International Neuropsychiatric Disease Journal

The Kinesthetic-motor Hypothesis in Developmental Dyslexia: A Systematic Review and Theoretical Model Proposition

Giovanna Azevedo Rodrigues — 2026-08-13

Introduction: Developmental dyslexia is traditionally explained by the acoustic phonological deficit theory, yet clinical observations suggest that reading difficulties may extend to motor and articulatory components, manifesting as phono-articulatory stalls during the decoding of phonotactically complex syllables.

Methodology: This systematic review, with a narrative qualitative synthesis, was conducted in accordance with PRISMA 2020 guidelines. Searches of PubMed/MEDLINE, Scopus, and Google Scholar identified 28 primary studies published between 1 January 2020 and 31 May 2026 addressing proprioception, sensorimotor integration, and speech motor control.

Results and Discussion: A risk-of-bias appraisal adapted from ROBIS indicated mixed evidence quality, with a subset of studies reporting associations between dyslexia and higher proprioceptive detection thresholds, magnocellular pathway alterations, structural/functional cerebellar variability, and atypical neuroimaging patterns during font-sound co-processing. Integrating these findings, the authors propose the Kinesthetic-Motor Hypothesis as a complementary, hypothesis-generating interpretative framework anchored in state-feedback speech motor control models, putting forward three concrete, falsifiable predictions regarding decoding uncertainty, reduced feedback gain, and prolonged error-correction latencies in a dissociable subgroup of dyslexic individuals.

Conclusion: This kinesthetic-motor model serves as a complementary explanatory layer for dyslexia heterogeneity rather than a replacement for established phonological or structured-literacy frameworks; it carries no immediate clinical practice recommendations and is intended to guide future controlled experimental interventions and hypothesis-driven physiological assessments.

Social Support Networks and Recovery from Depression: A Medical Sociological Study of Mental Health Patients in Ikpoba-Okha LGA, Edo State, Nigeria

Justus Chukwuka Iwegbu — 2026-08-08

Aim: This study aimed to determine the impact of social support networks on recovery from depression among patients with depression residing in Ikpoba-Okha LGA, Benin City, Edo State.

Methods: A descriptive cross-sectional survey design was adopted to examine the relationship between social support networks and recovery from depression among adults in Ikpoba-Okha Local Government Area, Edo State. A total of 200 clinically diagnosed patients with depression were selected through simple random sampling from a population of 450 patients. Data were collected using a structured, validated questionnaire and analysed using descriptive statistics and the chi-square test at a 5% level of significance.

Results: Family members, healthcare professionals and religious institutions were the major sources of social support. Social support positively influenced emotional well-being, treatment adherence, confidence and recovery, while community support was relatively low. Major barriers to accessing support included misconceptions about depression, financial constraints, inability to afford medication and stigma. A significant relationship was found between social support and recovery from depression (χ² = 24.56, df = 4, p < 0.001), indicating that stronger social support networks enhance recovery outcomes.

Conclusion: The study concludes that strong family, healthcare and religious support significantly enhance recovery from depression, while stigma, financial challenges, limited community support and cultural misconceptions hinder recovery, underscoring the need for comprehensive psychosocial and community-based interventions alongside medical treatment.

Association between Substance Use Disorders and 30-Day Readmission among Patients with Schizophrenia: A Retrospective Cohort Study Using MIMIC-IV

Onyedikachi Mmesoma Amagwu — 2026-08-10

Background: Schizophrenia is frequently accompanied by substance use disorders, which complicate clinical management and contribute to recurrent hospitalisation. Evidence regarding the association between substance use disorders and 30-day hospital readmission remains inconsistent.

Objective: To examine the association between substance use disorder (SUD) and 30-day hospital readmission among adults hospitalised with schizophrenia.

Methods: This retrospective cohort study used version 3.1 of the Medical Information Mart for Intensive Care IV (MIMIC-IV). Adults with schizophrenia were identified using International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM), and Tenth Revision, Clinical Modification (ICD-10-CM), diagnosis codes. Substance use disorder was the primary exposure, and 30-day all-cause hospital readmission was the primary outcome. Multivariable logistic regression was used to estimate adjusted odds ratios (aORs) and 95% confidence intervals (CIs) after adjustment for age, sex, race or ethnicity, insurance type, Charlson Comorbidity Index, hospital length of stay, and discharge location.

