When seeing depends on knowing: adults with Autism Spectrum Conditions show diminished top-down processes in the visual perception of degraded faces but not degraded objects.
Behavioural, neuroimaging and neurophysiological approaches emphasise the active and constructive nature of visual perception, determined not solely by the environmental input, but modulated top-down by prior knowledge. For example, degraded images, which at first appear as meaningless 'blobs', can easily be recognized as, say, a face, after having seen the same image un-degraded. This conscious perception of the fragmented stimuli relies on top-down priming influences from systems involved in attention and mental imagery on the processing of stimulus attributes, and feature-binding [Dolan, R. J., Fink, G. R., Rolls, E., Booth, M., Holmes, A., Frackowiak, R. S. J., et al. (1997). How the brain learns to see objects and faces in an impoverished context. Nature, 389, 596-599]. In Autism Spectrum Conditions (ASC), face processing abnormalities are well-established, but top-down anomalies in various domains have also been shown. Thus, we tested two alternative hypotheses: (i) that people with ASC show overall reduced top-down modulation in visual perception, or (ii) that top-down anomalies affect specifically the perception of faces. Participants were presented with sets of three consecutive images: degraded images (of faces or objects), corresponding or non-corresponding grey-scale photographs, and the same degraded images again. In a passive viewing sequence we compared gaze times (an index of focal attention) on faces/objects vs. background before and after viewers had seen the undegraded photographs. In an active viewing sequence, we compared how many faces/objects were identified pre- and post-exposure. Behavioural and gaze tracking data showed significantly reduced effects of prior knowledge on the conscious perception of degraded faces, but not objects in the ASC group. Implications for future work on the underlying mechanisms, at the cognitive and neurofunctional levels, are discussed.
Loth
Eva
E
MRC Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, United Kingdom. eva.loth@kcl.ac.uk
Gómez
Juan Carlos
JC
Happé
Francesca
F
D000328:Adult; D020817:Asperger Syndrome / Q000453:epidemiology*; D001321:Autistic Disorder / Q000453:epidemiology*; D003071:Cognition; D005145:Face; D005149:Facial Expression; D005260:Female; D006801:Humans; D008297:Male; D014794:Visual Fields / Q000502:physiology*; D014796:Visual Perception / Q000502:physiology*; D055815:Young Adult