² A medial malleolus adventitial bursa may mimic the morphology and signal intensity of a ganglion (Fig. 5.381). These bursa are associated with figure skating and skiing, which produce direct irritation over the malleolar prominences.

FIGURE 5.379 ● Red marrow conversion in sickle cell anemia. Note that the red marrow of the tibia does not extend to the physeal line. (A) Sagittal T1-weighted image. (B) Sagittal FS PD FSE image.

FIGURE 5.380 ● Fluid-filled ganglion originating from the calcaneocuboid articulation is hypointense on a coronal T1-weighted image (A) and hyperintense on corresponding FS PD FSE image (B).

FIGURE 5.381 ● (A) The medial malleolar subcutaneous bursa superficial to the tibialis posterior and deep to the skin. This bursa is located posterior to the inferior extensor retinaculum and superior to the flexor retinaculum. Lateral color illustration with axial insert. (B) Discrete medial malleolar subcutaneous bursa intermediate in signal intensity on axial PD FSE image.

If there is neither pain nor any other symptom, then treatment is usually unnecessary. Traditionally, ganglia were burst by hitting them with a heavy object, usually the family Bible. Today, if they do not resolve spontaneously they can be removed surgically.

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