Abstract
We describe seventeen patients (twenty-two limbs) who had snapping (dislocation) of both the ulnar nerve and the medial head of the triceps over the medial epicondyle. Two patients (two limbs) were seen because of painless snapping, four patients (five limbs) had snapping and pain in the medial aspect of the elbow, three patients (three limbs) had symptoms related to the ulnar nerve only, and six patients (seven limbs) had snapping and symptoms related to the ulnar nerve. In addition, snapping was identified incidentally on routine screening in five asymptomatic limbs in four patients, one of whom was seen because of snapping and symptoms related to the ulnar nerve on the contralateral side. The diagnosis was confirmed with magnetic resonance imaging or computerized tomography, or both, in all but the first three patients, in whom the operative findings were confirmatory.Only six patients (seven limbs) were sufficiently symptomatic to be managed operatively. Of these six patients, five (six limbs) who had symptoms related to the ulnar nerve had lateral transposition or excision of the dislocating medial head of the triceps in addition to decompression and transposition of the ulnar nerve. Two of these patients had had persistent symptoms immediately after a previous transfer of the ulnar nerve performed at another institution for symptoms related to, and well documented dislocation of, the ulnar nerve; we performed the index procedure to correct the postoperative snapping, which was the result of an unrecognized dislocation of the medial head of the triceps in one patient and the result of an accessory triceps tendon in the other. One patient who had pain in the medial part of the elbow, snapping (without symptoms related to the ulnar nerve), and cubitus varus had a valgus osteotomy of the distal aspect of the humerus that corrected the line of pull of the triceps and relieved the snapping.All of the patients who were managed operatively had an excellent result (no snapping, no symptoms related to the ulnar nerve, and a full range of motion), at an average of 4.5 years postoperatively. Non-operative treatment provided control of symptoms related to the ulnar nerve in four limbs and control of pain from the snapping in four limbs.Snapping on the medial side of the elbow, even if it is associated with symptoms related to the ulnar nerve, is not necessarily caused by dislocation of the ulnar nerve alone. Patients who have a transposition of the ulnar nerve, especially those who have dislocation of the ulnar nerve, should be examined intraoperatively with the elbow in flexion and extension so that the surgeon can be certain that the medial head of the triceps does not snap over the medial epicondyle. Failure to recognize concurrent dislocation of the ulnar nerve and the medial head of the triceps can result in persistent, symptomatic snapping after an otherwise successful transposition of the ulnar nerve.
Snapping of the medial head of the triceps has been reported rarely7,11,12,20,21 and probably has frequently gone unrecognized. To many physicians, a snapping elbow is synonymous with the relatively common recurrent dislocation of the ulnar nerve. However, the medial head of the triceps muscle or tendon also may dislocate over the medial epicondyle and result in snapping either as the elbow is flexed or as it is extended from a flexed position. Dislocation of the medial head of the triceps can occur in combination with dislocation of the ulnar nerve, producing the clinical finding of at least two snaps at the elbow, with or without discomfort on the medial side of the elbow and with or without ulnar neuropathy. Often snapping of the medial edge of the triceps over the epicondyle is subtle and is detected only with careful palpation, although occasionally it can be seen or heard. Misdiagnosis of this entity is common, and failure to recognize that the ulnar nerve and the medial head of the triceps can dislocate concurrently can result in persistent symptoms after an otherwise successful transposition of the ulnar nerve. The purpose of the present study was to emphasize the relatively common occurrence of snapping of the medial head of the triceps, its broad spectrum of presentation, and the frequency with which it is confused with better known disorders of the medial aspect of the elbow.
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Funds were received in total or partial support of the research or clinical study presented in this article. The funding sources were grants from the Duke Hand Club and the Piedmont Orthopaedic Society.
†Read at the Annual Meetings of the American Association of Clinical Anatomists, Seattle, Washington, June 17, 1993; The American Orthopaedic Association, White Sulphur Springs, West Virginia, June 13, 1995; the American Society for Surgery of the Hand, Nashville, Tennessee, October 2, 1996; and the American Society for Peripheral Nerve, Williamsburg, Virginia, June 6, 1997.
‡207 5th Avenue S.W., Apartment 505, Rochester, Minnesota 55902-3117. E-mail address: spinner.robert@mayo.edu.
§Duke University Medical Center, Box 3480, Durham, North Carolina 27702.
We evaluated seventeen patients (twenty-two limbs) who had snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve. The age of the fifteen male and two female patients averaged twenty-five years (range, ten to fifty-three years). The diagnosis was suspected clinically (Fig. 1) and was confirmed with magnetic resonance imaging or computerized tomography, or both, in all but the first three patients (in whom operative findings were confirmatory). Imaging24 was performed with the elbow in extension (Fig. 2-A) and in flexion (Fig. 2-B).
