AJR 2002; 179:989-997
© American Roentgen Ray Society
MR Imaging of Primary Skeletal Muscle Diseases in Children
Wing P. Chan1 and
Gin-Chung Liu2
1 Department of Radiology, Taipei Medical University, Municipal Wan Fang
Hospital, 111 Hsing-Long Rd., Sec. 3, Taipei 116, Taiwan, Republic of
China.
2 Department of Radiology, Kaohsiung Medical University Hospital, 100 Shih-Chuan
First Rd., Kaohsiung 807, Taiwan, Republic of China.
Received January 21, 2002;
accepted after revision March 28, 2002.
Address correspondence to G.-C. Liu.
Introduction
This article illustrates the MR imaging features of a spectrum of skeletal
muscle diseases in children. MR imaging with optimized protocols allows
localization of the extent of focal disease processes and assessment of
changes in tissue fat—water composition in children with skeletal muscle
diseases. Optimal imaging can minimize problems with sampling errors in
procedures performed blindly, such as biopsy and electromyography. We selected
patients with five types of diseases for illustration: muscular dystrophies
(Duchenne's, Becker's), congenital myopathies of unknown origin (congenital
muscular dystrophy), metabolic myopathies (Pompe's disease), inflammatory
disease (childhood dermatomyositis), and motor neuron disease (spinal muscular
atrophy).
Technical Aspects
The main goal in MR imaging of abnormal skeletal muscles is the delineation
of changes in tissue fat—water composition. T1-weighted imaging is
essential for depicting high-signal-intensity fat and low-signal-intensity
water. Short tau inversion recovery (STIR) sequences are sensitive for the
detection of edematous processes and specific by suppression of signal from
fat. Alternative T2-weighted chemical shift sequences offer sufficient fat
suppression and relatively short scanning times. However, fast T2-weighted
spinecho sequences should be avoided because they provide insufficient fat
signal suppression. Gadolinium-enhanced T1-weighted sequences may be helpful
in differentiating inflammatory or neoplastic lesions from edematous
fluid.
Coronal images provide the best overview of the longitudinal extent of the
disease and allow identification of palpable bony landmarks. Axial images
offer the best delineation of muscle groups and tissue characterization.
Circumferential body coils with large fields of view are essential to compare
symmetry of muscle involvement in the bilateral extremities. Surface coils are
optional to maximize the signal-to-noise ratio for imaging selected areas.
Sedation may be needed to prevent motion artifacts in infants and children.
The total scanning time can be limited to 20 min.
Muscular Dystrophies
Duchenne's Muscular Dystrophy
Duchenne's muscular dystrophy is a rapidly progressive primary degeneration
of skeletal muscle, with age at onset from 4 to 6 years and death at 10 to 20
years old. It is the most severe form of muscular dystrophy and is inherited
as an X-linked recessive disorder, predominantly in boys. An increase of more
than 10-fold in serum creatine kinase activity is noted in this disorder.
Duchenne's muscular dystrophy is characterized by an initial symmetric and
selective involvement of the proximal pelvic girdle muscles in the early stage
of the disease process, and the calf and proximal shoulder girdle muscles in
the late stage. Pseudohypertrophy of the calves is present in 80% of
patients.
T1-weighted MR images reveal hyperintense fatty infiltration interspersed
between the diseased muscles (Fig.
1A,1B,1C,1D,1E).
The mean fat mass is significantly higher in diseased muscle than in normal
muscle [1]. MR imaging enables
the radiologist to determine the severity of fatty infiltration, which
parallels declination in muscle strength
[2]. The muscle in the thigh
that is most resistant to disease is the gracilis, followed by the sartorius,
semitendinous, and semimembranous muscles
[2] (Figs.
2 and
3). Asymmetric involvement of
the thigh muscles is not unusual. The most characteristic histologic features
are the presence of hyaline fibers, adjacent parts of focal fiber necrosis,
and ongoing phagocytosis.
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Fig. 1A. —Duchenne's muscular dystrophy in 12-year-old boy with 3-year
history of unstable gait. Serum creatine kinase value was 4227 U/L. Coronal
T1-weighted spin-echo MR image (TR/TE, 300/20) shows longitudinal extent of
fatty infiltration of pelvic girdle and thigh muscles.
