Longitudinal evaluation of visual P300 amplitude in clinical high-risk subjects: An event-related potential study

Naoya Oribe, Neural Dynamics Laboratory, Research Service, VA Boston Healthcare System, and Department of Psychiatry, Harvard Medical School, Boston, USA.
Yoji Hirano, Neural Dynamics Laboratory, Research Service, VA Boston Healthcare System, and Department of Psychiatry, Harvard Medical School, Boston, USA.
Elisabetta Del Re, Departments of Psychiatry and Radiology, Veterans Affairs Boston Healthcare System, and Psychiatry Neuroimaging Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
Raquelle I. Mesholam-Gately, Massachusetts Mental Health Center, Division of Public Psychiatry, Beth Israel Deaconess Medical Center, Boston, USA.
Kristen A. Woodberry, Massachusetts Mental Health Center, Division of Public Psychiatry, Beth Israel Deaconess Medical Center, Boston, USA.
Takefumi Ueno, Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Kyushu, Japan.
Shigenobu Kanba, Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Kyushu, Japan.
Toshiaki Onitsuka, Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Kyushu, Japan.
Martha E. Shenton, Departments of Psychiatry and Radiology, Veterans Affairs Boston Healthcare System, and Psychiatry Neuroimaging Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
Kevin M. Spencer, Neural Dynamics Laboratory, Research Service, VA Boston Healthcare System, and Department of Psychiatry, Harvard Medical School, Boston, USA.
Margaret A. Niznikiewicz, Cognitive Neuroscience Laboratory, VA Boston Healthcare System, Department of Psychiatry, Harvard Medical School, Brockton, USA.

Abstract

AIM: We previously reported abnormal P300 and N200 in a visual oddball task, and progressive P300 amplitude reduction at 1-year follow-up in patients with first-episode schizophrenia. P300 reduction as well as intact P1/N1 were also observed in clinical high-risk subjects (CHR), but whether or not these components change over time is unknown. This study evaluates, longitudinally, the visual P300, as well as P1, N1, and N200, in CHR. METHODS: Visual event-related potentials (ERP) were recorded twice, once at baseline and once at 1-year follow-up in CHR (n = 19) and healthy comparison subjects (HC; n = 28). Participants silently counted infrequent target stimuli ('x') among standard stimuli ('y') presented on the screen while the 64-channel electroencephalogram was recorded. RESULTS: No CHR converted to psychosis from baseline to 1-year follow-up in this study. Visual P300 amplitude was reduced and the latency was delayed significantly in CHR at both time points compared with HC. Furthermore, CHR subjects who had more positive symptoms showed more amplitude reduction at both time points. P1, N1, and N200 did not differ between groups. CONCLUSION: Visual P300 amplitude was found to be reduced in CHR individuals compared with HC. We note that this finding is in subjects who did not convert to psychosis at 1-year follow-up. The association between visual P300 amplitude and symptoms suggests that for CHR who often experience clinical symptoms and seek medical care, visual P300 may be an important index that reflects the pathophysiological impairment underlying such clinical states.