Charcot first described neuropathic arthropathy in 1868, so it is also known as charcot arthropathy, charcot joint, or neuropathic arthritis. These diseases are caused by the absence of pain, and are also known as painless arthropathy. It can be caused by different types of neurological lesions. 1. Etiology This disease can occur in the central nervous system syphilis, spinal cord cavitation, diabetic neuropathy, spinal cord membrane bulge, congenital nociceptive deficiency, etc. In this case, the joints of shoulder, elbow, cervical spine, hip, knee, ankle and toe are damaged due to the absence of protective mechanisms for nociception leading to joint overuse and impact. In addition, the pathogenesis of medically induced joint destruction by long-term application of corticosteroids (e.g., in the treatment of rheumatoid arthritis, systemic lupus erythematosus, and after organ transplantation) and painkillers (botaxone, anti-inflammatory pain) is in the same manner. Spinal cord cavitation of the cervical medulla is a common neuropathic disorder involving the joints of the upper extremities. The shoulder, elbow, cervical spine and wrist are the most commonly affected sites. Spinal cord cavitation is associated with joint destruction in the upper extremities in about 25% of cases. In addition to joint lesions, there is also unilateral or bilateral loss of temperature sensation, so that scalding scars are visible on the skin of the upper extremities. Spinal syphilis, also called spinal consumption, often involves the knee, hip, ankle and lumbar spine. In addition to bone and joint changes, motor ataxia, deep sensory disturbances in the lower extremities Arggll-Robertson pupils, positive serum Convair reaction are seen. Spinal cord bulging, ankle and small foot joint involvement is common. Painless ulcers on the soles of the feet, soft tissue masses seen in the lumbosacral region, skin depression or hirsutism, loss of sensation in lower limb atrophy, and dysfunction of the extensor muscles. In diabetic neuropathy, painless swelling of the small joints of the foot (tarsometatarsal, metatarsal, interphalangeal, etc.) may occur, etc. 2, clinical manifestations Neuropathic arthropathy joints gradually swollen, unstable, fluid accumulation, the joint can wear out blood-like fluid. The swollen joints are mostly painless or only slightly distended, and the functional limitation of the joints is not obvious. Pain and functional limitation of the joint are not consistent with the swelling and destruction of the joint. In advanced stages, further joint destruction may lead to pathologic fracture or pathologic joint dislocation. Impairment of deep nociception or postural sensation affects the normal protective reflexes of the joint, often leading to trauma (especially recurrent small injuries) as well as fractures that occur unrecognized around small joints. In addition, increased bone blood flow due to reflex vasodilation results in bone resorption, which can cause fractures, joint damage and joint repair. The progression of the disease can be accelerated by the deposition of calcium pyrophosphate dihydrate or apatite crystals in large joints, loss of muscle tone, ligamentous laxity and swelling of the joint capsule due to exudation. 3, clinical diagnosis Based on the history of neurological primary disease, the presence of joint symptoms consistent with neurological symptoms and signs, and the exclusion of other arthritis such as osteoarthritis, the clinical diagnosis can be established. The primary disease can generally be identified, but about 20% of patients do not have signs and symptoms of the primary disease when the lesion appears in the joint, and need to be differentiated from other arthritis: neuropathic arthropathy is mostly painless, and although joint destruction and deformity are obvious, the degree of joint dysfunction is mild; whereas in other arthritis, joint pain, deformity, and destruction are consistent with joint dysfunction. Since a clear diagnosis of the primary cause is a guideline for clinical treatment, a detailed history, comprehensive physical examination and laboratory tests should be performed to identify the primary cause. The diagnosis of neurogenic arthropathy is mainly based on two questions: whether it is neurogenic arthropathy and what kind of neurogenic arthropathy. x-ray and CT examination can be a good aid in the diagnosis of neurogenic arthropathy. 4, treatment (1) diseased joints, upper limbs to avoid hard work, lower limbs to minimize weight bearing. (2) The heavily damaged joints (such as the knee, elbow and spine) can be protected by braces. (3) The foot can be amputated if the disease is severe and the ulcer does not heal. Young adult patients with severe destruction of the knee and ankle joints can undergo joint fusion, but the disease can occur again in adjacent joints. (4) Actively treat the primary disease. 5. Prevention For high-risk patients, prevention of arthrosis is possible. In patients with painless fractures, early diagnosis and fixation of painless fractures may prevent the occurrence of neuropathic arthropathy. For joints with significant structural damage, treatment with intra-articular fixation, compression techniques and appropriate bone grafting may be successful. When the disease is not in a progressive stage, total hip and knee arthroplasty can be performed with good results. However, loosening and dislocation of the artificial joint remains a major risk. Effective treatment of the primary neurologic disease will slow the progression of the joint lesion. If the joint destruction is still in its early stages, the arthropathy can be reversed.