Pupillary function in human amblyopia

Abstract

Quantitative measurements of pupillary function (response amplitude and latency) were made for normal eyes and for normal and fellow amblyopic eyes of groups of strabismic and anisometropic amblyopes. Stimuli consisted of luminance modulation of a large, evenly lit area (pupil light reflex) as well as contrast modulation of sinusoidal gratings (pupil grating response) of fixed, space-averaged luminance. Measurements were made of the direct and the consensual reflex under monocular stimulation. A comparison of the amplitude of the pupil light reflex as a function of luminance modulation showed no significant differences between normal and fellow amblyopic eyes for both the strabismic and anisometropic groups of amblyopes studied. A similar comparison of the associated response latencies showed significant difference between normal and fellow amblyopic eyes for both groups. In general, reductions in response amplitude and latency of the pupil grating response were found in individuals from each group when comparing the good and the affected eyes, although the observed group differences were only significant in the strabismic group. Interestingly, statistically significant reductions in both amplitude and latency for both the pupil light reflex and the pupil grating response were found between the eyes of normal observers and the so-called normal eyes of amblyopes in both groups studied. These results suggest that the type of pupillary deficit in amblyopia is a complicated one, depending not only on the type of amblyopia (strabismic or anisometropic) and the type of stimulus employed (light or pattern), but also on the parameter assessed (amplitude or latency) and whether the amblyopic result is referenced to its fellow normal eye or to the normal eye of a non-amblyopic observer. Since the pupil response to light flux changes is not mediated exclusively via the retinal projection to the midbrain and may also involve the activity of central visual pathways, the results obtained in this study cannot be used to provide definitive evidence for the site of abnormality in amblyopia.