The spring ligament complex (plantar calcaneonavicular ligaments) supports the head of the talus and stabilizes the longitudinal arch of the foot. Its components include the superomedial, inferoplantar longitudinal, and medioplantar oblique calcaneonavicular ligaments (14).
The major tendons about the ankle include the Achilles tendon posteriorly, the tibialis posterior, flexor hallicus longus, and flexor digitorum longus medially, the peroneus longus and brevis laterally, and the tibialis anterior, extensor hallicus longus, extensor digitorum longus, and peroneus tertius anteriorly. The tendons either are surrounded by fluid in a sheath or a peritenon (Achilles tendon).
The Achilles tendon is composed of the soleus and gastrocnemius tendons and is separated from the ankle joint by the pre-Achilles fat. As the Achilles tendon descends, its fibers rotate nearly 90° laterally with the soleus fibers located medially and the gastrocnemius contribution located laterally (24). The plantaris muscle originates from the lateral supracondylar line of the femur just superior to the origin of the lateral head of the gastrocnemius (7) and courses obliquely in a medial direction down the leg between the soleus and gastrocnemius muscles. It inserts on either the medial aspect of the distal Achilles tendon or medial aspect of the calcaneus.
Rather than being surrounded by a tendon sheath, the Achilles is surrounded by loose connective tissue termed a peritenon. This peritenon can be seen on magnetic resonance imaging (MRI) as an intermediate signal that encases the medial, posterior, and lateral aspects of the Achilles tendon (24).
The tibialis posterior tendon enters the foot passing deep to the flexor retinaculum and superficial to the deltoid ligament. The tibialis posterior tendon divides approximately 1.5 to 2 cm proximal to the navicular bone into an anterior, middle, and posterior component. The anterior component is a direct continuation of the main tendon that inserts onto the navicular tuberosity and medial cuneiform. The middle component inserts onto the intermediate and lateral cuneiforms, cuboid, and bases of the second, third, and fourth metatarsals. This component provides the origin of the flexor hallicus brevis muscle and also sends a slip to the crossing peroneus longus tendon near the base of the first metatarsal (22). The posterior component attaches onto the anterior aspect of the sustentaculum tali.
The flexor hallicus longus tendon descends into the foot passing inferior to the sustentaculum tali.
The imaging evaluation of sports-related injuries of the ankle should begin with plain radiographs. A proper ankle radiograph series includes weightbearing (if possible) anteroposterior (AP), lateral, and oblique (mortise) views. Computed tomography (CT) can be obtained to further evaluate a possible plain radiographic occult fracture, further delineation of complex fractures in treatment planning, for tarsal coalition, to assess fracture healing, or to evaluate hardware complications. CT imaging should be obtained with patient supine and the foot between neutral and 20° plantar flexion (8). Axial images should be obtained with at least 3-mm collimation.
MRI is the powerhouse of imaging when it comes to sports related injuries of the ankle. MRI should be obtained with the use of anatomy-specific and pathology-sensitive sequences (37). Sequences that are optimized for anatomy include T1-weighted or proton density-weighted. Sequences optimized for evaluating pathology include either T2-weighted with fat suppression or short tau inversion recovery (STIR). Although it is important to include a combination of both anatomy- and pathology-specific sequences, the particular imaging planes with which each are acquired varies between institutions.
Indirect magnetic resonance (MR) arthrography with the use of intravenous contrast rarely is used but may be helpful in postoperative cases or for better delineation of tenosynovitis or synovitis about the joints or bursa. Direct MR arthrography with intraarticular injection of contrast sometimes can be useful in the evaluation of osteochondral injury and suspected intraarticular bodies (6).
With the advent of higher-frequency transducers and technical advances, the role of ultrasound in the evaluation of ankle pathology is increasing. Advantages of ultrasound include its ability to image during dynamic maneuvers, availability of contralateral comparison, and ability to be used in patients who cannot undergo MR (those who have pacemakers, certain hardware, or claustrophobia). Further advantages include the use of Doppler, its flexibility of use in guided procedures, and ability to correlate with the site of pain in real time (9). In addition, ultrasound is not limited to three orthogonal planes as is MRI. A major disadvantage of musculoskeletal ultrasound is its unique reliance on the skill and experience of the operator, which can limit severely its diagnostic capacity.
In general, acute ligament sprains about the ankle manifest with prominent overlying soft-tissue edema. The key to diagnosing acute sprains on MR is identifying edema about the ligament. In chronic injury, the ligament may be thickened, but there should not be edema around the ligament (Fig. 4).
