Spina bifida is one of the most common human birth defects. In fetuses with open spina bifida, the spinal cord remains exposed to the amniotic fluid (AF) throughout gestation. Results of prenatal examinations suggest that affected fetuses exhibit leg movement until the third trimester but become paralyzed later in pregnancy, several months after the initial spinal cord defect occurred. Clinical observations suggest that after the initial defect in neural tube closure, the spinal cord may be subjected to continuous, progressive damage related to contact with the AF. We urge clinicians and scientists to test the AF damage hypothesis by studying prenatal fetal activity in humans and through experimental studies. If this hypothesis is correct, the onset of spinal paralysis in affected fetuses may be prevented by protecting the spinal cord tissues before major nerve damage occurs. If the course of this disease process could be altered, both the patient and family would benefit from the reduction in the misery of the disabling neurologic condition as well as from the acute and long-term cost of medical care.