Musculotendinous Magnetic Resonance Imaging of the Ankle

Musculotendinous Magnetic Resonance Imaging of the Ankle Brian Petersen, MD,* Jeff Fitzgerald, MD,† and Ken Schreibman, MD, PhD‡

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he ankle joint withstands tremendous pressure, supporting the entire body weight with every step. Unlike the hip and knee, however, the ankle joint uncommonly degenerates. Nature has performed well in designing a joint to withstand fantastic axial pressure, facilitate motion, and resist torsional stress. Despite its ability to resist chronic degenerative change, the ankle is the most commonly injured joint, with 1 million ankle injuries estimated per year by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Imaging of the acute or chronically injured ankle was historically limited to radiography, in a search for fractures or gross ankle instability. More recently, studies have shown magnetic resonance imaging (MRI) of the ankle to significantly alter clinical care, clarifying or changing preimaging clinical diagnosis, and, in some cases, helping to avoid surgery.1 This review will concentrate on MRI of tendons and accessory muscles about the ankle. MRI ankle protocol will be discussed with attention limited to issues that affect imaging of the tendons crossing the ankle joint. Normal MRI musculotendinous anatomy, imaging features of common disorders of tendons, and pathological normal variation will all be addressed.

MRI Ankle Protocol There are many ways to perform MRI of the ankle, and different protocols can be used based on the clinical scenario. A combination of fat-suppressed T2 or proton density-weighted sequences and fast spin-echo T1 or proton density usually provides sufficient anatomical detail and fluid sensitivity to make most diagnoses. At our institution, we perform direct axial proton density and proton density fatsuppressed sequences, followed by sagittal T1 and short tau *Department of Radiology and Orthopaedics, Musculoskeletal Radiology, University of Colorado Denver, Aurora, CO. †Department of Radiology, University of Colorado Denver, Denver, CO. ‡Department of Radiology, University of Wisconsin, Madison, WI. Address reprint requests to Brian Petersen, MD, Department of Radiology and Orthopaedics, Musculoskeletal Radiology, University of Colorado Denver, Mail Stop L954, 12401 East 17th Ave, Room 1618, Aurora, CO 80045. E-mail: [email protected]

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0037-198X/10/$-see front matter © 2010 Elsevier Inc. All rights reserved. doi:10.1053/j.ro.2009.12.003

inversion-recovery (STIR) sequences and a single fat-suppressed direct coronal proton density sequence. We place our patients in supine position using a chimney foot/ankle coil, with ankle flexed, and toes toward the ceiling (Fig. 1A). Some knee coils have a defect in the superior margin that allow the toes to protrude, and these can be used to produce fine images of the ankle as well (Fig. 1B). Having the technologist mark the site of pain has improved our accuracy tremendously, as subtle findings that may be typically ignored take on more importance if they correlate to the point of maximal pain. It is important to ask the patient to “point with one finger” to the point of maximal pain. Ankle pain is commonly perceived as diffuse by the patient, but when pressed, a more focally localized pain generator can usually be pin-pointed by the patient. In evaluating ankle tendons, magic angle artifact is a common confounder. Magic angle artifact is relative high T2 signal within collagen-rich tissues. This results from the intimate relationship of water to collagen in tissues, such as tendons, ligaments, and cartilage. Typically, the dipolar interactions of water molecules within the collagen-rich tissues result in rapid dephasing and very little signal within the structures; collagen-rich structures typically appear black. In sequences with low or intermediate echo times (TE ⬍ 37),2 T2 relaxation is delayed in collagen-rich tissue at an angle of 55° to the main magnetic field. This phenomenon was originally described in MRI of the supraspinatus, mimicking supraspinatus tendinosis. It is present, however, throughout the body and is prominent within the ankle tendons as they course around the ankle joint. This can be misinterpreted as pathological tendinosis if the interpreting radiologist is unfamiliar with this pitfall. However, locations that suffer from magic angle effect—the fibular turn of the peroneal tendons and the submalleolar location of the medial flexor tendons— are also common sites of pathology as well (Fig. 2). Magic angle effect can be countered in many ways. Using long TE, T2-weighted imaging can decrease magic angle effect (40 ms with spin-echo, 70 ms with fast spin-echo, and 30 ms with gradient echo imaging). Imaging the foot in mild plantar flexion (20°) or imaging with the patient prone, causing the peroneal and medial flexor tendons to lie straight, can obviate magic angle effect as well, but can distort other

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251 degeneration (thickening, high intratendinous T2 signal) all reflect the degenerative process, but may be asymptomatic and can only suggest clinical symptoms that may correlate (emphasizing the importance of clinical history and site of pain in evaluating MRI of ankle tendons). In this review, tendinosis will be used to describe the MRI signal abnormality that correlates to tendon degeneration, be it symptomatic or asymptomatic, and allow the term “tendinopathy” to reside in the clinical realm, describing a symptomatically degenerated tendon. Tendons that require angular gliding are invested by a lubricated sheath, termed the tenosynovium. Inflammatory change can be confined to the tenosynovium and is termed tenosynovitis. Tenosynovitis can occur with or without underlying tendinosis of the tendon.

Posterior Tendons: Achilles’ Tendon, Plantaris Tendon Normal Anatomy and Appearance Achilles’ tendon is the largest tendon in the human body. It originates from the myotendinous termination of the medial and lateral heads of the gastrocnemius muscles and the soleus muscle, inserting on the posterior calcaneus. The tendon should be uniformly low signal and, given its vertical orientation, should not suffer from magic angle artifact. Magic angle artifact, however, is occasionally encountered within the substance of the tendon, given the twisting of the individual muscle fascicles within the tendon. The gastrocnemius Figure 1 (A) This dedicated foot and ankle coil incorporates a chimney-like extension (white arrow) so the phalanges can be included in the field of view. (B) A knee coil can be used to scan the ankle. The open top on this knee coil allows the toes to extend through the coil while keeping the foot in neutral position.

important anatomy. Combining fluid sensitive, fat-suppressed sequences, multiple planes, clinical history, and site of pain, diagnostic pitfalls related to magic angle effect can be avoided without significant alterations to a neutral position ankle acquisition protocol.

Terminology Any review article of tendon MRI would be remiss without a brief kick to the dead horse of tendon disease terminology. The term “tendinitis” has long since been debunked, with numerous histopathologic studies demonstrating a conspicuous absence of inflammatory cells in injured tendons. The intratendinous disease process is one of degeneration, and at least 6 different patterns of collagen degeneration have been described as follows: hypoxic, hyaline, mucoid or myxoid, fibrinoid, lipoid, and calcifying/ossifying.3 The term “tendinosis” was implemented by Puddu et al4 to describe tendon degeneration without clinical or histologic signs of inflammation. Tendinopathy is the preferred clinical term for symptomatic tendon degeneration. The MRI findings of tendon

Figure 2 Sagittal T1-weighted image in a 23-year-old man imaged for follow-up of talar osteochondral lesion, demonstrates magic angle effect with focal high signal of the peroneal brevis tendon (arrows) at the point of orientation 55° to the main magnetic field (B␪).

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B. Petersen, J. Fitzgerald, and K. Schreibman 12-16 mm in width, 3 cm above the calcaneal attachment.6 The tendon should have flat ventral and dorsal margins on sagittal images (Fig. 3B), although Achilles’ tendon can normally appear bulbous just distal to the soleus myotendinous junction. Unlike the anterior extensor, medial flexor, and lateral peroneal tendons, whose functions rely on smoothly gliding at angular vectors over osseous structures, Achilles’ tendon has inline functionality, requiring no tenosynovial sheath. Achilles’ tendon is surrounded by a thin layer of vascular fibrous tissue that provides nutrients for the tendon, called the paratenon. The paratenon is made up of a fatty, highly vascularized single cell layer of areolar tissue, perfusing the adjacent tendon through a series of perforating vessels.7 It has been suggested that a relative paucity of these perforating vessels exists from 2 to 6 cm proximal to Achilles’ tendon insertion,7-10 predisposing the tendon to rupture in this area. A more recent angiographic study did not show significant changes in vascularity across the central portion of the tendon per cross-sectional volume, as the central portion of the tendon is thinner than the proximal and distal portions. It is likely that a combination of vascular compromise and relatively less cross-sectional thickness contributes to Achilles’ tendon predisposition to rupture in this area.7 Achilles’ tendon attaches to the dorsum of the calcaneus at the calcaneal tubercle. Enthesopathy and ossific degeneration of the Achilles’ attachment is common, commonly asymptomatic, and best appreciated on sagittal T1-weighted sequence.11 The retrocalcaneal bursa is the only anatomic bursa around the ankle, and a small amount of fluid in the retrocalcaneal bursa is normal (Fig. 4). Fluid in the acquired, pathologic, retro-Achilles’ bursa is always abnormal.