In the first week after injury, blood products (hematoma) may be present in the soft tissues, joints, and tendon sheaths, depicted as increased T1-weighted signal on MR. After 1 to 2 wk, the ligament often thickens or, if completely torn, it can scar down to the surrounding fascia appearing thickened but intact. At more than 2 months, the sprained ligament can appear absent, thickened, or normal (20). Potential sources of continued ankle pain after sprain include osteoarthritis, tenosynovitis or stenosing tenosynovitis, osteochondral injury, ankle instability, scarring within joint recesses (impingement), or scarring in the sinus tarsi or tarsal tunnel.
Medial Ligament Injuries
The medial collateral ligament (MCL) complex is an important stabilizer against valgus stress, anterior and lateral talar translation, and rotatory forces (19). The intimate association of the tibiospring, tibionavicular, and spring ligament support the talar head and the anterior subtalar joint (talocalcaneonavicular). Injuries of the MCL complex may lead to chronic instability and osteoarthrosis (23).
Injuries of the MCL complex account for approximately 15% of traumatic ligament ankle injuries (19). The most commonly injured medial ankle ligaments are the tibionavicular and tibiospring. Isolated MCL complex injuries are rare; rather, MCL complex injuries usually occur in association with lateral ligament injuries, syndesmotic ligament injury, and/or malleolar fractures (28).
On MRI, not all components of the MCL complex routinely are seen. However, the posterior portion of the deep deltoid ligament and the tibiospring portion of the superficial deltoid routinely are visualized (19). Portions of the MCL complex can have a variable appearance on MR, but the posterior portion of the deep deltoid usually is striated due to interposed fatty tissue (19). The absence of such striation with increased signal intensity is indicative of ligament injury. Medial ligament injury itself manifests as edema and discontinuity of the ligament fibers with overlying medial subcutaneous edema (20).
Lateral Ligament Injuries
The lateral collateral ligament complex is involved in 85% of ankle sprains with ATFL the most frequently injured lateral ankle ligament (31). With injury to the ATFL, the CF ligament is next at risk. The PTFL uncommonly is torn. Fluid tracking cephalad on coronal fluid-sensitive sequences suggests ATFL tear, while caudal extension of fluid suggests CF disruption (37). Fluid extending into the peroneal tendon sheath also is associated with tears of the CF ligament (20).
Tibiofibular syndesmotic ligament injury, often termed "high ankle sprain," can be difficult to diagnose on MRI. Axial images are the most beneficial with secondary signs including strain of the adjacent flexor hallicus longus muscle posterior to the syndesmosis (37). The anterior tibiofibular is the most commonly injured syndesmotic ligament in isolation.
Traumatic disruption of the spring ligament complex is uncommon. However, it has been reported to result in talonavicular dislocation with direct impaction between the talus and cuboid (14).
In the hands of a skilled operator, ultrasound imaging of ankle ligament injury can be advantageous. With ultrasound, mild ligament sprains show loss of the normal fibrillar architecture or ligament thickening. Discontinuous ligament fibers that remain taut with dynamic maneuvers are likely partially torn whereas complete tears on ultrasound are lax with any dynamic maneuver (9). Chronic tears show thickening and sometimes calcification.
Tendon injury often is due to chronic repetitive overuse injury or less commonly, acute injury. Altered biomechanics related to injury elsewhere in the ankle also may place additional stress on tendons. Complicating factors that can predispose to tendon injury and pathology include diabetes, gout, chronic renal failure, obesity, steroid, or fluoroquinolone use (20).
Many tendon sheaths about the ankle demonstrate a small amount of physiologic tenosynovial fluid. The flexor hallicus longus sheath can have a large amount of tenosynovial fluid as it normally communicates with the tibiotalar joint. The peroneal tendons, posterior tibialis tendon, and flexor digitorum longus can have a normal, small amount of fluid in their sheaths. More fluid than tendon is concerning for tenosynovitis (20).
Tendons that do not normally exhibit tenosynovial fluid include the anterior tendons and the Achilles tendon. As previously mentioned, the Achilles tendon does not possess a tendon sheath; rather, it is surrounded by a peritenon. Fluid about the Achilles tendon should be termed paratendinitis or peritendinitis, depending on where the fluid is located.
Injury of the peroneal tendons is a common cause of lateral ankle pain. Ankle inversion injuries and lateral malleolar fractures can lead to peroneal tenosynovitis. This also may occur in athletes who resume activity after a layoff or in ballet dancers who stand in half pointe (35).
Longitudinal tears (split tears) of the peroneal brevis commonly are encountered in young athletes. Several factors can predispose to peroneal brevis tears. These include thickening of the CF ligament, crowding in the retromalleolar groove by a peroneus quartus or low-lying peroneal brevis muscle, retromallolar groove bone irregularity, or superior peroneal retinacular insufficiency (35).
