Search Results (93)

(1) Background: Quantitative EEG (QEEG) offers potential for identifying objective neurophysiological biomarkers in psychiatric disorders and guiding neurofeedback interventions. This study examined whether three nonlinear QEEG metrics—Lempel–Ziv Complexity, Tsallis Entropy, and Renyi Entropy—can distinguish children with autism spectrum disorder (ASD) from typically developing (TD) peers, and assessed their relevance for neurofeedback targeting. (2) Methods: EEG recordings from 19 scalp channels were analyzed in children with ASD and TD. The three nonlinear metrics were computed for each channel. Group differences were evaluated statistically, while machine learning classifiers assessed discriminative performance. Dimensionality reduction with t-distributed Stochastic Neighbor Embedding (t-SNE) was applied to visualize clustering. (3) Results: All metrics showed significant group differences across multiple channels. Machine learning classifiers achieved >90% accuracy, demonstrating robust discriminative power. t-SNE revealed distinct ASD and TD clustering, with nonlinear separability in specific channels. Visual processing–related channels were prominent contributors to both classifier predictions and t-SNE cluster boundaries. (4) Conclusions: Nonlinear QEEG metrics, particularly from visual processing regions, differentiate ASD from TD with high accuracy and may serve as objective biomarkers for neurofeedback. Combining complexity and entropy measures with machine learning and visualization techniques offers a relevant framework for ASD diagnosis and personalized intervention planning. Full article

Mental disorders (MDs) constitute significant risk factors for self-harm and suicide. The incidence of MDs has been increasing annually, primarily due to inadequate diagnosis and intervention. Early identification and timely intervention can effectively slow the progression of MDs and enhance the quality of life. However, the high cost and complexity of in-hospital screening exacerbate the psychological burden on patients. Moreover, existing studies primarily focus on the identification of individual subcategories and lack attention to model explainability. These approaches fail to adequately address the complexity of clinical demands. Early screening of MDs using EEG signals and deep learning techniques has demonstrated simplicity and effectiveness. To this end, we constructed a Dual-Branch Network (DBN) leveraging resting-state Quantitative Electroencephalogram (QEEG) features. The DBN is designed to enable the detection of multiple categories of MDs. Firstly, a dual-branch feature extraction strategy was designed to capture multi-dimensional latent features. Further, we propose a Multi-Head Attention Mechanism (MHAM) that integrates dynamic routing. This architecture assigns greater weights to key elements and enhances information transmission efficiency. Finally, the diagnosis is derived from a fully connected layer. In addition, we incorporate SHAP analysis to facilitate feature attribution. This technique elucidates the contribution of significant features to MD detection and improves the transparency of model predictions. Experimental results demonstrate the effectiveness of DBN in detecting various MD categories. The performance of DBN surpasses that of traditional machine learning models. Ablation studies further validate the architectural soundness of DBN. The DBN effectively reduces screening complexity and demonstrates significant potential for clinical applications. Full article

This critical review synthesizes findings from quantitative electroencephalography (QEEG) to bridge the gap between systems-level neurophysiology and the underlying cellular pathology of Attention-Deficit/Hyperactivity Disorder (ADHD). As a prevalent neurodevelopmental disorder, ADHD diagnosis is challenged by symptomatic heterogeneity, creating an urgent need for objective biological indicators. Analysis of QEEG data reveals consistent neurophysiological patterns in ADHD, primarily an excess of Theta-band activity and a deficit in Beta-band activity. These findings have led to the proposal of specific biomarkers, such as the Theta/Beta Ratio (TBR), and serve as the basis for neurofeedback interventions aimed at modulating brainwave activity. While not a standalone diagnostic tool, this review posits that QEEG-based biomarkers and Neurofeedback responses are systems-level manifestations of putative cellular and synaptic dysfunctions. By outlining these robust macro-scale patterns, this work provides a conceptual framework intended to guide future molecular and cellular research into the fundamental biology of ADHD. Full article

