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Myasthenia gravis
Introduction
- Very rare disease in cats.
- Cause: failure of normal neuromuscular transmission due to a reduction in the number of functional nicotinic acetylcholine receptor; can be congenital or acquired.
- Signs: episodic or permanent muscular weakness, regurgitation, cervical ventroflexion, dropped jaw.
- Diagnosis: signs, presumptive diagnosis by clinical signs and edrophonium chloride (Tensilon) challenge test, anti-acetylcholine receptor antibodies, response to treatment.
- Treatment: pyridostigmine bromide, immunosuppressive therapy.
- Prognosis: guarded.
Print off the owner factsheet Myasthenia gravis Myasthenia gravis to give to your client.
Presenting signs
- Muscle weakness (most obvious in appendicular muscles) that is worse by activity and might be relieved with rest.
- Gait abnormalities.
- Regurgitation.
- Cervical ventroflexion.
- Dropped jaw.
- Voice changes/dysphonia.
Age predisposition
- <6 months for congenital form.
- Bimodal distribution for the age of onset of clinical signs of acquired form with peaks occurring at 2-3 and 9-10 years of age.
Breed/Species predisposition
- Abyssinians Abyssinian.
- Somalis Somali.
Pathogenesis
Etiology
Acquired
- Paraneoplastic syndrome Feline cutaneous paraneoplastic syndromes, eg associated with thymoma.
- Immune-mediated (development of antibodies against acetylcholine receptors).
- Drug-induced with treatment of hypothyroidism Hypothyroidism with methimazole Methimazole.
Congenital
- Structural or functional abnormality of acetylcholine receptors.
Pathophysiology
- Reduction in the number of functional nicotinic acetylcholine receptor results in failure of neuromuscular transmission.
- Acquired: aberrant immune process → development of heterogenous group of autoantibodies (mostly immunoglobulin class G) produced against the nicotinic acetylcholine receptor (AChR) antibodies → binds to the alpha-subunit nicotinic acetylcholine receptors at the neuromuscular junction → decreased number of functional receptors by causing endocytosis of AChR, activating complement-mediated destruction of postsynaptic muscle cell membrane near AChR, decreasing synthesis and membrane incoporation of new AChR, and directly interfering with AChR function by bound antibody.
- Congenital: result of a single or combination of presynaptic (mutations in choline acetyltransferase gene), synaptic (mutation of the acetylcholine esterase collagen gene) or postsynaptic (mostly deficient synthesis of AChR) defect(s).
Timecourse
- Often progress over weeks to months.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Shelton G D, Ho M, Kass P H (2000) Risk factors for acquired myasthenia gravis in cats - 105 cases (1986-1998). JAVMA 216 (1), 55-57 PubMed.
- Ducoté J M, Dewey C W, Coates J R (1999) Clinical forms of acquired myasthenia gravis in cats. Comp Cont Educ Pract Vet 21 (5), 440-447 VetMedResource.
- Shelton G D (1999) Acquired myasthenia gravis - what we have learned from experimental and spontaneous animal models. Vet Immunol Immunopathol 69 (2-4), 239-249 PubMed.
- Scott-Montcrieff J C, Cook J R Jr., Lantz G C (1990) Acquired myasthenia gravis in a cat with thymoma. JAVMA 196 (8), 1291-3 PubMed.
- Cuddon P A (1989) Acquired immune-mediated myasthenia gravis in a cat. JSAP 30 (9), 511-516 VetMedResource.
- Joseph R J, Carrillo J M & Lennon V A (1988) Myasthenia gravis in the cat. JVIM 2 (2), 75-79 PubMed.
- Indrieri R J, Creighton S R, Lambert E H et al (1983) Myasthenia gravis in two cats. JAVMA 182 (1), 57-60 PubMed.
Other sources of information
- Shelton G D (2002) Myasthenia gravis and disorders of neuromuscular transmission. In: Vet Clin North Am Small Anim Pract Ed G D Shelton, Philadelphia: W B Saunders. pp 189-206 PubMed.