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Fetal Origin of Epilepsy

  • Dan Xu,
  • Tao Jiang

摘要

Epilepsy is a neurological syndrome characterized by abnormally excessive synchronized neuronal electrical activity in the brain, which arises from multiple etiologies and complex pathogenesis. The incidence of epilepsy has increased in recent years, affecting people of all ages and leading to a serious decline in the quality of life for patients. It has been increasingly recognized that epilepsy has an intrauterine developmental origin, with multiple adverse factors during pregnancy leading to developmental impairment of the fetal nervous system and abnormal changes in neuronal ion channels. Furthermore, high-stress sensitivity of the hypothalamic-pituitary-adrenal axis after birth may also contribute to susceptibility to adverse external stresses that can trigger epilepsy. This chapter provides a comprehensive overview of the current pathogenesis and mechanisms of epilepsy, with a particular focus on the evidence of intrauterine origin of epilepsy and the mechanism of intrauterine programming of fetal-originated epilepsy mediated by altered epigenetic modifications. The aim is to explore and summarize early warning markers of offspring susceptibility to epilepsy caused by adverse environmental factors during pregnancy at the molecular level, which provides an important theoretical basis for further early prevention and treatment studies related to fetal-originated epilepsy.