MRI of Nontumorous Skeletal Muscle Disease: Case-Based Review

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1 MRI of Nontumorous Skeletal Muscle Disease: Case-ased Review Hyojeong Mulcahy 1, Felix S. Chew JR Integrative Imaging LIFELONG LERNING FOR RDIOLOGY Objective The educational objectives for this case-based review are to use case examples to improve skills in diagnostic radiology with regard to the interpretation of MRI of nontumorous skeletal muscle disease and to improve understanding of the pathophysiology and clinical features of each scenario. MRI is a useful tool for assessing muscle disease. In this article, multiple cases illustrating common and a few uncommon nontumorous skeletal muscle diseases will be presented. t the end of this article, readers will be able to generate a concise list of differential diagnoses for nontumorous skeletal muscle disease to make the correct diagnosis or to guide appropriate treatment. Scenario 1 Three days after a minor trauma, a 20-year-old man presented with continuous right thigh pain and swelling. The patient had a history of hypertension and had recently experienced acute gastric ulcer bleeding associated with nonsteroidal antiinflammatory drug use. n MRI examination of his right thigh was performed. The axial contrast-enhanced T1-weighted fat-saturated MR image (Fig. 1) shows a rim-enhancing cystic lesion in the adductor brevis, which shows a corresponding dark-signal-intensity rim that appears to bloom on the gradient-echo image (arrow in Fig. 1C). The axial T2-weighted fat-saturated image (Fig. 1) shows increased signal intensity not only of the cystic lesion but also at the insertion of the adductor brevis at the posterior femoral shaft (linea aspera). The surrounding muscle fibers within the adductor brevis show mild enhancement and mildly increased T2 signal intensity (Figs. 1 and 1). Muscle injuries that result in hemorrhage or the disruption of muscle fibers may reveal a masslike pattern on MR images. Moderate to severe muscle strain, laceration, and contusion are examples of such injuries. Intramuscular or intermuscular hematomas may be seen with any of these lesions or may occur spontaneously, especially in patients receiving anticoagulant therapy [1]. Most of the intramuscular hematomas that are evaluated with MRI between 2 days and 5 months after injury display characteristics of methemoglobin, with increased signal intensity on both T1- and T2- weighted images. Occasionally, serous-appearing fluid from a hematoma may linger within a connective tissue sheath, creating an intramuscular pseudocyst [2]. In this case, a lowsignal-intensity rim in all sequences (hemosiderin) may suggest the diagnosis of intramuscular hematoma. n intramuscular hematoma may mimic an intramuscular abscess, hemorrhagic neoplasm, or myonecrosis on MR images because all of these lesions may contain fluid-fluid levels and show surrounding muscle edema and enhancement. However, these conditions can be differentiated by clinical settings because intramuscular hematomas are usually seen after a muscle injury or in patients receiving anticoagulant therapy; the clinical history usually allows distinction among these conditions [1]. Hematomas are common after a myotendinous injury and may be predominantly intramuscular or intermuscular in location. Intramuscular hematomas often resorb spontaneously over a period of 6 8 weeks. With an equivocal or remote history of trauma, imaging may be indicated to assess a soft-tissue mass that is clinically suspected of being neoplastic. When the diagnosis of a probably benign hematoma is in doubt, clinical correlation and a follow-up MRI examination may be indicated to establish the appropriate evolution of the abnormality [2]. Differentiation between simple hematoma and hemorrhagic neoplasm may be difficult in some patients. oth of these lesions may contain fluid-fluid levels and show surrounding muscle edema and enhancement. Three potential diagnostic pitfalls must be recognized when interpreting the enhancement of a focal lesion after the IV administration of gadolinium contrast material. First, contrast enhancement is possible in the fibrovascular tissue of an evolving hematoma, Keywords: case-based learning, MRI, musculoskeletal imaging, nontumorous skeletal muscle disease, self-assessment, skeletal muscle DOI: /JR Received July 17, 2009; accepted after revision January 6, oth authors: Department of Radiology, University of Washington, ox , 4245 Roosevelt Way NE, Seattle, W ddress correspondence to H. Mulcahy (hyomul@u.washington.edu). JR 2011; 196:S77 S X/11/1966 S77 merican Roentgen Ray Society JR:196, June 2011 S77

