Schizophrenia is associated with deficits in higher order processing of visual information, steady state visual evoked potential responses recorded over the occipital cortex in patients with schizophrenia suggest a dysfunction of lower level visual pathways, which was more prominent for magnocellular than parvocellular biased stimuli. The magnocellular pathway helps in orienting towards salient stimuli [1]. A magnocellular pathwad deficit could contribute to higher level visual cognitive deficits in schizophrenia dysfunction of the magnocellular pathway may also account for other well described aspects of neurophysiological dysfunction in schizophrenia, for example, the magnocellular pathway projects predominantly to dorsal cortical stream (i.e. parietal lobe), which codes motion perception and spatial localization [2].

30 schizophrenic patients were recruited randomly from Alexandria University Hosiptal. They scored 4 or higher on the Clinical Global Impression Scale for Severity CGI-S. Visual Evoked Potential VEP was done to them and compared to healthy control group.

In the right eye the mean P100 was 104.55 ± 5.62 and 95 ± 5.27 msec in schizophrenic and healthy control group respectively with statistical significant difference. A finding that has been replicated in the left eye where the mean P100 was 105.8 ± 5.41 and 95.85 ± 5.4 msec in the same respective groups

P100 in both right and left eyes are more prolonged in schizophrenic patients compared to healthy control groups.