Posttraumatic stress disorder (PTSD) poses a major mental health threat in the Middle East, where people experience ongoing conflict, displacement, and trauma. This study summarizes the use of computational and data-driven approaches, including machine learning (ML), biomarker identification, network analysis, and factor analysis, to understand, diagnose, and treat PTSD in the Middle East. A detailed search of the Scopus database led to the inclusion of only relevant original/research studies that met strict inclusion criteria for human subjects, geographical focus, and use of computational approaches. Studies have suggested that computational models can predict PTSD onset, biomarkers from biology and neuroimaging, complex symptoms, and comorbidity networks. They enable the development of precision psychiatry and culturally adapted diagnostic measures for conflict-affected displaced population samples. The relevance of multimodal pre-trauma screening, as well as the importance of consistent biological markers (inflammation, gene expression), is underscored by a comparative analysis of predictive models (AUCs of 0.73-0.92). Nonetheless, the cross-cultural validity of PTSD symptoms and the presence of computer resources in the region remain concerning. This article describes the revolutionary potential of computational psychiatry for improving mental health research and practice in the Middle East. It emphasizes the importance of culture-sensitive, scalable application with respect to resources.
This narrative literature review aims to examine and hypothesize about the neurobiological effects of the Tesla Functional Magnetic Stimulation (FMS) chair through a comprehensive search of PubMed, Google Scholar, Scopus, Web of Science, and arXiv databases. A critical finding emerged: published research specifically investigating the Tesla FMS chair and its neurobiological mechanisms is extremely limited. Among the papers identified and ranked by relevance, only one study directly examined a Tesla-branded FMS chair system, which investigated a 3 Tesla electromagnetic chair for treating female urinary incontinence. The vast majority of the retrieved literature pertains to transcranial magnetic stimulation (TMS), a distinct neuromodulation technique that targets cortical brain regions rather than peripheral nervous system structures. This review also provides a detailed analysis of the available evidence on general FMS technology, contextualizes findings within the broader magnetic stimulation literature, and identifies critical gaps requiring future investigation. The limited evidence suggests FMS chairs operate through peripheral nerve depolarization and sacral neuromodulation, but comprehensive neurobiological characterization is lacking the published literature and requires more high-quality studies. This review should be interpreted as a hypothesis-generating narrative synthesis rather than as a definitive mechanistic or efficacy assessment. The comparison with TMS is used only as a conceptual framework. At the same time, the specific mechanisms of chair-based FMS remain to be directly demonstrated through dedicated peripheral, spinal, and supraspinal investigations.
Post-stroke ambulation demands significant cognitive regulation, particularly in complex environments that require concurrent motor and cognitive processing. Challenges in the coordination between cognitive functions and motor skills lead to reduced adaptability in walking, an increased fall risk, and limitations in moving around the community among stroke survivors. To integrate recent evidence on dual-task gait training post-stroke, with particular focus on the neurological mechanisms underlying cognitive-motor interference and their relationship to functional walking outcomes. A structured literature search was conducted using PubMed and Scopus to identify studies published between January 2015 and December 2025. Medical Subject Headings (MeSH) and related keywords on dual-task walking training, cognitive-motor interference (CMI), and stroke rehabilitation were used to retrieve relevant evidence. The review focused on the neurological mechanisms underlying gait coordination and the effects of dual-task interventions on walking performance in stroke survivors. The Scale guided the methodological rigor of the narrative review for the Assessment of Narrative Review Articles (SANRA). The examined studies indicated that participation in dual-task gait training was positively correlated with enhancements in walking speed, stride parameters, stability, and overall walking performance, even under cognitive load. Neuroimaging and neurophysiological investigations consistently reported increased recruitment of prefrontal and premotor-supplementary motor networks during dual-task walking, reflecting compensatory cortical recruitment and diminished gait automaticity post-stroke. Training-related modifications in cortical activation patterns imply enhanced neural efficiency and adaptive reorganization of cognitive-motor control networks. The use of dual-task gait training is considered a neurologically validated strategy to diminish the cognitive-motor obstacles that occur after stroke. By focusing on executive control and cortical network activation during ambulation, dual-task paradigms may facilitate functional gait recovery across the stroke phases/Further investigation integrating neurophysiological measures with clinical outcomes is warranted.
