Myelomeningocele (MMC) is the most common congenital defect of the central nervous system and results in devastating and lifelong disability. In MMC, the initial failure of neural tube closure early in gestation is followed by a progressive prenatal injury to the exposed spinal cord, which contributes to the deterioration of neurological function in fetuses. Prenatal strategies to control the spinal cord injury offer an appealing therapeutic approach to improve neurological function, although the definitive pathophysiological mechanisms of injury remain to be fully elucidated. A better understanding of these mechanisms at the cellular and molecular level is of paramount importance for the development of targeted prenatal MMC therapies to minimize or eliminate the effects of the injury and improve neurological function. In this review article, we discuss the pathological development of MMC with a focus on in utero injury to the exposed spinal cord. We emphasize the need for a better understanding of the causative factors in MMC spinal cord injury, pathophysiological alterations associated with the injury, and cellular and molecular mechanisms by which these alterations are induced.

脊髓膜腔积液（MMC）是中枢神经系统最常见的先天性缺陷，导致毁灭性和终生残疾。在MMC中，妊娠早期神经管闭合的最初失败是暴露的脊髓逐渐受到产前损伤，这导致胎儿神经功能的恶化。产前控制脊髓损伤的策略为改善神经功能提供了一种有吸引力的治疗方法，尽管损伤的确定的病理生理机制尚待充分阐明。在细胞和分子水平上更好地理解这些机制对于开发靶向产前MMC治疗方法至关重要，以最小化或消除损伤的影响并改善神经功能。在这篇评论文章中，在子宫内脊髓暴露损伤。我们强调需要更好地了解MMC脊髓损伤的病因，与损伤相关的病理生理学改变以及诱导这些改变的细胞和分子机制。