Although the neuromuscular disorder known as myasthenia gravis was first described in the seventeenth century,1 it was not until two centuries later that Erb2 and Goldflam3 firmly established the clinical features of this disease. During the next half century, references in the literature dealt mainly with the clinical and pathological aspects of the disease, and this information is well summarized by Keschner and Strauss.4 Relatively little progress was made in our understanding of the pathogenesis of myasthenia gravis until the advent of the theory of chemical mediation of nerve impulses at synaptic junctions. With the recognition of the importance of acetylcholine in the transmission of the nerve impulse at the motor end plate in striated muscles, there rapidly developed intense interest in both physiologic and pathophysiologic aspects of this mechanism. This interest has been maintained and has led to many significant advances in our knowledge with
SCHLEZINGER NS, FAIRFAX WA. Evaluation of Ocular Signs and Symptoms in Myasthenia Gravis. AMA Arch Ophthalmol. 1959;62(6):985–990. doi:10.1001/archopht.1959.04220060057010
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