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.
For example, typhus killed millions of prisoners in German Nazi concentration camps during World War II. The unhygenic conditions in camps such as Auschwitz, Theresienstadt, and Bergen-Belsen allowed diseases such as typhus to flourish. Situations in the twenty-first century with potential for a typhus epidemic would include refugee camps during a major famine or natural disaster. In the periods between outbreaks, when human to human transmission occurs less often, the flying squirrel serves as a zoonotic reservoir for the Rickettsia prowazekii bacterium. In 1916, Henrique da Rocha Lima proved that the bacterium Rickettsia prowazekii was the agent responsible for typhus; he named it after H. T. Ricketts and Stanislaus von Prowazek, two zoologists who had died from typhus while investigating epidemics. Once these crucial facts were recognized, Rudolf Weigl in 1930 was able to fashion a practical and effective vaccine production method. He ground up the insides of infected lice that had been drinking blood. It was, however, very dangerous to produce, and carried a high likelihood of infection to those who were working on it. A safer mass-production-ready method using egg yolks was developed by Herald R. Cox in 1938. This vaccine was widely available and used extensively by 1943. Diagnosis
IFA, ELISA or PCR positive after 10 days. Treatment
The infection is treated with antibiotics. Intravenous fluids and oxygen may be needed to stabilize the patient. There is a significant disparity between the untreated mortality and treated mortality rates: 10-60% untreated versus close to 0% treated with antibiotics within 8 days of initial infection.