2 Mulcahy and Chew potentially making differentiation from neoplasm difficult. Second, gadolinium may diffuse slowly into a fluid-filled space, such as a hematoma or an abscess. Consequently, imaging should be performed promptly after contrast administration to avoid spurious enhancement within a mass that might falsely suggest that it is solid. Third, minimal or no appreciable enhancement may be observed in myxoid lesions, Fig year-old man who presented with right thigh pain and swelling., xial contrast-enhanced T1-weighted fat-saturated image shows rim-enhancing lesion in adductor brevis., xial T2-weighted fat-saturated image shows high signal intensity of lesion. lso, there is increased signal intensity at insertion of adductor brevis along posterior femoral shaft (linea aspera). C, xial gradient-echo image shows some peripheral dark regions that appear to bloom (arrow). Scenario 2 38-year-old woman with a history of refractory myelodysplastic syndrome and acute myelogenous leukemia presented with febrile neutropenia and leg pain, which was treated with levofloxacin and vancomycin. physical examination revealed painful small red nodules on both feet, legs, arms, and trunk. MRI of the right lower extremity was performed. which then may be confused with cysts or lesions with a cystic component. When the lesion in question shows enhancing nodules, however, it may suggest the diagnosis of a neoplasm rather than a hematoma [3]. The diagnosis is adductor brevis hematoma due to injury. The axial contrast-enhanced T1-weighted fat-saturated (Fig. 2) and STIR (Fig. 2) MR images show numerous intramuscular ring-enhancing lesions, most of which measure 4 6 mm each. These lesions are seen within every compartment, and there is some edema. However, there is no mass effect in the surrounding muscles. lso, there is some fluid along the anterior fascia (arrow in Fig. 2). The imaging appearances of primary skeletal muscle infection vary according to whether the infection is confined to the muscle, whether there is secondary extension to the neighboring tissues, and whether abscesses have developed or myonecrosis has occurred. Most cases of infectious myositis are bacterial in cause, with Staphylococcus aureus being the most common causative organism. MRI commonly reveals nonspecific signs of inflammation, with changes in muscle signal (i.e., increased T2-weighted signal) and enhancement Fig year-old woman with history of refractory myelodysplastic syndrome and acute myelogenous leukemia who presented with febrile neutropenia and leg pain., xial contrast-enhanced T1-weighted fatsaturated image shows multiple small nodular ringenhancing lesions in anterior, posterior, and lateral compartments., xial STIR image shows high signal intensity corresponding to lesions shown in and small subfacial fluid collection along anterior fascia (arrow). There is no mass effect to surrounding muscles even though signal along some surrounding muscles is increased. C S78 JR:196, June 2011

3 Nontumorous Skeletal Muscle Disease Scenario 3 32-year-old man who was involved in a high-speed rollover motor vehicle accident was found several hours after the accident. During the course of resuscitation, he was found to have mild myoglobulinuria with associated rhabdomyolysis and underwent aggressive fluid resuscitation. fter resuscitation, a tense lag in the thigh led to a diagnosis of volume compartment syndrome. He underwent a fasciotomy of the left lateral thigh and a four-compartment fasciotomy of the calf. However, several days later, the patient developed severe pain in the calf and associated fever. MRI of the left lower extremity was performed to evaluate for possible postsurgical infection. Fig year-old man who recently underwent four-compartment fasciotomy of calf who presented with severe calf pain associated with fever., xial STIR image shows extensive high signal intensity of superficial posterior compartment muscles with fluid collection along superficial fascia circumferentially. Interestingly, central areas of those muscles (arrow) show relatively intermediate signal., xial contrast-enhanced T1-weighted fatsaturated image shows thick nodular peripheral contrast enhancement of superficial posterior compartment muscles. Interestingly, central areas of those muscles (arrow) are not enhanced. after gadolinium administration. Findings are usually limited to the muscles and the surrounding fascia, but inflammation (cellulitis) of adjacent soft tissues may also be seen [4]. fungal cause for infectious myositis is rare. When it occurs in immunocompromised hosts, the disease is frequently caused by Candida species. case of mucormycosis and one of fungal myositis caused by Fusarium species have been reported. Only six cases of spergillus-induced myositis or muscle abscess have been reported [5]. Schwartz and Morgan [6] reported multimodality imaging findings of the lower extremity of a patient with Candida tropicalis myositis. In that case, imaging revealed changes in the muscles typical of both myositis and solid-organ fungal disease. MRI showed these findings best, with good visualization of the numerous microabscesses similar in appearance to the lesions seen in solid-organ fungal disease. The microabscesses were superimposed on a background of diffuse muscular signal abnormality consistent with inflammation. Infections caused by spergillus species have dramatically increased in recent years; after Candida albicans, spergillus species are the most common causes of human opportunistic fungal infections in immunocompromised patients. Presentation of invasive aspergillosis is very varied throughout the patient population and includes multiple cutaneous ulcers and recurrent thoracic empyema. Fever unresponsive to broad-spectrum antibiotics is the earliest and most common sign of invasive aspergillosis. Cross-sectional imaging, such as MRI, is useful for the identification of intramuscular abscesses because these fluid collections are of high T2-weighted signal with a low-signalintensity rim that enhances after gadolinium administration. MRI also allows imaging of the full extent of muscle involvement, which CT is often unable to achieve. Treatment of spergillus fumigatus infection includes antifungal therapy in combination with surgical débridement [6, 7]. The diagnosis is fungal microabscesses due to spergillus species in a patient with systemic aspergillosis. The axial STIR image (Fig. 3) shows extensive high signal intensity of the superficial posterior compartment muscles of the left calf with a fluid collection along the superficial fascia circumferentially. The axial contrast-enhanced T1-weighted fat-saturated image (Fig. 3) shows a thick nodular peripheral contrast enhancement of the superficial posterior compartment muscles. Interestingly, however, the central areas (arrows in Figs. 3 and 3), which are not enhanced, show relatively intermediate signal intensity on the STIR image, indicating that these areas are not abscesses of fluid collections. Infarction of the skeletal muscle (myonecrosis) is relatively rare because skeletal muscle has a rich collateral blood supply. Myonecrosis generally results from ischemia caused by vasculitis, thromboembolic events, crush injury, and posttraumatic compartmental syndrome. Idiopathic myonecrosis occurs in the absence of obvious vascular compromise and has been associated with diabetes mellitus, alcoholism, infection, sickle cell crisis, intraarterial chemotherapy, and other causes [8]. It is an uncommon but well-recognized clinicopathologic entity in diabetes mellitus [1]. Kattapuram et al. [8] reported MRI findings of 14 patients with idiopathic and diabetic ischemic myonecrosis. T1-weighted images showed isointense swelling of the involved muscle, with mildly displaced fascial planes. Fat-suppressed T2-weighted images showed diffuse heterogeneous high signal intensity in JR:196, June 2011 S79

4 Mulcahy and Chew the muscles suggestive of diffuse edema. perifascial fluid collection was seen in eight patients. Subcutaneous edema was present in seven patients. fter IV gadolinium administration, MRI showed a focal area of a heterogeneously enhancing mass with peripheral enhancement. Within this focal lesion, linear dark areas were seen, with serpentine enhancing streaks separating the areas in eight patients. No focal fluid collection was noted. There was no association with calcification. Compartment syndrome refers to elevated pressure in a relatively noncompliant anatomic space that is associated with ischemia and may result in neuromuscular injury. The fundamental derangement in patients with compartment syndrome is elevated intracompartmental pressure. Regardless of the type of insult in any particular patient, the final common pathway to compartment syndrome involves a decreased arteriovenous gradient that can result in ischemia and, ultimately, tissue necrosis. Diagnostic tests used to evaluate for compartment syndrome include compartment pressure measurements, near-infrared spectroscopy, and imaging. lthough cross-sectional imaging is not the primary technique for diagnosing compartment syndrome, imaging may Scenario 4 54-year-old right-handed man presented with progressive weakness of the upper extremity. He first noticed weakness in his left hand about 2 years earlier. He works as an auto mechanic and had noticed that he was having trouble picking up his tools and holding them with a tight grip. His muscle weakness worsened slightly over the ensuing months, prompting him to seek medical treatment. The patient has never noticed weakness in other muscle groups, although he occasionally noted some fasciculation. On neurologic examination, he had motor weakness of both flexor digitorum profundus muscles without sensory involvement. n electromyogram was obtained and showed fibrillation changes in the forearm flexor muscle and some scattered forearm muscles