Borderline Personality Disorder (BPD) is marked by emotional dysregulation, instability in self-image and relationships, and high impulsivity. While functional magnetic resonance imaging (fMRI) studies have provided valuable insights into the disorder’s neural correlates, electroencephalography (EEG) may capture real-time brain activity changes relevant to BPD’s rapid emotional shifts. This review summarizes findings from studies investigating resting state and task-based EEG in individuals with BPD, highlighting common neurophysiological markers and their clinical implications. A targeted literature search (1980–2025) was conducted across databases, including PubMed, Google Scholar, and Cochrane. The search terms combined “EEG” or “electroencephalography” with “borderline personality disorder” or “BPD”. Clinical trials and case reports published in English were included if they recorded and analyzed EEG activity in BPD. A total of 24 studies met the inclusion criteria. Findings indicate that individuals with BPD often show patterns consistent with chronic hyperarousal (e.g., reduced alpha power and increased slow-wave activity) and difficulties shifting between vigilance states. Studies examining frontal EEG asymmetry reported varying results—some linked left-frontal activity to heightened hostility, while others found correlations between right-frontal shifts and dissociation. Childhood trauma, mentalization deficits, and dissociative symptoms were frequently predicted or correlated with EEG anomalies, underscoring the impact of adverse experiences on neural regulation—however, substantial heterogeneity in methods, small sample sizes, and comorbid conditions limited study comparability. Overall, EEG research supports the notion of altered arousal and emotion regulation circuits in BPD. While no single EEG marker uniformly defines the disorder, patterns such as reduced alpha power, increased theta/delta activity, and shifting frontal asymmetries converge with core BPD features of emotional lability and interpersonal hypersensitivity. More extensive, standardized, and multimodal investigations are needed to establish more reliable EEG biomarkers and elucidate how early trauma and dissociation shape BPD’s neurophysiological profile. Full article

Introduction: Learning disabilities (LD) compromise academic achievement in approximately 5–10% of school-aged children, yet the neurophysiological signatures that could facilitate earlier detection or stratification remain poorly defined. Resting-state electroencephalography (rs-EEG) offers millisecond resolution and is cost-effective, but its findings have never been synthesized systematically across pediatric LD cohorts. Methods: Following a PROSPERO-registered protocol (CRD420251087821) and adhering to PRISMA 2020 guidelines, we searched PubMed, Embase, Web of Science, Scopus, and PsycINFO through 31 March 2025 for peer-reviewed studies that recorded eyes-open or eyes-closed rs-EEG using ≥ 4 scalp electrodes in children (≤18 years) formally diagnosed with LD, and compared the results with typically developing peers or normative databases. Four reviewers independently screened titles and abstracts, extracted data, and assessed the risk of bias using ROBINS-I. Results: Seventeen studies (704 children with LD; 620 controls) met the inclusion criteria. The overall risk of bias was moderate, primarily due to small clinic-based samples and inconsistent control for confounding variables. Three consistent electrophysiological patterns emerged: (i) a 20–60% increase in delta/theta power over mesial-frontal, fronto-central and left peri-Sylvian cortices, resulting in markedly elevated θ/α and θ/β ratios; (ii) blunting or anterior displacement of the posterior alpha rhythm, particularly in language-critical temporo-parietal regions; and (iii) developmentally immature connectivity, characterized by widespread slow-band hypercoherence alongside hypo-connected upper-alpha networks linking left-hemisphere language hubs to posterior sensory areas. These abnormalities were correlated with reading, writing, and IQ scores and, in two longitudinal cohorts, they partially normalized in parallel with academic improvement. Furthermore, a link between reduced posterior/overall alpha and neuroinflammation has been found. Conclusions: Rs-EEG reveals a robust yet heterogeneous electrophysiological profile of pediatric LD, supporting a hybrid model that combines maturational delay with persistent circuit-level atypicalities in some children. While current evidence suggests that rs-EEG features show promise as potential biomarkers for LD detection and subtyping, these findings remain preliminary. Definitive clinical translation will require multi-site, dense-array longitudinal studies employing harmonized pipelines, integration with MRI and genetics, and the inclusion of EEG metrics in intervention trials. Full article

Alzheimer’s disease is the most prevalent neurodegenerative disorder leading to progressive cognitive decline and functional impairment. Although advanced neuroimaging and cerebrospinal fluid biomarkers have improved early detection, their high costs, invasiveness, and limited accessibility restrict universal screening. Quantitative electroencephalography (qEEG) offers a non-invasive and cost-effective alternative for assessing neurophysiological changes associated with AD. This review critically evaluates current evidence on EEG biomarkers, including spectral, connectivity, and complexity measures, discussing their pathophysiological basis, diagnostic accuracy, and clinical utility in AD. Limitations and future perspectives, especially in developing standardized protocols and integrating machine learning techniques, are also addressed. Full article