A torn peroneal brevis tendon assumes a C-shaped configuration on axial MRI or transverse ultrasound images with the central portion of the tendon markedly thinned, and the two split limbs of the tendon lying on either side of the peroneal longus tendon. Tendon thickening or increased intermediate signal in the tendon is consistent with tendinosis, while fluid signal within the tendon or nonvisualization of portions of the tendon are MR findings concerning for a tear.
Peroneal longus tears are seen in up to one third of cases that have peroneal brevis tears (35). Secondary findings of peroneal longus tendon pathology include marrow edema within a hypertrophied peroneal tubercle (Fig. 5) or marrow edema along the cuboid in the region of the cuboid tunnel.
The posterior tibialis tendon plays a major role in stabilizing the medial arch and contributing to proper hindfoot alignment. It should be twice the size of the flexor digitorum longus on axial MRI. Pathology of the posterior tibialis tendon can present as tendon thickening with intermediate signal consistent with tendinosis, focal fluid signal consistent with partial tearing, or tendon thinning or atrophy. The posterior tibialis tendon most often fails at the level of the medial malleolus (2) (Fig. 6).
Progressive pathology of the tibialis posterior tendon with resulting dysfunction can lead to pes planus, hindfoot valgus, and collapse of the medial longitudinal arch. In fact, posterior tibialis tendon tear is the most common cause of acquired pes planus. In a study by Balen and Helms, a high association was found between advanced tibialis posterior tendon injury and abnormalities of the spring ligament and ligaments of the sinus tarsi (2). A lower association was found in this study between posterior tibial tendon injury and plantar fascia abnormalities.
The Achilles tendon is the most commonly injured tendon in sporting activities. Because it lacks a tendon sheath, inflammation seen in a semicircumferential manner about the lateral, medial, and posterior aspects of the tendon should be termed peritendinitis as this distribution involves the peritenon. If inflammation involves the soft tissues around the tendon in the pre-Achilles fat, in particular, this should be termed paratendinitis. These terms often are interchanged in the literature, so description of the imaging findings is crucial.
Hypoxic degeneration of the Achilles tendon itself is termed tendinosis and usually occurs 2 to 7 cm proximal to its calcaneal insertion (37). The tendon can be enlarged with a convex anterior border on axial images and a fusiform shape on sagittal images. Histologic examination of such tendon degeneration has failed to demonstrate a significant inflammatory component; thus the term tendinosis, rather then tendinitis, is appropriate.
Achilles tendon tears usually occur in a region of hypovascularity approximately 5 cm above its calcaneal insertion (Fig. 7). Tears manifest as fluid signal on T2 or STIR sequences. Tears can be partial or complete, and MRI exquisitely demonstrates the amount of disrupted tendon, the gap between the proximal and distal portions of a complete tear, the margins of the torn fibers, and the integrity of the proximal and distal torn fibers.
Injuries of the anterior tendons can occur in athletes involved in kicking sports (20). The anterior tibialis tendon more commonly presents as a complete tear rather than partial tear. Patients often present complaining of a mass at the anterior aspect of the ankle joint related to the torn, retracted tendon fibers (Fig. 8).
Ultrasound is a useful modality for imaging tendon injuries about the ankle. With ultrasound, tendinosis is seen as tendon thickening and loss of the normal fibrillar pattern (9). Tenosynovitis is demonstrated as increased fluid within a tendon sheath and can demonstrate hypervascularity of the synovium surrounding the tendon with the use of doppler.
Partial thickness tears show linear or globular hypoechoic areas without retraction on ultrasound (34). Complete tendon rupture demonstrates fluid, debris, or hematoma with the tendon gap of an acute tear or hypoechoic granulation or scar tissue in chronic tears. Tendon subluxation or dislocation also can be readily evaluated with dynamic ultrasound imaging, particularly the peroneal tendons with the use of dorsiflexion and eversion (9).
Bone Stress Injuries
Stress reactions and stress fractures are a response to repetitive stress in which osteoclastic activity exceeds the compensatory rate of osteoblastic new bone formation (11). Plain radiographic findings of stress injuries can be seen after 2 to 8 wk of symptoms; however, the sensitivity of plain films is as low as 10% (11). The most common plain film finding is a focal area of periosteal new bone formation. A cortical area of decreased density (grey cortex sign) also can be seen early.
