Miosis from echothiophate in patients with total oculomotor nerve paralysis from intracranial abnormalities.
Seven subjects with intracranial pathologic abnormalities received bilateral instillations of echothiophate. Six had unilateral third (oculomotor) nerve paralysis; one had unilateral third nerve paresis. All 14 eyes became miotic. Miosis was greater in the defective eye in three subjects, greater in the normal eye in two subjects, and equal in two subjects. The neurons originating in the ciliary ganglion and terminating on the sphincter pupillae muscle may exhibit spontaneous activity. Echothiophate, by preventing acetylcholine hydrolysis, may have allowed this transmitter to accumulate and to produce miosis. The amount of maximal miosis in the abnormal eye after bilateral instillation of echothiophate drops may vary from that in the normal eye. The causes of this variation include denervation supersensitivity of the sphincter pupillae muscle, partial paresis of the dilator pupillae muscle, and increased drug penetration in the abnormal eye.[1]References
- Miosis from echothiophate in patients with total oculomotor nerve paralysis from intracranial abnormalities. Mindel, J.S. Am. J. Ophthalmol. (1981) [Pubmed]
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