Neuropathic pain (NP) refers to pain caused by injury or disease affecting the somatosensory nervous system. NP is usually chronic, with persistent or recurrent pain, causing great pain and functional impairment to patients. Various diseases that affect the peripheral or central nervous system, such as neurodegenerative diseases, autoimmune diseases, metabolic diseases, vascular diseases, tumors, infections, poisoning, trauma, genetic diseases, and unexplained neurological disorders, can all induce NP. The prevalence of NP in the general population is 3.0% to 17.0% .

The treatment of NP is full of challenges and difficulties. The Chinese pain community has proposed the principle of "treatment forward, early intervention, prevention of sensitization, and prevention and treatment of chronic pain", which has played a positive role in improving the clinical diagnosis and treatment level of NP. To standardize NP management, the Pain Medicine Branch of China Association of Health Care for the Elderly convened an expert panel to develop the ‘Chinese Guideline for Neuropathic Pain Diagnosis and Treatment’. This evidence-based guideline was formulated through systematic literature reviews of both domestic and international evidence, critical appraisal of expert recommendations through multiple rounds of expert evaluation.

The literature search period was from January 2014 to June 2024. The search terms included neuropathic pain, peripheral neuropathic pain, central neuropathic pain, etc. Data sourced from Wanfang, China National Knowledge Infrastructure (CNKI), PubMed, and Cochrane Library. Selectted high-grade evidence literatures such as systematic review, meta-analysis, randomized controlled trials (RCTs), expert consensus, and clinical guidelines as the basis. After multiple rounds of discussion and online voting using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology (Table 1 ) and consensus conference method, this guideline was ultimately developed.

The mechanism of NP is complex and not yet fully understood. Research has shown that pain transmission, modulation pathways, and pathological plasticity changes in cognitive and affective related brain regions caused by injury and disease play an important role . In peripheral sensory nerves, pathological plasticity changes are manifested by abnormal expression of multiple ion channels in dorsal root ganglion and trigeminal ganglion neurons, such as upregulation of sodium and calcium channels, while downregulation of potassium channels, causing abnormal increase in excitability and ectopic discharge, leading to hyperalgesia, hyperalgesia, and spontaneous pain , resulting in plastic changes in pain transmission at all levels of the central nervous system, from the spinal dorsal horn to the sensory cortex. In the early stage of NP, functional changes such as excitatory synaptic transmission efficiency and long term potentiation (LTP) are manifested. In the later stage, the number of excitatory synapses increases while the number of inhibitory synapses decreases, leading to neural circuit remodeling . The plasticity of the pain modulation system changes, leading to a decrease in the function of the descending inhibitory system and an increase in the activity of the descending facilitation system . The functional and structural changes in cognitive and affective related brain regions, such as the hippocampus and prefrontal cortex, lead to cognitive and affective disorders, and the changes in cognitive function enhance pain perception by interfering with the pain modulation system . Research has shown that activation of glial cells and overexpression of inflammatory cytokines such as TNF-α and IL-1β cause neuroinflammation, mediating chronic pain. Inflammatory cytokines regulate the expression of multiple ion channels, causing abnormal elevation of neuronal excitability. By differentially regulating synaptic plasticity in different brain regions, such as upregulating and downregulating the number of excitatory synapses in the spinal dorsal horn and hippocampus, chronic pain and cognitive or affective disorders can be caused. The destruction of the blood-brain barrier and blood-brain barrier caused by peripheral and central nervous system injury, leading to the infiltration of peripheral immune cells into peripheral nerves and brain tissue, is an important trigger of neuroinflammation .

Trigeminal neuralgia (TN) is divided into primary TN and secondary TN. Primary TN is the most common type in clinical practice, and is further divided into classic TN (with neurovascular compression) and idiopathic TN (with no underlying cause identified). Secondary TN (with potential pathology), also known as symptomatic TN, refers to TN caused by secondary damage to the trigeminal nerve caused by various organic diseases inside and outside the skull. The prevalence rate of TN is 182/100,000, and the annual incidence rate is 3-5/100,000, mostly in adults and the elderly .

