710 BIOL PSYCHIATRY 1989;25:710-716 Correlations Between Abnormal Auditory P300 Topography and Positive Symptoms in Schizophrenia: A Preliminary Report Martha E. Shenton, Steven F. Faux, Robert W. McCarley, Ruth Ballinger, Michael Coleman, Michael Torello, and Frank H. Duffy P300 component amplitude in the lef temporal scalp region, shown in three previous studies to differentiate normals from schizophrenics, was found to be significantly cor- related with the Thought Disorder Index (TDI) and the Scale for the Assessment of Positive Symptoms (SAPS). These correlations occurred primarily in the P300 waveform derived from the Goodin paradigm. These findings suggest a brain processing disturbance in positive symptom schizophrenia that may be reflected by electrophysiological abnormal- ities detectable in the temporal scalp region. Introduction In three separate topographic studies, our laboratory has reported a left temporal scalp region amplitude decrement of the auditory P300 in schizophrenics compared with age- matched normal controls (Goodin subtraction procedure, P3OOg waveform) (Morstyn et al. 1983; Faux et al. 1988a-c). As this left temporal feature was shown to differ- entiate schizophrenics from normal control subjects, and as there is little information regarding the relationship of evoked potentials to clinical variables in schizophrenia (e.g., Saletu et al. 1971; Roth and Cannon 1972; Roth et al. 1980a,b), we extended our analyses by examining the relationship between this feature and specific types of clinical symptoms in schizophrenia. We correlated the auditory event-related potential data from the same schizophrenic patients used in the replication study (see Faux et al. 1988a) with data collected concurrently from the Thought Disorder Index (TDI) (Johnston and Holzman 1979), the Scale for the Assessment of Negative Symptoms (SANS) (Andreasen 1981), the Scale for the Assessment of Positive Symptoms (SAPS) From the Department of Psychiatry, Massachusetts Mental Health Center, and Brockton VAMC, Harvard Medical School (M.S., S.F.F., R.W.McC., R.B.), Boston, MA; the Psychology Laboratory, (Mailman Research Center McLean Hospital, Harvard Medical School (M.C.), Boston, MA; Department of Psychiatry, Ohio State University (M.T.); and the Devel- opmental Neuropbysiology Laboratory, Children’s Hospital, Harvard Medical School (F.H.D.), Boston, MA. Supported in part by the Veterans Administration, NIMH 40,799, the Commonwealth of Massachusetts Research Center, and by NIMH Research Training Grant T32MH16259-04. Address reprint requests to Dr. Robert W. McCarley, Department of Psychiatry 116A, 940 Belmont Street. Brockton. MA 02401. Received December 28. 1987; revised May 31. 1988. This article 1s in the Public Domam 0006-3223/8Y/$OO.M~