Schizophrenia is often accompanied by a range of visual perception deficits, with many involving impairments in motion perception. The presence of perceptual abnormalities may impair neural processes that depend on normal visual analysis, which in turn may affect overall functioning in dynamic visual environments. Here, we examine the integrity of suppressive center-surround mechanisms in motion perception of schizophrenic patients. Center-surround suppression has been implicated in a range of visual functions, including figureground segregation and pursuit eye movements, visual functions that are impaired in schizophrenia. In control subjects, evidence of center-surround suppression is found in a reduced ability to perceive motion of a high-contrast stimulus as its size increases. This counterintuitive finding is likely a perceptual correlate of center-surround mechanisms in cortical area MT. We now show that schizophrenic patients exhibit abnormally weak center-surround suppression in motion, an abnormality that is most pronounced in patients with severe negative symptoms. Interestingly, patients with the weakest surround suppression outperformed control subjects in motion discriminations of large high-contrast stimuli. This enhanced motion perception of large high-contrast stimuli is consistent with an MT abnormality in schizophrenia and has a potential to disrupt smooth pursuit eye movements and other visual functions that depend on unimpaired center-surround interactions in motion.

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The social significance of imitation is that it provides internal tools for understanding the actions of others by simulating or forming internal representations of these actions. Imitation plays a central role in human social behavior by mediating diverse forms of social learning. However, imitation and simulation ability in schizophrenia has not been adequately addressed. The major aim of the present study was to investigate imitation ability in schizophrenia patients and healthy individuals by examining simple motor imitation that involved the replication of meaningless manual and oral gestures, and the imitation of emotional facial expressions, which has implications for mentalizing. A secondary aim of the present study was to investigate the relationships among imitation ability, social functioning, and working memory. Subjects were asked to mimic hand gestures, mouth movements, and facial expressions of others, online. Clinical symptoms, social competence, and working memory were also assessed. Patients with schizophrenia were significantly impaired on all imitation tasks. Imitation errors were significantly correlated with reduced social competence and increased negative symptoms. However, imitation ability was only weakly associated with working memory. To summarize, the present study examined the ability of patients with schizophrenia to imitate the behaviors demonstrated by others. The results indicate a fundamental impairment in imitation ability in schizophrenia and implicate a possible difficulty in simulation. Further research to determine the neural and developmental origins of this difficulty could be extremely helpful in elucidating the role of simulation in schizophrenia and to establish the complex relationships among mental representation, imitation, and social cognition.

Rats with medial prefrontal cortex or sham control lesions were tested on an eight-arm radial maze task to examine memory for the temporal order of a variable and a constant sequence of spatial locations as a function of temporal distance. During the study phase of each trial, rats were allowed to visit each of eight arms once in an order that was randomly selected or fixed for that trial. The test phase required the rats to choose which of two arms occurred earlier in the sequence of arms visited during the study phase. The arms selected as test arms varied according to temporal distance (0, 2, 4, or 6) or the number of arms that occurred between the two test arms in the study phase.For the variable sequences based on new information, control rats showed an increasing temporal distance function. Relative to control rats, medial prefrontal cortex-lesioned rats displayed a temporal order memory deficit across all distances. For the constant sequence based on familiar information, control rats performed well across all distances. Relative to controls, the medial prefrontal cortex-lesioned rats displayed a performance deficit. The results support the idea that the medial prefrontal cortex contributes to mnemonic operations associated with temporal order for new and familiar spatial location information.

Schizophrenia has been associated with impairment of counterfactual thinking (Hooker et al., 2000), defined as cognitions about alternatives to past outcomes (i.e., what might have been). Counterfactual thinking in healthy individuals is associated with effective problem-solving, behavioral regulation, and performance improvement (Camille et al., 2004; Ursu & Carter, 2005; Roese, 1997). Specifically, counterfactual thinking (e.g., "If only I had studied harder") contributes to behavior regulation via activation of intentions (e.g., "Next exam I will study harder"), which in turn elicit corresponding behavior (e.g., studying; see Figure 1). All three causal links in Figure 1 have been verified among healthy participants (Smallman & Roese, 2006). In schizophrenia patients, link 1 is impaired (Hooker et al., 2000), whereas link 3 is intact (Brandstätter et al., 2001). The present research examined whether impairment of link 2 (from counterfactuals to intentions) is associated with schizophrenia.