Canine myasthenia gravis

Decreased acetylcholine receptor content of the neuromuscular junction underlies the muscular weakness seen in both acquired and congenital myasthenia gravis. Immune mediated mechanisms account for the acquired defect while decreased membrane insertion of receptor leads to the congenital disorder. The congenital form typically presents in the first few weeks of life with generalised episodic weakness as the predominant sign. Although treatment with cholinesterase inhibitors may help temporarily, the prognosis is poor. Acquired myasthenia gravis can occur between eight months and 13 years of age and may present as megaoesophagus alone or as exercise-related weakness in conjunction with megaoesophagus. Although treatment of the immune mediated form is often successful and spontaneous remissions also occur, aspiration pneumonia secondary to megaoesophagus remains a major cause of mortality in affected dogs. Resolution of megaoesophagus must therefore be a major goal for future treatment regimes. The remarkable similarity between canine and human acquired myasthenia gravis suggests that the canine thymus gland warrants greater attention pathologically and perhaps therapeutically considering the value of thymectomy in human patients.