This review explores the integration of cognitive neuroscience principles into communication education, focusing on how neuroscience-informed curricular designs enhance skill acquisition and transfer. A comprehensive literature search was conducted across primary scientific databases, including PubMed, Scopus, Web of Science, and ERIC, to identify relevant studies published between 2014 and 2025. Following a multi-stage screening process based on predefined inclusion and exclusion criteria, 15 peer-reviewed scientific articles were selected for qualitative analysis. Advances in cognitive neuroscience illuminate the brain mechanisms supporting communication and learning. These insights enable educators to develop interventions such as working memory training, neurofeedback, and virtual reality simulations. Theoretical frameworks like Cognitive Load Theory and Social-Cognitive Neuroscience effectively guide curriculum design. However, despite reported cognitive improvements, evidence linking these neurological gains to real-world communication outcomes remains limited. This study underscores the importance of interdisciplinary approaches combining neuroscience, education, psychology, and technology. By embracing brain-based evidence, educators can manage cognitive load and deepen skill mastery, ultimately improving communication effectiveness across diverse contexts.
Death Education is an emerging field aimed at developing psychological and social competencies for engaging with death and dying. This qualitative study explored the experiences of 17 professionals—including psychologists, teachers, and spiritual counselors—implementing Death Education interventions in schools. Semi-structured interviews were analyzed thematically, revealing four key domains: (1) facilitators’ personal relationship with death and motivation; (2) children’s and adolescents’ representations of death; (3) perceived benefits and cultural or institutional resistance; and (4) essential elements for effective Death Education. Spirituality emerged as a central factor in fostering open, meaningful, and culturally sensitive discussions. Findings suggest that Death Education can support young people’s mental health by helping them process grief and engage with the reality of human finitude. However, cultural and familial resistance, along with limited teacher training, impede widespread implementation. Overall, the study underscores Death Education’s potential to enhance resilience and psychological well-being during developmental years.
Stress is a multifaceted response involving physiological, psychological, and behavioural processes, with neurotransmitters such as serotonin, dopamine, and norepinephrine playing key modulatory roles. This study aimed to map global research trends on stress and neurotransmitters, identify thematic clusters, and highlight emerging frontiers relevant to health and disease. A bibliometric analysis was conducted on 4,132 publications indexed in Scopus between 2000 and 2023. Data were retrieved and processed using Excel and Harzing’s Publish or Perish, and analyzed with VOSviewer to generate co-authorship, co-occurrence, and citation network visualizations. Publications on stress and neurotransmitters have shown a consistent upward trend over the past two decades. The United States, China, and Japan emerged as the leading contributors. Core keywords included stress, neurotransmitters, serotonin, dopamine, glutamate, depression, anxiety, and oxidative stress. Emerging terms such as antioxidants, neuroprotection, inflammation, BDNF, GABA, acetylcholinesterase, metabolism, and gene expression indicate growing interest in neurochemical pathways and their role in mental and neurodegenerative disorders. The network analysis revealed strong global collaboration and multidisciplinary research across neuroscience, psychology, and molecular biology. This study provides the first comprehensive bibliometric mapping of global research on the links between stress and neurotransmitters. By highlighting established themes and emerging areas such as BDNF-related signaling and metabolic-neurochemical interactions, the findings contribute to a deeper understanding of stress modulation mechanisms. These insights may guide future translational research and inform the development of targeted strategies for managing stress-related physical and mental health disorders.
