feline-clinical forms of acquired myasthenia gravis in cats

8/14/2019 FELINE-Clinical Forms of Acquired Myasthenia Gravis in Cats

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20TH ANNIVERSARY Vol. 21, No. 5 May 1999

Refereed Peer Review

FOCAL POINT

KEY FACTS

5Similar to the condition in dogs,acquired myasthenia gravis (MG)

in cats is an immune-mediated

disease of the neuromuscular

junction that presents in threedifferent clinical forms.

Clinical Forms ofAcquired MyastheniaGravis in Cats

Texas A&M UniversityJulie M. Ducot, DVMCurtis 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.

Acquired myasthenia gravis (MG) is an immune-mediated disease of theneuromuscular junction that is well recognized in humans and dogs.15

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 normalneuromuscular transmission include accelerated endocytosis of ACh receptors,complement-mediated destruction of the muscle cell membrane in the vicinityof ACh receptors, decreased synthesis and membrane incorporation of new AChreceptors, and direct interference with ACh-receptor function by bound anti-body.1,6,7 Skeletal muscle weakness is a clinical manifestation of the decreasednumber 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 muscleweakness. 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 beenidentified 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 thescientific literature have been sporadic,912 and the clinical forms of acquired MG

CE

s 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.

s Signs of generalized MG may

include appendicular muscle

weakness, exercise intolerance

and weakness, ventroflexion of

the neck, a dropped jaw, and

focal muscle weakness.

s Cats with acute fulminating MG

present with a rapid onset of

severe appendicular muscle

weakness that is often associated

with respiratory distress.

s 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.


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in cats have not been inves-tigated. We studied the caserecords of 20 cats diagnosed

with acquired MG via posi-tive serum ACh-receptor an-

tibody concentrations. Thepurpose of the study was toretrospectively describe thesignalment, historical andclinical findings, method(s)of treatment, and outcomein the typical feline MG pa-tient and to determine wheth-er feline MG presents in sev-eral clinical forms as it doesin dogs and humans.

MATERIALS ANDMETHODSThe medical records of 20

cats (seen from 1992 to 1995)were obtained from fourveterinary teaching hospitalsand seven veterinary referralpractices in the UnitedStates. The inclusion criteri-on for the study was a serum

ACh-receptor antibody titerof greater than 0.30 nM/L.13,14

This value was based on mea-surement of the serum ACh-receptor antibody concen-trations of 50 normal cats;the range of these values plusthree standard deviations

was used as the referencerange for normal cats.a

Records were reviewed andthe following information

was recorded: signalment;duration of clinical signs;

historical and clinical find-ings; results of intravenousedrophonium chloride ad-ministration, repetitive nervestimulation, and serum ACh-receptor antibody concentra-tion; method(s) of treatment;and outcome. Abnormalgait and exercise intolerance were considered indicative

of appendicular muscle weak-ness. A positive response tointravenous edrophoniumchloride was considered to bean improvement in muscle

strength as evidenced by animproved gait after adminis-tration. Repetitive nerve stim-ulation was considered ab-normal when the compoundmuscle action potential de-creased by 10% or more.15

Megaesophagus was deter-mined by survey thoracic ra-diography. The presence offacial muscle weakness wasascertained by evidence of a

decreased menace responseand palpebral reflex. Catswith a history of dysphonia(voice change) were consid-ered to have laryngeal muscledysfunction. Difficulty inswallowing was consideredevidence of pharyngeal mus-cle weakness.

Based on historical andclinical findings, cats wereclassified into one of three

categories: (1) cats withoutappendicular muscle weak-ness, (2) cats with appendic-ular muscle weakness, and(3) cats with an acute onsetand rapid progression of se-vere generalized muscle weak-ness. Mean ACh-receptorantibody concentration foreach group of cats was calcu-lated. Statistical analysis con-sisted of a Kruskal-Wallis anal-

ysis of variance (ANOVA)for nonparametric data; a Pvalue of .05 or less was con-sidered significant.

