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Vernier acuity determines the relative position of visual features with a precision better than the sampling resolution of cone receptors in the retina. Because Vernier displacement is thought to be mediated by orientation-tuned mechanisms, Vernier acuity is presumed to be processed in striate visual cortex (V1). However, there is considerable evidence suggesting that Vernier acuity is dependent not only on structures in V1 but also on processing in extrastriate cortical regions. Here we used functional magnetic resonance imaging-informed electroencephalogram source imaging to localize the cortical sources of Vernier acuity in observers with normal vision. We measured suprathreshold and near-threshold responses to Vernier onset/offset stimuli at different stages of the visual cortical hierarchy, including V1, hV4, lateral occipital cortex (LOC), and middle temporal cortex (hMT+). These responses were compared with responses to grating on/off stimuli, as well as to stimuli that control for lateral motion in the Vernier task. Our results show that all visual cortical regions of interest (ROIs) responded to both suprathreshold Vernier and grating stimuli. However, thresholds for Vernier displacement (Vernier acuity) were lowest in V1 and LOC compared with hV4 and hMT+, whereas all visual ROIs had identical thresholds for spatial frequency (grating acuity) and for relative motion. The cortical selectivity of sensitivity to Vernier displacement provides strong evidence that LOC, in addition to V1, is involved in Vernier acuity processing. The robust activation of LOC might be related to the sensitivity to the relative position of features, which is common to Vernier displacement and to some kinds of texture segmentation.

Behavioral studies have reported reduced spatial attention in amblyopia, a developmental disorder of spatial vision. However, the neural populations in the visual cortex linked with these behavioral spatial attention deficits have not been identified. Here, we use functional MRI-informed electroencephalography source imaging to measure the effect of attention on neural population activity in the visual cortex of human adult strabismic amblyopes who were stereoblind. We show that compared with controls, the modulatory effects of selective visual attention on the input from the amblyopic eye are substantially reduced in the primary visual cortex (V1) as well as in extrastriate visual areas hV4 and hMT+. Degraded attentional modulation is also found in the normal-acuity fellow eye in areas hV4 and hMT+ but not in V1. These results provide electrophysiological evidence that abnormal binocular input during a developmental critical period may impact cortical connections between the visual cortex and higher level cortices beyond the known amblyopic losses in V1 and V2, suggesting that a deficit of attentional modulation in the visual cortex is an important component of the functional impairment in amblyopia. Furthermore, we find that degraded attentional modulation in V1 is correlated with the magnitude of interocular suppression and the depth of amblyopia. These results support the view that the visual suppression often seen in strabismic amblyopia might be a form of attentional neglect of the visual input to the amblyopic eye.

Coherent motion responses of patients with mild to moderate strabismic amblyopia were compared to those of normals using visual-evoked potentials (VEPs). Responses were elicited by dynamic random-dot kinematograms that alternated at 0.83 Hz between globally coherent (left-right) and incoherent (random) motion states. Tuning curves were measured at the first harmonic of the global motion update rate (0.83 Hz) and at the first harmonic of the dot update rate (20 Hz) for spatial displacements 3.1 to 27.9 arcmin (1.6 to 9.3 deg/s). Responses locked to the changes in the global organization of the local direction vectors were an inverted U-shaped function of displacement/speed in the normal-vision observers and in the fellow eyes of the strabismus patients while the tuning function of the amblyopic eyes was shifted to larger displacements/higher speeds. Responses at the dot update rate were reduced in amplitude and altered in timing in both eyes of the patients. The results are consistent with both local and global deficits in motion processing in strabismic amblyopia.

Extended contours are a common feature of natural images. Most previous studies have considered contour integration as a two-dimensional process of linking like-oriented elements along their common orientation axis. Yet contours exist in a three-dimensional world, and one might therefore ask about the relationship between contour integration and binocular vision. Using an event-related potential assay of contour integration, we demonstrate that patients with strabismic amblyopia show a relative insensitivity to Gabor-defined contours in their dominant eyes, all of which had normal acuity. These deficits were not seen in the dominant eyes of patients with anisometropic amblyopia without strabismus, but were present in the amblyopic eyes of patients with either strabismus or anisometropia. Deficits were also found in both eyes of strabismus patients who had normal visual acuity in each eye, but who had strongly reduced or absent stereopsis. These results suggest that the maturation of contour detection mechanisms depends at least in part on the presence of normal binocular interaction during a developmental critical period.