Target audience:
Clinical radiologists involved in the interpretation of ankle MRI.

Learning objectives:
- To understand the etiology of ankle impingement syndromes;
- To learn about the most common sites of ankle impingements and the anatomic structures involved;
- To understand how MR imaging findings of ankle impingement can support the clinical diagnosis.

Outline of lecture
Repetitive trauma of the ankle can lead to osseous and soft tissue changes that cause mechanical impingement, leading to chronic ankle pain and limitation of movement. Common sites of impingement in the ankle include posterior, posteromedial, anteromedial, anterolateral, and less commonly, direct anterior. Although some of the osseous changes can be seen on plain radiographs, MR imaging and MR arthrography is the best imaging modality to evaluate impingement syndromes, and rule out other potential causes of chronic ankle pain. Initial treatment is almost always conservative, and ultrasound may be helpful for guiding therapeutic steroid injections. However, if this fails, arthroscopic debridement and synovectomy may be necessary, and can improve both symptoms and range of motion.

The majority of ankle sprains are due to inversion injuries, with concomitant lateral ligamentous damage. However, in a subset of patients, repetitive microtrauma can result in hypertrophied synovial tissue and fibrosis in the anterolateral gutter, causing anterolateral ankle pain and mechanical impingement. Occasionally the hypertrophied synovium can be remodeled between the fibula and talus to form a hyalinized meniscoid lesion. Other contributory factors include hypertrophy of the inferior portion of the anteroinferior tibiofibular ligament, or an accessory fascicle termed the ligament of Bassett, and occasional bony spurs. MR findings include an abnormal soft tissue mass or fibrous band in the anterolateral gutter, in association with lateral ligamentous injury, and chondral defects of the lateral talar dome. MR arthrography can demonstrate irregularity or nodularity of the anterolateral recess, or non-filling of the recess.

Anterior ankle impingement is relatively common in athletes subjected to repetitive microtrauma of the ankle in dorsiflexion, including soccer players, runners, high jumpers, and gymnasts. A large bony spur develops on the anterior aspect of the distal tibia, often with a corresponding bone spur on the apposing surface of the dorsal talus. These are thought to develop secondary to localized damage to the articular cartilage, with associated synovitis and scarring. Impingement occurs on dorsiflexion, leading to generalized anterior ankle pain and restricted motion, and there may be a “divot” on the anterior talar neck secondary to tibial spur abutment. Although these changes can be demonstrated on plain radiographs, MR imaging is helpful for evaluation of effusion, synovitis, chondral injury and bone marrow edema.

Syndesmotic sprains occur as a result of external dorsiflexion and hyperdorsiflexion, and can lead to syndesmotic impingement. Lateral ligamentous laxity can allow the talar dome to extrude anteriorly with dorsiflexion, which then impinges upon the distal anteroinferior tibiofibular ligament (AITF), particularly if Bassett’s ligament is present. This results in synovitis and synovial nodules around the AITF ligament, chondral degeneration of the talar dome, and ossification of the interosseous membrane.

Posterior impingement syndromes occur as a result of acute or repetitive plantar flexion of the foot, for example in ballet and gymnastics. Symptoms are thought to arise secondary to repeated compression of osseous and soft tissue structures between the posterior tibial plafond and superior surface of the calcaneus, likened to a nut in a nutcracker.

Bony factors predisposing to posterior impingement include an os trigonum, prominent posterior talar process (Stieda process), downsloping of the posterior tibia, and a prominent posterior calcaneal tuberosity. Soft tissue factors include a prominent posterior labrum (transverse tibiofibular/posterior intermalleolar ligament), posterior ligamentous injury, posterior ganglion cysts, synovitis of the posterior recess of the tibiotalar or subtalar joints, and tenosynovitis of the flexor hallucis longus tendon. Patients present with recurrent posterolateral ankle pain and swelling, with limited plantar flexion.

Medial impingement syndromes are less common. Anteromedial impingement can occur secondary to an inversion injury, with tearing of the anteromedial joint capsule and anterior tibiotalar ligament. This leads to thickening of the capsule and anterior tibiotalar ligament and synovitis, which can impinge on the anteomedial corner of the talus during ankle dorsiflexion, producing chondral injury and osteophytosis. Posteromedial impingement can arise after severe inversion injuries, causing a crush injury of the deep fibers of the posterior deltoid ligament. Inadequate healing can result in fibrotic scar tissue that can impinge between the medial talus and posterior medial malleolus.