RESULTSVarious breeds were repre-

sented in this study, includ-ing 12 domestic shorthair cats; 3 Abyssinians; and 1 eachof Somali, Siamese, Manx, Persian, and Himalayanbreeds. There were 13 neutered males, 4 spayed females,2 intact males, and 1 intact female. The animals ranged

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Figure 1Schematic of (A) a normal neuromuscular junctioncompared with (B) the neuromuscular junction of a patientaffected with myasthenia gravis. Note the decreased numberof acetylcholine (ACh) receptors and the abnormal junctionalfolds of the postsynaptic muscle cell membrane in B. (Cour-tesy of Anton G. Hoffman, DVM, PhD, Department of Vet-erinary Anatomy and Public Health, College of VeterinaryMedicine, Texas A&M University)

4

3

2

1

0

NumberofCats

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Age (years)

Figure 2A bimodal age distribution was seen in 20 cats af-fected with acquired myasthenia gravis.

aPersonal communication: Shelton GD, Comparative Neuro-muscular Laboratory, University of California San Diego, La

Jolla, CA, 1998.


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in age from 6 months to 15years (mean, 7.7 years; medi-an, 9 years). A bimodal agedistribution was noted, withthe majority being young

adult (2 to 3 years of age) ormiddle-aged (9 to 10 years ofage) cats (Figure 2). The du-ration of clinical signs beforepresentation ranged from 24hours to 8 months (mean,1.5 months).

Historical complaints andclinical findings are summa-rized in Tables I and II, re-spectively (Figure 3). Appen-dicular muscle weakness,

regurgitation or vomiting,decreased palpebral reflex,and decreased menace re-sponse were the most com-mon findings. Evidence ofappendicular muscle weak-ness was noted in 17 cats(85%), 3 of which wereseverely affected with acuteclinical signs that rapidlyprogressed to respiratorymuscle weakness and respi-

ratory distress. These 3 catsalso experienced regurgita-tion and dysphagia. Of theremaining 14 cats, 6 (30%)also had signs of regurgita-tion or dysphagia. Megaesophagus was confirmed ra-diographically in 8 cats (40%). Ventroflexion of the

neck was a presenting com-plaint in 4 cats (20%; Figure4). Three of 20 cats (15%)had no appendicular muscle

weakness and showed only

signs of esophageal or pha-ryngeal weakness. Aspira-tion pneumonia was foundin 4 cats with a history ofregurgitation. A cranial me-diastinal mass was seen onradiographs of 3 cats. Twocats underwent thoracoto-my, and histopathology re-vealed both masses to bethymoma. Cardiomegaly

was documented in 1 cat.

In addition to a serum ACh-receptor antibody con-centration, other diagnosticevaluation was performed in9 cats (45%). An intravenousedrophonium chloride chal-lenge test was performed in 8cats (40%) with appendicu-lar muscle weakness and wasconsidered positive in eachof them. Repetitive nervestimulation caused a decre-

mental response (20% to40%) in each of 4 cats tested(Figure 5); responses im-proved dramatically in 2 cats

when stimulation was repeat-ed after intravenous edrophonium chloride administra-tion. A muscle biopsy from 1 cat with appendicular

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TABLE I

Historical Complaints in 20 Cats withAcquired Myasthenia Gravis

Sign Number of Cats (%) Appendicular muscle weakness 17 (85)Vomiting/regurgitation 12 (60)Difficulty swallowing 7 (35)Coughing 6 (30)Ventroflexion of neck 4 (20)Dysphonia 4 (20)Nasal discharge 4 (20)Dropped jaw 3 (15)

Acute collapse 3 (15)Hypersalivation 2 (10)Labored breathing 1 (5)

TABLE II

Clinical Findings in 20 Cats withAcquired Myasthenia Gravis

Finding Number of Cats (%) Appendicular muscle weakness 17 (85)Decreased palpebral reflex 12 (60)Decreased menace response 10 (50)Megaesophagus 8 (40)

Aspiration pneumonia 4 (20)Cranial mediastinal mass 3 (15)Muscle fasciculations 3 (15)Decreased withdrawal reflexes 2 (10)Polymyositis 1 (5)Cardiomegaly 1 (5)Muscle atrophy 1 (5)

Figure 3A cat with a dropped jaw and hypersalivation,which may accompany other clinical signs of myastheniagravis.

