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The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD), for the first time, estimated stillbirth rate (SBR) by the WHO ICD-11 definition (≥22 weeks' gestation) for 204 countries, highlighting the extent of underestimation in stillbirth burden as compared with using only the late gestation (≥28 weeks' gestation) SBR estimation to understand the stillbirth burden. Given the size of its population, India accounted for the highest global burden of stillbirths for both gestation period cut-offs. Given the extent of state-level heterogeneity in disease burden in India, state-disaggregated SBR is necessary to enable policymakers and researchers to tailor strategies that are more responsive to local needs and institutional capacities, thereby enhancing the effectiveness of interventions and related resource allocation. Data were compiled from 122 sources, including surveys, published studies, and vital and sample registration systems, encompassing 2684 location-year observations. SBRs were estimated for 31 geographic units using spatiotemporal Gaussian process regression to model the ratio of SBR to neonatal mortality rate (NMR), integrating GBD 2023 fertility and all-cause neonatal mortality assessments. Estimates were produced for SBR and number of stillbirths for ≥22 and ≥28 weeks' gestation with 95% uncertainty intervals (UIs) for year 2023. Secondary analyses evaluated the relationship between SBR at the state-level with the Sustainable Development Goal 3 (SDG3; good health and wellbeing) state index score developed by the NITI Aayog and compared GBD results with India's Sample Registration System (SRS) for late gestation SBR and neonatal mortality rate (NMR) for 2023. An estimated 565,900 (462,600-702,900) and 347,300 (284,600-430,000) stillbirths occurred in India in 2023, corresponding to SBRs of 25.9 (95% UI 21.3-32.0) and 16.1 (13.2-19.8) at ≥22 weeks' and ≥28 weeks of gestation, respectively. SBR for both definitions varied four-fold between states, from 9.3 (6.8-12.6) in Mizoram to 38.2 (29.0-50.8) in Uttar Pradesh, with the latter and Bihar together accounting for nearly half of India's total stillbirths. A modest inverse correlation was observed between SBR and SDG3 index score (≥22 weeks p = 0.053, r = -0.350 and ≥28 weeks p = 0.034, r = -0.383). Comparison with SRS 2023 revealed substantial under-reporting in SBR, with national late-gestation SBR 2.3 times lower than GBD estimates, though NMR values were consistent across systems. India's true stillbirth burden is markedly underestimated using the ≥28-week definition. Improved surveillance, tracking stillbirths by the ≥22-week threshold, and integration of stillbirth prevention within broader maternal and newborn health initiatives are essential to address the stillbirth burden in India. Investments are also needed to improve both the availability and quality of data on the magnitude, causes, risk factors, and geographic disparities in stillbirth occurrences for appropriate action to address early gestation stillbirths in India. Gates Foundation.

Migraine is a widespread and debilitating disorder. Recent evidence suggests a role of seasonal and circadian rhythmicity in migraine episodes. We investigated the pattern of migraine attacks over 1 year in the North Indian population. A questionnaire was provided to 120 migraine patients at the end of each of the six seasons according to the Indian calendar. The frequency, pain intensity, and duration of migraine episodes were significantly higher during the hot summer (7.92 ± 0.70, 6.63 ± 0.17, and 8.73 ± 0.99, respectively) and monsoon (8.11 ± 0.72, 6.64 ± 0.17, and 8.00 ± 0.94, respectively) compared to the cold winter months. There was a gradual decrease from summer to winter, with 77.2% of patients reporting diurnal rhythmicity to their attacks, and 34.5% of patients reporting occurrences in the afternoons, increasing from colder to hotter months. Increased incidence during summer, monsoon, and afternoons should be considered in planning prophylactic and therapeutic interventions.

