December 2010
Volume 10, Issue 15
OSA Fall Vision Meeting Abstract  |   December 2010
Deficits in processing sensory context in schizophrenia
Author Affiliations
  • Steven Dakin
    Institute of Ophthalmology, University College London
  • Alice Seabright
    Cognitive, Perceptual & Brain Sciences Research Department, University College London
  • Bernice Wright
    Cognitive, Perceptual & Brain Sciences Research Department, University College London
  • Patricia Carlin
    Institute of Psychiatry, Kings college London
Journal of Vision December 2010, Vol.10, 31. doi:
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      Steven Dakin, Alice Seabright, Bernice Wright, Patricia Carlin; Deficits in processing sensory context in schizophrenia. Journal of Vision 2010;10(15):31.

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      © ARVO (1962-2015); The Authors (2016-present)

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The visual brain relies on context to make sense of images, a reliance that makes us vulnerable to illusions (where visual context interferes with our ability to make a perceptual judgment). People with schizophrenia (SZ) are less likely to be influenced by visual context and this can make them more accurate at matching the contrast of targets within disruptive visual contexts (Dakin, Carlin & Hemsley, 2005). We attribute this to a reduction in gain control (inhibitory interactions that optimize the operating range of neurons) in SZ.

In my talk I will describe several new results examining the idea that perceptual gain control is faulty in SZ. First, people with SZ experience weaker illusions when context is defined by attributes other than contrast (e.g. size) indicating a pervasive gain control deficit. Second, there are substantial individual differences in the extent to which controls experience these illusions. Third, the contrast-response function (inferred from contrast discrimination) is consistent with SZ leading to generally increased suppression of visual activity. Finally, ketamine - which induces positive symptoms of psychosis in healthy observers - interferes with contrast discrimination but does not induce changes in visual appearance we see in SZ.

We note that patients' results are essentially exaggerated versions of what we see in the control population (validating the use of schizotypy to probe perceptual deficits in SZ). The reliable and substantial differences in perceptual processing we observe are a promising new bio-marker for the diagnosis and treatment of SZ.


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