(Radiographics. 2000;20:S295-S315.)
© RSNA, 2000
Multiregional Pathologic Processes |
Abnormal Signal Intensity in Skeletal Muscle at MR Imaging: Patterns, Pearls, and Pitfalls1
David A. May, MD,
David G. Disler, MD,
Elizabeth A. Jones, MD,
Avinash A. Balkissoon, MD and
B. J. Manaster, MD, PhD, 2
1 From the Department of Radiology, Medical College of Virginia, Virginia Commonwealth University, 401 N 12th St, Richmond, VA 23298. Presented as a scientific exhibit at the 1999 RSNA scientific assembly. Received February 9, 2000; revision requested March 28 and received April 12; accepted April 19. Address correspondence to D.A.M. (damay@hsc.vcu.edu).
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Abstract
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Abnormal signal intensity within skeletal muscle is frequently encountered at magnetic resonance (MR) imaging. Potential causes are diverse, including traumatic, infectious, autoimmune, inflammatory, neoplastic, neurologic, and iatrogenic conditions. Alterations in muscle signal intensity seen in pathologic conditions usually fall into one of three recognizable patterns: muscle edema, fatty infiltration, and mass lesion. Muscle edema may be seen in polymyositis and dermatomyositis, mild injuries, infectious myositis, radiation therapy, subacute denervation, compartment syndrome, early myositis ossificans, rhabdomyolysis, and sickle cell crisis. Fatty infiltration may be seen in chronic denervation, in chronic disuse, as a late finding after a severe muscle injury or chronic tendon tear, and in corticosteroid use. The mass lesion pattern may be seen in neoplasms, intramuscular abscess, myonecrosis, traumatic injury, myositis ossificans, muscular sarcoidosis, and parasitic infection. Some of these conditions require prompt medical or surgical management, whereas others do not benefit from medical intervention. The ability to accurately diagnose these conditions is therefore necessary, and biopsy may be required to establish the correct diagnosis. Clues to the correct diagnosis and whether biopsy is necessary or appropriate are often present on the MR images, especially when they are correlated with clinical features and the findings from other imaging modalities.
Index Terms: Muscles, abscess, 40.242 • Muscles, denervation, 40.82 • Muscles, diseases, 40.614, 40.83 • Muscles, infection, 40.20 • Muscles, injuries, 40.40 • Muscles, neoplasms, 40.30 • Myositis, 40.22, 40.241
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- List the causes of abnormal signal intensity in skeletal muscle at MR imaging.
- Discuss the diagnostic and management issues pertinent to abnormal signal intensity in skeletal muscle.
- Recognize imaging and clinical findings that suggest a specific diagnosis or help narrow the differential diagnosis.
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Introduction
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Magnetic resonance (MR) imaging has an important role in detection and characterization of pathologic conditions of skeletal muscle that cause changes in muscle signal intensity. There are many conditions that may affect muscle signal intensity, such as inflammatory, infectious, traumatic, neurologic, neoplastic, and iatrogenic conditions. Some diseases that result in abnormal muscle signal intensity, such as polymyositis, require biopsy for appropriate therapy to be initiated; in other conditions, such as myositis ossificans, biopsy should be avoided because it may lead to an incorrect diagnosis of a neoplasm and thus to inappropriate therapy. Although the MR imaging findings of many conditions are similar, distinct patterns of signal intensity abnormality may be recognized. Recognition of MR imaging patterns can allow one to narrow the differential diagnostic possibilities. Additional clues to the diagnosis may also be present on the MR images, thus allowing the differential diagnosis to be further narrowed. Finally, correlation with the patient's clinical history and results of other imaging modalities can provide important clues to a single correct diagnosis.
In this article, we review many of the potential causes of altered signal intensity in skeletal muscle using a pattern recognition approach. We have found that alterations in muscle signal intensity seen in pathologic conditions usually fall into one of three recognizable patterns: muscle edema, fatty infiltration, and mass lesion. Emphasis is placed on findings that may assist in narrowing the differential diagnosis, determining whether biopsy is indicated, and directing biopsy when indicated. Imaging pitfalls that may lead to an incorrect diagnosis or inappropriate biopsy or therapy are also reviewed.
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Technical Considerations
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The signal intensity of normal skeletal muscle is generally slightly higher than that of water and much lower than that of fat on T1-weighted images and much lower than that of both fat and water on T2-weighted images. On inversion-recovery and fat-suppressed T2-weighted images, normal muscle signal intensity is much lower than that of water but higher than that of fat. Pathologic conditions that affect skeletal muscle may cause an alteration in muscle size, shape, or signal intensity. Abnormalities of muscle size and shape may be detected with virtually any MR imaging sequence. Alterations in muscle signal intensity may include alterations in muscle T1 and T2. Alteration in muscle T1, notably T1 shortening caused by fatty infiltration, methemoglobin, or proteinaceous material, may be detected with T1-weighted images. Alteration in muscle T2, notably T2 prolongation due to increased intracellular or extracellular free water (muscle edema), is best detected with inversion-recovery and fat-suppressed T2-weighted images (1,2). Thus, when one performs an MR imaging examination for a suspected skeletal muscle abnormality, both T1-weighted and fat-suppressed T2-weighted or inversion-recovery sequences should be performed.
