Transactions of the Twentieth Annual Meeting of the Society For Maternal-Fetal Medicine—Continued
Hindbrain herniation develops in surgically created myelomeningocele but is absent after repair in fetal lambs

Presented at the Twentieth Annual Meeting of the Society for Maternal-Fetal Medicine, Miami Beach, Florida, January 31–February 5, 2000.
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Abstract

Objective: The purpose of our study was to determine whether prenatal repair of myelomeningocele prevents or reverses hindbrain herniation in the sheep model. Study Design: A myelomeningocele was surgically created in fetal sheep. One group was repaired later in utero; the others were delivered without repair. After delivery, lambs were assessed for the presence of hindbrain herniation. Results: In all lambs that had not undergone repair of the myelomeningocele, severe hindbrain herniation developed, whereas the brains of all lambs that had undergone fetal repair were normal. Conclusion: Prenatal repair of myelomeningocele prevents or reverses development of hindbrain herniation in the fetal lamb model. (Am J Obstet Gynecol 2000;183:1119-23.)

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Material and methods

A surgical open-canal myelomeningocele-like spinal cord defect was created in fetal lambs at 75 days’ gestation (term, 147 days), modifying previously described techniques (Fig 1).6

. Surgical creation of myelomeningocele lesion.

Briefly, the lumbar region of the fetus was exposed through a hysterotomy. An oval skin excision over the lumbar portion of the spine and excision of soft tissue and the paraspinal muscles were performed. Subsequently, a laminectomy (first through fourth lumbar vertebrae)

Results

A myelomeningocele was surgically created in 20 fetal lambs (Fig 2).

. Groups of animals undergoing surgical creation and fetal repair of myelomeningocele lesion.

Four fetuses died shortly after creation of the lesion. One fetus was found to have a spontaneous closure of the defect 3 weeks after creation of the lesion. Five fetal sheep underwent an Alloderm repair, 4 underwent primary surgical repair, and 6 had no repair. Unfortunately, because of a preexisting infection of several ewes with

Comment

Infants with myelomeningocele always have magnetic resonance imaging evidence of hindbrain herniation.9 In addition to this hindbrain herniation, other anomalies of the central nervous system, such as enlargement of the massa intermedia, the presence of polymicrogyria, and the absence of the corpus callosum comprising the Chiari II malformation, are seen.2 Ultrasonography reveals the characteristic shape of the calvarium and frontal bones, referred to as the lemon sign, and the dysplastic

Acknowledgements

We thank William Hoffman, MD, and Bruce Storrs, MD, for their invaluable expertise and help in the primary repair of fetal myelomeningocele.

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Reprint requests: Bettina W. Paek, MD, The Fetal Treatment Center, University of California at San Francisco, San Francisco, CA 94143-0570.

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