Early-Stage Visual Processing Deficits in Schizophrenia

Abstract

Purpose of review-While cognitive dysfunction including memory and attentional deficits are well known in schizophrenia, recent work has also shown basic sensory processing deficits. Deficits are particularly prominent in the visual system and may be related to cognitive deficits and outcome. This article reviews studies of early-stage visual processing in schizophrenia published during the past year. These studies reflect the growing interest and importance of sensory processing deficits in schizophrenia.Recent findings-The visual system is divided into magnocellular and parvocellular pathways which project to dorsal and ventral visual areas. Recent electrophysiological and behavioral investigations have found preferential magnocellular/dorsal stream dysfunction, with some deficits in parvocellular function as well. These early-stage deficits appear to be related to higher level cognitive, social, and community function. Structural studies of occipital cortex and particularly optic radiations provide anatomical support for early visual processing dysfunction.Summary-These findings highlight the importance of sensory processing deficits, in addition to higher cognitive dysfunction, for understanding the pathophysiology of schizophrenia. Understanding the nature of sensory processing deficits may provide insight into mechanisms of pathology in schizophrenia, such as N-methyl-D-aspartate dysfunction or impaired signal amplification, and could lead to treatment strategies including sensory processing rehabilitation that may improve outcome.

Exploring intermediate phenotypes with EEG: Working memory dysfunction in schizophrenia

“…In a number of studies Butler et al [25,27,94 for review] have provided evidence for a specific impairment in the magnocellular pathway. This is a visual pathway which specialises in the processing of luminance information, while chromatic information is subserved by parvo-and koniocellular pathways [112].…”

Early Visual Processing Deficits in Dysbindin-Associated Schizophrenia

“…This is warranted because dysbindin is expressed throughout the brain, including sensory regions such as the occipital cortex. Early visual processing de cits have repeatedly been demonstrated in schizophrenia, particularly in the magnocellular system, which is glutamate/NMDA-dependent ( 9). Because dysbindin is implicated in glutamate/NMDA transmission, early visual processing may be a useful brain function in which to investigate dysbindin's impact.…”

Disintegration of sensorimotor brain networks in schizophrenia

“…This is in line with previous studies documenting sensory and perceptual deficits in various domains from early-stage processing to cognitive stimulus interpretation. 39,40 The strong sensory involvement overlaps with findings from electroencephalogram studies, associating schizophrenia with a broad range of sensory deficits reflected among various eventrelated potentials (eg, reduced pre-pulse inhibition (PPI), MMN [mismatch negativity], P1, P3). 40 Our data support both focal (within sensorimotor/ visual nodes) and distal (between sensorimotor/visual and thalamus/higher-order nodes) connectivity differences in schizophrenia, including edges implicating dorsal attention, default mode, frontoparietal, and thalamus nodes.…”