Congenital neural tube anomaly is a defect in the formation of the neuroembryo and is the most common birth defect with an incidence of 0.6 to 3.7 per 1000 live births. The pathogenesis includes both genetic and environmental factors. Possible environmental factors include geographic location, season of conception, socioeconomic level, maternal age, zinc and folic acid deficiency, maternal alcohol abuse, and maternal use of antiepileptic drugs. And genetics determines the susceptibility to environmental factors. They are classified as open and closed according to neural tissue exposure or not. ① Open neural tube malformation: Due to defective formation of primary neuroectoderm, neural tissue is exposed with cerebrospinal fluid leakage, e.g., with hydrocephalus, Chiari II malformation. ② Closed neural tube malformation: Due to defective formation of secondary neurogerm, neural tissue is not exposed and the defective area is covered with dysplastic skin tissue, including: anencephaly, cerebrospinal bulge (meningeal bulge or spinal cord bulge), craniospinal bifida, congenital dermal sinus, open spina bifida, spinal cord spinal membrane protrusion, meningeal bulge, spina bifida, spinal cord longitudinal bifida, caudal hypoplasia, etc. Open neural tube defects are visible at birth and the vast majority can be detected during gestation. Neural tube defects can cause progressive neurodegeneration, with symptoms appearing shortly after birth or later, due to concomitant hydrocephalus, Chiari II malformation, cystic masses of the spinal cord tethering, or fibrous bands compressing the neural tissue, which can be complicated by meningitis. Closed neural tube malformations have different presentations and can also have no skin markings, making them unrecognizable for many years. The most common manifestations are distinct abnormalities along the spine, such as fluid-filled cystic masses, hypopigmented, or hyperpigmented areas, dermal hypoplasia, congenital dermal sinuses, small hairy patches, skin appendages, and asymmetric gluteal clefts. Closed neural tube defects. This is followed by asymmetry of the lower extremities or feet, with one limb being thinner, smaller feet, high arched feet or claw toes. Other children present with progressive spinal deformities such as scoliosis. Some children present with progressive neurological deficits, including weakness of one distal lower extremity, sensory deficits, and bladder and rectal dysfunction, which are associated with spinal cord tethering. MRI is preferred for suspected neural tube deformities and can detect spinal or intracranial malformations. CT scans can show bony defects and anatomy, facilitating the detection of hydrocephalus or other intracranial malformations. Clinical manifestations Lumbosacral skin changes: bulging or depressed lumbosacral skin, possibly with secretions or infection; hypertrichosis; occult spina bifida, dermatomal sinus, spondylolisthesis, subcutaneous lipoma, etc. 1, manifesting as abnormal walking, weak lower limb strength, ankle deformation (clubfoot). 2, manifesting as abnormal sensation and pain in the lower limbs, perineum and low back. Open neural tube deformity surgical treatment includes: 1. early closure of the defect; 2. children with hydrocephalus should be closed with a tube for ventriculoperitoneal shunt; 3. symptomatic Chiari deformity should be decompression of the posterior cranial fossa under the occipital bone; 4. children with spinal cord tethering should undergo tethering release surgery as early as possible. Preferred surgical treatment is to loosen the tethered spinal cord. If there is a combination of lipoma, if it is easy to separate from the nerve tissue, it can be removed together with the end filaments, and a longitudinal shuttle incision is made for obviously bulging fatty masses. In order to reduce the strain on the spinal cord and nerve roots, the dura mater is incised and then the lipoma is resected intracapsularly, the pericardium is finally freed, the sides of the dural sac are explored, the adhesions on both sides of the dural sac are sharply freed, and the adherent spinal nerves are released. Cone-shaped dorsal, terminal filament, and fatty spinal cord bulging lipomas are relatively easy to manage. Cone-shaped ventral lipomas and compound lipomas are difficult to treat because the lipoma is located ventral to the spinal cord and because the lipoma is mixed with the spinal cord, with one or both nerve roots entering the lipoma. It is very difficult to remove the fat. In this case, most of the lipoma tissue can be aspirated by emulsifying the fat particles with a surgical ultrasound suction device without damaging the ventral nerve plate, and it is important to consider that the fat is not simply wrapped and adhered to the spinal cord, nerve roots and cauda equina, in which various forms of nerve fibers are distributed and grow together. The nerve stripper should be used to remove the adipose tissue in small pieces, and an electrical stimulator should be used to distinguish between the fibrous tract and the nerve. The dura should be repaired with artificial dura to prevent postoperative subarachnoid adhesions from re-tethering. The patient should be operated with a minimally invasive concept, insisting on microsurgery, and always with neurophysiological monitoring, in order to release the embolus as completely as possible, avoid nerve damage, reduce re-adhesion and embolus, and prevent postoperative wound complications. Postoperative patients are followed up for the prevention and treatment of urinary tract dysfunction, and with biofeedback rehabilitation, urinary and stool function can be restored by more than 75%. Restoration of lower limb motor and sensory rehabilitation, as well as correction of lower limb deformities are given as much guidance as possible. We believe that focusing solely on embolization surgery and neglecting proper guidance for the continued treatment of these dysfunctions is detrimental to patients.