Schizophrenia (SZ) is a complex neuropsychiatric disorder characterized by heterogeneous symptoms, relatively poor clinical outcome, and widespread disruptions in neural connectivity and oscillatory dynamics. This article attempts to review current evidence linking genomic and proteomic alterations with aberrant neural oscillations observed in SZ, including aberrations in all oscillatory frequency bands obtained via human EEG. The numerous genes discussed are mainly involved in modulating synaptic transmission, synaptic function, interneuron excitability, and excitation/inhibition balance, thereby influencing the generation and synchronization of neural oscillations at specific frequency bands (e.g., gamma frequency band) critical for different cognitive, emotional, and perceptual processes in humans. The review highlights how polygenic influences and gene–circuit interactions underlie the neural oscillatory and connectivity abnormalities central to SZ pathophysiology, providing a framework for future research on common genetic-neural function interactions and on potential therapeutic interventions targeting local and global network-level neural dysfunction in SZ patients. As will be discussed, many of these genes affecting neural oscillations in SZ also affect other neurological disorders, ranging from autism to epilepsy. In time, it is hoped that future research will show why the same genetic anomaly leads to one illness in one person and to another illness in a different person. Full article

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. Full article

Introduction: Huntington’s disease (HD) disrupts cortico-striato-thalamocortical circuits decades before clinical onset. Electroencephalography (EEG) offers millisecond temporal resolution, low cost, and broad accessibility, yet its mechanistic and biomarker potential in HD remains underexplored. We conducted a mechanistic review to synthesize half a century of EEG findings, identify reproducible electrophysiological signatures, and outline translational next steps. Methods: Two independent reviewers searched PubMed, Scopus, Google Scholar, ResearchGate, and the Cochrane Library (January 1970–April 2025) using the terms “EEG” OR “electroencephalography” AND “Huntington’s disease”. Clinical trials published in English that reported raw EEG (not ERP-only) in human HD gene carriers were eligible. Abstract/title screening, full-text appraisal, and cross-reference mining yielded 22 studies (~700 HD recordings, ~600 controls). We extracted sample characteristics, acquisition protocols, spectral/connectivity metrics, and neuroclinical correlations. Results: Across diverse platforms, a consistent spectral trajectory emerged: (i) presymptomatic carriers show a focal 7–9 Hz (low-alpha) power loss that scales with CAG repeat length; (ii) early-manifest patients exhibit widespread alpha attenuation, delta–theta excess, and a flattened anterior-posterior gradient; (iii) advanced disease is characterized by global slow-wave dominance and low-voltage tracings. Source-resolved studies reveal early alpha hypocoherence and progressive delta/high-beta hypersynchrony, microstate shifts (A/B ↑, C/D ↓), and rising omega complexity. These electrophysiological changes correlate with motor burden, cognitive slowing, sleep fragmentation, and neurovascular uncoupling, and achieve 80–90% diagnostic accuracy in shallow machine-learning pipelines. Conclusions: EEG offers a coherent, stage-sensitive window on HD pathophysiology—from early thalamocortical disinhibition to late network fragmentation—and fulfills key biomarker criteria. Translation now depends on large, longitudinal, multi-center cohorts with harmonized high-density protocols, rigorous artifact control, and linkage to clinical milestones. Such infrastructure will enable the qualification of alpha-band restoration, delta-band hypersynchrony, and neurovascular coupling as pharmacodynamic readouts, fostering precision monitoring and network-targeted therapy in Huntington’s disease. Full article

Introduction: Substance use disorders (SUDs) pose a significant public health challenge, with current treatments often exhibiting limited effectiveness and high relapse rates. Transcranial direct current stimulation (tDCS), a noninvasive neuromodulation technique that delivers low-intensity direct current via scalp electrodes, has shown promise in various psychiatric and neurological conditions. In SUDs, tDCS may help to modulate key neurocircuits involved in craving, executive control, and reward processing, potentially mitigating compulsive drug use. However, the precise neurobiological mechanisms by which tDCS exerts its therapeutic effects in SUDs remain only partly understood. This review addresses that gap by synthesizing evidence from clinical studies that used neuroimaging (fMRI, fNIRS, EEG) and blood-based biomarkers to elucidate tDCS’s mechanisms in treating SUDs. Methods: A targeted literature search identified articles published between 2008 and 2024 investigating tDCS interventions in alcohol, nicotine, opioid, and stimulant use disorders, focusing specifically on physiological and neurobiological assessments rather than purely behavioral outcomes. Studies were included if they employed either neuroimaging (fMRI, fNIRS, EEG) or blood tests (neurotrophic and neuroinflammatory markers) to investigate changes induced by single- or multi-session tDCS. Two reviewers screened titles/abstracts, conducted full-text assessments, and extracted key data on participant characteristics, tDCS protocols, neurobiological measures, and clinical outcomes. Results: Twenty-seven studies met the inclusion criteria. Across fMRI studies, tDCS—especially targeting the dorsolateral prefrontal cortex—consistently modulated large-scale network activity and connectivity in the default mode, salience, and executive control networks. Many of these changes correlated with subjective craving, attentional bias, or extended time to relapse. EEG-based investigations found that tDCS can alter event-related potentials (e.g., P3, N2, LPP) linked to inhibitory control and salience processing, often preceding or accompanying changes in craving. One fNIRS study revealed enhanced connectivity in prefrontal regions under active tDCS. At the same time, two blood-based investigations reported the partial normalization of neurotrophic (BDNF) and proinflammatory markers (TNF-α, IL-6) in participants receiving tDCS. Multi-session protocols were more apt to drive clinically meaningful neuroplastic changes than single-session interventions. Conclusions: Although significant questions remain regarding optimal stimulation parameters, sample heterogeneity, and the translation of acute neural shifts into lasting behavioral benefits, this research confirms that tDCS can induce detectable neurobiological effects in SUD populations. By reshaping activity across prefrontal and reward-related circuits, modulating electrophysiological indices, and altering relevant biomarkers, tDCS holds promise as a viable, mechanism-based adjunctive therapy for SUDs. Rigorous, large-scale studies with longer follow-up durations and attention to individual differences will be essential to establish how best to harness these neuromodulatory effects for durable clinical outcomes. Full article

