Closed spinal cord injury

　　1. Etiology

　　The cause of closed spinal cord injury is violence acting indirectly or directly on the spine, causing fractures and (or) dislocations, leading to compression, injury, of the spinal cord and cauda equina. Approximately 10% of spinal cord injury cases have no obvious radiographic changes in fractures and dislocations, known as spinal cord injuries without radiographic abnormalities, which are more common in children with strong spine elasticity and elderly individuals with pre-existing spinal canal stenosis or osteophytes.

　　Direct violence causing injury is relatively rare, seen in cases where heavy objects strike the back of the neck, back, lumbar region, corresponding vertebral plates, and spinous process fractures, with fracture fragments陷入 vertebral canal.

　　Indirect violence accounts for the majority of injuries, commonly occurring in traffic accidents, high-altitude falls, building collapses, cave collapses, and sports activities. The violence acts on other parts of the body and is then transmitted to the spine, causing it to exceed the normal limits of flexion, extension, rotation, lateral flexion, vertical compression, or traction (often a mixed motion), leading to the injury, rupture, fracture, and (or) dislocation of the tendons that maintain spinal stability, vertebral body fractures and (or) dislocations, articular process fractures and (or) dislocations, accessory fractures, intervertebral disc protrusion, yellow ligament folds, etc., causing compression and injury to the spinal cord.

　　Factors affecting the type of spinal fracture or ligament injury include: ① The intensity and direction of the external force, ② The point of application of the external force, ③ The posture of the body at the time of injury, ④ The anatomical and biomechanical characteristics of different segments.

　　Spinal cord injuries usually occur at the junction of a segment with a high degree of mobility and a segment with a low degree of mobility. The cervical and thoracolumbar junction (from the eleventh thoracic vertebra to the second lumbar vertebra) is the most frequently affected region in spinal cord injuries, followed by the incidence of the thoracic and lumbar segments. The reasons for the common types of injuries in different segments are as follows:

　　1, The cervical segment has poor mechanical stability and is more susceptible to injury than other segments, with a high proportion of combined spinal cord injury (40%), accounting for 50% of all spinal cord injuries.

　　(1) Flexion type injury: Commonly seen in sudden braking or collisions, where the head moves forward due to inertia, the posterior ligament complex is damaged, the anterior part of the vertebral body is compressed into a wedge shape, which is usually stable. However, excessive flexion can cause widespread injuries including intervertebral discs and joint capsules, or fracture of the articulating process, locking, and shearing forces can cause the vertebral bodies above the injury level to slide forward, with the spinal cord being compressed by the superior posterior part of the next vertebral body, even leading to rupture.

　　(2) Extension type injury: When falling, the chin or forehead hits the ground, or when hit by the rear vehicle while sitting in a car, the head is thrown back, with injuries most often occurring at the fourth to fifth cervical vertebrae. The anterior longitudinal ligament may rupture, the anterior part of the vertebral body may be torn off, the pedicle may be fractured, and in severe cases, the vertebral bodies above the injury level may posteriorly dislocate. The spinal cord may be compressed by the anterior vertebral body, intervertebral disc, and posterior vertebral lamina, yellow ligament, and those with cervical spondylosis are prone to such injuries.

　　(3) Vertical compression type injury: When the head is subjected to longitudinal force in an extended state of the neck, burst fractures or fractures of the pedicle may occur at the fourth and fifth cervical vertebrae.

　　(4) Special types of fractures: Jefferson fracture refers to the fracture of both sides of the anterior and posterior arches of the atlas under the action of axial pressure, where the spinal canal is wider and generally without spinal cord injury. Odontoid fracture is caused by excessive flexion or extension of the neck, with the fracture occurring at the tip, body, or base of the odontoid. Fractures in hanging or hanging from a gallows are caused by extreme hyperextension of the atlas, which can be accompanied by separation of the vertebral bodies of the second and third cervical vertebrae.