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Fig. 1B. —Duchenne's muscular dystrophy in 12-year-old boy with 3-year
history of unstable gait. Serum creatine kinase value was 4227 U/L. Axial
T1-weighted spin-echo MR image (500/20) shows widespread increased signal
intensity, denoting fatty infiltration, of all muscles in pelvic girdle with
exception of bilateral adductor minimus muscles (arrows), which are
relatively spared.
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Fig. 1C. —Duchenne's muscular dystrophy in 12-year-old boy with 3-year
history of unstable gait. Serum creatine kinase value was 4227 U/L. Axial
T1-weighted spin-echo MR image (500/20) shows selective bilateral fatty
infiltration of thigh muscles. Note sparing of bilateral gracilis (G),
sartorius (s), adductor magnus (arrow), and semitendinosus (St)
muscles.
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Fig. 1D. —Duchenne's muscular dystrophy in 12-year-old boy with 3-year
history of unstable gait. Serum creatine kinase value was 4227 U/L. Axial
T1-weighted spin-echo MR image (500/20) shows selective bilateral involvement
of calf muscles. Note less involvement of bilateral gastrocnemius
(straight arrows) and soleus (curved arrow) muscles.
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Fig. 1E. —Duchenne's muscular dystrophy in 12-year-old boy with 3-year
history of unstable gait. Serum creatine kinase value was 4227 U/L.
Photomicrograph of diseased muscle specimen shows varying fiber size, focal
muscle fiber necrosis, and phagocytosis. (H and E, x350)
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Fig. 2. —Duchenne's muscular dystrophy in 11-year-old boy. Axial
T1-weighted spin-echo MR image (TR/TE, 500/20) shows widespread bilateral
fatty infiltration of thigh muscles, resulting in mosaic pattern. Bilateral
gracilis muscles (G) are most resistant to disease.
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Fig. 3. —Duchenne's muscular dystrophy in a 7-year-old boy, brother of
patient in Figure 2. Axial
T1-weighted spin-echo MR image (TR/TE, 500/20) shows moderate fatty
infiltration with patchy pattern involving bilateral thigh muscles. Bilateral
semimembranosus (Sm), vastus intermedius (Vi), and vastus medialis (Vm)
muscles are less involved. Note sparing of bilateral gracilis (G), sartorius
(s), and semitendinosus (St) muscles.
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Becker's Muscular Dystrophy
Becker's muscular dystrophy is a slowly progressive primary degeneration of
skeletal muscle, with an onset age of approximately 11 years and age at death
up to the fourth decade. The disease is inherited as an X-linked recessive
disorder, predominantly in boys. Duchenne's and Becker's muscular dystrophies
affect the same dystrophin genetic system and have the same muscular
involvement, but the Becker type is less severe. Symptoms appear in the lower
limbs 5 to 10 years before they occur in the upper limbs. Serum creatine
kinase activity in Becker's muscular dystrophy is raised to a degree similar
to that found in the Duchenne type.
The selective muscular involvement in Becker's muscular dystrophy is
apparent on T1-weighted MR images (Fig.
4A,4B,4C).
The rectus femoris, adductor longus, gracilis, sartorius, semitendinosus, and
semimembranous muscles are relatively spared and even hypertrophied in the
thighs. Enlargement of the calves due to fatty infiltration (i.e.,
pseudohypertrophy) of the bilateral gastrocnemius and soleus muscles occurs in
the Becker type, but it is less severe than in Duchenne's muscular dystrophy.
The histology of Becker's muscular dystrophy resembles that of the Duchenne
type, except that in the Becker type the hyaline fibers are relatively
uncommon and regenerative fiber clusters are often seen.
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Fig. 4A. —Becker's muscular dystrophy in 13-year-old boy with proximal
muscle weakness. Serum creatine kinase value was 7600 U/L. Axial T1-weighted
spin-echo MR image (TR/TE, 400/20) of proximal thighs shows pattern similar to
that in Duchenne's muscular dystrophy, except for less severe involvement of
rectus femoris (Rf), adductor longus (Al), gracilis (G), and semitendinosus
(St) muscles. Involvement of bilateral thigh muscles is symmetric.
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Fig. 4B. —Becker's muscular dystrophy in 13-year-old boy with proximal
muscle weakness. Serum creatine kinase value was 7600 U/L. Axial T1-weighted
spin-echo MR image (400/20) shows pseudohypertrophy of bilateral calf muscles.
