I, distinguish two different types of lesions (a) the characteristics of the medical history 1, the impact of increased abdominal pressure on pain intravertebral lesions due to increased cerebrospinal fluid pressure and direct pressure on the nerve roots or dura mater, when the nerve is in an irritated state, forceful defecation, coughing, sneezing, etc. can intensify the pain. At this time, if the lumbar girth is worn to reduce the axial pressure of the lumbar spine, it will offset some of the increased abdominal pressure, thus relieving the resulting pain. Pain due to extravertebral soft tissue damage is less likely to be affected by changes in abdominal pressure. The second People’s Hospital of Lianyungang pain department Zhang Hongjin 2, a day of pain changes morning back and leg pain is obvious, and even woke up in the morning because of pain and can not lie down, must get up and move to relieve the pain, daytime work and activities generally do not hinder. This is the characteristic of soft tissue damage pain outside the lumbar spinal canal. In contrast, patients with lumbar spinal canal lesions have the best time of the day to wake up in the morning with no pain or slight pain, but the pain is most pronounced in the afternoon or evening when they go to bed, and the pain is aggravated more quickly by the sitting position. Obviously, this is closely related to the change of axial pressure on the lumbar intervertebral disc. 3, the nature of lower extremity pain Lower extremity pain can be caused by stimulation of the dura mater, posterior longitudinal ligament and ligamentum flavum area innervated by the sinus nerve in the spinal canal, and also by radicular pain caused by nerve root involvement, or radicular pain caused by stimulation of nerve trunk branches due to muscle and ligament damage outside the spinal canal and its own damage area. However, in the case of lower extremity radicular pain, the intra-vertebral lesions are mostly or only in a single segment and often involve the distal neurosensory distribution of the lower extremity, with a high chance of coexisting pain and numbness. In contrast, radiating pain in the lower extremities is also common in extravertebral soft tissue damage, but sensory loss in the distal lower extremities (feet) is less common. The location of lower extremity pain is blurred, and conduction to the foot is uncommon, usually from the lumbar region or buttocks to the posterior and lateral dispersion of the lower extremity to the N fossa. 4.The effect of lifting or supporting heavy objects caused by mechanical stimulation of the nerve endings in the vein wall of the lumbar spinal canal plexus, and this stimulation comes from increased venous pressure. Anatomical studies believe that the spinal venous system and thoracoabdominal, pelvic venous traffic. When the abdominal pressure rises, especially when holding weight at the waist, the thoracoabdominal muscles make strong contraction, which can almost make the venous pressure in the vertebral venous plexus extremely high, and if the epidural venous sinus branch or dorsal root branch in the lumbar spinal canal already has irritation damage (such as intravertebral tumor, disc herniation, vertebral fracture displacement), then it can increase the pressure of the affected dura and nerve root and aggravate the low back pain and lower limb pain. In a significant number of cases, the complaints describe episodes of pain due to lumbar weight-bearing, which do not easily resolve on their own. Although the soft tissue damage outside the spinal canal is also difficult to hold the weight, but the degree of impact is smaller, and the pain can generally disappear naturally after rest and braking. 5, the evolution of the disease process characteristics of extradural tissue damage pain can be sudden onset, but generally in a short period of time can be relieved, and the interval is long, self-limiting obvious, do not need special treatment. Intravertebral lesions cause sudden and frequent episodes of low back pain, and the interval becomes shorter as the number of episodes increases, and the episodes are long, usually requiring 2 to 6 weeks to be relieved by special treatment. If the symptoms of low back and leg pain are light and heavy at times, recurrent. There is no obvious cause, and the frequency of attacks becomes higher and the interval is shortened. If the episodes are not relieved by themselves at the beginning, a mixed lesion inside and outside the lumbar spinal canal should be considered. It is known that two different types of damage lead to the destruction of the stability of the lumbar spine, which is also a manifestation of the severity of the disease. 