Practically speaking, the choice between conventional spin-echo versus fast spin-echo techniques depends on the radiologist's preference. At our institution, we perform fast inversion-recovery and fat-suppressed T2-weighted fast spin-echo sequences, primarily because they require less imaging time than conventional spin-echo sequences. Inversion-recovery images also have the advantage of providing reliable, uniform fat suppression. When a masslike lesion is encountered at nonenhanced imaging, intravenous administration of gadolinium contrast material can assist in determining whether the lesion is cystic or necrotic (3). Enlarging the field of view to encompass both sides of the body allows assessment of muscle symmetry, which may assist in detection of subtle signal intensity abnormalities, particularly in focal disease.
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Muscle Edema
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The MR imaging finding in the edema pattern of abnormal muscle signal intensity is increased signal intensity on T2-weighted images superimposed on an otherwise normal appearance of the involved muscle or muscles. Muscle edema may be focal with ill-defined and poorly circumscribed margins or may diffusely involve a muscle. Muscle edema can be quite subtle and detectable only with inversion-recovery or fat-suppressed T2-weighted images (1,2,4–6). A finding of muscle edema on MR images is almost always due to increased intracellular or extracellular free water, that is, true muscle edema (6–8). However, the accumulation of abnormal metabolites that may occur in some pathologic conditions (9,10) might also contribute to T2 prolongation and thus
contribute to increased signal intensity on T2-weighted images. Nevertheless, because muscle edema is present in virtually all instances of increased muscle signal intensity on T2-weighted images, we use the term muscle edema to describe this pattern of abnormal muscle signal intensity.
Muscle edema may be seen in autoimmune conditions such as polymyositis and dermatomyositis (1,4,5,11–15), mild injuries (2,16–21), infectious myositis without phlegmon or abscess formation (15,22–25), radiation therapy (3), sub-acute denervation (26–29), compartment syndrome (30,31), early myositis ossificans (32–34), rhabdomyolysis (31,35), and sickle cell crisis (36) and as a transient, physiologic finding during and briefly following muscle exercise (37,38).
Polymyositis and dermatomyositis are autoimmune inflammatory conditions of skeletal muscle characterized by gradual onset of muscle weak-ness in the thighs and pelvic girdle that typically progresses to involve the upper extremities, neck flexors, and pharyngeal musculature (4). 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 4th decade of life. Dermatomyositis has a bimodal pattern of manifestation, with peaks during childhood and the 5th decade of life (4). Childhood-onset dermatomyositis tends to be more severe than the adult-onset form (4). 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 (4).
Typical MR imaging findings early in the course of polymyositis and dermatomyositis are bilateral and symmetric edema in pelvic and thigh musculature (Figs 1, 2), especially in the vastus lateralis and vastus intermedius muscles (1,4,5,10–15). Progression to fatty infiltration, often with atrophy, occurs over months to years. Myonecrosis or abscess formation is not a typical feature. The severity of muscle edema on MR images has been shown to correlate with the severity of the disease (1,10,14). Thus, MR imaging is useful in directing biopsy to actively involved muscles, thus increasing the diagnostic yield of the biopsy (1,10,14). Relative sparing of the rectus femoris and biceps femoris muscles has been noted in dermatomyositis (10), although exceptions may be seen. Sheetlike calcifications may develop, especially in dermatomyositis, which are best appreciated on radiographs.
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Figure 1a. Early polymyositis in a 31-year-old woman. (a) Axial T1-weighted MR image (repetition time msec/echo time msec = 650/19) shows a normal appearance of the thigh muscles, without fatty infiltration or atrophy. (b) Axial inversion-recovery MR image (3,950/29, 150-msec inversion time) shows edema in the bilateral thigh musculature, most prominently in the vastus lateralis muscles and left rectus femoris muscle (arrows). This pattern of muscle edema without fatty infiltration is consistent with early involvement. Also note the absence of abnormal signal intensity in the subcutaneous tissues, which are spared in polymyositis.
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Figure 1b. Early polymyositis in a 31-year-old woman. (a) Axial T1-weighted MR image (repetition time msec/echo time msec = 650/19) shows a normal appearance of the thigh muscles, without fatty infiltration or atrophy. (b) Axial inversion-recovery MR image (3,950/29, 150-msec inversion time) shows edema in the bilateral thigh musculature, most prominently in the vastus lateralis muscles and left rectus femoris muscle (arrows). This pattern of muscle edema without fatty infiltration is consistent with early involvement. Also note the absence of abnormal signal intensity in the subcutaneous tissues, which are spared in polymyositis.
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Figure 2a. Dermatomyositis in a 19-year-old woman. (a) Axial T2-weighted spin-echo MR image (3,500/80) shows edema in both the thigh musculature (open arrows) and the skin and subcutaneous tissues (solid arrows), an appearance that reflects inflammation of both skin and muscle. (b) Photograph shows the typical rash of dermatomyositis. (Courtesy of Julia Nunley, MD, Medical College of Virginia, Richmond.)
