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Exact incidence data are not available. The disorder occurs in 10% to 20% of children born to mothers with myasthenia gravis.

In some cases, the mother may be asymptomatic. Severity is generally not correlated with maternal disease but possibly with maternal antibody titers. Onset is usually within the first hours of life. Transient neonatal MG manifests as hypotonia, feeding difficulties, weak cry, facial diplegia and respiratory difficulties in affected neonates. With the gradual decrease in maternally-derived antibodies, the symptoms usually resolve. Subsequent births to the same mother are also at risk of this disorder. Risk factors for the condition are currently not clear. Rapid treatment usually enables resolution of the condition by 2 months of age.

The disorder is related to passive transplacental transfer of maternal anti-acetylcholine receptorantibodies (anti-AChR) or anti-muscle-specific tyrosine kinase antibodies (anti-MuSK) to the neonate. Circulating autoimmune antibodies are thought to damage the post-synaptic neuromuscular junction. The fetal onset form is related to antibodies directed against fetal AChR.