Several techniques facilitate examination and concurrently reproduce symptoms. The ulnar nerve can be palpated in the cubital tunnel with the elbow in extension and then the examiner can assess whether it or another structure (for example, the medial head of the triceps or an accessory tendon of the triceps) moves anteriorly over the medial epicondyle while the elbow is passively flexed and is extended from a flexed position. The dislocating structures can also be palpated while the patient actively flexes and extends the elbow. Proximal, posteriorly directed digital pressure on the nerve and the triceps also may accentuate the snapping when the elbow is flexed. Finally, the patient can contract the triceps, attempting to extend the elbow while allowing it to be passively flexed by the examiner.
Two limbs (Cases 7 and 8R) were seen because of painless snapping. Symptomatic snapping occurred in twelve limbs: pain was present about the medial aspect of the elbow in five limbs (Cases 6, 8L, 9L, 9R, and 14), and the symptoms were related to the ulnar nerve (pain and paresthesias or weakness) in seven (Cases 1L, 3, 4, 5L, 5R, 10, and 11). There were symptoms related to the ulnar nerve in three limbs (Cases 2, 12, and 13), but the patients were not aware of the snapping (Table I). In addition, snapping was identified in five asymptomatic limbs (Cases 1R, 15, 16, 17L, and 17R) in four patients who had been previously unaware of the snapping. Of these four patients, one had snapping and symptoms related to the ulnar nerve in the contralateral limb (Case 1L), which was treated operatively. The snapping in the remaining three patients (four limbs) was identified during routine examination by our institution's staff after they heard an oral presentation on this abnormality.
Both snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve were confirmed in all limbs. Two limbs (Cases 2 and 4) had been treated with a transfer of the ulnar nerve before they were evaluated by us, for symptoms related to, and well documented dislocation of, the ulnar nerve. At the time of our examination, the ulnar nerve in these two limbs remained anterior to the medial epicondyle while the medial head of the triceps dislocated over it with flexion of the elbow. Three limbs (Cases 1R, 4, and 6) had a cubitus varus deformity due to a previous supracondylar fracture. Specific athletic activities (such as weight lifting or pitching) reproduced the symptoms in ten limbs. No patient had a systemic disease that would predispose to a neuropathy.
Five patients had bilateral snapping of the medial head of the triceps (Cases 1L, 1R, 5L, 5R, 8L, 8R, 9L, 9R, 17L, and 17R). One of these patients had operative treatment of both limbs (Cases 5L and 5R). Another had snapping with symptoms related to the ulnar nerve in one limb (Case 1L), which was treated operatively; during the preoperative evaluation, snapping was discovered incidentally in the contralateral limb (Case 1R). The third patient had snapping with pain in one limb (Case 8L) and painless snapping in the other (Case 8R), and the fourth had snapping and pain in the medial aspect of the elbow in both limbs (Cases 9L and 9R). In the fifth patient, both limbs (Cases 17L and 17R) were asymptomatic; the bilateral snapping was found incidentally.
A three-to-six-month trial of non-operative treatment was offered to all patients who were seen because of snapping or symptoms related to the ulnar nerve, or both. Treatment options included avoidance of activities that required sustained or repeated flexion of the elbow with or without resistance, use of non-steroidal anti-inflammatory agents, and splinting of the elbow at approximately 75 degrees. The asymptomatic individuals who were found to have snapping of the triceps incidentally on clinical examination did not receive any treatment. Electromyography with nerve-conduction velocities was not performed for these patients, and long-term follow-up data are unavailable.
Seven limbs (Cases 1L and 2 through 6) were treated operatively (Table II). The indications for the operation were persistent pain in the medial aspect of the elbow and snapping in one limb (Case 6) and snapping with persistent symptoms related to the ulnar nerve in six (Cases 1L and 2 through 5R). In four limbs (Cases 1L, 3, 5L, and 5R), the compression of the ulnar nerve was grade I according to McGowan's system and mild according to Dellon's system6. In two limbs (Case 2 and 4), the compression was grade III (severe). Electrical studies supported the diagnosis of symptoms related to the ulnar nerve in five limbs (Cases 2 through 5R) and were not performed for two limbs (Cases 1L and 6). Of the six limbs in which the symptoms were related to the ulnar nerve, four (Cases 1L, 3, 5L, and 5R) were treated with lateral transposition and two (Cases 2 and 4), with excision of the dislocating part of the medial head of the triceps in addition to decompression and transposition of the ulnar nerve. Two patients had had persistent symptoms immediately after a previous transposition of the ulnar nerve. We performed the index procedure to correct persistent postoperative snapping, which was due to unrecognized dislocation of the medial head of the triceps in one of these limbs (Case 4) and due to an accessory triceps tendon in the other (Case 2). One patient (one limb; Case 6), who had pain in the medial aspect of the elbow, snapping, and cubitus varus deformity, had a valgus osteotomy of the distal aspect of the humerus to centralize the line of pull of the triceps.
All of the patients who had a symptomatic limb that was not treated operatively had originally been misdiagnosed at least once. The misdiagnoses included intra-articular abnormality (three limbs), Little Leaguer's elbow (two limbs), bicipital tendinitis (two limbs), medial epicondylitis (five limbs), and recurrent dislocation of the ulnar nerve as an isolated finding (six limbs). In addition, the diagnosis of snapping of the medial head of the triceps had not been made before the referral of any of the patients who were managed operatively.
