The spinal cord lesion in human fetuses with myelomeningocele: implications for fetal surgery.


Conference Paper

Recently produced experimental evidence suggests that secondary traumatic injury and degenerative changes, acquired in utero, to the openly exposed neural tissue may be primarily responsible for the massive neurological deficit associated with myelomeningocele (MMC). The goal of this study was to examine the morphology of human fetuses with MMC to determine if acquired trauma to the spinal cord could be identified. The MMC lesions with surrounding tissues from 10 human fetuses ranging in gestational age between 19 and 23 weeks were prepared with serial histological sections. The MMC lesions were characterized by an open vertebral arch, an open dura mater fused laterally to the dermis, and an open pia mater fused laterally to the epidermis. The spinal cord was exposed, without any meningeal, bony, or cutaneous covering, and was resting on the dorsal aspect of the abnormal arachnoid sac created by the fusion of the meninges to the cutaneous tissues. The exposed neural tissue had undergone varying degrees of recent traumatic injury as a result of its exposed position, ranging from nearly complete preservation of neural elements in four cases to nearly complete loss in two cases. The neural tissue remaining in the MMC with partial loss contained hemorrhages and abrasions from recent injury, suggesting that injury occurred during passage through the birth canal. The presence of dorsal and ventral parts of the cord with nerve roots and ganglia demonstrated that these structures had formed during development and that the loss of tissue by injury was a secondary change. The results support the concept that performing in utero surgery could protect the exposed but initially well-developed and uninjured cord, prevent secondary neural injury, and preserve neural function in the human fetus with myelomeningocele.

Full Text

Cited Authors

  • Meuli, M; Meuli-Simmen, C; Hutchins, GM; Seller, MJ; Harrison, MR; Adzick, NS

Published Date

  • March 1997

Published In

Volume / Issue

  • 32 / 3

Start / End Page

  • 448 - 452

PubMed ID

  • 9094015

Pubmed Central ID

  • 9094015

Electronic International Standard Serial Number (EISSN)

  • 1531-5037

International Standard Serial Number (ISSN)

  • 0022-3468

Digital Object Identifier (DOI)

  • 10.1016/s0022-3468(97)90603-5