Extraocular muscle motor weakness is a disorder of extraocular muscle movement due to various factors, muscle weakness, commonly seen in botulism, pediatric myasthenia gravis, and progressive muscular dystrophy. There is a certain Qi and blood deficiency and vitamin deficiency causing the problem. There may also be some relationship with loss of sinews and bones, lack of sleep, and congenital defects. Myasthenia gravis (MG) causing extraocular muscle weakness is a chronic autoimmune disease that involves acetylcholine receptors in the postsynaptic membrane at the nerve-muscle junction, resulting in impaired transmission of excitation between nerves and muscles, and has a tendency to recur and remit. The lesion causing myasthenia gravis is located at the nerve-muscle junction of the transverse striatum, and the symptoms resemble the action of arrow toxin, which impedes the conduction of nerve impulses. Nerve-muscle conduction occurs when a nerve generates an impulse that releases acetylcholine, causing a potential difference in the endplate membrane, which is then conducted to the muscle causing its fibers to contract. In patients with myasthenia gravis, the nerve impulse is transmitted with insufficient release of acetylcholine, or cholinesterase activity is so excessive that acetylcholine is destroyed too rapidly, resulting in impaired nerve-muscle excitation transmission and the onset of the disease. Certain antibiotics have a blocking effect on nerve-muscle conduction in patients with myasthenia gravis.Hokkane reported 6 cases of myasthenia gravis patients, in which the disease was aggravated by the addition of streptomycin antibiotics (15min~2h) after the condition was stabilized by drug treatment. Such drugs are: streptomycin, dihydrostreptomycin, neomycin, polymyxin, kanamycin, baronomycin, viomycin, etc. Lillmann et al. state that assuming a 1000 nerve-muscle blocking effect of d-tubocurarine (an argyrophilic toxin), polymyxin B is 5, neomycin is 2.5, streptomycin is 0.7, dihydrostreptomycin is 0.6, and kanamycin is 0.5. whereas the dose of antibiotics applied clinically is more than 100 times higher than that of argyrophilic toxins. Therefore, in patients with myasthenia gravis, the neuromuscular conduction is already blocked or relies on drugs to maintain the balance, in which case, once the above antibiotics are applied, it will certainly aggravate this blocking effect and further deteriorate the condition. Regarding the blocking effect of certain antibiotics on neuromuscular conduction, it is still unclear, and it is thought that streptomycin, like argyrophilic toxin, can reduce the sensitivity of the endplate to acetylcholine, and it is also thought that it can reduce the release of transmitter (transmitter).