When plain radiographs are negative, MRI often is the study of choice. It is highly sensitive for the detection of stress injuries with the added advantages of precise location, lack of ionizing radiation, multiplanar capability, and shorter imaging time than a three-phase bone scan. MR also can be used to grade the severity of stress injury using a four-stage grading system (10). Grade 1 demonstrates periosteal edema. Grade 2 shows additional increased T2 fat-suppressed signal, either intramedullary or endosteal. In Grade 3 injury, the signal abnormality also is present on T1-weighted images. Grade 4 injuries demonstrate the presence of a fracture line. Injuries graded 1, 2, or 3 on the basis of MR findings are termed stress reactions. Those with a fracture line (either on MR, x-ray, or CT) are diagnosed as true stress fractures.
Other imaging options include bone scans and CT. Tc 99 diphosphonate triple phase bone scan is sensitive, but nonspecific, detecting abnormality as early as 2 to 8 d after symptoms (27). All three phases are positive in acute stress fractures. CT can be used to rule out other possible causes of the patient's symptoms such as osteoid osteoma, Brodie's abscess, and neoplasm. CT is useful to elucidate a fracture line or periostitis.
In the ankle, bone stress injuries most commonly involve the calcaneus, or less often, the medial malleolus. Calcaneal stress injuries often occur subjacent to the calcaneal tuberosity or posterior subtalar joint, usually perpendicular to the trabecular lines (Fig. 9). Less commonly they involve the anterior process of the calcaneus.
Bone contusions demonstrate ill-defined low T1-weighted and high T2-weighted fat-suppressed signal on MRI. This abnormal signal is thought to be related to trabecular microfractures with edema and/or hemorrhage within the bone marrow (26). Bone contusions commonly are seen with ankle sprains, and their particular locations can provide clues to the mechanism of injury.
Osteochondral injuries can lead to detachment of an osteochondral fragment. Several terms have been used in the literature to describe this entity including osteochondral lesion, osteochondral defect, transchondral fracture, and osteochondritis dissecans. The exact etiology of osteochondritis dissecans is not known but is thought to be due to repetitive microtrauma (15). In the ankle, these lesions most often involve the talar dome. Berndt and Harty (4) classified these lesions into four stages based on the condition of the subchondral fragment and overlying cartilage. Stage I lesions are subchondral with preservation of the overlying articular cartilage. Stage II lesions demonstrate a partially detached but in situ fragment. Stage III lesions consist of a completely detached but in situ fragment. Stage IV lesions demonstrate a completely detached osteochondral fragment that is displaced.
MRI can provide detail regarding the size and location of the lesion, integrity of overlying cartilage, degree of healing at the donor site in chronic lesions, and location of a displaced fragment (26). Fluid signal between the fragment and the donor site and/or surrounding cystic change suggests instability; however, healing granulation tissue also can appear as fluid signal about a fragment simulating an unstable fragment. In such cases, MR arthrography is useful. There may be subchondral and surrounding edema, and/or cystic change, the degree of which may be related to symptoms (20) (Fig. 10). In addition, a detached but in situ fragment can rotate 180° and become inverted.
Impingement syndromes of the ankle are pathologic conditions that restrict movement at the tibiotalar joint. They are caused by osseous or soft-tissue hypertrophy, or by accessory ossification centers (13,32). Ankle impingement syndromes are classified based on their anatomic relationship to the tibiotalar joint.
Anterior impingement often is seen in ballet dancers and soccer players (13). Formation of bony prominences at the anterior aspect of the tibial plafond and dorsal aspect of the talus cause impingement within the anterior ankle joint with dorsiflexion. Such bony excrescences are thought to be either due to repetitive traction at the site of the joint capsule attachment or repetitive direct trauma. A recent anatomic study by Hayeri et al. (12) found that the talar outgrowths at the lateral aspect of the talar neck are enthesophytes, thus supporting the theory of repetitive and capsular traction on the lateral side. Alternatively, talar outgrowths on the medial part of the talar neck were osteophytes, thus supporting the theory of repetitive trauma on the medial side.
The diagnosis of anterior ankle impingement is predominately clinical. Imaging can raise the possibility of the diagnosis by demonstrating the anterior osteophytes and enthesophytes and also can exclude other causes of the chronic ankle pain.
Anterolateral ankle impingement is caused by entrapment of hypertrophied soft tissues in the anterolateral recess of the ankle joint (13). In more advanced cases, this hypertrophied soft tissue can form a connective tissue mass, historically termed a "meniscoid lesion" (36) (Fig. 11). It also may be caused by an accessory ligament or fascicle of the anteroinferior tibiofibular ligament (Bassett's ligament) (30).
