Paralysis seen in children with myelomeningocele has been attributed to congenital myelodysplasia. We suspected that paralysis may be due in part to a spinal cord injury caused by exposure of the neural tube to the amniotic fluid. This hypothesis was tested using a fetal rat model of surgically created dysraphism. Each pup from the experimental group of rats in which the spinal cord was intentionally exposed to the amniotic fluid was born with severe deformity and weakness of the hind limbs and tail. Control fetal rats, subjected to the same procedure without directly exposing the spinal cord to the intrauterine environment, were normal at birth. Histological studies of the exposed spinal cord revealed extensive erosion and necrosis, findings similar to those described in children with myelomeningocele. We therefore propose a “two-hit” hypothesis to explain the paralysis seen in children with myelomeningocele: congenital myelodysplasia complicated by an intrauterine spinal cord injury. Intrauterine protection of the exposed spinal cord might prevent some or all of the paralysis. The possible implications of these findings for the future treatment of myelomeningocele are discussed.
The paralysis seen in children with myelomeningocele has been attributed to congenital myelodysplasia. Clinical and pathological data, however, suggest that the paralysis may be due in part to a spinal cord injury caused by exposure of the neural tube to the intrauterine environment. This possibility has been supported by experimental data obtained using a fetal rat model of surgically created dysraphism. In this paper, we report the results of intrauterine treatment of experimental dysraphism in the fetal rat and the fetal pig. These studies confirm our earlier findings and suggest that both physical trauma and toxic injury may contribute to the spinal cord injury.
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