including the pronator teres. There was no evidence of any neuropathic component. Fibrillation potentials were also seen in the left anterior tibialis and in the complement direct pressure measurements by providing noninvasive data on the compartment or compartments that are involved, particularly in the nonacute setting. Imaging also assists in the evaluation for an underlying lesion (e.g., hematoma or neoplasm) that may contribute to compartment hypertension and needs to be addressed at surgery. Other potential indications for MRI include the diagnostic evaluation of atypical cases (e.g., an uncommon location or cause for compartment syndrome and borderline pressure measurements) and follow-up evaluations. The critical threshold at which myoneural necrosis occurs may vary according to the location of the compartment syndrome, its acuity and duration, and individual patient factors (e.g., hypotension and softtissue trauma). In general, surgical decompression is performed when acute compartment pressures reach mm Hg. Findings favoring fascial release include increasing compartment pressures over time, paresthesia, and paresis [2]. The diagnosis is posterior superficial compartment muscle infarct after acute compartment syndrome. right flexor pollicis longus. MRI of both thighs was performed to decide on a site for muscle biopsy. The axial T1-weighted image (Fig. 4) shows bilateral, asymmetric fatty atrophy along the mid to distal thigh. The axial STIR image (Fig. 4) shows corresponding high signal. The left thigh is worse than the right, mainly involving the vastus lateralis and intermedius and minimally involving the vastus medialis bilaterally. Idiopathic inflammatory myopathies are chronic systemic connective tissue diseases that are clinically characterized by symmetric proximal muscle weakness. lthough the idiopathic inflammatory myopathies share the characteristics of immune-mediated attacks on skeletal muscle, they are in fact heterogeneous diseases with distinct histopathologic and Fig year-old man who presented with chronic, progressive proximal upper extremity weakness. xial MR images of bilateral thighs were obtained., xial T1-weighted image shows bilateral, asymmetric fatty atrophy involving quadriceps muscles, mostly severe in vastus intermedius and lateralis along mid to distal thigh., xial STIR image shows corresponding high signal intensity. Left thigh is slightly worse than right. S80 JR:196, June 2011

5 Nontumorous Skeletal Muscle Disease clinical characteristics. The idiopathic inflammatory myopathies represent a treatable group of disorders, but their differential diagnosis is wide. Early and accurate diagnosis is essential before commencement of therapy. lthough muscle biopsy is the essential and definitive diagnostic modality for idiopathic inflammatory myopathies, MRI has assumed a major role in idiopathic inflammatory myopathy evaluation and management primarily because MRI is very sensitive to inflammation and edema, especially with the incorporation of fat-suppression sequences. MRI is thus very good for diagnosing the disease early, determining the extent and number of lesions, locating a biopsy site in an area of active disease, and monitoring therapy responses [9]. Sporadic inclusion body myositis (IM) is the most common chronic myopathy presenting after the age of 50 years and is a prominent cause of progressive muscular weakness and disability in elderly persons. lthough sporadic IM has traditionally been regarded as an inflammatory myopathy, a number of features distinguish it from the other varieties of immune-mediated inflammatory myopathy, such as polymyositis and dermatomyositis. Foremost among these are a characteristic selectivity of involvement of certain muscle groups in the upper and lower limbs, at least in the earlier stages of the condition, and a poor response to corticosteroids and other forms of immunotherapy, which usually fail to halt the progression of the myopathy [10]. Viral infection by paramyxovirus is the likely cause of IM. bscess formation is not seen in this condition. IM resembles polymyositis at clinical evaluation and MRI. Thus, a biopsy is required for reliable differentiation between these conditions. The distinction is important because IM is not associated with malignancy and is managed differently than polymyositis [1]. Polymyositis and dermatomyositis are autoimmune inflammatory conditions of skeletal muscle characterized by the gradual onset of muscle weakness in the thighs and pelvic girdle that typically progresses to involve the upper extremities, neck flexors, and pharyngeal musculature. These conditions are caused by a cell-mediated (type IV) autoimmune attack on striated muscle. Polymyositis involves only skeletal muscle; dermatomyositis involves both skeletal muscle and skin. However, these conditions can overlap