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.

Introduction: Depression is the most prevalent comorbid neuropsychiatric condition in individuals with Parkinson’s disease (PD), and its underlying mechanisms are not yet fully understood. Current treatment methods are characterised by moderate effectiveness and possible side effects, prompting the search for new non-invasive and safe treatment methods. Methods: This narrative review explores the use of transcranial direct current stimulation (tDCS) in the treatment of depression in PD, based on neuropsychological measures. Searches were conducted in the PubMed/Medline, Research Gate, and Cochrane databases. Results: Nine relevant studies were identified, where depression scores served as either primary or secondary outcomes. Stimulation protocols displayed heterogeneity, especially concerning choice of stimulation site. Patient samples were also heterogeneous. The majority of the studies incorporated anodal stimulation targeting the left dorsolateral prefrontal cortex (DLPFC). The results revealed a reduction in depression scores among PD patients following tDCS. Potential mechanisms through which tDCS may alleviate depression in PD were discussed and recommendations for future research were made. Conclusions: Preliminary evidence suggests that tDCS applied anodally to the left DLPFC reduces depression scores in people with PD; however, due to the heterogeneity of the studies analysed, the use of tDCS in this field should be approached with caution and warrants further validation and confirmation.

Introduction: Binge eating disorder (BED) is the most common eating disorder among those contributing to the development of obesity, and thus acts as a significant burden on the lives and health of patients. It is characterized by complex neurobiology, which includes changes in brain activity and neurotransmitter secretion. Existing treatments are moderately effective, and so the search for new therapies that are effective and safe is ongoing. Aim and Methods: This review examines the use of transcranial direct current stimulation (tDCS) in the treatment of binge eating disorder. Searches were conducted on the PubMed/Medline, Research Gate, and Cochrane databases. Results: Six studies were found that matched the review topic. All of them used the anodal stimulation of the right dorsolateral prefrontal cortex (DLPFC) in BED patients. tDCS proved effective in reducing food cravings, the desire to binge eat, the number of binging episodes, and food intake. It also improved the outcomes of inhibitory control and the treatment of eating disorder psychopathology. The potential mechanisms of action of tDCS in BED are explained, limitations in current research are outlined, and recommendations for future research are provided. Conclusions: Preliminary evidence suggests that the anodal application of tDCS to the right DLPFC reduces the symptoms of BED. However, caution should be exercised in the broader use of tDCS in this context due to the small number of studies performed and the small number of patients included. Future studies should incorporate neuroimaging and neurophysiological measurements to elucidate the potential mechanisms of action of tDCS in BED.

Occupational burnout is ubiquitous yet still debated as a disease entity. Previous reviews surveyed multiple biomarkers but left their neural substrate unclear. We therefore asked: What, if any, reproducible magnetic-resonance signature characterises burnout? Following PRISMA principles adapted for mechanistic synthesis, two reviewers searched PubMed, Scopus, Google Scholar, ResearchGate and Cochrane from January 2000 to May 2025 using “MRI/fMRI” AND “burnout”. After duplicate removal and multi-stage screening, 17 clinical studies met predefined inclusion criteria (English language, MRI outcomes, validated burnout diagnosis). In total, ≈1365 participants were scanned, 880 with clinically significant burnout and 470 controls. Uniform Maslach Burnout Inventory thresholds defined cases; most studies matched age and sex, and all excluded primary neurological disease. Structural morphometry (8/17 studies) revealed consistent amygdala enlargement—predominantly in women—and grey-matter loss in dorsolateral/ventromedial prefrontal cortex and striatal caudate–putamen, while hippocampal volume remained unaffected, distinguishing burnout from PTSD or depression. Resting-state and task fMRI (9/17 studies) showed fronto-cortical hyper-activation, weakened amygdala–ACC coupling, and progressive fragmentation of rich-club networks, collectively indicating compensatory executive overdrive and global inefficiency. Two longitudinal cohorts and several intervention sub-studies demonstrated partial reversal of cortical thinning and limbic hyper-reactivity after mindfulness, exercise, cognitive-behavioural therapy, neurofeedback, or rTMS, underscoring plasticity. Across heterogeneous paradigms and populations, MRI converges on a coherent, sex-modulated but reversible brain-networkopathy that satisfies objective disease criteria. These findings justify early neuro-imaging-based triage, circuit-targeted therapy, and formal nosological recognition of burnout as a mental disorder, with policy ramifications for occupational health and insurance parity.