Paroxysmal severe pain occurring in the trigeminal nerve distribution area, often accompanied by electric shock or needle puncture sensation, lasting for several seconds to minutes, with periodic pain and asymptomatic intervals. Pain is often triggered by touching the trigger point and is more common on one side, particularly in the maxillary and mandibular branches. When the pain is severe, it may be accompanied by ipsilateral muscle twitching, facial flushing, tears, and drooling.

Typical primary TN is diagnosed based on the third edition of International Classification of Headache Disorders (ICHD-3).

Trigeminal nerve attacks occur in one or more branches, without external radiating pain of the trigeminal nerve.

Include at least 3 of the following 4 items: Intermittent pain lasting for 1-2 minutes; Severe pain; Electric-shock-like pain, lightning-like pain, and lancinating pain; Trigger pain on the affected side.

No clinically significant neurological deficits.

Exclude other diagnoses listed in ICHD-3.

Must fulfill both criteria (i) and (ii), with documentation of ≥3 ipsilateral episodes.

TN needs to be differentiated from diseases such as glossopharyngeal neuralgia, toothache, cluster headache, atypical facial pain, sphenopalatine neuralgia, postherpetic neuralgia in the trigeminal nerve area, temporomandibular joint dysfunction syndrome, painful ophthalmoplegia syndrome, coronary heart disease, etc.

Postherpetic neuralgia (PHN) is defined as persistent pain lasting for ≥1 month after the resolution of herpes zoster rash, representing the most common complication of herpes zoster . PHN is more common in the elderly, and the incidence increases with age.

The most common areas of PHN are the chest and back, followed by the head, face, neck, and lumbar back, with the lowest incidence in the lumbar and sacral regions. The range of pain in patients often coincides or expands with the herpes area. Patients with PHN typically experience persistent baseline pain with paroxysmal worsening. The pain manifests in various neuropathic qualities, including electric-shock-like, lancinating, burning, or stabbing sensations. Frequent occurrences of spontaneous pain, hyperalgesia, hyperalgesia, and abnormal sensations.

PHN patients often have accompanying symptoms such as anxiety, depression, poor sleep, and decreased quality of life.

The diagnosis of PHN is primarily based on patient history and clinical presentation, typically requiring no additional specialized investigations. PHN needs to be differentiated from primary TN, glossopharyngeal neuralgia, occipital neuralgia, intercostal neuralgia, and pain caused by primary tumor compression.

Painful polyneuropathy refers to a kind of disease with pain symptoms caused by many reasons, such as aberrant metabolism, autoimmune response, family inheritance, infectious diseases, exposure to environmental or occupational toxins, or neurotoxic drug treatment . Common painful polyneuropathy included painful diabetes peripheral neuropathy (PDPN), chemotherapy induced peripheral neuropathy (CIPN), post radiotherapy pain, post-operative/traumatic pain, human immunodeficiency virus (HIV) infection painful polyneuropathy, etc. The prevalence of PDPN is 8.0%~26.0% , which is more likely to be chronic in type 2 diabetes. The prevalence of CIPN is about 40.0% . 13.0% to 50.0% of HIV patients may develop HIV infectious painful polyneuropathy .

PDPN most commonly affects the ends of the limbs, particularly the feet, and typically presents with persistent pain characterized by pricking, burning, or electric-shock-like sensations. The pain is often most prominent at rest and night.

CIPN is clinically characterized by sensory disturbances and neuropathic pain, including symmetric pain and numbness in the hands and feet, tingling, burning, or electric-shock-like sensations, which often worsen at night. Patients frequently experience muscle weakness, with advanced stages leading to motor impairment, such as muscle atrophy or coordination deficits.

Post radiotherapy pain refers to the pain caused by direct or delayed damage to nerves, bones, or soft tissues within the irradiation field during radiation therapy for primary tumors or tumor metastases. The most common form is chronic neuropathy caused by radiation.

Postoperative or posttraumatic pain refers to pain that occurs or intensifies due to surgery or tissue damage (including various injuries such as burns). The area of pain is often located within the surgical margin or tissue injury range, the corresponding nerve innervation area, and the skin segment area corresponding to surgery or injury of the deep body or visceral tissues.

