The proximal rectus femoris has two heads. The direct (or „straight”) head arises from the anterior-inferior iliac spine, and contributes to the anterior fascia of the muscle. The indirect (or „reflected”) head arises from the superior acetabular ridge and hip capsule, contributing to a long musculotendinous junction within the muscle [10]. Rectus femoris strains targeting this deep intramuscular musculotendinous junction (sometimes referred to as the central tendon or aponeurosis) can result in a „bull’s-eye sign” on MRI, and have a longer rehabilitation time than strains located at the muscle periphery [11].

The hamstrings are composed of the semimembranosus, semitendinosus and biceps femoris [12–14]. The semimembranosus origin is the superolateral facet of the ischial tuberosity. The semitendinosus and biceps femoris long head originate from a conjoint tendon at the inferomedial facet of the ischial tuberosity. High-grade or complete tendon rupture (or bony avulsion) at the proximal hamstring complex is considered an indication for surgical repair in active young adults, with better results in the acute setting [13].

The hamstrings are the most commonly injured muscles in sprinting and jumping athletes. Of the three hamstring components, the biceps femoris long head is the most commonly injured in the classic abrupt-onset hamstring strain. Less commonly, in some sports (e.g., dance), the onset of a stretching injury may occur more slowly, target the proximal semimembranosus tendon, and take much longer to heal [15]. Rehabilitation time may be suggested by the extent of hamstring injury seen by MRI. Convalescence periods reportedly vary widely from 2 weeks to 1.5 years before patients can return to vigorous activities. Recurrent injuries are common, occurring in one-quarter of athletes. Even minor hamstring injuries may double the risk of a more severe injury within 2 months.

Several muscles and tendons at the posterior aspect of the knee and calf may be subjected to strain injuries, including the gastrocnemius, soleus, plantaris, and popliteus muscles. „Tennis leg” may be defined clinically as the sudden onset of sharp pain in the mid-calf while participating in athletics (e.g., racket sports, running), typically in middle-aged persons [16]. Most commonly, these injuries are partial tears involving the (fast-twitch) medial head of the gastrocnemius muscle. Isolated strain of the (slow-twitch) soleus muscle is less common, usually occurring with endurance activities [17]. Treatment is almost always conservative, typically with relief of pain within 2 weeks and return to sports after at least 3 weeks. Clinical differential diagnosis may include a ruptured Baker’s cyst, overuse „tendinitis”, stress fracture, chronic exertional compartment syndrome, fascial herniation, venous thrombosis, nerve entrapment and popliteal artery entrapment syndrome.

Given that the physis is a weak link in the biomechanical chain for skeletally immature patients, we commonly see apophyseal avulsion fractures in adolescent athletes. The pelvis, with its many apophyses, is a common site for such avulsions. In one study of 203 adolescent athletes with acute pelvic avulsion fractures, the most common sites were: (1) the ischial tuberosity (origin of the hamstrings), (2) the anterior-inferior iliac spine (origin of the rectus femoris), and (3) the anterior-superior iliac spine (origin of the sartorius) [18]. Such avulsions generally are treated conservatively and have a good prognosis, although nonunions can occur. The imaging appearance of osseous avulsion injuries may be mistaken for a neoplastic or infectious process, especially in the nonacute setting when no history of trauma is provided. Knowledge of the major tendinous attachments to bone is indispensible in arriving at a correct diagnosis — and avoiding misdiagnosis of an osteochondroma or osteosarcoma.

Unlike muscle strains caused by indirect (noncontact) injury, contusions are caused by direct concussive trauma, usually by a blunt object. The resultant interstitial edema and hemorrhage correspond to the site of impact (rather than being localized to the myotendinous junction). Hemorrhage can be seen in the muscle, intermuscular fat planes or the subcutaneous tissues. Soft tissue hemorrhage can collect focally, resulting in a hematoma.

Several sequelae of musculotendinous injury may be observed, including hematoma, heterotopic ossification, fibrosis and atrophy. These sequelae are not specific to the post-traumatic setting, but rather reflect the limited pathological responses that muscle has when confronted with a wide array of insults.

