Antimyosin Scintigraphy Compared with Magnetic Resonance Imaging in Inflammatory Myopathies

ORIGINAL CONTRIBUTION Antimyosin Scintigraphy Compared With Magnetic Resonance Imaging in Inflammatory Myopathies

Mervi Lo¨fberg, MD; Kristian Liewendahl, MD, PhD; Antti Lamminen, MD, PhD; Ossi Korhola, MD, PhD; Hannu Somer, MD, PhD

Objective: To compare indium In 111 altumomab pen- or calves. After anti-inflammatory drug therapy, the mean tetate–labeled antimyosin scintigraphy with magnetic uptake of antibody and the mean signal intensity changes resonance imaging (MRI) in the diagnosis and fol- in T2-weighted MRI had decreased. However, in T1- low-up of patients with myositis. weighted MRI the signal intensity changes reflecting intramuscular fatty degeneration were more pronounced in Design and Methods: Sixteen patients with polymyo- the follow-up study. The level of serum creatine kinase had sitis and 1 patient with dermatomyositis, all verified with decreased markedly by the second examination except in biopsy samples, were examined during diagnostic evalu- 1 patient who also had more accumulation of antibody in ation with antimyosin antibody scintigraphy and low- the calves after than before treatment. The clinical condi- field MRI of the thighs and calves using T1- and T2- tion improved in 8 patients and remained unchanged in 9 weighted sequences. Both examinations were repeated patients. 6 to 22 months after therapeutic intervention with anti- inflammatory drugs. The performance of the 2 methods Conclusions: Antimyosin scintigraphy and T2- for the assessment of the severity of muscle inflamma- weighted MRI are feasible tools for the detection and tion was evaluated using comparison with clinical ex- follow-up of lesions in patients with myositis. Scintigra- amination and the serum creatine kinase level. phy findings correlate with serum creatine kinase activity and seem to reflect disease activity better than Results: At diagnosis all patients had increased uptake T2-weighted MRI changes, whereas secondary degenera- of antimyosin antibody in the thighs and/or calves. In T2- tive intramuscular lesions are only detectable using T1- weighted MRI images, increased signal intensity changes weighted MRI. reflecting intramuscular edema and inflammation were seen in all patients in at least 1 muscle group in the thighs Arch Neurol. 1998;55:987-993

OLYMYOSITIS AND dermato- fibers and intracellular amyloid deposits myositis are acquired muscle or 15- to 18-nm tubulofilaments shown us- diseases with proximal ing electron microscopy.2 muscle weakness, atrophy, Imaging methods have been used to and tenderness as the main characterize the distribution of mesenchy- Pclinical findings. Increased sarcoplasmic mal changes in myositis.3 Muscle wasting enzyme activities in the serum and typi- in advanced polymyositis can be detected cal findings from needle electromyogra- using computed tomography and ultrason- phy are the other characteristic features. ography. In childhood dermatomyositis, The diagnosis is confirmed histologically computed tomography can identify subcu- when inflammatory infiltrates are found taneous and intramuscular calcifications, in skeletal muscle. In polymyositis the in- which may also result in foci of increased From the Department flammatory cells are mainly T lympho- muscle echogenicity shown in ultrasonog- of Neurology, Institute of cytes attacking muscle cells, whereas in raphy. Computed tomography and ultra- Neurosciences (Drs Lo¨fberg dermatomyositis the pathomechanism is sonography are, however, less sensitive than and Somer), the Laboratory humoral immunity and the cells found in magnetic resonance imaging (MRI) in de- Department, Division of perivascular infiltrates in muscle are typi- tecting muscle edema, a typical sign of ac- Nuclear Medicine 1 3 (Dr Liewendahl), and the cally B lymphocytes. Inclusion body myo- tive inflammation in skeletal muscle. Department of Radiology sitis differs from other inflammatory my- Scintigraphy using technetium Tc (Drs Lamminen and Korhola), opathies clinically by simultaneous 99m chelates or gallium citrate Ga 67 has Helsinki University Central affection of distal muscles and histologi- been used in the diagnosis of inflamma- Hospital, Helsinki, Finland. cally by the presence of vacuolated muscle tory myopathies. In studies including 6 or

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 PATIENTS, MATERIALS, an echo time of 60 milliseconds, and 2 signal acquisitions were used. In patient 1, imaging only of the calves was per- AND METHODS formed at diagnosis.