Figure 3 Normal magnetic resonance imaging (MRI) appearance of Achilles’ tendon. (A) Normal axial proton density fast spin echo (PD FSE) image demonstrating slightly concave deep margin (black arrows). (B) Sagittal T1 image showing flat ventral surface (black arrows).

muscles and soleus contribute individual fascicles to Achilles’ tendon and separations between these fascicles are occasionally visible, and can mimic an interstitial tear.5 The fibers spiral in course with the medial-most fibers proximally, contributing the more posterior fibers at the attachment. In cross section, the tendon appears lentiform or comma-shaped, with a convex superficial margin and concave deep margin (Fig. 3A). In 10% of normal patients, the deep margin of Achilles’ tendon is slightly convex.6 Achilles’ tendon normally measures 5-7 mm in anteroposterior dimension and

Figure 4 A small amount of fluid is normal within the retrocalcaneal bursa (white arrow).

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Achilles’ Tendon Pathology The clinical syndrome of achillodynia is extremely common, resulting in activity limitation and pain in a broad spectrum of patient populations, from the young elite athlete to the elderly. Clinically differentiating different entities within the spectrum of disease affecting Achilles’ tendon and adjacent structures is difficult, yet clinical treatment for paratenonitis differs from that of partial tear. In a review of 118 patients with achillodynia by Karjalainen

Figure 5 (A) Axial PD FSE images showing normal location of the distal plantaris tendon (black arrow), medial to the distal Achilles’ tendon. (B) Common site of plantaris attachment (black arrow). Plantaris attachment site is somewhat variable.

The small plantaris muscle originates from the lateral meniscus and lateral femoral condyle. It rapidly converges at the myotendinous junction into the long, thin plantaris tendon, obliquely coursing deep to the medial head gastrocnemius muscle and superficial to the soleus to attach medial to Achilles’ tendon (Fig. 5). The plantaris attachment is variable, but commonly attaches to the medial calcaneal tuberosity with the Achilles’ or separately, slightly anterior and medial to the Achilles’ on the calcaneus. The plantaris tendon merges with the distal Achilles’ tendon in 20% of patients.6

Figure 6 Twenty-three years old runner with Achilles’ tendon pain. (A) Very mild paratenonitis with high signal and thickening of the paratenon (white arrows), accompanying mild Achilles’ tendinosis. Note slightly different position of the plantaris tendon in this patient compared with Fig. 5 (white arrowhead). (B) More severe paratenonitis with inflammation of Kager’s fat pad.

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B. Petersen, J. Fitzgerald, and K. Schreibman Noninsertional Tendinosis The MRI findings of Achilles’ tendinosis correlate to histologic degenerative changes within the substance of Achilles’ tendon. Hypoxic degeneration is most common and, if not isolated, combines with other forms of histologic degeneration to contribute to Achilles’ pathology. Some type of degenerative change (hypoxic ⬎ 75%) was found in all of 891 ruptured tendons in a series by Kannus and Jozsa.17 Although degenerative change is invariably the underlying pathologic process in Achilles’ tendon ruptures, partial tears are also related to histologic degeneration. The collagen fibers crosslinks

Figure 7 Sagittal T1-weighted sequence demonstrating hypoxic noninsertional Achilles’ tendinosis, in typical location, with bulbous thickening and intermediate signal within the substance of Achilles’ tendon.

et al,12 abnormal MR findings were demonstrated in 94% of cases. Imaging Achilles’ tendon with MRI has allowed specificity with regard to the varied Achilles’ pathology and is a valuable tool to guide treatment. Paratenonitis Most cases of clinically diagnosed acute Achilles’ “tendonitis” likely represent inflammation of the fibrovascular investment of the tendon—the paratenon. This manifests on MRI as a halo of high T2 signal around Achilles’ tendon (Fig. 6A). Depending on the severity of the inflammatory process, Kager’s fat pad, ventral to Achilles’ tendon, may become inflamed and demonstrate similar high T2 signal (Fig. 6B). Isolated paratenonitis is most commonly seen in a young athletic population, particularly in runners13,14; however, it has been reported with frequency in patients with rheumatoid arthritis, where it is commonly asymptomatic.15 Chronic inflammation of the paratenon results in connective tissue proliferation in, and around, the vessels of the paratenon, facilitating subsequent hypoxic degeneration of Achilles’ tendon.13,14,16 This can lead to coexistence of MRI findings of both paratenonitis and Achilles’ tendinosis. In fact, the original description of the histologic findings of paratenonitis and tendinosis by Puddu et al4 describes 3 predictable stages of Achilles’ tendon dysfunction as follows: stage 1, pure paratenonitis; stage 2, paratenonitis with tendinosis; and stage 3, tendinosis. Patients with chronic paratenonitis may have adhesions detectable with imaging, related to fibrinous exudates, and clinically manifest with crepitus as Achilles’ tendon attempts to move through the adhesive paratenon.

Figure 8 Severe mucoid degeneration. (A) Globular, near fluid signal, high T2 areas within the substance of the tendon are typical for mucoid degeneration. (B) Note adjacent paratenonitis, with high T2 signal extending into the adjacent Kager’s fat pad (black arrows).

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255 to retrocalcaneal bursitis, prominent posterior calcaneal process (Haglund’s bump), or retrocalcaneal bursitis, and commonly is a combination of all of these (Fig. 9). Insertional tendinosis is common in athletes participating in interval training and aggressive hill training.19 The retrocalcaneal bursa is the only anatomic bursa of the ankle and, when inflamed, leads to sympathetic adjacent inflammatory change of Achilles’ tendon. The normal retrocalcaneal bursa is commonly visible on MR, but is pathologic if it exceeds dimensions put forth by Bottger et al11 as 6 mm superior to inferior, 3 mm transverse, and 2 mm anteropos-

Figure 9 Achilles’ insertional tendinosis. Thickening of the distal Achilles’ tendon (white asterisk) is accompanied by retrocalcaneal bursitis (white arrow) and enthesopathic marrow edema of the calcaneal tubercle (black asterisk).

that lend strength to the tendon become brittle and break, allowing collagen fibers to crimp and slide against each other. The degenerated type-I collagen fibers can be replaced with by calcification, mucoid material, or fat.3 The MR appearance of Achilles’ tendinosis is quite broad. Thickening of the tendon with or without intrinsic high signal is likely related to isolated hypoxic degeneration, and most commonly occurs 4-6 cm proximal to the calcaneal insertion (Fig. 7). This correlates to the site of most common complete rupture and may be related to a relative hypovascularity, although this is controversial.7 Thickening of Achilles’ tendon may not be symptomatic and in a study comparing symptomatic to asymptomatic Achilles’ tendons, Haims et al found no significant statistical difference in tendon thickness,18 although those with symptoms and tendon tears had the thickest tendons. A complete tear that has subsequently healed can have a similar bulbous appearance and likely varies little in the histologic properties. Mucoid degeneration manifests on MRI as focal collections of high T2 signal material within the tendon (Fig. 8). This degenerative change is commonly asymptomatic, but can appear identical to acute interstitial/partial tear, making differentiation difficult without good history. This type of change likely accounts for the appearance of “partial tears” within asymptomatic patients; however, it has been postulated that the more intense the T2 signal within the tendon, the more likely it is to be symptomatic.18 Complete rupture of Achilles’ tendon may be the first indication of Achilles’ pathology in these patients. Insertional Tendinosis In the orthopedic literature, insertional Achilles’ tendinosis is considered a true inflammatory tendinitis. This can be related

Figure 10 A 45-year-old man clinically thought to have ruptured Achilles’ tendon. (A) Lateral radiograph demonstrating “fractured enthesophyte sign” (white arrow), large superior calcaneal tubercle (black arrow) that extends above the parallel pitch line represented by the dashed line (Haglund’s deformity), and soft tissue swelling about the insertion of Achilles’ tendon (white arrowheads). (B) Sagittal T2weighted MRI image of Haglund’s syndrome: Achilles’ insertional tendinosis (large white arrow), marrow edema of the superior calcaneal tubercle (asterisk), and retrocalcaneal bursitis (large black arrow).

