Theoretically, the local displacement of lumbar disc tissue beyond the limits of the intervertebral space is called disc herniation, in which the lumbar disc tissue includes the nucleus pulposus, cartilage, fibrous ring or a mixture of these tissues. The clinical term lumbar disc herniation usually refers to the rupture of the annulus fibrosus due to degenerative changes in the lumbar disc or trauma, and the nucleus pulposus is displaced from the rupture and compresses the nerve root or cauda equina nerve, resulting in a series of neurological symptoms such as radiating pain in the back and legs. The causes of lumbar disc herniation are mainly degenerative factors and traumatic factors. Patients with trauma-induced lumbar disc herniation usually have a history of varying degrees of trauma, commonly caused by heavy lifting, various forms of lumbar sprains (especially in intense sports), and direct external violence to the lumbar region. These traumatic violence can rupture the annulus fibrosus and herniate the nucleus pulposus in an instant, and trauma-induced disc herniation is more common in young adults. Degenerative factors are the main cause of lumbar disc herniation. The intervertebral disc is the largest avascular structure in the body and receives its nutrients mainly through the central cartilage end plate and the surrounding fibrous ring. The avascular nature of the disc means that the structural damage that occurs within the disc has no ability to heal; any fissures and breaks are unlikely to heal themselves, and these structural injuries persist. Typical structural disc degeneration begins in young adulthood and is manifested by the development of fissures within the disc. Histologic and biochemical analyses confirm that the water content of the disc decreases after degeneration and that the dehydrated nucleus pulposus tissue of the disc can rupture the posterior portion of the annulus fibrosus further, leading to disc tissue herniation. The herniated nucleus pulposus is the end of a series of pathophysiologic processes. Due to the lack of innervation within the disc, the presence of an intradiscal fissure is usually asymptomatic; however, progressive rupture of the annulus fibrosus can present with varying degrees of low back pain, which may manifest as mild pain or painful low back stiffness and limited motion. These acute low back pains are often accompanied by radiating pain in the pelvis and lower extremities, but this radiating pain differs from nerve root pain. Clinically, it is common for patients to experience relief of low back pain after the annulus fibrosus eventually ruptures completely and the nucleus pulposus enters the spinal canal, because the pressure on the annulus fibrosus is relieved by the entry of the nucleus pulposus into the spinal canal. If the nucleus pulposus enters the spinal canal and compresses the nerve roots, the characteristic radicular radiating pain of the lower extremities (commonly known as sciatica) replaces the predominant symptoms of low back pain. However, clinically, in the pathological process of rupture of the annulus fibrosus and herniated nucleus pulposus, some patients have no history of low back pain at all prior to the lower extremity radicular pain caused by the herniated disc, so the individual variation of symptoms in patients with lumbar disc herniation is very large. It is important as a surgeon to determine whether the patient’s symptoms are discogenic manifestations or the result of typical fibular annulus injury or neurologic symptoms resulting from nerve root compression due to herniated disc fragments. The mechanisms of sciatica in patients with lumbar disc herniation include both mechanical compression of the nerve root and local inflammatory irritation. Direct compression of the nerve roots after disc herniation can well explain the occurrence of sciatica, but the autoimmune microvascular response or inflammatory response that occurs when the herniated disc tissue (e.g., the nucleus pulposus) comes in contact with the nerve roots is also an important factor in the development of sciatica. Lumbar disc herniation can be classified as bulging, herniated and prolapsed according to the degree of protrusion. Bulging means that the disc fibrous ring dressing is uniformly beyond the intervertebral space, and there is no limited protrusion of disc tissue. Protrusion refers to local displacement of disc tissue beyond the intervertebral space, and the displaced disc tissue is still connected to the original disc tissue, and its basal continuous part is larger in diameter than the displaced disc part beyond the intervertebral space. Prolapse means that the diameter of the displaced disc tissue is greater than the basal contiguous portion and moves beyond the intervertebral space, and the prolapsed disc tissue is larger than the ruptured disc space and lies within the spinal canal through this fissure. Lumbar disc herniation can be divided into central canal herniation, lateral fossa herniation, foraminal herniation, and extradural herniation according to the anatomical location of the herniation. The first two are more common, and the nerve roots compressed by a herniated disc in this area are the downward traveling roots, such as the L4/5 disc herniation compressing the L5 nerve root. The latter two may also be collectively referred to as extreme lateral disc herniation, where the disc tissue compressed by the herniated disc at this site is the outward traveling exit root at the same level, such as the L4/5 extreme lateral disc herniation compressing the L4 nerve root. The common clinical