PATIENTS MRI INTERPRETATION

All patients except patient 17 had slowly progressive muscle Two radiologists (A.L. and O.K.) independently analyzed weakness for several months before the diagnostic exami- the MRI scans in both phases of the study without knowl- nations. Most patients could walk without assistance but edge of the clinical status, serum CK values, or scintigra- needed the aid of a handrail while climbing stairs. Patient phy findings of the patient. Synergistic muscle groups, ie, 14 felt weakness only in her thighs while walking longer extensors and flexors, were analyzed as a single entity for distances. Patients 8 and 11 needed support while walk- both thighs and calves. Interobserver agreement was first ing. Patient 17, the most affected, was diagnosed as hav- assessed using ␬ statistics; to facilitate further statistical ing an aggressive and rapidly progressing disease, and the evaluation, consensus grades were obtained using joint re- patient was bedridden and needed assistance in all activi- analysis and discussion in the cases in which there was ini- ties of daily living. The age of the patients ranged from 36 tial disagreement between the 2 readers. to 81 years (mean [ ± SD], 62 ± 13 years; SEM, 3 years). The MRI signal intensity changes were semiquantita- In all patients the serum creatine kinase (CK) level was tively graded as follows. The T1-weighted image sets: grade increased, and needle electromyography showed changes typi- 0, normal muscle signal intensity and homogeneous hypoin- cal of myositis or myopathy. The diagnosis was confirmed tense signal contrasting sharply with subcutaneous and in- using muscle biopsy samples; all patients except patient 2 had termuscular fat; grade 1, hyperintense, patchy but not con- inflammatory myopathy with T-lymphocyte predominance fluent intramuscular signal in a single muscle of a synergistic typical of polymyositis. Some histological features of inclu- muscle group; grade 2, hyperintense, patchy, and confluent sion body myositis (rimmed vacuoles or inclusion bodies) intramuscular signal, with widespread but less than total in- were seen in 5 of these patients (patients 5, 7, 10, 12, and volvement of the synergistic muscle group; and grade 3, ho- 16) but the diagnostic criteria for inclusion body myositis2 mogeneously hyperintense, confluent intramuscular signal, were not fulfilled. Patient 2 had skin lesions and B- with total involvement of the synergistic muscle group. lymphocyte predominance shown through analysis of muscle Because fat suppression sequences were unavailable biopsy samples and was therefore considered to have der- in the current imaging software, the T2-weighted image sets matomyositis. Magnetic resonance imaging and antimyosin were analyzed taking into account the signal changes caused antibody imaging were performed during the diagnostic evalu- by fatty degeneration in the exactly corresponding T1- ation before onset of drug therapy and repeated after 6 to 22 weighted slices: grade 0, normal and homogeneous hypo- months (mean [ ± SD], 10 ± 4 months; SEM, 1 month). intense signal; grade 1, limited changes and slightly in- The first choice of an anti-inflammatory drug was pred- creased morphologically localized intramuscular signal nisone, with a starting dose of 1 mg/kg. The initial re- intensity in T2-weighted images compared with T1- sponse to corticosteroid therapy was good in all patients weighted images; grade 2, moderate changes morphologi- as judged by a decrease in the serum CK level, but in some cally more widespread, but patchy increases in intramus- patients this therapy caused adverse effects. Therefore, to cular signal intensity in T2-weighted images; and grade 3, maintain good clinical response, sufficient levels of pred- widespread changes and extensive, homogeneous, and wide- nisone could not be continued for more than 4 to 6 weeks. spread increase in intramuscular signal intensity in T2- At this point azathioprine, 100 mg/d (in patient 9, only 50 weighted images. mg/d), was added to the therapy in 9 patients, and the corticosteroid dosage was lowered to a minimum. All pa- SCINTIGRAPHY tients were examined and treated at the Helsinki Univer- sity Central Hospital, Helsinki, Finland, in accordance with For scintigraphy, a 0.5 mg-dose of murine antimyosin Fab the Declaration of Helsinki II. fragments conjugated with diethylenetriaminepentaacetic acid (Myoscint, Centocor BV, Leiden, the Netherlands) and MAGNETIC RESONANCE IMAGING labeled with 111In (range, 65-140 MBq; mean, 102 MBq) was administered intravenously. This antibody, which was raised Magnetic resonance imaging of patients’ thighs and lower against cardiac myosin, has been found to cross-react with legs was performed with a 0.1-T MRI system (Merit, Picker skeletal myosin.4-6 No adverse effects were observed in the Nordstar Inc, Helsinki). Two sets of axial slices were ob- patients administered millipore-filtered labeled antibody. tained, one set positioned on thigh musculature and the Labeling was performed according to the instructions of other set on calf muscles, with a slice thickness of 10 mm, the manufacturer (Centocor BV). The labeling efficiency an interslice gap of 10 mm, and an imaging matrix of is 96% to 99% in thin-layer chromatography studies in our 256 ϫ 256. The field-of-view was 460 ϫ 460 mm. The num- laboratory. ber of slices was adjusted to cover the whole length of the Scintigraphy was performed with a single detector muscle bundles in the craniocaudal direction, usually with gamma camera (Picker SX 300), connected to a computer a set of 16 to 18 slices. Both T1- and T2-weighted images (PDP 11/74), or a single-head gamma camera (Picker were acquired with identical slice positioning. For T1- Prism XP 1500) connected to a computer (Odyssey VP com- weighted images a partial saturation sequence with a rep- puter, Picker International, Philadelphia, Pa). The cam- etition time of 150 milliseconds, an echo time of 15 milli- eras were equipped with medium-energy parallel-hole seconds, and 6 signal acquisitions was used, and for T2- weighted images, a repetition time of 1500 milliseconds, Continued on next page