Patients with severe neurological sequelae often experience profound motor deconditioning that, combined with impaired mucociliary clearance, reduced lung volume, and the presence of tracheostomy, predisposes them to pulmonary infections and serious respiratory complications. A 24-year-old male with spastic quadriplegia secondary to childhood cerebral hemorrhage from an arteriovenous malformation, tracheostomy with a cuffed cannula under mechanical ventilation, and hydrocephalus treated with a ventriculoperitoneal shunt, presented to the emergency department with fever unresponsive to paracetamol and ceftriaxone. Laboratory tests showed markedly elevated inflammatory indices (C-reactive protein 249.3 mg/dl), and chest computed tomography revealed extensive consolidation of the left lower lobe with an air bronchogram and endobronchial obstruction, consistent with aspiration pneumonia. Fibrobronchoscopy confirmed the presence of endobronchial material, and culture grew Acinetobacter baumannii. Given the patient’s clinical and functional status, the physiatrists prescribed an Individual Rehabilitation Project (motor and respiratory re-educational programs, including passive mobilization of major joints, cautious trunk stabilization, and lung volume recruitment maneuvers) to support the effects of positive-pressure ventilation. The case underscores the dual challenge of neurological impairment and pulmonary vulnerability, where immobilization further exacerbates respiratory compromise and infection risk, fostering sarcopenia and poor quality of life. In patients with spastic quadriplegia of cerebrovascular origin on long-term mechanical ventilation, a synergistic approach combining NIV optimization and individualized motor-respiratory rehabilitation may represent an effective strategy to control recurrent infections and maintain clinical stability. In this area, there is currently insufficient evidence, and urgent future research is needed.
Research has demonstrated the significant role of epidermal growth factor (EGF) in synaptic plasticity and the pathogenesis of Autism spectrum disorder (ASD). This study aimed to assess the correlation between EGF +61A/G (rs4444903) polymorphism and its serum level with ASD. Blood samples were collected from 200 ASD and 200 controls for DNA extraction, and genotyping was carried out using Restriction Fragment Length Polymorphism (RFLP). Additionally, EGF serum concentration was determined using enzyme-linked immunosorbent assay (ELISA). In ASD, the frequencies of GG, AG, and AA genotypes were 15%, 41%, and 44%, respectively, while in controls, they were 5%, 30%, and 65%. The genotypes of rs4444903 demonstrated an influential contribution to the susceptibility to ASD under co-dominant (GG versus AA), recessive (GG versus AA+AG), and dominant (AG+GG versus AA) models. Additionally, the frequencies of A and G alleles were 68.8% and 31.2% in ASD, and 79.8% and 20.2% in controls, respectively (P < 0.0001). Furthermore, the G allele was found to be associated with an increased risk of ASD (P = 0.0001). Notably, the EGF concentration in the serum samples of the ASD group was lower than in controls (792.65 ± 178.19 and 1265 ± 213.32 pg/ml, respectively; P = 0.0001). In ASD patients, the GG genotype is connected to lower serum EGF levels. The serum concentrations for carriers of GG, AG, and AA were measured at 515 ± 109.63, 716.22 ± 102.26, and 886.11 ± 119.69 pg/ml, respectively. The results of this project suggest that there may be a relationship between the EGF +61A/G (rs4444903) polymorphism and its serum levels with the risk of ASD. Furthermore, the GG genotype seems to be linked to decreased EGF expression in individuals with ASD.
