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MUSCLE DISORDERS

Diagnostic Approach to Muscle Disorders

Stephanie J. Valberg, DVM, PhD, Diplomate ACVIM

To identify a specific muscle disorder, a standardized approach of evaluating horses with potential
muscle disease should include accurate history, careful physical examination, and selection of diagnostic tests such as serum biochemistry, imaging techniques, exercise testing, electromyography,
muscle biopsy, and genetic testing. Authors address: Department of Veterinary Population Medicine, College of Veterinary Medicine, University of Minnesota, 1365 Gortner Avenue, St. Paul, MN
55108; e-mail: valbe001@umn.edu. 2006 AAEP.

1.

Introduction

The fundamental approach to diagnosing muscle

diseases in horses is based on a thorough history,
careful physical examination, complete blood count,
and serum biochemistry profile. After this evaluation, a diagnosis can be made if muscular signs are
part of a primary or secondary disease process.
Primary muscle disorders usually fall into one of five
broad clinical categories: (1) focal muscle strain,
(2) rhabdomyolysis, (3) weakness and exercise intolerance without rhabdomyolysis, (4) abnormal muscle contraction/conduction, and (5) muscle atrophy
(Table 1). Additional diagnostic tests can then be
selected to localize the muscle groups affected by the
disorder and to identify the disease process that is
causing the presenting clinical signs.
Localizing the extent and severity of muscle strain
or rhabdomyolysis may be assisted by thermography, ultrasonography, scintigraphy, or electromyography, and its specific cause may be determined by
historical information or in some cases, by muscle
biopsy. Exercise testing, electromyography, muscle biopsy, and molecular genetic testing may identify causes of exercise intolerance, weakness, and
abnormal muscle contractility. Determining if

muscle atrophy is myogenic or neurogenic in origin

can be assessed by electromyography and muscle
biopsy as well as other tests such as cerebrospinal
fluid (CSF) taps, Western blot for equine protozoal
myeloencephalitis (EPM), and serum vitamin E
concentrations. Detailed information regarding
specific diagnostic testing is provided in the accompanying sections.
2.

History and Physical Examination

A detailed history is often required when assessing

muscle disorders in horses, because many disorders
are intermittent in nature and triggered by certain
environmental stimuli. A careful description of the
horses muscle tone, muscle mass, gait, degree of
pain, exercise intolerance, and weakness when
showing clinical signs as well as the duration and
frequency of signs becomes important. Further
characterization of possible eliciting factors requires
a detailed account of the horses exercise schedule,
diet, vaccination history, signs of concurrent disease, and current medications.
Inspection of the horse at a distance while it is
standing with forelimbs and hindlimbs exactly
square is imperative in assessing muscle mass, symmetry, and signs of atrophy. Subsequently, palpa-

NOTES

340

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tion of the entire muscle mass of the horse provides

valuable information regarding muscle tone, heat,
pain, swelling, subtle muscle atrophy, and fasciculations. Firm and deep palpation of the lumbar,
gluteal, semimembranosus, and semitendinosus
muscles may reveal pain, cramps, or fibrosis. The
tricep, pectoral, gluteal, and semitendinosus muscles can be tapped with a fist or percussion hammer
and observed for prolonged contracture suggestive of
myotonia. Running a blunt instrument such as a
hemostat, needle cap, or pen over the lumbar and
gluteal muscles provides information regarding
back pain. Extension (swayback) followed by flexion (hogback) of the back is expected in healthy
animals. Guarding against movement may reflect
abnormalities in the pelvic or thoracolumbar muscles or pain associated with the thoracolumbar spine
or sacroiliac joints.
A lameness evaluation, including flexion tests, is
often indicated as part of evaluation of the muscular
system. Muscle pain may be secondary to changes
in movement caused by lower limb lameness. The
horse should be observed at a walk or trot for any
gait abnormalities and in some cases, lunged for 15
min or ridden until clinical signs are elicited. If the
horse shows any signs of neurologic disease, a detailed neurologic examination should also be
performed.
3.

