TENDON LESIONS IN RHEUMATOID ARTHRITIS

TENDON LESIONS IN RHEUMATOID ARTHRITIS

561 " " impaired it may use a sort of last ditch defence, blocking the id’s access to mental formulation Clinior motor expression of the intolerable...

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impaired it may use a sort of last ditch defence, blocking the id’s access to mental formulation Clinior motor expression of the intolerable impulses. cally, this condition shows itself in psychomotor retarda, weak

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massive form of outer defence characteristic of psychosis. The unquestionable benefit which these patients usually derive from shock treatment Abse attributes to the anxiety generated by the traumatic situation causing the ego to defend itself more vigorously, with the result therefore that psychomotor blocking can be discarded. Abse maintains that, in schizophrenia, treatment by insulin coma is more effective than other forms of shock treatment, owing to the emphasis in this technique on what he terms the " loving care " aspect of treatment. The patient receives longer and more assiduous attention, and the physiological disturbance is of a specifically hunger-producing kind. The patient experiences intense oral needs and may express feelings of gratitude towards the nurse who gives him a sugared drink on the termination of coma, re-experiencing emotions felt in early infancy at his mother’s breast. Abse refers to some disadvantages of shock treatment from the psychological angle. Masochistic trends may be reinforced and subsequent psychotherapy rendered more difficult. The patient may be rendered even more afraid of relinquishing inexpedient and self-sacrificing devices than he was before the onset of his illness. The presence in a patient of considerable ego assets, which are likely to render psychotherapy more rewarding, should be regarded as a contra-indication to shock treatment. Indeed, Abse believes that psychotherapy should always be first considered or given a trial, and that the choice of psychotherapy or a particular shock method should be based on careful appraisal of the individual case.

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is, in contrast, full and painless ; the joints themselves are not tender ;; and the nodule can be felt in the palm as the finger is moved. This disorder may improve spontaneously in early acute cases when the disease remits and the tendon thickening subsides, and also in progressive cases in which the fibrous bands soften.44 Kellgren and Ball4 believe that operative release of nodular or thickened tendons is useful where active movement has not been regained even after the disease has become relatively quiescent. When pain is prominent, relief may be obtained by applying a volar plaster slab with the wrist in extension and the fingers in partial flexion ; the plaster should be removed daily for gentle exercises. Wax baths followed by active and passive movement may also help, as also may injections of corticotrophin.1 Ansell and Bywaters point out that if these lesions are not treated secondary changes may develop in other tissues and thus lead to irremediable disability ; and they describe 3 cases in which contracture of fingers resulting from changes in tendons was the presenting abnormality. Ansell and Bywaters declare that this disorder must be distinguished from scleroderma : although the skin may be smooth from lack of use it is neither bound down nor thickened, and telangiectases or loss of pulp or bone in the terminal phalanx are not seen. Contracture of fingers due to lesions of nerve, muscle (Volkmann’s contracture, dermatomyositis), fascia (Dupuytren’s contracture), or joints should be easily distinguished. In rheumatic fever nodules may also form in the tendons of the palm, producing a sticking finger 5-7 ; but these nodules invariably resolve in a few days or weeks.8 Similar contractures occur in " palindromic " rheumatism,9and in lupus erythematosus. In gout, accumulation of uric acid in a tendon may produce similar symptoms. Snapping " finger is, of course, most commonly due

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TENDON LESIONS IN RHEUMATOID ARTHRITIS THE tendon lesions found in rheumatoid arthritis are usually inconspicuous and unimportant compared with the damage in nearby joints. Occasionally, however, these lesions contribute significantly to a patient’s disability; and, as Ansell and Bywaters1 point out, they may even be the main feature of the rheumatoid process. Such tendon lesions, first described by Helweg,2 are present in 40-50% of cases of rheumatoid arthritis.2-4 Most often the tendons of the long flexors of the fingers are affected, and less commonly the extensors of the fingers, the tendons round the ankle-joint, and the Achilles tendon. The long flexor tendons of the fingers enter the palm by passing under the volar carpal ligament, at which level they are surrounded by the palmar synovial sheath. In the distal half of the palm the synovial sheath is lacking, and each tendon is covered merely by a thin fibrous sheath containing three well-developed transverse bands.4 In rheumatoid arthritis the tendons may become thickened or even nodular, and symptoms develop when a nodule is jammed between the transverse bands. If the nodule is small it interferes with activee flexion and may give rise to a " snapping " finger, but the patient complains more often of weak and painful fingers. A large nodule may become completely impacted and prevent any active flexion of the interphalangea,l joints. In the exceptional cases where the joints are not greatly involved the clinical picture is easily recognised. The index and middle fingers are most commonly affected. On attempting to make a fist the patient flexes his metacarpo-phalangeal joints but his interphalangeal joints remain fully extended. Passive move1. Ansell, B. M., Bywaters, E. G. L. Ann. rheum. Dis. 1953, 12, 283. 2. Helweg, J. Klin. Wschr. 1924, 52, 2383. 3. Edström, G. Nord. Med. 1945, 25, 379. 4. Kellgren, J. H., Ball, J. Ann. rheum. Dis. 1950, 9, 48.

to trauma. The histological features of the tendon lesions of rheumatoid arthritis were established by Kellgren and Ball,4 who recognised the valuable opportunity of studying the collagen changes of rheumatoid arthritis in a tissue composed almost exclusively of collagen fibres and ground-substance. Changes in the tendon ranged from cedematous separation of the fibres to reduction of the compact tendon-fibre system into a swollen, homogeneous, granular mass, at first containing a reticulin network but later becoming completely afibrillar. In adjacent mesotenon or peritenon much granulation tissue was seen-the tendon nodule itself was an expression of the exuberant production of this tissue in the active stages of the disease. Not infrequently nodules on the surface of the tendon could be regarded as a mass of granulation tissue isolated from parent connective tissue ; and Kellgren and Ball, detecting in such nodules lesions identical with the subcutaneous necrobiotic foci of rheumatoid arthritis, suggested that one way in which such foci might be formed was by focal fibrinoid degeneration of preformed non-specific granulation tissue. Apparently, not only may collagen be involved by fibrinoid necrosis, but the associated granulation tissue is liable, at any stage in its development, to undergo similar degenerative changes, which in turn may stimulate further production of granulation tissue. THE

death

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announced

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Dr.

KLOTHiLDE

GOLLWITZER-MEIER, professor of pathological physiology in the University of Hamburg. In 1949 she lectured at King’s College, London, on Blood pH and Blood-flow during Muscular Activity. 5. 6. 7. 8.

Scheele. Keil, H.

Dtsch. med. Wschr. 1885, 11, 702. Medicine, Baltimore, 1938, 17, 261. Berkowitz, R. Arch. Kinderheilk. 1912, 59, 1. Bywaters, E. G. L. Modern Practice in Infectious Fevers. Edited by H. S. Banks. London, 1951 ; vol. 1, p. 156. 9. Bywaters, E. G. L. Ann. rheum. Dis. 1949, 8, 1.