20TH ANNIVERSARY
5 May 1999
CE Refereed Peer Review
FOCAL POINT
★Similar to the condition in dogs,
acquired myasthenia gravis (MG)
in cats is an immune-mediated
disease of the neuromuscular
junction that presents in three
different clinical forms.
KEY FACTS
■ Cats with focal MG display
weakness of esophageal, facial,
pharyngeal, or laryngeal muscles;
common signs include difficulty
in swallowing, hypersalivation,
regurgitation, inability to blink,
and dysphonia.
■ Signs of generalized MG may
include appendicular muscle
weakness, exercise intolerance
and weakness, ventroflexion of
the neck, a dropped jaw, and
focal muscle weakness.
■ Cats with acute fulminating MG
present with a rapid onset of
severe appendicular muscle
weakness that is often associated
with respiratory distress.
■ The prognosis for MG in cats
may be better than that in dogs,
probably because of the lower
incidence of megaesophagus and
aspiration pneumonia in cats.
Vol. 21, No.
Clinical Forms of
Acquired Myasthenia
Gravis in Cats
Texas A&M University
Julie M. Ducoté, DVM
Curtis W. Dewey, DVM, MS
Joan R. Coates, DVM, MS
ABSTRACT: Although much is known about acquired myasthenia gravis (MG) in dogs, rela-
tively little is known about the disease in cats. In an attempt to determine the signalment, clini-
cal findings, treatment, and outcome, we retrospectively studied the case records of 20 cats
diagnosed with acquired MG. Results of this study indicate that cats display several clinical
forms of acquired MG that are similar to those of dogs.
A
cquired myasthenia gravis (MG) is an immune-mediated disease of the
neuromuscular junction that is well recognized in humans and dogs.1–5
Primarily IgG autoantibodies are formed against nicotinic acetylcholine
(ACh) receptors on the postsynaptic membrane of skeletal muscles (Figure 1).
Several proposed mechanisms by which these antibodies interfere with normal
neuromuscular transmission include accelerated endocytosis of ACh receptors,
complement-mediated destruction of the muscle cell membrane in the vicinity
of ACh receptors, decreased synthesis and membrane incorporation of new ACh
receptors, and direct interference with ACh-receptor function by bound anti-
body.1,6,7 Skeletal muscle weakness is a clinical manifestation of the decreased
number of functional ACh receptors and the depletion of ACh stores.1
Several clinical forms of MG have been described in humans and dogs.1,3,6 Dogs
with focal MG exhibit localized weakness of esophageal, pharyngeal, laryngeal,
and/or facial muscle groups and have no clinical evidence of appendicular muscle
weakness. Dogs with generalized MG have evidence of appendicular muscle weak-
ness and may also display weakness of other skeletal muscles (e.g., megaesophagus).
Acute fulminating MG, a subtype of generalized MG in humans, has also been
identified in dogs.3,6 These patients present with a rapid onset and progression of se-
vere appendicular muscle weakness. Respiratory distress, which is common in pa-
tients with acute fulminating MG, is caused by intercostal and diaphragmatic mus-
cle weakness, often with concurrent aspiration pneumonia. Mortality data for dogs
with acute fulminating MG suggest a poor to grave prognosis.6,8
Acquired MG in cats is considered a rare disease. Reports of feline MG in the
scientific literature have been sporadic,9–12 and the clinical forms of acquired MG
Compendium May 1999 20TH ANNIVERSARY Small Animal/Exotics