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 2.0 2000 SEM ± collimators. Patients’ lower extremities were im- 1.8 1500 aged 3 to 4 hours and 20 to 24 hours after the injec- 1000 tion of radiolabeled antimyosin by collecting 400 000 1.6

SEM 500

to 600 000 counts per image (imaging time, 15 min- ± 0 utes) using 2 energy windows (171 keV and 245 keV; 1.4 20% windows). The lesion-to-nonlesion activity up- Serum CK, U/L, Mean Pre Post take ratio was higher at 24 hours than at 4 hours. The 1.2 scintigrams acquired at 24 hours were selected for comparison with MRI. 1.0 SCAN INTERPRETATION 0.8 Grade of Signal Intensity, Mean Grade of Signal Intensity, For grading of immunoscintigraphic findings in the lower extremities, the intensity of radioactivity in the 0.6 muscular areas above and below the knee were com- 0.4 pared with that in the main blood vessels in thighs and Pre Post Pre Post Pre Post calves, respectively. Blinded interpretation of images Scintigraphy T2 MRI T1 MRI taken at 20 to 24 hours was performed by 2 investiga- tors (M.L. and K.L.) with a 4-point scale (0 to +++) Figure 1. Serum creatine kinase (CK) levels and the grade of signal intensity of findings in antimyosin scintigraphy, T -weighted magnetic resonance Interobserver variation was assessed using ␬ statistics. 2 imaging (MRI), and T1-weighted MRI at diagnosis and at follow-up in 17 Discrepancies of interpretation were resolved using joint patients with myositis. Pre indicates before treatment; post, after treatment. reanalysis and discussion, and consensus values were used for statistics. For grade 0, the finding was considered normal if muscular radioactivity was homoge- U/L to 238 ± 59 U/L (mean ± SEM) (Figure 1). The neously distributed and the level of radioactivity was lower than in the blood vessels; grade + , patchy or fo- response to drug therapy was generally moderate as cal distribution of muscular radioactivity, the level of judged by the improvement of muscle strength. None of which was similar to that in the blood vessels; grade++, the patients’ conditions worsened during treatment and patchy or focal distribution of muscular radioactivity, the need for assistance decreased or remained the level of which was higher than in the blood ves- unchanged. The degree of disability evaluated by the sels; and grade+++,more widespread intense focal dis- Vignos grade7 initially created for muscular dystrophies tribution of muscular radioactivity, the level of which remained unchanged in 9 patients and improved in 8 was much higher than in the blood vessels. A stan- patients. dard source of radioactivity (0.74 MBq/100 mL of 111In) was inserted between the thighs and calves to facili- MAGNETIC RESONANCE IMAGING tate the comparison of intensities of pathological findings in different gamma camera fields. Before treatment all patients had increased signal inten- STATISTICAL EVALUATION sity on T2-weighted MRI scans in at least 1 muscle group. On T1-weighted MRI scans 5 patients had no signal ab- The nonparametric Spearman rank correlation test was normalities at diagnosis, and most of the other patients used for correlation of MRI signal intensity changes, had more widely distributed or more severe lesions in serum CK level, and uptake of antimyosin antibody. the T2-weighted than in the T1-weighted images. The re- Kappa statistics were used to assess interobserver grad- sults are presented in detail in Table 1. ing differences between the 2 observers. On the follow-up T2-weighted MRI scans, the signal intensity changes had decreased, but in only 1 patient had all lesions disappeared. On the contrary, on T1- weighted MRI scans, the average grade of signal intensity more patients with active myositis, the sensitivity of these changes had increased by the second examination. In pa- 3 scintigraphies was about 90%. Increased uptake of in- tients 3, 13, and 17, T1-weighted MRI findings had re- dium In 111 altumomab pentetate–labeled antimyosin mained normal. The results of the follow-up examina- antibody was reported by De Geeter et al4 in 2 patients tion are presented in Table 2. with dermatomyositis and by us5 in 2 patients with polymyositis and 1 patient with dermatomyositis. In this study SCINTIGRAPHY we compared 111In-labeled antimyosin scintigraphy with MRI in the diagnosis and follow-up of 17 patients with At diagnosis all patients had varying degrees of in- inflammatory mypathies. creased uptake of antimyosin antibody in the lower limbs. In some patients, the uptake was more pronounced in RESULTS the calves than in the thighs, and 7 patients also had increased uptake in the buttocks. SERUM CK AND CLINICAL EXAMINATION In the follow-up scans the muscular uptake of antimyosin antibody had decreased, but all patients still had By the time of the follow-up MRI and scintigraphy stud- increased antimyosin uptake in at least 1 limb. How- ies, the serum CK levels had decreased from 1664 ± 564 ever, patient 8, whose CK level had not changed during

