Neurogenic arthropathy (neuropathic arthropathy, Charcot joints) and back pain

Neurogenic arthropathy is a rapidly progressive destructive arthropathy, combined with a reduction in the perception of pain and positional sensitivity, which can be the result of various diseases, the most frequent of which are diabetes and stroke. Most often neurogenic arthropathy manifests with joint edema, hyperproduction of synovial fluid, deformity and instability. Pain may not correspond to the severity of neuropathy. Diagnosis requires radiographic confirmation; treatment involves the immobilization of the joint with slow progression, or, sometimes, surgical treatment if the disease progresses.

[1], [2], [3], [4]

Diseases that can lead to neurogenic arthropathy:

• Amyloid neuropathy (secondary amyloidosis)
• Arnold-Chiari malformation
• Congenital insensitivity to pain
• Degenerative diseases of the spine with compression of the spinal roots
• Diabetes
• Family inherited neuropathies
  • Family amyloid polyneuropathy
  • Family disautonomy (Riley-Dey's syndrome)
  • Hereditary sensory neuropathy
  • Hypertrophic interstitial neuropathy (Dejerine-Sott's disease)
• Peroneal muscular atrophy (Charcot-Marie-Tous disease)
• Gigantism with hypertrophic neuropathy
• Leprosy
• Spina bifida with menningomyelocele (in children)
• Subacute combined degeneration of the spinal cord
• Syringomyelia
• Dorsal articulation
• Tumors and injuries of peripheral nerves and spinal cord.

A defect in pain or proprioceptive sensitivity disrupts normal defensive articular reflexes, and often allows traumas (especially repeated small episodes) and minor periarticular lesions to go unnoticed. Increased bone flow due to the vasodilator reflex leads to activation of bone resorption, which causes damage to the bone and joints. Each new damage causes in the joint greater changes than in healthy individuals. Hemorrhages in the joint and multiple small fractures accelerate the progression of the disease. Weakness of the ligamentous apparatus, muscle hypotension, rapid destruction of articular cartilage are common phenomena that are predictors of joint dislocation, which also accelerates the progression of the disease.

[5], [6], [7], [8]

Diagnosis of neurogenic arthropathy

The diagnosis of "neurogenic arthropathy" should be suspected in patients with predisposing neurological diseases that lead to the development of destructive but rapid painless arthropathy, usually within a few years after the underlying neurological event. When suspected of neurogenic arthropathy, an X-ray examination is necessary. The diagnosis can be established in the presence of characteristic radiographic abnormalities in a patient with a predisposing disease and typical symptoms and signs.

X-ray anomalies at an early stage of neurogenic arthropathy are often similar to those in osteorthritis. The cardinal differences are: bone fragmentation, bone destruction, neo-osteopenia, and reduction of the joint space. It is also possible hyperproduction of synovial fluid, the development of joint subferaxation. Later the bone is deformed, the newly formed bone forms next to the cortical layer, beginning with the joint cavity and often extending beyond the main bone, especially in long bones. Less common is calcification and ossification of soft tissues. It is important that abnormal osteophytes can occur both along the edge of the joint, and inside it large curved osteophytes ("parrot's beak") often appear in the spine without a clinic of spinal disorders.

[9], [10]

Prophylaxis and treatment of neurogenic arthropathy

Prevention of arthropathy is possible in patients at risk of developing it. Early diagnosis of asymptomatic or minimally symptomatic fractures facilitates early treatment; immobilization (by a tire, special footwear or other devices) protects the joint from possible damage, can suspend the development of the disease. Treatment of a neurological disease that causes the development of neurogenic arthropathy can slow the progression of arthropathy and, at the destruction of the joint at an early stage, partially reverse the damage. If the joint is severely damaged, arthrodesis with internal fixation, compression, or the use of a bone pin can be helpful. With significant changes in the hip and knee joint, with the probability of a lack of progression of neurogenic arthropathy, a good result can be obtained with total replacement of the hip or knee joint. However, the high risk of instability and dislocation of the prosthesis persists.