Objectives: Despite advances in prenatal diagnosis, management of fetal myelomeningocele has been limited to abortion or supportive postnatal care. The rationale for fetal repair of myelomeningocele and initial clinical outcomes are discussed. Methods: A complete review of the literature concerning fetal myelomeningocele and repair was performed. Results: While myelomeningocele is a primary embryologic disorder, neurologic damage is also secondary to progressive in utero damage to the exposed spinal cord. Animal models with midgestational coverage of the spinal defect demonstrate near normal neurologic function at term. Early clinical results suggest that fetal closure can salvage neurologic function, reverse hindbrain herniation, and diminish the need for ventriculoperitoneal shunting. Conclusions: In utero repair of myelomeningocele may improve neurologic outcomes and reduce hindbrain herniation in selected patients.

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