6, cauda equina damage is a feature of intraspinal lesions lumbar spinal stenosis, giant disc herniation or intraspinal tumors can lead to compression damage of the cauda equina. The onset of the disease is initially ischemic limited arachnoiditis, resulting in functional impairment, with clinical manifestations of atypical lower extremity tingling or sunken pain, intermittent claudication in almost all patients, and lower extremity pain once walking for too long or just walking on the ground. When cauda equina damage is severe, the affected lower limb or bilateral lower limb foot drooping, step or step up and down the ladder appears to trigger the foot. Bladder and rectal dysfunction, from weakness in urination, constipation, and then progress to urinary and fecal incontinence, the patient’s perineum and perianal sensation is reduced or lost. If the low back pain or low back pain continues to develop and worsen progressively, and any non-surgical treatment does not help, and there is weakness, heaviness or atrophy of lower limbs, the existence of intra-vertebral tumor should be highly suspected, and palliation is not allowed. If there is a sudden onset of generalized or lower limb convulsions, or even loss of consciousness, neck strength, or severe pain in the low back during the course of the disease, the presence of subarachnoid hemorrhage in the lumbar spinal canal should be considered, which is a kind of risk in low back pain disease, and intradural extramedullary vascular tumor or variation should be further excluded. 8.involvement low back pain primary abdominal or pelvic organ lesions, accompanied by one or several superficial pains in the lumbar back or lumbosacral area, and at the same time there are segmental lumbar reflex muscle spasms, so the patient can also feel deep pain. Patients with so-called involved low back pain are often misdiagnosed and mistreated as primary low back pain and should be alerted. In these patients, the damage is not in the tissues at the site of pain, nor in the afferent fibers along the innervation of these tissues, but in some other visceral organ tissue whose innervation is segmentally related to the lumbosacral tissues. The injury receptor afferent fibers of this visceral tissue project to the junctional cells in layer V of the posterior horn of the spinal cord, which are the same as the junctional cells of the segmentally related cortical area. In this way, the visceral and cortical injury sensory transmission systems can be significantly converged in the junction cells in layer V of the posterior horn of the spinal cord, i.e., visceral injury sensory pain can be perceived in the cortical area. In clinical evidence, gynecological diseases (such as dysmenorrhea, ovarian lesions, uterine prolapse, cervical cancer, etc.), upper urinary tract lesions (such as pyelonephritis, kidney stones, etc.), posterior appendicitis, and prostate inflammation can all involve lower back pain or sacrococcygeal pain. (The “three clinical tests of the lumbar spine” proposed and recommended by Hsuan, Hsing, have distinctive specificity for lesions within the lumbar spinal canal, and can accurately differentiate from soft tissue damage outside the lumbar spinal canal in the diagnosis of low back pain. The three tests can be performed on herniated lumbar discs, lumbar spinal stenosis, nerve root and epidural sac inflammatory tissue reactions, and nerve tumors. The test is clinically specific and sensitive, and has a high detection rate. 1, thoracoabdominal pillow test (1) examination method: the patient in a prone position, the two upper limbs straight at the side of the body, the whole body relaxed. The examiner probes the deep lumbar muscles in the intervertebral space of the lumbar vertebrae 3 to sacral vertebrae 1 on the diseased side with fingers to find deep pressure points. ① Pressure pain measurement in the lumbar extension position (lying down). The patient was asked whether there was pain, radiating pain or tingling sensation in the lower limbs. ②Lumbar spine hyperextension pressure pain measurement. A 20-30 cm diameter pillow is placed on the anterior chest of the patient to make the lumbar spine in a hyperextended position. Then the examiner probes the pressure with the same pressure on the original pressure point with the thumb and asks the patient about the increase or decrease of pain, and whether there is any radiating pain or tingling sensation in the buttocks and lower limbs. (3) Measurement of pressure pain in the lumbar vertebrae in a hyper-anterior flexion position. The bolster is moved downward on the abdomen, roughly at the umbilicus, so that the lumbar vertebrae are in excessive forward flexion. Then the examiner uses the tip of the thumb to deeply press the original pain point and asks the patient about the increase or decrease of pain, and whether there is any radiating pain or tingling sensation in the buttocks and lower limbs. (2) Clinical significance: ①If the deep pressure pain, conduction pain or numbness in the lower limbs induced by the original hyperextension position disappears completely or is significantly reduced when measured in the hyperextension position of the lumbar spine, then it can be judged as a positive sign of lumbar spinal canal pathogenesis or lumbar leg pain with lumbar spinal canal pathology as the main cause. If the original pain and other symptoms are only mildly reduced, it should be judged as a mixed lesion caused by lumbar spinal canal and internal