symptoms of lumbar disc herniation are low back pain and radicular radiating pain of the lower extremities (commonly known as sciatica). Low back pain can be caused by a variety of diseases, so it is not a specific manifestation of lumbar disc herniation. Other diseases can also cause radicular reflex pain in the lower extremities, but it is rare compared to lumbar disc herniation, and care should be taken to differentiate it from tumors of the lumbar spine and pelvis, infections, and pyriform fossa syndrome, which cause radicular radiating pain in the lower extremities similar to the manifestations of disc herniation. The symptoms of lumbar radiculopathy are neurologically localized, and different lumbar radiculopathies may produce sensory or motor abnormalities in their respective areas of nerve root innervation. L5 radiculopathy is usually associated with pain radiating to the posterior lateral aspect of the calf to near the outer ankle, with weakness of the dorsal extension of the foot and toes (weakness of the dorsal foot upward or foot downward), and L4 radiculopathy with pain radiating from the buttock to the anterior aspect of the distal thigh and medial calf, with weakness of the quadriceps (weakness of the knee joint extension) and weakness or loss of the knee reflex. Most lumbar disc herniations occur in the L4/5 and L5/S1 discs, and disc herniations above the level of L3/4 (including L3/4) can often be referred to as high-grade disc herniations, which tend to have more mixed symptoms, and sometimes the symptoms and signs of nerve root damage localization are not very clear. There are a number of precipitating or exacerbating factors for lumbar disc herniation, and some patients experience a marked increase in symptoms with coughing, sneezing, or bending movements. The straight leg elevation test (Lasegue test) is the most common and highly specific sign of lumbar disc herniation, and the test is easy to master and can be performed at home for self-examination. The test is performed with the patient lying flat on the bed, the examiner holding the affected knee joint with one hand and keeping the knee extended with the other hand, and holding the affected ankle joint with the other hand and lifting it up, normal people can lift 80-90° without lower limb radiating pain, while patients with lumbar disc herniation tend to lift the lower limb <70°, which is a positive straight leg elevation test. However, it should be noted that L4/5 and L5/S1 disc herniations often show a positive straight leg elevation test, while patients with high lumbar disc herniation usually do not show a positive straight leg elevation test, so patients with a positive straight leg elevation test often indicate lumbar disc herniation, while those without a positive straight leg elevation test may still have lumbar disc herniation and need to be seen by a specialist. There are many imaging methods for lumbar disc herniation, including plain x-rays, CT, MRI, discography and spinal canalography. CT is a common method, which can show the disc herniation through the density difference of different tissues, but its ability to show the nerve structure is not clear, and the ability to judge the degree of pressure on the nerve structure is weak, and it is difficult to show the lesions such as tumor in the spinal canal. MRI can clearly show the degree of disc degeneration, the extent and location of herniation, the degree of compression of nerve structures and even intracanal tumors, which is extremely helpful for doctors to judge the condition and formulate surgical plans, and is therefore commonly used in the diagnosis of lumbar disc herniation. Discography and spinal canal imaging are invasive tests and are not currently used as routine tests for the diagnosis of lumbar disc herniation. The former can show lesions such as intravertebral disc fissures and rupture of the annulus fibrosus, which helps in the early diagnosis of lumbar disc herniation and is the golden diagnostic standard for the diagnosis of discogenic low back pain; the latter can show the dural sac and nerve root compression when the patient is unable to undergo lumbar MRI examination (such as placement of cardiac stents or pacemakers), and MRI is unclear for the local mechanism of the lumbar spine in patients after lumbar spine surgery, when intravertebral canal The MRI is not clear for the local mechanism of the lumbar spine after lumbar spine surgery. Electromyography can help identify nerve root damage or peripheral nerve damage, but it is not routinely used for lumbar disc herniation. In most cases of lumbar disc herniation, the neurological symptoms are progressive, but a small number of patients may experience a sharp increase in symptoms within a short period of time, and in the most severe cases, cauda equina syndrome may develop. Cauda equina syndrome is the result of acute compression of the entire cauda equina nerve by a herniated disc, which manifests as acute episodes of sudden pain in the lower back and lower extremities, numbness and even loss of sensation in the lower extremities and perineum, loss of muscle strength in the lower extremities (commonly known as paralysis), and incontinence. Once cauda equina syndrome is present, it is an indication for emergency surgery and must be examined and operated on urgently. Once cauda equina syndrome is present, the prognosis is poor, usually with incomplete recovery of neurological function and eventually with more or less neurological dysfunction (e.g., difficulty in bowel control, pain and numbness in the lower extremities, difficulty in walking).