Biochemical Profiles

Skeletal muscle necrosis may be identified by determining the activity in serum of creatine kinase (CK),
aspartate transaminase (AST), and lactate dehydrogenase (LDH). Carbonic anhydrase III1,2 and serum myoglobin have also been suggested as markers
of equine muscle necrosis.3,4 The permeability of
the muscle-cell membrane, rate of enzyme production, alternate tissue sources of the enzyme, and
rate of enzyme excretion/degradation may also influence serum-enzyme activities.5
Serum CK

Isoforms of CK are found in skeletal muscle (MM),

cardiac muscle (MB), and nervous tissue (BB).
CK, a relatively low molecular-weight protein
(80,000 Da), is liberated within hours of muscle
damage or increased cell-membrane permeability
into the extracellular fluid, and it usually peaks at
4 6 h after muscle injury.4 A three- to five-fold
increase in serum CK from normal values is believed
to represent necrosis of 20 g of muscle tissue.5
Rhabdomyolysis results in a proportionately greater
increase in the MM isoform than the MB isoform,
but some studies disagree about the tissue specificity of serum CK isoforms in the horse.6 8 Limited
elevations in CK (1000 U/l) may accompany training or transport. Extremely fatiguing exercise
(e.g., endurance rides or the cross-country phase of a
three-day event) may result in CK activities being
increased to 1000 U/l, but they are usually 5000
U/l. Under these circumstances, serum CK activi-

MUSCLE DISORDERS

ties rapidly return to baseline (i.e., 350 IU/l in

24 48 h). Recumbent animals may have slightly
elevated CK activities of 3000 U/l. In contrast,
more substantial elevations (from several thousand
to hundreds of thousands of U/l) in the activity of
this enzyme may occur with rhabdomyolysis.
Serum AST

Serum AST, previously known as serum glutamicoxaloacetic transaminase (SGOT), is a larger molecular-weight protein that has high activity in skeletal
and cardiac muscle as well as the liver, red blood
cells, and other tissues. Elevations in AST are not
specific for myonecrosis, and increases could be the
result of hemolysis or muscle, liver, or other organ
damage. AST activity rises more slowly in response to myonecrosis than does CK, often peaking
between 12 and 24 h after the insult.4 In addition,
AST is cleared slowly by the reticuloendothelial system and may persist for 23 wk after
rhabdomyolysis.
Comparing serial activities of CK and AST provides information concerning the progression of
myonecrosis. Combined elevations in CK and AST
reflect relatively recent or active myonecrosis; persistently elevated serum CK indicates that myonecrosis is likely to be continuing. Elevated AST
activity accompanied by decreasing or normal CK
activity indicates that myonecrosis has ceased.
The degree of elevation of CK and AST does not
necessarily reflect the severity of clinical signs.
Serum LDH

LDH is a tetramer made up of combinations of the M

and H subunits with five isoenzyme forms found in
various organs within the body. Electrophoretic
separation suggests that the M4 (LDH5) and M3H
(LDH4) isoforms are found predominantly in skeletal muscle.6 Elevations in LDH may be detected in
horses with rhabdomyolysis, myocardial necrosis,
and/or hepatic necrosis. Therefore, concurrent
measurement of serum CK is necessary to establish
if rhabdomyolysis is present.
Myoglobin

Elevation in plasma/serum myoglobin concentrations indicates acute muscle damage. Myoglobin is

a low molecular-weight protein (17.8 kDa) that leaks
into plasma immediately after muscle damage and
is rapidly cleared in the urine by the kidney; 200 g
of muscle or more must be damaged before it is
detectable in the urine in human patients.9
Normal serum concentrations in resting horses have
been determined by nephelometry (range 0 9 g/l),
and measured concentrations from horses with rhabdomyolysis range from 10,000 to 800,000 g/l.4,10
Vitamin E and Selenium Concentrations

Whole-blood selenium concentrations or glutathione

peroxidase measured in EDTA or heparin tubes are
of value in assessing muscle disorder in animals
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MUSCLE DISORDERS

housed in areas deficient in selenium. Vitamin E

concentration can be measured in serum samples;
however, variability in serum levels can be quite
large, and pooling of several samples is often recommended to accurately assess a deficiency.
4.

Urinalysis

Urine can be obtained free catch from horses placed

in stalls with fresh bedding or through catheterization of mares without tranquilization. Urinalysis
is particularly important in horses with myoglobinuria, elevations in creatinine, or suspected electrolyte imbalances. Urine specific gravity, protein
content, white blood cell count, red blood cell count,
and evaluation of cast formation should be performed to assess the potential for concurrent renal
disease. A positive hemastix test (orthotoluidine)
in the absence of hemolysis or red blood cells in
urine is highly suggestive of myoglobinuria. Further differentiation of myoglobin from hemoglobin is
sometimes warranted, and where available, electrophoresis, nephlometry, or spectroscopy may be used.
Renal Fractional Excretion of Electrolytes

