Charcot joint (CJ) is a collective term for joint lesions caused by various sensory nervous system pathologies. Typical cases caused by spinal cavities are less common and therefore have a higher rate of misdiagnosis. From January 2005 to January 2008, three patients with CJ caused by spinal cord cavity were admitted to the neurosurgery department of Beijing Military General Hospital, and the treatment results were good. The patient had no obvious cause for the swelling of the right shoulder joint, which was painless and accompanied by habitual dislocation, and improved after resetting and braking. A CT 3D reconstruction at a local hospital showed widening of the right shoulder joint gap, semi-dislocation and rough joint surface. Our MRI showed a small posterior cranial recess, the inferior border of the cerebellar tonsils was about 6 mm below the greater occipital foramen, and a spinal cord cavity was visible in the cervical medulla below the level of the C2 conus. 1A, B: CT reconstruction showed widening of the right shoulder joint gap with subluxation and rough joint surface; 1C: MRI T1 image showed a small posterior cranial recess, the inferior border of the cerebellar tonsils was lower than the foramen magnum, and a cavity was visible in the cervical medulla below the level of C2. Case 2: Male, 53 years old, presented with swelling, deformity and limitation of movement of the left elbow joint for 5 months. The patient presented with no obvious cause of swelling and hypertrophic deformity of the left elbow joint, accompanied by numbness of the left upper extremity, decreased sensitivity to heat sensation, and a history of unconscious left forearm scalding, which was only discovered when blistering occurred after the injury. He had a history of muscle atrophy in his left hand, no history of injury to the left elbow joint, no pain, and free movement of both lower extremities. An outpatient X-ray examination at a local hospital showed narrowing of the left elbow joint space, deformity of each bone end, uneven increase in bone density, and hyperplasia and sclerosis of the joint surface. A large amount of free bone-like density was seen in the joint, and the surrounding soft tissue was swollen (Figure 2A). In order to further diagnose the elbow joint lesion, he came to our hospital for cervical MRI examination, which showed that the cerebellar tonsils were lower than the foramen magnum by about 6 mm, the tip of the odontoid process was flattened along the palato-occipital line, C2 thickened the spinal cord from the lower level, continuous T1 low and T2 high signals were seen in the central part of the medulla, and the spinal cord parenchyma was thinned. 2A: X-ray showed that the joint space was narrowed, the bone ends were deformed, and the joint surface was hyperplastic and sclerotic. A large amount of free bone is seen in the joint and the surrounding soft tissue is swollen; 2B: MRI T1 shows cerebellar tonsils below the greater occipital foramen, and the spinal cord is hollow below C2. Case 3: Male, 43 years old, presented with 4 years of weakness in both hands and 2 years of weakness in both lower extremities, aggravated for 1 year. 4 years ago, numbness of 1.5 fingers on the ulnar side of both hands with no obvious cause, without pain, and accompanied by weakness in both hands, gradually aggravated, and in the last 1 year, atrophy of the internal muscles of both hands, obvious on the left side, and swelling of the elbow joint without redness and pain. In the past 2 years, he had weakness in both lower limbs, a feeling of stepping on cotton on the ground, and unstable walking, which could be relieved after bed rest, and weakness in standing up after sitting for a long time, with occasional neck pain and no upper limb radiating pain. MRI showed that the dentate process was located below the palato-occipital line, the cerebellar tonsils were below the inferior border of the foramen magnum, longitudinal T1 low and T2 high signals were seen in the cervical and upper thoracic medulla, and the spinal cord was compressed and thinned. 3A:The X-ray showed narrowing of the elbow joint space, deformed bone at each bone end, and hyperplasia and sclerosis of the joint surface. Free bone-like density shadow was seen in the joint. 3B: MRI T1 showed cerebellar tonsils below the greater occipital foramen, and cervical and upper thoracic segments of the spinal cord were cavernous. All three patients were diagnosed with spinal cord cavity-Chiari complex and Charcot’s arthropathy after admission to the hospital. The swelling of the joint subsided after two weeks. There was no recurrence of symptoms and normal joint movement at the follow-up every six months. CJ, also known as neurotrophic arthropathy, occurs in adults, mostly between the ages of 40 and 60, with a male to female ratio of about 3:1. It is commonly associated with spinal cord cavity, spinal cord consumption, spinal membrane bulge, polyneuritis, paraplegia, Potts’ disease, diabetes mellitus, pernicious anemia and other diseases. It occurs in large joints with a high level of activity and depends mainly on the innervated nerve segment. The pathogenesis is caused by much larger than normal shocks, jolts and torsional injuries to the joints during hyperalgesia. At the same time, due to neurotropic disorders, the broken cartilage surfaces, bone ends and ligaments are not effectively repaired, resulting in disorganized new bone formation, sometimes with fragmentation and resorption of bone ends, rapid joint destruction, joint capsule and ligament laxity, etc. In addition to sensory nerve damage, the related sympathetic nerves also lose their function, causing vasodilation, congestion and increased osteoclastic activity in the areas they innervate, which leads to bone resorption, fracture and fragmentation. This