　　2, The thoracic and lumbar segments from the first to the tenth thoracic vertebrae are protected by ribs, making them relatively stable with a low incidence of injury. However, when injury does occur, it is often complete due to the smaller spinal canal. The blood supply to the upper thoracic segment is poor, and if the injury involves the Adamkiewicz artery, the ischemic level can rise to the fourth thoracic vertebra. The lumbar joint surface is perpendicular, and the stability in the anterior-posterior direction is good. The lumbar canal is wider, and below the first and second lumbar vertebrae is the cauda equina. Therefore, injuries are often incomplete. The junction between the relatively stable thoracic vertebrae and the highly mobile lumbar vertebrae from the twelfth thoracic vertebra to the first lumbar vertebra is the most susceptible to injury.

　　(1) Flexion-type injury: When falling, if both feet or the buttocks land, and when bending over, the back is struck by a heavy object, it often causes flexion-type injury at the thoracolumbar segment. In mild cases, the anterior part of the vertebral body is compressed into a wedge shape, and in severe cases, it is accompanied by dislocation or separative injury to the posterior structure.

　　(2) Flexion-rotational injury: Caused by falling from a height, with the upper back and one shoulder landing, causing injury, which often involves the three-column structures of the front, middle, and back, with anterior vertebral body compression, vertebral body transverse fracture, vertebral arch and transverse process fracture, often accompanied by dislocation, leading to severe spinal cord injury.

　　(3) Vertical compression-type injury: When a falling object hits the upper thoracic segment or when falling, if both feet or the buttocks land, it can cause burst fractures of T10 to L2.

　　(4) Flexion-separation injury: Also known as seat belt fracture, the old-style car seat belt is horizontally fastened across the anterior abdominal wall without shoulder protection. In a traffic accident, the upper body is excessively flexed around this axis, and in severe cases, the three-column structure can be horizontally transversely cut, dislocated, and can be accompanied by abdominal visceral injury.

　　Second, pathogenesis

　　The mechanism of acute spinal cord injury includes primary spinal cord injury and secondary spinal cord injury that occurs subsequently. Primary injury refers to the initial mechanical spinal cord injury caused by local tissue deformation and trauma energy transmission; secondary spinal cord injury refers to the chain reaction process activated by the primary injury, including biochemical and cellular changes, which can cause progressive damage to nerve cells, even death, and lead to autolysis and destruction of the spinal cord, irreversible damage to intramedullary structures, and progressive expansion of the spinal cord injury area.

　　1. Primary spinal cord injury

　　(1) Cervical cord concussion: The mildest pathological injury among all spinal cord injuries, which results in transient, reversible spinal cord dysfunction after injury. Under the microscope, it can be seen that there is a small focal hemorrhage in the central gray matter, a few neurons or axons degenerate, and it can generally return to normal within a few weeks after injury, with hemorrhage absorption.

　　(2) Cervical cord contusion and laceration injury: The pathological changes in the early stage are mainly hemorrhage, exudation, edema, and degeneration of neurons. Under the microscope, it can be seen that small blood vessels rupture, red blood cells leak out, neurons swell, Nissl bodies disappear, the gap between the nerve axon and the myelin sheath increases, the myelin lamellae separate. With the development of the pathological process, necrosis, disintegration, and disappearance of neuronal structures gradually appear, gliocytes infiltrate, and connective tissue cells proliferate. The pathological changes of complete injury extend from massive hemorrhage in the central gray matter to hemorrhage in the white matter, and from central gray matter necrosis to complete spinal cord necrosis; while incomplete injury is mainly punctate hemorrhage, focal neuronal cell degeneration, disintegration, and a few axonal degenerative changes without central necrosis. There are qualitative and quantitative differences in pathological changes between the two.

　　(3) Cervical cord compression injury: Animal experiments have observed that long-term compression of the spinal cord can lead to cavities, cavities, and空洞 surrounded by phagocytes formed by fibrous tissue without obvious hemorrhage in the gray matter. Mildly compressed individuals often show no significant changes.

　　2, Secondary spinal cord injury:The concept of secondary injury was first proposed by Allen in 1911. In animal experiments, he observed that the neurological function of dogs with acute spinal cord injury improved after the hematoma was cleared, and he believed that there may be biochemical substances derived from local hematoma and necrosis that can cause further spinal cord injury. In the mid-1970s, Kobrine and Nelson respectively proposed the neurogenic theory and the vascular theory of secondary spinal cord injury. The former believes that the injury of the nerve membrane induces a series of pathophysiological metabolic changes, while the latter believes that the rupture of spinal cord microvessels, vasoconstriction, thrombosis, etc. cause spinal cord ischemia, ultimately leading to central hemorrhagic necrosis. In the following nearly 30 years, a large number of studies have successively proposed various factors related to secondary spinal cord injury, mainly including:

　　(1) Vascular changes, including local ischemia, microcirculatory disorders, vasoconstriction, thrombosis, and the loss of vascular autoregulation mechanisms.