in clinical and imaging features. Polymyositis most frequently manifests during the fourth decade of life. Dermatomyositis has a Scenario 5 55-year-old man suffered a stretch injury to the left sciatic nerve during hip replacement surgery about 1 year earlier. He now presents with complete motor deficits in the distribution of the left peroneal nerve. MRI of the left lower leg was performed. bimodal pattern of manifestation, with peaks during childhood and the fifth decade of life. Childhood-onset dermatomyositis tends to be more severe than the adult-onset form. However, the adult-onset form is associated with an increased prevalence of a variety of malignancies, including those of the breast, prostate, lung, adnexa, and gastrointestinal tract. Typical MRI findings early in the course of the inflammatory myopathies are bilateral and symmetric edemas in the pelvic and thigh musculature, especially in the vastus lateralis and vastus intermedius muscles [1]. Typical MRI findings early in the course of the inflammatory myopathies are bilateral and symmetric edemas in the pelvic and thigh musculature, especially in the vastus lateralis and vastus intermedius muscles. The severity of muscle edema indicated on MR images has been shown to correlate with the severity of the disease. Neither myonecrosis nor abscess formation is a typical feature of idiopathic inflammatory myopathies. Fatty infiltration may be seen in the chronic stages of inflammatory myopathies. MR images reveal increased quantities of fat with its characteristic high T1 signal intensity within the involved muscle, usually with a decreased volume of muscle tissue. Gadolinium enhancement in combination with fat-suppression imaging is superior to routine imaging. The theory behind this difference in techniques is that muscle inflammation results in increased vascularity, so this technique is potentially useful for detecting scattered areas of inflammation and increased vascularity within different muscles. MRI can show areas of active myositis, which are highlighted on T2-weighted images and STIR images, and can separate them from areas of fatty infiltration and atrophy, which are highlighted by T1-weighted images, thus minimizing the false-negative rate of muscle biopsy [9]. lthough muscle biopsy is the essential and definitive diagnosis modality for idiopathic inflammatory myopathies, MRI has assumed a major role in idiopathic inflammatory myopathy evaluation and management primarily because MRI is very sensitive to inflammation and edema, especially with the incorporation of fat-suppression sequences. MRI is thus very good for an early diagnosis of disease, determining the extent and number of lesions, locating a biopsy site in an area of active disease, and monitoring therapy responses [9]. The diagnosis is IM. The axial T1-weighted image (Fig. 5) shows fatty atrophy of the anterior and lateral compartments of the lower extremity, including the tibialis anterior, extensor digitorum longus, extensor hallucis longus, peroneus brevis, and longus muscles. The axial contrast-enhanced T1-weighted fat-saturated image shows diffuse contrast enhancement JR:196, June 2011 S81

6 Mulcahy and Chew (Fig. 5) and the STIR image shows corresponding high signal intensity of those muscles (Fig. 5C). Fig year-old man who came with complete motor deficits in distribution of left peroneal nerve., xial T1-weighted image shows fatty atrophy of muscles in anterior and lateral compartments., xial contrast-enhanced T1-weighted fat-saturated image shows diffuse contrast enhancement of anterior compartment muscles. C, xial STIR image shows corresponding high signal intensity. Muscle denervation results from a variety of causes including trauma, neoplasia, neuropathies, infections, autoimmune processes, and vasculitis. Traditionally, the diagnosis of muscle denervation was based on clinical examination and electromyography. MRI offers a distinct advantage over electromyography not only in diagnosing muscle denervation, but also in determining its cause. The most frequent mononeuropathy in the lower extremity involves the common peroneal nerve around the fibular head and neck area. The common peroneal nerve arises from the sciatic nerve at the upper level of the popliteal fossa. It descends obliquely along the lateral side of the popliteal fossa, posterior to the short head of the biceps femoris muscle, and then lateral and superficial to the lateral head of the gastrocnemius muscle. More inferiorly, it winds around the neck of the fibula, enters the anterior and lateral muscle compartments of the leg, and divides into the deep and superficial peroneal branches. The common peroneal nerve and its branches provide motor innervation to the anterior compartment of the leg (tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius muscles) and lateral compartment