Note that fatty infiltration in bilateral gastrocnemius (straight
arrows) and soleus (curved arrow) muscles is less severe in
Becker's dystrophy than in Duchenne type, resulting in patchy pattern.
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Fig. 4C. —Becker's muscular dystrophy in 13-year-old boy with proximal
muscle weakness. Serum creatine kinase value was 7600 U/L. Photomicrograph of
diseased muscle specimen shows abnormality resembling Duchenne type, except
that Becker type has more regenerative fiber clusters. (H and E,
x180)
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Congenital Muscular Dystrophy
Congenital muscular dystrophy is an uncommon genetically determined,
relatively nonprogressive necrotizing myopathy. It affects infants and occurs
with the same frequency in males and females. This dystrophy is characterized
by hypotonia, multiple joint contractures, and generalized muscular weakness,
with more severity proximally than distally.
The overall involvement of muscle in congenital dystrophy can be reliably
depicted on MR imaging (Fig.
5A,5B,5C,5D),
and it is less severe than the muscle involvement in patients with other
muscular dystrophies or inflammatory diseases
[3]. The sartorius and gracilis
muscles are relatively spared in the thighs
[4]. No selective sparing of
muscles occurs in patients with merosin-deficient congenital muscular
dystrophy [4]. Histologic
features of this disorder are typical of muscular dystrophy, consisting of
fibrosis and fat replacement with marked variability in fiber size, although
usually without active fiber necrosis and regeneration.
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Fig. 5A. —Congenital muscular dystrophy in 10-year-old girl with a
6-year history of muscular weakness. She had myopathic face and contractures
of both elbows. Her upper extremities were weaker than her lower extremities.
Coronal T1-weighted spin-echo MR image (TR/TE, 300/20) shows longitudinal
extent of diseased muscle. Findings of fatty degeneration are less severe than
those in patients with other dystrophies.
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Fig. 5B. —Congenital muscular dystrophy in 10-year-old girl with a
6-year history of muscular weakness. She had myopathic face and contractures
of both elbows. Her upper extremities were weaker than her lower extremities.
Axial T1-weighted spin-echo MR image (400/20) of bilateral thighs shows mildly
fatty infiltration of vastus lateralis (straight solid arrow)
muscles. Note selective sparing of bilateral vastus medialis (open
arrow) and gracilis (curved solid arrow) muscles.
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Fig. 5C. —Congenital muscular dystrophy in 10-year-old girl with a
6-year history of muscular weakness. She had myopathic face and contractures
of both elbows. Her upper extremities were weaker than her lower extremities.
Axial T1-weighted spin-echo MR image (400/20) shows moderate fatty
infiltration of all muscle groups in bilateral calves. Note that congenital
dystrophy has no sparing of muscles in either calf.
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Fig. 5D. —Congenital muscular dystrophy in 10-year-old girl with a
6-year history of muscular weakness. She had myopathic face and contractures
of both elbows. Her upper extremities were weaker than her lower extremities.
Photomicrograph of diseased muscle specimen shows fatty replacement, fibrosis,
varying fiber size, and fiber degeneration. (H and E, x350)
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Pompe's Disease (Acid Maltase Deficiency)
Local muscle glycogen is the main energy source for skeletal muscle
contraction. Glycogenoses or glycogen storage diseases are a group of
disorders characterized by deranged metabolism of glycogen, glucose, or both.
It is an autosomal recessive glycogenosis that may appear from infancy to
adulthood. For the infantile type, clinical manifestations include generalized
and rapidly progressive weakness and hypotonia and enlargement of the heart,
tongue, and liver. Pompe's disease presents in the first few months after
birth, and the age of death is before 2 years old. For the childhood type,
weakness is usually greater in proximal than distal limb muscles. Calf
enlargement may simulate muscular dystrophy. Onset occurs in early childhood,
with death before the second decade. For the adult type, onset can be at 20
years or older.
T1-weighted MR images show diffuse hypertrophy of muscle groups without
evidence of fatty infiltration (Fig.
6A,6B,6C,6D).
All muscle fibers contain large vacuoles in the infantile type. The vacuoles
tend to be less marked in the childhood type.
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Fig. 6A. —Pompe's disease in a 3-month-old boy with floppy infant
syndrome who had pneumonia and hypertrophic cardiomyopathy at admission.
Coronal T1-weighted spin-echo MR image (TR/TE, 300/20) shows diffuse muscle
hypertrophy of bilateral thighs.
