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Myasthenia gravis is an antibody-mediated disorder in which autoantibodies block the acetylcholine receptor at the neuromuscular junction[3] , reducing the muscle's response to nerve signals.
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Plate I · The proof
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Myasthenia gravis is an antibody-mediated disorder in which autoantibodies block the acetylcholine receptor at the neuromuscular junction[3] , reducing the muscle's response to nerve signals.
In the most common form of the disease, immunoglobulin G antibodies bind the acetylcholine receptor at the postsynaptic membrane, causing receptor loss and impaired neuromuscular transmission , which produces the characteristic fatigable weakness.
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Plate II · Source chat
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“What produces the fatigable weakness in myasthenia gravis?”
Autoantibodies bind the acetylcholine receptor at the postsynaptic membrane, reducing the number of functional receptors [Gilhus 2016, p. 214]. With fewer receptors, repeated nerve stimulation exhausts transmission, so the weakness worsens through the day and eases with rest [Vincent 2010, p. 1801].
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Plate IV · The roadmap
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Specimen · The output
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…the weakness characteristically worsens with sustained activity and improves after rest, a pattern that distinguishes it from most other neuromuscular disorders [3].
[3] Gilhus, N. E. (2016). Myasthenia gravis. New England Journal of Medicine, 375(26), 2570–2581.
Gilhus, Nils Erik. “Myasthenia Gravis.” New England Journal of Medicine, vol. 375, no. 26, 2016, pp. 2570–2581.
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