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Trigger finger syndrome in rheumatoid arthritis not caused by flexor tendon nodules
Trigger Finger Syndro~rne in Rheumatoid Arthritis not caused by Flexor Tendon Nodules --Gerhard Stellbrink
TRIGGER
F I N G E R S Y N D R O M E IN R H E U M A T O I D A R T H R I T I S N O T C A U S E D BY F L E X O R T E N D O N N O D U L E S
G E R H A R D STELLBR1NK, Hamburg INTRODUCTION
Triggering of the fingers is a very frequent symptom in rheumatoid arthritis. It is usually caused by a nodular tenosynovitis inside the fibrous tendon sheaths of the flexors of the fingers. While nodules in non-rheumatic hands usually occur in that part of the sheath formed by the proximal anular ligament, particularly in its dense part just distal to the base of the proximal phalanx, the cause of finger triggering in rheumatoid hands is not so uniform. It may be found at any level in the tendon sheath, from the proximal end as far as the proximal interphalangeal joint crease of the finger. Relaxation or herniation of parts of the pulley ligament wall and the sheath occurs, but some transverse bands of greater fibre strength may escape at any level. Nodular thickening of the tendons can be formed at any point on the surfaces of the superficial and the profundus tendons. Triggering may also arise from nodules of the profundus tendon gliding through a tight bifurcation of the superficial flexor tendon; this condition, recently described by Helal (1970) is a well known operative finding in rheumatoid hands. There is, however, a small number of cases of rheumatoid arthritis with a trigger phenomenon in the fingers where examination and palpation show no evidence of flexor tendon involvement at all and where the localisation and cause of the phenomenon are quite different. CLINICAL FINDINGS During the last three years trigger finger phenomenon not explainable by flexor nodules was found in fifteen fingers in nine patients. The findings were not completely uniform, but the common main characteristic was that the typical "snapping" during active finger movement was not felt on the palmar aspect of the palm or finger, but at the sides of the proximal interphalangeal joint when the examiner holds it in a slack pinch grip with two of his fingers. The common anatomical condition is that the temporary block of finger flexion movement and its sudden overcoming which characterises the trigger phenomenon is produced by disturbance of the volar gliding of the lateral bands of the extensor apparatus on the lateral aspects of the proximal interphalangeal joint. The clinical characteristics briefly summarised are the following: 1. The phenomenon has never been seen in other than rheumatoid hands. 2. It can be present in one patient in one or in several fingers. 3. The phenomenon has not been seen in the thumb. 4. It has never been found in obviously unaltered proximal interphalangeal joints. There is evidence of synovial involvement and swelling, either past or present, with the sequence of capsular thickening, and bony destruction or destruction and disorder of the extensor apparatus. 5. On X-ray examination bony destruction is present in most cases, but may be very localised. 6. The "snapping" at the sides of the proximal interphalangeal joints may be felt on one or both sides of the joint. 76
Vol. 3
No. 1
1971
Trigger Finger Syndrome in Rheumatoid Arthritis not caused by Flexor Tendon Nodules - - G e r h a r d Stellbrink
7. Like triggering caused by flexor tendon nodules this form can never be reproduced by passive flexion of the joints, but only by active flexion. Thus it cannot be reproduced during operation! 8. While in cases of flexor tendon nodules the block in flexion movement may occur in different positions of the joint in the course of the movement (according to different site of the nodules, and of the tunnel stenosis), in our cases the point of triggering was always just at the beginning of the movement, with no more than five to ten degrees of proximal interphalangeal joint flexion. 9. The trigger phenomenon is present only when active flexion of the proximal interphalangeal joint is performed with the metacarpo-phalangeal joint held in the extended position. It disappears when the same movement is performed with the metacarpo-phalangeal joint held in some twenty-five to forty degrees of flexion. The patient is able to make a fist when he begins with flexion of the metacarpo-phalangeal joint and flexes the distal joints later, but he is unable to do so when he commences with flexion of the proximal interphalangeal joint. 10. Even in the extended position of the metacarpo-phalangeal joint the phenomenon regularly disappears when the proximal phalanx is supported in this position either by the examiner or by the patient himself with his other hand. It is of no importance whether the proximal phalanx is held on the dorsal and volar aspects or on the sides, or even (with a stronger grip) at the side of the proximal interphalangeal joint. OPERATIVE F I N D I N G S
Since most patients are disturbed and alarmed by their finger triggering, it regularly requires operative intervention. The preliminary condition for successful operative treatment is an exact preoperative analysis of the point of trouble of the anatomical and kinesiological changes, since the phenomenon can never be reproduced during the operation due to the relaxation of muscle tension. The pathological findings in our nine patients which may serve for interpretation of the clinical characteristics are as follows: 1. Relaxed and distended fibres of the extensor apparatus between central and lateral bands, with the central band itself functionally intact, at the level of the proximal interphalangeal joint and the head of the proximal phalanx. This relaxation is enough to give the lateral bands an increased volar mobility over the lateral aspects of the joint, but not enough to lead to permanent volar displacement of these bands as in the buttonhole finger.
