Myasthenia gravis (MG) is an autoimmune
neuromuscular transmission disorder where well-defined
autoantibodies against muscle and muscle cell membrane molecules are directly pathogenetic. All MG patients should be defined for subtype, as such a subclassification has treatment consequences. Ocular MG, early-onset MG, late-onset MG, MG with
thymoma, MG with anti-muscle-specific
tyrosine kinase antibodies and MG with no defined
antibodies constitute the six MG categories. The MG diagnostic process includes neurophysiology, neuroimmunology, neuropharmacology and imaging. In addition to symptomatic
therapy with
acetylcholine esterase inhibitors, most patients need
thymectomy and/or immunosuppressive drugs. Today's treatment is not immunospecific and far from
antigen-specific, even if the pathogenesis is known in detail. Strategies for
acetylcholine receptor tolerance induction, manipulating
acetylcholine receptor antigen presentation or suppressing
acetylcholine receptor-specific B-cells or plasma cells work in experimental MG, but have not yet been attempted properly for the human disease, or they do not work. Apart from the 10-15% of patients with paraneoplastic MG, the cause of the disease is not known. Until curative or
antigen-specific
therapy become available, the well-established treatment gives good-to-excellent results in most patients, with acceptable quality of life and no increased mortality. Acute and
intensive care treatment during MG exacerbation is a cornerstone in the treatment.