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B. Petersen, J. Fitzgerald, and K. Schreibman Achilles’ and retrocalcaneal bursitis is commonly seen in Haglund’s syndrome associated with Haglund’s deformity (Fig. 10A). In Haglund’s syndrome, a large posterosuperior calcaneal tubercle is compressed within unforgiving footwear (most commonly seen in women wearing highheeled shoes—the “pump bump”) and contributes to retrocalcaneal and retro-Achilles’ bursitis as well as insertional tendinosis. The definition of Haglund’s deformity is a bursal projection of the posterosuperior calcaneus that extends above the parallel pitch line. The parallel pitch line is drawn as a plantar line tangential to the anterior calcaneal tubercle and plantar most portion of the medial tubercle of the calcaneus. A parallel line is then drawn contacting the dorsal margin of the calcaneal component of the posterior subtalar facet. Extension of the bursal calcaneal projection above this line is considered Haglund’s deformity. Although radiography is superior for measuring the parallel pitch line, MRI is commonly performed to assess the adjacent tendon for the need of intraoperative debridement concomitantly with the calcaneal osteoplasty (Fig. 10B). Insertional tendinosis is frequently associated with adjacent calcaneal marrow edema. This marrow edema was the most predictable sign of a symptomatic Achilles’ tendon in Haims’ MRI comparison of symptomatic and asymptomatic patients18 and has been shown to be a common associated finding in insertional tendinosis.20 The association of insertional tendinosis with Achilles’ insertional enthesophytes is debatable. Distal Achilles’ tendon ossification is extremely common radiographically (Fig. 11), and it has been suggested histologically that this is a phenomenon of endochondral ossification of the fibrocartilage of the enthesis, is age-related, and is not as a result of ongoing or

Figure 11 Ossification of the insertional enthesis of Achilles’ tendon is exceedingly common. If there is clear connection to the underlying calcaneus, it is unlikely to be related to an insertional tendinosis (A, B). This 72-year-old diabetic female had a normal Achilles’ tendon with large enthesophyte (black arrows) with clear marrow continuity with the underlying calcaneus. Intratendinous calcification (white arrows) on the radiograph was felt to be related to patient’s diabetes.

terior. Although it has been suggested that significant amounts of fluid in the retrocalcaneal bursa can be seen in asymptomatic individuals,6 the more fluid in the bursa, the more likely it is to be symptomatic.18 If the bursitis is severe, the adjacent distal Achilles’ tendon can be affected. The retro-Achilles’ bursa is an adventitial bursa caused by chronic, repetitive micromotion. Any amount of fluid in the retro-Achilles’ bursa is abnormal. The combination of retro-

Figure 12 A 32-year-old rugby player heard a “pop” while playing. Achilles’ tendon is ruptured approximately 6 cm from the calcaneal attachment (arrow). This patient had ruptured the contralateral Achilles’ tendon 2 years prior.

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previous inflammation or microtears.21 There is clearly a subset of patients who have marrow edema associated with enthesopathy and signs of distal Achilles’ tendinosis. Whether this enthesopathy is preexisting and unrelated, or a result of microtears is not completely known. The appearance of the “fractured enthesophyte” may be more specific for an inflammatory process (Fig. 10).22,23 Ossification within the tendon, clearly separate from the normal enthesis, would be expected to have a different histologic explanation than age-related endochondral ossification, and may be related to prior, or ongoing, microtears or inflammation.22 Partial or Complete Achilles’ Tendon Tear Achilles’ tendon tears are classified as partial thickness or full thickness. Full thickness tear of Achilles’ tendon is always associated with some form of underlying chronic degeneration.17 MRI can aid the clinician in deciding whether surgical repair is necessary. Complete tear of Achilles’ tendon has a high T2 signal gap between the tendon stump margins (Fig. 12). If the ends of the tendon can be approximated in a plantar flexed, casted position, surgery may not be necessary. Sagittal MRI sequences can be used to evaluate the margins of the tear after casting, predicting the success of a nonsurgical option. Irreversible fatty atrophy of the soleus muscle in the setting of complete Achilles’ tendon tear is important to report, as this finding can indicate a long-standing tear, making surgical repair more difficult and perhaps ultimately unsuccessful. Brief mention of a propensity for tendon rupture associated with particular systemic medications is necessary. Chronic steroid use predisposes to tendon disease. Fluoroquinolones, as a family of medications, have been reported to contribute to Achilles’ tendon rupture and may have a potentiating effect when combined with steroids.24-27 Partial tear of Achilles’ tendon is a difficult entity to diagnose with confidence. At our institution, we reserve the term for high T2 signal that extends to the surface of the tendon (Fig. 13). In the active individual, this is more common along the medial tendon because of repetitive distraction forces related to pronation of the ankle as the foot strikes the ground during running. High T2 signal within the substance of the tendon may be related to degenerative changes rather than true tearing, although attempts to separate these entities may not be necessary. Mucoid degeneration leads to separation of the collagen fibers and disruption of the collagen cross-links and, histologically, represents an interstitial tear, and attempting to separate “interstitial tear” from “mucoid degeneration” based on MRI is probably not a useful distinction.

Figure 13 Intrasubstance tear of the Achilles’ tendon in a 54 year old female with a history of rheumatoid arthritis and several months of persistent heel pain. T2 fat-suppressed images in the sagittal (A) and axial (B) planes reveal the distal Achilles’ tendon is abnormally swollen with increased intrasubstance signal (white arrow), extending to the surface of the tendon.

Systemic Disorders With Achilles’ Tendon Manifestations Manifestations of systemic disorders within Achilles’ tendon include hypercholesterolemia, rheumatoid arthritis, diabetes, and seronegative spondyloarthropathy. Abnormalities of Achilles’ tendon are common in patients with hyperlipidemia, detected in 92% of patients by MRI in 1 series.28 The MRI findings of Achilles’ xanthomas are similar to tendinosis with thickening of the tendon, but have a specific stippled pattern (Fig. 14A), related to infiltration of foamy histiocytes

between the normal collagen fibers28 and are typically bilateral, allowing some degree of differentiation from routine forms of intratendinous degeneration. In this author’s experience, there is commonly an extension of intermediate signal intensity material outside the confines of the tendon, supporting an infiltrative process over standard degenerative tear (Fig. 14B). The presence of Achilles’ tendon xanthomas does not predispose to rupture, but diagnosis of this entity is important, as it may be a sign of previously undiagnosed

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Figure 14 A 54-year-old woman with hypercholesterolemia. (A) Diffuse Achilles’ thickening demonstrates the typical stippled appearance on the axial PD FSE image (partially obscured by distance calibration bar). (B) Sagittal T1 image shows soft tissue extending outside the tendon (white arrows), also typical for Achilles’ tendon xanthoma. This patient had bilateral Achilles’ tendon xanthomas.

familial hypercholesterolemia. If the systemic hyperlipidemia is treated appropriately, xanthomas of the Achilles’ tendon may regress.29,30 Rheumatoid arthritis has been associated with the MRI findings of paratenonitis, but this is commonly asymptomatic.15 Of the inflammatory arthropathies, rheumatoid is least likely to have symptomatic manifestations of the Achilles’ complex, with rare retrocalcaneal bursitis being the only radiographically visible abnormality in a series of 100 rheumatoid arthritis patients.31 Chronic reactive arthritis (formerly known as Reiter’s disease) most commonly affects the enthesis of Achilles’ insertion and manifests as erosive disease of the adjacent calcaneus. Ankylosing spondylitis, although a common cause of enthesitis, less commonly involves Achilles’ attachment.31 Diabetics are at risk for the uncommon calcaneal insufficiency fracture, resulting in avulsion of the calcaneal tuberosity from the pull of Achilles’ tendon. This fracture type accounted for 66% of calcaneal fractures in a diabetic population studied by Kathol et al32 (Fig. 15).