　　(2) Ionic disorders, including increased intracellular calcium, extracellular hyperkalemia, and increased permeability of sodium ions.

　　(3) Neurotransmitters, such as 5-hydroxytryptamine, catecholamines, and the aggregation of excitatory amino acids, which can lead to excitotoxic injury to neurons.

　　(4) The release of arachidonic acid, the production of free radicals, and lipid peroxidation reactions.

　　(5) Endogenous opioid-like substances.

　　(6) Nitric oxide (N0).

　　(7) Edema.

　　(8) Inflammatory response.

　　(9) Abnormal cell energy metabolism.

　　(10) Programmed cell death, apoptosis, etc.

　　However, the mechanism of secondary spinal cord injury is still not very precise at present. Among these related factors, the most worthy of attention is still the ischemic changes caused by local microcirculatory disorders and the lipid peroxidation reaction caused by free radicals.

　　Due to the serious harm of secondary spinal cord injury, blocking and reversing this process in the early stage after injury is of great significance for the treatment of spinal cord injury. Effective treatment should target the pathophysiological mechanism of secondary spinal cord injury, protect the white matter tracts that have not been damaged, and achieve the purpose of preserving part of the neurological function.

　　Patients with acute spinal cord injury are affected by each system, atelectasis and accumulation of respiratory tract secretions often lead to pneumonia and other respiratory complications, congestion in the cardiovascular system often results in deep vein thrombosis, literature reports that 3% to 13% of cases of phlebitis or fatal pulmonary embolism caused by deep vein thrombosis, pressure on the skin without sensation can cause bedsores, ulcers, inability to move limbs can cause muscle atrophy and severe contracture of the soft tissues around the joints, congestion in the urinary tract system can cause frequent infections and calcification, inactivity of the skeletal system causes a large amount of calcium loss, leading to urinary tract stones, ectopic bones, severe osteoporosis, and ultimately pathological fractures, gastrointestinal paralysis causes intestinal obstruction, ulcers, bleeding, and chronic constipation, and sometimes pancreatitis may also occur.

　　In patients with acute spinal cord injury over 40 years of age who have arrhythmias due to neurogenic shock, and have a history of heart disease or direct heart injury, close cardiac monitoring should be provided. For younger patients in good general condition, a multi-lumen central venous pressure catheter and peripheral venous access should be provided, and continuous electrocardiogram monitoring can greatly reduce cardiovascular complications.

　　The most common complication of acute spinal cord injury is still the involvement of the respiratory system, caused by the paralysis of the intercostal muscles, leading to changes in pulmonary function. In patients with multiple trauma, there may be direct trauma to the ribs and lung parenchyma. Preventive tracheal intubation is often given to patients with high-level tetraplegia. Oxygen should be administered when there is insufficient arterial blood oxygen or respiratory distress, and chest physical therapy should be performed every 4 hours. Oxygen masks, nasal cannulas, or end-expiratory positive pressure masks may be used if necessary to maintain blood gas levels within the normal range. Tracheal intubation should be performed as nasally as possible to avoid tracheotomy. In patients with tetraplegia due to injury at C1-4, if there is no spontaneous breathing, tracheotomy should be performed early, and chronic airway support, intermittent ultrasound examination, electrical physiological examination of the diaphragm and phrenic nerve, and close monitoring of vital capacity, tidal volume, and other respiratory parameters should be carried out. If patients with acute spinal cord injury, especially those with tetraplegia, are extubated prematurely, they may experience mucus obstruction, atelectasis, and even respiratory distress.

