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

Neurogenic arthropathy is a rapidly progressive destructive arthropathy associated with decreased pain perception and positional sensitivity that may be due to a variety of diseases, the most common of which are diabetes and stroke. Neurogenic arthropathy most often manifests as joint swelling, hyperproduction of synovial fluid, deformity, and instability. Pain may not correspond to the severity of neuropathy. Diagnosis requires radiographic confirmation; treatment includes joint immobilization if progression is slow, or sometimes surgery if the disease progresses.

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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 spinal roots
• Diabetes mellitus
• Familial hereditary neuropathies
  • Familial amyloid polyneuropathy
  • Familial dysautonomia (Riley-Day syndrome)
  • Hereditary sensory neuropathy
  • Hypertrophic interstitial neuropathy (Dejerine-Sottas disease)
• Peroneal muscular atrophy (Charcot-Marie-Tooth disease)
• Gigantism with hypertrophic neuropathy
• Leprosy
• Spina bifida with menningomyelocele (in children)
• Subacute combined degeneration of the spinal cord
• Syringomyelia
• Tabes dorsalis
• Tumors and injuries of peripheral nerves and spinal cord.

Defects in pain or proprioceptive sensitivity impair normal protective joint reflexes, and often allow injuries (especially repeated minor episodes) and minor periarticular lesions to go unnoticed. Increased bone blood flow due to the vasodilation reflex leads to activation of bone resorption, which causes bone and joint damage. Each new injury causes greater changes in the joint than in healthy individuals. Bleeding into the joint and multiple minor fractures accelerate the progression of the disease. Ligamentous weakness, muscle hypotonia, rapid destruction of articular cartilage are common phenomena that predict joint dislocation, which also accelerates the progression of the disease.

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Diagnosis of neurogenic arthropathy

The diagnosis of neurogenic arthropathy should be suspected in patients with underlying neurologic diseases that result in destructive but rapid painless arthropathy, usually several years after the underlying neurologic event. If neurogenic arthropathy is suspected, radiographic examination should be performed. The diagnosis can be established by the presence of characteristic radiographic abnormalities in a patient with underlying disease and typical symptoms and signs.

Radiographic abnormalities in the early stages of neurogenic arthropathy are often similar to those in osteoarthritis. The cardinal differences are: bone fragmentation, bone destruction, neoosteogenesis, and a decrease in the joint space. Hyperproduction of synovial fluid and the development of joint subluxation are also possible. Later, the bone is deformed, newly formed bone is formed near the cortex, starting from 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 be found both along the edge of the joint and inside it; large curved osteophytes ("parrot beak") often occur in the spine without clinical signs of spinal disorders.

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Prevention 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 (with a splint, special shoes or other devices) protects the joint from possible damage and can stop the progression of the disease. Treatment of the neurological disease that causes the development of neurogenic arthropathy can slow the progression of arthropathy and, if the joint is destroyed at an early stage, partially reverse the damage. In case of significant joint damage, arthrodesis with internal fixation, compression or the use of a bone pin can be useful. In case of significant changes in the hip and knee joint, with the probability of no progression of neurogenic arthropathy, a good result can be achieved with total hip or knee replacement. However, a high risk of instability and dislocation of the prosthesis remains.