When the right eye was made miotic, the area under the stimulus-response curve decreased compared to pretreatment and compared to the fellow eye stimulation. The area under this curve ( shaded) essentially was the same no matter which eye was stimulated in the baseline state, as shown in the top graph. As the stimulus light was made brighter, the pupil contracted more, producing a sigmoid-shaped response curve (see Methods). The stimulus response curve is shown for the left, untreated eye's pupil contraction amplitude when the right eye was stimulated (as a function of light intensity) and also for the left eye's pupil contraction for left eye stimulation. This was necessary because at very small pupil sizes (<2.0 mm diameter), the computerized infrared pupillometer was not always able to track and measure the bright (infrared retro-illuminated) image of the pupil.Įxample of stimulus response curves plotted for baseline state before pilocaripin ( top) and after miosis ( bottom) was induced in the right eye by pilocarpine (same patient as example in Fig. The pupil diameter of the treated right eye was recorded before and after pilocarpine using a magnified infrared video camera with millimeter rule in the picture so that the entrance pupil size could be measured in all cases, even after profound miosis. Because of the induced miosis after instillation of pilocarpine, only the movement of the untreated left pupil was recorded and analyzed (sampling rate = 60 Hz) at the 90-minute posttreatment test time. Previous unpublished studies demonstrated that reversal of the stimulus order has no significant effect on the fitted response function due to retinal adaptation. The order of the stimuli was the same for each subject. Each subject was tested with the same protocol. The order of the stimuli was from dim to brightest stimuli for the stimulus protocol, the right eye received the same intensity as the left eye for each intensity step. Each stimulus was repeated six times during the test in staggered fashion. Eight stimulus intensities were presented over a 3.5 log unit range (35 dB range −44 to −9 dB of attenuation above a background of 3.1 apostilbs −44 dB attenuation = 0.13 cd/m 2, −0.9 dB = 400.7 cd/m 2). The stimulus duration was well within the latency time of the pupil light reflex so that the entrance pupil size was not affected during the time that the stimulus was on. The stimulus duration was 0.2 seconds and the time between light stimuli was 3.3 seconds. A flat black metal septum separated the right and left eye optical pathways to minimize stray light scatter. The refractive power of the instrument was adjusted by entering the refraction of the subject into the instrument's software so that the focal point was set at infinity to control accommodation. During the test, the stimulated eye was allowed to foveate on a small central cross before the ensuing light stimulus to control fixation. Each subject was adapted to a 3.1 apostilb background light for 30 seconds, then a sequence of light stimuli was presented alternately to each eye at varying intensities above the background level. Pupil responses to light stimuli were recorded using a computerized infrared pupillometer (Visual Pathways, Inc., Prescott, AZ) which presented a 30° radius light stimulus to each eye in non-Maxwellian view. This has important implications in understanding the potential influence of anisocoria on the RAPD and also greater susceptibility of lightly pigmented eyes to light toxicity. However, retinal illumination of lightly pigmented eyes is relatively independent of entrance pupil size, presumably due to extrapupillary transmission of light through the iris and sclera. In darkly pigmented eyes, entrance pupil size significantly influenced the retinal illumination. However, anisocoria correlated with RAPD only in subjects with darkly pigmented irides (Pearson correlation coefficient 0.793, P = 0.05). Induced anisocoria produced a significant change in RAPD from baseline (mean = 1.60 dB in the miotic eye, P = 0.007). The main outcome measure was the RAPD, determined by computerized pupillography, at baseline and after pilocarpine-induced anisocoria. The interocular difference in retinal illumination was assessed by computerized pupillometry from the stimulus response curve of the right and left eyes. Miosis was induced by topical 1% pilocarpine in the right eye of 14 healthy subjects with normal eyes. The influence of unilateral miosis on the magnitude of the pupil light reflex was studied to ascertain how a clinically significant anisocoria influences the relative afferent pupil defect (RAPD). We determined the effect of entrance pupil size on retinal illumination.
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