Our concept of myasthenia gravis has evolved from: (1) its recognition as a clinical syndrome first enunciated by T. Willis in the 17th century1; (2) its more precise exposition by Erb in 1879 and by Goldflam in 18931 (whence the designation Erb-Goldflam disease); (3) an effective treatment by anticholinesterase agents introduced by Walker in 19342; (4) its pharmacodiagnosis by means of intramuscular neostigmine (Prostigmine), described by Viets and Schwab in 1935,3 improved later by the use of intravenous edrophonium chloride (Tensilon)4; (5) its curious association with thymic hyperplasia and sometimes with thymomas5,6; (6) a significantly frequent association of a myasthenic syndrome with dysthyroidism, bronchogenic carcinoma,7 and with some of the autoimmune diseases8; and (7) a characteristic fatigue pattern demonstrable by electromyography, which may be of diagnostic significance.9
The extraocular muscles and orbicularis oculi are the muscles most commonly affected. Approximately half
COGAN DG. Myasthenia Gravis: A Review of the Disease and a Description of Lid Twitch as a Characteristic Sign. Arch Ophthalmol. 1965;74(2):217–221. doi:10.1001/archopht.1965.00970040219016
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