I. Pathological and anatomical basis of lumbar disc herniation causing low back pain Modern research shows that all spinal structures are rich in nerve distribution and are multi-segmental and overlapping, and only the inner fibrous ring of the intervertebral disc and the dorsal side of the dural sac lack innervation, and a variety of spinal tissue structures can cause pain directly or indirectly, but due to the compactness of spinal tissue and the richness and overlap of nerve distribution, it is difficult to distinguish clear The pain-causing tissues are discussed separately below. The intervertebral discs, intervertebral joints, nerve roots, and dorsal root nodes are discussed separately below. It is generally accepted that these tissues are responsible for the production of low back pain or are involved in the transmission and regulation of low back pain. (i) The intervertebral disc has multiple sensory innervation, with the lateral part and the anterior longitudinal ligament receiving innervation from the gray traffic branch and the posterior lateral part receiving innervation from the sinus vertebral nerve in addition to the gray traffic branch. The receptors of the intervertebral disc are unevenly distributed, with most of them on the lateral side and a small portion on the posterior side, while the anterior side should be more sparsely distributed, and its dense distribution area is also the part of the disc prone to injury. Since the intervertebral disc is innervated by multiple nerves, the spatial summation is formed and the afferent of pain impulses is accelerated. The afferent input of milder pain impulses under normal conditions may be modulated by diffuse pain inhibitory valves. Sympathetic mediation may also exacerbate pain. Autonomic nerve terminals are distributed on the spine and can cause nausea, sweating, and burning sensations, and this sympathetic afferent activity can excite the A-fiber mechanoreceptors and cause pain perception. Histological observations show that microtrauma of the intervertebral disc can be non-healing. Whether this phenomenon is due to the absence of blood vessels in the intervertebral disc is unclear. It is possible that the microtrauma is insufficient to elicit an inflammatory and healing response or that the avascular nature of the disc limits the inflammatory and healing response. Poor healing leads to decreased tissue strength and ease of re-injury, and repeated injury eventually leads to persistent inflammation, which in turn sensitizes pain receptors. (ii) Intervertebral joints The intervertebral joints and their associated structures are richly innervated by the inferior dorsal branches of the spinal nerves. The afferent fibers from the intervertebral joints are mainly type III and type IV fibers, whose abundant nerve terminals form a fine plexus in the joint capsule. The distribution of nociceptive nerves in the synovial folds is controversial. Recently, electron microscopy, silverophilic staining, and immunofluorescence staining have revealed nerve fibers and substance P in the subsynovial tissue within the internal saphenous fossa and synovial folds of the intervertebral joint, suggesting a pain-sensing function of the neuroreceptors in this region. Clearly, the multiple innervation of the intervertebral joint nerves is similar to that of the intervertebral disc, and thus all of the aforementioned pain mechanisms can occur in the intervertebral joint. However, the intervertebral joint also has its own peculiarities in that it is blood supplied and therefore has a greater vascular role in the inflammatory response, which is beneficial for healing, but can also lead to hyperplasia, causing degeneration of the intervertebral joint and narrowing of the intervertebral foramen with compression of the nerve roots. Synovitis, degeneration and ingrowth of synovial folds also contribute to the persistence and recurrence of intervertebral joint pain. (iii) Nerve roots The “tight” anatomy of the spinal canal means that inflammation or movement of one tissue will irritate or affect other tissues and create a secondary source of pain. Mechanical compression and the presence of inflammatory nociceptive agents can lower the pain threshold and thus cause pain. This tight configuration puts and nerve root at risk of becoming a secondary source of pain. Structurally, the nerve root is susceptible to injury, it is encased in a membrane with no outer nerve membrane to resist mechanical stress. Compressive injury to the nerve root can cause increased capillary permeability within the nerve, leading to edema formation; it also affects nutrient delivery to the nerve root due to elevated hydraulic pressure within the nerve. This mechanism is particularly important in nerve root segments that are tightly packed with connective tissue, so that nerve roots in the intervertebral foramen are more susceptible to so-called “impingement syndrome” than the central cauda equina. The blood supply to the nerve roots is derived proximally from the spinal vessels and distally from the intermediate branches of the segmental arteries. These two systems coincide in the outer third of the nerve root, where the vascular network is underdeveloped and is a vulnerable site for injury. In the capillary network within the peripheral nerves, there exists a blood-nerve barrier similar to the blood-brain barrier, and it is doubtful whether the nerve roots have a similar barrier. Experimental studies have shown that the plasma albumin within the capillaries of the nerve root runs less into the nerve than in the dorsal root ganglion and peripheral nerves. Parke et al. suggested that venous stasis is an important factor in radicular pain and found that in patients with severe spinal stenosis with intermittent claudication, the arteries in the nerve roots were not significantly and vascularly occluded, whereas the veins were significantly reduced and a large number of The arteries and veins of the nerve roots were not significantly and vascularly occluded, while the veins were significantly reduced and a large number of arterioles and veins were open. （From the anatomical point of view, the dorsal root ganglion is the link between the internal and external environment of the body and the spinal cord. The sensory cell bodies in the dorsal root ganglion are highly sensitive to mechanical displacement and can discharge spontaneously, and this spontaneous discharge is significantly affected by peripheral nerve injury. Lindblom first proposed the dorsal root ganglion as a regulator of low back pain, suggesting that given the characteristics of the blood supply to the dorsal root ganglion and the mechanical compression of its tense joint capsule could lead to intraneural edema and further reduce the blood supply to the cell bodies, which may be associated with dorsal root ganglion dysfunction and pain. Many neuropeptides are inflammatory precursors (e.g., substance