Inflammatory neuropathies are a heterogeneous group of disorders of the peripheral nerves. Pathogenic antibodies targeting various antigens at the node-paranode junctions, leading to its disorganization, are increasingly recognized as accounting for an important subset of inflammatory neuropathies. Among these, antibodies against neurofascin (NF)155 and NF186 are the most widely recognized. The current study aimed to determine the prevalence of NF155 and NF186 antibodies in an Indian cohort of patients with inflammatory neuropathies. Seventy-six patients with inflammatory neuropathies, including 44 with Guillain-Barré syndrome (GBS) and 32 with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and 32 healthy controls were recruited. NF155 and NF186 antibodies were tested in sera from all study participants. In this study, 8/76 (10.53%) patients with inflammatory neuropathies tested positive for NF186 antibodies, including 5 (11.36%) with GBS and 3 (9.37%) with CIDP. Given the small sample size, definitive differences between the NF186 antibody-positive and antibody-negative groups could not be established. None of the patients with GBS and NF186 antibody positivity required mechanical ventilation. None of the patients with CIDP and NF186 antibody positivity had an acute GBS-like onset. One patient in the NF186 antibody-positive CIDP group had the phenotype of combined central and peripheral demyelination. None of the study participants tested positive for NF155 antibodies. A higher proportion of GBS patients showed NF186 reactivity in the present study than in previous reports. The spectrum of other pathogenic antibodies remains to be tested, as the majority of patients with inflammatory neuropathies tested negative for the two NF antibodies.

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Toxoplasma gondii infects one-third of the global human population and invades and chronically persists in the central nervous system of the infected host. Chronic infection in the brain correlates with changes in the neuronal architecture and behavior. To the best of our knowledge, the association between T. gondii and neurological and psychiatric disorders has not been studied in the Indian population. Therefore, this study was conducted to determine the association between T. gondii in these patients. This cross-sectional study was conducted in a large Neuroscience Center by the Department of Microbiology in collaboration with the Psychiatry and Neurology Departments for 7 months from March to September 2025. A total of 281 neuropsychiatric patients and an equal number of controls were taken. They were further classified using the International Classification of Diseases, ICD-10 codes. After carefully explaining the procedure and goal of the study, informed written consent was taken. 3 mL of blood specimens was drawn under aseptic conditions by venipuncture, which was collected in sterile plain vials. Serum samples were tested for the presence of specific anti-T. gondii immunoglobulin G antibodies using a commercial qualitative enzyme-linked immunosorbent assay. Our results reveal a higher prevalence of T. gondii antibodies among schizophrenia (33.34%), mental and behavioral disorder due to substance abuse (30%), bipolar affective disorder (32%), Parkinson's disease (31.03%), and dementia (35%). Our results suggest that T. gondii seropositivity is higher among the psychiatric and neurological patients, but it is not significantly associated as compared to controls. Résumé Introduction:Toxoplasma gondii infecte un tiers de la population mondiale et envahit le système nerveux central de l’hôte infecté, où il persiste de façon chronique. L’infection chronique du cerveau est corrélée à des modifications de l’architecture neuronale et du comportement. À notre connaissance, l’association entre T. gondii et les troubles neurologiques et psychiatriques n’a pas été étudiée dans la population indienne. Par conséquent, cette étude a été menée afin de déterminer l’association entre T. gondii et ces troubles chez ces patients.Matériel et méthodes:Cette étude transversale a été menée dans un grand centre de neurosciences par le département de microbiologie, en collaboration avec les départements de psychiatrie et de neurologie, pendant 7 mois, de mars à septembre 2025. Au total, 281 patients neuropsychiatriques et un nombre égal de témoins ont été inclus. Ils ont ensuite été classés selon la Classification internationale des maladies (CIM-10). Après avoir expliqué en détail la procédure et l’objectif de l’étude, un consentement éclairé écrit a été obtenu. Un prélèvement sanguin de 3 mL a été effectué par ponction veineuse dans des conditions aseptiques, et recueilli dans des tubes stériles sans anticoagulant. Les échantillons de sérum ont été analysés pour la présence d’anticorps IgG anti-Toxoplasma gondii spécifiques à l’aide d’un test immuno-enzymatique (ELISA) qualitatif commercial.Résultats:Nos résultats révèlent une prévalence plus élevée d’anticorps anti-Toxoplasma gondii chez les patients atteints de schizophrénie (33,34 %), de troubles mentaux et comportementaux liés à la toxicomanie (30 %), de trouble bipolaire (32 %), de maladie de Parkinson (31,03 %) et de démence (35 %).Conclusion:Nos résultats suggèrent que la séropositivité à Toxoplasma gondii est plus élevée chez les patients psychiatriques etneurologiques, mais cette association n’est pas significative par rapport aux témoins.

