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Review
. 2024 Nov;44(12):1530-1535.
doi: 10.1002/pd.6681. Epub 2024 Oct 6.

Role of Amniotic Fluid Toxicity in the Pathophysiology of Myelomeningocele: A Narrative Literature Review

Yoann Athiel  1   2 , Jean-Marie Jouannic  1   3 , Matthieu Lépine  2 , Corentin Maillet  1   2 , Timothée de Saint Denis  4 , Jérôme Larghero  2 , Lucie Guilbaud  1   2   3
Affiliations
Review

Role of Amniotic Fluid Toxicity in the Pathophysiology of Myelomeningocele: A Narrative Literature Review

Yoann Athiel et al. Prenat Diagn. 2024 Nov.

Abstract

Myelomeningocele is a birth defect whose clinical manifestations are due both to incomplete neural tube closure and the progressive destruction of exposed neuroepithelium during pregnancy. Two hypotheses have been formulated to explain the spinal cord damage in utero: mechanical trauma and chemical factors. The objective of this review was to summarize the current insights about the potential role of amniotic fluid in spinal cord damage in myelomeningocele. Numerous histological and clinical data on animals and humans strongly suggest a progressive degeneration of neural tissue including loss of neural cells, astrogliosis, inflammation, and loss of normal architecture. However, few data have been published about the direct toxicity of amniotic fluid in this neural degeneration, including the potentially toxic effect of meconium. Finally, the chemical and cellular modifications of amniotic fluid composition in myelomeningocele could reflect both the process (toxic effect of meconium) and the consequences of neuroepithelium destruction (release of neural cells). Fetal surgery not only stops the leakage of the cerebrospinal fluid but also reduces the toxic effect of amniotic fluid by restoring the intrauterine environment. Identification of amniotic fluid neurotoxic factors could lead to the development of therapeutic agents designed to protect spinal tissue and improve fetal myelomeningocele outcomes.

Keywords: amniotic fluid; myelomeningocele; neuroepithelium; spinal cord damage; toxicity.

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