It is not uncommon for patients to experience no significant relief, exacerbation, or recurrence of pain in the low back after low back surgery. In recent years, there has been a gradual increase in the number of reports of postoperative low back pain syndromes. Postoperative low back pain syndrome is defined in a broad sense as intractable pain or other discomfort in the lower back, buttocks, or lower extremities that remains in the patient after laminectomy or lumbar disc removal. In a narrower sense, it refers only to the lack of any improvement in clinical symptoms after multiple surgeries. Due to the autoimmune inflammatory reaction and scar formation after surgery, the incidence of FBSS is high, about 10-40%, and the treatment is more difficult to be effective, the patient’s physical and mental pain is greater, and it is easy to lead to medical disputes. Causes There are many reasons for the occurrence of FBSS, but most of them are related to surgery, including the mastery of surgical indications, case selection, surgical methods, operating techniques, and mental factors, which can be divided into three aspects: preoperative, intraoperative, and postoperative. Preoperative factors: (1) Diagnostic error: only to meet the single diagnosis of lumbar disc herniation or lumbar spinal stenosis, while omitting other diagnoses, the corresponding treatment is inappropriate, resulting in FBSS; (2) Positioning error: the disc protrudes in which section and which one or more lumbar nerve roots are compressed in the wrong diagnosis. Intraoperative factors: (1) intraoperative localization errors; (2) lack of thoroughness of the operation: incomplete removal of the nucleus pulposus, which triggered reherniation; neglect of the prolapse and free disc herniation located in the anterior and posterior posterior longitudinal ligament; incomplete exploration and decompression of the lateral saphenous fossa, incomplete resection of the lateral wall of the ligamentum flavum that constitutes a fibrous canal on both sides of the arch on either side of the root of the vertebral body, and stenosis caused by the coalescing of the articular eminences; neglect of the fibrous fasciculation of the dural membrane; (3) failure to remove the fibrous bony material at the posterior edge of the vertebral body. Unused curved chisel for removal of the bony cords at the posterior margin of the vertebral body; insufficient decompression of the spinal canal stenosis. Postoperative factors: (1) excessive surgical scope caused postoperative lumbar instability and slippage: according to the literature, the incidence of lumbar instability and slippage in extensive laminectomy was reported to be 34%, especially for the removal of the articular eminence, which was generally limited to 1/2~1/3 of the articular eminence; (2) re-protrusion of other segments, which was mainly caused by degeneration of adjacent segments; (3) formation of scar in the epidural cavity, i.e., epidural fibrosis, scar formation, according to the literature, in the case of FDA, the epidural fibrosis is not completely removed. (3) Scar formation in the epidural space, i.e., epidural fibrosis, scar formation, which is reported to account for 5%~24% in FBSS; (4) regeneration of the vertebral plate, etc., leading to spinal stenosis; (5) infection factors leading to the aggravation of adhesion: due to the expansion of the surgical damage to the fibrocartilage plate, resulting in intervertebral hemorrhage caused by an increase in intervertebral space infections. Pathogenesis (1) autoimmune response studies have confirmed that with the aging and degeneration of the intervertebral disc, the nucleus pulposus in the matrix lysozyme increase, this enzyme can make the proteoglycans and linkage proteins cleaved into highly heterogeneous molecules, with antigenic properties. Recent studies have also found that type I and II collagen and cartilage plate matrix of intervertebral disc tissues are also autoantigenic. After disc herniation or surgery, these autoimmune antigenic substances leak out and are exposed to the immune system to produce an immune response, mediating radiculitis and causing low back pain and leg pain in patients. (2) Inflammatory response of tissues Numerous studies have found that the nucleus pulposus, phospholipase A2 (PLA2), IgG, IgM, proteoglycan ions, ATP and other intervertebral disc inflammation-causing substances can leak out of the intervertebral discs with disc herniation and surgery, stimulating the sinusocele nerve endings to cause pain. When the chemical substances cause impulses in the injury receptors to produce pain, the neurons themselves can synthesize and release neuropeptides, such as substance P, vasoactive intestinal peptide (VIP), etc., forming a positive feedback loop that exacerbates the inflammatory