Contrast sensitivity was measured in 12 subjects for different spatial frequencies of sinusoidal grating patterns, generated by oscilloscope, for pupil diameters 2-8 mm and for defocus of +1-4 D, following homatropine eyedrops. Changes in pupil diameter, without correction for the change in retinal illumination, had no significant effect on contrast sensitivity, except at 0.5 and 1 c deg-1 when a significant reduction occurred with the 2 mm pupil. Defocus caused a large reduction in contrast sensitivity at spatial frequencies higher than the peak of the contrast sensitivity function (3 c deg-1) and a smaller reduction below the peak. In both individual and group results, there was no significant effect of defocus in causing a disproportionately greater reduction in contrast sensitivity at higher spatial frequencies nor were the zero mimina predicted by optical theory observed. The results were confirmed in eight subjects viewing with the natural eye, though the reduction in contrast sensitivity caused by +1 D defocus was not significant: this was attributed to the relaxation of accommodation in response to defocus. To predict the performance of the visual system, multiple regression equations were derived to incorporate terms for pupil diameter, defocus and spatial frequency. These equations reflected the lack of effect of pupil diameter, while defocus caused a 51% loss in contrast sensitivity per dioptre at higher spatial frequencies (3-38 c deg-1) and a 19% reduction at low spatial frequencies.

SUMMARYInstillation 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.

The effects of a single intramuscular injection of 2 mg atropine sulphate on visual function were studied in volunteer subjects. The well-known effects of increased heart rate, dryness of the mouth, ncreased pupil diameter and reduced accommodative range were confirmed. Visual acuity, stereoacuity, red-green colour balance and reaction time to a visual stimulus were unaffected by atropine, while extraocular muscle balance (horizontal heterophoria and cyclophoria) underwent a transient change. There was no significant change in contrast sensitivity measurements to stationary sinusoidal grating patterns of spatial frequencies 1-30 c/deg; however contrast sensitivity o moving grating patterns of spatial frequencies 1-5 c/deg showed a sustained reduction which was ,till present at 6 h post-injection. It is concluded that atropine adversely affects movement letection but not stationary visual function.

SUMMARYAn 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 phasereversed grating pattern was actually diminished by atropine, though this was not statistically significant. By contrast, 2 % homatropine hydrobromide eyedrops did effectively anatagonize 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.