Determination of electrolyte, mineral, and creatinine concentrations in urine and blood may be useful to identify electrolyte balance in horses with
muscle cramping or exertional rhabdomyolysis.1113
Ideally, urine should be collected as a freely voided
sample at a standardized time of day before exercise
and feeding. Ion-specific electrodes commonly used
for analyses in small animals are useful in determining creatinine and chloride concentrations in
horses. They are of limited value for testing sodium concentrations, because the high urinary-potassium content of equine urine often interferes with
analysis for sodium. Use of flame photometry or
emission spectrophotometry can provide more accurate measurements of Na, K, Ca, Mg, and
P. Where Ca, P, and Mg are to be analyzed, samples should not be centrifuged before analysis but
acidified to dissolve urine crystals.11 Values below
the reported ranges are suggestive of conservation
and possibly inadequate dietary intake that may
require supplementation; however, wide variations
can occur between and within individual
horses.1114
Renal fractional excretions (FE) can be calculated
using the following formula (x measured electrolyte and Cr creatinine).
FE%X

Crplasma
Xurine
100

Crurine
Xplasma

Normal values for FE of electrolytes are dependant

on a horses diet. Normal values in acidified urine
for horses consuming grass hay and a sweet-feed
mix with available salt are FENa 0.04 0.08%,
FEK 35 80%, FECl 0.4 1.2%, FECa 5.3
14.5%, FEP 0.05 4.1%, and FEMg 14.221.4%.11
342

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5.

Exercise-Response Test

Diagnosing chronic exertional rhabdomyolysis may

be problematic in horses that do not have acute
clinical signs and have normal serum AST and CK
at rest. In such cases, an exercise challenge can be
helpful in detecting subclinical exertional rhabdomyolysis. In addition, quantifying the extent of
rhabdomyolysis during mild exercise is helpful in
deciding how rapidly to put a horse back into training. Blood samples should be taken before exercise
and 4 6 h after exercise to evaluate peak changes
in CK.4,5 Serum CK activity measured immediately post-exercise will not reflect the amount of
damage occurring during the exercise test.4 Small
fluctuations in serum CK activity may occur with
exercise because of enhanced muscle-membrane
permeability, particularly if exercise is prolonged or
strenuous and the horse is untrained.6,15,16 A submaximal exercise test is often valuable for detecting
rhabdomyolysis, because it provides more consistent
evidence of subclinical rhabdomyolysis than maximal exercise tests.4 Fifteen minutes of trotting is
often sufficient to produce subclinical muscle damage in horses prone to exertional myopathies.17
If signs of stiffness develop before this time, exercise
should be concluded. A normal response would be a
three- to four-fold increase from basal CK.
6.

Imaging

Thermography

Thermography may be useful for identification of

superficial abnormal temperature changes caused
by muscle damage, but it has limited value in deeper
injuries; there are many potentially confusing issues
such as recent removal of a rug or tack or grooming.
Careful comparisons of the left and right sides
should be made. Muscle inflammation is seen as a
hot spot in the skin directly overlying the affected
muscle. The most common sites of muscle strain
identified thermographically include the longissimus dorsi, the origin or body of the middle gluteal,
the insertion of the gluteals on the greater and third
trochanters of the femur, biceps femoris, semitendinosus, semimembranosus, and adductor.18
Nuclear Scintigraphy

Nuclear scintigraphy is particularly useful for identification of areas of deep muscle damage that had
not been suspected based on clinical examination.
Scintigraphy has been used most commonly in
horses with a history of poor performance, with or
without stiffness after exercise, to confirm a diagnosis of equine rhabdomyolysis.19 Technetium 99m
methylene diphosphonate (MDP) is taken up in
damaged muscle in the horse and is best seen in the
bone-phase images (i.e., 3 h after injection). The
mechanism of MDP binding is unknown, but the
release of large amounts of calcium from damaged
muscle or the exposure of calcium binding sites on
protein macromolecules in the damaged muscle may

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be responsible.20 The use of scintigraphy for the

diagnosis of other muscle injuries has not been documented in the horse, but it can be helpful in some
cases involving either proximal forelimb or hindlimb
muscles. Uptake of the radiopharmaceutical tends
to be much more focal and much less intense than in
cases of equine rhabdomyolysis.21
Ultrasonography

If there is physical disruption of the muscle, diagnostic ultrasonography is potentially very useful for
identification of muscle trauma and fibrosis. Careful comparisons must be made between similar sites
in contralateral limbs in both transverse and longitudinal images, because the typical striated echogenic pattern varies according to the muscle
group.22 The appearance of muscle is also sensitive
to the way the horse is standing and the tension on
the muscle, so it is important that the horse is standing squarely and bearing weight evenly. Muscle
fascia appears as well-defined relatively echo-dense
bands. Care must be taken in identifying large
vessels and artifacts created by them.
In an acute injury, muscle-fiber disruption is seen
as relatively hypoechoic areas within muscle with
loss of the normal muscle striation. The jagged
edge of the margin of the torn muscle may be increased in echogenicity. Tears in the muscle fascia
may be identified. The defect in muscle may be
filled by a loculated haematoma that is slowly replaced by hypoechoic granulation tissue. Muscle
repair shows a progressive increase in echogenicity.
Relatively hyperechoic regions may develop because
of fibrous scarring. Hyperechoic regions causing
shadowing artefacts reflect mineralization.
7.