　　Acute gastrointestinal bleeding in patients with acute spinal cord injury is often fatal, and therefore, hydrogen ion antagonists should be administered intravenously, a gastric tube should be placed, and low-pressure drainage of gastric secretions should be maintained. The pH value should be tested every 4 hours. Patients with acute spinal cord injury at the level of the cervical spine often have neurogenic shock, which is often manifested as a sympathectomy-like syndrome, such as increased gastric acid secretion, relative ischemia and weakness of the gastrointestinal tract, which are prone to cause stress ulcers.

　　In addition to cardiovascular and pulmonary complications, another major cause of death in patients with acute spinal cord injury is urinary tract infection complicated with sepsis. The management of the genitourinary system begins in the emergency room, with the insertion of a Foley catheter, monitoring urine output, and paying attention to the presence of gross and microscopic hematuria. Patients with catheters should undergo a urine bacterial culture every 4 days, as there may be an asymptomatic urinary tract infection. Almost all patients with acute spinal cord injury have detectable bacteria in their paralytic bladders. In addition, there are many invasive catheters in the ICU, such as intravenous catheters, arterial catheters, even heart catheters, and cranial traction clamps, all of which carry a high risk of sepsis. Therefore, strict aseptic procedures should be followed for all diagnostic and therapeutic measures, and relevant nursing protocols should be implemented.

　　Patients with multiple system trauma usually present with a catabolic state, which is not conducive to healing and immune response. Therefore, within 24 hours after admission, all acute spinal cord injury patients should be given central venous hyperalimentation support, high-calorie intravenous infusion, until bowel sounds return. After the bowel sounds return, oral or nasogastric liquid food should be administered, and the diet should be gradually changed until normal diet is achieved as soon as possible.

　　Patients with quadriplegia lose skin sensation and the ability to turn over actively. After a long period of lying down, bone protrusions are prone to cause bedsores, the most common sites being: sacrum, spinous process of the spine, scapula, greater trochanter of the femur, heel, and fibula head, etc. Severe bedsores can reach the bone, causing osteomyelitis, leading to long-term fatigue and death. Therefore, air cushions or rubber pads should be used, and the patient should be turned every 2 hours. The skin of bony prominences should be kept clean and dry. If the wound does not heal for a long time, plastic surgery can be performed. During the acute phase, many authors recommend the use of Roto-Rest treatment beds. For patients with acute spinal instability, this movable Roto-Rest treatment bed is the best treatment device, which can move any part of the body without affecting spinal stability. It is safe for most acute spinal cord injury patients. Ideally, each patient should be rotated continuously on the bed, at least 20 times every 24 hours, and the device should only be stopped during meals, cleaning, physical therapy, respiratory therapy, neurological examination, and radiological examination. This device can also be used for patients with high risks of cardiovascular, skin, and other systemic syndromes after surgery, as well as early surgery patients. Continuous activity can reduce complications in patients with acute spinal cord injury who are in a fixed state.

　　After spinal cord injury, there is complete flaccid paralysis below the injury level, with the disappearance of various reflexes, sensation, and sphincter function. Recovery begins within a few hours, and is complete within 2 to 4 weeks. In severe injuries, there is a process of spinal shock, usually appearing gradually after 3 to 6 weeks. It is difficult to determine whether the spinal cord injury is functional or organic during the period of spinal shock, but complete sensory loss occurs immediately or within a few hours after injury, especially with paralysis of the limbs accompanied by the loss of vibration sensation, indicating organic injury. The longer the duration of spinal shock, the more severe the degree of spinal cord injury.

　　In completely injured spinal cord, all sensations below the injured level are lost, while in partially injured individuals, some sensation is retained depending on the degree of injury.

　　The motor function of the injury is transverse and extensive, after the period of spinal shock, the motor function below the injured level is completely absent, but with high muscle tone and hyperreflexia; in some cases, partial muscle spontaneous activity appears gradually after the shock period. The appearance of atrophy, muscle relaxation, and disappearance of tendon reflexes in the支配muscles of the injured segment after spinal cord injury has the significance of localization diagnosis for lower motor neuron injury.

　　Four, after the shock period of reflex activity, the reflexes below the level of injury gradually change from disappearance to hyperactivity, and tension changes from flaccidity to spasm. Complete spinal cord injury is flexion paraplegia, and partial injury presents as extension paraplegia. Sometimes stimulation of the lower limbs can cause irresistible flexion and urination, known as overall reflex.