Results: A total of 7,968 eligible hospital admissions were included, of which 2,728 (34.2%) had substance use disorder and 2,461 (30.9%) experienced a 30-day readmission. After adjustment, substance use disorder was associated with lower odds of 30-day readmission (aOR, 0.85; 95% CI, 0.76 to 0.95; p = 0.004). Higher Charlson Comorbidity Index scores were associated with increased odds of readmission (aOR, 1.06; 95% CI, 1.03 to 1.09; p < 0.001), whereas discharge to a psychiatric facility was associated with markedly higher odds of readmission than discharge to home (aOR, 5.95; 95% CI, 4.72 to 7.50; p < 0.001).

Conclusions: Substance use disorder was associated with lower adjusted odds of 30-day hospital readmission among adults hospitalised with schizophrenia. Patient characteristics, comorbidity burden, insurance type, and discharge destination were also associated with readmission, highlighting the importance of comprehensive discharge planning and continued follow-up. Additional multicentre studies are needed to examine clinical and social factors that may influence readmission after hospitalisation for schizophrenia.

The Role of High-Dose Vitamin A on the Amygdala of Adult Male Wistar Rats Exposed to Toxic Doses of Methamphetamine

Ezejindu Damian Nnabuihe — 2026-08-19

The amygdala, a major limbic structure, regulates emotional response, anxiety, and memory formation. Methamphetamine is known to trigger oxidative stress and neurodegeneration, whereas vitamin A possesses potent antioxidant properties that may offer neuroprotection. This study evaluated the effect of high-dose vitamin A on the amygdala of adult male Wistar rats exposed to toxic doses of methamphetamine. Twenty (20) adults male Wistar rats were randomly assigned into four groups and received as follows: Group A (control), Group B (METH-only; 5 mg/kg at 3-hours interval within 12 hours in a day), group C (Vitamin A-only; 2.5 mg/kg), while, group D (combined METH 5 mg/kg at 3-hours interval within 12 hours in a day + Vitamin A-only; 2.5 mg/kg). All experimental groups received feed and water. The administration was done orally using intubation method for a period of twenty-eight days. Body weight result revealed a significant reduction in the methamphetamine-only group compared with the control suggesting metabolic disturbance and appetite suppression. Co-treatment with vitamin A improved body weight, indicating a restorative metabolic effect. Biochemical findings showed elevated malondialdehyde (MDA) and decreased glutathione (GSH) and superoxide dismutase (SOD) levels in the methamphetamine group, confirming oxidative damage within the amygdala. Vitamin A treatment markedly reduced MDA and preserved GSH and SOD activities, demonstrating enhanced antioxidant defense. Behavioral testing using the Elevated Plus Maze indicated anxiety-related alterations following methamphetamine exposure, while vitamin A co-administration protected these behavioral changes. Histological results showed that methamphetamine caused neuronal degeneration, vacuolation, and necrosis, whereas vitamin A preserved neuronal integrity and promoted partial structural recovery. In conclusion, high-dose vitamin A significantly mitigated methamphetamine-induced oxidative and structural damage in the amygdala, highlighting its antioxidative and neuroprotective potential against psychostimulant toxicity.

Internet Gaming Disorder and Sleep Quality among Medical Residents in Eastern Province, Saudi Arabia: A Cross sectional Study

Abdulelah Almuqaytif — 2026-08-19

Background: Internet Gaming Disorder (IGD) is an emerging behavioural health concern globally, yet its association with sleep quality among medical residents in Saudi Arabia remains understudied.

Objectives: This study aimed to estimate the prevalence of IGD, assess sleep quality, and identify associated sociodemographic and lifestyle factors among medical residents in the Eastern Province of Saudi Arabia.

Methods: A cross-sectional survey was conducted using a convenience sample of 292 medical residents. Validated instruments included the Internet Gaming Disorder (IGD-20) questionnaire to assess gaming behaviour and the Pittsburgh Sleep Quality Index (PSQI) to evaluate sleep quality. Data were analysed using SPSS version 26, with statistical significance set at *p* < 0.05.

Results: Among the 292 participants, 167 (57.2%) played online games, and the prevalence of disordered online gaming (IGD-20 cut-off ≥71) among gamers was 20.4% (n = 34). More than half of the total sample (55.5%) exhibited disturbed sleep (global PSQI score >5). Disordered online gaming was significantly associated with poorer subjective sleep quality (*p* = 0.006) and greater use of sleep medication (*p* = 0.005). The IGD-20 total score correlated positively with the global PSQI score (*r* = 0.268, *p* < 0.001), subjective sleep quality (*r* = 0.265, *p* = 0.001), and sleep disturbance (*r* = 0.202, *p* = 0.009). Playing online games was significantly associated with age (*p* = 0.002), gender (*p* < 0.001), marital status (*p* < 0.001), parenthood (*p* = 0.001), and caffeine consumption (*p* = 0.039). IGD-20 category was significantly associated with gaming duration on weekdays (*p* = 0.002) and weekends (*p* = 0.005).