Fig. 1 Lateral tendon will snap over thickened bony contour or ca ~sular structures. .
A deepened bony groove for the lateral bands at the dorso-lateral aspects of the base of.the middle phalanx, which gives some resistance to the gliding-out of the bands during proximal interphalangeal joint flexion when these bands
Vol. 3
No. 1
1971
77
Trigger Finger Syndro,me in Rheumatoid Arthritis not caused by FIe3for Tendon Nodules - - G e r h a r d SteIIbrink
are tight. A deepened groove may be caused by bone attrition or synovial bone erosion or by chronic inflammatory swelling and induration of lateral capsular structures and collateral ligaments (volar to lateral bands) (Fig. 1), by synovial swelling of the distal lateral joint recess, lying volar to the lateral bands as well or by reactive osteophytic prominence of the lateral tubercles at the base of middle phalanx. MECHANISM
It is very clear that it needs a combination of the conditions one and two for the development of this type of triggering phenomenon: and increased volar mobility of the lateral bands and an increased prominence volar to the normal position of these bands at the sides of the base of the middle phalanx. There is temporary resistance to the gliding movement of these bands out of their bone grooves at a certain stage of commencing flexion of this joint, either on one side of the joint or on both. The first condition is usually caused by a long standing swelling of the dorsal joint space in the past. The second condition may be produced by bone erosion which has deepened the grooves or by chronic inflammation with subsequent thickening of bone contours or of capsular structures (Fig. 1). Some of the clinical characteristics are well understandable, for example the fact that the phenomenon cannot be reproduced passively, either at operation or with the proximal phalanx supported. Snapping of the lateral band out of its bone groove, can take place only when the band is strained by muscle pull. When released the band will glide out also, during proximal interphalangeal joint flexion, easily and without resistance, and no block of movement will result. Furthermore, active flexion of the proximal interphalangeal joint does not require action of the long flexor muscle only, but the antagonist long extensor participates with some amount of counteraction in order to stabilise the metacarpo-phalangeal joint and to make the grip powerful. The lateral bands, though the intrinsic muscles do not act, are tightened by this extensor action, namely by transmission of the long extensor pull through the lateral slips of the central tendon (Fig. 2a). This strain on the lateral bands is, of course, relaxed at operation, and also by passive support of the proximal phalanx, which stabilises the metacarpo-phalangeal joint, and makes long extensor action unnecessary.
Fig. 2a Snapping can occur when the long tendon is under tension. Fig. 2b When the laterM bands are relaxed, snapping will not occur. 78
Vol. 3
No. 1
1971
Trigger Finger Syndro,rne in Rheumatoid Arthritis not caused by Flexor Tendon Nodules - - G e r h a r d Stellbrink
It is more difficult to explain why the phenomenon disappears when the metacarpo-phalangeal joint is in a flexed position, i.e. when active flexion of the interphalangeal joint is performed from the so-called "intrinsic position" of the fingers (flexed metacarpo-phalangeal and extended distal joints). This position is typically produced by intrinsic muscle action: and possibly the lateral bands, in this position of the fingers, should be under strain while the fully extended position of all finger joints is held by action first and foremost of the long extensors, these muscles do not participate much in holding the "intrinsic position" of the fingers, which is produced by the almost isolated action of the small muscles of the hand. Their pull is almost exclusively transmitted up to the dorsum of the middle phalanx by the spiral fibres and by the "wing fibres" of the aponeurosis, The long extensors (and consequently their lateral slips descending down to the lateral bands) remain relatively lax in this position. The tension in the lateral bands is provided only by the intrinsic muscles, and as these muscles relax immediately flexion commences the trigger phenomenon does not occur. SUMMARY
A trigger finger phenomenon in rheumatoid hands has been described which is not caused by flexor tendon nodules but by disturbance of volar gliding of the lateral bands of the extensor apparatus over the lateral aspects of the proximal interphalangeal joint. The clinical and anatomical characteristics are demonstrated and discussed and an explanation is put forward for the different aspects of the clinical signs.