in cats have not been inves- of appendicular muscle weak-

tigated. We studied the case ness. A positive response to
records of 20 cats diagnosed intravenous edrophonium
with acquired MG via posi- chloride was considered to be
tive serum ACh-receptor an- an improvement in muscle
tibody concentrations. The strength as evidenced by an
purpose of the study was to improved gait after adminis-
retrospectively describe the tration. Repetitive nerve stim-
signalment, historical and ulation was considered ab-
clinical findings, method(s) normal when the compound
of treatment, and outcome muscle action potential de-
in the typical feline MG pa- creased by 10% or more.15
tient and to determine wheth- Megaesophagus was deter-
er feline MG presents in sev- mined by survey thoracic ra-
eral clinical forms as it does diography. The presence of
in dogs and humans. facial muscle weakness was
ascertained by evidence of a
MATERIALS AND decreased menace response
METHODS and palpebral reflex. Cats
The medical records of 20 with a history of dysphonia
cats (seen from 1992 to 1995) (voice change) were consid-
were obtained from four ered to have laryngeal muscle
veterinary teaching hospitals dysfunction. Difficulty in
and seven veterinary referral swallowing was considered
practices in the United evidence of pharyngeal mus-
States. The inclusion criteri- Figure 1—Schematic of (A) a normal neuromuscular junction cle weakness.
on for the study was a serum compared with (B) the neuromuscular junction of a patient Based on historical and
ACh-receptor antibody titer affected with myasthenia gravis. Note the decreased number clinical findings, cats were
of greater than 0.30 nM/L.13,14 of acetylcholine (ACh) receptors and the abnormal junctional classified into one of three
This value was based on mea- folds of the postsynaptic muscle cell membrane in B. (Cour- categories: (1) cats without
surement of the serum ACh- tesy of Anton G. Hoffman, DVM, PhD, Department of Vet- appendicular muscle weak-
erinary Anatomy and Public Health, College of Veterinary
receptor antibody concen- Medicine, Texas A&M University) ness, (2) cats with appendic-
trations of 50 normal cats; ular muscle weakness, and
the range of these values plus (3) cats with an acute onset
three standard deviations 4 and rapid progression of se-
was used as the reference vere generalized muscle weak-
range for normal cats.a 3 ness. Mean ACh-receptor
Number of Cats

Records were reviewed and antibody concentration for

the following information 2 each group of cats was calcu-
was recorded: signalment; lated. Statistical analysis con-
1
duration of clinical signs; sisted of a Kruskal-Wallis anal-
historical and clinical find- ysis of variance (ANOVA)
0
ings; results of intravenous 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
for nonparametric data; a P
edrophonium chloride ad- value of .05 or less was con-
Age (years)
ministration, repetitive nerve sidered significant.
stimulation, and serum ACh-
receptor antibody concentra- Figure 2—A bimodal age distribution was seen in 20 cats af- RESULTS
fected with acquired myasthenia gravis.
tion; method(s) of treatment; Various breeds were repre-
and outcome. Abnormal sented in this study, includ-
gait and exercise intolerance were considered indicative ing 12 domestic shorthair cats; 3 Abyssinians; and 1 each
a
Personal communication: Shelton GD, Comparative Neuro- of Somali, Siamese, Manx, Persian, and Himalayan
muscular Laboratory, University of California San Diego, La breeds. There were 13 neutered males, 4 spayed females,
Jolla, CA, 1998. 2 intact males, and 1 intact female. The animals ranged