and external lumbar leg pain. ③No change or increase of the original pain and other symptoms. If the possibility of intra-lumbar spinal canal pathogenesis is basically excluded, it can be considered as extra-spinal canal soft tissue damage low back pain. 2, lumbar scoliosis test (1) examination method: the patient stands in a standing position, with arms naturally hanging down. Lower limbs upright, heels together, so that the patient’s trunk to maintain a moderate posterior position. The examiner stands behind the patient and presses one hand on the upper part of the shoulder on the healthy side and the other hand on the lateral part of the hip on the affected side of the pelvis. Then, one hand presses the pelvic brake and the other hand pushes the healthy shoulder to the direction of the diseased side, so that the trunk and the head are slowly bent to the affected side. When bending to the extreme, ask the patient if there is lumbosacral pain on the affected side or concurrent lower limb conduction pain and soreness, and ask the patient to indicate the pain area. Then the examiner switches the position of both hands and gradually bends the lumbar spine to the healthy side by the same method, and when it reaches the extreme, asks if there are any painful symptoms in the affected lumbar region. (2) Clinical significance: ① If the spine bends to the diseased side and causes deep pain in the lumbosacral region or is complicated by radiating pain or numbness in the buttocks and lower extremities, the test is a positive sign and can be judged to have intraspinal pathogenesis. ② When the spinal curvature to the healthy side is extreme, the deep lumbosacral pain and lower extremity symptoms induced by the original lateral curvature test disappear completely, and the test is also judged to be positive. If the spine bends to the healthy side and the affected side of the back pain appears, it can be judged as soft tissue damage outside the lumbar spinal canal. If the pain in the lumbar or lumbosacral region is caused by either the bending of the spine to the affected side or the healthy side, the test is judged to be a mixed type of lesion inside or outside the lumbar spinal canal causing lumbago. (C) Imaging features 1. X-ray plain film The following changes are for reference. (1) Disc changes. The height of the intervertebral disc becomes narrower. The posterior edge of the vertebral body becomes worn (obtuse angle) or hyperplasia, the joint surface of the intervertebral disc hardens, the posterior longitudinal ligament calcifies and ossifies, the intervertebral pseudoslip and the disc is missing and other morphological changes. (2) The sequence/curve of the intervertebral body in the frontal and lateral position is changed. Lumbar intradiscal lesions (lumbar disc herniation) can occur in lumbar scoliosis and lumbar kyphosis, as well as in cases of severe soft tissue damage to the lumbar region or buttocks, often manifesting clinically as severe mixed lesions within and outside the lumbar spinal canal. The following conditions can cause lumbar kyphosis to the diseased side: unilateral damage mainly to the sacrospinous muscle, damage to the multifidus and rotator spinae muscles in the lumbar 4 to sacral 1 area, and unilateral damage to the gluteus medius. Excessive anterior lumbar spine convexity is caused by severe damage to the posterior lumbar dorsal fascia and sacrospinous muscles in the deep lumbar muscles. Reduced, straightened, or retroverted physiological lumbar lordosis is caused by severe damage to the multifidus, rotator spinae, and anterior lumbar dorsalis fasciae. In cases of excessive anterior convexity, the pain is limited in forward flexion and increased, while in cases of posterior extension, the pain is reduced in forward flexion and limited in posterior extension, and the pain is increased. 2.CT scan or MRI examination The measurement of the size of the spinal canal, that is, the presence of stenosis (central canal, lateral canal, intervertebral foramen) and changes in the structure and morphology of the contents can be used as a hint. The diagnosis can be made more clearly for the form, size, location, segmental range and the relationship with the dural sac and nerve roots of the herniated disc. The detection rate of spinal canal tumors is also high and has important reference value. (D) electromyography can be distinguished between neurogenic damage and myogenic damage, both of which indicate lesions from the spinal canal. If a large number of fibrillation potentials and positive phase potentials are found in the tibialis anterior muscle (L4-5) and peroneus longus muscle (L5-S1), and at the same time the action potential decreases without significant changes in wave amplitude and wave width, it indicates that the L5 spinal nerve may be involved. If the loss of innervation potentials was also found in the sacrospinous muscle innervated by L5, the involvement of the L5 nerve root segment could be confirmed. If no abnormal potentials are found in the sacrospinal muscles innervated by L5, a peripheral lesion should be