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Psychophysical assessment of magno- and parvocellular function in schizophrenia

Published online by Cambridge University Press:  06 September 2006

SANDRINE DELORD
Affiliation:
Université Bordeaux 2, Equipe de Psychologie Cognitive, Laboratoire de Psychologie (EA 3662), Bordeaux, France
MARIA GIOVANNA DUCATO
Affiliation:
CNRS FRE 2726, Laboratoire de Neurosciences Fonctionnelles et Pathologies, Lille, France Université Lille 2, CHRU de Lille, Lille, France
DELPHINE PINS
Affiliation:
CNRS FRE 2726, Laboratoire de Neurosciences Fonctionnelles et Pathologies, Lille, France Université Lille 2, CHRU de Lille, Lille, France
FRÉDÉRIC DEVINCK
Affiliation:
Section of Neurobiology, Physiology and Behavior, Department of Ophthalmology, University of California at Davis, Davis, California
PIERRE THOMAS
Affiliation:
CNRS FRE 2726, Laboratoire de Neurosciences Fonctionnelles et Pathologies, Lille, France Université Lille 2, CHRU de Lille, Lille, France
MURIEL BOUCART
Affiliation:
CNRS FRE 2726, Laboratoire de Neurosciences Fonctionnelles et Pathologies, Lille, France Université Lille 2, CHRU de Lille, Lille, France
KENNETH KNOBLAUCH
Affiliation:
INSERM, U371, Cerveau et Vision, Department of Cognitive Neuroscience, Bron, France Université Claude Bernard Lyon 1, Lyon, France

Abstract

Recently developed psychophysical techniques permit the biasing of the processing of the stimulus by early visual channels so that responses reflect characteristics of either magno- or parvocellular pathways (Pokorny & Smith, 1997). We used such techniques to test psychophysically whether the global magnocellular dysfunction reported in schizophrenia also affects early processes. Seven schizophrenic patients and 19 normal controls participated. The task was a four-alternative forced-choice luminance discrimination, using a 2 × 2 configuration of four 1-deg squares. Target luminance threshold was determined in three conditions: the stimulus, including the target, was pulsed for 17 ms (pulse paradigm); the target was presented on a steady background of four squares (steady paradigm), or the target was presented alone (no background paradigm). We replicated previous results demonstrating magnocellular and parvocellular signatures in control participants. No evidence for an early magnocellular deficit could be detected as the thresholds of all schizophrenic observers were higher both in the steady paradigm (presumed magnocellular mediation) and in the pulse paradigm (presumed parvocellular mediation). Magnocellular dysfunction, if present in schizophrenia, must concern more integrated processes, possibly at levels at which parvocellular and magnocellular paths interact.

Type
CLINICAL PSYCHOPHYSICS
Copyright
© 2006 Cambridge University Press

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