This narrative review explores the pathophysiological consequences, neuroendocrine processes, and treatment approaches aimed at reducing the cardiometabolic adverse effects linked to antipsychotic medications; in particular, it highlights recent mechanistic advances in receptor-mediated metabolic dysregulation and emerging therapeutic implications. Schizophrenia, which is a long-term and debilitating disorder, correlates with a substantially shorter life expectancy (15-20 years less than that of the general populace) and elevated all-cause mortality rates. This underscores that psychotic disorders are systemic illnesses involving various physiological systems. Antipsychotics play a crucial role in the treatment of schizophrenia; however, their use can lead to serious side effects, including cardiometabolic dysfunction and metabolic syndrome (MetS). These complications elevate the risk of obesity, diabetes, and dyslipidemia. The underlying mechanisms contributing to these side effects are complex and multifaceted, involving interactions with various receptors, such as D2, H1, M3, and 5-HT2C, as well as influences from gut microbiota, neurohormonal pathways, and genetic predispositions. Furthermore, individual patient characteristics—including lifestyle choices and genetic factors—interact with specific medications, resulting in varied metabolic responses. Weight gain is a common concern for patients receiving treatment, often intensified by unhealthy lifestyle habits that frequently accompany schizophrenia. This rise in weight can adversely affect quality of life, increase the risk of premature mortality, and impede treatment adherence. This article discusses the importance of consistent clinical monitoring, comprehensive patient evaluations, and tailored interventions to effectively balance the therapeutic benefits of antipsychotics with the necessity of managing metabolic risks. It examines both pharmacological and non-pharmacological strategies to improve treatment tolerability and mitigate cardiometabolic complications for individuals with psychotic disorders.
Autism is a neurodevelopmental disorder characterized by persistent challenges in social interactions and repetitive behaviors. This study aimed to investigate the prevalence of autism and autism spectrum disorder(ASD) in normal and abnormal groups, such as premature infants or seizure patients, using an umbrella review and meta-analysis. This study was conducted in accordance with the PRISMA guidelines. Scientific sources included PubMed, Scopus, Web of Science, and Google Scholar, and searches were conducted without time limits until the end of September 2024. Meta-analysis was performed using a random-effects model and heterogeneity using an I2 index. Of the 799 articles identified, 30 were included in the meta-analysis. The prevalence of autism was 15.8 per 10,000 (CI = 10.5-21.0, P < 0.001) in normal samples and 600 per 10,000 (CI = 412-793, P = 0.77) in abnormal samples. The overall prevalence of autism was 18.1 per 10,000 (CI = 10.9-25.4, P < 0.001). The prevalence of ASD in normal samples was 48.9 per 10,000 (CI = 31.6-66.1, P < 0.001) and in abnormal samples 900 per 10,000 (CI = 680-1121, P < 0.001). The overall prevalence of ASD was estimated to be 153 per 10,000 (CI = 125-180, P < 0.001). Given the prevalence of ASD and its link to environmental and genetic factors, increased public awareness and better diagnostic tools are needed. In addition, timely and accurate screening is recommended to prevent delays in diagnosis and treatment.
The study aimed to compare the effects of neurobic and aerobic approaches in Dementia care. Dementia is a progressive brain disorder that leads to a decline in cognitive abilities, including thinking, reasoning, and memory. In India, it is estimated that 74% of adults aged 60 and older are affected, totaling around 8.8 million individuals. Neurobics refers to exercises designed to enhance oxygen flow and invigorate the brain by engaging in novel activities, situations, or experiences. This may include attending live performances, trying a new sport, exploring new locations, or taking a different route home. Conversely, aerobic exercise, such as walking or jogging, focuses on oxygen consumption to satisfy the body’s metabolic needs. Both neurobics and aerobics support the elderly by fostering cognitive and physical health, respectively. This study seeks to raise awareness about how exercise can help prevent the onset of cognitive decline in older adults. This cross-sectional comparative study was conducted in elderly homes around Anakaputhur, Chennai, over 6 months, with an intervention duration of 12 weeks. A total of 50 participants aged 60 years and above were selected using simple random sampling. Both male and female participants were included in the study. Inclusion criteria: individuals with mild to moderate dementia as diagnosed by a neurologist on the Dementia severity scale score 18-36, the ability to follow simple instructions, the capability for light to moderate physical activity, and no history of psychiatric disorders. Exclusion criteria included severe dementia (Dementia severity scale score 37-54), severe cardiovascular disease, uncontrolled psychiatric conditions, mobility issues, and severe hearing or vision loss. Based on the inclusion and exclusion criteria, the participants were randomly divided into two equal groups of 25 each: one group underwent neurobics training, and the other underwent aerobics training. Both groups participated in 30-minute sessions, five times per week, for 12 weeks. The intervention aimed to enhance cognitive function and memory. Pre- and post-intervention assessments were conducted using standardized tools, including the Montreal Cognitive Assessment (MoCA), the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE), and the Digit Span Test. On comparing pre- and post-test within Group A and Group B, the Group B intervention was found to be more effective than Group A on IQCODE, MoCA, and Digit span test, with significant differences in mean values at P < 0.05.
