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.

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.

Psychic activity relies on the physiological processes occurring in the brain. When disruptive factors, such as alcohol consumption or hallucinogenic substances intervene, the product of nervous activity, known as the psyche, becomes disturbed, resulting in perception, thought, and behavioral disorders. The psyche can be considered a fascinating mechanism oscillating between extremes: it can be both objective and subjective; both material and ideal. Additionally, the psyche manifests itself both normally and pathologically. Regarding the ways the psyche manifests, distinct categories can be identified. Appropriate behavior exhibited by individuals defines the normal psyche, while the pathological psyche exhibits unusual behavioral disorders often deemed immoral. The term "normality" is ambiguous and encompasses several meanings:It can refer to a person's discernment in psychiatric expert evaluations for judicial purposes; It can be associated broadly with individual health; It represents physical, mental, and social well-being; Psychiatrically, it is defined by the absence of mental illness. Medico-legal psychiatric examinations play a crucial role in justice, providing data to assess the responsibility of individuals who have committed criminal acts. To promote ethical principles and lawful conduct, preventive and intervention measures must be devised for cases involving antisocial defiance and social maladaptation. The pathological psyche is characterized by biological and/or psycho-behavioral changes that cause distress, disability, or a high risk of such outcomes (according to the American Psychiatric Association, 1994).

Turner syndrome (TS), a disorder caused by the complete or partial absence of an X chromosome, exhibits significant clinical variability that cannot be fully explained by chromosomal anomalies alone. This narrative review highlights the crucial role of epigenetic mechanisms, particularly X-chromosome inactivation (XCI), in shaping the TS phenotype. The haploinsufficiency of genes that normally escape XCI is a primary driver of TS features. The specific epigenetic consequences depend on the chromosomal anomaly. In complete monosomy (45,X), the absence of escape-mediated dosage compensation genes from a second X chromosome amplifies haploinsufficiency across X-linked escape genes. Isochromosome Xq (i(Xq)) variants involve the loss of the short arm (Xp) and duplication of the long arm (Xq), creating a dual dosage imbalance with extreme XCI skewing. Carriers of i(Xq) also have a heightened risk for autoimmune disorders compared to those with 45,X TS. For ring-X chromosomes (r(X)), which are mitotically unstable, the functional status of the XIST gene is critical. If the ring is XIST-negative, it remains transcriptionally active, resulting in functional disomy and a more severe phenotype with pronounced neurodevelopmental and craniofacial features. Ultimately, the clinical heterogeneity in TS arises from a complex interplay of the specific chromosomal structure, tissue-specific mosaicism, XIST function, and variable escape from XCI, defining TS as a disorder of epigenetic and gene-regulatory imbalance. However, future research requires a better understanding of the complex mechanism of X-chromosome inactivation.

A renowned psychiatrist once remarked that “paranoid manifestations have become as prevalent as depression.” This paper examines the clinical features, progression, and medico-legal implications of paranoia, with a particular focus on its potential for violence and social risk. We analyze the mechanisms through which violence may emerge in individuals with paranoia, the behavioral patterns of violent paranoid patients, and the underlying factors predisposing them to aggressive acts. Furthermore, we address the natural course of the disorder, its age of onset, and the demographic groups most vulnerable to become paranoid.