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Figure 2b. Dermatomyositis in a 19-year-old woman. (a) Axial T2-weighted spin-echo MR image (3,500/80) shows edema in both the thigh musculature (open arrows) and the skin and subcutaneous tissues (solid arrows), an appearance that reflects inflammation of both skin and muscle. (b) Photograph shows the typical rash of dermatomyositis. (Courtesy of Julia Nunley, MD, Medical College of Virginia, Richmond.)
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Muscle contusions are caused by a direct blow. MR images reveal edema at the injured site, frequently due to interstitial hemorrhage as well as edema (19). More severe contusions may contain hematomas and thus reveal a masslike lesion in addition to edema. Muscle strains are injuries of the musculotendinous junction caused by overly forceful muscle contraction (18–20). Muscle strain occurs most frequently in muscles that cross two joints, contain fast-twitch fibers, and contract during elongation (eccentric contraction). The hamstring, gastrocnemius, and biceps brachii muscles have these features and are the most frequently strained. MR images of a mild muscle strain may reveal edema centered along the musculotendinous junction (Figs 3–5). More severe muscle strains contain fluid collections such as hematomas and may contain grossly interrupted muscle fibers and thus may show masslike features on MR images in addition to muscle edema.
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Figure 3. Acute popliteus muscle strain in a 40-year-old man. Sagittal T2-weighted fast spin-echo MR image (3,000/45) obtained with inhomogeneous fat suppression shows edema in the popliteus muscle (arrow) due to a strain associated with an acute tear of the anterior cruciate ligament (not shown).
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Figure 4. Extensive hip adductor strain due to a fall in a 65-year-old woman. Coronal inversion-recovery MR image (2,200/60/150) shows extensive edema in the adductor muscles of the left thigh (large *) and the bilateral obturator internus and externus muscles (small *) and a subtle incomplete intertrochanteric fracture of the left femur (arrow), which was confirmed with additional, high-resolution images.
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Figure 5a. Strain of the pronator quadratus muscle in a 15-year-old boy. Axial intermediate-weighted spin-echo (2,000/20) (a) and inversion-recovery (2,300/17/140) (b) MR images show increased signal intensity due to mild intramuscular hemorrhage and edema centered along the musculotendinous junction (arrows). R = radius, U = ulna.
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Figure 5b. Strain of the pronator quadratus muscle in a 15-year-old boy. Axial intermediate-weighted spin-echo (2,000/20) (a) and inversion-recovery (2,300/17/140) (b) MR images show increased signal intensity due to mild intramuscular hemorrhage and edema centered along the musculotendinous junction (arrows). R = radius, U = ulna.
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An acute mild muscle strain may be simulated on MR images by other causes of muscle trauma (Fig 6), including delayed-onset muscle soreness (DOMS). DOMS is a type of overuse injury that does not become symptomatic until hours or days after the overuse episode, in contrast with a
muscle strain or contusion, which usually is immediately painful. Mild DOMS is frequently seen in recreational athletes. Severe forms may progress to rhabdomyolysis (19,21).
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Figure 6. Muscle edema in a 37-year-old woman who underwent aspiration of the right shoulder via a posterior approach 2 days earlier. Axial inversion-recovery MR image (3,000/30/130) shows edema in the posterior deltoid muscle (arrows).
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Muscle infection (myositis) without abscess or necrosis may produce edema as the sole abnormality on MR images. Bacterial myositis may result from direct extension of infection in tissues adjacent to a muscle, such as osteomyelitis or a subcutaneous abscess (23) (Fig 7). The MR images and clinical history may suggest the presence of such an infection. Bacterial myositis frequently progresses to abscess formation and thus often has a masslike appearance on MR images (23). Viral infection by paramyxovirus is the likely cause of inclusion body myositis (24,25). The pathognomonic histologic feature of this condition is the presence of inclusion bodies in the nucleus and cytoplasm of affected muscle cells. Abscess formation is not seen in this condition. Inclusion body myositis resembles polymyositis at clinical evaluation and MR imaging (Fig 8). Thus, biopsy is required for reliable differentiation between these conditions. The distinction is important because inclusion body myositis is not associated with malignancy and is managed differently than polymyositis (24,25).
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Figure 7a. Staphylococcal osteomyelitis of the right femur and myositis of the adjacent quadriceps muscles in a 52-year-old man. Coronal inversion-recovery MR image (3,950/29/150) (a), axial T2-weighted fast spin-echo MR image (4,000/105) obtained with inhomogeneous fat suppression (b), and axial fat-suppressed T1-weighted MR image (735/17) obtained after intravenous administration of gadolinium contrast material (c) show edema in the marrow of the right femur with enhancement (white arrow), edema and enhancement of the quadriceps muscles (*), and a small cloaca through the lateral femoral cortex (black arrow).
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Figure 7b. Staphylococcal osteomyelitis of the right femur and myositis of the adjacent quadriceps muscles in a 52-year-old man. Coronal inversion-recovery MR image (3,950/29/150) (a), axial T2-weighted fast spin-echo MR image (4,000/105) obtained with inhomogeneous fat suppression (b), and axial fat-suppressed T1-weighted MR image (735/17) obtained after intravenous administration of gadolinium contrast material (c) show edema in the marrow of the right femur with enhancement (white arrow), edema and enhancement of the quadriceps muscles (*), and a small cloaca through the lateral femoral cortex (black arrow).
