Neural Correlates of Burnout Syndrome Based on Electroencephalography (EEG)—A Mechanistic Review and Discussion of Burnout Syndrome Cognitive Bias Theory

Introduction: Burnout syndrome, long described as an “occupational phenomenon”, now affects 15–20% of the general workforce and more than 50% of clinicians, teachers, social-care staff and first responders. Its precise nosological standing remains disputed. We conducted a mechanistic review of electroencephalography (EEG) studies to determine whether burnout is accompanied by reproducible brain-function alterations that justify disease-level classification. Methods: Following PRISMA-adapted guidelines, two independent reviewers searched PubMed/MEDLINE, Scopus, Google Scholar, Cochrane Library and reference lists (January 1980–May 2025) using combinations of “burnout,” “EEG”, “electroencephalography” and “event-related potential.” Only English-language clinical investigations were eligible. Eighteen studies (n = 2194 participants) met the inclusion criteria. Data were synthesised across three domains: resting-state spectra/connectivity, event-related potentials (ERPs) and longitudinal change. Results: Resting EEG consistently showed (i) a 0.4–0.6 Hz slowing of individual-alpha frequency, (ii) 20–35% global alpha-power reduction and (iii) fragmentation of high-alpha (11–13 Hz) fronto-parietal coherence, with stage- and sex-dependent modulation. ERP paradigms revealed a distinctive “alarm-heavy/evaluation-poor” profile; enlarged N2 and ERN components signalled hyper-reactive conflict and error detection, whereas P3b, Pe, reward-P3 and late CNV amplitudes were attenuated by 25–50%, indicating depleted evaluative and preparatory resources. Feedback processing showed intact or heightened FRN but blunted FRP, and affective tasks demonstrated threat-biassed P3a latency shifts alongside dampened VPP/EPN to positive cues. These alterations persisted in longitudinal cohorts yet normalised after recovery, supporting trait-plus-state dynamics. The electrophysiological fingerprint differed from major depression (no frontal-alpha asymmetry, opposite connectivity pattern). Conclusions: Across paradigms, burnout exhibits a coherent neurophysiological signature comparable in magnitude to established psychiatric disorders, refuting its current classification as a non-disease. Objective EEG markers can complement symptom scales for earlier diagnosis, treatment monitoring and public-health surveillance. Recognising burnout as a clinical disorder—and funding prevention and care accordingly—is medically justified and economically imperative.