　　Five, during the spinal shock period of bladder function, it is a flaccid neurogenic bladder; after the spinal shock gradually recovers, it is manifested as a reflex neurogenic bladder and intermittent urinary incontinence; when the spinal cord recovers to the appearance of reflexes, stimulation of the skin will cause involuntary reflexive urination. In the late stage, it is manifested as a contractile neurogenic bladder.

　　Six, autonomic dysfunction can often lead to abnormal penile erection, Horner syndrome, paralytic ileus, lack of sweating below the level of injury, and fever, etc.

　　Seven, some patients have specific manifestations or syndromes after spinal cord injury that are helpful for diagnosis. In 1985, the Brown-Séquard syndrome was proposed. Typical injuries of this kind are caused by penetrating or penetrating injuries that result in the anatomical transection of one side of the spinal cord. Although this type of injury is not common in clinical practice, there are often patients with similar symptoms, functionally presenting as a hemisection of the spinal cord. Other more common syndromes include:

　　1. Central spinal cord injury syndrome: It is the most common cervical syndrome, mainly seen in older individuals, especially middle-aged and elderly males. These patients often have spondylosis and spinal canal stenosis before injury, and the injury is usually hyperextensional. In addition to some primary changes such as spondylosis, there are few or no abnormal findings on X-rays. Clinical manifestations include quadriplegia, but the paralysis of the upper limbs is more severe than that of the lower limbs. The upper limbs present with flaccid paralysis, while the lower limbs present with spastic paralysis. There is immediate dysfunction of defecation and sexual function, and most patients can recover and gradually progress to a stable level of nerve function. During the recovery process, the lower limbs recover first, followed by bladder function, and the upper limbs, especially the fingers, recover more slowly.

　　The central spinal cord injury syndrome was initially proposed by Schneider, who believed it was caused by central gray matter hemorrhage and periventricular white matter edema. Scholars at the University of Miami through anatomical studies believe this is not absolute, more scattered white matter injury on the dorsal side, new data consistent with pre-death and post-death magnetic resonance imaging results suggest that the thickening and hypertrophy of the yellow ligament can produce a cutting injury to the underlying spinal cord tissue when it is hyperextended.

　　2. Anterior spinal cord syndrome: This kind of injury is often caused by excessive flexion or vertebral axis loading mechanism, and is often accompanied by vertebral fractures and (or) dislocations and intervertebral disc herniation. CT, myelography, or magnetic resonance imaging can often show compression of the anterior part of the spinal canal and the spinal cord. Clinical manifestations include the loss of overall motor function below the level of injury, and the loss of lateral bundle sensory function (pain and temperature), while the function of the posterior bundle (proprioception and position sense, etc.) is not affected. The prognosis is worse than that of the central spinal cord injury syndrome.

　　3. Conus medullaris syndrome: The conus syndrome is often accompanied by thoracolumbar spinal cord injury, characterized by the concurrent involvement of the spinal cord and nerve roots (such as conus and cauda equina), with both upper and lower motor neuron injuries. The prognosis of conus component injury is similar to that of higher-level spinal cord injury, that is, complete injury has a poor prognosis, incomplete injury has a better prognosis, and the prognosis of cauda equina nerve root injury is better, similar to peripheral nerve injury. However, complete conus or spinal cord injury, incomplete cauda equina or nerve root injury is not uncommon. These patients may recover to the ability to walk if they have sufficient decompression, but if there is a long-term complete conus injury syndrome, patients will not be able to defecate and will have sexual dysfunction.

　　4. Cauda equina syndrome: The injury in the圆锥损伤综合征 is often from the level of T11 to L1, while the cauda equina syndrome is seen from the level of L1 to the sacral level. These patients present with simple lower motor neuron injury, not only with decreased lower limb reflexes but also with decreased reflexes in the intestines and bladder. Clinically, they often show incomplete and asymmetric symptoms and have a good prognosis. Severe conus and cauda equina injuries are often accompanied by chronic refractory pain, which is more common than high-level injuries.