Dextromethorphan-associated neurotoxicity with cerebellar edema syndrome is a recently described clinico-radiological condition resembling pediatric opioid use-associated neurotoxicity with cerebellar edema syndrome. To describe two children with dextromethorphan-associated neurotoxicity with cerebellar edema syndrome from a tertiary care hospital in North India. The clinical details were obtained from the medical case records of the children admitted with dextromethorphan-associated neurotoxicity with cerebellar edema syndrome during the month of August and September 2025. We report two children (3 years and 13 months) who presented with encephalopathy following ingestion of dextromethorphan-containing cough syrup for viral prodrome. Magnetic resonance imaging showed T2/FLAIR hyperintensities in bilateral cerebellar hemispheres with diffusion restriction, suggestive of cytotoxic edema. With supportive treatment and intravenous methylprednisolone, both patients recovered rapidly with no residual neurologic deficits. These two cases highlight the occurrence of dextromethorphan-associated neurotoxicity with cerebellar edema syndrome in young children. Sensitization of healthcare providers about dextromethorphan-associated neurotoxicity with cerebellar edema syndrome, early clinical suspicion, confirmation of diagnosis with neuroimaging, and supportive care, may be associate with good neurological recovery. Dextromethorphan-associated neurotoxicity with cerebellar edema syndrome is a new clinico-radiological condition that occurs following ingestion of dextromethorphan in young children. Similar to the recently published report and cases presented here, early identification and treatment may be associated with favorable neurological recovery. Therefore, this syndrome should be considered in the differential diagnosis at an early stage. There is a need to increase awareness among healthcare providers to avoid prescribing dextromethorphan-containing cough syrups to younger children.

This article is a structured narrative review that synthesizes empirical findings and expert consensus and provides policy guidance to outline implementation pathways for integrating Yoga into mainstream healthcare systems, with India as a case example. Yoga is an ancient health practice traditionally used as a holistic approach to health management and wellbeing. However, the acceptance of Yoga as an evidence-based practice in the modern healthcare delivery requires systematic reassessment for its implementation within the healthcare system to make healthcare more affordable, improve prevention, rehabilitation, and resilience thus reduce strain on medical resources. In this review, we have organized the literature review and practical insights around three core themes: stakeholder configurations and governance, economic and quality management, and implementation strategies and evaluation to develop an actionable framework for an optimal care system responsive to patients' needs and adaptable to different community settings. This article has incorporated peer-reviewed studies on the effectiveness of Yoga, its implementation in mainstream healthcare, along with relevant publicly available policy, accreditation, and practice standard sources, to emphasize constructs of implementation science and evidence-based practice. The review identifies a know-do gap between growing evidence for Yoga and its system-level adoption, proposing a staged framework that integrates stakeholder engagement, economic evaluation, quality management, and monitoring to support evidence-based implementation. We propose a comprehensive, context-sensitive model that combines traditional wisdom with contemporary behavioral, clinical, and systems-based approaches. By embedding Yoga within an implementation science framework, we advocate for its role as a mainstream, evidence-informed system. Adoption of Yoga as a therapeutic and preventive modality can be accelerated through standardized protocols, transparent evaluation and regulation, and tripartite governance among state actors, healthcare institutions, and Yoga professionals; however, the feasibility hinges on context-sensitive financial support, stakeholder management, and workforce development.

