Reductions in the N1 and P2 Auditory Event-Related Potentials in First-Hospitalized and Chronic Schizophrenia

Abstract

The N1 auditory event-related potential (ERP) is reduced in chronic schizophrenia, as is the P2 to attended tones. N1 reduction may be endophenotypic for schizophrenia, being reduced in twins of schizophrenic patients and showing heritability. Results in family members, however, are equivocal, with abnormally small N1 (consistent with an endophenotype) and abnormally large N1 (inconsistent with an endophenotype) reported. P2 has been little studied in schizophrenia or family members. One crucial step in establishing endophenotypes is to rule out causal chronicity factors. We examined schizophrenia patients within 1 year of first hospitalization (most within 2 wk), chronically ill patients, and matched controls to examine N1 and P2 reductions and disease stage. Two active target detection oddball tasks were used, one with 97-dB tones against 70-dB white masking noise, the second with 97-dB tones without noise. Results from 8 samples are reported: first-hospitalized patients and matched controls and chronic patients and matched controls for the 2 tasks. N1 and P2 were measured from the standard stimuli. N1 and P2 were significantly reduced in chronic patients, as expected, and reduced in first-hospitalized patients. Because N1 and P2 are reduced even at the first hospitalization for schizophrenia, they may serve as viable electrophysiological endophenotypes for the disorder. However, deficit early in the disease is necessary but not sufficient to establish these ERPs as endophenotypes. Deficits must next be demonstrated in at least a subset of unaffected family members, a crucial criterion for an endophenotype.

Clinical high risk and first episode schizophrenia: Auditory event-related potentials

“…The data confirm findings of reduced N100 amplitude in FESZ (Salisbury et al, 2010; Foxe et al, 2011) and indicate similar deficits in CHR individuals. Although no N100 group differences to standard stimuli in an oddball paradigm in at-risk individuals were reported in other studies (Bramon et al, 2008; van Tricht et al, 2010), gating studies have shown S1 and S1-S2 N100 deficits in prodromes but not in at-risk individuals (Brockhaus-Dumke et al, 2008).…”

Early auditory processing evoked potentials (N100) show a continuum of blunting from clinical high risk to psychosis in a pediatric sample

“…Significant differences were followed by 2 × 2 Fisher’s exact tests with Bonferroni corrected p threshold for categorical variables and Student–Newman–Keuls (SNK) tests for continuous variables. Consistent with prior studies (del Re et al, 2015; Salisbury et al, 2010), a one-way ANOVA revealed no significant association between clinical group and N100 mean latency [F(2, 65) = 0.020, p = 0.980]; thus, N100 latency was not considered further.…”

Genetic Sources of Subcomponents of Event-Related Potential in the Dimension of Psychosis Analyzed From the B-SNIP Study

“…ERP component E1 (a linear combination of standard N1, P2, frontal and parietal target N1) showed overall increased loadings (less change from baseline) in SZ and PBP compared to controls reflecting deficits in early sensory processing, consistent with prior SZ (18, 20, 34) and PBP (13) studies. The primary source of N1 and P2 is the auditory cortex (35, 36) (Heschl's gyrus); we identified reduction in gray matter regions surrounding this structure.…”

“…P300 amplitude abnormalities in PBP may be proband-specific (17). Deficits in ERP subcomponents N1, P2 and N2 are found in SZ patients (18, 19) and their relatives (20). Both N1 and P2 amplitude abnormalities (13) and their endophenotypic status are less studied in PBP.…”