Objectives: Despite advances in prenatal diagnosis, management of fetal mye
lomeningocele has been limited to abortion or supportive postnatal care. Th
e rationale for fetal repair of myelomeningocele and initial clinical outco
mes are discussed. Methods: A complete review of the literature concerning
fetal myelomeningocele and repair was performed. Results: While myelomening
ocele is a primary embryologic disorder, neurologic damage is also secondar
y to progressive in utero damage to the exposed spinal cord. Animal models
with midgestational coverage of the spinal defect demonstrate near normal n
eurologic function at term. Early clinical results suggest that fetal closu
re can salvage neurologic function, reverse hindbrain herniation, and dimin
ish the need for ventriculoperitoneal shunting. Conclusions: In utero repai
r of myelomeningocele may improve neurologic outcomes and reduce hindbrain
herniation in selected patients. Copyright (C) 2001 S.Karger AG, Basel.