The glymphatic system is a glia-dependent network surrounding blood vessels that facilitates the exchange of cerebrospinal fluid (CSF) and interstitial fluid, playing a crucial role in clearing neuro-metabolites from the brain. This system’s efficiency in transporting waste significantly increases during non-rapid eye movement non-REM sleep. Recent findings suggests that malfunctioning of the glymphatic system might be linked to neurodevelopmental disorders such as attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and schizophrenia (SCZ), all of which often correlate with disturbed sleep patterns. Furthermore, various environmental toxicants have been shown to affect neurodevelopment negatively. Exposure to these toxicants early in life disrupts the sleep/Blood-Brain Barrier (BBB)/Aquaporin-4 connections, impairs the glymphatic system’s ability to clear substances like amyloid-beta (Aβ), tau proteins, and inflammatory mediators, ultimately skewing neurodevelopment toward an increased risk of disorders. In summary, this narrative review consolidates existing evidence. It highlights key priorities for examining the relationship between the exposome, the glymphatic system, and neurodevelopmental pathways, aiming to pave the way for future research and therapeutic interventions.
The study explores the crucial biological function of nitrogen in cyclic and acyclic structures with resonance potential, including tetrazoles, pyrroles, piperidines, and carbamates, within the realm of chemical neuroscience. It highlights the importance of these compounds for their biological properties and their ability to cross the blood-brain barrier (BBB) to reach the central nervous system (CNS). The study emphasizes the necessity for neurochemical drugs, like morphine, to effectively cross the BBB, as modifications to their nitrogen structure can significantly impact their pharmacological effects. Additionally, the research explores the biochemical mechanisms of opioid and opioid-like analgesics, focusing on the impact of nitrogen heteroatoms and resonance on the stability of drug structures. The results highlight the importance of nitrogen-containing compounds in drug development, especially in pain management and other central nervous system applications. This document provides a thorough overview of the synthesis, characterization, and uses of different nitrogen heterocycles in medicinal chemistry.
Personalized psychopharmacotherapy remains a critical yet underdeveloped frontier in psychiatry, as traditional approaches often fail to address substantial interindividual variability in drug efficacy and tolerability. While demographic, clinical, and genetic factors have improved treatment precision, they do not fully account for observed heterogeneity. Recent advances highlight the promise of personality traits, particularly as operationalized by Cloninger’s Seven-Factor Model, as novel biomarkers for treatment optimization. This model distinguishes between temperament—biologically-based, heritable predispositions—and character, which is shaped by environmental, developmental, and cultural factors. Mapping these dimensions to neurochemical pathways offers a framework for tailoring pharmacological interventions to individual neurobiological profiles, potentially enhancing symptom control, tolerability, and adherence. Integrating personality assessment with pharmacogenomics, neuroimaging, and computational phenotyping may enable more holistic patient stratification, fostering the development of precision psychiatry. However, significant methodological, practical, and ethical challenges persist, including inconsistent findings, concerns regarding validity and generalizability, and the risk of stigmatization or misuse of sensitive data. Future research should prioritize large-scale, diverse, and longitudinal studies that leverage advances in artificial intelligence and integrative biomarker platforms. Interdisciplinary collaboration and rigorous ethical oversight are essential to translate the theoretical promise of personality-informed psychopharmacotherapy into effective, equitable, and patient-centered clinical practice. Ultimately, incorporating personality biomarkers may redefine the landscape of individualized psychiatric care and advance the goals of precision psychiatry.
