High-resolution ultrasound and MRI in the evaluation of the forefoot and midfoot

Stress fractures typically occur in young to middle-aged individuals undertaking unaccustomed high levels of exercise over an extended period. The 2^nd and, less frequently, the 3^rd metatarsal mid-shafts are commonly affected sites⁽¹⁾ (Fig. 1). The base of the 2^nd metatarsal is splinted between the distal end of the medial cuneiform and the 3^rd metatarsal bone. It is also a key weight-bearing bone, making it more susceptible to injury. The 1^st, 2^nd and 5^th metatarsal bases, the navicular, cuneiform, cuboid, and medial sesamoid bones are additional common sites of stress fractures in the mid- and forefoot^(1,2) (Fig. 2). Radiographs are normal in the earliest stages of stress fracture. US at this juncture may reveal a cuff of echogenic thickening due to thickened periosteum (‘periostitis’) around the cortex of the affected bone area. The cortex may be less distinct than usual, together with juxtacortical soft tissue edema and hyperemia (Fig. 1). While such findings are non-specific, they are usually diagnostic in the appropriate clinical setting without the need for additional imaging other than radiographic follow-up. MRI will provide even earlier detection of stress fracture than US, revealing focal bone marrow edema (BME) at the affected site, often with a thin hypointense fracture line⁽¹⁾ (Fig. 2). In the appropriate clinical setting, BME on fat-suppressed, fluid-sensitive sequences without a visible fracture line is termed a ‘stress reaction’ rather than a ‘stress fracture’⁽¹⁾. Radiographs and US will typically be normal in stress reaction. It is important to correlate any BME with clinical symptoms, as BME may occur due to physiological bone remodeling without necessarily being reflective of an injurious stress reaction⁽³⁾.

Fig. 1.

Fig. 2.

Sesamoid pathology is quite common and includes osteoarthritis of the sesamoid-first metatarsophalangeal (MTP) articulation, traumatic sesamoid bone fracture, and sesamoid bone stress fracture and sesamoid bone inflammation, known as sesamoiditis, which may be secondary to either stress reaction or osteonecrosis⁽⁴⁾. Osteoarthritis between the sesamoid and the undersurface of the first metatarsal head articulation is usually assessed radiographically. Sesamoid fracture is also evaluated by radiography and should be distinguished from a bipartite sesamoid bone (Fig. 3). In bipartite sesamoid, the summated size of both sesamoid components is greater than the expected size of the sesamoid bone. Also, the opposing bone edges are smooth and corticated, with a transversely orientated partition, as opposed to the often irregular, obliquely orientated margins of a sesamoid fracture (Fig. 4). Sesamoiditis is seen on MRI examination as diffuse edema of the affected sesamoid bone.

Fig. 3.

Fig. 4.

Freiberg’s disease is an infraction that most likely follows a subchondral fracture, leading to progressive flattening and collapse most commonly of the second metatarsal head, though the other lesser metatarsal heads may also be affected (Fig. 5). It is about five times more common in females. The diagnosis is usually made radiographically and supported, if necessary, by CT or MRI as a prelude to osteotomy⁽⁵⁾. US may potentially help in detecting Freiberg’s disease when radiographs are not available with assessment of inflammation, synovial hypertrophy and hyperemia on Doppler imaging, at the 2^nd metatarsophalangeal joint. Otherwise, the role of US in Freiberg’s disease is limited.

Fig. 5.

Injury to the 1^st MTP joint, which is broadly termed ‘turf toe’, is common among athletes⁽⁴⁾. As the anatomy of the first MTP joint differs from that of the lesser MTP joints, the injury spectrum also differs. The first MTP joint contains the paired sesamoid bones which are held in place by a framework of ligament, tendon, capsule, and fibrocartilaginous plantar plate attachments (Fig. 10, Fig. 11). The plantar plate is a trapezoidal-shaped thickening on the plantar aspect of the MTP joint (Fig. 10, Fig. 11). Distally, it is attached to the proximal phalanx and proximally to the inter-sesamoid ligament (Fig. 10, Fig. 11). As the 1^st MTP joint anatomy is rather complex, plantar plate and ligament injury is usually best assessed with MRI rather than with US.