of the leg (peroneus longus and brevis muscles) and sensory innervation to the distal two thirds of the leg [11]. MRI shows characteristic signal intensity patterns depending on the stage of muscle denervation. The acute and subacutely denervated muscle shows a high-signal-intensity pattern on fluid-sensitive sequences and normal signal intensity on T1-weighted MR images. In chronic denervation, muscle atrophy and fatty infiltration show high signal changes on T1-weighted sequences in association with volume loss [12]. In clinical studies, abnormal signal intensity within the denervated muscles has been shown within 4 days of injury. These changes, however, may evolve over several weeks. Characteristic MRI signal intensity patterns in acute or subacute muscle denervation include high signal intensity of the muscles on fluidsensitive MRI sequences such as STIR or T2-weighted sequences and normal signal intensity on T1-weighted MR images. fter gadolinium administration, significant enhancement may be seen in the denervated muscles on T1-weighted images. lthough contrast enhancement can be appreciated in denervated muscles, contrast administration is not necessary in all patients because STIR and T2 fat-saturated sequences are sensitive in diagnosing muscle denervation. The signal abnormality on T2- weighted images and enhancement on contrast-enhanced T1- weighted images could last for up to 3 months after denervation. The denervated muscle sometimes results in denervation pseudohypertrophy, where the affected muscle paradoxically enlarges in response to the denervation. In true muscle hypertrophy, the enlarged muscle retains the normal signal intensity of the innervated muscle on all MRI sequences. However, in pseudohypertrophy, MRI shows an excessive amount of fat interspersed throughout the denervated muscle. Eventually, the volume loss resulting in muscle atrophy becomes apparent. Chronic denervation is often best seen on T1-weighted spinecho images as loss of muscle bulk and widespread areas of increased signal intensity resulting from fatty infiltration [12]. The diagnosis is denervation myopathy secondary to common peroneal neuropathy. C Scenario 6 61-year-old man was treated for a high-grade leiomyosarcoma in his right thigh. He received four cycles of neoadjuvant chemotherapy and subsequent surgery. He then completed an additional two cycles of adjuvant chemotherapy and subsequent radiation between 60 and 70 Gy to this region over 6 weeks. He presented with skin S82 JR:196, June 2011

7 Nontumorous Skeletal Muscle Disease blistering, pain, and stiffness in his right thigh. MRI of the right thigh was performed. The axial T2-weighted fat-saturated image (Fig. 6) shows increased T2 signal throughout the lateral muscles of the thigh involving the vastus lateralis, vastus intermedius, and rectus femoris anteriorly and the biceps femoris long head and semitendinosus posteriorly. The axial unenhanced and contrastenhanced T1-weighted fat-saturated images (Figs. 6 and 6C) show diffuse contrast enhancement of those muscles. Note the straight, sharp margins of the edematous tissue that correspond to the margins of the radiation field and the uniformly abnormal signal intensity of all tissues in the radiation field (arrows in Figs. 6 and 6C). lthough radiation-induced muscle injury is observed in experimental animal studies, it is infrequently reported in the clinical literature. Skeletal muscle has been considered relatively resistant to radiation injury, and damage induced by conventional external beam radiotherapy is infrequently observed. Radiation therapy causes vasculitis and tissue injury that may Scenario 7 33-year-old right hand dominant woman presented with right forearm pain. It was accompanied by a slowly enlarging soft but tender mass over her proximal dorsal forearm. The axial T1-weighted image (Fig. 7) shows an isointense, ill-defined lesion with mild mass effect to the surrounding muscles in the dorsal forearm centered between Fig year-old man who presented with skin blistering, pain, and stiffness in his right thigh., xial T2-weighted fat-saturated image shows increased T2 signal intensity throughout vastus lateralis, vastus intermedius, and rectus femoris anteriorly and throughout biceps femoris long head and semitendinosus posteriorly. Collection of small amount of subfascial fluid is seen along long head of biceps and semitendinosus. Note straight sharp margins of edematous tissue (arrows), which correspond to margins of radiation field, and uniformly abnormal signal intensity of all tissues in radiation field., xial T1-weighted image shows diffuse enlargement of involved muscles. C, xial contrast-enhanced T1-weighted fat-saturated image shows corresponding contrast enhancement. Like, this image also shows straight sharp margins of edematous tissue (arrows) and uniformly