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Figure 7c. Staphylococcal osteomyelitis of the right femur and myositis of the adjacent quadriceps muscles in a 52-year-old man. Coronal inversion-recovery MR image (3,950/29/150) (a), axial T2-weighted fast spin-echo MR image (4,000/105) obtained with inhomogeneous fat suppression (b), and axial fat-suppressed T1-weighted MR image (735/17) obtained after intravenous administration of gadolinium contrast material (c) show edema in the marrow of the right femur with enhancement (white arrow), edema and enhancement of the quadriceps muscles (*), and a small cloaca through the lateral femoral cortex (black arrow).
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Radiation therapy causes vasculitis and tissue injury that may be seen on MR images as fairly uniform muscle edema (3). 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 (3) (Fig 9). Changes due to radiation should be distinguished from an enhancing nodule or nodules in the surgical bed, a finding suggestive of recurrent or residual tumor (39).
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Figure 9a. Muscle edema in a 60-year-old woman after radiation therapy for metastatic breast cancer in the left shoulder region. Axial T2-weighted spin-echo MR image (2,150/80) (a) and axial T1-weighted MR image (617/16) obtained after intravenous administration of gadolinium contrast material (b) show edema with enhancement (arrows). Note the straight, sharp margins of the edematous tissue (arrowheads), which correspond to the margins of the radiation field, and the uniformly abnormal signal intensity of all tissues in the radiation field, including muscle. A necrotic lymph node (X) does not demonstrate enhancement.
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Figure 9b. Muscle edema in a 60-year-old woman after radiation therapy for metastatic breast cancer in the left shoulder region. Axial T2-weighted spin-echo MR image (2,150/80) (a) and axial T1-weighted MR image (617/16) obtained after intravenous administration of gadolinium contrast material (b) show edema with enhancement (arrows). Note the straight, sharp margins of the edematous tissue (arrowheads), which correspond to the margins of the radiation field, and the uniformly abnormal signal intensity of all tissues in the radiation field, including muscle. A necrotic lymph node (X) does not demonstrate enhancement.
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Subacute muscle denervation causes edema uniformly throughout an involved muscle (6,26–29). This finding usually does not become evident on MR images until approximately 2–4 weeks after denervation has occurred (6), although such signal intensity changes have been observed as early as 2–4 days after denervation (8). The mechanism of this finding is not completely understood but appears likely to reflect shifting of water from intracellular to extracellular spaces (8). If normal innervation is restored, the MR imaging findings eventually return to normal. However, if innervation is not restored, atrophy with fatty infiltration develops after a period of months, indicating irreversible changes in the muscle (6). Acutely denervated muscle does not demonstrate signal intensity alterations at MR imaging (6). This observation may allow distinction of denervation from acute traumatic muscle injury, which tends to have abnormal signal intensity at MR imaging that can be seen within hours or days after the injury. Another finding that may be seen in muscle trauma but is not associated with denervation is the presence of edema in other injured tissues, in particular overlying subcutaneous tissues (Figs 4, 6).
Potential mechanisms of denervation are numerous, including spinal cord injury, poliomyelitis, peripheral nerve injury or compression (26,27,29) (Fig 10), Graves disease (ocular muscles) (40), and neuritis (28,29) (Fig 11). Peripheral nerves, particularly in the upper extremities, are vulnerable to entrapment in narrow anatomic spaces and compression by mass lesions (26). One role of MR imaging in the setting of suspected peripheral nerve injury is detection of a surgically correctable cause of nerve compression such as a bone spur or ganglion cyst (Fig 10). Correlation with clinical and electromyelographic findings may be helpful in such cases because the level of nerve dysfunction can be localized to a specific anatomic region, thus allowing a focused MR imaging examination.
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Figure 10. Infraspinatus muscle denervation caused by compression of the suprascapular nerve by a glenoid labral cyst in a 53-year-old man. The patient presented with the clinical features of a rotator cuff tear. Axial fat-suppressed T2-weighted fast spin-echo MR image (3,500/105) shows a lobulated ganglion in the spinoglenoid notch of the scapula (small *) and diffuse infraspinatus edema (large *). The ganglion was due to a glenoid labral tear (not shown). The motor nerve to the infraspinatus muscle, which courses through this notch, was compressed by the ganglion. The pain and weakness of the infraspinatus muscle resolved after the ganglion was resected.
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Figure 11. Parsonage-Turner syndrome (idiopathic inflammation of the brachial plexus) resulting in denervation of the infraspinatus and supraspinatus muscles in a 25-year-old man. Oblique sagittal fat-suppressed T2-weighted fast spin-echo MR image (5,000/64) shows edema in the infraspinatus (large black *) and supraspinatus (small black *) muscles, in contrast with the normal appearance of the subscapularis (small white *) and teres minor (large white *) muscles. Parsonage-Turner syndrome manifests as acute onset of shoulder girdle pain and weakness in young men and is caused by inflammation of the brachial plexus. It is usually self-limited, and uneventful full recovery is the rule. MR imaging findings include edema in the infraspinatus or supraspinatus muscle. An identical appearance on MR images could be caused by an isolated suprascapular nerve injury. (Courtesy of Clyde Helms, MD, Duke University, Durham, NC.)