Another painful polyneuropathy, such as HIV-infected painful polyneuropathy, typically manifests as abnormal sensory pain in the distribution area of stocking-glove, mainly affecting the feet and hands. Vitamin B deficiency causes painful polyneuropathy, with clinical manifestations mainly including lower limb burning pain or numbness, progressive aggravation, decreased muscle strength, and even muscle atrophy, seriously affecting walking. Patients with alcoholic polyneuropathy often complain of burning or numbness in the soles of the feet, fever, and spasmodic pain in the gastrocnemius muscle.

PDPN is diagnosed according to the Toronto Consensus Criteria for Diabetic Neuropathy : Possible existence of PDPN History of diabetes, PDPN related symptoms, such as painful stocking-glove distribution sensory changes; Probable PDPN is diagnosed when two or more of the following criteria are met: neuropathic pain symptoms, distal sensory impairment, and/or diminished/absent ankle reflexes.; Definitive diagnosis of PDPN requires abnormal nerve conduction studies (NCS). If NCS findings are normal, small fiber nerve function testing may be employed to support diagnosis.

CIPN There are no clearly established diagnostic criteria. Chemotherapeutic agents, particularly oxaliplatin- or paclitaxel-based regimens, are more likely to induce neuropathic pain, which is more severe and lasts longer. It is recommended to use cotton swabs or wooden sticks to evaluate tactile sensation, use hot and cold objects to evaluate thermal sensation, and use tuning fork tests to evaluate vibration sensation.

Other painful polyneuropathy There are no clearly established diagnostic criteria, and diagnosis is mainly based on medical history and clinical characteristics. Vitamin B complex deficiency is common in obesity, tumors, and long-term chronic gastroenteritis after gastrointestinal surgery. Alcohol-related polyneuropathy is more common in chronic heavy alcohol use for 10 years or more.

NP after peripheral nerve injury is a persistent or recurrent NP caused by peripheral neuropathy . Peripheral nerve injury is often caused by trauma such as traction injury, compression injury, and cutting injury. Incomplete or poor functional recovery after nerve damage can lead to NP. Depending on the affected area, NP after peripheral nerve injury can be divided into phantom limb pain, residual limb pain, nerve entrapment syndrome, brachial plexus nerve injury, and other nerve trunk injuries . Residual limb pain refers to pain occurring in the remaining stump after amputation, whereas phantom limb pain is the perception of pain in the amputated portion of the limb. The incidence of NP following peripheral nerve injury ranges from 8.0% to 26.0% .

NP resulting from peripheral nerve injury is characterized by prolonged duration and complex clinical manifestations, including sensory deficits, motor dysfunction, and autonomic nervous system disturbances. The clinical manifestations mainly include spontaneous pain, allodynia, hyperalgesia, persistent pain, or paresthesia. The pain may manifest in various forms, including lancinating, lightning-like, burning, tearing, shooting, electric-shock-like, or needle-pricking sensations. These diverse presentations can be either deep-seated or superficial, with most patients experiencing two or more distinct pain qualities simultaneously. Symptom exacerbation commonly occurs with physical activity, fatigue, psychological stress, or changes in environmental/climatic conditions. Patients may experience symptoms such as muscle spasms, stiffness, weakness, and atrophy. Physical examination shows decreased muscle tone, muscle atrophy, weakened or absent tendon reflexes, and sensory abnormalities. Notably, the pain often persists chronically even after resolution of the original etiology, complete tissue healing, or effective disease control, significantly impairing quality of life and frequently accompanied by affective disorders.

The diagnosis of NP after peripheral nerve injury primarily relies on a detailed understanding of the medical history, systematic physical examination, and necessary neurophysiological testing, as no unified diagnostic criteria currently exist. The main diagnostic standards currently employed are as follows : The medical history clearly indicates the presence of related trauma or diseases in the peripheral nervous system; The onset of pain shows a clear temporal correlation with the traumatic incident; The pain distribution corresponds to the anatomical territory of somatosensory nerves; The neurological examination confirms objective signs consistent with nerve damage or disease; At least one auxiliary examination confirms the presence of related damage or disease in the somatosensory system.