Plantaris Tendon Injury: Tennis Leg Tear of the plantaris tendon is an increasingly common injury, as it is now imaged with MRI and has characteristic MRI findings. It is important for the radiologist to accurately diagnose plantaris tear, as the rest and rehabilitation necessary to recover from this injury is far shorter than partial tear of one of the components of the triceps surae (medial and lateral head gastrocnemius and soleus muscles). Complete tear of the plantaris tendon as it courses between the medial head of the gastrocnemius and soleus muscles results in insignificant long-term sequelae. MRI shows a characteristic location of

edema along the normal course of the plantaris tendon (Fig. 16). If the entire lower extremity is imaged, the proximal muscle belly of the plantaris can be localized and the tendon followed inferiorly to a blind ending stump. Commonly, the tendon is indistinguishable from adjacent edema, but no contiguous tendon can be identified to the normal insertion medial with the Achilles’ attachment. Tears of the medial head of the gastrocnemius are often called “tennis leg,” and may coexist with plantaris tendon tears. Given its intimate association with the distal Achilles’ tendon, the plantaris tendon can simulate an intact portion of an otherwise complete rupture of the Achilles’ tendon. The plantaris can also hypertrophy in cases of chronic, neglected Achilles’ rupture.33

Peroneal Muscles and Tendons Normal Anatomy and Appearance The primary function of the peroneal musculature is eversion and pronation of the foot. These muscles also play a secondary role in plantar flexion and help in providing the stability to the lateral ankle joint.34 The peroneus longus muscle originates from the proximal fibula, interosseous membrane, and posterolateral tibial condyle. Deep to the peroneus longus, the peroneus brevis has its origin off the distal fibula and interosseous membrane. These tendons share a common tendon sheath that originates approximately 4 cm above the lateral malleolus and extends distally to the calcaneocuboid joint region.35 The peroneus brevis muscle and tendon lie anteromedial to the peroneus

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259 bony protuberance called the peroneal tubercle is seen off the lateral calcaneus at this level (Fig. 17B). This holds the peroneal tendons separate from each other, with the peroneus brevis tendon lying anterosuperior and the peroneus longus tendon inferoposterior to this structure.39 Distally, the peroneus longus tendon courses medially through the peroneal groove of the cuboid and inserts on the plantar aspect of the medial cuneiform and first metatarsal. The peroneus brevis tendon courses laterally to insert on the fifth metatarsal base. The peroneal tendons are normally uniformly low signal intensity on all pulse sequences. As they course underneath the lateral malleolus however, tendon orientation can suffer from magic angle artifact.40 Normally, the peroneal tendons are oval. At the level of the lateral malleolus, however, they can take on a flattened or crescentic morphology (particularly the peroneus brevis) but should not be thinner centrally than peripherally.41 Peroneal tendon size should be less than the posterior tibial tendon at the same level. If they are the same size or larger, they should be considered thickened.42 Fluid can normally be present within the common peroneal tendon sheath and thus care should be taken when diagnosing peroneal tenosynovitis.42-44 Ankle joint fluid can communicate with the peroneal tendon sheath in the presence of a torn calcaneofibular ligament. Additionally, a peroneal effusion can accompany a calcaneus fracture and other mechanical abnormalities.45 If, however, the fluid is circumferential about the tendon and greater than 3 mm in thickness from tendon edge to synovial sheath, it should be considered pathologic.42 Smaller amounts of fluid within the tenosynovial sheath may take on added significance if correlating to the patient’s point of maximal pain.

Peroneal Tendon Pathology

Figure 15 A 51-year-old diabetic female with calcaneal insufficiency avulsion (A, B). Sagittal MRI was performed 3 months following injury to assess for osteomyelitis.

longus as these structures course distally underneath the fibula within a fibro-osseous tunnel called the retromalleolar groove (Fig. 17A). They are held in place behind the fibula within the retromalleolar groove by the superior peroneal retinaculum (SPR), a thin fibrous band of tissue that is identifiable on MR as a low T1/T2 structure approximately 1 mm in thickness.36 The SPR arises from the lateral malleolus and attaches onto the lateral aspect of the calcaneus and Achilles’ tendon.37 Often, there is a small triangular fibrous ridge associated with the SPR at its fibular attachment that acts to deepen the retromalleolar groove and keep the peroneal tendons normally located.38 Distal to the ankle joint, the peroneal tendons are held against the lateral calcaneus by the inferior peroneal retinaculum. In 40% of patients, a small

As the primary evertors of the foot and ankle, the peroneal brevis and longus are prone to injury with excessive inversion and dorsiflexion.46-48 Additionally, because of the anatomic constraints created by both normal and variant anatomy along the posterolateral ankle, they are prone to attrition and excessive mechanical wear. Clinically unsuspected pathology involving these structures can be a cause of chronic pain, instability, and functional limitation in both athletic activities and daily life. MR is able to identify pathology and variant anatomy in this region and thereby guide management, either conservative or surgical. Peroneal Tendinosis, Tenosynovitis Peroneal tendinosis is a degenerative, noninflammatory condition affecting the peroneal tendons. This condition can be symptomatic or asymptomatic and affects both young and old. It is a frequent finding in individuals who repeatedly place great demand on their lateral ankle tendons. Two hallmarks of tendinosis in general are tendon thickening and increased intrasubstance signal (Fig. 18). The individual peroneal tendons should be considered thickened if they are equal to or larger in size than the posterior tibial tendon at the same level.42 Tendon thickening, however, is a relatively insensitive finding of symptomatic peroneal tendinosis.42 In their study of 24 patients with symptomatic per-

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Figure 16 Plantaris tear. (A) Edema (asterisk) is present interposed between the medial head of the gastrocnemius muscle (MG) and soleus (S) on axial T2 fat-suppressed image. (B) The proximal stump of the plantaris is demonstrated well on large field of view coronal short tau inversion-recovery (STIR) image (white arrow).

oneal tendinosis and tenosynovitis, Kijowski et al42 described intermediate signal intensity within the peroneal tendons on 3 consecutive axial proton density-weighted images as being the most sensitive (92%) finding of symptomatic peroneal tendinosis. Corresponding increased intratendinous T2 signal adds specificity to this finding, but by itself is relatively insensitive. Peroneal tenosynovitis describes inflammation and fluid within the common peroneal tendon sheath. This finding can be seen with recent inversion injury, peroneal tendon pathology, lateral malleolus/calcaneal fractures, infection, and inflammatory or crystalline arthropathies.49-51 A small amount of fluid within the peroneal tendon sheath can be normal. If, however, the fluid circumferentially surrounds the peroneal tendons with a tendon edge to synovial sheath diameter of 3 mm or greater, the diagnosis of peroneal tenosynovitis can be made with high specificity42 (Fig. 19). When chronic, peroneal tenosynovitis can result in a thickened, low T1/T2 signal intensity tendon sheath, and is then referred to as stenosing tenosynovitis.45 Peroneus Brevis Split Tear Peroneus brevis tears can occur in young, athletic individuals, as well as the elderly people. Symptoms include pain, swelling, ankle instability, and sometimes a clicking or popping sensation along the posterolateral ankle. Peroneus brevis tendon tears are usually longitudinal in orientation, also called “split” tears (Fig. 20). Although most isolated tears are the result of an acute inversion injury, the peroneus brevis is particularly prone to chronic attrition because of its anatomical position within the retromalleolar groove. With foot dorsiflexion, the peroneus brevis tendon is sandwiched between the lateral malleolus, superior peroneal retinaculum, and the peroneus longus tendon. When repetitive and chronic, this action can cause the peroneus longus to “saw” into the peroneus brevis, thereby leading to mechanical attrition and eventually resulting in tear. When torn, the peroneus longus

can insinuate itself into a peroneus brevis tear, thus preventing healing.41,45-47 Rosenberg et al41 described reliable MR findings of longitudinal tears of the peroneus brevis. In their series of patients, tears were centered at the retromalleolar groove and commonly demonstrated proximal and distal extension. When torn, the peroneus brevis commonly takes on a C-shaped configuration that partially envelopes the peroneus longus tendon. In partial split tears, the central portion of the tendon anterior to peroneus longus is thinned with 2 globular limbs located medial and lateral to the peroneus longus tendon. With extensive longitudinal split tears, separate divisions of the peroneus brevis are present medial, lateral, and sometimes posterior to the peroneus longus tendon. In all cases, reconstitution into a single nonsplit tendon was noted distally, usually as the peroneal tendons descended along the lateral calcaneal wall. Other reliable findings of peroneus brevis split tears in their series of surgically proven cases included clefts, tendon contour abnormalities, and increased signal on proton density-weighted images.41 Care should be taken in diagnosing a split peroneus brevis tear as the peroneus brevis tendon can be bifid. Identification of muscle fibers about each of the bifurcated tendons allows recognition of this normal variant.38 Because of its constrained anatomic space within the retromalleolar groove, anything that decreases or “crowds” this space can lead to mechanical attrition of the peroneus brevis tendon. Causes include the presence of an accessory peroneus quartus muscle, a low-lying peroneus brevis muscle belly, and a flat or convex retromalleolar groove. These are described in more detail later in the text. Peroneus Longus Tears Isolated tears of the peroneus longus tendon are uncommon.34 They may, however, accompany peroneus brevis tendon tears in a maximum of one-third of patients.38 Acutely, they usually result from direct trauma (ie, calcaneal fracture, crush

