Dysfunction of early-stage visual processing in schizophrenia

Citation
Pd. Butler et al., Dysfunction of early-stage visual processing in schizophrenia, AM J PSYCHI, 158(7), 2001, pp. 1126-1133
Citations number
57
Categorie Soggetti
Psychiatry,"Clinical Psycology & Psychiatry","Neurosciences & Behavoir
Journal title
AMERICAN JOURNAL OF PSYCHIATRY
ISSN journal
0002953X → ACNP
Volume
158
Issue
7
Year of publication
2001
Pages
1126 - 1133
Database
ISI
SICI code
0002-953X(200107)158:7<1126:DOEVPI>2.0.ZU;2-M
Abstract
Objective: Schizophrenia is associated with deficits in higher-order proces sing of visual information. This study evaluated the integrity of early vis ual processing in order to evaluate the overall pattern of visual dysfuncti on in schizophrenia. Method: Steady-state visual-evoked potential responses were recorded over t he occipital cortex in patients with schizophrenia and in age- and sex-matc hed comparison volunteers. Visual-evoked potentials were obtained for stimu li composed of isolated squares that were modulated sinusoidally in luminan ce contrast, number of squares, or chromatic contrast in order to emphasize magnocellular or parvocellular visual pathway activity. Results: Responses of patients to magnocellular-biased stimuli were signifi cantly lower than those of comparison volunteers. These lower response leve ls were ob served in conditions using both low luminance contrast and large squares that biased processing toward the magnocellular pathway. In contra st, responses to stimuli that biased processing toward the parvocellular pa thway were not significantly different between schizophrenia patients and c omparison volunteers. A significant interaction of group and stimulus type was observed in the condition using low luminance contrast. Conclusions: These findings suggest a dysfunction of lower-level visual pat hways, which was more prominent for magnocellular than parvocellular biased stimuli. The magnocellular pathway helps in orienting toward salient stimu li. A magnocellular pathway deficit could contribute to higher-level visual cognitive deficits in schizophrenia.