Painful radiculopathy is a disease that causes peripheral neuropathic pain through nerve root lesions, characterized by persistent or recurrent pain resulting from pathologies affecting cervical, thoracic, lumbar, or sacral nerve roots, and classified as peripheral neuropathic pain. Degenerative spinal changes are the most common cause of painful radiculopathy, while trauma, tumors, neoplastic meningitis, infections, hemorrhage or ischemia, diabetes, rheumatoid arthritis, and iatrogenic conditions may also contribute .

The main clinical manifestations are spontaneous pain, hyperalgesia, and sensory abnormalities in the corresponding nerve root innervation area. The pain may present as persistent or paroxysmal, with qualities including lancinating, burning, tearing, electric-shock-like, or needle-stabbing sensations, often leading to functional impairment.

The diagnosis primarily relies on medical history, physical examination, assessment scales, imagings, neurophysiological tests, and diagnostic interventions.

Glossopharyngeal neuralgia (GPN) is a disease characterized by brief, paroxysmal episodes of unilateral pain, occurring in the distribution area of the glossopharyngeal nerve (mandible, ears, tonsil fossa, and tongue base). When involving the pharyngeal and auricular branches of the vagus nerve, symptoms are often triggered by swallowing. The annual incidence rate of GPN is about 0.7/100000, with increasing prevalence in older populations.

The diagnostic criteria for GPN in ICHD-3 are as follows.

Recurrent and paroxysmal pain attacks in the distribution area of unilateral glossopharyngeal nerve.

Pain should have all of the following characteristics: The pain lasts from a few seconds to 2 minutes; The degree of pain is severe; The pain is characterized as sharp, stabbing, or electric shock-like sensations; Pain is triggered or exacerbated by coughing, yawning, swallowing, or speaking.

Pain cannot be explained by any other ICHD-3 diagnosis.

The diagnosis requires excluding other diseases that may cause similar symptoms, such as TN, temporal arteritis, temporomandibular joint dysfunction, etc. Diagnostic blockade via pharyngeal topical anesthesia is commonly used in clinical practice to assist in differential diagnosis.

The central NP associated with spinal cord injury, abbreviated as spinal cord injury pain (SCIP), is one of the common sequelae of spinal cord injury. SCIP is divided into two categories.

The first category is nociceptive pain, which can be further divided into musculoskeletal pain and visceral pain.

The second category is neuropathic pain, which can be further divided into pain above the injury plane, pain below the injury plane, and pain below the injury plane. Numerous studies have shown that approximately 2/3 of spinal cord injury patients develop SCIP. Apart from motor dysfunction and sphincter disturbances, SCIP is often the greatest source of suffering for these patients.

Musculoskeletal pain is the most common type of pain during the acute phase after spinal cord injury. Pain episodes are often associated with muscle contractions, limb movements, or changes in posture, and may radiate into the limbs and trunk.

Visceral pain following spinal cord injury is primarily characterized in the thoracic, abdominal, or pelvic regions. The pain is typically diffuse, poorly localized, and often described as dull, colicky, or aching. It usually emerges months or even years after the spinal cord injury and tends to occur intermittently.

Spinal cord injury induced NP is often characterized by severe, shooting, burning, cutting, or stabbing pain, frequently accompanied by band-like dysesthesia.

Clear history of spinal cord injury, including traumatic spinal cord injury, iatrogenic spinal cord injury, or other confirmed causes.

At least one auxiliary examination confirming that the pain corresponds to a neuroanatomical distribution.

At least one auxiliary examination demonstrating relevant structural damage or pathology.

Chronic pain is a common sequela and one of the most frequent complaints in patients with traumatic brain injury (TBI). The prevalence of chronic pain exceeds 50.0% in TBI patients, reaching as high as 75.0% in mild TBI cases . In most instances, chronic pain localizes to the bodily region of tissue injury. However, some chronic pain occurs in non-traumatized areas or body parts without apparent pathology, potentially arising from central mechanisms—termed ‘central pain’ . Post-TBI chronic pain encompasses headache, musculoskeletal pain, central pain, and other types .

