Lumbosacral radicular pain or sciatica is commonly associated with various degenerative diseases of the lumbar spine such as lumbar disc herniation. Mechanical compression of nerve roots or dorsal root ganglia is certainly an important pathological factor in lumbosacral radicular pain, however, nerve root compression is not the only pain-causing factor. The fact that free disc prolapse is more painful than other types of disc herniation suggests that there is a correlation between the production of radicular pain and the protrusion of the nucleus pulposus: the corresponding discography shows that the degenerated nucleus pulposus has access to the adjacent nerve roots and triggers chemical radiculitis, venous congestion, fibrosis and fibrinolysis, which proves that the biochemical factors of the nucleus pulposus This proves that the biochemical factors of the medulla are also a significant factor in the pathology of pain. (2) The arterial network of spinal nerve roots is not as rich as that of peripheral nerves and is susceptible to ischemic injury. (3) The plasma proteins in the capillaries of the spinal nerve roots are less transported to the spinal nerve than to the peripheral nerve, and the “blood-nerve” barrier is not as strong as that of the peripheral nerve, making it susceptible to edema and dystrophy. (4) The dorsal root of the spinal nerve is more sensitive to various stimuli than the nerve root itself, and is the main factor in the perception of pain. (2) Changes in the compressed nerve root 1. Nerve dystrophy: Compression produces a direct mechanical effect on the nerve root, and can also damage the nerve blood supply and produce indirect effects. The degree of damage to the nerve is related to the applied pressure. When the applied pressure reaches 0.6—1.33 Kpa, the nerve root arterial blood flow terminates the dystrophy. 2, nerve conduction damage 3, inflammation: (1) mechanical inflammatory damage to the nerve root. (2) Chemical stimulation (3) Natural immune response (3) Pathophysiological mechanism of producing radicular pain (injury receptors, activation of injury receptors) 1. Injury receptors are free nerve endings that receive pain stimulus conduction. 2.After tissue injury caused by chemical or physical factors, the injured tissue releases chemical substances to activate the injury receptors. These substances that activate the injury receptors include non-neurogenic (bradykinin, serotonin, histamine, prostaglandin) and neurogenic mediators (neuropeptide, substance P, calcitonin, etc.) 3, the nerve root “tolerance” and “escape” phenomenon