Schizophrenia is a neuropsychiatric disorder affecting approximately 1 in 300 people worldwide. It is characterized by a range of symptoms, including positive symptoms (delusions, hallucinations, and formal thought disorganization), negative symptoms (anhedonia, alogia, avolition, asociality, and blunted affect), and cognitive impairments (impaired memory, attention, executive function, and processing speed). Current treatments, such as psychopharmacology and psychotherapy, often do not fully address these symptoms, leading to impaired everyday functionality. In recent years, there has been a growing interest in neuromodulation due to computer and engineering science making extraordinary computational advances. Those put together have reinitiated the spark in the field of neurofeedback (NF) as a means for self-regulation and neuromodulation with the potential to alleviate the daily burden of schizophrenia. We review, in a systematic way, the primary reports of electroencephalogram (EEG)-based NF as a therapeutical tool for schizophrenia. The main body of research consists mostly of case studies and case reports. The results of a few randomized controlled studies, combined with case studies/series, underscore the potential use of NF as an add-on treatment option for improving the lives of suffering individuals, being sustained by the changes in brain function and symptomatology improvement. We aim to provide important evidence of neuromodulation using NF in patients with schizophrenia, summarizing the effects and conclusions found in several clinical trials.

Transcranial direct current stimulation (tDCS) came into consideration in recent years as a promising, non-invasive form of neuromodulation for individuals suffering from mild cognitive impairment (MCI). MCI represents a transitional stage between normal cognitive aging and more severe cognitive decline, which appears in neurodegenerative diseases, such as Alzheimer’s disease. Numerous studies have shown that tDCS can have several useful effects in patients with MCI. It is believed to enhance cognitive functions, including memory and attention, potentially slowing down the progression of neurodegeneration and cognitive decline. tDCS is believed to work by modulating neuronal activity and promoting synaptic plasticity in the brain regions associated with cognition. Moreover, tDCS is generally considered safe and well-tolerated, making it an attractive option for long-term therapeutic use in MCI. However, further research is needed to determine the optimal stimulation parameters and long-term effects of tDCS in this population, as well as its potential to serve as a complementary therapy alongside other interventions for MCI. In this review, we included 16 randomized clinical trials containing patients with MCI who were treated with tDCS. We aim to provide important evidence for the cognitive enhancement using tDCS in patients with MCI, summarizing the effects and conclusions found in several clinical trials, and discuss its main mechanisms.

Pediatric acute-onset neuropsychiatric presentations occurring in the context of prior streptococcal exposure remain clinically important but diagnostically inconclusive, particularly at the interface between PANS and PANDAS. This observational cohort study examined whether serological, psychometric, and electroencephalographic findings converged within a clinically selected pediatric psychiatric sample. Children and adolescents presenting with acute-onset or abruptly worsened neuropsychiatric symptoms and a history suggestive of prior streptococcal exposure were recruited over a 12-month period through inpatient and outpatient child psychiatric services. Of 154 screened cases, 96 with analyzable baseline data were retained and stratified by ASO status. Symptom burden was quantified using the Pediatric Acute-onset Neuropsychiatric Syndrome 31-Item Symptom Rating Scale (PANS-31) and examined in relation to ASO titers, time since the last reported streptococcal infection, EEG findings, and selected developmental and clinical-history variables. Higher ASO values were strongly associated with greater PANS-31 symptom burden, whereas a shorter interval since the last reported streptococcal infection was associated with both higher ASO titers and higher symptom scores. PANS-31 showed good total-scale internal consistency and meaningful domain-level convergence with age-appropriate CSI-4 and ASI-4 domains. These findings do not support a disease-specific biomarker model, but suggest that higher antistreptococcal serology, more recent streptococcal exposure, and greater neuropsychiatric burden may cluster within a more clearly expressed clinical phenotype in a real-world psychiatric environment.

