Ischiofemoral impingement (IFI) syndrome results from narrowing of the space between the femur and the ischial tuberosity [10–12]. Clinical symptoms and signs are often nonspecific and require correlation with MR findings.

Numerous factors may predispose to IFI. Developmental etiologies include coxa valga, lesser trochanteric prominence, abnormal femoral torsion and variation in pelvic morphology. Acquired etiologies include hip instability, postural imbalances, extreme hypermobility, post-traumatic deformity and ossific enthesopathy.

The distance between the lesser trochanter and ischium depends on patient positioning, which is difficult to standardize during MR imaging. This distance is narrowed when the hip is adducted, internally rotated and extended, but widened when the hip is abducted, externally rotated and flexed. Because of variations in patient positioning, distance measurements in IFI diagnosis remain unvalidated. Asymmetric narrowing of the ischiofemoral space improves specificity when the left and right hips have identical positioning.

Besides narrowing of the ischiofemoral space, major MR findings associated with IFI include edema of quadratus femoris muscle, fatty atrophy of quadratus femoris muscle, edema or bursal fluid involving ischiofemoral fat, and elongated, hook-shaped lesser trochanter (Fig. 2). Less specific findings include hamstring tendon tear, bony proliferative change at ischial tuberosity, and unbalanced adductor-abductor musculature (e.g. asymmetric atrophy of gluteal musculature and tensor fascia lata).

Diagnostic injection can help to confirm the diagnosis of IFI. Using CT or US guidance, a needle is inserted into the ischiofemoral space for administration of anesthetic (with or without corticosteroid). A positive injection test occurs when concordant symptoms are produced during needle placement, or post-injection symptoms are substantially decreased.

Athletic pubalgia results from overuse activity. The prevelance of athletic pubalgia is greatest in sports that require rapid changes in speed and direction such as soccer, American football, ice hockey, fencing and certain track and field events.

Groin pain is common in athletes and poses diagnostic challenges because of numerous, complicated etiologies [13]. In clinical practice, patients with athletic pubalgia complain of the insidious onset of exertional pain and tenderness over the pubic, inguinal and adductor regions. Structural abnormalities include adductor longus tear, common adductor-rectus abdominis dysfunction, osteitis pubis and inguinal wall disruption (Sportsman’s hernia).

On MR images, functionally related structures include the pubis and pubic symphysis, rectus abdominis, adductor longus, adductor brevis and gracilis [14, 15]. The sheath of rectus abdominis passes over the pubis and pubic symphysis, forming a thick aponeurosis. This aponeurosis creates a prepubic aponeurotic complex (P-PAC) by providing a common adductor longus-rectus abdominis attachment site that also anchors the posterior wall of the inguinal canal.

In athletic pubalgia, MR abnormalities typically involve the adductor longus tendon at the pubic and P-PAC attachment sites. Adductor longus enthesopathy may be associated with adjacent bone marrow edema in the pubis. As the tendons strip away from bone, enthesopathy progresses to a fluid-filled tear best characterized in the coronal or sagittal plane. The secondary cleft sign indicates communication between the adductor tear and the symphyseal joint space (Fig. 3). Adductor tears may propagate along the P-PAC into the attachment site of rectus abdominis.

The spectrum of athletic pubalgia includes altered mechanics, P-PAC insufficiency, symphyseal instability and osteitis pubis characterized by bone marrow edema on MR images. MR signs of chronic instability include fatty infiltration of bone marrow, thickening of the superior pubic ligament, and degenerative changes such as symphyseal sclerosis and subchondral cysts.

Just as pre-existing hamstring tear predisposes to spontaneous tendon rupture, pre-existing adductor tear and symphyseal instability predispose to the avulsion of common adductors, gracilis and rectus abdominis. They also lower the threshold for acute myotendinous strain of parasymphyseal musculature, including pectineus, obturator externus and adductors. Once the first strain occurs, weakened muscle is susceptible to repeated injury.

The condition called Sportsman’s hernia encompasses two distinct inguinal pathologies [13] and insertional fascial deficiencies. In posterior inguinal wall deficiency, the posterior wall of the inguinal canal is weakened due to tearing of the conjoint tendon and transversalis fascia. In Gilmore’s groin, the anterior wall and superficial ring of the inguinal canal are weakened due to tearing of the external oblique aponeurosis. No hernia is present in either condition. MR imaging findings are minimal or absent unless the injury is acute, in which case edema and hemorrhage may be detectable in the inguinal canal [14, 15]. Skilled operators may be able to identify subtle inguinal defects using ultrasound.

The surface of the greater trochanter consistently shows four distinct facets—the anterior, lateral, posterior and postero-superior facet [16]. All these facets serve as tendon attachments (anterior, lateral, and postero-superior facet) or are covered by a bursa (posterior facet).

The gluteus medius tendon is a tendon which has attachments all around the greater trochanter. The strong main tendon attaches to the postero-superior facet. The lateral part of the gluteus medius tendon attaches to the lower portion of the lateral facet. The anterior part of the gluteus medius tendon is a muscular attachment onto the gluteus minimus tendon.

In contrast to the gluteus medius tendon, the gluteus minimus tendon is a purely anterior structure. The lateral part attaches to the peripheral areas of the anterior facet, the medial part attaches onto the hip joint capsule.