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Instillation of 0.25% physostigmine sulphate eyedrops in twelve subjects caused a sustained miosis, a transient reduction in near-point and a transient increase in the amplitude of accommodation. The latter had a peak at 30 min and had recovered by 90 min, though its amplitude varied widely between subjects. Contrast sensitivity to stationary grating patterns of 3-30 cycles/deg and phase-reversed grating patterns of 0.5-3 cycles/deg was reduced transiently with a time course similar to that of the increase in accommodation. The peak reduction in contrast sensitivity was correlated significantly with the peak amplitude of accommodation. Contrast sensitivity to laser interference fringes, observed in Maxwellian view where the effects of defocus are bypassed, was also reduced, indicating that physostigmine also had a direct deleterious action on the visual system.

An intramuscular injection of 2 mg atropine sulphate was given at either 8 or 120 min prior to instillation of 0.25% physostigmine sulphate eyedrops. In this way, the maximum accommodative change and the concomitant reduction in contrast sensitivity caused by physostigmine coincided with, respectively, the peak plasma atropine concentration or the fully developed mydriasis and reduction of near-point accommodation caused by atropine. Atropine at both times did not affect the miosis, the reduction in near-point, the increase in accommodation or the reduction in contrast sensitivity caused by physostigmine. Contrast sensitivity to a phase-reversed grating pattern was actually diminished by atropine, though this was not statistically significant. By contrast, 2% homatropine hydrobromide eyedrops did effectively antagonize physostigmine's actions. This indicates that the rate of delivery of atropine from the intramuscular injection was insufficient to compete against the ocular effects of physostigmine.