Neurofeedback (NF) is an emerging treatment for Major Depressive Disorder (MDD). NF is a training approach that enables individuals to self-regulate brain activity patterns associated with emotional and cognitive dysfunction. While interest is increasing, research results vary, and clinical implementation does not follow standardized protocols. This scoping review aimed to map and synthesize the existing peer-reviewed evidence on electroencephalography (EEG)-based neurofeedback interventions for MDD, with a focus on training protocols, neurophysiological targets, reported clinical outcomes, and methodological limitations. A systematic scoping review was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews (PRISMA-ScR) guidelines (OSF registration): https://doi.org/10.17605/OSF.IO/NQ3BW. Electronic searches were performed across Embase, PubMed, Web of Science, and ClinicalTrials.gov. Studies were included if they evaluated EEG-based neurofeedback interventions in adults with MDD and reported clinical or neurophysiological outcomes. Of 1299 records identified, 11 studies met the inclusion criteria, encompassing outcome data from 175 patients who received active EEG-NF. The studies observed a reduction in depressive symptoms following neurofeedback, most commonly using frontal alpha asymmetry protocols (k = 5). Potential improvements in cognitive performance were reported in 4 studies, particularly those incorporating upper-alpha or beta/theta modulation. Connectivity-based approaches using low-resolution electromagnetic tomography Z-score neurofeedback (low-resolution electromagnetic tomography (LORETA); k = 2) suggested possible effects on deep brain networks involved in emotional regulation, though replication remains limited. This scoping review outlines the existing evidence on EEG-based neurofeedback in major depressive disorder, highlighting the diversity of protocols, targets, and reported outcomes. While preliminary findings suggest potential clinical relevance, substantial methodological limitations and heterogeneity remain. These observations emphasize the need for more rigorous, standardized, and longitudinal research to better define the role of EEG-based neurofeedback in the treatment of MDD.

Pediatric acute-onset neuropsychiatric presentations occurring in the context of prior streptococcal exposure remain clinically important but diagnostically inconclusive, particularly at the interface between Pediatric Acute-onset Neuropsychiatric Syndrome (PANS) and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS). This cross-sectional observational study examined whether serological, psychometric, and electroencephalographic findings converged within a clinically referred pediatric psychiatric cohort at the index assessment. Children and adolescents evaluated for neuropsychiatric symptoms in the context of caregiver- or record-supported history suggestive of prior streptococcal exposure were recruited over a 12-month period through inpatient and outpatient child psychiatric services. Out of 154 screened cases, 96 with analyzable index assessment data were retained and stratified by antistreptolysin O (ASO) status. Symptom burden was quantified using the Pediatric Acute-onset Neuropsychiatric Syndrome 31-Item Symptom Rating Scale (PANS-31) which was treated primarily as a continuous dimensional outcome and examined in relation to ASO titers, time since the last reported streptococcal infection, electroencephalography (EEG) findings, and selected developmental and clinical-history variables. Higher ASO values were associated with greater PANS-31 symptom burden, whereas a shorter interval since the last reported streptococcal infection was associated with both higher ASO titers and higher symptom scores. PANS-31 showed good total scale internal consistency and meaningful domain-level convergence with age-appropriate Child Symptom Inventory-4 (CSI-4) and Adolescent Symptom Inventory-4 (ASI-4) domains. Exploratory within-cohort stratification using an operational PANS-31 threshold and alternative post hoc thresholds suggested that higher symptom burden subgroups were largely confined to the ASO-positive stratum; however, these threshold-based patterns were interpreted descriptively and not as diagnostic performance or predictive classification. These findings do not support a disease-specific biomarker model, but suggest that higher anti-streptococcal serology, more recent streptococcal exposure, and greater neuropsychiatric burden may cluster as a clinically interpretable association pattern in a selected real-world psychiatric sample.

Background/Objectives: Pediatric neuropsychiatric presentations in the context of suspected previous streptococcal exposure remain clinically heterogeneous. This study examined whether a predefined clinical–serological profile could be reconstructed within a naturalistic psychiatric cohort using interpretable supervised models and whether discrimination persisted after removing endpoint-proximal predictors. Methods: This secondary exploratory analysis included 96 children and adolescents evaluated in Romanian psychiatric inpatient and outpatient settings. The operational endpoint required PANS-31 > 36, antistreptolysin O (ASO) > 200 IU/mL, abrupt symptom onset or worsening, and a reported streptococcal episode within six months; 24 participants met all four conditions. Infection history was derived from caregiver reports and available medical documentation. Logistic Regression, Random Forest, and XGBoost were evaluated using stratified five-fold cross-validation and a 70/30 training–test split. Full-feature models included 27 predictors, whereas restricted-feature models were refitted after excluding continuous ASO, infection recency, and abrupt onset. SHAP was used to examine feature attribution. Results: Full-feature models achieved held-out ROC-AUC values of 0.909–0.961, compared with 0.630–0.792 after feature restriction. The held-out sample comprised 29 participants, including seven endpoint-positive cases. Full-feature attribution emphasized serological, temporal, and onset-related variables, whereas restricted-feature attribution shifted toward symptom-domain, age-related, and contextual variables. Conclusions: High full-feature discrimination primarily reflected internal reconstruction of the rule-defined profile rather than independent diagnostic prediction. The attenuation following feature restriction indicates substantial dependence on information related to endpoint construction. These exploratory findings do not establish streptococcal causality, disease specificity, or generalizable diagnostic performance.