Fig. 10.

Fig. 11.

The plantar plate is the most frequently injured component of the 1^st MTP joint though other supporting structures can also be torn either in isolation or in conjunction with a plantar plate tear. Plantar plate injury may be acute from traumatic hyperextension or chronic. The relative prevalence of acute or chronic tears seen is largely dependent on the referral population. Chronic tears occur in degenerative attenuated plantar plates from repetitive overload (Fig. 12). On MRI, degenerated plantar plates will tend to have intermediate rather than low signal intensity on all pulse sequences⁽¹¹⁾. Partial tears are more common than complete tears. If complete tears are accompanied by tearing of the supporting sesamoid ligaments, proximal migration of one or both sesamoid bones may occur. Unlike plantar plate tears of the lesser MTP joints, 1^st MTP joint plantar plate tears tend not to induce exuberant reactive capsular/pericapsular fibrosis.

Fig. 12.

Even more so than the 1^st MTP joint, the plantar plates of the lesser MTP joints resist joint hyperextension and provide sagittal stability⁽¹¹⁾. Distally, the plantar plates are firmly attached to the proximal phalangeal bases while proximally, they are loosely attached to the metacarpal necks by fibro-synovial tissue⁽¹²⁾. On either side, the plantar plates are firmly attached to the medial and lateral accessory collateral ligaments (Fig. 13) and, as such, co-existent injury of the plantar plate and accessory ligaments commonly occurs⁽¹²⁾. Plantar plate tear can lead to MTP joint medial or lateral deviation, dorsal subluxation, and hammer toe⁽¹³⁾. The normal plantar plate and plate tears are shown on US and MRI in Fig. 14 and Fig. 15. As with the 1^st MTP joint, a midline hyperintense zone, measuring up to 2.5 mm long, at the phalangeal base is a normal anatomic recess⁽¹¹⁾ (Fig. 10). This is less frequently appreciated on US as a hyperechoic zone.

Fig. 13.

Fig. 14.

Fig. 15.

The 2^nd, followed by the 3^rd, MTP joint plantar plates are the most frequently injured⁽¹²⁾. Plantar plate tears typically occur at the junction between the plantar plate and the accessory collateral ligament close to the phalangeal attachment, most commonly at the inferolateral aspect of the joint (Fig. 13). On US, most plantar plate tears are seen as discrete partial or full thickness hypoechoic defects in the plate substance^(13,14). Flattening or attenuation may occur with plantar plate degeneration. When the plantar plate is completely torn, the flexor digitorum tendon may directly contact the metatarsal head^(13,14). In the chronic setting, reactive pericapsular fibrosis can be seen as a non-compressible hypoechoic cuff of tissue abutting the plantar and inferolateral (or inferomedial) aspects of the MTP joint^(13,14). US should be performed in both longitudinal and transverse planes, scanning the plantar aspect of the MTP joint slowly from lateral to medial and from distal to proximal, with angling of the transducer to avoid anisotropy. Most injuries occur at the distal attachment of the plate. Longitudinal US is best to detect and characterize tears while transverse US is useful to delineate the eccentric location of pericapsular fibrosis and to exclude subluxation of the flexor digitorum tendon. Longitudinal US during toe dorsiflexion can improve tear detection and appreciation of MTP joint subluxation⁽¹⁴⁾.