　　5. Acute Dejerine onion skin-like syndrome: This type of injury is located at the high cervical level and is caused by damage to the trigeminal spinal tract. There is numbness and decreased sensation in the face and forehead, with a ring-like sensation of numbness and decreased sensation around the mouth and nose. The level of sensory decrease in the body is still below the clavicle, and there is paralysis to varying degrees in the limbs.

　　In 1983, Deniss, based on the CT findings of thoracolumbar injuries, proposed the concept of the spine being divided into three columns: anterior, middle, and posterior. The anterior column includes the anterior longitudinal ligament, the anterior part of the vertebral body, and the anterior part of the annulus fibrosus of the intervertebral disc; the middle column includes the posterior part of the vertebral body, the posterior part of the annulus fibrosus, the posterior longitudinal ligament, and the vertebral arch; the posterior column includes the vertebral arch, the small joints, and the posterior ligament complex (supraspinous ligament, interspinous ligament, yellow ligament, joint capsule). Un stability is considered when two or three columns are damaged, the key being whether the integrity of the middle column is maintained, and this standard also applies to the lower cervical spine.

　　Prevent traffic accidents and violent incidents, prevent accidental falls that may cause damage, and take preventive measures for work and sports-related injuries. This disease severely affects the daily life of patients, so it should be actively prevented.

　　1. X-ray film:Generally, anteroposterior, lateral, and oblique views should be taken, but excessive movement of the patient should be avoided in pursuit of good imaging results. It is advisable to first take a lateral view, and when reviewing the films, the following should be observed: ① The overall alignment and arrangement of the spine; ② Types of vertebral fractures and dislocations; ③ Presence of fractures in the appendages; ④ Narrowing or widening of the vertebral interspaces (indicating disc protrusion and anterior longitudinal ligament rupture), and widening of the spinous process gaps (indicating interspinous ligament injury). The first two items are of the greatest significance, but sometimes dislocation is severe at the moment of injury and can recover alignment later. Overextension and overflexion positions can be observed for stability, but caution should be exercised.

　　2. CT scan:Axial CT can show the shape of the spinal canal, whether there are fractured fragments protruding, and after injecting a water-soluble contrast agent into the lumbar puncture, CT can clearly show the protruding intervertebral disc and the situation of the spinal cord being compressed and displaced. When the spinal cord edema thickens, the annular subarachnoid space can become narrow or disappear.

　　3. Spinal cord iodine water myelography:Can show whether there is obstruction in the subarachnoid space, the degree and direction of compression of the spinal cord, and whether the nerve roots are involved.

　　4. Magnetic Resonance Imaging:Is the only means to observe the morphology of the spinal cord so far, which helps to understand the nature, degree, and extent of spinal cord injury, discover the location of hemorrhage and traumatic spinal cord cavities, and thus can help judge the prognosis. The magnetic resonance signal characteristics of the early lesion area of spinal cord injury and their relationship with pathological types and prognosis are displayed, showing characteristic changes in the signal on the T2-weighted image in different types of injuries. The T1-weighted image often only shows the thickening of the spinal cord, which has a localization significance. A significant drawback is that magnetic resonance imaging is not clear in observing changes in bone structure.

　　5. Somatosensory evoked potential:When stimulating the peripheral nerves, potential changes can be recorded in the corresponding sensory areas of the cerebral cortex. During spinal cord injury, this examination can be used to judge the integrity of spinal cord function and structure. If no evoked potential can be induced after 24 hours of injury, and there is no recovery even after several weeks of continuous examination, it indicates a complete injury; if an evoked potential can be induced immediately after injury, or if an abnormal potential wave can be induced after a period of time, it indicates an incomplete injury. The drawback of this examination is that it only reflects sensory function and cannot evaluate motor function.

　　The choice of daily diet intake should be high-fiber, low-fat, low-cholesterol, and adjusted for calories, in order to reduce triglycerides and neutral fats in the blood, thus achieving the goal of controlling weight and maintaining the energy consumption required for long-term rehabilitation treatment.

　　In terms of diet intake, high-calorie foods such as fried foods, fatty meat, desserts, cakes, ice cream, sodas, black tea drinks, and other beverages should be avoided. When cooking, it is advisable to avoid using lard and to reduce the intake of high-cholesterol foods such as egg yolks, internal organs, and excessive seafood, and to increase the intake of high-fiber foods such as vegetables, grains, fruits, and sufficient water.