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. Full article

Background/Objectives: Gamma oscillations (30–100 Hz), which are essential for memory, attention, and cortical synchronization, remain underexplored in Alzheimer’s disease (AD) research. While resting-state EEG studies have predominantly examined lower frequency bands (delta to beta), gamma activity may more accurately reflect early synaptic dysfunction and other mechanisms relevant to AD pathophysiology. AD is a common age-related neurodegenerative disorder frequently associated with altered resting-state EEG (rEEG) patterns. This study analyzed gamma power spectral density (PSD) during eyes-open (EOR) and eyes-closed (ECR) resting-state EEG in AD patients compared to cognitively normal (CN) individuals. Methods: rEEG data from 534 participants (269 CN, 265 AD) aged 40–90 were analyzed. Quantitative EEG (qEEG) analysis focused on the gamma band (30–100 Hz) using PSD estimation with the Welch method, coherence matrices, and coherence-based functional connectivity. Data preprocessing and analysis were performed using EEGLAB and Brainstorm in MATLAB R2024b. Group comparisons were conducted using ANOVA for unadjusted models and linear regression with age adjustment using log₁₀-transformed PSD values in Python (version 3.13.2, 2025). Results: AD patients exhibited significantly elevated gamma PSD in frontal and temporal regions during EOR and ECR states compared to CN. During ECR, gamma PSD was markedly higher in the AD group (Mean = 0.0860 ± 0.0590) than CN (Mean = 0.0042 ± 0.0010), with a large effect size (Cohen’s d = 1.960, p < 0.001). Conversely, after adjusting for age, the group difference was no longer statistically significant (β = −0.0047, SE = 0.0054, p = 0.391), while age remained a significant predictor of gamma power (β = −0.0008, p = 0.019). Pairwise coherence matrix and coherence-based functional connectivity were increased in AD during ECR but decreased in EOR relative to CN. Conclusions: Gamma oscillatory activity in the 30–100 Hz range differed significantly between AD and CN individuals during resting-state EEG, particularly under ECR conditions. However, age-adjusted analyses revealed that these differences are not AD-specific, suggesting that gamma band changes may reflect aging-related processes more than disease effects. These findings contribute to the evolving understanding of gamma dynamics in dementia and support further investigation of gamma PSD as a potential, age-sensitive biomarker. Full article

