Eye movement dysfunction as a biological marker of risk for schizophrenia.

Abstract

Our aim was to review smooth pursuit eye movement (SPEM) studies in schizophrenia and groups at high risk for schizophrenia, with a view to evaluating the utility of SPEM dysfunction as a biological marker of risk for schizophrenia. Smooth pursuit eye movement studies, related saccade function and the unresolved issues in this area of schizophrenia research were addressed. The different perspectives on the trait marker status of SPEM dysfunction, provided by both high-risk studies and related developmental research were considered. Attention was also given to the relationship between eye movement dysfunction and symptom profiles. Converging evidence points to the robust and specific nature of SPEM dysfunction in schizophrenia, and highlights the role of frontal lobe and a related network dysfunction. The vast majority of 'high risk' studies support the view that SPEM dysfunction is also genetically specific to schizophrenia, and is not simply due to the overt expression of this illness. Studies assessing SPEM in relation to symptomatology show an association with the Disorganisation syndrome in particular. Evidence for the specificity of SPEM dysfunction to diagnosed schizophrenia, as well as to healthy individuals with a genetic vulnerability to schizophrenia, suggests that the SPEM task has efficacy as a test of gene carrier status in schizophrenia, and therefore as a trait marker of risk for schizophrenia. Future studies should seek to explore the relationships between SPEM and other eye movement dysfunctions (antisaccades, express saccades), in view of evidence that some of these dysfunctions also show specificity for schizophrenia.