SERUM ACh-RECEPTOR ANTIBODY CONCENTRATION ■ HISTORICAL AND CLINICAL FINDINGS

Small Animal/Exotics 20TH ANNIVERSARY Compendium May 1999

in age from 6 months to 15 neck was a presenting com-

years (mean, 7.7 years; medi- plaint in 4 cats (20%; Figure
an, 9 years). A bimodal age 4). Three of 20 cats (15%)
distribution was noted, with had no appendicular muscle
the majority being young weakness and showed only
adult (2 to 3 years of age) or signs of esophageal or pha-
middle-aged (9 to 10 years of ryngeal weakness. Aspira-
age) cats (Figure 2). The du- tion pneumonia was found
ration of clinical signs before in 4 cats with a history of
presentation ranged from 24 regurgitation. A cranial me-
hours to 8 months (mean, diastinal mass was seen on
1.5 months). radiographs of 3 cats. Two
Historical complaints and cats underwent thoracoto-
clinical findings are summa- Figure 3—A cat with a dropped jaw and hypersalivation, my, and histopathology re-
rized in Tables I and II, re- which may accompany other clinical signs of myasthenia vealed both masses to be
spectively (Figure 3). Appen- gravis. thymoma. Cardiomegaly
dicular muscle weakness, was documented in 1 cat.
regurgitation or vomiting, In addition to a serum
decreased palpebral reflex, ACh-receptor antibody con-
and decreased menace re- centration, other diagnostic
sponse were the most com- evaluation was performed in
mon findings. Evidence of 9 cats (45%). An intravenous
appendicular muscle weak- edrophonium chloride chal-
ness was noted in 17 cats lenge test was performed in 8
(85%), 3 of which were cats (40%) with appendicu-
severely affected with acute lar muscle weakness and was
clinical signs that rapidly considered positive in each
progressed to respiratory of them. Repetitive nerve
muscle weakness and respi- stimulation caused a decre-
ratory distress. These 3 cats mental response (20% to
also experienced regurgita- Figure 4—Cats affected with myasthenia gravis may display 40%) in each of 4 cats tested
tion and dysphagia. Of the appendicular muscle weakness and cervical ventroflexion. (Figure 5); responses im-
remaining 14 cats, 6 (30%) proved dramatically in 2 cats
also had signs of regurgita- when stimulation was repeat-
tion or dysphagia. Megaesophagus was confirmed ra- ed after intravenous edrophonium chloride administra-
diographically in 8 cats (40%). Ventroflexion of the tion. A muscle biopsy from 1 cat with appendicular

TABLE I TABLE II
Historical Complaints in 20 Cats with Clinical Findings in 20 Cats with
Acquired Myasthenia Gravis Acquired Myasthenia Gravis
Sign Number of Cats (%) Finding Number of Cats (%)
Appendicular muscle weakness 17 (85) Appendicular muscle weakness 17 (85)
Vomiting/regurgitation 12 (60) Decreased palpebral reflex 12 (60)
Difficulty swallowing 7 (35) Decreased menace response 10 (50)
Coughing 6 (30) Megaesophagus 8 (40)
Ventroflexion of neck 4 (20) Aspiration pneumonia 4 (20)
Dysphonia 4 (20) Cranial mediastinal mass 3 (15)
Nasal discharge 4 (20) Muscle fasciculations 3 (15)
Dropped jaw 3 (15) Decreased withdrawal reflexes 2 (10)
Acute collapse 3 (15) Polymyositis 1 (5)
Hypersalivation 2 (10) Cardiomegaly 1 (5)
Labored breathing 1 (5) Muscle atrophy 1 (5)

INTRAVENOUS EDROPHONIUM CHLORIDE CHALLENGE TEST ■ REPETITIVE NERVE STIMULATION

Compendium May 1999 20TH ANNIVERSARY Small Animal/Exotics

muscle weakness revealed used in 4 cats with a history

multifocal mononuclear cell of regurgitation or vomit-
infiltrates; focal necrosis; fi- ing. One cat with appendic-
brosis; and angular cell atro- ular muscle weakness was
phy, especially of type II treated with pyridostigmine
fibers. The histopathologic and corticosteroids and im-
diagnosis was polymyositis. proved initially, relapsed 1
Cranial mediastinal masses year later, and improved
were identified in thoracic again after cyclosporine ad-
radiographs in 3 cats and ministration (25 mg every
were confirmed as thymoma 12 hours).
in 2 of them. Outcome at both 2 months
Treatment commonly con- after diagnosis and at the
sisted of supportive care and time of this study were re-
pyridostigmine (0.10 to 0.25 corded for each cat. At 2
mg/kg/day). Fourteen cats months after diagnosis, 11
were also treated with im- of 20 cats (55%) had shown
munosuppressive cortico- some clinical improvement,
steroid therapy (prednisone 6 (30%) were unchanged,
Figure 5—Recording of the response to repetitive stimulation
[1 to 4 mg/kg/day] or dex- of the left tibial nerve in a cat with acquired myasthenia and 3 (15%) had died. Twelve
amethasone [0.25 to 2.0 gravis. A stimulus of 3 Hz was repeated 10 times. The com- cats (60%) were eventually
mg/kg/day]). Antibiotics pound muscle action potential decreases by 40%. lost to follow-up. Two of the
were administered if neces- remaining 5 cats were known
sary for aspiration pneumo- to be alive and doing well.
nia. Cimetidine (3.0 to 7.5 mg/kg every 8 hours) and Three cats had died or were euthanatized at least 1 year
metoclopramide (0.2 to 0.4 mg/kg every 8 hours) were after presentation for apparently unrelated causes