　　First, treatment

　　Mastering the correct transportation methods during on-site first aid is of crucial importance for preventing further injury. According to statistics, 25% of the neural function damage secondary to spinal cord injury is caused by improper transportation. Untrained individuals should not manually move patients with possible spinal or spinal cord injuries, unless there is an emergency situation that threatens the patient's life, such as the patient lying in a burning car or the head and face submerged in water. The correct method for transporting paraplegic patients is: three people on one side of the patient, lifting it horizontally at the same time, placing it on a wooden board, and sending it to a specialized hospital as soon as possible.

　　The modern treatment principles for closed spinal cord injury are: early treatment, comprehensive treatment, reduction and immobilization, relieve pressure, prevent and treat complications, and rehabilitation training.

　　1. Non-surgical treatment

　　(1) Cervical traction: Applicable to cervical fractures, dislocations, or upper thoracic segment fractures and dislocations in the early stage of treatment. It is also often performed during surgery. Commonly used traction devices include Crutchfield traction forceps and Gardner-Wells traction bow (with screws that can be rotated into both sides of the bone plates at both ends, which are more convenient and less likely to slip). The initial traction weight is about 1kg per vertebral body, increasing by 2kg every 10 minutes, not exceeding 20kg. After confirming the reduction by X-ray, if no immediate surgical treatment is needed, maintain 5-8kg for 1-2 months, and then switch to other bracing devices for immobilization after fibrous healing, such as a collar, cervicothoracic brace, for about 3 months.

　　(2) Cervicothoracic brace (also known as craniocervical orthosis): Particularly suitable for incomplete cervical segment injuries, which can allow early ambulation, and is also used for external fixation after cervical fusion surgery. This method is widely used abroad.

　　(3) Manual reduction: Applicable to thoracic vertebral fractures and dislocations. For patients with anterior and posterior dislocations, the patient lies on his stomach, each lower limb is pulled by one person and gradually elevated to extend the spine, then press the back to reduce it, and then turn over to lie on his back, locally padded with a pillow to maintain the extended position. If there is also a lateral dislocation, the patient lies on his side (the side to which the upper vertebral body moves is on the bottom), with a pillow under the bottom to pull each lower limb upwards to bend the spine, the operator presses the lower vertebral body, and after reduction, turn to lie on his stomach, reduce the anterior and posterior dislocations as described above, and finally lie on his back to maintain the extended position.

　　(4) Postural reduction: Applicable to thoracolumbar segment dislocation. The British famous spinal cord injury expert Cuttmann advocates this method. The patient lies on his back, the fractured part of the back is padded with a soft pillow, so that the spine is in an extended position, and it is gradually padded up to increase the extension to achieve reduction. Generally, it takes 2 months to stabilize the reduction, during which time the patient should be turned regularly and maintain the extended position.

　　The aforementioned methods (3), (4) are not applicable to fractures of the spinous process and lamina.

　　2. Drug therapy

　　(1) Methylprednisolone: Its main function is to inhibit the lipid peroxidation reaction of the cell membrane, stabilize lysosome membranes, improve the tolerance of neurons and their axons to secondary injury, reduce edema, and prevent secondary spinal cord damage, thus gaining time for surgical treatment. The 1990 NASCIS II National Acute Spinal Cord Injury Study in the United States confirmed that the early and high-dose application of methylprednisolone is an effective method for treating human acute spinal cord injury. The application should start within 8 hours after the injury, with an initial dose of 30mg/kg, followed by 5.4mg/(kg·h) × 23h. The recent NASCIS III study shows that the effect of giving medication within 3 hours after the trauma is significantly improved, but the application of high-dose hormones must pay close attention to the occurrence of complications such as stress ulcers. 21-oxyl steroids, as a new type of preparation, have a stronger ability to inhibit lipid peroxidation than methylprednisolone and are less likely to cause the side effects associated with hormones. Animal experiments have shown good results, and it has been included in the third American Acute Spinal Cord Injury Study (NASCIS III) plan.

　　(2) Mannitol, furosemide (Lasix), and other diuretics can alleviate spinal cord edema and should be used early.

