Myasthenia gravis precipitated by trauma: latent myasthenia and the concept of 'threshold'.

Myasthenia gravis is caused by antibodies to post-synaptic neuromuscular junction proteins, most commonly nicotinic acetylcholine receptors. Evidence indicates that acetylcholine receptor antibodies must be present in the circulation prior to the development of clinical or neurophysiological manifestations of myasthenia. We describe the onset of seropositive myasthenia within minutes of minor trauma to the chest and neck in a previously asymptomatic 68-year-old man, followed by protracted disease with persistent antibodies. Such rapid evolution of myasthenia following an identifiable stimulus has not been reported previously and suggests a humoral mechanism. We speculate that the remote effects of autoinflammation secondary to tissue microtrauma led to a sudden increase in muscle permeability and greater exposure of receptors to antibody, with resulting acute impairment of neuromuscular transmission. We also suggest that the trauma might have resulted in increased antibody production by remnant thymic tissue, leading to chronic isease.