Myasthenia results from dysfunction of the neuromuscular synapse (ie, the neuromuscular junction [NMJ]), causing clinical “fatigue,” which is defined as muscle weakness that worsens with muscle use and improves with rest. Electrodiagnostic testing demonstrates either decremental compound muscle action potentials in response to repetitive nerve stimulation at slow rates, generally 2 to 3 Hz, or increased synaptic jitter measured by single fiber electromyography. The majority of the myasthenic disorders result from dysfunction of the postsynaptic component of the NMJ, although involvement of either the synaptic cleft or the presynaptic motor nerve terminal can occasionally produce myasthenia.
Richman DP. The Future of Research in Myasthenia. JAMA Neurol. 2015;72(7):812–814. doi:https://doi.org/10.1001/jamaneurol.2014.4740
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