Chronic headache following brain injury most commonly manifests in three types: tension-type headache, migraine, and mixed symptoms of both. The headaches are typically of moderate intensity, with 65.0% of patients describing bilateral pain localized to the frontal region, characterized by a combination of throbbing and pressure-like qualities. Among moderate to severe TBI patients, approximately 12.0% may develop complex regional pain syndrome (CRPS), primarily presenting with limb spasms. Some TBI patients experience delayed-onset pain syndromes, often emerging weeks to months post-injury, predominantly unilateral, with persistent pain and paroxysmal exacerbations.

The diagnosis is established based on a history of TBI, combined with characteristic symptoms, physical examination findings, and relevant imaging studies.

Central Post-Stroke Pain (CPSP) refers to somatic pain and sensory abnormalities associated with ischemic or hemorrhagic stroke lesions. The incidence of CPSP ranges from 1.0% to 12.0% , typically emerging 3–6 months post-stroke. The development of CPSP is closely linked to sensory deficits, with younger age, smoking, depression, and stroke severity identified as high-risk factors .

The pain is often located in the contralateral limb, face, or trunk of the central lesion, and may also occur in ipsilateral hemiparesis, but the pain symptoms are milder than those on the contralateral side. The pain manifests with qualities such as burning, stabbing, lightning-like, crushing, freezing, or tearing sensations. The location of pain is basically consistent with the distribution of sensory abnormalities.

Diagnosis primarily relies on stroke history, pain characteristics, and sensory abnormality symptoms, while excluding other potential conditions. The diagnostic criteria for CPSP proposed by Klit et al. include the following essential components.

Pain localized to somatic areas corresponding to the central nervous system lesion.

History of stroke, with pain onset coinciding with or following the stroke.

Clinical examination reveals sensory deficits consistent with the lesion.

Neuroimaging confirms a relevant causative lesion.

Exclusion of alternative pain etiologies.

Multiple sclerosis (MS) related central NP is a chronic inflammatory demyelinating disease of the central nervous system, frequently manifests with pain secondary to neurological damage. Pain is highly prevalent in MS, typically resulting from neurological damage, with the majority being central NP and a minority presenting as peripheral neuropathic pain or musculoskeletal pain. Between 50.0% and 75.0% of MS patients experience chronic pain at some point during the disease course, and in some cases, pain may be the initial symptom of MS. The type of pain in MS patients generally correlates with the specific regions of the nervous system affected.

Painful numbness is the most common type of pain in MS, present in 45.0% of patients. It is characterized by persistent burning pain that worsens with high temperatures or weather changes, and may be accompanied by allodynia and hyperalgesia. The pain is typically bilateral, affecting the legs and feet, and is more severe at night. Physical activity can exacerbate the pain. Patients with primary progressive MS may also experience brief, electric-shock-like or radiating pain lasting less than 2 seconds in the posterior neck, lower back, or other body areas, triggered by neck flexion and immediately relieved upon cessation of movement.

The diagnosis of MS is primarily based on comprehensive analysis of clinical symptoms and ancillary test results, while requiring exclusion of other potential diseases.

NP is a persistent condition that may involve recurrent exacerbations, requiring long-term therapeutic management. NP treatment should be based on safety, efficacy, and cost-effectiveness, guided by the principles of ‘moving the checkpoint forward, early intervention, prevention of sensitization, and prevention of chronic pain’. Pharmacotherapy is generally the first-line approach, with timely incorporation of minimally invasive procedures when indicated, and general treatment, physical therapy, traditional Chinese medicine treatment, psychological therapy, etc. should be combined as appropriate.

Environmental factors and emotional changes can worsen NP, highlighting the importance of patient education and self-management. Patients should maintain healthy habits, avoiding sleep deprivation, overexertion, excessive eating/drinking, smoking, and overly spicy foods. Guide patients to self-regulate their emotions. Regular exercise and social engagement are encouraged. A strong, trusting physician-patient relationship fosters better treatment adherence and outcomes. Evidence-based recommendations for general therapies, including quality grading and strength of evidence, are summarized in Table 2 .

