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ANTIBIOTICS produce weakness by interfering with neuromuscular transmission. Apnea in experimental animals was observed first in 1941 with tyrothricin, the first antibiotic tested for clinical application.¹In 1956, the first case of prolonged apnea in man was reported after intraperitoneally infected neomycin sulfate.²Since 1956, a syndrome characterized by respiratory weakness, flaccid paralysis, and pupillary and visual changes has been recognized in association with a number of antibiotics.³⁻⁵⁰As defined, this "myasthenic syndrome" occurs in patients who do not have myasthenia gravis, although some myasthenics become weaker when given certain antibiotics.⁵¹Recent reviews of antibiotic toxicity do not emphasize this syndrome⁵²⁻⁵⁴Electromyographic (EMG) studies were mentioned in only four patients. In one, neuromuscular transmission and nerve conduction velocities were normal.⁴⁹A "currarelike"³⁰or nondepolarizing³⁴,⁵⁰effect occurred in the others. In one patient⁵⁰the block was not altered by edrophonium chloride. Profound
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McQuillen et al. (1968) studied this question.
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