For MR imaging, T1-weighted (T1W) coronal images are usually the most helpful as routine sagittal forefoot images do not always image the plantar plate in a true sagittal plane⁽¹²⁾ (Fig. 15). Performing MRI in the prone position, with the foot in plantarflexion, results in less magic angle artifact and less movement artefact potentially facilitating assessment of the plantar plate⁽¹¹⁾. Prone positioning also leads to slight plantar shift of the interdigital soft tissues improving assessment of Morton’s neuroma⁽¹⁵⁾. Dynamic US assessment during MTP joint dorsiflexion or during dorsal drawer (Lachman) testing can help assessment of plantar plate integrity and MTP joint stability. Compared with surgical findings, the pooled sensitivity (93%) of US for detecting plantar plate tears is comparable to that of MRI (89–95%), though MRI has a higher specificity (54–83%) than US (33–52%)⁽¹⁶⁾. A negative US examination makes plantar plate injury very unlikely. If US is positive or equivocal, MRI can provide more specificity as to the nature of the injury and yield a more global assessment of the MTP joint⁽¹⁷⁾.

Additional indirect MRI signs of plantar plate tear are joint effusion, subarticular BME, flexor tenosynovitis, an elongated 2^nd metatarsal bone, and reparative pericapsular fibrosis while intermetatarsal bursitis and Morton’s neuroma are quite common accompaniments. Pericapsular fibrosis is a useful indirect sign of chronic plantar plate tear which often mimics Morton’s neuroma (i.e. ‘pseudoneuroma’)⁽¹¹⁾ (Fig. 16). Helpful features to distinguish between pericapsular fibrosis and Morton’s neuroma are listed in Tab. 3. It is likely that as pericapsular fibrosis/plantar plate tear becomes more widely recognized, less Morton’s neuromas and more chronic plantar plate tears will be diagnosed.

Fig. 16.

The intermetatarsal bursae have a synovial lining and are located in the superior intermetatarsal space, dorsal to the intermetatarsal ligament⁽¹⁸⁾. Bursal enlargement of >3 mm in the axial plane is considered significant. Intermetatarsal bursitis may be seen on MRI in early RA before clinical joint swelling in patients with clinically suspected arthralgia⁽¹⁹⁾ (Fig. 17).

Fig. 17.

Adventitial bursitis can occur at any pressure point (Fig. 12) and is often seen alongside the 1^st and 5^th metatarsal heads. If inferior to the metatarsal heads, it is known as submetatarsal bursitis (Fig. 18). Adventitial bursae have no synovial lining. Active bursitis is seen on MRI and US as a sharply demarcated area with variable soft tissue inflammation, hyperemia, and contrast enhancement. Chronic inactive bursitis can appear like reactive fibrosis with no discernible fluid and localized soft tissue thickening, low in signal on both T1W and T2-weighted (T2W) imaging. Submetatarsal bursitis is more common in RA patients than in patients with other arthritides or healthy volunteers, and tends to occur plantar deep to the 1^st and 5^th metatarsal heads⁽¹⁸⁾.

Fig. 18.

Diffuse submetatarsal alteration (DSMA) or metatarsal fat pad atrophy is a common cause of metatarsalgia. It is seen plantar to the metatarsal heads, with thinning and poorly defined edema of the metatarsal fat pads either on US or MRI examination with or without diffuse contrast enhancement⁽¹⁸⁾ (Fig. 19). Hyperemia is not usually a feature. No discrete bursitis is present. Any of the metatarsal heads may be affected. Occurrence under the first and fifth metatarsal heads is most likely due to mechanical loading. In rheumatoid arthritis, DSMA occurs mainly under the 2^nd, 3^rd, and 4^th metatarsal heads⁽¹⁸⁾. Metatarsal fat pad atrophy is currently a subjective assessment, based on a general perception of submetatarsal tissue thickness, as no reliable age-related normative data are available (Fig. 19).

Fig. 19.

A ganglion cyst is connected to a joint or, less commonly, a tendon sheath. It contains synovial fluid, though the cyst itself has no synovial lining. Visualizing a deep connection, which may be thin and serpiginous, enables a more definitive diagnosis and is helpful for surgical excision (Fig. 21). Occasionally, only a suggestion of a tract pointing towards the joint of origin is apparent. On MRI, a ganglion cyst is seen as a demarcated mass with a high signal intensity on fluid-sensitive sequences, which may be multilobular with septae, and display peripheral enhancement after intravenous gadolinium administration.