response and further aggravates the symptoms. (3) Degenerative changes in the lumbar spine Postoperative lumbar spine instability, slippage, causing biomechanical dysfunction, aggravating the degenerative changes in the lumbar spine, such as small articular eminences, intervertebral joints degeneration, ligamentum flavum hyperplasia and hypertrophy caused by re-stenosis, resulting in new compression symptoms. (4) Extravertebral soft tissue injury and inflammation FBSS caused by soft tissue injury and aseptic inflammation due to lumbar spine surgical process. (5) Nerve root adhesion On the basis of the original immune-inflammatory reaction, coupled with the surgical trauma and hemorrhagic mechanization, scar formation, the transverse root is adhered and stuck, and pain and numbness appear in the area of the distribution of the affected nerve. (6) Increased sympathetic nerve excitability Inflammatory reaction and abnormal immune response in the vertebral canal can agitate the sinusoidal spinal nerves and reflexively cause increased sympathetic nerve excitability, and the patient may feel soreness and numbness in the lumbar, buttock and leg areas, and fear of cold and chills. (7) Non-bony lateral crypt stenosis Non-bony lateral crypt stenosis, due to anterior disc protrusion or bulging and posterior ligamentum flavum hypertrophy caused by the narrowing of the spinal canal. Clinical manifestations (1) Low back pain mainly in the lower lumbar or lumbosacral region, mostly at or adjacent to the site of surgery. The nature of the pain is mostly chronic dull pain or acute severe pain, and some patients have nociceptive hypersensitivity and touch-induced pain. Pain is generally heavier at night, cold and damp, exertion can aggravate the pain so that patients can not stand and walk. (2) Lower extremity pain is mostly radiating, from the buttock, posterior lateral thigh, lateral calf to the dorsum or sole of the foot; patients with high intervertebral space lesions show anterior thigh pain, and some even show pain in the lower abdomen. (3) Intermittent claudication FBSS patients cause more factors of spinal stenosis, so intermittent claudication is not uncommon, manifested as walking distance increase caused by low back pain or discomfort, at the same time, the affected limbs appear pain and numbness or the original pain and numbness symptoms aggravated, squatting or lying down for a few moments, the symptom gradually relieved. (4) Neurological damage: atrophy of the muscles of the waist and buttocks and the muscles of the lower limbs innervated by the affected nerves, loss of muscle strength, and foot drop; the waist and buttocks and the legs can be allergic to sensation, hyperalgesia or disappearance of sensation, and hyperalgesia is more common. If the patient’s cauda equina nerve compression or injury inflammation, can cause sphincter and sexual dysfunction, manifested as constipation, urinary frequency, urinary urgency, urination difficulties and other symptoms, male patients can occur impotence and other sexual dysfunction. (5) Patients often have weakened or involved knee tendon reflex or (and) Achilles tendon reflex. (6) Pressure pain may be present in the lumbar and hip interspinous, paraspinous, and gluteal external cutaneous nerve projections, mostly radiating to the thighs. (7) There may be positive straight leg raising test, straight leg raising strengthening test and femoral nerve pulling test. (8)Magnetic resonance enhancement examination is currently the best means of examination to assess FBSS, manifested as nucleus pulposus protrusion or prolapse, remnants of prolapsed nucleus pulposus, epidural scar adhesion, scar tissue compression of the dural sac, intradural cysts, and dural rupture; CT, as a better means of assessing intervertebral foraminal stenosis and other osseous anomalies, manifested as proliferation of the lesser synovial process combined with lateral saphenous fossa stenosis, disc protrusion or prolapse, and lateral saphenous fossa stenosis; of which CT has a better means of assessing foraminal stenosis and other bony abnormalities. stenosis; of these, myelography with CT is considered the best method to detect arachnoiditis and epidural fibrous rings, as evidenced by deformation of the dural sac with thinning or complete obstruction, loss of the nerve root cuffs, and still having a filling defect in the surgical space with contrast. Diagnosis For patients with low back pain, the importance of the correct diagnosis of this disease should be emphasized, and awareness of this disease should be improved, especially for those with multiple complaints and heavy symptoms and unclear localization and diagnosis, a careful history and detailed examination should be performed, and auxiliary examinations such as CT and MRI are effective