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.