Fig. 21.

US is the method of choice for examining suspected ganglion cysts and shows a well-defined anechoic lesion, occasionally multilocular, and usually non-compressible (Fig. 21). Occasionally, echogenic colloid aggregates suspended within the myxoid cyst fluid may be visible. Emptying or reducing the size of the cyst by US-guided aspiration with a large bore needle and intra-cystic corticosteroid injection is sometimes helpful. Some cysts may be too viscous to aspirate. In the absence of intracystic suspensions, it is not possible to gauge cyst content viscosity. A smaller, and usually less symptomatic, cyst remnant often persists following aspiration⁽²⁴⁾.

Plantar fibromatosis is a benign condition with focal nodular fibrous enlargement of the plantar aponeurosis (i.e. plantar fibroma). Classically, a nodule is felt by the patient at the medial side of the middle one-third of the sole. US shows a typical uniform hypoechoic fusiform thickening in continuity with the plantar fascia, which may be multifocal in the same foot in one-quarter and bilateral in one-third of patients^(25,26) (Fig. 22). It can be differentiated from the much less common plantar fascial tears, which show focal reparative fibrosis with or without plantar fascial discontinuity at a site of previous injury, or the more common plantar fasciitis, which is located at the calcaneal insertion. Plantar fibromas can also be seen on MRI (Fig. 23), though US examination alone is generally satisfactory. On MRI, plantar fibromas are seen as small to medium-sized fusiform-shaped nodule or clustered nodules attached to and extending along the plantar aponeurosis (‘fascial tail sign’), usually the medial cord. T2 hyperintense (relative to muscle) lesions with avid contrast enhancement tend to be actively growing lesions, containing proliferative fibroblastic tissue, that are more responsive to electron beam irradiation therapy, while T2 isointense or hypointense lesions with poor enhancement tend to be quiescent lesions, containing mature collagenous tissue⁽²⁷⁾.

Fig. 22.

Fig. 23.

This entity usually occurs in the subcutaneous fat on the plantar aspect of the foot. The patient often recalls a history of penetrating trauma. Radiopaque foreign bodies, such as metal and large pieces of glass, can be detected on radiographs. US is the preferred investigation to detect radiolucent foreign bodies, such as wood, plastic, or small glass splinters. US also allows the location of the foreign body to be precisely defined, and detects injury to structures such as tendons, nerves, and vessels⁽²⁸⁾. All foreign bodies are echogenic⁽²⁸⁾. Smooth, flat surfaces will lead to a hypoechoic, ‘dirty’ acoustic shadowing, while irregular, curved surfaces will lead to echogenic, ‘clean’ shadowing⁽²⁸⁾. Often, the US is performed weeks or months following initial penetrating injury. In such instances, US reveals a hypoechoic halo of granulation tissue on greyscale imaging, either with or without hyperemia, close to or encasing the hyperechoic foreign body on Doppler imaging (Fig. 24). The size of the hypoechoic halo will vary depending on the intensity of foreign body reaction induced. Such reactions may occasionally be seen after 24 hours⁽²⁸⁾. Abscess is infrequently present.

Fig. 24.

Two-thirds of leiomyomas (or angioleiomyomas) occur in the lower leg, ankle, or foot region. This is a benign solitary smooth muscle tumor that mostly occurs in the subcutaneous tissues. Most are <2 cm in diameter and occur close to neurovascular bundles⁽²⁹⁾. On US, they are well-defined, homogenously hypoechoic, or ovoid, with a smooth margin, even though no discernible capsule is seen. About half of leiomyomas will have small hypoechoic protrusions at one or both ends of the mass, most likely due to extension along the vessel of origin⁽²⁹⁾. Mild to moderate posterior enhancement is usually seen⁽²⁹⁾. Most tend to be moderately hypervascular, occasionally with peripheral vascular convergence (Fig. 25). Many of these features can also be seen in small subcutaneous peripheral nerve sheath tumors arising from small subcutaneous nerves and, as such, do not have a visible neural tail. Consequently, the distinction between leiomyoma and nerve sheath tumor is often difficult.

