Contrast perception above threshold is only minimally impaired in human amblyopia

Abstract

Amblyopia is a condition occurring at birth, or in early childhood, which affects up to 5% of the population and is characterized by degraded vision in one eye not able to be corrected by spectacles and having no observable lesion in the eye itself. Its cause is therefore uncertain, yet indirect evidence suggests a neural one, very likely in the visual areas of the brain. Ambyopia is usually associated with either a strabismus (eye misalignment) or anisometropia (unequal refractive error). Investigation into its neural basis has involved two approaches: psychophysical research in humans with amblyopia^1–6 has shown marked contrast deficits for threshold stimuli, suggesting deficient contrast coding at and above threshold in amblyopia. Neurophysiological research on animals deprived in early life with either a surgically induced squint or an optically induced anisometropia has suggested that ‘blur’ may be the common etiological basis for these two amblyopias⁷. We have investigated here whether amblyopes exhibit contrast deficiencies for other than threshold stimuli. Our measurements show that the threshold deficits measured in amblyopia bear no simple relationship to what happens above threshold. There is no contrast coding abnormality in amblyopia in the high-contrast range typical of everyday vision. We also give suprathreshold evidence for anisometropic and strabismic amblyopia having different neural bases.