I. Definition: Failedbacksurgerysyndrome (FBSS) specifically refers to persistent or recurrent chronic pain that occurs after 1 or more lumbar or sacral spine surgeries. Although it more accurately describes persistent back pain that occurs after nonspecific treatment, failed back surgery syndrome usually represents the same category of disorders. The term “back treatment failure” usually has a 2-tiered meaning, implying back dysfunction and the corresponding treatment or surgical failure. Epidemiology Like other diseases with a medical component, FBSS has a corresponding incidence in lumbosacral spine surgery. In the United States, more than 300,000 spine surgeries are performed each year, and FBSS occurs in approximately 10% to 40% of lumbar spine surgery cases. correspondingly, 25% of surgical cases and 80% of the total population will experience low back pain during their lifetime, and the implications of these numbers are of concern. The earliest reports of FBSS appeared only 1 year after the initial surgical treatment of lumbar disc disease. The advent of new invasive treatments, such as percutaneous discectomy and chemical lysis of the nucleus pulposus, while reducing the incidence of some complications and further relaxing the indications for treatment, has also increased the number of new types of treatment failures. We should keep in mind Finneson’s maxim that “no matter how severe or intractable the pain is, surgical treatment often makes it worse”. (a) Patient selection Selecting patients who are not suitable for surgical treatment or who should not be operated on prematurely is the most frequent cause of FBSS. In a retrospective survey of patients with FBSS, it was found that less than half of the patients initially treated with surgery met the standard surgical indications. Fearing neurosurgical complications from inappropriate surgery, patients continue to visit the “doctor’s store” until they find a satisfactory surgeon. The natural history of low back and sciatic pain, including herniated discs, has a good prognosis in most cases, so when the indications for surgery are not clear, surgery should usually be postponed and treated conservatively or with more time to develop a treatment plan with minimal impact on the body in terms of long-term outcome. (ii) The second common cause of FBSS is persistent pain due to irreversible nerve injury, which can also occur in patients who meet the indications for surgery and have successful surgery. Preoperatively, it should be made clear to the patient that the primary goal of surgery is to prevent further deterioration rather than to reverse the existing injury. In patients who require surgical treatment (and who are not expected to heal spontaneously), it is unrealistic to expect complete pain freedom and full return to pre-morbid function after surgery. There should be in-depth communication between the physician and patient regarding the extent of postoperative pain relief. If the prognosis is viewed realistically, then partial relief of postoperative pain should be considered quite satisfactory compared to FBSS. Persistent nerve injuries are divided into 2 types, which can be either single or concurrent. The first type greatly affects the dorsal roots of the spinal nerve, which includes direct injury or neuronal necrosis (e.g., due to compression of the nerve root by a herniated disc), and the primary risk factors for injury include severe lesions, closer proximity to the neuronal cell, and longer lesion duration. We have noted that cases with a delay of more than 6 months in decompression after an acute disc herniation episode are more prone to postoperative pain. The general condition of the patient, including age, concurrent neuropathy, and other medical factors, can affect the recovery of neurological function after decompression. In conclusion, after the onset of several types of neuronal injury, severe loss of primary afferent neurons has been shown to be 1 risk factor for the development of chronic neuropathic pain (17, 18). In contrast, a second type of chronic neurological injury can continue to improve postoperatively. It consists of trans-synaptic alterations in higher sensory neurons located in the central nervous system. It has long been known that repeated stimulation of receptor nerve endings can cause local sensory and nociceptive sensitization, but recent findings suggest that it can also affect spinal cord and brain cells. Studies of chronic changes in the connectivity and composition of nerves have progressed in reliable animal models of neuropathic pain, but have not yet been confirmed in the central nervous system tissue of human patients with neuropathic pain. Descriptions of post-injury responses include reversible and irreversible physiological alterations, such as central sensitization, compound pharmacological alterations, and apparent anatomical alterations in the brain and spinal cord (growth of non-injury sensory mechanosensory neurons in the glial-like material of the injurious sensory transmission pathway). It is very important to explain to the patient after surgery that since it takes months for their muscles and bones to recover, it will also take months or years for the injured nerve tissue to return to normal. We can also expect that the partial relief of pain after surgery will enhance the patient’s psychosocial functioning, i.e., improve the patient’s tolerance of the remaining pain (perhaps by reducing the antinociceptive allergic effect). Sometimes 1 aggressive pharmacological regimen is sufficient to reverse the downturn in FBSS patients and thus improve their quality of life. Antidepressant treatment with pain medication is more likely to be the key to treatment in a rehabilitation program than secondary surgery. (iii) 1 uncommon cause of successful surgical technique for FBSS is inappropriate surgery. Examples include insistence on surgery for unrecognized lateral saphenous fossa stenosis or lateral disc protrusion. 