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Fig. 6B. —Pompe's disease in a 3-month-old boy with floppy infant
syndrome who had pneumonia and hypertrophic cardiomyopathy at admission. Axial
proton-weighted spin-echo MR image (1500/20) shows no evidence of fatty
involvement in pelvic girdle muscles.
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Fig. 6C. —Pompe's disease in a 3-month-old boy with floppy infant
syndrome who had pneumonia and hypertrophic cardiomyopathy at admission. Axial
T2-weighted spin-echo MR image (1500/90) shows hypertrophy of all muscle
groups in bilateral thighs with no edematous changes.
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Fig. 6D. —Pompe's disease in a 3-month-old boy with floppy infant
syndrome who had pneumonia and hypertrophic cardiomyopathy at admission.
Photomicrograph of diseased muscle specimen shows marked vacuolar myopathy. (H
and E, x200)
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Childhood Dermatomyositis
Childhood dermatomyositis is a multisystemic disease of unknown cause. It
is characterized by diffuse nonsuppurative inflammation of muscle fibers and
skin. The primary targets of the disease process are blood vessels, and thus
it is actually a systemic vasculopathy. The earliest manifestation is proximal
lower extremity weakness, followed by proximal upper limb weakness.
Contractures in joints frequently occur. Typically, the skin lesions appear as
discoloration of the upper lids and malar aspect of the face.
MR images reveal increased water content of the infarcted muscle because of
vasculitis [5] (Fig.
7A,7B,7C,7D,7E).
T2-weighted and STIR MR imaging are important for depicting the infarcted
muscles of the disease. However, children with dermatomyositis may also have
extensive subcutaneous and intermuscular calcium-laden fluid collections;
gadolinium-enhanced MR imaging allows differentiation of these collections,
which have minimal peripheral enhancement, from abscesses with marked
enhancement [6].
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Fig. 7A. —Childhood dermatomyositis in 4-year-old girl with 3-month
history of waddling with progressive deterioration. Gottron's sign and
arthralgia were noted 1 month earlier. Serum creatine kinase value was 384
U/L. Axial T1-weighted spin-echo MR image (TR/TE, 500/20) shows unremarkable
MR signal changes in pelvic girdle muscles.
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Fig. 7B. —Childhood dermatomyositis in 4-year-old girl with 3-month
history of waddling with progressive deterioration. Gottron's sign and
arthralgia were noted 1 month earlier. Serum creatine kinase value was 384
U/L. Axial T2-weighted spin-echo MR image (1500/90) of pelvic girdle shows
increased signal intensity, denoting edemalike changes in vastus lateralis
(VI), vastus intermedius (Vi), and adductor (Ad) muscles. Note that band of
high signal intensity at muscle—fat interface indicates enhanced
chemical-shift artifact (arrow).
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Fig. 7C. —Childhood dermatomyositis in 4-year-old girl with 3-month
history of waddling with progressive deterioration. Gottron's sign and
arthralgia were noted 1 month earlier. Serum creatine kinase value was 384
U/L. Axial T1-weighted spin-echo MR image (500/20) shows no evidence of fatty
replacement in thigh muscles.
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Fig. 7D. —Childhood dermatomyositis in 4-year-old girl with 3-month
history of waddling with progressive deterioration. Gottron's sign and
arthralgia were noted 1 month earlier. Serum creatine kinase value was 384
U/L. Axial T2-weighted spin-echo MR image (1500/90) shows edematous changes of
all muscle groups in bilateral thighs. Note presence of enhanced chemical
shift artifact (arrows).
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Fig. 7E. —Childhood dermatomyositis in 4-year-old girl with 3-month
history of waddling with progressive deterioration. Gottron's sign and
arthralgia were noted 1 month earlier. Serum creatine kinase value was 384
U/L. Photomicrograph of diseased muscle specimen shows prominent focal
lymphocytic infiltration in muscle fascicle in relation to thickened blood
vessel. (H and E, x200)
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Spinal Muscular Atrophy
Spinal muscular atrophy is inherited as autosomal recessive disorders
affecting anterior horn cells in the spinal cord and brain stem nuclei. It
manifests as proximal muscular weakness and wasting with varying age of onset,
progression, and severity. Spinal muscular atrophy can be classified as mild,
intermediate, or severe on the basis of the patient's ability to walk,
inability to walk, or inability to sit, respectively. The mild type has fatty
infiltration of muscle bundles and increased intramuscular fat planes (Fig.
