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Pupillary dysfunction in myasthenia gravis
Author(s) -
Lepore Frederick E.,
Sanborn George E.,
Slevin John T.
Publication year - 1979
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410060107
Subject(s) - myasthenia gravis , ocular myasthenia , neuromuscular junction , reflex , medicine , constriction , pyridostigmine , neuromuscular transmission , pupillary light reflex , pupillary response , anesthesia , pupil , neuroscience , psychology
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.