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Small Animal/Exotics 20TH ANNIVERSARY Compendium May 1999

(chronic renal failure, gastrointestinal lymphosarcoma,
and fibrosarcoma, respectively).
Serum ACh-receptor antibody concentrations in the
20 cats ranged from 0.31 to 15.5 nM/L (mean and me-
dian, 5.4 nM/L). The mean ACh-receptor antibody
concentration was 4.3 nM/L for cats without appendic-
ular muscle weakness, 10.0 nM/L for cats with appen-
dicular muscle weakness, and 19.0 nM/L for cats with
severe and rapid onset of clinical signs. A Kruskal-Wal-
lis ANOVA test for nonparametric data was performed
to determine whether there was a significant difference
among mean ACh-receptor antibody concentrations for
each group of cats. The mean concentration of the cats
with acute severe clinical signs was significantly higher
than that of the cats in the other two groups (P = .008).
However, no significant difference was found between
the remaining two groups.
DISCUSSION
Clinical signs manifested by the cats in this report
support the classification of feline acquired MG into
three forms—focal, generalized, and acute fulminating.
These findings parallel those in dogs6 and humans.1,7
The classic human myasthenic patient suffers from ex-
ercise-related skeletal muscle weakness that affects the
appendicular and ocular muscles most profoundly.1 A
is theorized that the thymoma cells express antigenic
epitopes similar to those of nicotinic ACh receptors.
The immune response to these epitopes results in the
lack of functional ACh receptors in skeletal muscle. Al-
though there may be an association between MG and
the presence of thymoma in cats,17–19 there does not ap-
pear to be a resultant increase in the severity of MG
when thymoma is found. Polymyositis was document-
ed in 1 cat in this study. The presence of thymoma has
also been associated with polymyositis in cats,20 al-
though an association between polymyositis and MG
has not been documented.
A significantly higher mean ACh-receptor antibody
concentration was observed in cats with acute fulminat-
ing MG than was found in either the focal or general-
ized group. Based on this finding, it is tempting to as-
sume that cats with higher titers will have more severe
disease and cats with lower titers will have less severe
disease. However, a linear relationship between ACh-re-
ceptor antibody concentration and disease severity was
not found between focal and generalized MG in cats.
Most cats in this study received both anticholin-
esterase and immunosuppressive corticosteroid therapy.
Although anticholinest-
erase drugs remain the pri-
ENDIU
mary means of treating MP

M’
20th

CO
substantial number of dogs with acquired MG do not MG, immunosuppressive

S

9 9 9
9 - 1

show generalized appendicular muscle weakness 3,6; drug therapy has become 1 9 7

ANNIVERSARY
however, exercise-associated weakness and appendicular an important component
muscle weakness were more common signs in cats. In of therapy in humans.1,21–25
this study, a smaller percentage of cats than that report- Immunosuppressive drugs A LookBack
ed in dogs were found to have the focal form of MG. have also been shown to be
In a recent study,6 9 of 25 dogs (36%) had focal MG associated with a positive The most important advance in
26–28 the past 20 years in the study of
compared with 3 of 20 of the cats (15%) in this study. outcome in dogs. The
Clinical signs were associated with esophageal and pha- lower mortality rate in the myasthenia gravis in dogs and
ryngeal muscle weakness and, occasionally, laryngeal cats in this study suggests a cats has been the development
muscle weakness. The relatively lower percentage of potentially important role of a readily available,
cats with focal MG could be related to the minimal for immunosuppressive noninvasive, and reliable
amount of skeletal muscle in the feline esophagus as therapy in cats. There have
diagnostic test for the disease.
compared with that in dogs. been reports of prednisone
There was an apparent overrepresentation of pure- administration increasing The immunoprecipitation
bred cats in this study (8 of 20 cats [40%]) as com- neuromuscular weakness radioimmunoassay quantitates
6 the circulating serum antibodies
pared with the pet cat population in general, although in dogs with acquired MG.
this was not statistically significant. Three of the 8 However, this was not re- directed against the
purebred cats were Abyssinians, which may support the ported in any of the cats in acetylcholine receptor. The assay
suspicion of a breed predilection of Abyssinians to ac- this study. has been adapted for use in dogs
quired MG.13 A bimodal age distribution was found in The 1-year mortality and cats.
these cats that was similar to that described in dogs and rate of 15% is much lower
humans.1,3,6 than that reported for dogs
Acquired MG was associated with a cranial mediasti- with acquired MG (60%),6
nal mass in 3 cats in this study. In humans, there is perhaps suggesting a better
thought to be an association between the presence of prognosis for successful
thymoma and the severity of clinical signs of MG.1,16 It management of MG in