Fig. 25.

Osteoarthritis may affect any joint in the mid- to forefoot, but it most commonly involves the joints of the medial longitudinal arch. The medial column, which is composed of the 1^st MTP joint, or middle column, which comprises the 2^nd and 3^rd MTP joints, are usually affected more than the lateral column, which includes the 4^th and 5^th MTP joints⁽³⁰⁾. Patients present with pain aggravated by prolonged weight-bearing. Radiography is the first line of investigation. US is usually undertaken to establish osteoarthritis as the likely cause of dorsal midfoot pain and swelling. Dorsal foot swelling in such instances is typically caused by hypertrophic dorsal osteophytes and capsular/soft tissue swelling, though paraarticular ganglia are also common. US reveals joint space narrowing with marginal osteophytosis, capsular thickening, and mild surrounding soft tissue swelling, possibly with hyperemia on Doppler imaging (Fig. 26)⁽³⁰⁾. As the curvature of the articular surfaces and marginal osteophytosis limits accurate US assessment of joint space narrowing, radiographic correlation is useful in this regard. If surgery is considered, CT optimizes delineation of osseous anatomy, disease extent, and severity, as well as alignment. Cone beam CT is a small footprint, self-shielded device, producing high-quality localized CT images of the mid- and forefoot, and is a useful emerging imaging modality for foot osteoarthritis, not least that the examination can be obtained in the weightbearing position⁽³⁰⁾. MRI is advantageous in showing subchondral BME, which is moderately associated with pain with or without focal articular cartilage defects. MRI, however, is usually not required to investigate suspected mid- and forefoot osteoarthritis.

Fig. 26.

Gravity and the relatively colder temperatures of the mid- and forefoot encourage uric acid crystal deposition. This deposition mainly occurs in periarticular tissues and ligamentous insertions. Intratendinous or peritendinous deposition is also common (Fig. 27). The first MTP joint is the most affected. Patients may present acutely with a painful joint similar to septic arthritis, or chronically with an intermittently painful mass or an enlarged joint due to gouty tophi. A diagnosis of gouty arthritis/gouty tophi can usually be adequately established with radiographs and US. There is usually little benefit to performing MRI examination. Dual energy CT is helpful to establish the presence of uric acid accumulations, though it is falsely negative in gouty arthritis without uric acid accumulation.

Fig. 27.

Calcium pyrophosphate deposition (CPPD) can also occur in the foot. The presentation is similar to gout, though tophi tend to be less prevalent, and crystal deposition occurs in the mid-zone articular cartilage layer, as opposed to the cartilage surface, though such delineation is generally not feasible in the thin articular cartilage of the foot.

Hallux valgus is excessive adduction at the first MTP joint. This diagnosis is made clinically, with supportive radiographs⁽³¹⁾. US is usually not necessary, though it may reveal osteoarthritis of the first MTP joint. MRI is usually not indicated. The normal hallux angle is 8–12°⁽³¹⁾. Adventitial bursitis is a relatively uncommon complication of hallux valgus that can be assessed by US.

Pes planus, or flatfoot, results from variable collapse of the medial longitudinal arch. This can be associated with posterior tibialis tendinosis either at its insertion or along the course of the posterior tibialis tendon (Fig. 28). Tendinosis and tendon tears can be evaluated well with US, as can the presence of an often accompanying accessory navicular bone or cornuate configuration to the medial pole of the navicular bone. MRI allows a more comprehensive assessment of navicular configuration, medial longitudinal arch flattening, talar head support, heel valgus, sub-talar and sub-fibular impingement, as well as reactive ligamentous thickening and tears.

Fig. 28.