Alcoholic neuropathy
Cerebral palsy
Leprosy
Syphilis (tabes dorsalis), caused by the organism Treponema pallidum
Spinal cord injury
Myelomeningocele
Syringomyelia
Intra-articular steroid injections
Congenital insensitivity to pain
Peroneal muscular atrophy

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. 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, 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. Diagnosis
Clinical findings
Clinical findings include erythema, edema and increased temperature in the affected joint. In neuropathic foot joints, plantar ulcers may be present.
Duration and aggressiveness of offloading (non-weight-bearing vs. weight-bearing, non-removable vs. removable device) should be guided by clinical assessment of healing of neuropathic arthropathy based on edema, erythema, and skin temperature changes. It can take six to nine months for the edema and erythema of the affected joint to recede. Outcome
Outcomes vary depending on the location of the disease, the degree of damage to the joint, and whether surgical repair was necessary. Average healing times vary from 55 to 97 days, depending on location. Up to one to two years may be required for complete healing. Further reading
Neuropathic osteoarthropathy by Monica Bhargava, M.D., University of Washington Department of Radiology
John R. Crockarell; Daugherty, Kay; Jones, Linda Winstead; Frederick M. Azar; Beaty, James H; James H. Calandruccio; Peter G. Carnesale; Kevin B. Cleveland; Andrew H. Crenshaw (2003). Campbells Operative Orthopedics (10th ed.). Saint Louis, MO: C.V. Mosby. ISBN 0-323-01248-5. Gupta R (November 1993). "A short history of neuropathic arthropathy". Clinical Orthopaedics and Related Research (296): 43–9. PMID 8222448. Sommer TC, Lee TH (November 2001). "Charcot foot: the diagnostic dilemma". American Family Physician. 64 (9): 1591–8. PMID 11730314. References


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