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 Table 1. Clinical, MRI, and Immunoscintigraphic Data at Diagnosis of Patients With Polymyositis or Dermatomyositis*

MRI Signal Intensity Changes

T1, R/L T2, R/L

Location of Thighs Calves Thighs Calves Scintigraphic Lesions, R/L Patient No./ Sex/Age, y CK Level, U/L EFEFEFEFThighs Calves 1/M/68 2079 NA NA 2/2 2/2 NA NA 2/2 2/2 +/+ ++/++ 2/M/65 5050 0/0 0/1 0/0 0/0 0/0 3/3 0/0 0/0 ++/++ +/+ 3/F/51 170 0/0 0/0 0/0 0/0 0/0 0/0 0/0 1/1 +/+ ++/++ 4/F/36 1554 0/0 0/0 0/0 1/1 2/1 1/0 0/0 2/2 ++/+ ++/++ 5/F/79 541 1/1 1/1 0/2 2/2 2/2 2/2 3/2 2/2 ++/+ +++/+++ 6/F/77 3286 0/0 0/0 0/0 0/0 1/1 1/1 1/0 1/1 ++/++ ++/++ 7/M/48 1167 2/2 1/1 2/2 2/2 2/2 1/1 2/2 1/1 ++/++ ++/++ 8/F/81 680 0/0 0/0 0/0 2/1 3/3 2/2 1/1 2/2 ++/++ ++/++ 9/M/68 321 2/2 1/1 0/0 2/2 1/1 1/1 1/0 0/0 +/+ ++/++ 10/M/55 731 0/0 0/0 1/0 2/1 0/0 1/1 3/0 2/2 +/0 +/+++ 11/F/70 460 2/2 2/2 3/3 2/2 1/1 1/1 1/1 3/3 +/+ ++/++ 12/M/52 493 0/0 1/1 0/0 0/0 2/2 2/2 1/1 1/1 +/+ ++/+ 13/F/55 515 0/0 0/0 0/0 0/0 1/1 1/1 2/2 1/1 +/+ ++/++ 14/F/51 673 0/0 0/0 0/0 1/2 1/0 0/0 0/0 1/1 +/+ ++/++ 15/F/71 1057 1/1 0/0 0/0 2/2 2/2 1/1 3/3 3/3 +/++ ++/++ 16/M/73 272 1/1 1/1 0/0 2/2 3/3 1/1 2/2 2/2 ++/++ ++/+ 17/F/53 9242 0/0 0/0 0/0 0/0 3/3 2/2 3/3 2/1 +++/+ ++/++

*MRI indicates magnetic resonance imaging; CK, creatine kinase; R/L, right/left; E, extensors; F, flexors; and NA, data not available. Grades of MRI signal intensity changes: 0, normal; 1, limited changes; 2, moderate changes; and 3, widespread changes. Intensity of radioantibody uptake: 0, no uptake; 1 plus sign, weak; 2 plus signs, moderate; and 3 plus signs, intense.

