W. KING ENGEL, M.D.; BARRY W. FESTOFF, M.D.; BERNARD M. PATTEN, M.D.; MICHAEL L. SWERDLOW, M.D.; HAROLD H. NEWBALL, M.D.; MARY D. THOMPSON, R.N.
In myasthenia gravis, fatigability and persistent, often fatal weakness of voluntary muscles are attributable to dysfunction at the neuromuscular junction. The overall dysimmune state of the patient probably causes the junctional defect. Seventy percent of patients have thymic hyperplasia and 10%, thymoma. The atrophy of muscle fibers usually looks like denervation atrophy, and there are morphologic abnormalities of motor axon endings and the postsynaptic region of the muscle fiber. Electromyographic studies detect the neuromuscular junction defects: fatigue on repetitive stimulation and post-tetanic exhaustion. "Open-biopsy EMG" confirms that the commonly found electromyographic pattern comes from regions showing only denervation-like atrophy of muscle fibers. Other diagnostic tests include benefit from anticholinesterases and worsening by d-tubocurarine; the worsening of weakness by lactate infusion might serve as a diagnostic test. Treatment includes anticholinesterases, thymectomy, and the recently introduced long-term, high single dose, alternate-day prednisone program. Experienced 24-hour nursing surveillance is essential to treatment of the severely myasthenic patient.
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ENGEL WK, FESTOFF BW, PATTEN BM, SWERDLOW ML, NEWBALL HH, THOMPSON MD. Myasthenia Gravis. Ann Intern Med. 1974;81:225–246. doi: 10.7326/0003-4819-81-2-225
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Published: Ann Intern Med. 1974;81(2):225-246.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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