The editors of OBM Neurobiology would like to express their sincere gratitude to the following reviewers for assessing manuscripts in 2025. We greatly appreciate the contribution of expert reviewers, which is crucial to the journal's editorial process. We aim to recognize reviewer contributions through several mechanisms, of which the annual publication of reviewer names is one. Reviewers can download a certificate of recognition directly from our submission system. Additionally, reviewers can sign up to the Web of Science Reviewer Recognition Service (formerly Publons) (https://webofscience.com/wos/) to receive recognition. Of course, in these initiatives we are careful not to compromise reviewer confidentiality. Many reviewers see their work as a voluntary and often unseen part of their role as researchers. We are grateful for the time reviewers donate to our journals and the contribution they make.
Super Skills for Life (SSL) is a transdiagnostic psychoeducational program designed for children with anxiety and depressive symptoms based on cognitive-behavioral therapy. Empirically documented studies to date have demonstrated its immediate and long-term effectiveness in different contexts. The aim of this study was to assess the efficacy of the SSL program to reduce emotional and behavioral difficulties in a clinical sample of Greek-speaking primary school children aged 6 to 12. The program was implemented over 2 years in a community child mental health unit of the NHS. The sample consisted of 23 children attending elementary school who had been diagnosed with at least one anxiety disorder (AD). Small groups of 4 to 6 children with a similar age range were formed, and each session was held once a week for 1 hour. Assessments were conducted before and after the 8-week intervention by using the Strengths and Difficulties Questionnaire parent form. After the intervention, a reduction was observed in children's hyperactivity (Z = -2.83, p = 0.01), peer problems (Z = -2.69, p = 0.01), as well as total scores of SDQ parent form (Z = -2.31, p = 0.02). A statistically significant increase in children's prosocial skills was also observed (Z = -2.470, p = 0.01). The findings of this study imply an immediate effect of the Greek adaptation of SSL, suggesting that it could be a valuable resource for early reduction, not only of emotional but also of comorbid symptoms in young Greek-speaking children. Finally, these results suggest that the intervention could be delivered by a non-mental health specialist since the program coordinator was a special educator. Clinical implications of these findings are discussed further in this report.
The inbred Krushinsky-Molodkina (KM) rat strain, characterized by latent genetic epilepsy, reduced social motivation, and a high propensity for freezing, is a promising model for translational research of social deficits in autism spectrum disorder (ASD). In clinical practice, social deficits often lead to social withdrawal and can be accompanied by aggression. It was unknown if KM rats exhibit such aggression during inescapable social encounters. We assessed intraspecific aggression in KM and control rats using the resident-intruder test, and autonomic nervous system responses were evaluated via heart rate variability analysis in a small separate cohort using a modified social-challenge paradigm that prevented direct physical contact. In the resident-intruder test, KM rats displayed significantly less aggression toward unfamiliar intruders than controls, exhibiting fewer attacks, fights, and competitive wins. Electrocardiographic analysis during the social preference test further revealed that the social challenge triggered parasympathetic, rather than sympathetic, nervous system activation in KM rats. Together, these findings indicate that social load in KM rats evokes a stress response, marked by a hypolocomotion and an atypical autonomic reaction. Conversely, control rats, which displayed a typical fight response to unfamiliar intruders, exhibited marked sympathetic activation during the sociability test. These findings suggest the KM strain may help model specific aspects of ASD-relevant social behavior alongside autonomic dysregulation.
