J Psychiatry Neurosci 2009; 34(6): 459-464
Sherlyn Yeap, MRCPsych; Simon P. Kelly, PhD ; Richard B. Reilly, PhD; Jogin H. Thakore, MD, PhD; John J. Foxe, PhD
Yeap, Kelly, Reilly, Thakore, Foxe — The Cognitive Neurophysiology Laboratory, St. Vincent’s Hospital, Richmond Road, Fairview, Dublin, Republic of Ireland; Kelly, Foxe — The Cognitive Neurophysiology Laboratory, Nathan S. Kline Institute for Psychiatric Research, Program in Cognitive Neuroscience and Schizophrenia, Orangeburg, NY; Reilly — School of Engineering and School of Medicine, Trinity College, University of Dublin, Dublin, Republic of Ireland; Foxe — Program in Cognitive Neuroscience, Departments of Psychology and Biology, City College of the City University of New York, New York, NY
Background: Etiological commonalities are apparent between bipolar disorder and schizophrenia. For example, it is becoming clear that both populations show similar electrophysiological deficits in the auditory domain. Recent studies have also shown robust visual sensory processing deficits in patients with schizophrenia using the event-related potential technique, but this has not been formally tested in those with bipolar disorder. Our goal here was to assess whether early visual sensory processing in patients with bipolar disorder, as indexed by decreased amplitude of the P1 component of the visual evoked potential (VEP), would show a similar deficit to that seen in those with schizophrenia. Since the P1 deficit has already been established as an endophenotype in schizophrenia, a finding of commonality between disorders would raise the possibility that it represents a measure of common genetic liability.
Methods: We visually presented isolated-check stimuli to euthymic patients with a diagnosis of bipolar disorder and age-matched healthy controls within a simple go/no-go task and recorded VEPs using high-density (72-channel) electroencephalography.
Results: The P1 VEP amplitude was substantially reduced in patients with bipolar disorder, with an effect size of f = 0.56 (large according to Cohen’s criteria).
Limitations: Our sample size was relatively small and as such, did not allow for an examination of potential relations between the physiologic measures and clinical measures.
Conclusions: This reduction in P1 amplitude among patients with bipolar disorder represents a dysfunction in early visual processing that is highly similar to that found repeatedly in patients with schizophrenia and their healthy first-degree relatives. Since the P1 deficit has been related to susceptibility genes for schizophrenia, our results raise the possibility that the deficit may in fact be more broadly related to the development of psychosis and that it merits further investigation as a candidate endophenotype for bipolar disorder.
Submitted Jul. 27, 2008; Revised Sept. 8, 2008; Jul. 7, Aug. 3, 10, 2009; Accepted Aug. 25, 2009.
Acknowledgements: This work was supported in part by a grant from the National Institute of Mental Health (MH65350) to Professor John Foxe. Dr. Yeap was supported by a fellowship from the Irish Health Research Board. The authors thank the Chief Executive Officer at St. Vincent’s Hospital, Mr. Edward Byrne and the Director of Nursing, Mrs. Phil Burke, for their support of the Cognitive Neurophysiology Laboratory (CNL). Thanks also to Mícheál Mac an tSionnaigh and Máire Nic an tSionnaigh for their essential help in establishing and maintaining the CNL facilities at St. Vincent’s.
Competing interests: None declared for Drs. Kelly, Thakore and Foxe. Dr. Yeap has received speaker fees and travel assistance from the Irish Health Research Board. Dr. Reilly has received travel assistance from Unilever.
Contributors: Dr. Foxe designed the study. Drs. Yeap and Thakore acquired the data, which Drs. Yeap, Kelly, Reilly and Foxe analyzed. Drs. Yeap, Kelly and Foxe wrote the article, which all authors reviewed and approved for publication.
Correspondence to: Professor J.J. Foxe, Director, Program in Cognitive Neuroscience, Department of Psychology, City College of the City University of New York, 138th St. and Convent Ave., New York, NY 10031; fax 845 398-6545; email@example.com