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Compartment syndrome results from increased pressure within an indistensible space (41). Trauma, burns, heavy exercise, extrinsic pressure, or intramuscular hemorrhage may initiate a vicious cycle of increasing pressure within confining fascia that leads to venous occlusion, muscle and nerve ischemia, arterial occlusion, and tissue necrosis. Acute and less severe chronic subtypes are seen (Figs 12, 13). Clinical findings include severe pain and dysfunction of sensory and motor nerves that pass through the affected compartment. Early MR imaging findings include extremity swelling and diffuse edema within the affected compartment (30,31). If an acute compartment syndrome is clinically suspected, direct measurement of intracompartmental pressure should not be delayed (30,41).
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Figure 12. Acute compartment syndrome in a 50-year-old man. One day earlier, the patient's right leg was placed in a stirrup during surgical reduction of a contralateral femoral fracture. Axial T2-weighted spin-echo MR image (2,000/80) shows edema in the deep posterior compartment of the right leg (arrowheads). The stirrup compressed the posterior compartment, resulting in ischemia and edema, which led to increased intracompartmental pressure. Fasciotomy was required to decompress the compartment. T = tibia.
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Figure 13a. Chronic compartment syndrome in a 19-year-old male soccer player with a 6-month history of bilateral anterior leg pain during running. (a) Axial inversion-recovery MR image (4,705/126/150) obtained at the level of the proximal leg with the patient at rest shows normal signal intensity in both legs. (b) Corresponding MR image obtained with the sequence initiated as rapidly as possible ( 2-3 minutes) after the patient ran for 15 minutes shows subtle edema in the anterior compartments of both legs (arrows). The patient elected to undergo bilateral anterior compartment fasciotomy. His symptoms did not recur, and he was able to resume his soccer career. T = tibia. (Courtesy of Thomas McCauley, MD, Yale University, New Haven, Conn.)
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Figure 13b. Chronic compartment syndrome in a 19-year-old male soccer player with a 6-month history of bilateral anterior leg pain during running. (a) Axial inversion-recovery MR image (4,705/126/150) obtained at the level of the proximal leg with the patient at rest shows normal signal intensity in both legs. (b) Corresponding MR image obtained with the sequence initiated as rapidly as possible (2-3 minutes) after the patient ran for 15 minutes shows subtle edema in the anterior compartments of both legs (arrows). The patient elected to undergo bilateral anterior compartment fasciotomy. His symptoms did not recur, and he was able to resume his soccer career. T = tibia. (Courtesy of Thomas McCauley, MD, Yale University, New Haven, Conn.)
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Muscle edema may also be seen in the earliest stages of myositis ossificans, infiltrating neoplasms, and rhabdomyolysis. These conditions usually progress to the mass pattern and are
therefore discussed in that section. We have also observed muscle edema in idiopathic muscle inflammation (Fig 14). Experimental study has demonstrated that edemalike signal intensity occurs as a transient, physiologic finding during and briefly following vigorous muscle exercise (37,38) (Fig 15).
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Figure 14. Idiopathic myositis in a 50-year-old woman with muscle weakness and malaise. She denied a history of trauma and had no neurologic deficits. Axial T2-weighted spin-echo MR image (2,500/90) through the left thigh shows edema in the vastus lateralis muscle (*). Muscle biopsy revealed only "nonspecific myositis" without features of dermatomyositis, inclusion cell myositis, or infection. The symptoms resolved over several months. No diagnosis was made.
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Figure 15a. Physiologic signal intensity changes in the tibialis anterior muscle in a 26-year-old man during and shortly after exercise of the muscle. Axial fat-suppressed T2-weighted echo-planar MR images (9,000/60) of the midcalf obtained at the beginning of (a), at completion of (b), and shortly after (c) 3 minutes of continuous ankle dorsiflexion against resistance show increased signal intensity in the tibialis anterior muscle (*) during exercise (b), with subtle partial resolution seen in the final image (c). The causes of the change in signal intensity in this experiment are not completely understood, but the change probably reflects accumulation and clearing of metabolites of anaerobic exercise rather than increased intracellular and extracellular water or increased perfusion. The severity of the signal intensity changes has been shown to correlate with the intensity of the exercise. T = tibia. (Reprinted, with permission, from reference 38.)
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Figure 15b. Physiologic signal intensity changes in the tibialis anterior muscle in a 26-year-old man during and shortly after exercise of the muscle. Axial fat-suppressed T2-weighted echo-planar MR images (9,000/60) of the midcalf obtained at the beginning of (a), at completion of (b), and shortly after (c) 3 minutes of continuous ankle dorsiflexion against resistance show increased signal intensity in the tibialis anterior muscle (*) during exercise (b), with subtle partial resolution seen in the final image (c). The causes of the change in signal intensity in this experiment are not completely understood, but the change probably reflects accumulation and clearing of metabolites of anaerobic exercise rather than increased intracellular and extracellular water or increased perfusion. The severity of the signal intensity changes has been shown to correlate with the intensity of the exercise. T = tibia. (Reprinted, with permission, from reference 38.)