Retinal artery occlusion (RAO) shares vascular pathophysiology with cerebrovascular disease, and its relationship to incident dementia remains unsettled. Reported associations may reflect shared vascular pathology, differential ascertainment along the intensive workup pathways that RAO patients enter, or both. No prior study has calibrated RAO-dementia estimates against prespecified negative-control outcomes spanning distinct ascertainment pathways. Among 129,279 All of Us participants aged 50 years or older and free of prevalent dementia (controlled-tier release R2024Q3R9, OMOP common data model), strict RAO was defined by seven verified SNOMED concept identifiers (n = 339). Incident dementia required two or more codes at least 30 days apart (Wilkinson algorithm), with prespecified vascular and Alzheimer subtypes. Cox models used age as timescale with left truncation and time-varying exposure; 1:5 propensity-score matching was the primary confounder-adjusted analysis. Cataract, benign paroxysmal positional vertigo (BPPV), and inguinal hernia were prespecified negative controls for ophthalmology, neurology, and general-contact pathways. There were 1,506 incident dementia events. RAO was not associated with all-cause dementia (unmatched hazard ratio (HR) 0.81, 95% confidence interval (CI) 0.40-1.64; matched HR 1.33, 95% CI 0.72-2.47; 10 exposed events). The vascular dementia estimate remained elevated but imprecise (unmatched HR 1.93, 95% CI 1.02-3.66; matched HR 1.81, 95% CI 0.66-4.94; 3 exposed events). Cataract was elevated (HR 1.87, 95% CI 1.45-2.42), whereas BPPV (HR 1.27, 95% CI 0.90-1.79) and hernia (HR 1.10, 95% CI 0.68-1.78) were not. We found no evidence that RAO is independently associated with incident dementia, replicating a large European null finding in a diverse United States cohort. The cohort was underpowered to exclude clinically meaningful effects, particularly for vascular dementia. Detection bias in this dataset was demonstrably pathway-specific, but same-pathway calibration accounts for only part of the residual vascular dementia estimate.

BHLHE22 encodes a basic helix-loop-helix transcription factor expressed exclusively in the retina and central nervous system and functions as an important regulator of neuronal differentiation. However, BHLHE22 has not yet been associated with a Mendelian neurodevelopmental or neurological disorder. 15 individuals from 13 unrelated families carrying BHLHE22 variants identified by exome sequencing were collected through an international collaboration. De novo missense variants located in the highly conserved helix-loop-helix domain of the protein were found in six individuals, and one recurrent homozygous frameshift variant, NP_689627.1:p.Gly74AlafsTer18, was found in nine individuals. Frequent clinical features include absent or limited speech (10/13), delayed or impaired motor abilities (11/13), intellectual disability (ID; 9/12), partial or complete agenesis of the corpus callosum (12/15), involuntary movements and/or stereotypies (11/13) and abnormal muscle tone (13/13), depending on data availability. Two individuals developed spastic paraplegia, without ID or callosal anomalies. One individual had moderate developmental delay and ID but without callosal anomalies. Collectively, our data establish BHLHE22 as a previously unrecognized neurodevelopmental disease gene. Disruption of BHLHE22, through either dominant or recessive variants, results in a distinct syndrome characterised by abnormalities in brain development, cognition, tone and movement.

Blood-brain barrier (BBB) dysfunction is an early feature of Alzheimer's disease (AD). Fibrinogen represents a sensitive marker of BBB leakage, but whether it modifies longitudinal tau progression in cognitively unimpaired (CU) individuals remains unknown. CU older adults underwent clinical evaluation and cerebrospinal fluid (CSF) assessment of fibrinogen, Aβ42, total tau (tTau), phosphorylated tau 181 (pTau181), and YKL-40. Linear regression tested baseline associations. Linear mixed-effects models tested whether baseline fibrinogen predicted longitudinal pTau181 change. Among 169 CU participants with baseline fibrinogen, 87 had longitudinal pTau181 measurements (mean follow-up 2.5-years). Higher fibrinogen was associated with elevated YKL-40 (β = 0.28, 95% confidence interval [CI] [0.11, 0.45]) but not Aβ42, tTau, or pTau181 at baseline. Baseline fibrinogen modified longitudinal pTau181 trajectories (interaction β = 0.11, 95% CI [0.04, 0.19]), with only participants above the median showing significant pTau181 increases (β = 0.13, 95% CI [0.08, 0.18]). CSF fibrinogen associates cross-sectionally with glial inflammation and predicts accelerated tau accumulation in preclinical AD.

