A vision science perspective on schizophrenia

Perceptual impairments in schizophreniawere described as long ago as 1903, when Kraepelin (1903) reported that patients demonstrated incomplete perception of briefly exposed objects on a laboratory task. Despite this early beginning, and despite the fact that the visual system is the most heavily researched area of cognitive neuroscience, there have been far fewer studies of vision in schizophrenia than of other cognitive functions (e.g., memory, cognitive control) (Silverstein and Keane, 2011b). In recent years, however, reports have accumulated indicating that visual processing impairments are both prevalent among individuals with schizophrenia, and significant in terms of advancing knowledge regarding etiology, pathophysiology, phenomenology, and course of illness. For example, approximately 25–30% of individuals with schizophrenia report visual hallucinations (Waters et al., 2014), and the number of patients reporting visual distortions (of brightness, motion, form, and color) is over twice that high (Phillipson and Harris, 1985). Importantly, reliable and valid laboratorymeasures of processing in these domains are available, and they have long histories of demonstrating specific impairments in schizophrenia (Cadenhead et al., 2013; Chen, 2011; Green et al., 2011; Silverstein and Keane, 2011a). These subjective and laboratory manifestations of visual abnormality are clinically significant. For example, visual distortions are associated with subjective distress and suicidal ideation (even after controlling for other factors such as psychotic symptoms and auditory distortions) (Grano et al., 2015). Laboratory-based markers of visual processing impairments have been shown to be related to poorer detection of facial affect (Tso et al., 2015; Turetsky et al., 2007), impaired reading ability (Martinez et al., 2012), poorer real-world functioning (Green et al., 2012; Rassovsky et al., 2011), and reduced short(Silverstein et al., 2013) and long-term (Silverstein et al., 1998) treatment response. Visual abnormalities can also be observed in children, adolescents, and young adults at high-risk for schizophrenia (Hebert et al., 2010; Koethe et al., 2009; Mittal et al. in press; Revheim et al., 2014; Schubert et al., 2005), and findings suggest that they may be particularly sensitive (compared to other clinical phenomena) for predicting conversion to the disorder among high-risk (Klosterkotter et al., 2001) and generalpopulation (Schubert et al., 2005) samples. Nevertheless, despite this growing body of evidence, visual processingmeasures are still rarely included in clinical trials or high-risk studies. Because, as noted above, visual functioning is relatively well understood in the normal brain, it has the potential to shed light on many aspects of brain dysfunction in conditions such as schizophrenia. For example, because the basic architecture of local integrative circuitry, involving pyramidal cells and inhibitory interneurons, is the same in all regions of the cortex (Phillips and Singer, 1997), but expressed far less densely (i.e., with less associated complexity) in visual cortex compared to other regions (e.g., the frontal cortex) (Monaghan et al., 1989), visual cortex can serve as a useful model of broader aspects of coordinated