Table 2. Clinical, MRI, and Immunoscintigraphic Data at Follow-up of Patients With Polymyositis or Dermatomyositis*

MRI Signal Intensity Changes

T1, R/L T2, R/L

Location of Thighs Calves Thighs Calves Scintigraphic Lesions, R/L

Patient No. Therapy CK Level, U/L EFEFEFEF Thighs Calves Follow-up, mo 1 Prednisone and azathioprine 434 3/3 0/0 2/2 2/2 1/1 0/0 1/1 0/0 +/+ ++/+ 16 2 Prednisone and azathioprine 109 0/0 2/2 0/0 0/0 0/0 1/1 0/0 0/0 +/+ +/+ 7 3 Prednisone and azathioprine 107 0/0 0/0 0/0 0/0 0/0 0/0 0/0 0/0 +/+ +/+ 13 4 Prednisone and azathioprine 290 0/0 0/0 0/0 0/0 2/1 1/0 0/0 2/2 +/+ +/+ 22 5 Prednisone 89 2/2 2/3 1/2 2/2 1/1 0/0 2/2 1/1 +/+ ++/++ 9 6 Prednisone and azathioprine 454 0/0 1/1 0/0 0/0 1/0 1/1 0/0 0/0 ++/++ ++/++ 9 7 Prednisone 764 2/2 1/1 2/2 2/2 1/1 0/0 1/1 0/0 +/+ ++/+ 11 8 Prednisone 682 1/1 2/2 0/0 2/1 3/3 2/2 0/0 2/2 ++/++ +++/+++ 7 9 Prednisone and azathioprine 42 2/2 1/1 0/0 2/2 1/1 0/0 1/1 1/1 0/0 +/+ 8 10 Prednisone and azathioprine 510 0/0 0/0 1/0 3/1 1/1 1/1 2/2 1/1 +/0 +/++ 10 11 Prednisone 172 2/2 2/2 3/3 2/2 0/0 0/0 0/0 2/2 +/+ ++/++ 11 12 Prednisone and azathioprine 20 1/1 1/1 1/1 1/1 0/0 0/0 1/1 1/1 0/0 +/0 7 13 Prednisone 50 0/0 0/0 0/0 0/0 0/0 0/0 1/1 0/0 0/0 0/+ 6 14 Prednisone 201 0/0 0/0 0/0 1/2 0/0 0/0 1/1 1/1 +/+ +/+ 8 15 Prednisone 44 2/2 1/1 1/1 2/2 2/1 1/1 1/1 1/1 0/0 +/+ 7 16 Prednisone 20 2/2 2/2 1/0 1/1 3/3 2/2 0/0 1/1 +/+ +/+ 7 17 Prednisone and azathioprine 53 0/0 0/0 0/0 0/0 2/2 1/1 2/2 1/1 0/0 +/+ 8

*MRI indicates magnetic resonance imaging; CK, creatine kinase; R/L, right/left; E, extensors; and F, flexors. Grades of MRI signal intensity changes: 0, normal; 1, limited changes; 2, moderate changes; and 3, widespread changes. Intensity of radioantibody uptake: 0, no uptake; 1 plus sign, weak; 2 plus signs, moderate; and 3 plus signs, intense.

therapy, actually had more accumulation of antibody in CORRELATION BETWEEN SERUM CK, her calves in the second study. Magnetic resonance im- SCINTIGRAPHY, AND MRI aging and scintigraphy findings of patient 2 and patient 17 at diagnosis and at follow-up are presented (in There was a tendency for positive correlation between Figure 2 and Figure 3, respectively). T2-weighted MRI imaging and uptake of antimyosin an-

