Incidence The incidence of complex localized pain syndrome (CRPS) in the normal population is extremely small; the incidence of complex localized pain syndrome (CRPS) after trauma has been reported by various authors, generally ranging from 4% to 8%. Nerve injury is more prone to burning pain (CRPS type II) than other tissue injuries, with a prevalence of 1% to 15%, depending on the degree of nerve injury; some observations have shown that 20% of patients with nerve injuries have transient symptoms of burning pain, and 2% of the symptoms persist even after 12 days; other reports have shown that, for those who have had injuries to the brachial plexus, median, ulnar, sciatic, and tibial nerves, 8.2% of the patients have persistent type II symptoms. Symptoms. In terms of distribution, adults tend to be upper extremity, and 2/3 of type II lesions are located in the upper extremity; pediatric patients are less likely to present with complex localized pain syndrome (CRPS); the age of patients is between 40 and 60 years old; and the incidence of both sexes is generally considered to be higher in females, which may be related to psychological status. Classification Complex localized pain syndrome (CRPS) encompasses two typical types of sympathetic pain disorders, reflex sympathetic dystrophy and burning neuralgia, known as CRPS Type I and CRPS Type II. Type I is a cluster of symptoms consistent with the traditional description of RSD symptoms, i.e., abnormal neuromodulation (vasodilatory sweating dysfunction), hypersensitivity or dullness of sensation, and tissue dystrophy. Type II refers particularly to burning pain, and this type refers specifically to sympathetically dependent persistent pain (SMP), which should be distinguished from sympathetically nondependent persistent pain, i.e., independent pain (SIP). Because the latter is the pain of the nerve injury itself, does not belong to the complex localized pain syndrome (CRPS) category. Clinical features 1, pain: most patients are induced by mechanical, warm, mental and emotional stimuli, and such pain includes spontaneous pain, nociceptive hypersensitivity and nociceptive allergy and other neurogenic pain. In some cases, 3 to 6 months or even longer after the injury, the pain can still be persistent and spread to the surrounding area. 2.Nutritional disorders: In the injury site and its surrounding tissues, often accompanied by vasomotor nerve function disorders, swelling. Sometimes, although the edema is not obvious, it often complains of swelling. The skin begins to sweat, mostly in the form of wetness and flushing. Skin temperature may be high or low and variable, with a tendency for the skin temperature to decrease in the later stages, showing ischemic changes. With the progressive development of the disease, the growth rate of hair and nails changes from accelerated to slowed down, and gradually appear thin skin, curled nails and loss of luster. 3.Motor function: Grip strength and fine motor function can be reduced in the early stage. As the range of motion decreases, the joints become stiff due to muscle wasting atrophy. Patients often in the course of 6 months later, due to subcutaneous tissue atrophy, skin thinning and shiny, affected skin sweating increased or decreased. If myofascial hypertrophy is present, it may lead to joint contracture and osteoporosis, which can be seen on X-ray. Diagnostic Criteria ①History of long or recent injury or disease. ② Persistent burning pain, with neurogenic pain manifestations. ③ There is vascular and sweating dysfunction, trophic changes such as muscle atrophy, limb edema or dehydration, and hypersensitivity to cold and other stimuli. ④ Diagnostic sympathetic nerve block test is mostly positive. Treatment Complex localized pain syndrome (CRPS) treatment Once diagnosed, pain relief methods should be sought as early as possible, while rehabilitation therapy is actively carried out. 1.Preventive treatment: The perfect treatment of trauma and adequate analgesia in the early stage of injury is very important. That is to say, perfect control of pain in the acute stage, to prevent it from developing in the direction of chronicity, and at the same time, combined with the treatment of mental aspects, it is generally believed that a better therapeutic effect can be achieved. 2, transcutaneous electrical stimulation (TENS): transcutaneous electrical stimulation is through the activation of endogenous opioid peptide and analgesia, but also can stimulate the pain site of the thick fiber nerves, change the sensory impulses transmitted to the central nervous system, to achieve the purpose of reducing pain. 3, drug therapy: ① antidepressants: commonly used amitriptyline, promethazine, doxepin, mepitriptyline and other three (four) cyclic antidepressants. ② Anti-spasmodic drugs: representative drugs are carbamazepine, phenytoin sodium, sodium valproate, which is effective for nerve shock-like pain. The more widely used abroad is gabapentin, which can significantly relieve neuralgia caused by diabetes or herpes zoster. ③ Non-steroidal anti-inflammatory analgesic drugs, neurotropin, prostaglandin preparations, hormones, morphine drugs and so on. 4.Neuroblock treatment: sympathetic nerve block is the main. Commonly used nerve block: SGB, thoracic sympathetic nerve block, lumbar sympathetic nerve block, intraventricular local nerve block, epidural block, subarachnoid space block. The sympathetic nerve block performed in the clinic mainly plays a role by blocking the pain mediated by it and dilating the blood vessels in the area of its innervation. 5.When there is no improvement or only temporary improvement of pain symptoms after anesthetic block, the use of nerve-destroying drugs, nerve destruction or sympathectomy should be considered. 6.When the above treatments are ineffective, implantation of analgesic pacemaker or subarachnoid analgesic pump can be considered.