At the November and December meetings of the London Clinical Society in 1884, an interesting debate unfolded: was a ‘new’ disease appearing in England? A number of patients had been seen in hospitals and asylums in the preceding years who exhibited unusual joint affections. It was a sudden phenomenon, characterised by severely swollen but usually painless joints. Though any joints of the body might be affected, knees and ankles tended to fare worst. The lack of pain and generally dulled sensations that were experienced impacted on the everyday actions of sufferers, who dropped objects, frequently fell, or had difficulty walking. Other bodily manifestations appeared in the form of ulcers, often on the feet. Many patients also reported that they suffered from ‘neuralgia’, ‘flying gout’, and gastric crises.

Deformity of the knee in Charcot’s disease.
© Wellcome Images/St Bartholomew’s Hospital Archives & Museum.
The condition was first properly identified by neurologist Jean-Martin Charcot in 1868, earning it the moniker ‘Charcot’s joint’ (Charcot noted that the condition had also received attention from J.K. Mitchell in the 1830s). In 1880s England, though, according to W. Hale White of Guy’s Hospital, ‘discussion about Charcot’s joint [had] waxed very warm’. Alienist interest in the condition stemmed from its appearance in tabes dorsalis (nerve degeneration in the spinal cord due to untreated syphilis) patients, who were often seen in asylums before the incidence of syphilis was vastly reduced with the use of penicillin in the 20th century. Charcot said he had only ever seen the condition in tabes dorsalis patients, and other asylum doctors related similar cases. Conolly Norman at Dublin’s Richmond Asylum hosted a meeting of the Irish division of the Medico-Psychological Association in 1896 at which delegates viewed two cases of Charcot’s joints on Richmond’s wards, both occurring in general paralytic (neurosyphilitic) patients. In syphilitic conditions, nerve degeneration impaired patients’ reflexes and sensations whilst muscle wastage reduced the natural protection around the joints. The result was that patients became increasingly vulnerable to injury (discussions of the disease often noted spontaneous fractures), or their bones literally ‘wore away’ as they ground together.

Dissected knee joint exhibiting Charcot’s disease.
© Wellcome Images/St Bartholomew’s Hospital Archive & Museum.
Alongside syphilis, physical injuries were also cited by some as an immediate, exciting cause. (Whilst syphilis was the condition most commonly associated with Charcot’s disease by nineteenth-century doctors, it was gradually recognised as a condition with much wider aetiological factors. It may be present in diabetic neuropathies, for example, where nerve damage affects the weight-bearing joints.) J. Wallace Anderson related the case of a patient at Glasgow Royal Infirmary. Admitted to the hospital due to his difficulty in walking, the 45 year old gardener ‘ascribe[d] his complaint to a stroke of lightning … twelve years ago’, following which he began to experience ‘tingling’ pains and weakness in the hips, until finally his right hip “went out”. Though he was discharged from the hospital able to walk with the aid of sticks, he remained prone to ‘unusual variations in his general condition’. Charcot’s disease was, ultimately, untreatable, and little could be done for patients other than try to assist their mobility in various ways.
Ascertaining if Charcot’s disease was indeed novel to the late nineteenth century was difficult. One stumbling block was the apparent lack of such specimens in pathological museums: if it wasn’t a new disease, why were there no samples from previous years? At the London Clinical Society meeting, Sir James Paget suggested that museum curators – even if they were able to secure a specimen of a comparatively rare condition – tended to collect normal rather than abnormal specimens for teaching purposes. Interpretations of the disease ranged from osteo-arthritis to ‘modified’ chronic rheumatic arthritis, though such diagnoses were complicated by the sudden onset of the joint affection.
Although W. Hale White said that discussion about the disease had ‘waxed very warm’ and ‘everyone [had] had an opportunity of expressing his opinion’, he doubted if ‘exact knowledge of the subject [had] been much advanced’. At a point in time when doctors were increasingly keen to pinpoint the physical lesions of disease, Charcot’s joint seemed a perfect opportunity to trace a visible physical deformity to minute changes in the nerves. This was complicated by its resemblance to other conditions, however: was it just a form of rheumatism? Was it a ‘new’ disease? Or a ‘new compound of diseases’? These were – and are – fascinating questions that bring to mind current historical debates about retrospective diagnoses, the ‘framing’ of disease, and how we assess medical knowledge of the past: giving a condition a name didn’t necessarily mean that its identity was static, or signal a ‘pinnacle’ of understanding.
Further reading
D. Ferrier, On Tabes Dorsalis: the Lumelian Lectures, delivered before the Royal College of Physicians, London, March, 1906 (London: John Bale, son & Danielsson, 1906).
W.J.M.A. Maloney, Locomotor Ataxia (Tabes Dorsalis): An Introduction to the Study and Treatment of Nervous Diseases, for Students and Practitioners (London: D, Appleton, 1918).
L.C. Rogers et al, ‘The Charcot Foot in Diabetes‘, Diabetes Care 34 (2011).
L.J. Sanders, ‘Jean-Martin Charcot (1825 – 1893): The Man Behind the Joint Disease‘, Journal of the American Podiatric Medical Association 92 (Jul./Aug. 2002).
H. Waldo, ‘A Case of Charcot’s Joint Disease, with Perforating Ulcer of the Foot in a Tabetic Patient‘, BMJ (1 Dec. 1894).
R. Waterhouse, ‘Remarks on the Arthropathies of Acquired Syphilis‘, BMJ (10 Oct. 1908).























