High velocity transient visual processing deficits diminish ability of patients with schizophrenia to recognize...

Early information processing deficits are consistently reported for patients with schizophrenia. A growing number of studies have applied a transient (magnocellular) or sustained (parvocellular) explanation to account for deficient processing of briefly presented visual stimuli, moving stimuli, and stimuli requiring eye movements in patients with schizophrenia. This reasoning is based on research that makes the distinction between a magnocellular channel, which primarily responds to low spatial frequency and moving or rapidly presented visual information, and a parvocellular channel, which is primarily responsive to high spatial frequency and detailed information.

Although the preponderance of findings offer support for transient ("where is it") as opposed to sustained ("what is it") deficit in patients with schizophrenia, there remains a need for more specific depiction of the deficit.

The present study evaluated normal control subjects and patients with schizophrenia recruited from in-patient and out-patient settings. A Motion Defined Letter task was used, owing to its sensitivity to transient (magnocellular) activation.

Twenty-three patients with schizophrenia and sixteen normal control subjects were tested on eight dot velocity levels, ranging from 88 arc min/sec to 0.69 arc min/sec. A repeated measures analysis of variance indicated that the performance of patients with schizophrenia was significantly poorer than that of their normal counterparts on the three fastest dot velocity conditions (88 arc min/sec, p < 0.0001, 44 arc min/sec, p < 0.00001, and 22 arc min/sec, p < 0.00003), but performance did not differ on the five slower dot velocity conditions. A regression analysis revealed that the dosage of medication was positively associated with performance on three middle range dot velocity conditions (11 arc min/sec F (1,22) = 6.99; p < 0.025; 5.5 arc min/sec, F (2,20) = 0.379; p = 0.05, and 2.25 arc min/sec F (2,20) = 7.37; p < 0.005).

The findings afford support for an early information processing deficit in schizophrenics. These data also support the neurophysiologic model that explains the poor performance of patients with schizophrenia as it relates to a transient channel deficiency.