leads to bone resorption, dissolution and fragmentation. The combination of these factors eventually leads to subluxation or complete dislocation of the joint, or even complete destruction of the entire joint, which no longer has its original function [1]. Spinal cord cavities are often due to developmental malformations of the crico-occipital region, mostly due to Chiari malformation, and are known as the spinal cord cavity-Chiari complex, which is one of the main causes of Charcot’s joints. Since spinal cord cavities are most commonly found in the lower cervical spinal cord, especially at the base of the posterior horn of cervical expansion, causing CJ is more common in neurosurgery in the upper extremities. There are four main manifestations of CJ caused by the spinal cord cavity-Chiari complex: (1) manifestations due to compression of the medulla oblongata and upper cervical spinal cord, such as dysphagia and limb dysfunction; (2) manifestations of the spinal cord cavity itself: limb sensory separation phenomenon, high cervical muscle tone, inflexibility, and atrophy of bilateral interosseous muscles, etc. The appearance of these manifestations is mainly related to the location and size of the cavity; (3) Local manifestations of the affected joints: swelling, softness or cystic sensation on patting, local sensation loss or disappearance, redness, painlessness and weakness of the joint, normal or increased mobility, progressive joint deformity, bone rubbing sensation or bone rubbing sound when moving, or even fracture, fluid accumulation in the joint cavity or adjacent parts of the joint, skin breakdown or sinus tract formation. It has also been reported that more than half of the patients had arthralgia; (4) secondary damage of bone and joint destruction; for example, CJ of the elbow joint can invade and compress the ulnar nerve, causing loss of sensation and movement of the ulnar innervation [2]. All cases in this group had hyperalgesia, painless joint swelling, and in case 3 there was also a sign of ulnar nerve compression. The diagnosis of CJ caused by the spinal cavity-Chiari complex is focused on the following: (1) clinical manifestations with painless swelling and increased mobility of the skeletal joints and sensory separation of the limbs; (2) imaging with destruction of articular cartilage, osteoporosis or/and fractures, subchondral sclerosis, bone flab formation, with cartilage or bone fragments filling the joints, chronic bursitis with a large amount of exudate, with joint signs of joint instability such as loosening and dislocation; (3) MRI examination to confirm the presence of Chiari malformation and spinal cavity; (4) normal serology and cerebrospinal fluid examination to exclude the presence of rheumatic, rheumatoid, or bacterial arthritis [3,4]. Charcot arthropathy is mainly differentiated from the following joint lesions: (1) degenerative osteoarthropathy: pain is often the main symptom, affecting mobility. radiographs show unequal width or narrowing of the joint space, osteoporosis, osteophytes or joint enlargement at the joint, and even joint deformation, subchondral bone plate sclerosis and bone redundancy formation. (2) Rheumatoid joint: symmetrical small joint pain, morning stiffness, joint deformation and muscle atrophy are common, and rheumatoid factor is positive. Early X-ray examination shows soft tissue swelling and joint cavity exudate, and after several months, osteoporosis of joint parts, reduction of joint space and erosion of bone, suggesting the loss of joint cartilage. Subluxation, dislocation and bony ankylosis appear in the later stage. (3) Gout: It is common in [toe joints and often starts with acute joint pain that attacks at night. The pain worsens progressively and is severe. Signs resemble acute infection, with swelling, localized fever, redness and marked tenderness. The skin is tense, hot, shiny, and dark red or purplish in appearance, and gouty nodules may appear in the soft tissue around the joint. X-rays: Initially, there may be osteoporosis, decalcification, disturbance of bone trabeculae, blurring of joint images, and narrowing of joint cavities. The soft tissue around the joint is swollen. In the extreme stage, the joint cavity is narrowed or disappears, and the surrounding soft tissue shadows are widened. Extensive bone decalcification, bone destruction and defects, cavity formation and dead bone occur. Erosion of the epiphysis may cause dislocation of the joint. In the resting phase, the bone ends are clearly imaged, and the edges of the lesion are densely bony, with osteophytes visible. Abscess resorption or calcification may be seen. The joint may heal fibrously, or bony. Sometimes cavities and dead bone may persist for a long time. [5] CJ emphasizes early treatment of the primary pathology. CJ due to spinal cavity-Chiari complex is mainly treated by posterior cranial recess decompression, and spinal cavities are usually left untreated, while larger cavities are drained [6]. The lesioned joints are prone to poor incision healing and infection due to the lack of innervation, so surgical treatment is not possible, and temporary braking can be used to protect the lesioned joints, which can largely prevent deformities. The three patients in this group only used posterior cranial recess decompression and temporary braking of the joint, and achieved good results after four weeks. Since the pain of CJ patients is not obvious, they are seldom treated formally at the early stage of the disease, and they are mostly referred to orthopedics and rheumatology departments for arthritis, so they should not only pay attention to the joint manifestations and ignore the neurological symptoms and signs, but should ask detailed medical history, examine the body carefully and analyze comprehensively to avoid misdiagnosis.