P), which are released from fine primary afferent nerves and then act on mast cells to cause the release of a series of other inflammatory factors, such as histamine, serotonin, and leukotrienes, which cause vasodilation and increased permeability, promote inflammation, and at the same time sensitize pain receptors. This shows that DRG is associated with radiocutaneous pain and nociceptive hypersensitivity. Second, the pathological type of lumbar disc herniation and its regression LDH pathological typing has important guiding significance for judging the prognosis and choosing the treatment method. There are many classification methods, such as Spengler’s classification of LDH into three types: protruded, extruded, and free (sequestered). In China, Zhou Bingwen combined pathological observation and clinical practice and proposed the classification of protruded, ruptured and free types. The International Society for the Study of the Lumbar Spine (ISSLS) and the American Academy of Orthopaedic Surgery (AAOS) put forward six types of classification: degenerative (such as DARK DISC), bulging, protruding, prolapsed (under the posterior longitudinal ligament), prolapsed (behind the posterior longitudinal ligament) and free. Regardless of the classification, there are four pathological patterns and basic concepts as follows. (a) bulging (bulging) is a physiological degeneration in which the fibrous ring is relaxed but intact and the nucleus pulposus is dehydrated and crumpled. It is manifested by the uniformity of the fibrous ring beyond the edge of the vertebral body end plate, and often appears as a distraction of the anterior edge of the vertebral body, generally without clinical symptoms, sometimes due to narrowing of the intervertebral space, segmental instability, secondary changes in the articular eminence, recurrent back pain, and rarely radicular symptoms. If combined with developmental spinal stenosis, it is manifested as spinal stenosis, which should be decompressed, such as the nucleus pulposus removal is bound to expand more serious, the more serious the clinical results of treatment. (B) protrusion (protrusion) is the nucleus pulposus breaking into the annulus fibrosus but the outer layer of the annulus fibrosus is still intact, manifested as a limited protrusion of the intervertebral disc into the spinal canal, most asymptomatic, some patients appear typical radicular symptoms and signs. This type can be retracted by conservative methods such as traction and bed rest, but due to the poor healing ability of the ruptured annulus fibrosus, it may continue to break through the annulus fibrosus and become a prolapsed or free type. (C) Extrusion: The posterior longitudinal ligament is still intact, but the annulus fibrosus is completely ruptured, due to the limited retraction of the posterior longitudinal ligament and the difficulty of healing the annulus fibrosus! For the prolapse with obvious symptoms, it is difficult to heal by itself, and the effect of conservative treatment is relatively poor, so surgery is needed. There are a few cases of reabsorption of the herniated tissue. Depending on the location of the protrusion (postero-lateral, central), its size and its relationship to the nerve root, it can break through the posterior longitudinal ligament and become a free type. （The herniated nucleus pulposus is not attached to the corresponding intervertebral disc, and may be free to the epidural area or to the upper or lower segment of the lesion, or to the intervertebral foramen, etc. Its regression is either adhesion to the nerve root or resorption, and the corresponding clinical manifestations are persistent radicular symptoms, spinal stenosis, or self-resolution. This type often requires surgical treatment. In addition, there are some special types of LDH, such as intradural, intradural or extradural (extreme lateral type), endplate and intravertebral body herniation, all of which have their special corresponding manifestations. Third, the indications for surgery of lumbar disc herniation 1, when conservative treatment fails, surgery should be considered. 2.Patients most suitable for surgery are those with unilateral leg pain or pain mainly concentrated on one side, whose pain radiates below the knee joint and whose symptoms persist for more than 6 weeks and are relieved by rest, anti-inflammatory therapy or epidural hormone therapy, but after at least 6-8 weeks of conservative treatment, the symptoms recur to the initial severity. 3.The presence of cauda equina syndrome with significant neurological impairment, especially when large and small bowel dysfunction, necessitates emergency surgery. 4.In cases with intermittent claudication, there is mostly spinal stenosis at the same time, and non-surgical treatment is generally ineffective, so surgery should be performed as early as possible. 5, combined with lumbar isthmic fracture and lumbar spine slippage or lumbar instability, the protruding disc tissue should be surgically removed, and lumbar fusion should be performed at the same time. 6, surgery for lumbar disc herniation, the main purpose is to relieve the symptoms of lumbar and leg pain, and the main pain of patients who mainly manifest lumbar pain may not be eliminated after surgery, such patients should be carefully selected. Fourth, the choice of surgical methods for lumbar disc herniation (a) disc nucleus pulposus removal, nerve root decompression surgery 1, traditional open disc nucleus pulposus removal The classic posterior surgery for lumbar disc herniation has been carried out in China for more than half a century. The authors have reported the excellent rate of 104 cases with 8-20 years (average 12.66 years) of postoperative follow-up, 83.8% in the open group, 77.3% in the hemi-laminectomy group and 43.5% in the total laminectomy group. In the Affiliated Hospital of Qingdao University Medical College, the overall excellent rate was 85.71% for 273 cases of lumbar disc herniation with classical surgery at 3-10 years of follow-up, 95.58% at 3-4 years of follow-up (mid-term follow-up), 85.82% at 5-9 years of follow-up (long-term follow-up), and 75% at 10 years of follow-up. These two groups reported that posterior classical surgery for lumbar disc herniation has good long-term outcomes. However, in the follow-up cases of the good group, X-ray examination revealed varying degrees of intervertebral space narrowing in the operated segment. For this reason, in recent years, some people in China have been performing classical surgery for lumbar disc herniation with arch fixation on one or both sides and short-segment lumbar fusion to maintain the height of the intervertebral space and the stability of the lumbar spine. In fact, spinal stenosis may not have symptoms of low back pain, and spinal stenosis does not necessarily have symptoms of lumbar instability and nerve root impingement. The diameter of the L4 and L5 nerve roots in adults.