REFERENCE
HELAL, B. (1970) Distal Profundus Entrapment in Rheumatoid Disease. The Hand. 2: 48. Vol. 3
No. 1
1971
79
TRIGGER
F I N G E R S Y N D R O M E IN R H E U M A T O I D A R T H R I T I S N O T C A U S E D BY F L E X O R T E N D O N N O D U L E S
G E R H A R D STELLBR1NK, Hamburg INTRODUCTION
Triggering of the fingers is a very frequent symptom in rheumatoid arthritis. It is usually caused by a nodular tenosynovitis inside the fibrous tendon sheaths of the flexors of the fingers. While nodules in non-rheumatic hands usually occur in that part of the sheath formed by the proximal anular ligament, particularly in its dense part just distal to the base of the proximal phalanx, the cause of finger triggering in rheumatoid hands is not so uniform. It may be found at any level in the tendon sheath, from the proximal end as far as the proximal interphalangeal joint crease of the finger. Relaxation or herniation of parts of the pulley ligament wall and the sheath occurs, but some transverse bands of greater fibre strength may escape at any level. Nodular thickening of the tendons can be formed at any point on the surfaces of the superficial and the profundus tendons. Triggering may also arise from nodules of the profundus tendon gliding through a tight bifurcation of the superficial flexor tendon; this condition, recently described by Helal (1970) is a well known operative finding in rheumatoid hands. There is, however, a small number of cases of rheumatoid arthritis with a trigger phenomenon in the fingers where examination and palpation show no evidence of flexor tendon involvement at all and where the localisation and cause of the phenomenon are quite different. CLINICAL FINDINGS During the last three years trigger finger phenomenon not explainable by flexor nodules was found in fifteen fingers in nine patients. The findings were not completely uniform, but the common main characteristic was that the typical "snapping" during active finger movement was not felt on the palmar aspect of the palm or finger, but at the sides of the proximal interphalangeal joint when the examiner holds it in a slack pinch grip with two of his fingers. The common anatomical condition is that the temporary block of finger flexion movement and its sudden overcoming which characterises the trigger phenomenon is produced by disturbance of the volar gliding of the lateral bands of the extensor apparatus on the lateral aspects of the proximal interphalangeal joint. The clinical characteristics briefly summarised are the following: 1. The phenomenon has never been seen in other than rheumatoid hands. 2. It can be present in one patient in one or in several fingers. 3. The phenomenon has not been seen in the thumb. 4. It has never been found in obviously unaltered proximal interphalangeal joints. There is evidence of synovial involvement and swelling, either past or present, with the sequence of capsular thickening, and bony destruction or destruction and disorder of the extensor apparatus. 5. On X-ray examination bony destruction is present in most cases, but may be very localised. 6. The "snapping" at the sides of the proximal interphalangeal joints may be felt on one or both sides of the joint. 76
Vol. 3
No. 1
1971
Trigger Finger Syndrome in Rheumatoid Arthritis not caused by Flexor Tendon Nodules - - G e r h a r d Stellbrink
7. Like triggering caused by flexor tendon nodules this form can never be reproduced by passive flexion of the joints, but only by active flexion. Thus it cannot be reproduced during operation! 8. While in cases of flexor tendon nodules the block in flexion movement may occur in different positions of the joint in the course of the movement (according to different site of the nodules, and of the tunnel stenosis), in our cases the point of triggering was always just at the beginning of the movement, with no more than five to ten degrees of proximal interphalangeal joint flexion. 9. The trigger phenomenon is present only when active flexion of the proximal interphalangeal joint is performed with the metacarpo-phalangeal joint held in the extended position. It disappears when the same movement is performed with the metacarpo-phalangeal joint held in some twenty-five to forty degrees of flexion. The patient is able to make a fist when he begins with flexion of the metacarpo-phalangeal joint and flexes the distal joints later, but he is unable to do so when he commences with flexion of the proximal interphalangeal joint. 10. Even in the extended position of the metacarpo-phalangeal joint the phenomenon regularly disappears when the proximal phalanx is supported in this position either by the examiner or by the patient himself with his other hand. It is of no importance whether the proximal phalanx is held on the dorsal and volar aspects or on the sides, or even (with a stronger grip) at the side of the proximal interphalangeal joint. OPERATIVE F I N D I N G S
Since most patients are disturbed and alarmed by their finger triggering, it regularly requires operative intervention. The preliminary condition for successful operative treatment is an exact preoperative analysis of the point of trouble of the anatomical and kinesiological changes, since the phenomenon can never be reproduced during the operation due to the relaxation of muscle tension. The pathological findings in our nine patients which may serve for interpretation of the clinical characteristics are as follows: 1. Relaxed and distended fibres of the extensor apparatus between central and lateral bands, with the central band itself functionally intact, at the level of the proximal interphalangeal joint and the head of the proximal phalanx. This relaxation is enough to give the lateral bands an increased volar mobility over the lateral aspects of the joint, but not enough to lead to permanent volar displacement of these bands as in the buttonhole finger.