considered. The localization of radicular pain in most limbs can be determined on this basis. If a large number of spontaneous nerve potentials are found in the atrophic muscle group, and there is a decrease in motor units, but the conduction velocity is normal, and the action potential amplitude is high and wide, it indicates the possibility of spinal cord lesion. The average time frame of motor potentials of sacrospinous muscle measured by EMG was significantly shorter than normal, and there were no or rarely (occasionally) abnormal waveforms of denervation such as positive phase potentials and fibrillation potentials. If there is also no reduction in action potential and the waveform amplitude is low, the width is narrow and the nerve conduction velocity is normal, then the disease is more likely to be myopathy. A simple shortening of the mean time frame of the action potential indicates a dysfunction of the muscle tissue due to a sterile inflammatory response to nerve root stimulation. Second, determine the site of the lesion (a) lumbar spinal canal lesions 1, lumbar forward flexion and back extension functional activities The lumbar forward flexion activities first by the hip flexion to complete 50%, followed by the real lumbar spine itself to complete 50%. About 75% of the lumbar forward flexion activity depends mainly on the function of the L5-S1 intersegment (the remaining 25% function is completed by L2-5). When the L5-S1 intervertebral disc is herniated or the lumbosacral and sacrospinous muscles are damaged, the forward flexion activity will be significantly limited. In the case of lumbar posterior extension, on the one hand, the volume of the lumbar spinal canal becomes smaller, the posterior fibrous ring of the disc is extruded backward, the ligamentum flavum is folded forward, and the compression and stimulation of the small articular prominence increases on the dural sac or nerve roots, which may induce clinical symptoms; on the other hand, the posterior extension is mainly completed by the lumbar spine segments 2 to 5. The above situation makes the L5-S1 segment less affected, but if the posterior extension activity of the lumbar region is limited and neurological symptoms arise, the lesion of the L3-4/L4-5 segment should be considered. Similarly, the motor segment that affects sitting work should also be L5-S1. 2, pressure pain in the paravertebral or median area of the lumbar spine can indicate segmental damage in the spinal canal. Interspinous pressure pain along with paraspinous intervertebral plate pressure pain and lower extremity radicular pain indicates central lateral disc herniation; if only interspinous pressure pain or paraspinous intervertebral plate pressure pain and lower extremity radicular pain is present, then central or lateral disc herniation should be considered. Of course, the site of pressure pain is of great value in distinguishing damage to different segments of the spine, especially spinal percussion pain is meaningful for the detection of intraspinal occupying lesions, and can be used as a screening method before imaging. 3, neurological localization signs, with high diagnostic value (1) sensory loss or loss: the distribution of sensory nerves in the low back is mainly innervated by the posterior branch of the spinal nerve; the distribution of sensory fibers in the spinal canal is innervated by the sinus nerve from its posterior branch, and the limbs are innervated by the sensory branches from the plexus composed of the anterior branch of the spinal nerve. Therefore, the sensory disorders in the cortex innervated by the affected nerve roots can be used as a reference for the diagnosis and localization of lesions in the lumbar spinal canal (such as lumbar disc herniation and lumbar spinal stenosis). However, the prerequisite is that the two lesions within and outside the spinal canal are first distinguished. When the sciatic nerve trunk and its branches are compressed by spasm or degenerative contracture of the soft tissues of the lumbar and hip lesions, the same hypesthesia or loss of sensation in the innervated dermatomal areas as in the case of compression of the lumbar nerve root can occur. The sciatica and hyperalgesia or hyperalgesia of the lateral calf seen clinically are signs that are common to both intradural and extradural damage. (1) Lateral thigh dermatomes. Nerve branches from the lumbar plexus (L2, 3). (2) Anterior medial calf skin area. From the lumbar plexus (L.4) nerve branch. (iii) Posterior lateral thigh, lateral calf cortex, lateral ankle, dorsal foot and medial three toe cortex. Nerve branches from the sacral plexus (L5 to S1). ④Posterior thigh, posterior calf, plantar or lateral edge of the foot and the lateral two toe skin areas. Nerve branches from the sacral plexus (L5 to S1 and 2). (2) Muscle weakness: muscle weakness in different areas reflects the involved nerve segments. For example, weakened quadriceps muscle reflects segmental involvement of L2, 3, 4 (knee extension ↓); weakened anterior tibial muscle reflects segmental involvement of L4 (dorsiflexion ↓); weakened