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C D

E F

Figure 2. Increased uptake of antimyosin antibody in scintigraphy (A), increased signal intensity in T2-weighted magnetic resonance imaging (MRI) (B), and pathological signal intensity in T1-weighted MRI (C) in the thighs of patient 2 at diagnosis. At follow-up the findings in scintigraphy (D) and T2-weighted MRI (E) decreased, but the lesions in T1-weighted MRI (F) are slightly more pronounced.

tibody before treatment (Rs = 0.36; P = .15) when using a vided information on the efficacy of drug therapy to sup- mean value for all the muscle groups studied in each pa- press inflammation in these patients. However, the good tient. At follow-up this correlation could not be found. correlation between the uptake of antimyosin antibody Uptake of antimyosin correlated with serum CK levels and serum CK activity was not found between T2- both at diagnosis (Rs = 0.48; P = .05) and at follow-up weighted MRI and CK levels, favoring scintigraphy as the (Rs = 0.71; P = .004). There was no correlation between method of choice for the assessment of the severity of findings of T2-weighted MRI and CK activity. The agree- inflammation. The plausible explanation for increased up- ment between the mean pretherapy and posttherapy uptake of antimyosin antibody is that the inflammatory pro- take of antibody and mean signal intensity on T2- cess disturbs the integrity of muscle cell membranes and weighted MRI is shown in Figure 1. reveals the insoluble myosin to the antibody. Notably, The ␬ values for interobserver variation were 0.71 the progression of intramuscular fatty degeneration caus- (good) for MRI grading and 0.55 (moderate) for scintig- ing increased signal intensity on T1-weighted MRI scans raphy grading. was not reflected in antimyosin scintigraphy. A further advantage of MRI compared with scintigraphy was the COMMENT possibility of distinguishing between lesions in exten- sor and flexor muscles. 8 Both scintigraphy with antimyosin antibody and T2- Kaufman et al identified abnormalities in T1- weighted MRI were capable of detecting inflammatory weighted MRI signal intensity and fat replacement that lesions in muscles of patients with polymyositis and der- were claimed to correlate with clinical disease activity in matomyositis. Scintigraphy and T2-weighted MRI also pro- 13 patients with polymyositis and dermatomyositis.

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C D

E F

Figure 3. Accumulation of antimyosin antibody (A) and increased signal intensity in T2-weighted sequences in magnetic resonance imaging (MRI) (B) in the calves of patient 17 at diagnosis when the patient was bedridden, and 8 months later at follow-up (C and D) when she was mostly independent in activities of daily living

and able to walk small distances without support. T1-weighted MRI findings remained normal (E and F).

Fujino et al9 concluded from studies on 8 patients with showed definitive changes at follow-up in imaging com- active myositis that the high-intensity lesions in the T2- pared with the first study, an observation that corre- weighted images represented both inflammation and lated with clinical and biochemical findings in 2 of them.12 edema of muscles and that, therefore, T2-weighted im- In juvenile dermatomyositis, changes in T2-weighted imaging appeared to be more important for the diagnosis aging that rapidly parallel disease activity or with a de- 13-15 of inflammatory myopathies than T1-weighted images. lay of 2 months have been reported. Reimers et al,10 assessing the value of gadolinium– Antimyosin scintigraphy, which has an established gadopentetate dimeglumine in inflammatory myopa- role in the evaluation of cardiac muscle damage, has also thies of adults, found T2-weighted images to be more sen- been used to detect traumatic skeletal muscle le- 5,16 sitive than contrast-enhanced T1-weighted images. Of 58 sions. The accumulation of antimyosin antibody is fo- patients, the sensitivity of MRI for detection of abnor- cal and often quite intensive in rhabdomyolysis, com- mal muscle structure was about 80%, with this method pared with the more diffuse or patchy antibody being especially sensitive for the detection of edemalike accumulation in myositis. In muscular dystrophies the abnormalities. better preserved muscle bulk in the calves accumulated Only a few patients with inflammatory myopathies more antibodies than the atrophic thigh muscles, which have been serially followed up with MRI. Fraser et al11 had more pronounced increases in signal intensity in reported that the increased signal intensity in fat sup- T1-weighted MRI, reflecting replacement of muscle by pressive images paralleled disease activity using needle fat.5 Similar observations on the effect of fatty degenera- biopsy in the 3 patients studied. When 10 patients with tion on MRI findings were made in our study on polymyositis were examined twice with MRI, 3 patients patients with myositis.