Mycotoxins, toxic secondary metabolites produced by fungi and molds, have negative health impacts on both humans and animals. They are commonly found in foods such as nuts, coffee, cereals, and grains, particularly in regions with warm, humid climates. Among the most prevalent mycotoxins in these foods are aflatoxin B1, ochratoxin A, zearalenone, patulin, and deoxynivalenol (DON). The presence of mold capable of producing mycotoxins within food contributes to an elevated risk of various illnesses, including those related to the nervous system, due to their known neurotoxicity. When mycotoxins cross the blood-brain barrier (BBB), they can damage brain cells, induce inflammation, and disrupt the balance of neurochemicals. A growing body of evidence suggests a link between these harmful compounds and neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Additionally, they are posited as potential factors in psychiatric conditions, contributing to cognitive deficits, anxiety, and depression. Numerous pathways through which neurotoxicity occurs have been explored, such as mitochondrial dysfunction, oxidative stress, neuroinflammation, compromise of the BBB, and the activation of glial cells, which collectively lead to neuronal apoptosis and disturbance of the normal operations within the central nervous system. This thorough review examines the role of mycotoxins as environmental catalysts in the development of neurodegenerative and psychological disorders, elucidates the underlying mechanisms, and evaluates strategies to mitigate their effects in driving these conditions.
Difficult-to-treat depression (DTD) with inflammatory features (e.g., hs-CRP ≥3 mg/L and/or elevated IL-6) may represent a clinically and biologically distinct presentation characterized by chronicity, functional impairment, prominent cognitive-motivational symptoms, and suboptimal response to conventional treatments. Classical anti-inflammatory strategies (e.g., COX-2 inhibitors or cytokine-targeting biologics) have shown signals of efficacy in selected biomarker-enriched subgroups; however, overall evidence remains heterogeneous, with modest effect sizes and substantial limitations for real-world implementation. This Commentary advances a complementary perspective, proposing that in many patients “inflamed DTD” reflects not only increased pro-inflammatory drive but also impaired physiological resolution mechanisms across immune, autonomic, circadian, and metabolic systems. Within this “resolution failure” framework, we discuss emerging therapeutic targets and multimodal strategies and their integration into endotype-guided immunopsychiatric care. We further address limitations of the current evidence base, outline biomarker-enriched trial designs with patient-centred outcomes (functioning, quality of life, cognition), and highlight real-world barriers, including access to biomarkers, reimbursement, and equity of care. Overall, this perspective argues for moving beyond single-pathway anti-inflammatory approaches towards pragmatic, mechanistically informed interventions for inflamed DTD.
The "Sama Code" is a protocol implemented in Iranian pre-hospital emergency services to manage time and treat patients with suspected stroke symptoms based on the FAST criteria. This study aims to analyze the workflow of patients with stroke symptoms transferred under the Sama Code. All patients with neurological symptoms who were brought to Imam Reza Hospital by pre-hospital emergency services after activating the Sama Code during the years 2021 and 2022 were included in the study. Data were collected from pre-hospital emergency records and registries, including patient age and gender, time of emergency contact, code activation, arrival of personnel at the patient’s side, clinical findings recorded in pre-hospital files, time to emergency department arrival, CT scan (Computed tomography scan), thrombolytic therapy initiation, reasons for treatment cancellation, and patient outcomes. A total of 880 patients were included in the study, with a mean age of 69.24 years (CI 95%: 68.30-70.17). The median age was 71 years, with most patients aged 61-80 years. Among the patients, 505 (57.4%) were male, and 375 (42.6%) were female. The number of patients transferred by pre-hospital emergency services under the Sama Code was roughly equal over the two years studied. The median time from emergency notification to mission start was 1 minute, while the median time from care plan initiation to patient arrival was 10 minutes. The median time from the patient’s side to transfer was 18 minutes, and from transfer initiation to hospital arrival was 10 minutes. The median time from hospital arrival to CT scan was 17 minutes. Of 880 patients, 750 were admitted to the hospital, and 13 Sama Codes were canceled during triage due to other diagnoses. Of the remaining 737 patients, only 20 received thrombolytic treatment, with a median time from CT scan to treatment of 20 minutes. According to this study’s findings, a small percentage of patients receive thrombolytic treatment; however, patient transfers in accordance with the Sama Code guidelines are well implemented, ensuring rapid CT scanning and timely decision-making.