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injury) or an inversion injury. Like peroneus brevis tears, they are usually longitudinal in orientation and frequently occur at sites where the tendon changes direction. Consequently, most tears are found underneath the lateral malleolus (within the retromalleolar groove) or underneath the cuboid within the peroneal groove5 (Fig. 21A). Not uncommonly, associated cuboid marrow edema is seen and this finding should alert the radiologist to possible peroneus longus pathology.38

Figure 18 Peroneal tendinosis. Both the peroneal longus (PL) and peroneal brevis (PB) tendons are thickened with intrasubstance high signal on axial PD FSE sequence.

The presence of a hypertrophied peroneal tubercle may predispose to peroneus longus injury (Fig. 21B). This is thought to cause increased friction on the adjacent peroneus longus tendon, thus leading to premature tendinopathy and tearing.38,52 High T2 signal within the hypertrophied peroneal tubercle may also be seen. Additionally, peroneus longus tendon tears can be associated with an accessory peroneus quartus

Figure 17 Peroneal tendon anatomy. (A) At the level of the fibular retromalleolar groove, the peroneal brevis (PB) is deep to the peroneal longus (PL) and the tendons are covered by the superior peroneal retinaculum (thick white arrow). (B) Distally, the tendons are separated by the peroneal tubercle with the peroneal longus posterior to the peroneal brevis. The inferior peroneal retinaculum covers the tendons at this level (white arrowheads).

Figure 19 Severe common peroneal tenosynovitis. Tenosynovial filling defects likely represent long-standing inflammation, with hemorrhage or fibrinous exudate (arrows).

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B. Petersen, J. Fitzgerald, and K. Schreibman with peroneal longus degeneration, tenosynovitis, and/or tear.54 When associated with peroneal tubercle hypertrophy, an os peroneum may be a cause of peroneal longus entrapment.34 Clinically, peroneal symptomatology associated with an os peroneum is referred to as painful os peroneum syndrome or POPS (Fig. 22).

Figure 20 Peroneal brevis split tear. The peroneal brevis (PB) has separated into distinct parts due to longitudinal split tear on this axial PD FSE image (A). Axial, fat suppressed PD sequence demonstrating tenosynovitis associated with the severe tendon disease (thick white arrows) (B).

and inflammatory arthropathies, such as rheumatoid arthritis and psoriasis.34,38 Present in approximately 25% of ankles, the os peroneum is a sesamoid bone found within the peroneus longus tendon in the region of the cuboid bone.53 This can be ossified (20%) or cartilaginous.53 Knowledge of this normal variant is important on MR because a nonossified os peroneum could be mistaken for a peroneus longus tear. The os peroneum can be single or multipartite and may fracture, diastase (when multipartite), or be associated

Figure 21 Sagittal PD FSE sequence demonstrating complete tear of the distal peroneal longus tendon with retraction (A). The distal stump of the peroneus longus (black arrow) is retracted and there is severe underlying peroneal tendinosis. Axial fat suppressed PD FSE image in a different patient showing isolated peroneal longus tenosynovitis (white arrow) related to hypertrophied peroneal tubercle (asterisk) (B).

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Figure 22 Painful os peroneum syndrome (POPS) in a 58-year-old man who developed chronic lateral foot pain after ballroom dancing. Oblique radiograph (A) demonstrates an os peroneum (white arrow) below the calcaneal-cuboid joint, a common normal variant. Short axis axial STIR (B) and long axis axial STIR images (C) show edema of the os peroneum (white arrow) and the underlying portion of the cuboid (white arrowhead). (D) Bone scan demonstrates focal increased uptake of the os peroneum (white arrow).

Peroneal Tendon Subluxation/Dislocation Peroneal tendon subluxation and/or dislocation most commonly results from sudden, reflexive contraction of the peroneal muscles either during an acute inversion injury to the dorsiflexed ankle or during forced dorsiflexion of the everted foot.52,55,56 Frequently, this is associated with injury to the SPR.52 Chronic lateral ligamentous injuries can also lead to laxity of the SPR, thus predisposing to peroneal tendon subluxation.57 Patients often describe pain along the posterolateral fibula, sometimes accompanied by a “popping” or clicking sensation. On physical examination, there is focal tenderness along the posterolateral ankle, often with palpable snapping/crepitus of the tendons during dorsiflexive maneuvers as the tendons slip over the lateral malleolus.52

Ankle radiographs may show a small avulsion fracture off the lateral malleolus, termed the “fleck sign.”52 When physical examination findings are equivocal, MR can be helpful (Fig. 23A). To determine subluxation, a vertical line can be drawn at the lateral margin of the inferior fibula on axial images (Fig. 23B). If the tendons touch this line, this should be considered subluxation. If they cross this line, they should be considered dislocated.37 MR also defines the extent of associated SPR injury and retromalleolar groove morphology, as a flat or convex groove may predispose to recurrent subluxation.37,38,52,58 The retromalleolar groove is evaluated 1 cm proximal to the fibular tip and is smooth and concave in 82% of people.38 Less commonly, the groove takes on a flat or convex morphology

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B. Petersen, J. Fitzgerald, and K. Schreibman digitorum longus (FDL) tendons (Fig. 24). Their order is counterintuitive as the FHL and the FDL tendons cross at the master knot of Henry, located at the plantar surface of the foot, to arrive at their distal insertions. The mnemonic of Tom, Dick ANd Harry is useful to remember the order of the tendons, from medial to lateral, at the level of the ankle joint. By emphasizing the ANd, the important contents of the tarsal tunnel—the posterior tibial artery and the tibial nerve, located between flexor digitorum longus and flexor hallucis longus—are not forgotten. Attention to the contents of the tarsal tunnel is required during the interpretation of ankle MRI studies. Tibialis Posterior The tibialis posterior muscle has a broad origin that spans the proximal tibia and fibula within the interosseous space. Origins are found at the lateral aspect of the proximal tibia, the medial aspect of the fibula, and the posterior surface of the interosseous membrane. The tibialis posterior tendon (PTT) coalesces to appear solely as a tendinous structure at the level of the ankle joint. The PTT runs behind and under the medial malleolus, deep and medial to the FDL, along the medial border of the talus. Medial to the talus, the PTT is intimately associated with the superomedial calcaneonavicular ligament, one of three ligaments that make up the spring ligament complex. The PTT courses along the plantar surface of the medial arch to predominantly insert on the medial navicular tubercle. Slips of the tendon pass under the foot to insert on all the cuneiforms and the second through fourth metatarsal bases. The PTT functions as a dynamic stabilizer of the

Figure 23 (A) Peroneal tendon dislocation. The peroneal tendons are dislocated laterally from the retromalleolar groove (asterisk). Superior peroneal retinaculum (black arrows) is detached from the fibula. (B) Normal retromalleolar groove. The peroneal tendons do not contact or extend past a vertical line drawn along the lateral margin of the distal fibula.

with or without irregular contour, which can predispose to peroneal tendon subluxation/dislocation and mechanical attrition.59

Medial Flexor Tendons Normal Anatomy and Appearance The medial flexor tendons consist, from medial to lateral, of the tibialis posterior, flexor hallucis longus (FHL), and flexor

Figure 24 Normal medial flexor and tarsal tunnel anatomy. Medial flexor tendons: tibialis posterior tendon (PTT), flexor digitorum longus (FDL), flexor hallucis longus (FHL). Other tarsal tunnel contents: posterior tibial artery (PTa), posterior tibial veins (PTv), and tibial nerve (Tn).

