De Quervain tenosynovitis is the most common tendinopathy of the wrist in athletes. It is caused by a shearing stress injury of the first extensor compartment tendons along the radial styloid. Repetitive wrist motion with radial or ulnar deviation and flexion or extension may result in tenosynovitis or even tearing of the extensor pollicis brevis and abductor pollicis longus tendons (Bancroft 2013; Davis and Blankenbaker 2010).

Two types of intersection syndrome have been described. The first is an overuse injury as a result of repetitive microtrauma. The condition is also known as oarsmen’s wrist, squeaker’s wrist, or crossover syndrome (Bancroft 2013; Lee et al. 2009). MRI demonstrates peritendinous edema of the first and second extensor compartment tendons (abductor pollicis longus and extensor pollicis brevis) in the distal forearm as they cross over each other, hence the term crossover syndrome. Distal intersection syndrome results in peritendinous edema of the second and third extensor compartment tendons as they cross over each other (Fig. 21.6) (Bancroft 2013; Parellada et al. 2007).

Three bursal groups are found about the hip: the trochanteric, ischiogluteal, and iliopsoas bursae. The trochanteric bursa consists of the subgluteus maximus, subgluteus medius, and subgluteus minimus bursae. Hip bursopathy is also known as greater trochanteric pain syndrome as the trochanteric bursa is most commonly affected. It is often associated with gluteus medius and minimus tendinopathy. It is more commonly seen in women, likely because of the wider pelvis in women. Running on a cambered road, an unusually prominent trochanter and excessive adduction are further risk factors. MRI demonstrates fluid distention of the bursae. Signs of inflammation and/or hemorrhage include synovial thickening, internal debris, septations, and fluid-fluid levels (Fig. 21.7) (Spiker et al. 2012; Pan and Bredella 2013; Cho et al. 2004).

Snapping hip syndrome is also known as coxa saltans, iliopsoas tendinopathy, or dancer’s hip. It presents as an often painful snapping sensation and/or audible snapping sound that occurs at the hip during a specific motion. It is more common among younger athletes. External and internal types have been described (Spiker et al. 2012). External snapping hip syndrome is caused by either the iliotibial band, tensor fascia lata, or tendon of the gluteus maximus muscle rapidly sliding over the greater trochanter. External snapping is often a clinical diagnosis and rarely requires imaging. Internal snapping hip syndrome is more complex and may occur when the iliopsoas tendon slides over the iliopectineal eminence, femoral head, lesser trochanter, or the anterior hip capsule. It may also occur when the biceps femoris tendon slides over the ischial tuberosity or the iliofemoral ligament slides over the femoral head (Pan and Bredella 2013). Ultrasound is the investigation of choice for dynamic evaluation of the iliopsoas tendon in internal snapping. It is seen as a sudden lateral-to-medial movement of the tendon as it passes over the iliopectineal eminence. Ultrasound can also be used as a therapeutic modality for guided injection of a combination of a local anesthetic agent and a corticosteroid into the iliopsoas bursa (Deslandes et al. 2008; Pelsser et al. 2001). Further causes of internal snapping include labral tears, intra-articular loose bodies, synovial osteochondromatosis, and fracture fragments all of which can be well evaluated by means of arthrographic MRI (Fig. 21.8) (Spiker et al. 2012; Pan and Bredella 2013).

Piriformis syndrome is still a poorly understood clinical entity. Patients present with isolated sciatic pain affecting the buttock with radiation to the upper thigh, but without sensory fallout. Described radiological features include piriformis muscle hypertrophy and an anomalous course of the S2 nerve root, most notably an intramuscular course traversing through the piriformis muscle. There is also a lack of more common causes of sciatica such as lumbar disk herniation (Russell et al. 2008; Lee et al. 2004; Papadopoulos and Khan 2004). Image-guided injection of the piriformis muscle initially with air (marker) followed by local anesthetic and cortisone can be used as a diagnostic test. If successful, intramuscular injection of Botox has shown good medium term results as the abnormal piriformis muscle atrophies (Fig. 21.9) (Filler et al. 2005).

Osteitis pubis is part of the entity known as athletic pubalgia (Galloway 2013; Lovell et al. 2006). It occurs as a result of repetitive vertical shearing forces across the pubic symphysis (Tuite 2010). MRI demonstrates bone marrow edema at the pubic symphysis. It may be associated with adductor tendinopathy, posterior abdominal wall weakness, and incipient inguinal hernia (Gilmores groin) (Fig. 21.10) (Tuite 2010; Galloway 2013; Lovell et al. 2006).

A cyclist’s nodule represents a focal mass-like lesion of the perineum associated with cycling. It is also known as a biker’s nodule or third testicle (Van de Perre et al. 2009). It is characterized by focal fibroblastic and myofibroblastic proliferation and myxoid degeneration of adipose and collagenous tissue overlying the ischial tuberosities, resulting from pressure, friction, and vibration between the tuberosities and the bike saddle (McCluggage and Smith 2001). Ultrasound demonstrates a hypoechoic hypovascular superficial soft tissue nodule of the perineum. Small focal internal cystic areas may also be present. MRI shows a hypointense, irregular, non-enhancing lesion in the subcutaneous fat (Fig. 21.11) (Van de Perre et al. 2009).