Electromyography

A specific diagnosis of the cause of muscle atrophy,

muscle fasciculations, or myotonic dimpling after
tapping the muscle can be aided by performing electromyography (EMG).23,24 EMG of normal skeletal
muscle shows a brief burst of electrical activity when
the needle is inserted in muscle and then quiescence; this is not the case if motor units are recruited
(motor-unit action potentials) or the needle is very
close to a motor-end plate (miniature end-plate potentials). Normal muscle shows little spontaneous
electrical activity unless the muscle contracts or the
horse moves. Horses with abnormalities in the
electrical-conduction system of muscle or denervation of motor units show abnormal spontaneous electrical activity in the form of fibrillation potentials,
positive sharp waves, myotonic discharges, or complex repetitive discharges. Specific patterns of
waveforms may indicate specific disorders such as
denervation atrophy, hyperkalemic periodic paralysis (HYPP), or myotonia.2529
8.

Fig. 1. The open surgical-biopsy technique is used to remove a

tissue sample through a vertical incision that runs parallel to the
fibers of the semimembranosus muscle. The muscle sample is
grasped in one corner only to avoid crushing the tissue and
creating artifacts.

Muscle Biopsy

There have been many recent advances in obtaining

diagnostic information regarding specific muscle

disease by using the muscle-biopsy technique.30 34

Specialized laboratories are often most helpful in
processing frozen muscle biopsies and interpreting
muscle pathology to provide a specific diagnosis and
treatment.
To obtain the best diagnostic information, it is
important to select an appropriate muscle to biopsy.35 With exertional rhabdomyolysis, samples of
the semimembranosus muscle and gluteus medius
muscle are often examined because of their consistent involvement in exertional rhabdomyolysis and
the ease of collection with open- and needle-biopsy
techniques, respectively.32,34 An open-surgical biopsy of the semimembranosus muscle is usually obtained in veterinary practice because of the ease of
orienting a longitudinal biopsy and ease of treating
complications such as dehiscence. A site 8 cm
distal to the tuber ischii provides ample muscle tissue without leaving a readily evident scar should
dehiscence occur (Figs. 1 and 2). The biopsy is performed using sedation and local anesthesia directed
into the SC, but not muscle, tissue. After a vertical
incision in the skin and muscle fascia, two parallel
incisions 2 cm apart and 4 5 cm long are made in
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MUSCLE DISORDERS

Fig. 3. The muscle sample that is a 2-cm cube is placed on

saline-moistened gauze in a hard container on ice packs and
shipped to a specialized laboratory. Alternatively, samples for
formalin fixation are pinned longitudinally on a tongue depressor
or allowed to sit in air for 5 min before they are placed in 10%
buffered formalin.

Fig. 2. The biopsy incision is closed with two layers of absorbable sutures in the fascia and SC tissue. Staples can be used for
closure of the skin.

the muscle. The muscle is grasped in one dorsal

corner using forceps to avoid crushing other portions
of the biopsy (Fig. 1). A cross-secting incision is
made dorsally; the muscle sample is then excised in
a ventral direction to a depth of 12 cm, and the
sample is excised ventrally. Preparation of the
sample for shipment is described below. Good closure of fascia and SC tissue is the key to prevent
dehiscence. Staples or non-absorbable skin sutures are used to close the skin. Horses need to be
stall rested for 2 4 days after this biopsy procedure,
and sutures should be removed in 10 14 days.
Another technique that decreases recuperation
time uses a specialized 6-mm outer diameter percutaneous biopsy needle.a A 1-cm skin incision is
made through a bleb of local anesthetic, and the
needle is inserted into the gluteus muscle to a depth
of 6 cm. If necessary, repeated needle insertion is
performed to obtain enough muscle to form at least
a 1.5-cm2 sample. Samples obtained using the needle biopsies do not tolerate shipment on ice packs to
an outside laboratory as well as samples obtained by
surgical biopsy.
A few muscle disorders are amenable to evaluation using Trucut biopsy samples. This is best applied to diffuse disorders like immune-mediated
344

myopathies that affect muscles such as epaxial or

gluteal muscles that are difficult to sample using
open surgical techniques. Several Trucut biopsies
placed in formalin are required. Trucut samples
are not of value in assessing samples from horses
with exertional rhabdomyolysis or equine motorneuron disease, because they do not provide an adequate sample size to make a diagnosis.
Sample Preparation

