Pupillary dysfunction in myasthenia gravis.

The constriction-dilation cycles of pupils exposed to a stationary, discrete slit-lamp beam were significantly prolonged in 25 myasthenic patients (1,060.4 +/- 45.8 msec) undergoing therapy with steroids, anticholinesterases, or both, compared to normal controls (801.9 +/- 8.6 msec) or subjects receiving steroids for nonneurological disease (860.9 +/- 14.9 msec). The duration of myasthenia correlated with the slowing of the cycle time. Myasthenia gravis may affect ectodermally derived smooth muscle or the autonomic neuromuscular junction or both, and not be restricted to the well-demonstrated alterations of neuromuscular junction in striated muscle of mesodermal origin. Alternatively, prolonged pupillary cycles could be attributed to dysfunction of central pathways of the pupillary light reflex.