Conclusion: IGD was prevalent among medical residents in the Eastern Province and was significantly associated with poorer subjective sleep quality and greater use of sleep medication. These findings support consideration of targeted screening, awareness, and sleep-health education for residents, particularly those reporting prolonged gaming. However, causal inference is limited by the cross-sectional design and convenience sampling.

Sociodemographic and Socioeconomic Determinants of Adherence to Antiepileptic Medication among Patients in Kitui Central Sub-County, Kenya

Rebecca Nyaguthii Mwengi — 2026-08-25

Aim: The aim of this study was to assess sociodemographic and socioeconomic factors associated with adherence to epilepsy treatment.

Methods: The study was conducted in Kitui Central Sub-County among adult patients with epilepsy. The study adopted a cross-sectional design, and a sample of 192 respondents was recruited. A two-stage sampling technique was used, whereby purposive sampling was used to identify Kitui Level 4 Hospital in Kitui Township and Wanzoa, Itoleka, Miambani, and Katulani health centres in Kyangwithia East, Kyangwithia West, Miambani, and Mulango wards, respectively. This was followed by random sampling of 39 patients with epilepsy attending the inpatient and outpatient departments in each health facility. Descriptive statistics were used to summarise the prevalence of adherence to antiepileptic medication and the sociodemographic and socioeconomic factors. Chi-square tests were used to assess sociodemographic and socioeconomic factors associated with the prevalence of adherence to epilepsy medication. Ethical clearance was sought from the Chuka University Research and Ethics Committee (IERC) and NACOSTI. Permission was sought from the Kitui County Commissioner, the Chief Officer in the Ministry of Health and Sanitation, the County Director of Education, and the Medical Officer of Health in Kitui Central Sub-County.

Results: The prevalence of adherence to antiepileptic medication was 45.3%. Sociodemographic and socioeconomic factors associated with adherence to antiepileptic medication were age (χ2 (5, N=190) =11.389, p= 0.044), residence (χ2 (3, N=190) =11.296, p= 0.010), level of education (χ2 (3, N=190) =11.789, p= 0.008), and monthly income (χ2 (4, N=190) =16.183, p= 0.003).

Conclusion: Improving adherence to antiepileptic medication requires a multifaceted approach that extends beyond medication provision alone. Strengthening patient education, improving access to epilepsy care in underserved areas, ensuring the consistent availability of antiepileptic medicines, and reducing financial barriers to treatment may substantially improve adherence and long-term seizure control.

The General Psychiatric Syndrome as a Transdiagnostic Hypothesis: A Critical Appraisal of Evidence, Interpretation and Clinical Reach

Luiz Costa — 2026-08-25

Persistent comorbidity, diagnostic instability and the scarcity of disorder-specific causes have encouraged the proposal that a single superordinate dimension underlies liability to all common mental disorders. This proposition, expressed empirically as the general factor of psychopathology and framed conceptually as a general psychiatric syndrome, now shapes nosological reform, aetiological research and the design of youth mental health services. Its status remains contested. This critical narrative review evaluates the hypothesis across five domains of evidence: psychometric modelling, quantitative and molecular genetics, structural neuroimaging and neurocognition, developmental epidemiology, and clinical translation. Literature published between January 1999 and June 2026 was identified through structured searching of biomedical and multidisciplinary scholarly sources, supplemented by citation tracking of recent reviews and of a 2026 target-article exchange devoted to the topic. Sources were appraised for design adequacy, sample independence, replication, and the correspondence between statistical models and the substantive claims drawn from them. Evidence for a strong and replicable general dimension at the phenotypic level is robust. It accounts for the majority of reliable symptom variance from early childhood to adulthood, aggregates within families, and predicts impairment more consistently than narrower factors. Evidence bearing on its interpretation is considerably weaker. Competing accounts framing the dimension as negative emotionality, disinhibition, thought dysfunction, low cognitive ability or an index of impairment are only partially separable empirically, and several are close to statistically equivalent. Molecular genomic analyses supply the strongest disconfirming signal, repeatedly favouring several correlated genomic factors over a single dimension of genetic risk. Neuroimaging associations are modest, derive from a small number of overlapping cohorts, and have not produced diagnostic or prognostic utility. Transdiagnostic psychological treatments perform comparably to disorder-specific protocols, although this parity does not establish a shared causal mechanism. The general dimension is best regarded at present as a well-replicated descriptive summary of liability and impairment rather than a demonstrated syndrome with unitary aetiology. Clinical adoption should follow evidence of incremental decision-making value, which has not yet been generated.