Before obtaining a muscle biopsy, the laboratory

where samples will be evaluated should be contacted
to determine their preferred method of fixation.
Many laboratories specializing in neuromuscular
diseases prefer to obtain samples that are fresh
within 24 h of sampling, because frozen sections
provide better preservation and visualization of
muscle properties. On arrival in the laboratory,
these fresh samples are prepared for freezing in
isopentane suspended in liquid nitrogen. Preparation of samples for shipment includes wrapping the
muscle in gauze moistened with saline (damp but
not soaking wet) and placing it in a small plastic
container (Fig. 3). Samples are shipped overnight
on icepacks in a Styrofoam container. If placing
samples in formalin, either stretch the sample by
pinning it on a tongue depressor or allow the sample
to sit in open air for 25 min before fixing; this
minimizes contraction bands within fibers. Laboratories that use formalin fixation avoid the more
intensive preparation that is required for frozen
samples; however, formalin fixation has the disadvantage of creating a number of artifacts including
cracking, sedimentation, and leaching of glycogen
that make it less than ideal.

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Table 1.

Classification of Muscle Disorders

1. Non-exercise associated rhabdomyolysis

i. Inflammatory myopathies
Clostridial myositis
Influenza myositis
Sarcocystis myositis
Immune mediated myopathy
ii. Nutritional myopathy
Vitamin E and selenium deficiency
iii. Toxic myopathy
Ionophore toxicity
Pasture myopathies
Rayless golden rod/white snake root
Cassia occidentalis
Atypical myoglobinuria
iv. Traumatic myopathy
Compressive anesthetic myopathy
Trauma
v. Metabolic myopathy
Glycogen branching enzyme deficiency in Quarter
Horses
Polysaccharide storage myopathy
2. Exertional rhabdomyolysis
i. Focal muscle strain
ii. Sporadic tying-up (historically first episode, normal AST)
iii. Chronic tying-up
Dietary imbalances, vitamins, minerals, electrolytes
Polysaccharide storage myopathy
Recurrent exertional rhabdomyolysis
Idiopathic chronic exertional rhabdomyolysis
3. Exertional myopathy with normal CK
i. Mitochondrial myopathy
4. Muscle atrophy
i. Myogenic atrophy
Severe rhabdomyolysis
Disuse
Cushings disease
Immune-mediated myositis (rapid atrophy)
ii. Neurogenic atrophy
Equine protozoal myelitis
Local nerve trauma
Equine motor neuron disease
5. Muscle fasciculations
i. Pain, fear
ii. Electrolyte abnormalities
iii. Hyperkalemic periodic paralysis
iv. Otobius Megnini ear tick infestation
v. Myotonic dystrophy
vi. Stiff horse syndrome
vii. Shivers

Staining

A number of basic pathologic responses can be detected in hematoxylin and eosin (H&E), periodic aid
Schiffs (PAS), and amylase PAS stains of muscle
tissue. Further histochemical stains of frozen sections include acid and alkaline phosphatases for
necrosis and degeneration, myosin adenosine
triphosphatase stains for fiber typing, mitochondrial
stains, lipid stains, and immunohistochemical
stains. Although not routinely performed because
of expense, glutaraldehyde fixation of small muscle
samples can be of value for electron microscopy.

9.

MUSCLE DISORDERS

Genetic Testing

A DNA test36 is available to identify horses carrying

the mutation for HYPP found in the extended pedigree of Impressive descendants. Mane or tail
hairs with intact roots are submitted for analysis to
determine if horses are normal, heterozygous, or
homozygous for HYPP. Other genetic mutations in
other bloodlines that might cause HYPP are not
detected by this test. A DNA test3 is also available
to identify if horses are carriers of glycogen-branching enzyme deficiency (GBED) or if foals or aborted
feti are homozygous for this disorder. Testing is
performed on hair samples with intact roots or liver
samples.
Based on the information obtained by this type of
thorough evaluation, a diagnosis can usually be obtained. A classification system may be helpful in
narrowing down muscle diseases in horses, such as
GBED, immune-mediated myopathies, exertional
rhabdomyolysis, polysaccharide storage myopathy,
and shivers.
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a
Jrgen Kruuse A/S, Marslev Byvej 35, Marslev 5290, Denmark.

2006 Vol. 52 AAEP PROCEEDINGS

Proceedings of the Annual Convention of the AAEP - San Antonio, TX, 2006