Figure 4Cats affected with myasthenia gravis may displayappendicular muscle weakness and cervical ventroflexion.


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muscle weakness revealedmultifocal mononuclear cellinfiltrates; focal necrosis; fi-brosis; and angular cell atro-phy, especially of type II

fibers. The histopathologicdiagnosis was polymyositis.Cranial mediastinal masses

were identified in thoracicradiographs in 3 cats and

were confirmed as thymomain 2 of them.

Treatment commonly con-sisted of supportive care andpyridostigmine (0.10 to 0.25mg/kg/day). Fourteen cats

were also treated with im-

munosuppressive cortico-steroid therapy (prednisone[1 to 4 mg/kg/day] or dex-amethasone [0.25 to 2.0mg/kg/day]). Antibiotics

were administered if neces-sary for aspiration pneumo-nia. Cimetidine (3.0 to 7.5 mg/kg every 8 hours) andmetoclopramide (0.2 to 0.4 mg/kg every 8 hours) were

used in 4 cats with a historyof regurgitation or vomit-ing. One cat with appendic-ular muscle weakness wastreated with pyridostigmine

and corticosteroids and im-proved initially, relapsed 1year later, and improvedagain after cyclosporine ad-ministration (25 mg every12 hours).

Outcome at both 2 monthsafter diagnosis and at thetime of this study were re-corded for each cat. At 2months after diagnosis, 11of 20 cats (55%) had shown

some clinical improvement,6 (30%) were unchanged,and 3 (15%) had died. Twelvecats (60%) were eventuallylost to follow-up. Two of theremaining 5 cats were knownto be alive and doing well.

Three cats had died or were euthanatized at least 1 yearafter presentation for apparently unrelated causes


Figure 5Recording of the response to repetitive stimulationof the left tibial nerve in a cat with acquired myastheniagravis. A stimulus of 3 Hz was repeated 10 times. The com-pound muscle action potential decreases by 40%.

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is theorized that the thymoma cells express antigenicepitopes similar to those of nicotinic ACh receptors.The immune response to these epitopes results in thelack of functional ACh receptors in skeletal muscle. Al-though there may be an association between MG and

the presence of thymoma in cats,

1719

there does not ap-pear to be a resultant increase in the severity of MGwhen thymoma is found. Polymyositis was document-ed in 1 cat in this study. The presence of thymoma hasalso been associated with polymyositis in cats,20 al-though an association between polymyositis and MGhas not been documented.

A significantly higher mean ACh-receptor antibodyconcentration 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 severedisease. However, a linear relationship between ACh-re-ceptor antibody concentration and disease severity wasnot 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-mary means of treatingMG, immunosuppressivedrug therapy has becomean important component

of therapy in humans.

1,2125

Immunosuppressive drugshave also been shown to beassociated with a positiveoutcome in dogs.2628 Thelower mortality rate in thecats in this study suggests apotentially important rolefor immunosuppressivetherapy in cats. There havebeen reports of prednisoneadministration increasing

neuromuscular weaknessin dogs with acquired MG.6

However, this was not re-ported in any of the cats inthis study.

The 1-year mortalityrate of 15% is much lowerthan that reported for dogs

with acquired MG (60%),6

perhaps suggesting a betterprognosis for successfulmanagement of MG in

(chronic renal failure, gastrointestinal lymphosarcoma,and fibrosarcoma, respectively).

Serum ACh-receptor antibody concentrations in the20 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 withsevere and rapid onset of clinical signs. A Kruskal-Wal-lis ANOVA test for nonparametric data was performedto determine whether there was a significant differenceamong mean ACh-receptor antibody concentrations foreach group of cats. The mean concentration of the cats

with acute severe clinical signs was significantly higherthan that of the cats in the other two groups (P= .008).However, no significant difference was found betweenthe remaining two groups.

