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Updated: May 22, 2026

Analyzing Neural Activity and Connectivity Using Intracranial EEG Data with SPM Software
Published on: October 30, 2018
Amblyopic deficits in the timing and strength of visual cortical responses to faces
Éva M Bankó1, Judit Körtvélyes, János Németh
1Faculty of Information Technology, Pázmány Péter Catholic University, Budapest, Hungary. banko@digitus.itk.ppke.hu
Abstract:
Behavioral research revealed that object vision is impaired in amblyopia. Nevertheless, neurophysiological research in humans has focused on the amblyopic effects at the earliest stage of visual cortical processing, leaving the question of later, object-specific neural processing deficits unexplored. By measuring event-related potentials (ERPs) to foveal face stimuli we characterized the amblyopic effects on the N170 component, reflecting higher-level structural face processing. Single trial analysis revealed that latencies of the ERP components increased and were more variable in the amblyopic eye compared to the fellow eye both in strabismic and anisometropic patent groups. Moreover, there was an additional delay of N170 relative to the early P1 component over the right hemisphere, which was absent in the fellow eye, suggesting a slower evolution of face specific cortical responses in amblyopia. On the other hand, distribution of single trial N170 peak amplitudes differed between the amblyopic and fellow eye only in the strabismic but not in the anisometropic patients. Furthermore, the amblyopic N170 latency increment but not the amplitude reduction correlated with the interocular differences in visual acuity and fixation stability. We found no difference in the anticipatory neural oscillations between stimulation of the amblyopic and the fellow eye implying that impairment of the neural processes underlying generation of stimulus-driven visual cortical responses might be the primary reason behind the observed amblyopic effects. These findings provide evidence that amblyopic disruption of early visual experience leads to deficits in the strength and timing of higher-level, face specific visual cortical responses, reflected in the N170 component.
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