Steven Silverstein

Professor of Psychiatry and Director of the Division of Schizophrenia Research at Rutgers Biomedical and Health Sciences
Dr. Silverstein's research has included both laboratory and clinical studies.  This includes studies of low-, mid-, and high-level visual processes in the disorder (e.g., retinal function, contrast sensitivity, perceptual organization, and Bayesian effects in reduced illusion susceptibility).  These psychophysical and brain imaging studies have clarified aspects of altered neural circuitry, suggested a basic computational algorithm dysfunction involved in perceptual and conceptual disorganization, and clarified which impairments are state vs. trait related, thereby assisting with biomarker development.  In addition, he has developed and tested a psychological treatment for attentional impairment in schizophrenia.   As primary chair of the 2012 Ernst Strüngmann Forum on schizophrenia at the Frankfurt Institute for Advanced Studies in Germany, he organized a conference of schizophrenia scholars for the purpose of translating current developments in psychology and behavioral neuroscience into a transformed concept of mental illness and schizophrenia.
Cognitive organization as a dimension of individual differences and psychopathology

Visual processing impairments are well established in schizophrenia. These include abnormalities in contrast sensitivity; various excitatory and inhibitory effects, including those involved in masking and surround suppression; and in form, motion, brightness, and color processing. Many of these effects have been demonstrated using sophisticated psychophysical paradigms that avoid generalized deficit confounds, and many have known neurobiological correlates as revealed by EEG/ERP or functional MRI. Recently, the clinical importance of these impairments has become clearer, with research indicating that they predict conversion to psychosis and are associated with poorer functional outcomes in patients. Moreover, it has been demonstrated that the disturbances in the computational mechanisms and neural circuitry involved in specific visual impairments in schizophrenia are clear examples of more widespread failures in: 1) predictive coding, which is thought to be the basis of positive symptoms; or 2) cognitive coordination, which is thought to be the basis of disorganized symptoms. As would be predicted by these models, positive and disorganized symptoms are significantly and differentially correlated with visual impairments that can be viewed as exemplars of their basic mechanisms. Several studies have also clarified the state/trait status of specific impairments, thereby increasing their utility for studies of treatment-related biomarkers or endophenotypes, respectively. Finally, recent evidence indicates that changes in the retina – the only neural tissue that can be viewed directly in fully awake subjects – are associated with illness progression and poorer cognitive functioning – suggesting their use as a proxy for brain structure and function, as has been demonstrated with other CNS diseases. Additionally, several known visual impairments in schizophrenia suggest either illness- or medication-related retinal effects. This presentation will review data on selected visual processing impairments to demonstrate their different neural bases (from retina to occipital lobe to frontal cortex), computational mechanisms, status as biomarkers, and treatment implications.