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Figure 15c. Physiologic signal intensity changes in the tibialis anterior muscle in a 26-year-old man during and shortly after exercise of the muscle. Axial fat-suppressed T2-weighted echo-planar MR images (9,000/60) of the midcalf obtained at the beginning of (a), at completion of (b), and shortly after (c) 3 minutes of continuous ankle dorsiflexion against resistance show increased signal intensity in the tibialis anterior muscle (*) during exercise (b), with subtle partial resolution seen in the final image (c). The causes of the change in signal intensity in this experiment are not completely understood, but the change probably reflects accumulation and clearing of metabolites of anaerobic exercise rather than increased intracellular and extracellular water or increased perfusion. The severity of the signal intensity changes has been shown to correlate with the intensity of the exercise. T = tibia. (Reprinted, with permission, from reference 38.)
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Fatty Infiltration
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Fatty infiltration involves abnormal deposition of fat diffusely within a muscle. Fatty infiltration occurs in the late stages of many pathologic conditions involving skeletal muscle. Pathologic fatty infiltration is usually seen in association with muscle atrophy. MR images reveal increased quantities of fat with its characteristic signal intensity within the involved muscle, usually with a decreased volume of muscle tissue.
Fatty infiltration may be seen in the chronic stages of muscle denervation (6), in chronic disuse, as a late finding after a severe muscle injury or chronic tendon tear, and as a consequence of corticosteroid use (42).
Fatty infiltration due to chronic denervation is usually accompanied by muscle atrophy and represents irreversible muscle injury (6) (Fig 16). Paradoxically, fatty infiltration may contribute to apparent hypertrophy of a chronically denervated muscle (43), but this association is rare. T2-weighted and inversion-recovery images show variable findings in chronic denervation (6) and thus are less reliable than T1-weighted images in revealing changes of chronic muscle denervation.
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Figure 16. Chronic muscle denervation in a 52-year-old man who contracted poliomyelitis as a child from the vaccine. Coronal T1-weighted MR image (300/19) shows nearly total fatty replacement of the left pelvic and thigh muscles (*).
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Muscle atrophy with fatty infiltration may be seen in nonneurologic conditions that may mimic chronic denervation on MR images. Chronic muscle disuse leads to atrophy with fatty infiltration (Fig 17). A specific example is disuse of a single muscle due to a chronic tendon tear (Figs 18, 19). Potential clues to this diagnosis include identification of the tendon interruption and retraction of the muscle belly.
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Figure 17. Chronic disuse in a 73-year-old man with painful osteoarthritis of the right knee and right hip that resulted in limited use of his right leg. Coronal T1-weighted MR image (700/17) shows atrophy and fatty infiltration (*) of the right gluteus maximus due to disuse. Similar findings could be seen in cases of chronic partial denervation. Contrast the appearance in this case with the more severe fatty infiltration in Figure 16.
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Figure 18. Chronic tear of the semimembranosus tendon in a 54-year-old woman. Axial intermediate-weighted spin-echo MR image (2,000/10) shows extensive fatty infiltration and atrophy of the left semimembranosus muscle (arrows). Interruption of the tendon was confirmed on other MR images.
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Figure 19. Chronic partial tear of the subscapularis tendon in a 70-year-old man. Oblique sagittal intermediate-weighted fast spin-echo MR image (3,000/20) shows atrophy and fatty infiltration of the superior two-thirds of the subscapularis muscle (arrowheads) with relative sparing of the inferior one-third (arrows). Axial images demonstrated interruption of the superior two-thirds of the subscapularis tendon, the intact inferior portion of the tendon, and retraction and atrophy of the upper portion of the subscapularis muscle.
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Corticosteroids, especially when used in high doses for long periods, are associated with truncal muscle atrophy and fatty infiltration (42) (Fig 20). Prominent fat deposition diffusely in subcutaneous fat is also seen, and involvement is bilateral and regional rather than unilateral, as may be seen in chronic denervation due to poliomyelitis, stroke, or peripheral nerve injury.
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Figure 20. Fatty infiltration in a 63-year-old woman receiving long-term high-dose corticosteroid therapy. Coronal T1-weighted MR image (650/17) shows atrophy and fatty infiltration of the pelvic girdle muscles (arrows) as well as diffuse subcutaneous and pelvic fat deposition.
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Intramuscular hemangiomas may contain fat (44) (Fig 21). Hemangiomas may be readily distinguished from fatty infiltration on MR images because hemangiomas do not conform to the shape of the muscle, frequently cross fascial planes with involvement of adjacent tissues, and often contain well-circumscribed, serpiginous blood-filled spaces that may demonstrate flow voids. Hemangiomas may also be associated with phleboliths on radiographs (44).