abnormal signal intensity of all tissues in radiation field. be seen on MR images as fairly uniform muscle edema. cute changes on MRI, characterized by bright T2-weighted signal intensity, indicate edema or inflammation within the treatment fields. Characteristic findings on MR images include edema throughout the radiation field and straight, sharp margins of edema that extend uninterrupted across muscle and subcutaneous fat. Chronic changes are mainly seen as discrete areas of muscle atrophy and fibrosis, often with overlying volume deficits corresponding to the radiation treatment ports [1]. These radiographic findings are generally more pronounced after neutron therapy than after conventional photon therapy [13]. s with inflammation-related pain from other causes, nonsteroidal antiinflammatory drugs are a reasonable initial intervention for active radiation myositis. The value of corticosteroids for radiation myositis is anecdotal and extrapolated from the utility of prednisone in other subacute radiation-related inflammatory conditions such as radiation pneumonitis. Hyperbaric oxygen therapy is beneficial in the treatment of extensive muscle tissue breakdown due to various causes, including radiation injury [13]. The diagnosis is radiation-induced myositis. the radius and ulna (arrow in Fig. 7). The axial fat-saturated T2-weighted image (Fig. 7) shows heterogeneous iso- to high signal intensity to muscle with surrounding edema. The radius shows high-signal-intensity marrow edema. The axial contrast-enhanced T1-weighted fat-saturated image (Fig. 7C) shows a mainly peripheral area of contrast enhancement. The corresponding axial CT image (Fig. 7D) shows the lesion with a central low density and peripheral dense ossification rim that is typical zonal phenomenon. C JR:196, June 2011 S83

8 Mulcahy and Chew C D Fig year-old, right-hand-dominant woman who presented with right forearm pain. Pain was accompanied by slowly enlarging soft but tender mass over her proximal dorsal forearm. xial MR ( C) and CT (D) images of right forearm were obtained., xial T1-weighted image shows isointense ill-defined lesion (arrow) with mild mass effect to surrounding muscles in dorsal forearm centered between radius (R) and ulna (U). Marrow of radius shows low-signal-intensity edema., xial fat-saturated T2-weighted image shows lobulated masslike lesion with heterogeneous iso- to high signal intensity to muscle with surrounding edema. Radius shows high-signal-intensity marrow edema. C, xial contrast-enhanced T1-weighted fatsaturated image shows mainly peripheral area of contrast enhancement. D, Corresponding axial CT image shows lesion with central low-density and peripheral dense ossification rim that is typical zonal phenomenon. R = radius, U = ulna. Myositis ossificans traumatica typically manifests as a soft-tissue mass that develops characteristic peripheral calcification over the next 6 8 weeks. This condition usually results from trauma but may also be seen in patients with paralysis, burns, tetanus, or an intramuscular hematoma or may develop spontaneously [1]. The radiographic pattern of posttraumatic myositis ossificans parallels the histologic pattern of maturation. Conventional radiographs may be normal at the outset. The earliest radiographic change, occurring within 7 14 days of trauma, is a soft-tissue mass that may be accompanied by faint periosteal new bone formation. y the third to fourth week, as the osteoid becomes mineralized, floccular calcification can be noted within the soft-tissue mass. The maximum opacity of the lesion is located at the periphery, with the central zone being relatively radiolucent. periosteal reaction is frequently evident in the adjacent bone and may precede opacification of the soft-tissue mass. The zoning pattern of peripheral maturation is the most important diagnostic feature and indicates that the lesion is benign. t 6 8 weeks, a lacy pattern of new bone with a sharp peripheral cortex is formed. From 10 weeks to 6 months, the central region may enlarge to produce the appearance of an eggshell at the end stage. t 5 6 months, the mass shrinks and a radiolucent zone of soft tissue separating the lesion from the underlying cortex appears. The lesion may eventually form a dense ossified mass. Trabecular bone formation may also be seen in chronic lesions [14]. The CT appearance of posttraumatic myositis ossificans has been well described. CT usually will show a rim of mineralization around lesions 4 6 weeks after injury. Even when densely mineralized on CT, this rim is much less apparent on MRI. The center of the mass may have decreased CT tissue attenuation, reflecting its similarity to nodular fasciitis and corresponding to areas of increased signal intensity on T2-weighted MRI. Mature lesions may show diffuse ossification with corresponding regions of decreased signal