• A Hubault.
• Rev Neurol France. 1982 Jan 1; 138 (12): 1009-17.

AbstractIn 1868, J.M. Charcot published his memoir "sur quelques athropathies qui paraissent dépendre d'une lésion du cerveau ou de la moelle épinière "based on 4 cases of tabes dorsalis. This work was subsequently developed and presented in London in 1881 when Sir James Paget acknowledged the significance of this entity. "Charcot's joint" has come in use to mean that particular joint disease which results, from nervous lesions, whatever its nature. A controversy lasted between those who thought, e.g. Volkman, that mechanical trauma is the significant pathophysiological factor and those, e.g. Charcot, who ascribed a trophic role to the spinal cord. At the beginning, Charcot thought that lesions of the anterior horn were responsible but finally concluded that be could not bring a precise answer to that point. Subsequently Raymond, Dejerine (who insisted on the absence of pain), Foix and Alajouanine, Alajouanine and his collaborators extended Charcot's observations. Alajouanine proposed that lesions of the sympathetic nervous system played a major pathophysiological role. In 1960 Castaigne and Cambier proposed a unified theory with complementary roles ascribed to trauma and to nervous lesions. In 1936, diabetic neuropathy was described by W. Jordan. In 1942, Thevenard described "acropathie ulcéro-mutilante" now widely known as hereditary sensory neuropathy. Amyloidosis, familial dysautonomia, congenital insensitivity to pain were added to the list of causes of Charcot's joint. Less well known are the works of Charcot on joint diseases in hemiplegics. These were later studied by Alajouanine and Thurel and de Sèze and Ryckewaert have proposed to call them "algoneurodystrophies décalcifiantes réflexes" a topic which nowadays arises much interest in rheumatology.

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