PUREBRED CATS ■ IMMUNOSUPPRESSIVE DRUGS ■ MORTALITY RATE

Compendium May 1999 20TH ANNIVERSARY
cats. The high mortality rate for this disease in dogs is
thought to result from the high incidence of aspiration
pneumonia related to megaesophagus.3,6 Megaesopha-
gus was radiographically confirmed in a previous study
in 21 of 25 dogs (84%) with acquired MG.6 In this
study, 8 cats (40%) had radiographically confirmed
megaesophagus, and an additional 4 cats exhibited clin-
ical signs of regurgitation possibly associated with
esophageal dysfunction. The lower incidence of
esophageal dysfunction in cats (12 of 20 [60%]) com-
pared with dogs (84%)6 likely results from the smaller
proportion of skeletal muscle in the feline esophagus
and probably contributes to the lower mortality rate in
cats with acquired MG.
SUMMARY
Feline acquired MG has historically been considered
an uncommon disease.11 It may be more common than
previously reported, however, because of the nonspecif-
ic signs of weakness and lower incidence of megaesoph-
agus as a clinical finding. It is important for clinicians
to recognize the historical and clinical signs of acquired
MG in cats and to maintain a high index of suspicion
when evaluating a cat with the primary complaint of
weakness. Three distinct clinical forms of the disease
are encountered. Cats with focal MG present with signs
isolated to the esophageal, pharyngeal, laryngeal, or fa-
cial muscles. Generalized MG is characterized by ap-
pendicular muscle weakness, with or without
esophageal, pharyngeal, laryngeal, or facial muscle dys-
function. Acute fulminating MG is a severe form of
generalized MG in which cats present with an acute
onset and rapid progression of severe appendicular
muscle weakness, often associated with respiratory
muscle paresis or paralysis. This severe form of MG is
associated with a grave prognosis. Treatment of feline
MG patients typically includes anticholinesterase and
immunosuppressive drug therapy. The prognosis for
cats with acquired MG appears to be better than that
previously reported in dogs.
ACKNOWLEDGMENTS
The authors thank Margaret Slater for her help with
statistical analysis; Anton Hoffman for his illustrations;
David Lipsitz, Anne Chauvet, Stacey Sullivan, Jason
Berg, Allen Sisson, David Sweet, Anthony Basher,
Timothy McAughan, John Meeks, Alan Potthoff,
Mark Hitt, and Billy Thomas for their contributions
of case material; and the Comparative Neuromuscular
Laboratory, University of California San Diego, La Jol-
la, California, for assisting in locating cases for this
study.
MEGAESOPHAGUS ■ RECOGNIZING SIGNS ■ PROGNOSIS
Small Animal/Exotics
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Compendium May 1999
About the Authors
Drs. Ducoté, Dewey, and Coates are affiliated with the
Department of Small Animal Medicine and Surgery, Col-
lege of Veterinary Medicine, Texas A&M University, Col-
lege Station, Texas. Dr. Dewey is a Diplomate of the
American College of Veterinary Internal Medicine (Neurol-
ogy) and the American College of Veterinary Surgeons,
and Dr. Coates is a Diplomate of the American College of
Veterinary Internal Medicine (Neurology).