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Losartan, a commonly prescribed angiotensin II receptor blocker, is generally well-tolerated but can rarely cause severe drug-induced liver injury (DILI), leading to acute liver failure. We report a 43-year-old man with hypertension and type 2 diabetes who developed jaundice, fatigue, and right upper quadrant pain six weeks after starting losartan (50 mg daily). Despite prompt discontinuation of the drug, he progressed to acute liver failure with hepatic encephalopathy, coagulopathy (international normalized ratio (INR): 2.8), and a Model for End-Stage Liver Disease (MELD) score of 28, meeting King's College criteria for poor prognosis. Comprehensive workup, including viral hepatitis panel (A, B, C, and E), cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus (HSV), autoimmune markers, Wilson disease screening, acetaminophen levels, and exclusion of ischemic and metabolic causes, was negative. Liver biopsy showed severe centrilobular necrosis, eosinophilic infiltrate, portal inflammation, interface hepatitis, and cholestasis. Causality assessment using the Roussel Uclaf Causality Assessment Method (RUCAM) yielded a score of 8 (Probable DILI). The patient ultimately required liver transplantation despite early drug withdrawal. This case highlights that losartan-induced hepatotoxicity, although rare, can be life-threatening and underscores the importance of early recognition and a high index of suspicion in patients with unexplained liver injury.

Alzheimer's disease (AD) develops silently for years before symptoms emerge, making early identification of at-risk individuals essential for prevention trials and early intervention. We tested whether combining neurophysiological, imaging, and blood biomarkers improves prediction of progression to mild cognitive impairment (MCI) in cognitively unimpaired older adults with a family history of AD (n = 102; 31 progressors; mean follow-up of 5.9 years). Magnetoencephalography, magnetic resonance imaging, plasma biomarkers, and amyloid and tau positron emission tomography each captured complementary aspects of disease biology. Multimodal models predicted progression more accurately than demographic and genetic factors alone. Higher MEG alpha power was associated with increased near-term risk, whereas higher gamma activity predicted lower near-term risk; both effects weakened over time. Higher neocortical amyloid burden predicted increasing risk over follow-up, whereas plasma biomarkers and entorhinal tau predicted higher risk without significant time-varying effects. These findings support a time-sensitive multimodal framework for identifying cognitively unimpaired individuals at risk of MCI due to AD.

Paradoxical reactions (PR) in pediatric HIV-negative CNS tuberculosis remain underexplored. This study prospectively analyzes incidence and pattern of PR and its impact on functional outcome. Children (6 months-14 years) with newly diagnosed CNS Tuberculosis using the Lancet Consensus Scoring System, were enrolled. All participants received standard anti-tubercular therapy (ATT). Clinical evaluation, CSF analysis and neuroimaging were performed at baseline, during clinical worsening, or at 8 weeks. PR patterns defined as worsening or new tuberculosis lesions or symptoms following initial improvement after ≥10 days of ATT, were documented. Functional outcomes were assessed at 6-months using the Pediatric Cerebral Performance Category (PCPC) scale. Of the 57 participants enrolled [04 with rifampicin resistance were excluded; 24/53 had deterioration within initial 12-weeks of which 17 children qualified for PR (32%; median onset-3.5 weeks; range: 2-7 weeks). Two children developed late-onset PR beyond 12 weeks. [Total PR = 19 (Early-17; Late-2)] Common clinical features included focal neurological deficits (47%) and fever (42%). Prominent radiological patterns were infarction (47%), new or enlarging tuberculomas (37%) and spinal arachnoiditis (37%). Thirteen of 19 cases required additional anti-inflammatory treatment. BMRC Stage 2 and 3 independently predicted PR. PR was associated with unfavourable outcome on PCPC scale (adjusted OR = 34.3; 95% CI: 3.42-343.71; p = 0.001). PR occurs in approximately one-third of pediatric HIV-negative CNS tuberculosis cases, typically early in treatment. Early recognition is essential to distinguish PR from disease progression or drug resistance and to avoid inappropriate treatment modifications.