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Figure 21. Hemangioma extensively involving the distal thigh and knee in a 13-year-old boy. Sagittal T1-weighted MR image (700/20) shows widely distributed, smoothly marginated, serpiginous low-signal-intensity masses infiltrating the regional muscles and subcutaneous tissues (solid arrows). The masses demonstrated high signal intensity on T2-weighted images and enhanced uniformly after intravenous administration of gadolinium contrast material. Note the stippled regions of increased signal intensity within the regional muscles (open arrows), which are due to fat deposition. This finding supports a diagnosis of hemangioma and is not necessarily related to muscle atrophy. Radiographs revealed phleboliths.
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Mass Lesion
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In the mass lesion pattern, a localized masslike region with morphology and signal intensity different than those of normal muscle is found with all sequences. This pattern may be seen in neoplasms (3), intramuscular abscess (15,22,23), any condition associated with myonecrosis (30,31,36,45–48), traumatic injury (2,18–20), myositis ossificans (32–34), muscular sarcoidosis (49), and parasitic infection (23,50).
Careful attention to the signal intensity characteristics of the mass and findings from other imaging modalities may reveal clues to its nature. If a fluid-fluid level is seen, necrosis, blood, or purulent material is likely to be present. Uniform high signal intensity on T1-weighted images suggests the presence of the blood breakdown product methemoglobin, proteinaceous material, or fat. Intramuscular hematomas and myositis ossificans may demonstrate peripheral calcification on radiographs. If intravenous gadolinium contrast material is administered and enhancement is observed within central portions of the mass, then myonecrosis or liquefaction is unlikely. Rather, a solid neoplasm, granulation tissue, or myositis ossificans is likely to be present. Correlation with the clinical history may support
one of these diagnoses and assist in determining whether biopsy is indicated or may be deferred. However, absence of central enhancement does not allow exclusion of a neoplasm because central necrosis or an avascular tumor may be present (3). Also, gadolinium contrast material may slowly diffuse into a fluid-filled space such as an abscess or hematoma. Thus, it is important to complete imaging promptly after administration of gadolinium contrast material to avoid enhancement within a mass that would falsely suggest it to be solid.
Neoplasms may cause apparent edema in adjacent skeletal muscle. This signal intensity alteration may reflect muscle edema, tumor invasion, or both (51). The presence or absence of this finding on static MR images does not enable reliable distinction between benign and malignant processes, nor does it allow assessment of the true location of the tumor margins (3,51) (Fig 22). Infiltrating tumors may cause muscle enlargement and alterations in signal intensity (Fig 23). However, a review of the types of neoplasms that occur in skeletal muscle is beyond the scope of this article.
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Figure 22. Forearm sarcoma in a 58-year-old woman. Axial fat-suppressed T2-weighted fast spin-echo MR image (2,500/45) shows a mass that appears to have sharp margins (arrows); no edema is seen in the adjacent muscles. However, microinvasion into the adjacent muscles was shown at histologic analysis. This example illustrates the important observation that absence of signal-intensity changes in tissues around a neoplasm does not allow exclusion of microinvasion. The converse of this observation is also true: The presence of edema around a mass is not a reliable indicator of tumor extension into the adjacent tissue.
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Figure 23a. Lymphoma in a 74-year-old woman. Coronal inversion-recovery (4,000/30/130) (a) and axial fat-suppressed intermediate-weighted fast spin-echo (4,500/15) (b) MR images show abnormal marrow signal intensity in both femurs (small *) and an enlarged left vastus intermedius muscle with edema (large *). Biopsy of the vastus intermedius muscle revealed non-Hodgkin lymphoma.
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Figure 23b. Lymphoma in a 74-year-old woman. Coronal inversion-recovery (4,000/30/130) (a) and axial fat-suppressed intermediate-weighted fast spin-echo (4,500/15) (b) MR images show abnormal marrow signal intensity in both femurs (small *) and an enlarged left vastus intermedius muscle with edema (large *). Biopsy of the vastus intermedius muscle revealed non-Hodgkin lymphoma.
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Focal myositis (benign inflammatory pseudotumor) may simulate a neoplasm on MR images (15). Focal myositis is a localized inflammatory process of unknown origin that manifests as a small intramuscular mass. MR images reveal a small masslike lesion with high signal intensity on T2-weighted images and intense enhancement after intravenous administration of gadolinium contrast material. Resection is often curative (15).
An intramuscular abscess may be caused by a variety of infectious agents, frequently Staphylococcus aureus (Fig 24). Bacterial infection causes fever, swelling, and marked tenderness. The infection may be initiated by direct extension from adjacent infected tissues or hematogenous seeding from a remote site (22,23). If MR imaging is performed before a phlegmon or abscess is formed, the only finding may be muscle edema. Fungal infections are less common but may also cause abscess formation. Necrotizing fasciitis is often associated with myonecrosis and abscess formation in adjacent muscles.
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Figure 24a. Abscess of the right quadriceps in a 16-year-old boy with a 6-month history of night sweats and progressive pain and swelling of the right thigh. Coronal T2-weighted spin-echo MR image (2,000/80) (a) and coronal T1-weighted MR image (567/10) obtained after intravenous administration of gadolinium contrast material (b) show an abscess (*) in the right quadriceps muscles with surrounding edema and enhancement (arrows). Cultures of the abscess grew S aureus.
