TCS is a syndrome in which the spinal cord is stretched and the cone is 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, urinary and fecal disorders, etc. TCS can develop at any age. The clinical manifestations of TCS vary depending on the type of pathology and age. The spinal cord is located in the spinal canal, which grows faster than the spinal cord during development, so the lower end of the spinal cord gradually rises in relation to the lower end of the spinal canal. Spinal cord tethering is a condition in which the lower end of the spinal cord cannot rise normally due to various reasons, making its position lower than normal. It is one of the main pathological mechanisms of various congenital developmental abnormalities leading to neurological symptoms, resulting in a series of clinical manifestations called spinal cord tethering syndrome, also known as spinal cord tethering syndrome. Etiology Causes 1, various congenital spinal developmental abnormalities such as spondylolisthesis, spina bifida, spinal cord spondylolisthesis caused by atresia of the neural tube ends. Most cases are repaired within a few days after birth. The aim is to repair the abnormal neural tissue to a normal state as much as possible, and it is important to prevent cerebrospinal fluid leakage, but the adhesions generated during the healing process after the reconstruction of the spinal dural canal cause embolism at the end of the spinal cord. 2. Spinal cord lipoma and intradural and extradural lipomas are caused by premature separation of the neuroectoderm from the epidermal ectoderm, where fat cells from the mesoderm enter the neuroectoderm that has not yet been occluded. The adipose tissue can enter the central part of the spinal cord, or it can connect to the subcutaneous adipose tissue through the separated vertebral arch, fixing the spinal cord cone. And in cases after early childhood, it is associated with embolism due to inflammation of the fat present in the subarachnoid space, causing fibrosis and adhesive scarring around the nerve roots. Spinal cord embolism syndrome 3, latent hair sinus is a local formation of cord-like tissue from the skin through the subcutis and spine, causing embolism to the spinal cord cone because the neural ectoderm and epidermal ectoderm fail to differentiate well. Dermatomal cysts and epidermal cysts and teratomas can also be produced by the enlargement and proliferation of tissue in the wall of the latent hair sinus, which can encircle or pull on the spinal cord nerves and cause embolism. 4, spinal cord longitudinal fracture The mechanism of spinal cord longitudinal fracture is thought to be caused by factors other than the nerve, namely abnormal development of the vertebrae; others think it is caused by abnormal development of the vertebrae as a result of the abnormal occurrence of the nerve. The spinal cord is separated from the left and right, and there are two types of dural canal with and without division. In this case, the spinal cord is completely separated by fibers, cartilage, or bony crests at the longitudinal fissure, and is divided into two, each with its own dura and arachnoid membranes, and the spinal cord is pulled by the separators, causing symptoms. Type II: common spinal capsule double spinal cord type, the spinal membrane at the longitudinal fissure, mostly separated by the fiber septum, for two parts, but there is a common dura and arachnoid membrane, generally no clinical symptoms. 5.Tension of the terminal filaments is due to the degeneration of the terminal filaments of the immature spinal cord terminal part of the process of formation of obstruction, and make the terminal filaments than the normal terminal filaments thick, the remaining part of the spinal cord embolism caused. 6, neurogenic intestinal cyst The so-called neurogenic intestinal cyst is a state in which the mesenteric margin of the intestinal canal forms a traffic with the tissue in front of the spinal column due to the non-closure of the notochordal duct. Depending on the degree of non-closure and communication of the spinal ducts, there can be associated with bony defects in front of the spine, called spinal-enteric fistula and intestinal cysts inside and outside the spinal canal. 7, lumbosacral spinal expansion postoperative adhesions and other complications Some scholars statistics such can account for 10% to 20% of all surgical cases. Pathogenesis Some scholars believe that the spinal cord embolization restricts the movement of the cauda equina cone and results in a series of clinical symptoms, and they emphasize that it is therapeutic to raise the cauda equina cone after releasing the spinal cord embolization at the time of surgery. However, others argue that although there is no gap in the tension involved, the mechanical effects caused by this static extension are not in themselves the primary cause of symptoms and their significance varies according to the pathology. Repeated flexion and extension of the spine during daily motor movements also causes repeated relaxation and tension of the tethered spinal cord. In fact, it is mainly dynamic factors that play an important role in the appearance and aggravation of symptoms due to posture. In cases of lumbosacral fatty spinal bulge, as the disease progresses, fibrosis due to adhesive arachnoiditis develops, causing not only embolization due to attachment and invasion of the lipoma in the conus, but also contractures around the nerve roots that prevent the spinal cord from ascending. In this case relying only on surgical removal of the lipoma from the conus and allowing little rise of the conus does not make a lot of sense. When the position of the spinal cord cone was observed clinically by MRI after