The laboratory diagnosis of mild myasthenia gravis
✍ Scribed by Dr John J. Kelly Jr; Jasper R. Daube; Vanda A. Lennon; Frank M. Howard Jr; Brian R. Younge
- Publisher
- John Wiley and Sons
- Year
- 1982
- Tongue
- English
- Weight
- 496 KB
- Volume
- 12
- Category
- Article
- ISSN
- 0364-5134
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
We report our experience with single‐fiber electromyogrphy (SF‐EMG), acetylcholine receptor antibody assays, and Lancaster Red‐Green tests of ocular motility with edrophonium chloride in the diagnosis of myasthenia gravis (MG). Over a period of almost 3 years, 43 patients in whom repetitive‐stimulation nerve conduction tests were nondiagnostic had SF‐EMG studies; 34 (79%) were positive. Examination of more proximal muscles yielded a higher likelihood of positive results. Anti‐acetylcholine receptor antibodies were detected in 25 (71%) of 35 patients whose sera were assayed, and Lancaster Red‐Green tests of ocular motility were positive in 13 (81%) of 16 patients studied. No single test was superior in diagnosing MG, but the three were complementary. If patients with mild MG are tested by all three methods, at least 95% should have laboratory confirmation of MG.
📜 SIMILAR VOLUMES
Myasthenia gravis (MG) and its animal model experimental autoimmune myasthenia gravis (EAMG) are caused by autoantibodies against nicotinic acetylcholine receptor (AChR) in skeletal muscle. The production of anti-AChR antibodies is mediated by cytokines produced by CD4+ and CD8+ T helper (Th) cells.
The annual scientific session of the Myasthenia Gravis Foundation of America (MGFA) was held on October 9, 1999 in Seattle, Washington. Dr. James F. Howard, Jr. organized the meeting which contained 17 international presentations that covered six topics: 1) autoantibodies in myasthenia gravis (MG);
## Abstract A 26‐year‐old woman was in spontaneous clinical remission from myasthenia gravis (MG) for six months, yet gave birth to a full‐term infant with typical neonatal MG. It is believed that transplacental transfer of anti‐acetylcholine (ACh) receptor antibodies is responsible for neonatal MG