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Figure 24b. Abscess of the right quadriceps in a 16-year-old boy with a 6-month history of night sweats and progressive pain and swelling of the right thigh. Coronal T2-weighted spin-echo MR image (2,000/80) (a) and coronal T1-weighted MR image (567/10) obtained after intravenous administration of gadolinium contrast material (b) show an abscess (*) in the right quadriceps muscles with surrounding edema and enhancement (arrows). Cultures of the abscess grew S aureus.
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Myonecrosis can occur in sickle cell crisis (36), diabetic myonecrosis (45–48), compartment syndrome (30,31,41), crush injury (31), severe ischemia (31,41), intraarterial chemotherapy (52), and rhabdomyolysis (31,35). Any condition that can cause myonecrosis can simulate an abscess at both clinical evaluation and MR imaging. Clinical correlation for evidence of an underlying condition associated with myonecrosis may allow an unnecessary aspiration to be deferred (36,47,48).
Diabetic myonecrosis is a distinctive myopathy associated with poorly controlled diabetes mellitus (45–48) (Figs 25, 26). Clinical features include severe pain, most frequently in the thigh muscles, with comparatively mild physical examination findings and occasionally a low-grade fever. Cultures of the involved muscles are negative. MR images demonstrate marked edema and enhancement around often irregular masslike regions of muscle necrosis.
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Figure 25a. Diabetic myonecrosis of the left soleus and gastrocnemius muscles in a 30-year-old woman. Axial T2-weighted spin-echo MR image (2,500/60) (a) and axial T1-weighted MR image (500/13) obtained after intravenous administration of gadolinium contrast material (b) show edema (solid arrows) and enhancement (open arrows) surrounding an irregular region of myonecrosis (*). F = fibula, T = tibia.
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Figure 25b. Diabetic myonecrosis of the left soleus and gastrocnemius muscles in a 30-year-old woman. Axial T2-weighted spin-echo MR image (2,500/60) (a) and axial T1-weighted MR image (500/13) obtained after intravenous administration of gadolinium contrast material (b) show edema (solid arrows) and enhancement (open arrows) surrounding an irregular region of myonecrosis (*). F = fibula, T = tibia.
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Figure 26a. Diabetic myonecrosis of the left quadriceps muscles in a 43-year-old man with poorly controlled diabetes mellitus and an extremely painful and tender left thigh. Axial T1-weighted MR image (600/18) (a), axial T2-weighted fast spin-echo MR image (7,869/96) obtained with inhomogeneous fat suppression (b), coronal fat-suppressed T2-weighted fast spin-echo MR image (6,995/96) (c), and axial fat-suppressed T1-weighted MR image (576/13) obtained after intravenous administration of gadolinium contrast material (d) show enlargement of the left quadriceps muscles, especially the vastus medialis (arrows), as well as diffuse edema throughout the left quadriceps muscles with enhancement (*). There is a region of absent enhancement (X) in the left vastus medialis muscle, a finding consistent with myonecrosis. Although the patient was febrile, recognition that his diabetes was poorly controlled and that the pain and tenderness seemed to be disproportionately severe allowed aspiration of the region of myonecrosis to be appropriately deferred.
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Figure 26b. Diabetic myonecrosis of the left quadriceps muscles in a 43-year-old man with poorly controlled diabetes mellitus and an extremely painful and tender left thigh. Axial T1-weighted MR image (600/18) (a), axial T2-weighted fast spin-echo MR image (7,869/96) obtained with inhomogeneous fat suppression (b), coronal fat-suppressed T2-weighted fast spin-echo MR image (6,995/96) (c), and axial fat-suppressed T1-weighted MR image (576/13) obtained after intravenous administration of gadolinium contrast material (d) show enlargement of the left quadriceps muscles, especially the vastus medialis (arrows), as well as diffuse edema throughout the left quadriceps muscles with enhancement (*). There is a region of absent enhancement (X) in the left vastus medialis muscle, a finding consistent with myonecrosis. Although the patient was febrile, recognition that his diabetes was poorly controlled and that the pain and tenderness seemed to be disproportionately severe allowed aspiration of the region of myonecrosis to be appropriately deferred.
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Figure 26c. Diabetic myonecrosis of the left quadriceps muscles in a 43-year-old man with poorly controlled diabetes mellitus and an extremely painful and tender left thigh. Axial T1-weighted MR image (600/18) (a), axial T2-weighted fast spin-echo MR image (7,869/96) obtained with inhomogeneous fat suppression (b), coronal fat-suppressed T2-weighted fast spin-echo MR image (6,995/96) (c), and axial fat-suppressed T1-weighted MR image (576/13) obtained after intravenous administration of gadolinium contrast material (d) show enlargement of the left quadriceps muscles, especially the vastus medialis (arrows), as well as diffuse edema throughout the left quadriceps muscles with enhancement (*). There is a region of absent enhancement (X) in the left vastus medialis muscle, a finding consistent with myonecrosis. Although the patient was febrile, recognition that his diabetes was poorly controlled and that the pain and tenderness seemed to be disproportionately severe allowed aspiration of the region of myonecrosis to be appropriately deferred.
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Abstract
LEARNING OBJECTIVES 
