Observations on the physiology and pathology of hemi-chorea / by J. Hughlings-Jackson, M.D.

  • John Hughlings Jackson
Date:
1868
Catalogue details

Licence: Public Domain Mark

Credit: Observations on the physiology and pathology of hemi-chorea / by J. Hughlings-Jackson, M.D. Source: Wellcome Collection.

Provider: This material has been provided by The University of Glasgow Library. The original may be consulted at The University of Glasgow Library.

    10/16 page 8
    cHoreiform movements are rare, and they are not quite like tliose seen in choreaic children, and in most cases they are only developed when the patient voluntarily uses the affected limbs. (5.) The Particular Nature of the Local Change.—The speculation advanced, as to the supposed particular nature of the local change, is in harmony with (a.). It is admitted by.all that we find in chorea, at least frequently, a condition for embolism. In some cases there is valvular mur- mur. In others there is a history of rheumatic or of scarlet fever. The movements will sometimes begin with joint affection; this being either what would be commonly called acute rheumatism, or slight pain and swelling in a few joints. Add to this that, according to Kirkes, Wilks, and Andrew, vegetations are invariably found on the cardiac valves at post-mortem examinations on those who have died of chorea. I am aware, however, that there have been exceptions. Dr Kirkes long ago put forward the view that chorea is associated not so much with rheumatism as with valvular disease of the heart, a thing which rheumatism often induces. Then chorea occurs with pregnancy and parturition, states under which it is admitted that paralysis from embolism results. To complete what I have to say on this part of the question, I will quote one of our best clinical observers. Dr Hillier, in his recently published work on Diseases of Chil- dren (1868), writes :— The late Dr Kirkes, in one of his last papers [Medical Times and Gazette^ June 1863), proposes a very ingenious and plausible theory to explain this connexion. He dwells upon the frequent presence of a systolic murmur in chorea, and states that valvular disease often exists without the presence of a murmur to indicate its existence, especially when granulations occur on the auricular surface of the flaps of the mitral or tricuspid valve. He also calls attention to the fact that a condition, v/hich has not been uncommonly found post-mortem in fatal cases of chorea, is softening of parts of the cord or of the cerebrum, and occasionally intense capillary congestion of other parts, more or less simulating haemor- rhage. The patients who suffer from chorea are very impressible and emotional, and very liable to derangement of the nervous system. Putting these facts together, he asks, may not endocarditis be the first link in the chain, causing fibrinous exudation on the cardiac valves ? Particles of this exudation are carried forward into the smaller vessels of the cord and brain, giving rise to deranged function in these parts, and sometimes leading to local softening of nerve-tissue. However, Dr Hillier adds—the italics are mine :— A forcible objection to this theory is, that we do not find symptoms like those of chorea 'produced by embolism^ when it is proved to exist^ or when experimentally induced in animals^ I do not consider this argument to be so forcible as it appears at first glance.
    digitised image 1
    digitised image 2
    digitised image 3