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Bicuspid Aortic Valve (BAV) is the most common congenital heart disease and often causes aortic stenosis in younger adults. There are few prospective randomized trials comparing Transcatheter Aortic Valve Replacement (TAVR) and Surgical Aortic Valve Replacement (SAVR) in BAV patients, since these patients are usually excluded from major studies because of their complex anatomy. A meta-analysis to compare clinical outcomes between TAVR and SAVR in people with BAV was conducted. PubMed, Google Scholar, and SCOPUS were searched for studies published up to December 2023 that compared TAVR and SAVR in patients with BAV. The main outcomes that were examined were mortality, atrial fibrillation, permanent pacemaker implantation, stroke, respiratory complications, and acute kidney injury. Forward and backward citation searches were also used. Random-effects models were used to calculate pooled odds ratios (ORs) with 95% confidence intervals, and heterogeneity was assessed using the I² statistic. Sensitivity analyses were performed by removing one study at a time. The analysis included seven studies with a total of 96,430 BAV patients. Of these, 41,110 had TAVR and 55,320 had SAVR. Patients who had TAVR were less likely to experience in-hospital respiratory complications, bleeding or need for transfusion, and new-onset atrial fibrillation. However, they were more likely to need a permanent pacemaker. There were no significant differences between the groups in short-term mortality, stroke, or acute kidney injury. Lower peri-procedural morbidity with TAVR likely reflects its minimally invasive nature, whereas higher pacemaker rates may relate to bicuspid valve anatomy and conduction system vulnerability. TAVR appears to be a reasonable alternative to SAVR in carefully selected BAV patients, but randomized trials and long-term follow-up remain necessary.

Transthyretin amyloid cardiomyopathy (ATTR-CM) is a progressive and life-threatening condition caused by extracellular deposition of misfolded transthyretin protein in cardiac tissue. Once considered rare and universally fatal, ATTR-CM has emerged as an increasingly recognized cause of heart failure, particularly among older adults. Recent therapeutic advances have transformed the management landscape from purely symptomatic care to disease-modifying interventions targeting multiple pathogenic mechanisms. This narrative review synthesizes current evidence on pharmacologic strategies for ATTR-CM, including transthyretin stabilizers such as tafamidis and acoramidis, gene-silencing therapies including patisiran, vutrisiran, and eplontersen, fibril disruptors, and emerging amyloid-depleting monoclonal antibodies and gene-editing approaches. We examine pivotal trial data demonstrating improvements in survival, functional capacity, and quality of life, alongside ongoing challenges related to safety, cost, and equitable access. The convergence of early diagnosis through improved imaging and biomarker strategies with targeted therapeutics has substantially changed the outlook for patients with a previously untreatable disease. Future directions emphasize combination therapies, biomarker-guided treatment selection, and precision medicine approaches tailored to disease genotype and phenotype.

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Cardiogenesis is an exquisitely complex developmental process that unfolds through a series of tightly regulated and dynamic morphogenetic events. Proper heart development demands meticulous coordination of multiple signaling pathways, transcription factors and epigenetic mechanisms at every stage of cardiogenesis. Better understanding of the molecular regulation of cardiac development and the advances in the field of stem cell technology have paved way to the development of robust differentiation strategies to generate cardiomyocytes from pluripotent stem cells. This review provides a concise overview of key processes underlying human cardiac development, with a focus on their genetic and epigenetic regulation. It further discusses the generation of cardiomyocytes from human pluripotent stem cells, highlighting state-of-the-art differentiation protocols and detailing the genetic and epigenetic mechanisms that govern in vitro cardiomyocyte formation. By integrating insights from both in vivo human cardiac development and in vitro pluripotent stem cell-derived cardiomyocyte models, this article offers a comprehensive perspective on how embryonic cardiogenesis can be recapitulated in vitro, deepening our understanding of the molecular framework governing cardiomyocyte formation. Importantly, these insights hold significant translational potential for advancing disease modeling, drug discovery, and regenerative therapies for cardiovascular diseases.