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265 Flexor Hallucis Longus The FHL muscle originates from the dorsal margin of the mid to distal fibular diaphysis. The musculotendinous unit is long, and the muscle belly is the lowest lying of the medial flexor ankle tendons, commonly visible to the level of the ankle joint. The FHL tendon courses medial to the tarsal tunnel, in a groove between the medial and trigonal processes of the posterior talus. The tenosynovial sheath communicates with the ankle joint in approximately 20% of patients,44,61-63 and ankle joint effusions can result in large volumes of fluid within the FHL tendon sheath. Beneath the ankle joint, the FHL tendon courses inferior to the sustentaculum tali, communicates with the FDL tenosynovial sheath at the master knot of Henry, courses between the great toe sesamoids, and inserts at the base of the great toe distal phalanx.

Medial Flexor Tendon Pathology

Figure 25 Posterior tibial tendon can normally be thickened distally near the navicular insertion (black arrow). This patient had lateral ligamentous injury without symptoms referable to the distal tibialis posterior tendon.

foot, and, along with the spring ligament complex, is crucial to maintaining the arch of the foot. The PTT has normal areas of intratendinous high signal. As the PTT curves around the medial malleolus, it can suffer from magic angle artifact on short TE sequences. In addition, near its insertion on the navicular, the PTT commonly broadens with intratendinous signal.60 This can be due to interposed connective tissue within the tendon (Fig. 25) or presence of an os tibiale externum, a common and usually asymptomatic sesamoid within the substance of the distal PTT. The PTT is normally twice as large as the adjacent FDL tendon, and this relationship can be useful in assessing for tendinosis or chronic thinning. Flexor Digitorum Longus FDL muscle belly originates along the posterior surface of the middle third of the tibial diaphysis. The FDL tendon coalesces rapidly and is visualized as a tendinous structure at the level of the ankle joint. The FDL tendon lies posterior to the PTT as they both course posterior and under the medial malleolus, but maintain separate tenosynovial sheaths. FDL turns laterally, across the plantar arch, and crosses superficial to the flexor hallucis longus (FHL). It is at this point that the FDL and FHL tenosynovial sheaths communicate at the master knot of Henry. The FDL tendon progresses to insert on the plantar base of all lesser toe distal phalanges. It is not unusual to see a small amount of fluid in the FDL tendon sheath at the level of the ankle44 and fluid at the master knot of Henry is acceptable as well, particularly if there is FHL tenosynovial fluid more proximally.

Tibialis Posterior Tendon The PTT is the most commonly diseased tendon of the medial flexor tendons. Posterior to the medial malleolus is the area of greatest friction and combines with relative hypovascularity,64 to make this area particularly susceptible to injury. The area of greatest injury is somewhat controversial; however, as a series by Schweitzer et al60 showed greatest incidence of injury distally, near the navicular attachment. It is safe to say that PTT pathology occurs from the medial retromalleolar groove to the navicular insertion. PTT dysfunction is a broad term that has been used to describe the spectrum of PTT disease; from tenosynovitis to tendinosis to partial and complete tear.65 Isolated tenosynovitis of the PTT is most commonly seen in young, active individuals (Fig. 26). There is a clear

Figure 26 Tibialis posterior tendon tenosynovitis (black arrows). Fluid distends the sheath of the tibialis posterior tendon (white arrow).

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Figure 27 Tibialis posterior tendon tears. (A) Type I: fusiform thickening of the PTT (white arrow) correlating well to the patient’s point of maximal pain as represented by skin marker (asterisk). The PTT is more than twice the size of the adjacent flexor digitorum tendon. Accessory flexor digitorum accessorius also noted (black arrowheads). (B, C) Type II: The PTT is partially torn and thin. On axial PD fat-suppressed image, the PTT is thin (white arrow), smaller compared with adjacent FDL. Sagittal T1 image shows partial tear of the PTT with distal stump fibers (black arrowhead) and thin residual PTT (black arrows). (D-F) Type III: Complete PTT tear with retraction. The normal location of the PTT at the level of the ankle joint is empty (white arrow, D) and the tendon is retracted proximally (black arrows, E). This patient’s PTT dysfunction was associated with an accessory navicular (asterisk, F).

propensity for tenosynovitis of the PTT in patients with inflammatory arthridites, such as rheumatoid, seronegative arthropathies, lupus, and gout.66-68 A small amount of tenosynovial fluid can be seen in normal individuals,44 but it has been suggested that circumferential 2-mm radial diameter of the tenosynovial fluid is abnormal.45 At our institution, we rely heavily on the MR technologist to mark the site of maximal pain with a skin marker, and this influences our interpretation with regard to how much tenosynovial fluid is pathologic. Tendinosis and partial tendon tears are most common in middle-aged or elderly women.65 The presence of inflammatory arthritides, diabetes, hypertension, previous surgery, local steroid injection, and obesity increases the risk of PTT

dysfunction.67,68 Patients are likely to suffer from chronic dysfunction and typically present late, with changes of tendinosis or partial tearing apparent on MRI. Tear of the PTT can result in hindfoot valgus and pes planus deformities, but is the cause of such deformity in only some cases. In patients with diabetes or rheumatoid who present with acute painful flatfoot, spontaneous rupture of the PTT is likely the cause. In the majority, however, the degree of hindfoot valgus exceeds the PTT disease, and likely chronically contributes to PTT dysfunction instead of PTT dysfunction being the primary cause of the hindfoot valgus and flat foot. For the purposes of this article, tendinosis and partial tear will be considered part of a continuum, grouped together, and separated into three types, as originally described by

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267 ants. These variants include the os tibiale externum (referred to as type I accessory navicular in some of the published data), the accessory navicular (sporadically referred to as type 2 accessory navicular), and the cornuate navicular (occasionally referred to as type 3 accessory navicular). Navicular variants likely reflect a developmental spectrum of size and degree of ossification of the cartilaginous anlage of the navicular tubercle. For the purposes of this article, the numbered types will not be used and the proper names of the individual variants will be favored;

Figure 28 Four tendon sign of longitudinal split in the posterior tibial tendon (PTT) in a 39 years old. Axial PD FSE shows what appears to be four medial tendons, the so-called “4-tendon sign,” where 1 and 2 are the 2 halves of the split PTT, while 3 and 4 are the normal FDL and FHL tendons.

Rosenberg et al.69,70 This imaging classification system mirrors that which is put forth in the surgical literature. Type I injury is fusiform enlargement of the tendon (Fig. 27A) with or without internal high signal or accompanying tenosynovitis.65,70 Abnormal enlargement of the tendon can be judged by comparing it with the adjacent, and rarely diseased, FDL tendon, which should be approximately half the size of a normal PTT. Discrete longitudinal split tears may be a severe form of type I injury. This type of PTT tear can present with the MRI finding of the “4 tendon sign,” with the 2 discrete halves of PTT combining with the FDL and FHL to give the appearance of 4 medial flexor tendons (Fig. 28). Type II injury is chronic thinning of the PTT, and correlates to partial tear at surgery (Fig. 27B, C). These are commonly undercalled with MR imaging, with larger than suspected tears found at surgery. Close attention to the morphology of the tendon is necessary when evaluating the PTT. In a small series of MR and surgical correlation by Khoury et al,65 none of these types of tears were described. The tendon is commonly hypertrophied proximal and distal to the area of thinning, presumably because of long-standing type I injury with focal progression to type II. Type III injury is complete rupture of the PTT and is demonstrated on MRI as a tendon gap (Fig. 27D-F). Important factors with regard to the navicular tubercle contribute to PTT dysfunction. The reported prevalence of accessory navicular is 4%-21%.71 In this author’s opinion, the incidence is at the higher end of that range, when all navicular variants are included. There is some confusion with regard to terminology of the accessory navicular vari-

Figure 29 AP radiograph (A) and axial PD FSE image (B) showing small os tibiale externum (white arrow). This accessory ossicle is a sesamoid within the tibialis posterior tendon (PTT). The os tibiale externum does not cause PTT dysfunction, although its presence can lead to a thickened appearance to the distal PTT.