DISCUSSIONClinical signs manifested by the cats in this report

support the classification of feline acquired MG intothree formsfocal, 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 theappendicular and ocular muscles most profoundly.1 Asubstantial number of dogs with acquired MG do notshow generalized appendicular muscle weakness3,6;however, exercise-associated weakness and appendicular

muscle weakness were more common signs in cats. Inthis study, a smaller percentage of cats than that report-ed in dogs were found to have the focal form of MG.In a recent study,6 9 of 25 dogs (36%) had focal MGcompared with 3 of 20 of the cats (15%) in this study.Clinical signs were associated with esophageal and pha-ryngeal muscle weakness and, occasionally, laryngealmuscle weakness. The relatively lower percentage ofcats with focal MG could be related to the minimalamount of skeletal muscle in the feline esophagus ascompared with that in dogs.

There was an apparent overrepresentation of pure-

bred cats in this study (8 of 20 cats [40%]) as com-pared with the pet cat population in general, althoughthis was not statistically significant. Three of the 8purebred cats were Abyssinians, which may support thesuspicion of a breed predilection of Abyssinians to ac-quired MG.13A bimodal age distribution was found inthese cats that was similar to that described in dogs andhumans.1,3,6

Acquired MG was associated with a cranial mediasti-nal mass in 3 cats in this study. In humans, there isthought to be an association between the presence ofthymoma and the severity of clinical signs of MG. 1,16 It


P U R E B R E D C A T S s I M M U N O S U P P R E S S I V E D R U G S s M O R T A L I T Y R A T E

The most important advance in

the past 20 years in the study of

myasthenia gravis in dogs and

cats has been the development

of a readily available,

noninvasive, and reliable

diagnostic test for the disease.

The immunoprecipitation

radioimmunoassay quantitates

the circulating serum antibodies

directed against the

acetylcholine receptor. The assay

has been adapted for use in dogs

and cats.

A LookBack

COMP

ENDIUMS

20thANNIVERSARY

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M E G A E S O P H A G U S s R E C O G N I Z I N G S I G N S s P R O G N O S I S

REFERENCES1. Drachman DB: Myasthenia gravis. N Engl J Med330:

17971810, 1994.2. Amann JF: Congenital and acquired neuromuscular disease

of young dogs and cats. Vet Clin North Am Sm Anim Pract17(3): 617639, 1987.

3. Dewey CW: Acquired myasthenia gravis in dogs. Part I.Compend Contin Educ Pract Vet19(12):13401353, 1997.4. Shelton GD: Canine myasthenia gravis, in Kirk RW, Bona-

gura JD (eds): Current Veterinary Therapy XI. Philadelphia,WB Saunders Co, 1992, pp 10391042.

5. Shelton GD, Schule A, Kass PH: Risk factors for acquiredmyasthenia gravis in dogs: 1154 cases (19911995).JAVMA211(11):14281431, 1997.

6. Dewey CW, Bailey CS, Shelton GD, et al: Clinical forms ofacquired myasthenia gravis in dogs: 25 cases (19881995).JVet Intern Med11(2):5057, 1997.

7. Drachman DB, Adams RN, Josifek LF, et al: Functional ac-tivities of autoantibodies to acetylcholine receptors and theclinical severity of myasthenia gravis. N Engl J Med307(13):

769775, 1982.8. King LG, Vite CH: Acute fulminating myasthenia gravis infive dogs.JAVMA212(6):830834, 1998.

9. Mason KV: A case of myasthenia gravis in a cat.J Sm AnimPract17:467472, 1976.

10. Indrieri RJ, Creighton SR, Lambert EH, et al: Myastheniagravis in two cats.JAVMA182(1):5760, 1983.

11. Joseph RJ, Carrillo JM, Lennon VA: Myasthenia gravis inthe cat.J Vet Intern Med2:7579, 1988.

12. Cuddon PA: Acquired immune mediated myasthenia gravisin a cat.J Sm Anim Pract30:511516, 1989.

13. Shelton GD: Disorders of neuromuscular transmission.Semin Vet Med Surg4(2):126132, 1989.

14. Shelton GD, Cardinet GH, Lindstrom JM: Canine and hu-

man myasthenia gravis autoantibodies recognize similar re-gions on the acetylcholine receptor. Neurology 38:14171423, 1988.

15. Sims MH, McLean RA: Use of repetitive nerve stimulation toassess neuromuscular function in dogs: A test protocol for sus-pected myasthenia gravis. Prog Vet Neurol1(3):311319, 1990.

