Melbourne Neuropsychiatry Centre, Department of Psychiatry, University of Melbourne, Australia
ORYGEN Research Centre, Department of Psychiatry, University of Melbourne, Australia
Melbourne Neuropsychiatry Centre, Department of Psychiatry, University of Melbourne and Department of Psychology, Australian Catholic University, Australia
Department of Psychology, University of Melbourne, Australia
Research Centre, Department of Psychiatry, University of Melbourne, Australia
Department of Psychology, University of Melbourne, Australia
ORYGEN Research Centre, Department of Psychiatry, University of Melbourne, Australia
Melbourne Neuropsychiatry Centre, Department of Psychiatry, University of Melbourne, Australia
Correspondence: Dr Stephen Wood, Melbourne Neuropsychiatry Centre, c/o National Neuroscience Facility, 161 Barry Street, Carlton South, VIC 3053 Australia. tel: +61 3 8344 1877; fax: +61 3 9348 0469; email: sjwood{at}unimelb.edu.au
Declaration of interest None. Funding detailed in Acknowledgements.
Background The origin of cognitive impairments in psychotic disorders is still unclear. Although some deficits are apparent prior to the onset of frank illness, it is unknown if they progress.
Aims To investigate whether cognitive function declined over the transition to psychosis in a group of ultra-high risk individuals.
Method Participants consisted of two groups: controls (n=17) and individuals at ultra-high risk for development of psychosis (n=16). Seven of the latter group later developed psychosis. Neuropsychological testing was conducted at baseline and again after at least a 12-month interval.
Results Both the Visual Reproduction sub-test of the Wechsler Memory Scale-Revised and Trail-Making Test B showed a decline over the follow-up period that was specific to the group who became psychotic. In addition, both high-risk groups showed a decline in digit span performance. No other task showed significant change over time.
Conclusions These preliminary data suggest that as psychosis develops there may be a specific decline in visual memory and attentional set-shifting, reflecting impairments in efficient organisation of visual stimuli. This may be caused by either the illness itself or treatment with antipsychotic medication.