1 free necrotic disc fragment may have been left behind during surgery. In this regard spinal radiography as well as postoperative magnetic resonance imaging (MRI) can make the diagnosis. In addition, spinal instability that occurs after fusion is usually due to fusion failure. Although instrumentation (tipped bolts, plates, meshes cages) reduces the incidence of such technical problems, the clinical benefit is more uncertain. Smoking is the 1 major risk factor for difficult bone healing. Unless smoking is stopped, bone fusion will be delayed. In a few cases, although the anterior or posterior spines are superficially successfully fused, some sort of activity will still occur, necessitating a repeat fusion procedure. (iv) New damage to the nerves or spine Another category of FBSS includes pain syndromes resulting from a pathological process triggered by the initial surgery. Complications of spinal surgery are known to include nerve, dural, joint, and muscle damage, all of which can produce pain. Examples include segmental instability following 1 extensive laminectomy (laminectomy), incomplete fractures, or pseudarthrosis formation following inadequate fusion. Movement of the spine adjacent to the level of spinal fusion is thought to cause and accelerate the onset of degeneration here (transition syndrometransitionsyndrome), although the onset of degeneration after fusion is inevitable. X-rays of the spine in flexion and extension are often of value in the diagnosis of this syndrome. In addition, based on the above discussion of persistent nerve injury, there is a risk of injury to the nerve roots or spinal cord at the time of surgery. The issue of the risk of pain from this nascent action on the spinal nerve roots and discs has been discussed at length. Appropriate techniques, including the use of intraoperative electronic monitoring when necessary, will minimize complications. (v) Extensive fusion Extensive fusion or extensive instrumentation can cause secondary postural deficits, such as loss of normal lumbar lordosis (flat spine syndrome). Abnormal posture can induce or accelerate degeneration and lead to new pain problems. Postural dysplasia can be easily diagnosed with X-rays, and periodic X-rays are needed for unclear history because of the potential risk of these syndromes in postoperative patients. (vi) Non-surgical complications It is important to note that not all perioperative painful complications are due to the surgery itself. Invasive diagnostics or x-ray fluoroscopy can occasionally lead to chronic painful complications. This would include infection or arachnoiditis, such as with invasive discography. The application of epidural interstitial corticosteroids, myelography, these can change the contrast agent from fat soluble to water soluble, thus partially relieving the pain. Postoperative scarring or inflammation of the cerebrospinal membrane (arachnoid fibrosis or arachnoiditis) can lead to irregular neurological findings that are difficult to interpret. Although routine MRI can sometimes show masses of lumbosacral spinal nerve roots, spinal radiography can show them more clearly. The value of long-term steroid use in the epidural space is not as clear as the effect of distant surgery or percutaneous manipulation in an attempt to “get rid of the scar”. V. Pseudo-failed back surgery syndrome After the postoperative pain-free interval, if previous or new pain occurs, the patient or internist may incorrectly assume that the surgery was unsuccessful. This may indicate a recurrence of the surgical plane or other planes of lesion. It is helpful to explain to the patient that surgery will neither prevent an underlying degenerative process such as osteoarthritis nor prevent the need for a second surgery in the future. There is a risk of underlying biological changes such as structural changes in collagen that can cause recurrence of back disorders in some individuals (or families) after surgery. Any patient who has undergone a single low back surgery will be at increased risk for a second surgery in the future. Whether this represents a basic characteristic of susceptibility to FBSS or a higher incidence remains unclear, but it may be a reflection of both. Identifying the biological risk factors that predict poor outcomes in back surgery can help minimize the risk of developing FBSS. Pain associated with axonal regeneration may be mistaken for FBSS. Although neuronal cell bodies do not regenerate in adults, they can regenerate if the axon is not severely damaged (e.g., in the case of spinal nerve root compression). If the sensory neuron cytosol in the dorsal root ganglion survives the trauma, a new axonal regeneration process may occur once the pressure is surgically relieved. Axonal regeneration is associated with the persistence or worsening of pain. This is due to the accumulation of sensory transmission molecules at the distal (neoplastic) end of the regenerating axon. Clinicians can determine the length of a nascent axon by tapping along the peripheral nerve walk until sensory abnormalities appear (Tinel’ syndrome). The maximum growth rate of the neoplastic axon is the same as that of the paracrine fast axon (approximately 1 mm/d), so the recovery phase may last for several months or more than a year. This pain and sensory anomalies must be distinguished from FBSS pain, because it is in fact a sign of recovery. It should not be considered as a deterioration, much less as a result of further surgery. Once the distal axonal innervation is restored, the pain is completely or nearly completely relieved, and it is rare for patients to have persistent radicular pain for months after surgery.