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Figure 30 Accessory navicular. (A) Radiograph showing accessory navicular with degenerative changes at the synchondrosis with the underlying native navicular (black arrow). Note overlying soft tissue swelling (asterisk). (B, C) Axial PS FSE and axial fat-suppressed PD image in the same patient with marked marrow edema surrounding the accessory navicular synchondrosis (white arrows). (D) Tibialis posterior dysfunction often accompanies accessory navicular. Sagittal T2 fat-suppressed image demonstrates mild PTT tenosynovitis as well (white arrowheads).

however, the reader should note that the numbered types and individual names are interchangeable in the literature. The os tibiale externum is an accessory ossicle that is embedded within the PTT, within 5 mm of the navicular, and lacks a cartilaginous connection to the navicular72 (Fig. 29). This makes up 30% of navicular variants72,73 but anecdotally, is the most commonly encountered variant at the author’s institution. This variant is typically asymptomatic. Some make a distinction between os tibiale externum and a PTT sesamoid,74 but these will be grouped together for the purposes of this article. The accessory navicular is a triangular-shaped bone that represents ossification of the cartilaginous anlage of the navicular tubercle. It has a synchondrosis with the underlying native navicular that consists of fibrocartilage or hyaline car-

tilage.72,75 The chronic tug of the PTT can lead to degenerative changes at the synchondrosis, bone marrow edema, and result in focal pain76 (Fig. 30). Surgical excision can be curative.76 MR evaluation is excellent for demonstrating the marrow edema associated with a symptomatic accessory navicular synchondrosis.76 Altered biomechanics on the PTT result in increased incidence of PTT dysfunction with the presence of an accessory navicular.60,77 The cornuate navicular results when there is complete ossification and fusion of a large navicular tubercle cartilaginous anlage. There is no synchondrosis in this case, so patients with cornuate navicular do not suffer from the synchondritis and marrow edema pattern seen with accessory navicular. PTT dysfunction resulting from biomechanical alterations is similar60,77 (Fig. 31).

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269 Flexor Hallucis Longus Pathology of the FHL is uncommon78 compared to Achilles’, peroneal, and PTT disorders of the ankle. Tenosynovitis and tendinosis of the FHL are typically seen in patients participating in activities requiring repetitive extreme plantar flexion and results from physical impingement of the tendon and tenosynovial sheaths at one of several locations. The fibroosseous tunnel between the medial and lateral tubercles of the talus, below the sustentaculum tali, at the master knot of Henry, and the passage through the great sesamoids are all sites of potential impingement. Evaluation of FHL tenosynovitis is difficult, as the tenosynovial sheath communicates with the ankle joint in 20% of patients, and there is commonly tenosynovial fluid present. This is particularly true in the presence of an ankle effusion (Fig. 32A, B), and the diagnosis of tenosynovitis of FHL should be reserved for a constellation of findings that includes heterogeneous tenosynovial fluid, absence of ankle effusion (in particular the anterior recess), and abrupt cutoff of the tenosynovial fluid at the level of physical impingement78 (Fig. 32C). Diagnosis of FHL tenosynovitis is important because, untreated, FHL tenosynovitis can progress to a stenosing tenosynovitis in which the tendon and tenosynovial sheath become thickened and fibrous exudates results, preventing smooth function of the FHL.45 Entrapment of the FHL at the level of the ankle joint is commonly related to the presence of an os trigonum.78 When present, the os trigonum, the unfused lateral tubercle of the posterior talus, is just lateral to the FHL at the level of the ankle joint. Ballet dancers, who are required to perform multiple forceful extreme plantar flexion maneuvers, seem to be most susceptible to this type cause of posterior impingement. The size of the os trigonum is not predictive of impingement.78 On MRI, marrow edema of the os trigonum, adjacent calcaneus, and/or posterior tibial lip can indicate os trigonum syndrome. The presence of an os trigonum can contribute to FHL tenosynovitis (Fig. 33). Post-traumatic impingement was also common in the small series studied by Lo et al,78 with half of the FHL impingement related to entrapment by osseous or soft tissue scar related to fracture. Flexor Digitorum Longus Pathology of the FDL is rare. MRI findings of tenosynovitis are similar to other tendons about the ankle. It should be noted, however that the FDL and the FHL have communicating tenosynovial sheaths at the master knot of Henry, and severe tenosynovitis of the FHL or normal communication of a large ankle joint effusion with the FHL can both result in fluid within the tenosynovial sheath of the FDL.

Extensor Tendons Figure 31 Cornuate navicular. (A, B) Radiograph and axial PD FSE sequence show cornuate morphology to the navicular (white arrows). (C) Axial T2-weighted image more proximally shows PTT dysfunction in the form of tenosynovitis (black arrow).

Normal Anatomy and Appearance There are usually four tendons found anterior to the ankle. These include (from medial to lateral) the tibialis anterior tendon (ATT), extensor hallucis longus (EHL), extensor digitorum longus (EDL), and the variable peroneus tertius (Fig. 34). Their primary function is to dorsiflex the foot and ankle.

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B. Petersen, J. Fitzgerald, and K. Schreibman The ATT, EHL, and EDL are invested by their own tenosynovial sheaths. All four tendons are held tight against the anterior surface of the ankle and foot by two thin, fibrous, transversely orientated aponeurotic bands called the superior and inferior extensor retinacula. The superior extensor retinaculum is present just above the ankle joint with insertions laterally onto the lateral malleolus and medially onto the anterior tibial and medial malleolus.79 Usually, all four tendons pass beneath this structure; however, in 25% of ankles, there is a separate tunnel for the tibialis anterior tendon created by superficial and deep layers of the superior extensor retinaculum.79 The inferior extensor retinaculum is a Y-shaped aponeurotic band along the anterior foot and ankle. Its anatomy is more complex than its superior counterpart, with contributions from four separate fibrous components.79 Tibialis Anterior The tibialis anterior muscle has a broad origin off the proximal half of the anterolateral tibia and interosseous membrane. The ATT begins at approximately the middle third of the tibia and courses toward the medial foot, inserting onto the first metatarsal base and medial cuneiform in 84%-96% of individuals.79-81 At the ankle, the ATT is typically round or oval, becoming flat distally. Normally, the tendon should be 5 mm or less in thickness within 3 cm of its insertion. If greater, tendinopathy should be considered.81 The primary function of the tibialis anterior muscle is to dorsiflex and evert the foot. Extensor Hallucis Longus The extensor hallucis longus originates from middle third of the anterior fibula and interosseous membrane with its tendon inserting onto the dorsal aspect of the distal first phalangeal base. This tendon extends the first toe and helps dorsiflex the foot.82 Extensor Digitorum Longus The EDL has a long origin off the lateral tibial condyle as well as proximal three-fourths of the medial fibula and interosseous membrane. Its tendons insert onto the dorsal aspect of the second through fifth middle and distal phalanges. The primary function of EDL is to extend the second through fifth toes and dorsiflex the foot.82

Figure 32 (A, B) Flexor hallucis longus tenosynovitis. Note tibial talar posterior joint recess effusion, absence of anterior recess effusion (A, black arrows, sagittal STIR image), and heterogenous fluid in the FHL tenosynovial sheath (B, black arrowhead, axial T2-weighted image). (C) FHL tenosynovitis in a different patient appears as significant amount of fluid within the sheath (white arrow) in absence of an effusion. This patient has severe common peroneal tenosynovitis as well (asterisk).

Peroneus Tertius When present, the peroneus tertius originates from the distal third of the anterior fibula and interosseous membrane. Its muscle belly is usually inseparable from the EDL and ends proximal to the inferior extensor retinaculum. It may be invested by its own synovial sheath or share one with the adjacent EDL.83 Nonetheless, its tendon passes alone beneath the inferior extensor retinaculum and lateral to the EDL to insert onto the dorsal aspect of the fifth metatarsal base. Variations in peroneus tertius insertional anatomy do exist, the most common being an accessory slip that inserts onto the fourth metatarsal base.83 The peroneus tertius helps dorsiflex and evert the foot.82

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Figure 33 Twenty-eight year-old male basketball player with ankle pain. The presence of an os trigonum (A, sagittal T1-weighted image, black arrow) can contribute to FHL tenosynovitis (B, axial T2-weighted image, white arrows).