Neuroinflammation, Oxidative Stress and Mitochondrial Dysfunction in Epilepsy: An Integrated Critical Review of Molecular Mechanisms and Therapeutic Opportunities

Kolawole Oluwaseyi Emmanuel — 2026-09-01

Epilepsy is a heterogeneous brain disorder in which recurrent seizures arise from diverse genetic, structural, metabolic, immune and unknown causes. Neuroinflammation, oxidative stress and mitochondrial dysfunction have each been implicated in seizure generation and epileptogenesis, but their importance depends on whether they are initiating mechanisms, amplifiers of an established epileptic network, consequences of seizures, or markers of tissue injury. This critical narrative review integrates molecular, animal and human evidence to evaluate the bidirectional neuroimmune-redox-mitochondrial network and its therapeutic relevance. Literature from 1990 to 28 June 2026 was selected through live scholarly searching, citation tracing and bibliographic verification, with emphasis on peer-reviewed mechanistic studies, human biomarker or tissue investigations, clinical trials, consensus statements and high-quality reviews. The strongest causal evidence comes from experimental models in which interleukin-1 signalling, high-mobility group box 1-Toll-like receptor 4 signalling, blood-brain barrier transforming growth factor-beta pathways, reactive oxygen species generation, impaired antioxidant defences and mitochondrial respiratory defects can alter seizure threshold, neuronal injury or epileptogenesis. Human evidence confirms activation of several corresponding pathways, including glial and cytokine responses, translocator protein positron-emission tomography signals and mitochondrial respiratory abnormalities, but is often cross-sectional and vulnerable to confounding by recent seizures, antiseizure medicines and end-stage surgical tissue. Mitochondria appear to be a mechanistic convergence point because energetic failure and calcium dysregulation increase reactive oxygen species, while mitochondrial damage can release danger signals that recruit innate immunity. Recent experimental evidence linking mitochondrial DNA leakage to cyclic GMP-AMP synthase-stimulator of interferon genes signalling further sharpens this connection, although clinical validation is lacking. Therapeutically, ketogenic dietary therapies have established antiseizure efficacy, whereas anti-inflammatory and redox-directed approaches range from phenotype-specific clinical experience to predominantly preclinical disease-modification evidence. Future progress depends on mechanistic endotyping, longitudinal biomarkers, target-engagement measures and trials that separate acute seizure suppression from durable modification of epileptogenesis and comorbidity. The integrated pathway is therefore biologically credible and therapeutically attractive, but its clinical value will depend on identifying the patients, disease stages and molecular states in which each node is causal rather than merely reactive.

Envisioning a Path Forward: A Critical Narrative Review of the Brain Disease Model of Addiction (BDMA) after Three Decades of Debate

Prakat Karki — 2026-09-05

For nearly three decades, the Brain Disease Model of Addiction (BDMA) has strongly influenced scientific, clinical, and public understandings of addiction while remaining the focus of sustained debate. This critical narrative review reassesses the BDMA by integrating evidence from addiction neuroscience, genetics, neuroimaging, behavioural economics, recovery research, stigma studies, and philosophical critique. The review examines evidence supporting a neurobiological basis for addiction alongside concerns regarding causation, agency, responsibility, social context, treatment implications, and stigma. The synthesis indicates that much of the continuing disagreement reflects differing definitions of “brain disease” rather than wholly incompatible evidence. Neurobiological findings demonstrate consistent involvement of reward, motivation, learning, and control systems, but they do not by themselves establish that addiction can be fully explained at a biological level. Conversely, psychosocial and choice-based accounts do not negate the relevance of neurobiological mechanisms. The reviewed literature therefore supports an integrative interpretation in which addiction emerges from interactions among biological vulnerability, learning history, socioeconomic conditions, environmental contingencies, and individual agency. This perspective has practical implications for prevention and treatment, favouring approaches that combine mechanism-specific and precision-oriented interventions with psychosocial support, recovery resources, and attention to stigma and social disadvantage. The review concludes that future progress depends less on defending a single explanatory label than on clarifying the meaning and limits of the brain-disease concept and applying multiple levels of explanation to research, clinical care, and public health.