release of the embolus, it was found that the rise of the cone was very limited and there was no significant correlation between the improvement of symptoms and the rise of the cone seen by MRI. The significance of the surgery is rather to free the caudal part of the spinal cord and to relieve the local obstruction of blood circulation to the cone caused by motion with repeated stretching. Considering the impaired blood circulation in the tethered tissue as an important pathogenesis, the practice has been confirmed by experiments on animals causing spinal cord tethering, and the observation and follow-up of somatosensory evoked potentials as an indicator has shown progressive neurological pathological abnormalities. Clinical manifestations The clinical manifestations of spinal cord embolism syndrome (spinal cord tethering syndrome) have similarities to spina bifida in the following ways: lumbosacral skin changes bulging or depressed lumbosacral skin, possibly with discharge or infection; hypertrichosis; bulging large masses ……. These predict the presence of occult spina bifida, latent hair sinus, and spinal bulge, which may be combined with spinal cord embolism. Motor disorders of the lower extremities manifest as abnormal walking, weakness, deformity and pain in the lower extremities, and may be combined with scoliosis. Sensory disorders of the lower extremities include abnormal sensation and pain in the lower extremities, perineum and low back. Urinary and fecal dysfunction commonly manifests as urinary retention, difficulty in urination, urinary incontinence, frequent urination, less than normal volume each time, etc.; constipation, constipation, or incontinence. Diagnosis and examination Magnetic resonance imaging (MRI) is the main method to diagnose spinal cord embolism, which can not only clarify the presence of spinal cord embolism, but also other coexisting pathological changes, such as lipoma, spinal cord longitudinal bifida, etc. X-ray can determine the presence of spina bifida. Ultrasound of the urinary tract and urodynamics are performed in conjunction with urinary and fecal function to evaluate the degree of urinary tract involvement and spinal cord neurological impairment. Treatment principles Early surgery – attention to staging – microsurgery – complete release – end-pool molding – prevention of re-adhesion The sooner embolism release surgery is done once the diagnosis is confirmed, the better. The spinal cord embolism is already organically altered by the time symptoms appear, and we cannot restore it to normal, but can only treat it appropriately so that it does not continue to develop. The symptoms of spinal cord embolism may be the result of destructive damage to the nervous system, which is usually irreparable, and treatment is simply to keep the damage from getting worse. It may also be the result of irritative or incomplete damage to the nervous system, where surgery may have the dual effect of reducing symptoms and preventing progression. Therefore, the fundamental purpose of surgical treatment for spinal cord embolism syndrome is to prevent the progression of the disease, and the degree of improvement is as follows: pain relief or disappearance > recovery of sensory-motor function > recovery of urinary and defecation function > cessation of the deformity and self-correction. In contrast, cases with early onset, severe symptoms and late treatment have relatively poor results, with some having no effect; or the condition recurs after surgery and requires reoperation. Surgery usually does not improve the deformities of the lower extremities and feet, but may improve the pain and incomplete muscle strength to some extent. The deformities of the lower extremities and feet can be partially improved by orthopedic surgery. For patients with normal spinal cord embolism, including those found to have lumbosacral skin changes and sensory and motor deficits in the lower extremities, we recommend early systematic examination, evaluation, and surgery; for patients who have already developed urinary and fecal dysfunction, surgery should be chosen in the context of their general condition and related investigations, and most of these patients can and will require surgery. The outcome of surgery for adult spinal cord embolism syndrome is relatively inferior to that of children. There are many factors that determine the prognosis, which may be related to age, disease duration, etiology, degree of neurological damage, surgical operation and preoperative and postoperative care. Surgery should be performed by a neurosurgeon with experience in spinal surgery and microsurgery. Some children have had previous surgery but only the large lumbosacral pouch (i.e., the bulging spinal capsule and lipoma) was removed without dealing with the spinal cord lesion in the spinal canal. The result is ineffective or aggravated; some doctors even think that the disease is untreatable and wait passively for it to develop, which is a painful lesson. When operating on patients, we should implement the concept of minimally invasive surgery, insist on microsurgery, and cooperate with neurophysiological monitoring if necessary, so as to completely release the embolism as much as possible, avoid nerve damage, reduce re-adhesion and embolism, and prevent postoperative wound complications. Postoperative patients are followed up and given the best possible guidance on the prevention and treatment of urinary tract dysfunction, rehabilitation of lower limb movement and sensation, and correction of lower limb deformities. We believe that focusing solely on embolization surgery and neglecting proper guidance for the continued treatment of these dysfunctions is detrimental to the patient.