On MR, thickening of the anterior talofibular ligament and soft-tissue fullness in the lateral gutter suggest the diagnosis of anterolateral impingement. The findings are more conspicuous in the setting of an ankle joint effusion. MR arthrography can be helpful to more accurately evaluate the anterolateral recess. In addition, ultrasound can be used to assess the lateral aspect of the ankle, with some studies concluding its evaluation is nonspecific (1), while others show it can accurately diagnose the anterolateral mass (18).
Anteromedial ankle impingement rarely occurs in isolation. At MRI, irregular soft-tissue thickening is demonstrated anterior to the anterior tibiotalar portion of the deep deltoid ligament. A study by Vann and Manoli (33) suggested a relatively common occurrence of medial ankle impingement in young, competitive gymnasts with intraoperative findings that included thickening of the anterior tibiotalar ligament, localized synovitis, and talar osteophytes. MRI can demonstrate irregular soft-tissue thickening anterior to the anterior tibiotalar ligament, consistent with synovitis (25).
Soft-tissue abnormality impinging between the posterior aspect of the medial malleolus and the medial talus suggests posteromedial impingement syndrome. MRI can demonstrate loss of normal fat striations within the posterior tibiotalar portion of the deep deltoid ligament, posteromedial synovitis, posteromedial joint capsule thickening, and displaced or entrapped medial tendons (13).
Posterior ankle impingement is characterized by posterior ankle pain particularly with chronic repetitive stress in plantar flexion. It commonly occurs in ballet dancers due to the en pointe plantar flexed position they often maintain. Soccer players and downhill runners also are affected often. There is impingement of soft tissue or bone abnormalities about the posterior aspect of the talus between the posterior tibia and calcaneus. Other terms that have been used to describe the constellation of the signs and symptoms of posterior ankle impingement include talar compression syndrome, posterior block, and os trigonum syndrome.
The most common cause of posterior ankle impingement is the os-trigonum-talar process (13). As mentioned previously, the posterior process of the talus projects posteromedially and is made up of a medial and lateral tubercle. The posterior talus forms from a secondary ossification center with mineralization beginning between 7 and 13 yr and fuses within the next 12 months when it then forms the lateral tubercle (13). In 14% to 25% of people, the lateral tubercle fails to fuse to the talar body, forming a separate ossicle known as the os trigonum (16). The os trigonum is bilateral in 1.4% of people. It articulates with the talar body via a cartilaginous synchondrosis. The posterior facet of the os trigonum serves as the attachment site of the posterior talofibular ligament. An elongated lateral tubercle is termed a Steida process.
Plain radiographs in posterior ankle impingement can demonstrate a Steida process or os trigonum. The size of the os trigonum has shown not to be an accurate predictor of symptoms (17). CT can better delineate a fractured lateral tubercle or separation of the synchondrosis of an os trigonum. Ultrasound also can show thickening of the posterior joint capsule.
MRI in posterior ankle impingement demonstrates posterior capsule thickening and synovial proliferation. It also can show marrow edema, fracture, fragmentation of the lateral tubercle-os trigonum, or a psuedoarthrosis (5). Involvement of the posterior malleolus and superior aspect of the calcaneus also can be seen (Fig. 12).
SINUS TARSI SYNDROME
The sinus tarsi is an anatomic space located anterior to the posterior subtalar joint between the inferior aspect of the talus and the superior aspect of the calcaneus. The sinus tarsi contains the interosseous talocalcaneal and cervical ligaments as well as the roots of the inferior extensor retinaculum, neurovascular structures, and fat. Hemorrhage or inflammation of the synovial recesses about the sinus tarsi can lead to sinus tarsi syndrome even without tears of the ligaments (26). Inversion injury, either related to chronic repetitive or acute trauma, also can tear the ligaments within the sinus tarsi, leading to progressive inflammation and subtalar instability (29).
Sinus tarsi syndrome can be associated with tears of the lateral collateral ligaments, rheumatologic disorders, tumors and masses such as ganglion cysts, and abnormal biomechanics such as posterior tibial tendon dysfunction, pes planus, and hindfoot valgus deformities. MRI features of sinus tarsi syndrome include obliteration of the normal sinus tarsi fat replaced by fluid or fibrosis, or disruption of the ligaments (3). In advanced cases, sinus tarsi syndrome may lead to osteoarthrosis of the subtalar joints.
Sports-related ankle injuries are common, and their incidence is increasing. Technological advances in imaging now provide exquisite anatomic detail with higher sensitivity for pathology. Armed with a detailed understanding of anatomy and familiarity with the imaging features of sports-related ankle injuries, one can provide accurate imaging diagnoses, leading to more efficient and successful injury management.
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