Extensor Tendon Pathology Because of their relatively straight course, the extensor tendons are not typically subjected to attritional injury at points of tendon direction change like the peroneal tendons. In fact, extensor tendon injury is relatively rare, and hence rarely reported in the orthopedic and radiological literature.84 Tibialis Anterior Tendon Injury The tibialis anterior is the primary dorsiflexor of the foot and the most commonly injured extensor tendon. Injuries are generally

Figure 34 Normal extensor tendon anatomy. Tibialis anterior (TA), extensor hallucis longus (EHL), extensor digitorum longus (EDL), anterior tibial artery (ATA).

divided into acute and acute-on-chronic.85 Acute injuries are usually the result of a penetrating injury or laceration (Fig. 35), either from external causes or a tibial shaft fracture.86 The mechanism of acute-on-chronic injuries is less well understood. One possible etiology is chronic frictional wear against the inferior extensor retinaculum. Others include mechanical attrition against an adjacent navicular spur or prominent medial tarsometatarsal joint osteophyte eventually resulting in rupture, oral or local steroid administration, diabetes, gout, and inflammatory arthropathies.81,84,87,88 Acute-onchronic injury often presents with little to no functional limitation because of the compensatory action of the other extensor tendons in dorsiflexion. Sometimes the ruptured tendon can present as a focal mass along the anterior ankle raising the clinical suspicion of neoplasm. In these cases, MR is useful in demonstrating the true nature of the abnormality. ATT tears usually involve the distal 0.5-3 cm of tendon, often occurring where the tendon passes underneath the inferior extensor retinaculum or near its medial cuneiform insertion.79,84,85 Again, this may relate to chronic attrition against the inferior peroneal retinaculum or adjacent bony structures and/or the fact that the anterior half of the tendon is relatively avascular and thus less well able to heal.89 On MR, complete rupture is seen as frank tendon discontinuity with or without tendon retraction. The degree of tendon retraction with a complete tear may be significant to the level of the ankle joint and present clinically as a soft tissue mass. Tendon attenuation suggests partial tear. Tendon thickening and increased intrasubstance signal may be seen with tendinopathy or partial tear.84 As with the peroneals, care should be made in diagnosing tibialis anterior tendinopathy as artificial increased intrasubstance signal may be seen due to the magic angle effect on short TE sequences. Extensor Digitorum Longus and Hallucis Longus Injury Like the ATT, penetrating trauma and tibial shaft fractures may injure the EHL and EDL tendons. Additionally, tendon

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Figure 35 Axial T2 (A) and sagittal STIR (B) images showing complete absence of the tibialis anterior tendon on single axial image (A, arrow) and retraction of tendon stump (B, arrow) in a 36-year-old man following penetrating trauma to the ankle.

degeneration, tearing, and/or tenosynovitis may also occur from abnormal friction against adjacent osteophytes, fracture fragments, and orthopedic hardware.90 Overall, however, EHL and EDL pathology should be considered rare.

a compartment syndrome or demand ischemia related to the additional muscle mass.94,95

Peroneus Tertius Impingement A peroneus tertius muscle is present in approximately 83%95% of cadaveric studies.91 Rarely, its tendon may become impinged and symptomatic as it crosses over the cuboidometatarsal joint.92 Additionally, it may be a cause of lateral ankle pain and snapping as its tendon courses over the lateral talar dome.83 In these cases, resection of the involved portion of muscle and/or tendon can be curative.

The peroneus quartus muscle is a relatively common anatomic variant with a reported incidence of 22% in cadaveric dissections.96 Most commonly, it originates from the peroneus brevis muscle but can also arise from the peroneus

Peroneus Quartus

Accessory Muscles There are several accessory muscles around the ankle. Although they are variations of normal development, an awareness of them is necessary as they can cause pathology related to crowding of adjacent tendons or compression of neurovascular structures.

Accessory Soleus The accessory soleus (AS) (Fig. 36) muscle originates from either the normal soleus origin at the proximal tibia and fibula or from the ventral margin of the soleus muscle itself. The AS has variable insertions, but usually inserts on Achilles’ tendon or the medial calcaneus.93 The AS is usually unilateral and has an incidence of 0.7%-5.5% based on cadaveric studies.94 On MRI, the muscle is deep to Achilles’ tendon and outside the tarsal tunnel. Despite its location superficial to the tarsal tunnel, symptomatic AS has been reported to contribute to tarsal tunnel syndrome. Symptoms are rare, but usually occur in young, athletic males, and may be related to

Figure 36 Large accessory soleus (asterisk). Note location deep to Achilles’ tendon but superficial to the retinaculum of the tarsal tunnel (white arrow).

Musculotendinous MRI of the ankle

273

Figure 37 A 29-year-old man with lateral ankle pain. Peroneus quartus lies posterior and medial to the peroneal tendons at the level of the retromalleolar groove (A, axial PD FSE, asterisk). As a space occupying lesion it can contribute to peroneal tenosynovitis, as seen in this patient (B, axial fat-suppressed PD, white arrows).

longus muscle or posterior fibula. Within the retromalleolar groove, the peroneus quartus lies posterior or medial to the peroneus brevis and longus (Fig. 37A). Distally, the tendon most commonly inserts onto the retrotrochlear eminence, a bony protuberance along the lateral calcaneus posterior to the peroneal tubercle,97 often causing hypertrophy of the retrotrochlear eminence.38,98 This has been termed the peroneocalcaneus externus, and other names vary based on the multiple insertion sites of peroneus quartus (peroneoperoneolongus, peroneoperoneobrevis, peroneocuboideus).98 All of these variations will be grouped under the term peroneus quartus for the purposes of this review. Rarely is an accessory peroneus quartus muscle symptomatic.99 Because it occupies space deep to the SPR, it can contribute to tenosynovitis (Fig. 37B), chronic lateral ankle pain, swelling, and instability, especially in the athlete following an inversion injury.100,101 This is thought to be due to an “overcrowding” effect within the retromalleolar groove predisposing to SPR insufficiency and thus peroneal tendon subluxation and mechanical attrition.102 When symptomatic, complete resection of the peroneus quartus usually results in total recovery.100

allows distinction from the accessory soleus. FDAL is frequently unilateral, seen more often in males, and has a reported prevalence of 6%-8%.103,104

Peroneocalcaneus Internus The peroneocalcaneus internus muscle (Fig. 39) has variable proximal origin but a distinctive location, course, and insertion at the ankle to allow accurate diagnosis. The myotendinous unit lies deep to the flexor retinaculum, lateral to the FHL, displacing the FHL toward the tarsal tunnel.105 The

Flexor Digitorum Accessorius Longus The flexor digitorum accessorius longus (FDAL) (Fig. 38) has a variable proximal origin, but distally inserts onto either the quadratus plantae muscle or FDL tendon. Peroneocalcaneus internus and tibiocalcaneus internus (accessory muscles that lay deep to the flexor retinaculum) both insert on the calcaneus, distinguishing them from the FDAL. The FDAL can be symptomatic as it is intimately associated with the posterior tibial neurovascular bundle, lying deep to the flexor retinaculum, and can compress the contents of the tarsal tunnel. The location deep to the flexor retinaculum

Figure 38 Flexor digitorum accessorius longus (FDAL, arrows). The FDAL can contribute to tarsal tunnel as it lies deep to the tarsal tunnel retinaculum (arrowheads).

274

Figure 39 Peroneocalcaneus internus (asterisk). This accessory muscle accompanies the FHL and inserts characteristically on the medial calcaneus, beneath the sustentaculum tali. This muscle can be indirectly symptomatic by displacing the FHL into the contents of the tarsal tunnel.

tendon travels with the FHL between the lateral and medial tubercles of the talus, beneath the sustentaculum tali, to insert uniquely on the medial aspect of the calcaneus, distal to the sustentaculum tali.105 The muscle is rare, with a prevalence estimated at 1% and is frequently bilateral.105 It may not be commonly symptomatic as it is usually purely tendinous at the level of the ankle joint, but may displace the FHL medially and indirectly compress the tarsal tunnel contents.105

Tibiocalcaneus Internus The tibiocalcaneus internus muscle is rare, and its appearance has not been described in detail in the radiologic literature. It is deep to the flexor retinaculum, similar in location to the FDAL, but inserts on the medial calcaneus, anterior to the Achilles’ insertion.106 The location deep to the flexor retinaculum likely predisposes to tarsal tunnel compression.

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