Adult-onset myasthenia gravis is an acquired autoimmune disorder of
neuromuscular transmission in which acetylcholine receptor
antibodies attack the postsynaptic membrane of the neuromuscular
junction. Although the cause of this disease is unknown, the role of
immune responses in its pathogenesis is well established.
Circulating acetylcholine receptor antibodies are present in 80% to
90% of patients with the generalized form of myasthenia gravis. Most
patients have ptosis, diplopia, dysarthria and dysphagia. The weakness
and fatigue worsen on exertion and improve with rest. Respiratory
muscle and limb weakness are rare at the onset of the disease.
For the past two decades, there has been considerable progress in
understanding the diagnosis and management of myasthenia gravis.
The diagnosis is based on clinical presentation, neurologic examination,
and confirmation by means of electrophysiologic testing and
immunologic studies. Myasthenia gravis mimics many neuromuscular
diseases and even illnesses such as depression and chronic fatigue
syndrome. One should always exclude drug-induced myasthenia gravis
for all patients.
With the introduction of new modalities of treatment, particularly
immunosuppressive or immunomodulating drugs, plasma exchange and
thymectomy, the morbidity and mortality of myasthenia gravis have
decreased dramatically to the point that myasthenia gravis should not
be considered as serious a disease as it once was. Although the several
therapeutic options are usually effective and have meant independence in
daily life to many patients with myasthenia gravis, well-designed,