Patellar tendinopathy is also known as jumper’s knee. It usually presents with acute onset anterior knee pain during running and cycling. During cycling, the high extension forces during the down stroke places strain on the patellar tendon. It often occurs due to a low cadence with high resistance, associated with hill climbing and cycling while standing (Bailey et al. 2003). Tendinopathy usually occurs at the proximal enthesis (Tuite 2010; Deakon 2012; Ostlere 2013). Ultrasound is the initial imaging modality and shows a hypoechoic focus in the tendon. There is usually associated increased echogenicity in the adjacent Kager fat pad. The abnormal focus of tendinosis may demonstrate increased Doppler signal, in keeping with neovascularization. MRI reveals thickening of the tendon with increased signal intensity on fluid-sensitive sequences. Bone marrow edema may be present in the inferior pole of the patella (Fig. 21.12) (Ostlere 2013).

Patellofemoral stress syndrome is also called runner’s or biker’s knee (Tuite 2010; Ostlere 2013). Causes are multifactorial and usually include a combination of overuse, trauma, and abnormal biomechanics. It is described more often in female athletes. It is postulated that the latter is due to a greater Q angle resulting in an increase in the lateral displacement forces and patellar maltracking. Excessive load is placed on the patellofemoral joint. X-rays may be normal or may demonstrate a patella alta, lateral subluxation of the patella, and/or features of trochlear dysplasia. Quadriceps muscle imbalance with relative deficiency of the vastus medialis obliquus muscle group may be a further etiological factor. MRI is the investigation of choice to assess the patellofemoral chondral surfaces. Chondral degeneration, delamination, chondral defects with a bone stress reaction, and eventually patellofemoral osteoarthrosis may occur (Figs. 21.13 and 21.14) (Ostlere 2013).

ITBS occurs with repetitive friction between the distal iliotibial band and the lateral femoral condyle. The condition presents as lateral knee pain. It usually occurs between 10 and 30° of knee flexion. Both running and cycling may result in and cause aggravation of ITBS (Tuite 2010; Spiker et al. 2012; Farrell et al. 2003). Factors that may increase the risk of occurrence include suboptimal seat position, especially when the seat is too high or too far back. Running on a cambered road, downhill running, treadmill running, leg length discrepancy, and a too rapid increase in distance per week are further risk factors. Weak hip abductors are also associated with an increased risk of ITBS. MRI findings include poorly defined high signal intensity or a circumscribed fluid collection deep to the iliotibial band on fluid-sensitive sequences (Fig. 21.15) (Deakon 2012; Galloway 2013).

Meniscal tears may occur due to repetitive impaction forces during running. They are more common in older athletes (Tuite 2010; Shellock et al. 2003). The posterior horn of the medial meniscus is most commonly affected (Fig. 21.16).

Plicae are normal anatomic structures without a known function. They represent remnants of synovial membrane from embryologic development. They may become symptomatic, resulting in pain and discomfort. (García-Valtuille et al. 2002) Plica syndrome is defined as painful impairment of knee function with a thickened and fibrotic plica. This is thought to be secondary to the hyperflexion position of the knee during extended periods in the aero position. It may be associated with a joint effusion and synovitis. It may also result in erosion about the femoral condyles and/or patellar cartilage damage. Most common plicae include the infrapatellar, suprapatellar, and mediopatellar plicae. The mediopatellar plica most commonly becomes symptomatic (Fig. 21.17) (García-Valtuille et al. 2002; Boles et al. 2004; Dirim et al. 2008; Jee et al. 1998).

Popliteal artery entrapment syndrome represents a further vascular compression syndrome. It is characterized by compression of the popliteal artery between the two heads of the gastrocnemius muscle. Compression may result in thrombosis with or without distal embolization as well as aneurysm formation. The underlying etiology is anatomic variation in the relationship between the gastrocnemius muscle and the popliteal artery. Six types have been described. Type 3 is the most common, characterized by an abnormal accessory slip of the gastrocnemius muscle (Fig. 21.18) (Eliahou et al. 2012; Kim et al. 2006).

Cystic adventitial disease is characterized by luminal compression secondary to the formation of mucoid cysts in the adventitia (Tomasian et al. 2008). It was first described by Atkins and Key in 1947 and has an incidence of approximately 1 in 1200 of patients presenting with claudication (Wright et al. 2004). Less than 350 cases have been described worldwide. The disease typically affects men between 20 and 50 years without atherosclerotic risk factors. Involvement of the external iliac, femoral, popliteal, radial, and ulnar arteries as well as veins has been described. The popliteal arteries are most commonly affected, involved in approximately 85 % of described cases. It is hypothesized that repetitive adventitial microtrauma may be an etiological factor. Cystic adventitial disease has been described in conjunction with popliteal artery entrapment syndrome, supporting the microtrauma hypothesis (Tomasian et al. 2008; Wright et al. 2004). Athletes present with rapidly progressive calf claudication. Ultrasound and MRI may demonstrate focal cystic lesions in the adventitia with associated luminal narrowing (Fig. 21.19).