Intramuscular hematomas evaluated between 5 days and 5 months after injury commonly display characteristics of methemoglobin, with increased signal intensity on both T1- and T2-weighted images. Most intramuscular hematomas tend to diminish in size over a period of 6– 8 weeks. Differentiation between a simple hematoma and a hemorrhagic neoplasm may be difficult in some patients both clinically and with imaging. Administration of contrast material aids in excluding a neoplasm when the lesion in question shows no enhancement. Conversely, the presence of an enhancing nodule in a muscle lesion may suggest the diagnosis of a neoplasm rather than a hematoma (Fig. 2). When the diagnosis of a probably benign hematoma is in doubt, clinical correlation and a follow- up MRI examination are indicated to confirm lesion stability or resolution. In the chronic setting, serous-appearing fluid may linger within a connective tissue sheath, creating an intramuscular pseudocyst or „seroma”. Heterotopic ossification also may occur.

The most common type of heterotopic ossification occurs in muscle, and commonly is referred to as myositis ossificans. Risk factors for heterotopic ossification include traumatic insults (e.g., contusion, surgery, burns), neurological insults (e.g., paraplegia, traumatic brain injury, stroke), or bleeding dyscrasias (e.g., hemophilia). In the clinical and radiological arenas, three typical phases of evolution occur: (1) an acute or pseudo-inflammatory phase; (2) a subacute or pseudotumoral phase; and (3) a chronic, self-limited phase that may (or may not) undergo spontaneous healing. In the acute and subacute stages of myositis ossificans, imaging examinations have a notoriously nonspecific appearance. CT is the single best imaging examination for showing the characteristic ossific matrix. In the final stage, the imaging findings that permit confident differentiation of myositis ossificans from neoplasm are: (1) the ossific mass is well-defined, sharply marginated, and appears more mature peripherally than centrally with architecture that approximates native bone (an area of cancellous bone centrally surrounded by compact bone peripherally); (2) the lesion generally decreases in size with the passage of time; and (3) there is no destruction in the underlying bone.

Imaging findings evolve over time, and are typically nonspecific in the acute and subacute stages. The involved muscle is enlarged and underlying periostitis is common. With MRI, the muscle exhibits nonspecific intermediate T1 and high T2 signal intensity. As the lesion matures, T2 hyperintensity and contrast enhancement progressively decrease. The signal intensity of the lesion may remain inhomogeneous, although areas of signal intensity equivalent to marrow fat and cortical bone increase [19]. Mature myositis ossificans is easiest to recognize when there is a low signal rim and fat signal centrally, although persistent granulation-type tissue may make the diagnosis difficult by MRI.

Myositis ossificans has been designated a „don’t touch” lesion that should not be biopsied injudiciously. Treatment for myositis ossificans may include physical therapy, nonsteroidal antiinflammatory agents, bisphosphonates, low-dose irradiation therapy and, in uncommon cases, surgical resection for a bulky area of ossification that causes nerve entrapment or limits range of motion. Surgical resection of myositis ossificans traditionally is performed after the mass „matures” in the hopes of minimizing the risk of recurrence.

Fibrosis is characteristically displayed as low signal intensity tissue in muscle on T2-weighted images after a nonacute insult. Recognized sites of muscle fibrosis include the deltoid, gluteus maximus and the vastus lateralis. Evaluation of the clinical impact and treatment of fibrosis is an active area of research.

Muscle atrophy may occur after certain musculotendinous injuries, disuse or other insults. The cardinal feature of muscle atrophy is decreased muscle volume, which is often accompanied by fatty infiltration. The most frequent site of muscle atrophy is in the shoulder girdle after a rotator cuff tear. After a supraspinatus tendon tear, adjacent muscle atrophy is recognized as a negative prognostic factor for patients undergoing cuff repair. Atrophy of other shoulder girdle muscles also can occur, even when the rotator cuff tendons are intact. Muscle atrophy begins to develop within 10 days after immobilization. After bed rest for 20 days, the muscle cross-sectional area decreases approximately 10% in healthy men [20]. Muscle atrophy may be partially irreversible by 4 months.