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14-September-2008 12:50:26 - Neuropathic joint disease Redirected from Charcot joint Neuropathic joint disease Classification and external resources DiseasesDB 2344 eMedicine orthoped/381 radio/476 Neuropathic osteoarthropathy refers to progressive degeneration of a weight bearing joint, a process marked by bony destruction, bone resorption, and eventual deformity. Onset is usually insidious. It is also known as Charcot joint. If this pathological process continues unchecked, it could result in joint deformity, ulceration and/or superinfection, loss of function, and in the worst case scenario: amputation. Early identification of joint changes is the best way to limit morbidity. Contents 1 Pathogenesis 1.1 Underlying Mechanisms 1.2 Joint Involvement 2 Clinical Findings 3 Radiologic Findings 4 Treatment 5 References Pathogenesis Basically, any condition resulting in decreased peripheral sensation, proprioception, and fine motor control: Diabetes mellitus neuropathy the most common in the U.S. today, resulting in destruction of foot and ankle joints, with Charcot joints in 1/600-700 diabetics. Related to long-term poor glucose control. Alcoholic neuropathy Cerebral palsy Leprosy Syphilis tabes dorsalis, caused by the organism Treponema pallidum Congenital insensitivity to pain Spinal cord injury Myelomeningocele Syringomyelia Intra-articular steroid injections Underlying Mechanisms Two primary theories have been advanced: Neurotrauma: Loss of peripheral sensation and proprioception leads to repetitive microtrauma to the joint in question; this damage goes unnoticed by the neuropathic patient, and the resultant inflammatory resorption of traumatized bone renders that region weak and susceptible to further trauma. Indeed, it is a vicious cycle. In addition, poor fine motor control generates unnatural pressure on certain joints, leading to additional microtrauma. Neurovascular: Neuropathic patients have dysregulated autonomic nervous system reflexes, and de-sensitized joints receive significantly greater blood flow. The resulting hyperemia leads to increased osteoclastic resorption of bone, and this, in concert with mechanical stress, leads to bony destruction. In reality, both of these mechanisms probably play a role in the development of a Charcot joint. Joint Involvement Diabetes is the foremost cause in America today for neuropathic joint disease,citation needed and the foot is the most affected region. In those with foot deformity, approximately 60% are in the tarsometatarsal joints medial joints affected more than lateral, 30% Metatarsophalangeal joints and 10% have ankle disease. Over half of diabetic patients with neuropathic joints can recall some kind of precipitating trauma, usually, minor. Patients with neurosyphilis tend to have knee involvement, and patients with syringomyelia of the spinal cord may demonstrate shoulder deformity. Hip joint destruction is also seen in neuropathic patients. Clinical Findings Clinical findings include erythema, edema and increased temperature in the affected joint. In neuropathic foot joints, plantar ulcers may be present. Note that it is often difficult to differentiate osteomyelitis from a Charcot joint, as they may have similar tagged WBC scan and MRI features joint destruction, dislocation, edema. Definitive diagnosis may require bone or synovial biopsy. Radiologic Findings First, it is important to recognize that two types of abnormality may be detected. One is termed atrophic, in which there is osteolysis of the distal metatarsals in the forefoot. The more common form of destruction is hypertrophic joint disease, characterized by acute peri-articular fracture and joint dislocation. The natural history of the joint destruction process has a classification scheme of its own, offered by Eichenholtz decades ago: Stage 0: Clinically, there is joint edema, but radiographs are negative. Note that a bone scan may be positive before a radiograph is, making it a sensitive but not very specific modality. Stage 1: Osseous fragmentation with joint dislocation seen on radiograph acute Charcot. Stage 2: Decreased local edema, with coalescence of fragments and absorption of fine bone debris Stage 3: No local edema, with consolidation and remodeling albeit deformed of fracture fragments. The foot is now stable. Destroyed TMT joints in the medial left foot, with fracture and dislocation of fragments; these are classic findings. Also note loss of the foot arch and acquired flat foot pes planus deformity. Treatment Once the process is recognized, immobilization with a total contact cast will help ward off further joint destruction. Pneumatic walking braces are also used. Surgical correction of a joint is rarely successful in the long-term in these patients. It can take 6-9 months for the edema and erythema of the affected joint to recede. References Neuropathic osteoarthropathy by Monica Bhargava, M.D., University of Washington Department of Radiology Canale: Campbell's Orthopaedics, 10th ion, 2003 Mosby, Inc. Gupta, R. 1993. A short history of neuropathic arthropathy. Clinical Orthopaedics, 296, pp. 43-49. Sommer, Todd C., and Lee, Thomas H. Charcot Foot: The Diagnostic Dilemma. American Family Physician. Vol. 64, No. 9, Nov. 1, 2001. Retrieved from http://en..org/wiki/Neuropathic_joint_disease Categories: RheumatologyHidden categories: All articles with statements | Articles with statements since June 2008 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page This page was last modified on 27 June 2008, at 14:45
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