Introduction: Chewing gum is a widespread, seemingly mundane behaviour that has been linked to diverse benefits such as improved cognitive performance, reduced stress, and enhanced alertness. While animal and human research indicate that mastication engages extensive sensorimotor networks and may also modulate higher-order cognitive and emotional processes, questions remain about the specific neural mechanisms involved. This review combines findings from neuroimaging studies—including fMRI, fNIRS, and EEG—that investigate how chewing gum alters brain activity in humans. Methods: Using a targeted search strategy, we screened the major databases (PubMed/Medline, Scopus, ResearchGate, Google Scholar, and Cochrane) from January 1980 to March 2025 for clinical studies published in English. Eligible studies explicitly measured brain activity during gum chewing using EEG, fNIRS, or fMRI. Results: After a title/abstract screening and a full-text review, thirty-two studies met the inclusion criteria for this review: 15 utilising fMRI, 10 using fNIRS, 2 using both fNIRS and EEG, and 5 employing EEG. Overall, the fMRI investigations consistently reported strong activation in bilateral motor and somatosensory cortices, the supplementary motor area, the insula, the cerebellum, and the thalamus, during gum chewing, with several studies also noting involvement of higher-order prefrontal and cingulate regions, particularly under stress conditions or when participants chewed flavoured gum. The fNIRS findings indicated that chewing gum increased oxygenated haemoglobin in the prefrontal cortex, reflecting heightened cortical blood flow; these effects were often amplified when the gum was flavoured or when participants were exposed to stressful stimuli, suggesting that both sensory and emotional variables can influence chewing-related cortical responses. Finally, the EEG studies documented transient increases in alpha and beta wave power during gum chewing, particularly when flavoured gum was used, and reported short-lived enhancements in vigilance or alertness, which tended to subside soon after participants ceased chewing. Conclusions: Neuroimaging data indicate that chewing gum reliably engages broad sensorimotor circuits while also influencing regions tied to attention, stress regulation, and possibly memory. Although these effects are often short-lived, the range of outcomes—from changes in cortical oxygenation to shifts in EEG power—underscores chewing gum’s capacity to modulate brain function beyond simple oral motor control. However, at this time, the neural changes associated with gum chewing cannot be directly linked to the positive behavioural and functional outcomes observed in studies that measure these effects without the use of neuroimaging techniques. Future research should address longer-term impacts, refine methods to isolate flavour or stress variables, and explore potential therapeutic applications for mastication-based interventions.

Transcranial direct current stimulation (tDCS) can modulate cortical excitability in a polarity-specific manner, yet identical protocols often produce inconsistent outcomes across sessions or individuals. This narrative review proposes that much of this variability arises from the brain’s intrinsic temporal landscape. Integrating evidence from chronobiology, sleep research, and non-invasive brain stimulation, we argue that tDCS produces reliable, polarity-specific after-effects only within a circadian–homeostatic “window of efficacy”. On the circadian (Process C) axis, intrinsic alertness, membrane depolarisation, and glutamatergic gain rise in the late biological morning and early evening, whereas pre-dawn phases are marked by reduced excitability and heightened inhibition. On the homeostatic (Process S) axis, consolidated sleep renormalises synaptic weights, widening the capacity for further potentiation, whereas prolonged wakefulness saturates plasticity and can even reverse the usual anodal/cathodal polarity rules. Human stimulation studies mirror this two-process fingerprint: sleep deprivation abolishes anodal long-term-potentiation-like effects and converts cathodal inhibition into facilitation, while stimulating at each participant’s chronotype-aligned (phase-aligned) peak time amplifies and prolongs after-effects even under equal sleep pressure. From these observations we derive practical recommendations: (i) schedule excitatory tDCS after restorative sleep and near the individual wake-maintenance zone; (ii) avoid sessions at high sleep pressure or circadian troughs; (iii) log melatonin phase, chronotype, recent sleep and, where feasible, core temperature; and (iv) consider mild pre-heating or time-restricted feeding as physiological primers. By viewing Borbély’s two-process model and allied metabolic clocks as adjustable knobs for plasticity engineering, this review provides a conceptual scaffold for personalised, time-sensitive tDCS protocols that could improve reproducibility in research and therapeutic gain in the clinic.