TCS is a syndrome in which the spinal cord is stretched and coned low due to congenital or acquired factors, resulting in ischemia, hypoxia, neurodegeneration, and other pathological changes in the spinal cord, resulting in sensory and motor dysfunction or deformity of the lower extremities, and urinary and fecal impairment. The clinical manifestations of TCS vary depending on the type of pathology and age. There are various causes of spinal cord embolism, such as congenital spina bifida, intradural and extradural lipomas, spinal cord bulge, spinal cord adhesions after lumbosacral surgery, and spinal cord longitudinal bifida deformity. The site of spinal cord embolism is, in most cases, the conus or terminal filum of the spinal cord. The common feature is the fixation effect of the lesion on the distal spinal cord and nerve roots. Etiology of primary TCS At the beginning of embryonic development, the spinal cord and the spinal canal are equal in length, and then the spinal column grows faster than the spinal cord, so the spinal cord moves relatively upward due to cephalad fixation of the spinal cord. At 20 w of embryonic life, the spinal cord cone moves up to the level of L3-4 vertebrae, and at 40 w it is located at the level of L3 vertebrae, and the end of the spinal cord is located at the level of L1-2 in birth infants. Three months after birth, the spinal cord rises to the adult level, i.e., the cone ends at the L1 level. The cone of the spinal cord becomes thin and moves to the end filament (less than 2 mm in diameter in adults). In the process of spinal cord upward migration, if there are pathological changes such as neural tube closure insufficiency, intradural lipoma, spinal cord cone dermatomal cyst or teratoma, or spinal cord longitudinal fracture that leads to spinal cord traction and cone hypoplasia, it will cause poor retraction of the spinal cord ends, and the cauda equina terminal filaments are adhered and bound, resulting in dysplasia, which is called primary spinal cord embolism syndrome. Secondary causes of TCS Mostly after lumbosacral spina bifida repair or intradural spinal canal surgery, the scar tissue in this area adheres to the spinal cord and cauda equina, and scar contraction leads to spinal cord traction, also seen in adhesions formed after local bleeding from arachnoiditis, called secondary spinal cord embolism syndrome. After the spinal cord is embolized and fixed, it causes ischemia and hypoxia due to impaired blood circulation to the spinal cord or nerves, and gradually degenerates and necroses or shows degenerative changes. In the lipoma type, the adipose tissue embolizes the spinal cord through the defective vertebral plate and dura mater, and the adipose tissue infiltrates the spinal cord and the nerve fibers penetrate deep into the lipoma, often without a clear boundary between the two. This results in a low metabolic rate at the embolization site and progressive neurological damage, and about 20% of spinal cord emboli are combined with hydrocephalus. Patients with spinal cord embolism syndrome often have characteristic cutaneous manifestations, such as small depressions in the lumbosacral skin, cutaneous sinus tracts, localized hairy or dermal sinuses, hemangiomas in the midline of the waist, and asymmetric gluteal clefts. Lumbosacral subcutaneous lipomas are suggestive of fatty spinal cord spondylolisthesis (lipomyelomeningocele). MRI: MRI is the preferred method for diagnosing TCS. MRI clearly shows the location of the spinal cord cone and thickened end filaments, and it is generally considered abnormal for the spinal cord cone to be below the lower edge of the lumbar 2 vertebral body and for the end filaments to be >2 mm in diameter. MRI can also detect other abnormalities such as spina bifida, split spinal cord deformity, and spinal cord cavity. X-ray plain film: It can understand the presence of spina bifida, scoliosis and vertebral segmentation insufficiency and other deformities, and it is suggestive for the diagnosis of TCS, but it can only show bone abnormalities and cannot directly show neurological deformities and abnormalities. CT: CT myelography can show the relationship between lipomas, spinal cones, cauda equina and dura mater. In addition, CT can show skeletal deformities, spina bifida, and intraspinal tumors. However, the sensitivity and reliability of CT diagnosis of spinal cord embolism syndrome is not as good as MRI, and CT spinal canal imaging is invasive, so for typical spinal cord embolism syndrome patients, MRI diagnosis is sufficient. For complex spinal cord embolism syndromes, especially those with complex bony deformities, MRI and CT can be used in combination. Surgical treatment of spina bifida is required for all cases of manifest spina bifida, and the timing of surgery is 1-3 months after birth. Simple spina bifida, or other types with mild neurological symptoms, should be operated as early as possible. If surgery is postponed for reasons such as systemic conditions, local protection should be provided, especially for those with exposed spinal cord, to prevent infection. The principle of surgery is to divide and release the surrounding adhesions, incorporate the posteriorly protruding spinal cord or nerve roots back into the spinal canal, remove the excess dural sac, close the spinal opening with tight sutures, repair the fascial overlap on both sides of the fissure, and repair the defect in the vertebral plate (bone graft, etc.). In patients with spinal cord embolism syndrome, spinal canal exploration, release of adhesions and severance of the end filaments are feasible. On the other hand, because the barrier function of the skin is fragile, and the skin contains more water and has a higher pH value, which is conducive to the growth of pathogenic bacteria, the skin care of the child should be strengthened, turning the child every l to 2 hours, turning gently, avoiding dragging, etc., paying attention to keeping the bed unit clean and tidy, without folds, and to the bone Protruding parts should be massaged after each turning, and attention should be paid to axial turning when turning to avoid excessive distortion of the torso.