Biomarkers currently used to diagnose dementia, including Alzheimer’s disease (AD), primarily detect molecular and structural brain changes associated with the condition’s pathology. Although these markers are pivotal in detecting disease-specific neuropathological hallmarks, their association with the clinical manifestations of dementia frequently remains poorly defined and exhibits considerable variability. These biomarkers may show abnormalities in cognitively healthy individuals and frequently fail to accurately represent the severity of cognitive and functional impairments in individuals with dementia. Research indicates that synaptic degeneration and functional impairment occur early in the progression of AD and exhibit the strongest correlation with clinical symptoms. This identifies brain functional impairment measurements as promising early indicators for AD detection. Electroencephalography (EEG), a non-invasive and cost-effective method with high temporal resolution, is used as a biomarker for the early detection and diagnosis of AD through frequency-domain analysis of quantitative EEG (qEEG). Many researchers demonstrate that qEEG measures effectively identify disruptions in neuronal activity, including alterations in activity patterns, topographical distribution, and synchronization. Specific findings along the stages of AD include impaired neuronal synchronization, generalized EEG slowing, and an increase in lower-frequency bands accompanied by a decrease in higher-frequency bands of resting state EEG. Moreover, qEEG helps clinicians effectively correlate indicators of AD neuropathology and distinguish between various forms of dementia, positioning it as a promising, low-cost, non-invasive biomarker for dementia. However, additional clinical investigation is required to clarify the diagnostic and prognostic significance of qEEG measurements as early functional markers for AD. This narrative review examines time-frequency domain qEEG analysis as a potential biomarker across various types of dementia. Through a structured search of PubMed and Scopus, we identified studies assessing spectral and connectivity-based qEEG features. Consistent findings include EEG slowing, reduced functional connectivity, and network desynchronization. The review outlines key methodological challenges, such as lack of standardization and limited longitudinal validation, and recommends integrative, multimodal approaches to enhance diagnostic precision and clinical applicability. Full article

Quantitative electroencephalography (QEEG) has emerged as a promising tool for detecting Alzheimer’s disease (AD). Among QEEG measures, Multiscale Fuzzy Entropy (MFE) shows great potential in identifying AD-related changes in EEG complexity. However, MFE is intrinsically linked to signal amplitude, which can vary substantially among EEG systems, and this hinders the adoption of this metric for AD detection. To overcome this issue, this study investigates different preprocessing strategies to make the calculation of MFE less dependent on the specific amplitude characteristics of the EEG signals at hand. This contributes to generalizing and making more robust the adoption of MFE for AD detection. To demonstrate the robustness of the proposed preprocessing methods, binary classification tasks with Support Vector Machines (SVMs), Random Forest (RF), and K-Nearest Neighbor (KNN) classifiers are used. Performance metrics, such as classification accuracy and Matthews Correlation Coefficient (MCC), are employed to assess the results. The methodology is validated on two public EEG datasets. Results show that amplitude transformation, particularly normalization, significantly enhances AD detection, achieving mean classification accuracy values exceeding 80% with an uncertainty of 10% across all classifiers. These results highlight the importance of preprocessing in improving the accuracy and the reliability of EEG-based AD diagnostic tools, offering potential advancements in patient management and treatment planning. Full article

Introduction: Combat sport athletes are exposed to repetitive head impacts yet also develop distinct performance-related brain adaptations. Electroencephalography (EEG) provides millisecond-level insight into both processes; however, findings are dispersed across decades of heterogeneous studies. This mechanistic review consolidates and interprets EEG evidence to elucidate how participation in combat sports shapes brain function and to identify research gaps that impede clinical translation. Methods: A structured search was conducted in March 2025 across PubMed/MEDLINE, Scopus, Cochrane Library, ResearchGate, Google Scholar, and related databases for English-language clinical studies published between January 1980 and March 2025. Eligible studies recorded raw resting or task-related EEG in athletes engaged in boxing, wrestling, judo, karate, taekwondo, kickboxing, or mixed martial arts. Titles, abstracts, and full texts were independently screened by two reviewers. Twenty-three studies, encompassing approximately 650 combat sport athletes and 430 controls, met the inclusion criteria and were included in the qualitative synthesis. Results: Early visual EEG and perfusion studies linked prolonged competitive exposure in professional boxers to focal hypoperfusion and low-frequency slowing. More recent quantitative studies refined these findings: across boxing, wrestling, and kickboxing cohorts, chronic participation was associated with reduced alpha and theta power, excess slow-wave activity, and disrupted small-world network topology—alterations that often preceded cognitive or structural impairments. In contrast, elite athletes in karate, fencing, and kickboxing consistently demonstrated neural efficiency patterns, including elevated resting alpha power, reduced task-related event-related desynchronization (ERD), and streamlined cortico-muscular coupling during cognitive and motor tasks. Acute bouts elicited transient increases in frontal–occipital delta and high beta power proportional to head impact count and cortisol elevation, while brief judo chokes triggered short-lived slow-wave bursts without lasting dysfunction. Methodological heterogeneity—including variations in channel count (1 to 64), reference schemes, and frequency band definitions—limited cross-study comparability. Conclusions: EEG effectively captures both the adverse effects of repetitive head trauma and the cortical adaptations associated with high-level combat sport training, underscoring its potential as a rapid, portable tool for brain monitoring. Standardizing acquisition protocols, integrating EEG into longitudinal multimodal studies, and establishing sex- and age-specific normative data are essential for translating these insights into practical applications in concussion management, performance monitoring, and regulatory policy. Full article