Reflex sympathetic dystrophy (rsds) RSDS was first reported 127 years ago by Mitchell et al. After a Medline search, no reports on this disease have been seen in China so far. Early studies of patients with RSDS showed that there are certain predisposing factors for the development of the disease, but not all of them are traumatic, and renal transplantation, myocardial infarction and cerebrovascular accidents have been reported to sometimes cause the disease. In addition, emotional stress may also be an important predisposing factor. The fact that the patient in this case started after soft tissue injury also indicates the importance of precipitating factors in the development of this disease. The pathogenesis of RSDS is unclear. First, the disease may be related to the formation of a post-traumatic reflex arc. This reflex arc is modulated by the cortex and causes peripheral vascular disturbances. The abnormal pain response may indicate an increased sensitivity of the injured axons to sympathetically related substances such as adrenaline, which can be blocked by anti-sympathetic drugs. Second, quantitative EEG and limb sensory arousal potentials may be impaired in RSDS patients, which, together with the fact that unilateral sympathetic blockade yields improvement in bilateral skin abnormalities and limb pain, suggests the involvement of cortical pathways in the pathogenesis. In addition, HLA-A3, B7, and DR2 were twofold higher in RSDS patients than in controls. The above suggests that RSDS may be a neuroimmune disease. The disease can be divided into three clinical stages: Stage 1 patients present with pain in the affected limb (including burning sensation, throbbing pain, and diffuse pain and discomfort), with local edema and varying degrees of vasoconstriction disorders, resulting in changes in limb color and temperature. x-rays may be normal or may show patchy bone hypodensity. If left untreated, the disease may progress to stage 2 in 3-6 months. stage 2 is a progressive stage, highlighted by progressively increasing soft tissue swelling, skin and joint thickening, muscle wasting and skin stiffness. Stage 3 is the most severe and is characterized by limited mobility, shoulder-hand syndrome, finger flexion, waxy dystrophy-like skin changes, and fragile nail crests, with severe osteoporosis seen on bone radiographs. Although the history of this patient is only 3 months old, the significant arthralgias and muscle atrophy indicate that the disease has progressed to stage 2. Autonomic tests can provide clues for early diagnosis, including static sweating, static skin temperature, and a quantitative axonal reflex test for pro-sweating. Increased static sweating suggests a diagnosis of RSDS, with a sensitivity and specificity of 94% and 98%, respectively, if accompanied by abnormal results of the quantified axonal reflex test. Imaging is important for the diagnosis of RSDS, and radiographs show osteoporosis, joint destruction and subluxation, new bone formation and degenerative changes. Bone scan is more reliable than plain radiographs in stage 1 RSDS. A pertechnetate bone scan with technetium 99m immediately after injury showed decreased perfusion at the involved site, and a delayed scan 6 weeks later showed increased uptake at the involved joint. The bone scan was highly sensitive (97% versus 57%) and specific (86% versus 57%) compared to plain radiographs. In stage 2 RSDS, both bone scan and plain radiographs are of high value, with an accuracy of 86% and 81%, respectively. MRI is useful for early diagnosis: changes such as skin thickening, tissue contrast enhancement and soft tissue swelling can be seen in stage 1 patients; in stage 2 additional skin thinning can be seen; muscle atrophy is only seen in stage 3 patients. The best treatment for this disease is prevention. Once the disease has developed, protective exercise of the affected limb can prevent disuse atrophy, physical therapy can effectively relieve limb pain, and tricyclic antidepressants can reduce pain and help with sleep. If the disease is in stage 1, NSAIDs can be given on top of painful spot injections and physical therapy. In addition, prazosin (1 to 6) mg?d-1, tretinoin (30 to 60) mg?d-1, nifedipine (30 to 60) mg?d-1, guanethidine or phenoxybenzamine (10 to 30) mg?d-1, and topical capsaicin may also be effective. Patients with skin changes or persistent activity restriction with sympathetic-dependent pain are suitable for sympathetic blockade, and sympathectomy is feasible if accompanied by significant skin changes or contractures. Prednisone (30-80) mg?d-1 in divided oral doses is effective in patients with active inflammation on radiographic technetium bone scan. The dose should be reduced promptly after the onset of action and should be maintained with a small dose of prednisone in severe cases. The treatment of pain in affected peripheral innervation sites by implantation of metal-like electrical nerve stimulation devices and the use of diphosphonates to prevent bone resorption and calcitonin for pain can also be effective. This patient was effectively treated with neurotoxin.