extensor hallucis longus muscle reflects segmental involvement of L5 (bunion ↓); weakened plantarflexor and flexor hallucis longus muscle reflects segmental involvement of S1 (plantarflexion ↓); but it should be noted that muscle weakness or atrophy is also a common sign of lesions inside and outside the spinal canal. Clinically, a single foot supporting trunk movement (golden chicken independence) can indicate the involvement of S1 segment or not. (3) Reflex disorders: tendon reflexes of the lower limbs have a more accurate localization. In intraspinal lesions, the involved nerve segment can be identified. Reduced or absent knee tendon reflexes reflect lesions of L3 and 4 segments. A decreased or absent Achilles reflex reflects a lesion in the S1 segment. If pathological reflexes such as Babinski’s sign appear, the intracanalicular lesion should be considered as a vertebral bundle sign in the cervicothoracic spine, which is mostly caused by a damaging spinal cord lesion. 4, prone knee and hip flexion test: this test was originally a sign of femoral nerve tension, but due to the anatomical variation of the spinal nerve can appear lower back pain or sciatica. The reason for lower back pain is that the afferent branch of the second lumbar nerve travels downward and is buried in the posterior longitudinal ligament, along the posterior edge of the vertebral body and down to the plane of the fifth lumbar vertebra, so when the knee is flexed and the hip is extended, the dorsal root of the L2 nerve and its inferior branch may be involved, and when it is irritated and damaged, pain can be induced. The reason for sciatica is that in many cases, there is a traffic branch between the fourth lumbar nerve and the fifth lumbar nerve, and when the knee is flexed and the hip is extended, the dorsal root of the L4 nerve and its traffic branch are stretched, causing irritation of the L5 nerve root. If the L4-5 disc herniation stimulates and compresses the L5 nerve root, this test can be positive. However, if the L5-S1 disc herniation stimulates and compresses the S1 nerve root, this test does not cause radiating pain in the lower extremities, so it can distinguish nerve damage in the L4-5 segment from that in the L5-S1 segment. (2) soft tissue damage outside the lumbar spinal canal 1. pressure points and involvement pain (1) pressure points in the lumbar hip and lower extremities: pressure points in the lower thoracic or lumbar interspinous process, paraspinous process, and mid-sacral crest (supraspinous and interspinous ligaments); pressure points at the inner edge of the posterior superior iliac spine and the posterior 1/3 of the iliac crest (sacrospinous muscle); pressure points at the upper edge of the pubic symphysis (rectus abdominis and proneus muscle); pressure points at the iliac crest (lumbar square, external and internal oblique muscles); pressure points in the thoracolumbar spine plate and small (lumbar deep muscle spinae, multifidus, and small joint capsule); lumbar transverse process and lower border of the 12th rib (lumbar square and lumbar dorsal fascia); posterior superior iliac spine and lower outer border of sacrococcyx and gluteus maximus (gluteus maximus); sacroiliac joint (long and short ligaments, joint capsule); iliac wing and upper border of the greater sciatic foramen and intertrochanteric fossa (gluteus medius and minimus); posterior superior iliac spine and lateral femoral pressure points (anterior superior iliac spine and lateral femoral pressure points) and lateral femoral pressure points (vastus lateralis, iliotibial bundle); lateral sciatic tuberosity pressure point (femoral square); superior medial sciatic tuberosity pressure point (sacral tuberosity ligament); apical femoral greater trochanter pressure point (pear-shaped muscle); small trochanter muscle attachment pressure point (iliopsoas muscle); inferior and inferior pubicis branch muscle attachment pressure point (femoral adductor group); superior gluteal cutaneous nerve pressure point; inferior sciatic nerve pear-shaped muscle outlet pressure point; pressure point of superior gluteal nerve at the superior outlet of the pear-shaped muscle; pressure point of inferior gluteal nerve at the inferior outlet of the pear-shaped muscle; pressure point of tibial nerve at the slapping fossa; pressure point of submental fat pad; pressure point below the inner ankle (posterior tibial tendon and tendon sheath); pressure point below the outer ankle (peroneal long and short tendons and tendon sheath). Tarsal sinus (extensor digitorum brevis, ankle pad), heel spine (metatarsal tendon membrane, metatarsal long ligament) (2) Involvement pain: soft tissue damage in the area innervated by the distribution of the sinus nerve or posterior branch of the spinal nerve can produce lower extremity discharge pain similar to that of spinal nerve root involvement. Usually, the pathway of dissemination is vague and not necessarily distant, but in a few cases it can reach the end of the limb. (1) Inflammatory adhesions, hyperplasia and contracture of soft tissues in the lumbar or lumbosacral