Neurogenic arthropathy (also called Charcot's arthropathy) is most common in men over age 40. It's a progressively degenerative disease of peripheral and axial joints that results from impaired sensory innervation. Trauma or disease results in loss of sensation in the joint, which damages the supporting ligaments. Eventually, the affected joint disintegrates.
The specific joints affected vary. Diabetes mellitus usually attacks joints and bones of the feet. Tabes dorsalis affects large, weight-bearing joints, such as the knee, hip, ankle, or lumbar and dorsal vertebrae. Syringomyelia involves the shoulder, elbow, or cervical intervertebral joint. Neurogenic arthropathy caused by intraarticular corticosteroid injections may develop in the hip or knee joint.
In adults, the most common cause of neurogenic arthropathy is diabetes mellitus. Other causes include syringomyelia (which progresses to neurogenic arthropathy in about one of four patients). myelopathy of pernicious anemia, spinal cord trauma, paraplegia, hereditary sensory radicular neuropathy, and CharcotMarie-Tooth disease. Rarely, tabes dorsalis, amyloidosis, peripheral nerve injury, myelomeningocele (in children), leprosy, or alcoholism cause neurogenic arthropathy.
Frequent intraarticular injection of corticosteroids has also been linked to neurogenic arthropathy. The analgesic effect of the corticosteroids may mask symptoms and allow continuous damaging stress to accelerate joint destruction.
Signs and Symptoms
While peripheral neuropathy develops over decades, the progression of Charcot foot (ligament tears, small fractures, subluxation, dislocation, deformity) can occur in a matter of weeks or months. A minor trauma, such as twisting the foot, can initiate the process. Increased bone resorption makes the joints in the foot susceptible to small fractures.
Because of the loss of pain perception and the loss of the sense of position of the foot, joints receive repeated injuries, such as torn ligaments and bone fractures.
Early signs that may present soon after injury include the following:
X-rays confirm the diagnosis and allow evaluation of damage. Early in the disease, soft-tissue swelling or effusion may be the only overt effect. Late in the disease. X-rays may display articular fracture, subluxation, and cartilaginous erosion; periosteal new bone formation; and excessive growth of marginal loose bodies (osteophytosis). Bone resorption may also be evident.
Vertebral examination shows narrowed disk spaces, vertebral deterioration, and osteophyte formation, leading to ankylosis and deforming kyphoscoliosis.
Synovial biopsy detects bony fragments and bits of calcified cartilage.
Neuromuscular tests may reveal motor and sensory deficits and diminished deep tendon reflexes.
Pain relief - the immediate treatment goal- may be achieved with analgesics, nonsteroidal antinflammatory drugs, and joint immobilization (crutches, splints, braces, and weight-bearing restrictions). Surgical correction, such as joint fusion or amputation, may be necessary in severe disease although surgical treatment has a high failure rate because of nonunion, infection, or dislocation.
Prevention of arthropathy may be possible in a patient at risk. Early diagnosis of asymptomatic or minimally symptomatic fractures facilitates early treatment; immobilization (with splints, special boots, or calipers) protects the joint from further injury, possibly stopping disease evolution.
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