Fig. 1 Lateral tendon will snap over thickened bony contour or ca ~sular structures. .
A deepened bony groove for the lateral bands at the dorso-lateral aspects of the base of.the middle phalanx, which gives some resistance to the gliding-out of the bands during proximal interphalangeal joint flexion when these bands
Vol. 3
No. 1
1971
77
Trigger Finger Syndro,me in Rheumatoid Arthritis not caused by FIe3for Tendon Nodules - - G e r h a r d SteIIbrink
are tight. A deepened groove may be caused by bone attrition or synovial bone erosion or by chronic inflammatory swelling and induration of lateral capsular structures and collateral ligaments (volar to lateral bands) (Fig. 1), by synovial swelling of the distal lateral joint recess, lying volar to the lateral bands as well or by reactive osteophytic prominence of the lateral tubercles at the base of middle phalanx. MECHANISM
It is very clear that it needs a combination of the conditions one and two for the development of this type of triggering phenomenon: and increased volar mobility of the lateral bands and an increased prominence volar to the normal position of these bands at the sides of the base of the middle phalanx. There is temporary resistance to the gliding movement of these bands out of their bone grooves at a certain stage of commencing flexion of this joint, either on one side of the joint or on both. The first condition is usually caused by a long standing swelling of the dorsal joint space in the past. The second condition may be produced by bone erosion which has deepened the grooves or by chronic inflammation with subsequent thickening of bone contours or of capsular structures (Fig. 1). Some of the clinical characteristics are well understandable, for example the fact that the phenomenon cannot be reproduced passively, either at operation or with the proximal phalanx supported. Snapping of the lateral band out of its bone groove, can take place only when the band is strained by muscle pull. When released the band will glide out also, during proximal interphalangeal joint flexion, easily and without resistance, and no block of movement will result. Furthermore, active flexion of the proximal interphalangeal joint does not require action of the long flexor muscle only, but the antagonist long extensor participates with some amount of counteraction in order to stabilise the metacarpo-phalangeal joint and to make the grip powerful. The lateral bands, though the intrinsic muscles do not act, are tightened by this extensor action, namely by transmission of the long extensor pull through the lateral slips of the central tendon (Fig. 2a). This strain on the lateral bands is, of course, relaxed at operation, and also by passive support of the proximal phalanx, which stabilises the metacarpo-phalangeal joint, and makes long extensor action unnecessary.
Fig. 2a Snapping can occur when the long tendon is under tension. Fig. 2b When the laterM bands are relaxed, snapping will not occur. 78
Vol. 3
No. 1
1971
Trigger Finger Syndro,rne in Rheumatoid Arthritis not caused by Flexor Tendon Nodules - - G e r h a r d Stellbrink
It is more difficult to explain why the phenomenon disappears when the metacarpo-phalangeal joint is in a flexed position, i.e. when active flexion of the interphalangeal joint is performed from the so-called "intrinsic position" of the fingers (flexed metacarpo-phalangeal and extended distal joints). This position is typically produced by intrinsic muscle action: and possibly the lateral bands, in this position of the fingers, should be under strain while the fully extended position of all finger joints is held by action first and foremost of the long extensors, these muscles do not participate much in holding the "intrinsic position" of the fingers, which is produced by the almost isolated action of the small muscles of the hand. Their pull is almost exclusively transmitted up to the dorsum of the middle phalanx by the spiral fibres and by the "wing fibres" of the aponeurosis, The long extensors (and consequently their lateral slips descending down to the lateral bands) remain relatively lax in this position. The tension in the lateral bands is provided only by the intrinsic muscles, and as these muscles relax immediately flexion commences the trigger phenomenon does not occur. SUMMARY
A trigger finger phenomenon in rheumatoid hands has been described which is not caused by flexor tendon nodules but by disturbance of volar gliding of the lateral bands of the extensor apparatus over the lateral aspects of the proximal interphalangeal joint. The clinical and anatomical characteristics are demonstrated and discussed and an explanation is put forward for the different aspects of the clinical signs.
REFERENCE
HELAL, B. (1970) Distal Profundus Entrapment in Rheumatoid Disease. The Hand. 2: 48. Vol. 3
No. 1
1971
79