intensity on all MR pulse sequences [15]. MRI is the technique of choice for evaluating soft-tissue lesions. However, an important limitation of MRI is its relative inability to detect soft-tissue calcification. Consequently, conditions such as myositis ossificans that may be readily apparent on radiographs can remain nonspecific on MRI. The MRI appearances of myositis ossificans are variable and depend on the maturity of the lesion. In the early phase, T1-weighted images either may be normal or may show the lesion as isointense to muscle. The lesion is often recognizable only by mass effect displacing fascial planes, particularly because the borders of the lesion can be difficult to separate from surrounding edema. On T2-weighted images, the lesion appears as an inhomogeneous focal mass with high central signal intensity greater than fat. lowsignal-intensity rim corresponding to peripheral ossifica- S84 JR:196, June 2011

9 Nontumorous Skeletal Muscle Disease tion may be present. If no ossification is detected at the periphery, the appearances are nonspecific, and it may be difficult to distinguish a lesion at this stage from a sarcoma. Extensive muscle edema is a typical feature of myositis ossificans. This finding is unusual in most primary neoplasms that have not been biopsied or undergone hemorrhage. fter IV contrast administration, myositis ossificans may show rim enhancement in the acute phase. However, abscesses and necrotic tumors can also show rim enhancement. Diffuse enhancement may also be seen. In the subacute phase, the center of the lesion on T1-weighted images may be isointense or slightly hyperintense relative to muscle. Less frequently, fluid-fluid levels corresponding to hemorrhage within the immature central portion of the lesion are apparent. Occasionally, adjacent bone marrow edema is identified. MRI can also show periostitis and reactive joint. Chronic lesions are well defined and the signal intensity is similar to that of bone with a lack of adjacent edema. On T1- and T2-weighted images, chronic myositis ossificans may show a central area of high signal intensity representing fat between bony trabeculae, with peripheral and central low-signal-intensity areas of ossification. reas of fibrosis and hemosiderin may also contribute to the decreased signal intensity on T1- and T2-weighted images. When the degree of mineralization is minimal, the most important differential diagnosis is soft-tissue sarcoma, and in the mature stage, the main differential diagnosis is parosteal or extraskeletal osteosarcoma [14]. The diagnosis is myositis ossificans traumatica. References 1. May D, Disler DG, Jones E, alkissoon, Manaster J. bnormal signal intensity in skeletal muscle at MR imaging: patterns, pearls, and pitfalls. RadioGraphics 2000; 20[spec no]:s295 S outin RD, Fritz RC, Steinbach LS. Imaging of sports-related muscle injuries. Radiol Clin North m 2002; 40: , vii 3. Maldjian C, dam R, onakdarpour, Robinson TM, Shienbaum J. MRI appearance of clear cell hidradenoma. Skeletal Radiol 1999; 28: Soler R, Rodríguez E, guilera C, Fernández R. Magnetic resonance imaging of pyomyositis in 43 cases. Eur J Radiol 2000; 35: Javier RM, Sibilia J, Lugger S, Natarajan-me S, Kuntz JL, Herbrecht R. Fatal spergillus fumigatus myositis in an immunocompetent patient. Eur J Clin Microbiol Infect Dis 2001; 20: Schwartz DM, Morgan ER. Multimodality imaging of Candida tropicalis myositis. Pediatr Radiol 2008; 38: Mekan SF, Saeed O, Khan J. Invasive aspergillosis with polyarthritis. Mycoses 2004; 47: Kattapuram TM, Suri R, Rosol MS, Rosenberg E, Kattapuram SV. Idiopathic and diabetic skeletal muscle necrosis: evaluation by magnetic resonance imaging. Skeletal Radiol 2005; 34: Curiel RV, Jones R, rindle K. Magnetic resonance imaging of the idiopathic inflammatory myopathies: structural and clinical aspects. nn N Y cad Sci 2009; 1154: Phillips, Cala L, Thickbroom GW, Melsom, Zilko PJ, Mastaglia FL. Patterns of muscle involvement in inclusion body myositis: clinical and magnetic resonance imaging study. Muscle Nerve 2001; 24: Vieira RL, Rosenberg ZS, Kiprovski K. MRI of the distal biceps femoris muscle: normal anatomy, variants, and association with common peroneal entrapment neuropathy. JR 2007; 189: Kamath S, Venkatanarasimha N, Walsh M, Hughes PM. MRI appearance of muscle denervation. Skeletal Radiol 2008; 37: Welsh JS, Torre TG, DeWeese TL, O Reilly S. Radiation myositis. nn Oncol 1999; 10: Parikh J, Hyare H, Saifuddin. The imaging features of post-traumatic myositis ossificans, with emphasis on MRI. Clin Radiol 2002; 57: Kransdorf MJ, Meis JM, Jelinek JS. Myositis ossificans: MR appearance with radiologic-pathologic correlation. JR 1991; 157: FOR YOUR INFORMTION The reader s attention is directed to the Self-ssessment Module for this article, which appears on the following page. JR:196, June 2011 S85