Pharmacotherapy forms the foundation of treatment and should utilize recommended drugs at effective doses . Combination therapy is well-tolerated and can enhance analgesic efficacy in patients with inadequate pain control from monotherapy . Upon achieving effective pain relief, abrupt discontinuation should be avoided, with maintenance treatment continued for at least 2 weeks .

(i) Common drug classification

Calcium channel-targeting agents: Primary representative medications include pregabalin, gabapentin, crisugabalin, and mirogabalin .

Sodium channel modulators: Key representative drugs comprise carbamazepine, oxcarbazepine, lidocaine, and bulleyaconitine A.

Tricyclic antidepressants (TCAs): The main representative drugs include amitriptyline, imipramine, desipramine, and nortriptyline. However, there is little evidence to support the use of imipramine , desipramine , or nortriptyline for treating NP.

Serotonin and norepinephrine reuptake inhibitors (SNRIs): Key representative drugs include duloxetine and venlafaxine.

Opioids: Main representative drugs include morphine, oxycodone, fentanyl, buprenorphine, tapentadol, methadone, and hydromorphone. However, there is insufficient evidence to support or refute the efficacy of morphine , fentanyl , or hydromorphone in NP treatment.

NMDA receptor antagonists (e.g., ketamine, memantine, dextromethorphan).

Botulinum toxin type A (BTX-A) and the novel anti-inflammatory drug tetrandrine can be effectively used in the comprehensive management of NP.

Platelet-rich plasma (PRP) : Perineural PRP injection is an effective therapy for alleviating pain and numbness in PDPN and improving peripheral nerve function.

Other medications: such as tramadol, capsaicin patch, cannabinoids, antiepileptic drugs (e.g., lamotrigine, topiramate), vaccinia virus-inoculated rabbit skin inflammatory extract, traditional Chinese medicines (e.g., Jingshu Granules ), glucocorticoids, vitamins, muscle relaxants (e.g., baclofen), etc.

(ii) The quality grading and recommendation strength of evidence-based medicine for common NP treatment drugs (Table 3).

Pregabalin has the widest and highest level of evidence support. For PHN , PDPN , CIPN, post radiotherapy pain , postoperative or posttraumatic pain , SCIP , CPSP, the evidence level of pregabalin is A1. In contrast, the strength of evidence for Gabapentin varies. Its evidence level for TN is B2 , but its evidence level for PHN and PDPN is A1. For CIPN and post radiotherapy pain , the evidence level drops to B1. For SCIP, the level of evidence returned to A1, but for CPSP , the level of evidence was downgraded to B1. The new drug Crisugabalin showed A1 level evidence for both TN and PHN . Another new drug, Mirogabalin, has an evidence level of A1 for PHN and PDPN , B1 for CIPN, A1 for postoperative or posttraumatic pain and SCIP , and B1 for CPSP .

In the category of sodium channel blockers, carbamazepine , is a classic A1 level recommended drug for TN, but its evidence level for PHN is only B2 . Oxcarbazepine is also an A1 level recommended drug for TN , but the evidence level for PHN is B2 , and the evidence level for SCIP is also B2 . Lidocaine has an evidence level of B2 for TN but shows A1 evidence for PHN , and an evidence level of B2 for SCIP .

Among tricyclic antidepressants, amitriptyline has an evidence level of B2 for PHN , but an evidence level of A1 for SCIP . Duloxetine has extensive A1 level evidence among SNRIs, including PDPN , CIPN , postoperative or posttraumatic pain , SCIP, and CPSP . The evidence level of Venlafaxine for PDPN and CIPN is A1, but the evidence level for SCIP is B2 .

In opioid drugs, the evidence level for buprenorphine on PHN and PDPN is B2.In NMDA receptor antagonists, the evidence level of ketamine for PHN and SCIP[62, 63] is B2, with references and , respectively. In the category of others, the level of evidence for multiple drugs is generally not high. Type A botulinum toxin (BTX-A) has an evidence level of B2 in TN, PHN , PDPN , and SCIP . 8% capsaicin has an evidence level of B2 in PHN PDPN , CIPN , and SCIP . Lamotrigine has an evidence level of B2 in TN , SCIP , and CPSP . The evidence level of vaccinia virus immune globulin for PHN is A1 , but for PDPN is B2 .