8A,8B,8C,8D,8E).
The intermediate type has ragged atrophy of muscle bundles of the thigh and
the calf with selective preservation of the adductor longus muscle (Fig.
9A,9B,9C,9D,9E).
The severe type shows severe atrophy of the entire muscle bundles of the thigh
and the calf.
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Fig. 8A. —Spinal muscular atrophy (mild type) in 10-year-old boy in
whom waddling was noted at 5 years old. Serum creatine kinase value was 573
U/L. Coronal T1-weighted spin-echo MR image (TR/TE, 300/20) shows longitudinal
extent of pronounced intermuscular fat planes of bilateral thighs.
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Fig. 8B. —Spinal muscular atrophy (mild type) in 10-year-old boy in
whom waddling was noted at 5 years old. Serum creatine kinase value was 573
U/L. Axial T1-weighted spin-echo MR image (350/20) shows fatty infiltration of
gluteus maximus and vastus lateralis muscles. Adductor muscles (Ad) are
spared.
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Fig. 8C. —Spinal muscular atrophy (mild type) in 10-year-old boy in
whom waddling was noted at 5 years old. Serum creatine kinase value was 573
U/L. Axial T1-weighted spin-echo MR image (350/20) shows mild atrophy and
fatty infiltration of thigh muscles, with exception of sartorious (s),
semitendinosus (St), and semimembranosus (Sm) muscles, which are spared.
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Fig. 8D. —Spinal muscular atrophy (mild type) in 10-year-old boy in
whom waddling was noted at 5 years old. Serum creatine kinase value was 573
U/L. Axial T1-weighted spin-echo MR image (350/20) shows fatty infiltration of
soleus and peroneal group of calf muscles. Note asymmetric severity of
involvement of bilateral calf muscles. Anterior tibialis (straight
arrow) and gastrocnemius (curved arrow) muscles are spared.
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Fig. 8E. —Spinal muscular atrophy (mild type) in 10-year-old boy in
whom waddling was noted at 5 years old. Serum creatine kinase value was 573
U/L. Photomicrograph of diseased muscle specimen shows large groups of
atrophic fibers next to bunches of hypertrophic fibers. (H and E,
x400)
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Fig. 9A. —Spinal muscular atrophy (intermediate type) in 13-year-old
girl who was never able to stand up. Serum creatine kinase value was 120 U/L.
Coronal T1-weighted spin-echo MR image (TR/TE, 500/14) of bilateral thighs
shows fascicular appearance of entire muscle bundles.
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Fig. 9B. —Spinal muscular atrophy (intermediate type) in 13-year-old
girl who was never able to stand up. Serum creatine kinase value was 120 U/L.
Coronal short tau inversion recovery image (1800/100; inversion time, 160
msec) shows saturation of signal from fat and no edematous changes of thigh
muscles.
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Fig. 9C. —Spinal muscular atrophy (intermediate type) in 13-year-old
girl who was never able to stand up. Serum creatine kinase value was 120 U/L.
Axial T1-weighted spin-echo MR image (500/14) shows severe fatty infiltration
of all muscles of pelvic girdle, which are ragged.
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Fig. 9D. —Spinal muscular atrophy (intermediate type) in 13-year-old
girl who was never able to stand up. Serum creatine kinase value was 120 U/L.
Axial T1-weighted spin-echo MR image (500/14) shows diffuse ragged atrophy of
all thigh muscles. Note selective sparing of adductor longus muscle
(arrow).
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Fig. 9E. —Spinal muscular atrophy (intermediate type) in 13-year-old
girl who was never able to stand up. Serum creatine kinase value was 120 U/L.
Photomicrograph of diseased muscle shows prominent groups of small atrophic
fibers occupying several fascicles and nearby hypertrophied fibers. (H and E,
x200)
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The common characteristic MR imaging finding is asymmetry of muscle
involvement in the lower extremities. Findings on MR imaging can be in
agreement with histologic changes
[7].
In summary, a highly selective involvement of muscle groups is noted in
various primary skeletal muscle diseases in children. MR imaging enables the
radiologist to assess the distribution and severity of the diseased muscles
and thereby provides a powerful tool for guiding tissue diagnosis and
monitoring treatment response.
Acknowledgments
We thank Yuh-Jyh Jong for providing well-prepared photomicrographs and
clinical data for this article.
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