Cortical deficits in human amblyopia: their regional distribution and their relationship to the contrast detection deficit

Abstract

Purpose: The understanding of the site and nature of the cortical processing deficit in human amblyopia awaits the resolution of three fundamental questions about which there is, at present, much controversy: First, is area V1 affected as the present animal models would predict, but some imaging studies argue against? Second, how extensive is the loss of extrastriate function, and does it simply follow as a consequence of an impaired V1 input? Third, does the brain imaging deficit, be it striate or extrastriate, correlate with the well-documented psychophysical loss?--a fundamental issue on which previous brain imaging studies are divided.

Methods: A spatially broadband stimulus was used to determine the functional MRI responses from the different retinotopically identified visual cortical areas in a group of normal (n = 6) and a group of amblyopic (n = 11) observers. Responses were compared between the amblyopic and fellow fixing eyes of amblyopes and between the dominant and nondominant eyes of normal subjects, in central and peripheral parts of the visual field. Psychophysical acuity and contrast sensitivity was also measured and its correlation with the brain imaging deficit determined.

Results: V1 was affected in most but not all cases; the brain-imaging deficit involved extensive regions of extrastriate cortex and, at least with the stimuli used in the study, correlated with the V1 loss, suggesting a strong V1 influence; and neither the striate nor the extrastriate deficits correlated with the psychophysical contrast threshold losses at either high or low spatial frequencies.

Conclusions: The results suggest that there are significant suprathreshold processing deficits that are not a consequence of the well-known threshold deficit. Our preoccupation over the past 30 years with the contrast detection deficit in amblyopia limited to the processing within a circumscribed part of V1 may have to be modified to include not only processing deficits for high-contrast stimuli but also the involvement of multiple extrastriate areas.