diagnostic methods. Diagnostic criteria: (1) history of lumbar laminectomy; (2) ≥1 year from the time of surgery; (3) persistent pain in the lumbar, hip, and leg regions or ≥4 episodes of pain per year, with pain that affects normal life and work; and (4) CT (or enhancement) and MRI suggesting recurrent disc herniation or epidural tissue proliferation. Treatment The treatment of this disease is quite difficult, patients often lose confidence, resulting in psychological disorders, and cause systemic dysfunction. In the treatment, it is necessary for doctors and patients to build up confidence, be patient, and choose different treatments or a combination of different treatments for different causes (discogenic, neurogenic, extradural soft tissueogenic, etc.) and pathogenesis of FBSS in order to achieve the therapeutic purpose of inhibiting or eliminating inflammation, improving microcirculation of local tissues, removing necrotic tissues, and accelerating tissue repair. 1.Anti-inflammatory and analgesic therapy If FBSS is mainly caused by inflammation, non-steroidal anti-inflammatory and analgesic drugs can be applied systemically, and O3 and anti-inflammatory and analgesic liquid can be injected into the lateral saphenous fossa to inhibit autoimmune reaction, reduce inflammatory reaction of the nerve root, and alleviate inflammation and analgesia, and then relieve the symptoms and signs. After injection of anti-inflammatory and analgesic solution or O3, the internal or external orifice of the intervertebral foramen or the combined internal and external orifice can be loosened by needle knife, followed by the nerve root loosening technique: a small needle knife can be used through the internal or external orifice of the intervertebral foramen to tightly adhere to the bony surface to reach the adhesion place of the nerve root, and then the scar tissues and compression bands of adhesion and compression of the nerve root are loosened or cut off to loosen the nerve root, and then the nerve root is loosened and free, and the knee-extension technique can be used to stretch the nerve root after hip flexion and knee extension, which can enhance the effect of loosening. The effect of relaxation can be enhanced by stretching the nerve root downward after bending the hip and knee. The anti-inflammatory and analgesic liquid and O3 injected around the nerve root can not only play the role of liquid and gas stripping for the adherent nerve root, but also prevent the re-adhesion after the release. Postoperative intravenous drip of mannitol 250ml, plus dexamethasone 5~10mgqd×3d can prevent the occurrence of reactive edema after nerve root stimulation. 3.Sympathetic inhibition therapy FBSS has typical sympathetic excitation symptoms (such as feeling soreness and numbness in the waist, buttocks and legs, and fear of cold and chills), the feasibility of deep thermal therapy-intra-disc radiofrequency, sympathetic nerve block. The use of sympathetic nerve block or radiofrequency ablation can inhibit the excessive excitation of the sympathetic nerves, and relieve the patient of symptoms such as coldness of the lower limbs caused by increased sympathetic excitability. 4. Treatment of lumbar disc herniation For those who have symptoms caused by disc herniation (confirmed by CT or MR), the herniated disc needs to be treated. When treating FBSS, it is necessary to recognize the pathogenesis of FBSS and take targeted treatment. Whether it is recurrent or new disc herniation, different treatment methods or combinations of different methods should be chosen according to the location, shape, size, intra-disc pressure, integrity of the annulus fibrosus, and concomitant symptoms of the herniated disc. 5.Anti-infection treatment Systemic application of effective antimicrobial agents, intralesional injection of O3, once every 5 days, 3 times so that the symptoms are significantly reduced. Because of the serious low back pain caused by postoperative disc infection, it was difficult to reach the diseased area with simple application of antibiotics in the past, so the treatment effect was not good. The addition of intravertebral injection of O3 can play a strong anti-inflammatory and anti-infectious role in the infected space, so the effect is better. 6. Non-invasive treatment Non-invasive treatment can be used as auxiliary treatment of minimally invasive treatment to strengthen the effect of minimally invasive treatment; non-invasive treatment can be applied to promote recovery during the recovery period after minimally invasive treatment, and non-invasive treatment can be applied to treat diffuse soft tissue lesions outside the vertebral canal and inflammatory lesions inside the vertebral canal in the course of minimally invasive treatment or after the course of minimally invasive treatment.