region → pain in the buttocks, posterior thigh, lateral calf, below the outer ankle, lateral heel bone and anterolateral dorsum of the foot. (2) Inflammatory adhesions, hyperplastic degeneration and contracture between the soft tissues of the hip and its muscle intervals → posterior or lateral thigh, lateral calf, upper knee, heel or dorsum of the foot. (3) Inflammatory adhesion, hyperplasia and contracture of the broad fascia tensor muscle at the attachment of the anterior superior iliac spine muscle → pain outside the knee, pain in front of the knee, pain in front of the tibia, dorsum of the foot or heel; pain below the outer ankle, pain in the lateral aspect of the heel, pain in the lateral aspect of the forefoot. ④Chronic inflammatory damage to the pubic bone attachment of the adductor muscle group → hip, lateral calf, and foot; medial thigh, medial knee, medial calf, medial heel, and medial foot pain. ⑤ Chronic inflammatory damage at the attachment of the iliac crest such as the external and internal oblique muscles and transversus abdominis → pain in the lateral thorax, abdominal wall, and sudden twitching of the affected lower extremity. (6) Chronic inflammatory damage to the upper edge of the pubic symphysis of the rectus abdominis and proneural muscles → lower abdominal pain, or urethral pain. (7) Inflammatory damage to the iliolumbar ligament → pain in the lumbar groin, iliac crest and medial thigh root. (8) Inflammatory damage to the sacroiliac ligament → pain in the lateral thigh (short sacroiliac ligament), the posterior side of the large and small legs, and the lateral edge of the foot (long sacroiliac ligament). Inflammatory damage of the sacral nodal ligament → posterior medial thigh, posterior medial calf, and heel pain. 2.Functional examination can localize the pressure pain points. (1) straight leg elevation test; (2) flexion knee and hip splitting test; (3) hip abduction test: gluteus medius; (4) iliotibial tension test; (5) hip internal rotation test: pear-shaped muscle; (6) sacroiliac joint test: “4” test; (7) infraspinatus fat pad extrusion sign; (8) drawer test; (9) femoral nerve tension test. The nature of the lesion can be clarified based on clinical features, imaging and laboratory diagnosis. (1) Intraspinal disorders (1) Tumors: neurofibroma, nerve sheath tumor, nerve root cyst, dermatomal cyst, ventricular meningioma, metastatic carcinoma (liver, kidney, prostate, ovary), spinal cord glioblastoma, neuroblastoma, etc. (2) Angiomas and variants: arteriovenous tumors, spinal membrane bulge. (3) Spinal cord cavernous disease, multiple sclerosis. 2.Common disorders (1)Lumbar disc herniation (central type, lateral paracentral type, lateral type, extreme lateral type, anterior type). (2) Thoracolumbar spinal stenosis (congenital, developmental, degenerative, traumatic, medical, mixed). (3) Lumbar spinal slippage (leading to secondary spinal stenosis). (4) Soft tissue damage (hypertrophy of the ligamentum flavum, calcification of the posterior longitudinal ligament, degenerative contracture of fatty connective tissue, etc.). (B) Extra-vertebral lesions 1. extreme or specific lesions (1) spinal tumors, tuberculosis, eosinophilic granuloma. (2) sequelae of spinal injury: crush fracture, splinter fracture, fracture dislocation. (2) Rheumatoid arthropathy. Rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, Liet’s syndrome, systemic lupus erythematosus, gouty arthritis, dermatomyositis and reactive arthritis, sacroiliac joint disorders, ischemic necrosis of the femoral head, etc. 3.Organ disorders and systemic disorders. Hepatobiliary and digestive system, genitourinary disorders, gynecological disorders, endocrine disorders (hypothyroidism, diabetes mellitus, aldosteronism). 4. Vascular disorders. Thrombo-occlusive vasculitis, thrombotic deep phlebitis, common iliac artery or external iliac artery thrombosis. 5, soft tissue damage (including fibromyalgia syndrome). Roughly divided into lumbar muscle group, gluteal muscle group, internal femoral retractor group, ventral muscle group, slapping cord muscle group, medial and lateral heads of gastrocnemius, submental fat pad, peroneal long and short muscles, posterior tibial muscle group, tarsal sinus soft tissue, metatarsal tendon membrane and various joint ligaments of the lower extremities, and other parts of the injury aseptic inflammatory reaction. 6, infectious. Herpes zoster, lymphangitis. The above ideas of diagnostic procedures have been verified by clinical cases with high accuracy and are not easy to be missed. From the current status of pain diagnosis and treatment, it is not appropriate to include CT, MRI and electrophysiological examination in the routine items. The authors believe that a clear diagnosis can be made by careful history taking, thorough physical examination and routine X-ray or necessary laboratory tests, and MRI and electromyography will be done only when extreme or specific lesions inside or outside the spinal canal are suspected. The diagnostic ideas provided in this article are useful in selecting the correct clinical treatment.