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Ocular Myasthenia Gravis TreatmentThe Case Against Prednisone Therapy and Thymectomy
Molly E. Gilbert, MD;
Eduardo A. De Sousa, MD;
Peter J. Savino, MD
Arch Neurol. 2007;64(12):1790-1792.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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Myasthenia gravis (MG) is an autoimmune disorder that affects the postsynaptic neuromuscular junction membrane. Acetylcholine receptor (AChR) antibodies are frequently present, and the number of functioning postsynaptic receptors is reduced. Muscle-specific kinase antibodies may be identified in individuals with and without AChR antibodies.1 Ptosis or diplopia due to ocular muscle involvement are frequently the first symptoms of the disease.2 Approximately half of the patients are first seen with purely ocular MG (OMG); of these, 53% develop generalized MG (GMG) within 2 years (> 80% in the first year). Furthermore, a spontaneous remission rate of 30% has been reported in patients with OMG during a 15-year period.3 Both AChR and muscle-specific kinase antibodies may be present in OMG.4
The goal of therapy for OMG and GMG is to minimize the patient's symptoms. Another recently discussed goal is to prevent . . . [Full Text of this Article] AUTHOR INFORMATION
Author Affiliations: Neuro-ophthalmology Service, Wills Eye Institute (Drs Gilbert and Savino), and Department of Neurology, Thomas Jefferson University (Dr De Sousa), Philadelphia, Pennsylvania. Dr Gilbert is now with the Department of Neuro-Ophthalmology, Illinois Eye and Ear Infirmary, Chicago.
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