Self-referential Processing in Remitted Depression: An Event-Related Potential Study

BACKGROUND: Identifying mechanisms of major depressive disorder that continue into remission is critical, as these mechanisms may contribute to subsequent depressive episodes. Biobehavioral markers related to depressogenic self-referential processing biases have been identified in adults with depression. Thus, we investigated whether these risk factors persisted during remission as well as contributed to the occurrence of stress and depressive symptoms over time. METHODS: At baseline, adults with remitted depression (n = 33) and healthy control subjects (n = 33) were administered diagnostic and stress interviews as well as self-report symptom measures. In addition, participants completed a self-referential encoding task while electroencephalography data were acquired. Stress interviews and self-report symptom measures were readministered at the 6-month follow-up assessment. RESULTS: Drift diffusion modeling showed that compared with healthy individuals, adults with remitted depression exhibited a slower drift rate to negative stimuli, indicating a slower tendency to reject negative stimuli as self-relevant. At the 6-month follow-up assessment, a slower drift rate to negative stimuli predicted greater interpersonal stress severity among individuals with remitted depression but not healthy individuals while controlling for both baseline depression symptoms and interpersonal stress severity. Highlighting the specificity of this effect, results were nonsignificant when predicting noninterpersonal stress. For self-relevant positive words endorsed, adults with remitted depression exhibited smaller left- than right-hemisphere late positive potential amplitudes; healthy control subjects did not show hemispheric differences. CONCLUSIONS: Self-referential processing deficits persist into remission. In line with the stress generation framework, these biases predicted the occurrence of interpersonal stress, which may provide insight about a potential pathway for the re-emergence of depressive symptoms.