Tag Archives: Charcot’s joint

Horses and humans in the history of neurology

Towards the end of the 19th century, there was increasing interest in comparative pathology, comparative neurology or – let’s use this one for simplicity’s sake – comparative neuro-pathology. This was the idea that, by studying the brain and nervous system of an animal, one could extrapolate the knowledge gained in such investigation to human subjects. The Journal of Comparative Neurology, for example, published its first issue in 1891. In an era captivated by evolutionary theory, an animal’s brain offered to reveal something of cerebral development, demonstrating ‘by what steps the lower faculties of animals may have passed by natural process of development into the higher faculties of man’. The use of animals in scientific research at this time has previously been discussed on this blog by Mike Finn, who highlighted popular responses to the cerebral localisation work of David Ferrier (often using monkeys or cats), whilst Liz Gray has examined the work of William Lauder Lindsay, who was interested in the ‘psychopathology’ of animals.

From C. Watson, 'The Pathogenesis of Tabes and Allied Conditions in the Cord' (1901).

From C. Watson, ‘The Pathogenesis of Tabes and Allied Conditions in the Cord’ (1901). The horse’s hind legs assume an unusual position and the right rear knee joint is prominent.

Animals might also be used to reveal something of the nature of neurological disorders which had distinct physical symptoms. In 1901, Chalmers Watson of the Scottish Asylums tried to advance existing knowledge about tabes, a degenerative condition of the spinal cord: ‘If the etiology of tabes were accurately determined,’ he said, ‘a large and important chapter in neurology could be written’. In setting about this task, Watson presented a clinical case study not of a human patient, but of a horse. He had seen a horse that exhibited tabes-like symptoms, with an unusual gait and prominent knee-joint that recalled the Charcot’s knee seen in humans. The horse went on to suffer a seizure, afterwards developing the signs of ‘Stringhalt’. Stringhalt is a condition affecting horses in which the hind legs flex whilst walking. It may be most marked when the animal is frightened, turns, or has to back up slowly. (You can see a video of a horse with the condition here.)

In ‘On “Stringhalt” and “Shivering” in Horses’, Watson presented his horse much as one would present a human case study, setting out the animal’s age, appearance, and occupation:

The subject was a light-legged, well-bred horse, 15½ hands, aged 15 years or more, that had been able for work up to three months before the date at which he came under observation. His work was light, that of going in a fishmonger’s cart in a level country. His owner informed me that the animal had occasionally been off work for a few days or so from “lameness.”

Detail from a Muybridge study of a horse and its rider. © Wellcome Library, London.

Detail from a Muybridge study of a horse and its rider. © Wellcome Library, London.

Watson had earlier presented a cinematograph film of this horse to a meeting of the British Medical Association, which documented the animal’s unusual movement (and which also recalls the motion studies of Eadweard Muybridge). The horse’s physical symptoms – ‘spastic movements of the hind limbs’, elevated and quivering tail, inco-ordination – were observed for a few days by Watson, at the end of which the case took a rather different course than that of a human case study: ‘the animal was shot’.

Watson was particularly keen to conduct a post-mortem on the horse in the hope that the pathological appearances found would reveal something about the progress of disease. The advantage of using animals was that their ‘tissues … [exhibited] evidence of nervous disease … at an early stage of the morbid process when the pathological picture [was] as yet unobscured by the secondary and non-essential changes which so frequently complicate[d] the picture in the human subject’. The post-mortem and subsequent microscopical examinations led Watson to conclude the horse’s Stringhalt had been caused by ‘a chronic interstitial neuritis with secondary degeneration of the nerve fibres in the main nerves of the hind limbs’, with the ‘shivering’ symptoms explained by nerve fibre degeneration.

Appearance of the (human) spinal cord in advanced tabes. This was interestingly presented beneath the photograph of the horse in Watson's 'Pathogenesis of Tabes' article.

Appearance of the (human) spinal cord in advanced tabes. This was interestingly presented directly beneath the photograph of the horse in Watson’s ‘Pathogenesis of Tabes’ article.

Whilst Watson recognised the difficulty of formulating any general conclusions from a single case, he considered his findings to be of interest to both the veterinary and human sciences. He concluded that the post-mortem exam both threw light upon ‘common diseases of the horse’, and held some ‘suggestive lessons for the student of pathological processes in the human subject’. On the latter point, he pointed to the importance of vascular lesions (such as thickened blood vessels) in the horse, suggesting this might also be at the root of tabes in human subjects. He further suggested a possible cause for such changes, ‘toxaemia, probably of bacterial origin’, reflecting the interest in bacteriological matters that ran through much of his work. (Watson’s obituary demonstrates that his interests in bacteriology and animals often complemented one another: ‘in [his] later years [he] devoted himself to rearing cattle for [the] production of pure and safe milk’.)

By using animal case studies, then, investigators could make deductions about neurological development, but also neurological disease. Such studies reveal the often surprising scope of asylum-based research at this time, with Watson thanking the President of the Royal College of Veterinary Surgeons and referencing publications such as the Veterinary Record in his research. In addressing degenerative conditions like tabes, animals offered doctors and pathologists a way in to uncovering the ‘truth’ of diseases that caused many asylums to fill up with chronic (human) cases.


C. Watson, ‘The Pathogenesis of Tabes and Allied Conditions in the Cord’, BMJ (1 Jun. 1901).

C. Watson, ‘Cinematograph and Lantern Demonstration upon Nervous Diseases in the Lower Animals’, BMJ (27 Sept. 1902).

C. Watson, ‘On “Stringhalt” and “Shivering” in Horses. A Study in Comparative Neuro-pathology’, Brain 26 (1903).

A ‘new’ disease?

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.

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.

L0061441 Dissected knee joint, the subject of marked locomotor ataxy

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.

N0008052 Charcot's knee

X-ray of a Charcot’s knee.
© Wellcome Images.

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).