Perceptual processing deficits are commonly observed in schizophrenia, and one of the most thoroughly investigated perceptual tasks in schizophrenia is visual masking. In visual masking, the ability to identify a visual target is disrupted by the presence of a mask that occurs briefly before or after the target (Breitmeyer, 1984
; Breitmeyer and Ogmen, 2000
). Forward masking occurs when a mask precedes a target; backward masking occurs when a mask follows a target. It has long been noted that schizophrenic patients have more difficulty than comparison subjects in identifying the target in the presence of a mask (Saccuzzo and Braff, 1981
; Green and Walker, 1986
; Rund, 1993
; Cadenhead et al., 1998
Visual masking performance is frequently viewed as the interaction between two key visual channels that form the basis for complex visual processing (Van Essen et al., 1992
). The two pathways are known by the functionally based terms “sustained channel” and “transient channel”, or by the anatomically based terms “parvocellular pathway” and “magnocellular pathway”. According to this model, the sustained or parvocellular activity elicited by a target conveys detailed information that is needed to identify targets, while the transient or magnocellular activity provides more rapid information that allows location of a stimulus but not identification. Masking results from disruption of this target information by the magnocellular or parvocellular pathways of the mask (Breitmeyer and Ganz, 1976
; Breitmeyer, 1984
Moving out from neural circuits to everyday functioning, visual masking deficits have been linked to performance on a measure of social perception (i.e., ability to perceive a social context from brief vignettes, Sergi and Green, 2002
) and have served as a key component of a model of community functioning (Sergi et al., 2006
). Hence, improved understanding of visual masking deficits in schizophrenia may provide a useful lynchpin in mapping pathways from neural circuits to community functioning.
Emerging evidence suggests that performance on visual masking tasks may be a trait marker that reflects vulnerability to schizophrenia rather than a reflection of a symptomatic state. For example, masking deficits have been reported in schizophrenia patients who are in clinical remission (Miller et al., 1979
; Green et al., 1999
). In addition, first-degree relatives of schizophrenia patients often show similar, but milder, masking deficits than patients (Green et al., 1997
; Keri et al., 2001
; Green et al., 2006
), though specific task parameters may affect the magnitude of the group differences (e.g., Bedwell et al., 2003
). Similarly, masking deficits have been observed in individuals who are considered to be psychosis-prone (Merritt and Balogh, 1989
; Cadenhead et al., 1996
Beyond these demonstrations that visual masking deficits occur in individuals who are at heightened risk for schizophrenic episodes but who are not currently symptomatic, a reasonable degree of stability over time would be expected if visual masking deficits are vulnerability markers for schizophrenia (Zubin and Spring, 1977
; Nuechterlein and Dawson, 1984
; Nuechterlein et al., 1994
). Surprisingly, however, little is known about the stability of masking performance deficits in schizophrenia.
Only one study to our knowledge examined visual masking in schizophrenia over an extended follow up period. Rund et al. (1993)
reported no significant effect of time on a backward masking performance in a sample of 22 schizophrenia patients tested over a 2-year period. Although this study suggests that visual masking performance in schizophrenia is relatively stable over a 2-year period, the conclusions are limited by the use of a very basic masking procedure (i.e. only two stimulus onset asynchronies, limited temporal resolution, no forward masking, and only a single high-energy condition). The study also included patients with a wide range of ages and illness chronicity, so it is difficult to determine whether the stability suggested in this initial study applies to the initial phase of schizophrenia in which clinical fluctuations are often more marked over time.
The goal of the current study was to examine in a thorough manner the stability of visual masking performance in schizophrenia. To do so, we prospectively assessed a sample of recent-onset schizophrenia patients at baseline, 6 months, and 18 months. The visual masking procedures included multiple SOAs for forward and backward masking for four different masking conditions that differed in the extent to which they relied on the magnocellular and parvocellular pathways.