　　(3) Ganglioside (GM-1): It is a type of ganglioside (Ganglioside, Gg), where Gg is a sialic acid-containing glycosphingolipid on the cell membrane of tissue cells. Ganglioside (GM-1) contains a high amount in the cell membranes of the central nervous system of mammals, especially in myelin, synapses, and synaptic clefts, which can provide raw materials for the repair of damaged spinal cord (especially axons). In animal experiments, it has the activity to activate Na-K-ATPase, adenylate cyclase, and phosphorylase, prevent cellular edema in neural tissue due to ischemic injury, improve the survival rate of neural cells under hypoxic conditions, and promote the axonal and dendritic sprouting and regeneration of neural cells. Ceisler summarized in 1992 that the average Frankel score of the treatment group with ganglioside (GM-1) after spinal cord injury increased by 2～3 levels, and the combined use of low-dose methylprednisolone and ganglioside (GM-1) is better than single use. However, further research is still needed on the timing of application, administration time, and the optimal matching dose of MP for ganglioside (GM-1).

　　(4) Others: There are many drugs such as excitatory amino acid antagonists, opiate peptide receptor antagonists, free radical scavengers, etc., which are still in the animal experiment stage and are considered to have certain application prospects.

　　3. Hyperbaric Oxygen and Local Hypothermia Therapy:Hyperbaric oxygen therapy can increase blood oxygen partial pressure and improve the ischemic condition of the spinal cord. Local低温 can reduce the metabolism of the injured site, reduce oxygen consumption, and can be performed using open or closed systems, epidural or subdural cooling fluid irrigation, with a temperature of 5～15℃.

　　4. Surgical Treatment:The purpose of surgical treatment is to preserve the patient's life and improve the impairment of neural function. Surgery usually involves decompression, removal of foreign bodies and hematomas, and prevention of infection and cerebrospinal fluid leakage. For the treatment of paralysis after spinal cord injury, there are options such as intercostal nerve transplantation, omental transplantation, and spinal cord tissue transplantation, but these are still in research and have not yet been applied in clinical practice.

　　Second、Surgical Indications:

　　1. Patients with open spinal cord injury.

　　2. Progressive worsening of neurological signs in patients with closed spinal cord injury.

　　3. Subarachnoid space obstruction.

　　4. Spinal X-ray shows bone fragments陷入椎管内.

　　Patients with extrinsic compression of the spinal cord shown by neuroradiography, who cannot undergo traction (thoracic or lumbar segment) or decompression failure (cervical segment), should be admitted to the operating room within 24 hours, to reconstruct the patency of the spinal canal and the integrity of the spine, which includes the repositioning of the spine, decompression of the spinal cord and nerve roots, fusion surgery or other methods for spinal fixation. Most of these patients are injured in the thoracic and lumbar segments, and only a few patients in the cervical spine require acute decompression surgery, such as: cervical burst fractures, intervertebral disc herniation, epidural hematoma, severe spinal avulsion that cannot be treated with halo device, neck brace, or those without immediate surgical fixation.

　　Patients with penetrating injuries of the neck, chest, or abdomen, and whose organ damage is more severe than neurological dysfunction: these patients should be immediately admitted to the operating room for exploration and initial treatment by general surgeons, and then neurosurgeons should perform surgery at an appropriate time or simultaneously with general surgery.

　　Patients with penetrating injuries of the spine and surrounding soft tissues, but without damage to vital organs that threaten life, do not need to undergo exploratory surgery.

　　Patients with central hemorrhagic necrosis of the spinal cord should undergo surgery, through the incision in the middle of the dorsal side of the spinal cord, remove the hemorrhage and exclude catecholamine substances, and at the same time, use cold saline solution for repeated washing.

　　Three, Prognosis

　　In 1927, Cushing summarized his experience during World War I, believing that 80% of patients would die within the first week after injury, and survivors of acute trauma would die within two years due to complications, including urinary tract infections, renal failure, and sepsis, etc. In the mid-20th century, with the development of antibiotics, the advancement of medical technology, and the accumulation of experience in treating a large number of spinal cord injuries during World War II, the long-term survival status after acute spinal cord injury has improved. Currently, the focus of research after injury is how to restore self-care, return to work, and improve the quality of life.