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 The follow-up of patients with inflammatory 3. Fleckenstein JL, Reimers CD. Inflammatory myopathies: radiologic evaluation. myopathies is based on clinical examination and serum Radiol Clin North Am. 1996;34:427-439. 1 4. De Geeter F, Deleu D, Debeuckelaere S, De-Coninck A, Somers G, Bossuyt A. CK levels. Repeated muscle biopsy is not used often Detection of muscle necrosis in dermatomyositis by 111 In-labelled antimyosin since it is an invasive and expensive method for evaluat- Fab fragments. Nucl Med Commun. 1989;10:603-607. ing the efficacy of therapy. Muscle imaging has the 5. Lo¨fberg M, Liewendahl K, Savolainen S, et al. Antimyosin scintigraphy in pa- advantage of noninvasiveness and the capability to tients with acquired and hereditary muscular disorders. Eur J Nucl Med. 1994; reveal changes in all muscles of interest. Antimyosin 21:1098-1105. 6. Kairemo KJ, Wiklund TA, Liewendahl K, et al. Imaging of soft-tissue sarcomas scintigraphy correlated with serum CK levels, both at with indium-111-labeled monoclonal antimyosin Fab fragments. J Nucl Med. 1990; diagnosis and at follow-up, in our patients with myosi- 31:23-31. tis. T1-weighted MRI images were required for revealing 7. Archibald KC, Vignos PJ. A study of contractures in muscular dystrophy. Arch secondary changes, particularly fatty degeneration, in Phys Med Rehabil. 1959;40:150-157. 8. Kaufman LD, Gruber BL, Gerstman DP, Kaell AT. Preliminary observations on patients with chronic myositis. In conclusion, our study the role of magnetic resonance imaging for polymyositis and dermatomyositis. has demonstrated that relevant information on the Ann Rheum Dis. 1987;46:569-572. extent and severity of lesions in patients with myositis 9. Fujino H, Kobayashi T, Goto I, Onitsuka H. Magnetic resonance imaging of the can be obtained with antimyosin scintigraphy and low- muscles in patients with polymyositis and dermatomyositis. Muscle Nerve. 1991; field MRI, reducing the need for follow-up muscle 14:716-720. 10. Reimers CD, Schedel H, Fleckenstein JL, et al. Magnetic resonance imaging of biopsy. skeletal muscles in idiopathic inflammatory myopathies of adults. J Neurol. 1994; 241:306-314. Accepted for publication December 1, 1997. 11. Fraser DD, Frank JA, Dalakas M, Miller FW, Hicks JE, Plotz P. Magnetic reso- This work was supported by a grant from the Paulo nance imaging in the idiopathic inflammatory myopathies. J Rheumatol. 1991; Foundation, Helsinki, Finland (Dr Lo¨fberg). 18:1693-1700. Reprints: Mervi Lo¨fberg, MD, Institute of Neurosci- 12. Stiglbauer R, Graninger W, Prayer L, et al. Polymyositis: MRI-appearance at 1.5 ences, Department of Neurology, Helsinki University Cen- T and correlation to clinical findings. Clin Radiol. 1993;48:244-248. 13. Keim DR, Hernandez RJ, Sullivan DB. Serial magnetic resonance imaging in ju- tral Hospital, 00290 Helsinki, Finland. venile dermatomyositis. Arthritis Rheum. 1991;34:1580-1584. 14. Chapman S, Southwood TR, Fowler J, Ryder AJ. Rapid changes in magnetic reso- REFERENCES nance imaging of muscle during the treatment of juvenile dermatomyositis. Br J Rheumatol. 1994;33:184-186. 15. Huppertz HI, Kaiser WA. Serial magnetic resonance imaging in juvenile derma- 1. Dalakas MC. Polymyositis, dermatomyositis, and inclusion-body myositis. N Engl tomyositis–delayed normalization. Rheumatol Int. 1994;14:127-129. J Med. 1991;325:1487-1496. 16. Malki AA, Elgazzar A, Ashqar T, Owunwanne A, Abdel-Dayem H. New tech- 2. Griggs RC, Askanas V, DiMauro S, et al. Inclusion body myositis and myopa- nique for assessing muscle damage after trauma. J R Coll Surg Edinb. 1992; thies. Ann Neurol. 1995;38:705-713. 37:131-133.

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