(iii) Recommended NP drug therapy (Table 4 ).

(iv) TN drug therapy recommendations (Table 5 ).

(v) Recommendations for drug treatment of diabetes peripheral neuropathic pain (Table 6).

(vi) Recommendations for drug treatment of central neuropathic pain (Table 7).

Abbreviations: TN, trigeminal neuralgia; PHN, postherpetic neuralgia; PDPN, painful diabetes peripheral neuropathy; CIPN, chemotherapy induced peripheral neuropathy; CRPS, complex regional pain syndrome; BTX-A, botulinum toxin type A.

Physical therapy is a common non-invasive, non-pharmacological treatment approach widely used in NP management. It primarily includes photobiomodulation therapy (PBMT), low-level laser therapy (LLLT), transcutaneous electrical nerve stimulation (TENS), scrambler therapy (ST), extracorporeal shockwave therapy (ESWT), repetitive transcranial magnetic stimulation (rTMS) , transcranial direct electrical stimulation (tDCS) , cryotherapy, whole-body vibration (WBV), yoga, etc. (Table 8 ).

Abbreviations: PHN, Postherpetic neuralgia; PDPN, Painful diabetic peripheral neuropathy; CIPN: Chemotherapy-induced peripheral neuropathy; CPSP, Central post-stroke pain; PBMT, Photobiomodulation therapy; LLLT, Low-level laser therapy; TENS, Transcutaneous electrical nerve stimulation; ST, Scrambler therapy; ESWT, Extracorporeal shock wave therapy; rTMS, Repetitive transcranial magnetic stimulation; tDCS: Transcranial direct current stimulation; BWV, Whole-body vibration

Minimally invasive intervention therapy refers to the use of imaging equipment such as CT, ultrasound, digital subtraction angiography (DSA), C-arm, etc. to guide the observation, diagnosis, and treatment of lesions in the body with the smallest incision path and minimal tissue damage. It mainly includes nerve block, nerve damage (chemical and physical damage), nerve regulation, etc. Specific treatment methods include stellate ganglion block (SGB), continuous radio frequency (CRF), pulsed radio frequency (PRF), pulsed combined continuous radio frequency (PCRF), and percutaneous balloon compression (PCF). Balloon compression (PBC), spinal cord electrical stimulation (SCS) . Deep brain stimulation (DBS) , motor cortex stimulation (MCS), peripheral nerve stimulation (PNS), dorsal root ganglion stimulation (DRGS), intrathecal drug delivery system (IDDS), etc. (Table 9).

Neuroblock (NB) has shown A1 levels of evidence for PHN and painful radiculopathy. Percutaneous balloon compression (PBC) is an A1 level recommended method for treating TN . Condensed radiofrequency (CRF) is also an A1 level method for treating TN . In addition, its evidence level for postoperative or post-traumatic pain is A2 , and its evidence level for painful radiculopathy is B2. Pulse radiofrequency (PRF) therapy has a wide range of A1 level evidence and is suitable for trigeminal TN, PHN , postoperative or posttraumatic pain , and painful radiculopathy . Pulse combined with condensing radiofrequency (PCRF) has also received A1 level recommendation in the treatment of TN [233, 238, 248-250]. Spinal cord electrical stimulation (SCS) has shown strong evidence support in multiple fields, with A1 level recommendations for PHN, PDPN , CIPN [261], postoperative or post-traumatic pain . However, for SCIP [266], the evidence level is weak, at B2 level. The deep brain stimulation (DBS) has B2 level evidence for postoperative or post-traumatic pain and SCIP , but with evidence level A1 for CPSP. The evidence strength for motor cortex stimulation (MCS) is generally not high, with a grade of B2 for TN and postoperative or post-traumatic pain , with A2 grade for CPSP. Peripheral nerve stimulation (PNS) has B2 level evidence for TN, and CIPN . But its evidence level for PHN and postoperative or post-traumatic pain is A1. The level of evidence for root ganglion stimulation (DRGS) is relatively low, with B1 grade for PDPNand B2 grade for CIPN and CPSP . The intrathecal drug infusion system (IDDS) only showed B2 level evidence in SCIP .