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In spina bi da occulta, the cord remains inside the canal and there is no external sac, although a subcutaneous lipoma or a dimple or wisp of hair on the overlying skin may mark the site of the lesion. In meningocele, there is a protrusion of only the dura and arachnoid through the defect in the vertebral laminae, forming a cystic swelling usually in the lumbosacral region; the cord remains in the canal, however. In meningomyelocele, which is 10 times as frequent as meningocele, the cord (more often the cauda equina) is extruded also and is closely applied to the fundus of the cystic swelling. The incidence of spinal dysraphism (myeloschisis), like that of anencephaly, varies widely from one locale to another, and the disorder is more likely to occur in a second child if one child has already been affected (the incidence then rises from 1 per 1000 to 40 to 50 per 1000). Exogenous factors (e.g., potato blight in Ireland) have been implicated in the genesis of both myeloschisis and anencephaly. Folic acid, given before the 28th day of pregnancy, can be protective; vitamin A may also have slight protective bene t. As with anencephaly, the diagnosis can often be inferred from the presence of -fetoprotein in the amniotic uid (sampled at 15 to 16 weeks of pregnancy) and the deformity con rmed by ultrasound in utero, as mentioned earlier in this chapter. Blood contamination is a source of error in the fetoprotein test (Milunsky). Acetylcholinesterase immunoassay, done on amniotic uid, is another reliable means of con rming the presence of neural tube defects. Some parents, on receiving this information, request abortion. In the case of meningomyelocele, the child is born with a large externalized lumbosacral sac covered by delicate, weeping skin. It may have ruptured in utero or during birth, but more often the covering is intact. There is severe dysfunction of the cauda equina roots or conus medullaris contained in the sac. Stroking of the sac may elicit involuntary movements of the legs. As a rule the legs are motionless; urine dribbles, keeping the patient constantly wet; there is no response to pinprick over the lumbosacral zones; and the tendon re exes are absent. In contrast, craniocervical structures are normal unless a Chiari malformation is associated (see further on). Differences are noted in the neurologic picture depending on the level of the lesion. If it is entirely sacral, bladder and bowel sphincters are affected but legs escape; if lower lumbar and sacral, the buttocks, legs, and feet are more impaired than hip exors and quadriceps; if upper lumbar, the feet and legs are sometimes spared and ankle re exes retained, and there may be Babinski signs. The two dreaded complications of these severe spinal defects are meningitis and progressive hydrocephalus from a Chiari malformation, which is often associated (see below). The subject of neural tube defects has been reviewed by Botto and colleagues. Treatment Opinions as to proper management vary considerably. Excision and closure of the coverings of the meningomyelocele in the rst few days of life is advised if the objective is to prevent a fatal meningitis. After a few weeks or months, as hydrocephalus reveals its presence by rapid increase in head size and enlargement of the ventricles on the CT scan, a ventriculoatrial or ventriculoperitoneal shunt is required. Patients with high spinal lesions and total paraplegia, kyphosis, hydrocephalus, and other major congenital anomalies are usually not accepted for treatment. Less than 30 percent of such patients survive beyond 1 year, and the long-term results of treating these patients have not been encouraging. Lorber and others report that 80 to 90 percent of their surviving patients are mentally retarded to some degree and are paraplegic thus totally dependent on others for their care. The decision to undertake
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