16. Hebra AH, Reed CE, Heldmann M, Black MJ: Myastheniagravis: A review with emphasis on the potential role ofthymectomy.J S Carolina Med AssocJuly:392395, 1990.

17. Malik R, Gabor L, Hunt GB, et al: Benign cranial mediasti-nal lesions in three cats.Aust Vet J75:183187, 1997.

18. Vos JH, Stolwijk J, Ramaekers FCS, et al: The use of keratinantisera in the characterization of a feline thymoma.J CompPathol102:7177, 1990.

19. Gores BR, Berg J, Carpenter JL, Aronsohn MG: Surgicaltreatment of thymoma in cats: 12 cases (19871992).JAVMA204(11):17821785, 1994.

20. Kornegay J: Lower motor neuron tetraparesis. Prob Vet Med3(3):384, 1991.

21. Johns TR: Long-term corticosteroid treatment of myasthe-nia gravis.Ann NY Acad Sci505:568583, 1987.

22. Cosi V, Lombardi M, Erbetta A, Piccolo G: Azathioprine asa single immunosuppressive drug in the treatment of myas-thenia gravis.Acta Neurol15:123131, 1993.

23. Matell G: Immunosuppressive drugs: Azathioprine in thetreatment of myasthenia gravis. Ann NY Acad Sci505:588594, 1987.

24. Sommer N, Sigg B, Melms A, et al: Ocular myasthenia


cats. The high mortality rate for this disease in dogs isthought to result from the high incidence of aspirationpneumonia related to megaesophagus.3,6 Megaesopha-gus was radiographically confirmed in a previous studyin 21 of 25 dogs (84%) with acquired MG. 6 In this

study, 8 cats (40%) had radiographically confirmedmegaesophagus, and an additional 4 cats exhibited clin-ical signs of regurgitation possibly associated withesophageal dysfunction. The lower incidence ofesophageal dysfunction in cats (12 of 20 [60%]) com-pared with dogs (84%)6 likely results from the smallerproportion of skeletal muscle in the feline esophagusand probably contributes to the lower mortality rate incats with acquired MG.

SUMMARYFeline acquired MG has historically been considered

an uncommon disease.11 It may be more common thanpreviously reported, however, because of the nonspecif-ic signs of weakness and lower incidence of megaesoph-agus as a clinical finding. It is important for cliniciansto recognize the historical and clinical signs of acquiredMG 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 diseaseare encountered. Cats with focal MG present with signsisolated 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 ofgeneralized MG in which cats present with an acuteonset and rapid progression of severe appendicularmuscle weakness, often associated with respiratorymuscle paresis or paralysis. This severe form of MG isassociated with a grave prognosis. Treatment of felineMG patients typically includes anticholinesterase andimmunosuppressive drug therapy. The prognosis forcats with acquired MG appears to be better than thatpreviously reported in dogs.

ACKNOWLEDGMENTS

The authors thank Margaret Slater for her help withstatistical analysis; Anton Hoffman for his illustrations;David Lipsitz, Anne Chauvet, Stacey Sullivan, JasonBerg, Allen Sisson, David Sweet, Anthony Basher,Timothy McAughan, John Meeks, Alan Potthoff,Mark Hitt, and Billy Thomas for their contributionsof case material; and the Comparative NeuromuscularLaboratory, University of California San Diego, La Jol-la, California, for assisting in locating cases for thisstudy.


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About the AuthorsDrs. Ducot, 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).

gravis: Response to long term immunosuppressive treatment.J Neurol Neurosurg Psych62:156162, 1997.

25. Niakan E, Harati Y, Rolak LA: Immunosuppressive drug ther-apy in myasthenia gravis.Arch Neurol43:155156, 1986.

26. Dewey CW, Coates JR, Ducot JM, et al: Azathioprine ther-apy for acquired myasthenia gravis in five dogs. JAAHA(inpress).

27. Van Heerden J, Van Schouwenburg SJ: The use of cortico-steroids in a dog with myasthenia gravis. J S Afr Vet Assoc54(2):135137, 1983.

28. Dewey CW: Acquired myasthenia gravis in dogs. Part II.Compend Contin Educ Pract Vet20(1):4757, 1998.


feline-clinical forms of acquired myasthenia gravis in cats

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