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Neurology 1997;48(Suppl 5):S1-S7
This article is an overview of myasthenia gravis and a background for the other articles that follow in this issue. Other reviews have appeared since 1992. [1-7]
Pathogenesis.
Myasthenia gravis (MG) is probably the best understood autoimmune disorder. None other has captured the attention of so many generations of neurologists and neuroscientists. It is instructive for students of myasthenia gravis to appreciate the historical achievements in the order of their occurrence, and the many individuals who have contributed to the understanding of the disease.
The ancient history of MG is controversial. Possibly the first description of a patient with myasthenia gravis appeared in 1644 in correspondence from colonial Jamestown, Virginia, pertaining to Indian Chief Opechankanough. [8] In 1685, Sir Thomas Willis described a patient with bulbar symptoms that could have been psychogenic. [9] The clinical syndrome was identified by Wilks in 1877, [10] Erb in 1879, [11] and Goldflam in 1893. [12] In 1895, Jolly [13] named the disease "myasthenia gravis pseudoparalytica." By 1900, Campbell and Bramwell [14] had reported 60 cases. In 1934, the efficacy of physostigmine was shown by Walker. [15] One year later, Dale and colleagues [16] described the chemical nature of neuromuscular transmission at motor end-plates. Harvey and Masland [17] summarized the salient electrophysiologic features of MG in 1941. In the same year, Blalock, [18] and later Keynes, [19] described trans-sternal thymectomy in myasthenia gravis that included as complete a removal of the gland as possible, whether or not a tumor was suspected preoperatively.
In 1960, an autoimmune cause of MG was suggested by Simpson [20] and by Nastuk et al. [21] However, the immunologic basis of MG awaited basic understanding of acetylcholine (ACh) release at motor end-plates, as described by Katz and Miledi. [22] Nature provided two gifts that facilitated characterization of the …
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