Elevation of the intraocular pressure in humans causes a mydriasis. When the pressure exceeds the systolic ophthalmic artery pressure, an afferent pupillary defect develops due to the transient retinal ischemia. Iris sphincter function is clearly impaired with pressurization and can even be noted at intraocular pressures below the diastolic ophthalmic artery pressure. Further sphincter impairment occurs with higher intraocular pressures. The iris sphincter muscle itself, and not the neuromuscular junction, appears to be effected by the elevated pressure. The iris dilator function seems to be relatively resistant to the effects of increased intraocular pressure. These findings may be of clinical significance in cases of angle-closure glaucoma.
Rutkowski PC, Thompson HS. Mydriasis and Increased Intraocular Pressure: I. Pupillographic Studies. Arch Ophthalmol. 1972;87(1):21–24. doi:10.1001/archopht.1972.01000020023004
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