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Background: Exposure to general anesthetics (GA) in early childhood is associated with developmental disorders. However, few studies have addressed in-utero exposure to anesthetics during delivery and subsequent developmental disorders in the offspring. This study aimed to investigate whether GA for cesarean delivery is associated with developmental disorders in children.
Methods: Using data retrieved from the National Health Insurance Research Database linked to the Birth Reporting Database and the Maternal and Child Health Database between 2015 and 2020, this nationwide retrospective cohort study compared the incidence of developmental disorders following cesarean delivery under GA with that under neuraxial anesthesia (NA). Developmental disorders were diagnosed using the corresponding International Classification of Diseases codes traced 2-6 years after delivery.
Results: After excluding twins, children born with congenital anomalies or diseases and those with missing data, 325,309 eligible singleton pregnancies delivered through cesarean section under either GA or NA were enrolled. Of the total, 6973 of them were delivered under GA and 318,336 under NA. After propensity score-based fine stratification weighting with a model including age, socioeconomic deprivation, gestational status, infant sex, preterm delivery, low birth weight, and cesarean delivery duration, children delivered under GA were associated with a higher risk of developmental disorders diagnosed within 2 years (adjusted odds ratio [aOR], 1.17; 95% confidence interval [CI], 1.07-1.28), 3 years (aOR, 1.12; 95% CI, 1.04-1.21), and 4 years (aOR, 1.12; 95% CI, 1.04-1.21) compared with those under NA. This association was no longer present when the confounding effect of Apgar scores was included in the propensity-score model.
Conclusions: GA for cesarean delivery may be associated with developmental disorders diagnosed within 2-4 years after birth manifested through poorer 1- and 5-min Apgar scores. There is no evidence of a direct relationship between GA-related neurotoxicity and subsequent developmental disorders.
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http://dx.doi.org/10.1186/s12916-025-03886-6 | DOI Listing |
J Med Genet
September 2025
Department of Pediatrics, Danish Epilepsy Center, Dianalund, Denmark
Rare variants in , the gene encoding the GluA3 subunit of amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors (AMPARs), are associated with defects in early brain development. Disease-causing variants are generally categorised as either loss of function (LoF) or gain of function (GoF) that appear to be linked to different symptoms. Here, we reported a de novo variant (N651D) that has mixed LoF and GoF in a female patient with a devastating developmental and epileptic encephalopathy, parkinsonism and cortical malformation.
View Article and Find Full Text PDFBMJ Case Rep
September 2025
Department of Pathology and Lab Medicine, All India Institute of Medical Sciences Jodhpur, Jodhpur, Rajasthan, India.
Gaucher's disease (GD) is the most common lysosomal storage disorder inherited in an autosomal recessive pattern. It occurs due to a deficiency of the enzyme glucocerebrosidase owing to a mutation in the acid-β-glucosidase () gene resulting in accumulation of glucocerebrosides in lysosomes of cells. It presents with abdominal distension, hepatosplenomegaly, developmental delay, pancytopenia, neurological manifestations and bone diseases.
View Article and Find Full Text PDFBrain Res Bull
September 2025
Department of Neuroscience of Disease, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan. Electronic address:
Mutations in the UBE3A gene are responsible for neurodevelopmental disorders (NDDs), including Angelman syndrome (AS), which is characterized by developmental delays, impaired motor coordination, and cognitive disabilities. In recent years, UBE3A mutations have also been linked to autism spectrum disorders (ASD), due to their significant role in synaptic plasticity and cognitive function. Although substantial research has utilized mammalian models, the zebrafish (Danio rerio) provides unique opportunities to investigate gene functions owing to their transparent embryos, rapid development, and suitability for large-scale genetic and behavioral studies.
View Article and Find Full Text PDFBiol Psychiatry
September 2025
Developmental Neuroscience and Neurogenetics Program, The Saban Research Institute, Los Angeles, CA; Child and Brain Development Program, Canadian Institute for Advanced Research, Toronto, Canada; Division of Endocrinology, Children's Hospital LA, Los Angeles, CA; Department of Pediatrics, Keck Scho
Background: Exposure to early life adversity (ELA), including childhood maltreatment, is one of the most significant risk factors for the emergence of psychosomatic disorders in adolescence and adulthood. Most investigations into biological processes that have been perturbed by ELA have profiled DNA methylation in whole blood and coalesced around perturbations of immunobiology being centrally insulted by ELA.
Methods: To identify novel molecular signatures that are enduringly perturbed by childhood maltreatment, we isolated circulating extracellular vesicles (EVs) from plasma collected from adolescent rhesus macaques that had either experienced nurturing maternal care (CONT, n = 7, 4M 3F) or maltreatment in infancy (MALT, n = 6, 3M 3F).
Biol Psychiatry Cogn Neurosci Neuroimaging
September 2025
Developmental Imaging and Psychopathology Laboratory, University of Geneva School of medicine, Geneva, Switzerland; Department of Genetic Medicine and Development, University of Geneva School of Medicine, Geneva, Switzerland.
Background: Recent epidemiological evidence links early-life obesity and metabolic dysregulation to adult psychosis vulnerability, though a causal relationship remains unclear. Establishing causality in highly heritable psychotic disorders requires: 1) demonstrating that early-life metabolic factors mediate between genetic vulnerability and psychosis trajectory, 2) dissecting mechanisms leading to early-life obesity in genetically vulnerable individuals, and 3) clarifying downstream neurodevelopmental pathways linking early-life obesity to psychosis symptoms.
Methods: Here we investigated bidirectional pathways linking behavioral, BMI, and neurodevelopment trajectories in a unique longitudinal cohort of 184 individuals at high genetic risk for psychosis, due to 22q11.