Neurophysiology of Sleep-Deprivation Part 1: Effects of Sleep-Deprivation on Event-Related Potentials...

Background: Sleep deprivation is one of the major public health and performance risk factors, with documented effects on vigilance, executive function, emotional regulation, and safety-critical behaviour. This review examines how event-related potentials (ERPs)-which provide millisecond-level resolution of cognitive processing stages-can clarify which neural processes are most affected by sleep loss, from early sensory encoding to later evaluative and control-related stages. Materials and Methods: This study was conducted as a systematic review of human studies on sleep deprivation and ERPs. Eligible studies included human participants, focused primarily on acute/total sleep deprivation, and reported ERP outcomes (e.g., amplitude, latency, topography, or related event-locked EEG measures). Searches were performed in major biomedical/psychology databases using sleep deprivation and ERP terms, with additional forward/backward citation searching. Data was extracted in a structured format (participant characteristics, deprivation protocol, ERP methods, behavioural outcomes, ERP findings, and recovery/countermeasure effects). Due to substantial heterogeneity in paradigms, protocols, and ERP methods, findings were synthesised narratively rather than meta-analysed. Risk of bias was assessed with RoB 2 and ROBINS-I. Results: The search identified 854 records, of which 82 studies were included following deduplication, screening, full-text review, and citation chasing. Samples were typically small, highly selected, and dominated by healthy young adults, with frequent attrition related to prolonged wakefulness and EEG data-quality constraints. Across studies, sleep deprivation produced stage-specific and task-dependent ERP effects rather than a single uniform pattern. The most consistent findings involved mid-to-late components. These components typically showed prolonged latency and reduced amplitude. In some cases, amplitude increases were observed and interpreted as compensatory recruitment. Early sensory/pre-attentive components (e.g., P1/N1/MMN/P50) were often relatively preserved, but showed selective vulnerability, including latency slowing, reduced filtering/gating, or decreased phase locking. A recurring observation was a behaviour-ERP dissociation, where ERP abnormalities were detectable even when behavioural impairment was modest, indicating covert neural inefficiency or compensation. Recovery sleep, naps, and countermeasures (e.g., modafinil, caffeine) produced partial, component-specific recovery, with amplitude and latency often recovering at different rates. Conclusions: The evidence indicates that sleep deprivation primarily disrupts higher-order, late-stage, and temporally coordinated neural processing, while earlier sensory processing is often preserved but becomes slower and less stable. Among ERP markers, the P300/P3 family is the most robust and informative signature of sleep loss effects and recovery. ERPs are therefore a sensitive tool for detecting neural dysfunction and compensation under sleep deprivation, including changes that may precede overt behavioural decline. Future research must improve the generalisability and reproducibility of ERP findings by employing larger, more diverse samples, alongside more standardised methodological, recording, and reporting practices.