The symptoms were adequately controlled by non-operative treatment in eight limbs, including four (Cases 8L, 9L, 9R, and 14) of the five that had snapping and pain (without symptoms related to the ulnar nerve), two (Cases 10 and 11) of the seven that had snapping and symptoms related to the ulnar nerve, and two (Cases 12 and 13) of the three that had isolated symptoms related to the ulnar nerve. Neither pain nor symptoms related to the ulnar nerve developed in the two limbs (Cases 7 and 8R) that had snapping alone at presentation or in those (Cases 1R, 15, 16, 17L, and 17R) that were found to have snapping on screening. The patients who were asymptomatic did become more conscious of the snapping after it was demonstrated to them. The clinical findings of snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve persisted in all of the limbs that were treated non-operatively or that were not treated at all.
Anatomical variations were confirmed in all of the operatively treated limbs at the time of the operation and included hypermobility of the ulnar nerve (seven limbs; Cases 1L and 2 through 6), abnormal configuration of the triceps (five limbs; Cases 1L, 2, 3, 5L, and 5R), and osseous abnormalities at the elbow (two limbs; Cases 4 and 6). In all limbs, varying amounts of triceps-muscle fibers extended distal to the level of the medial epicondyle and dislocated over the medial epicondyle with the elbow in flexion. In three limbs (Cases 4, 5L, and 5R), thickening of the fascial edge of the medial head of the triceps was noted to produce the snapping. Two limbs (Cases 1L and 2) had an accessory triceps tendon. Two limbs (Cases 1L and 3) had snapping of a prominent medial head of the triceps; one of these limbs (Case 1L) also had an accessory tendon. Two limbs (Case 5L and 5R) had supernumerary bands of the medial head of the triceps with separate insertions. Two limbs (Cases 4 and 6) that had post-traumatic cubitus varus deformity had snapping of a normal-sized medial head (Table II).
Of the ten limbs that had symptoms related to the ulnar nerve, six (Cases 1L and 2 through 5R) were treated operatively. Compression was found within the cubital tunnel in both limbs (Cases 5L and 5R) of one patient. No visible area of localized neural compression could be identified in the other four limbs; the ulnar neuropathy probably was due to a combination of factors, including chronic irritation or friction caused by the ulnar nerve dislocating over the medial epicondyle or by compression by the medial head of the triceps, the accessory triceps tendon, or the medial intermuscular septum during flexion of the elbow.
The result was excellent (no snapping, no symptoms related to the ulnar nerve, and a full range of motion) an average of 4.5 years (range, 2.5 to 8.0 years) postoperatively for all of the patients who had been managed operatively (Table II). Postoperative magnetic resonance images were made for three limbs and showed that no structures had dislocated.
CASE 1L. A twelve-year-old boy, who was left-hand dominant, was seen because of pain in the left elbow and a snapping sensation with flexion that had begun three years earlier. During the year preceding presentation, he had noted intermittent dysesthesias in the left little finger, especially with pitching and weight lifting.
On physical examination, the patient had a normal carrying angle and a full range of motion of the elbow and forearm. There were three distinct snaps with flexion of the elbow. With palpation, the ulnar nerve was felt to snap at 90 degrees of flexion; the edge of the triceps muscle, at 105 degrees of flexion; and a tendinous band, at 120 degrees of flexion. Flexion of the elbow reproduced the dysesthesias in the hand; the findings of the motor and sensory examination were otherwise normal, and percussion over the cubital tunnel did not produce discomfort. The findings on routine anteroposterior and lateral radiographs were normal.
The operative findings consisted of a dislocating ulnar nerve and a shallow ulnar groove (Figs. 3-A and 3-B), a prominent medial head of the triceps inserting into the olecranon (Fig. 3-C), and a five-centimeter by five-millimeter accessory tendon (Figs. 3-D and 3-E) that arose from a muscle belly deep to the medial head of the triceps (most likely an accessory band of the triceps muscle) and that inserted onto the proximal-medial portion of the olecranon. The three separate snaps could be reproduced and were due to the ulnar nerve, the medial edge of the prominent head, and dislocation of the accessory tendon over the medial epicondyle with flexion of the elbow. The medial head of the triceps pushed the ulnar nerve anteromedially with flexion. No site of focal compression of the ulnar nerve was identified.
External neurolysis of the ulnar nerve was performed; it included release of the arcade of Struthers, excision of the intermuscular septum adjacent to the nerve, and release of the flexor carpi ulnaris and deep flexor-pronator aponeuroses. There was no cubital tunnel retinaculum. Both the accessory tendon and the prominent medial head of the triceps were transposed laterally into the triceps12 in order to restore a more normal anatomical configuration. An anterior subcutaneous transposition of the ulnar nerve was done, and the nerve was stabilized with a fascial sling8. At the end of the procedure, there was no snapping or dislocation over the medial epicondyle with flexion of the elbow (Fig. 3-F) and the ulnar nerve was free of compression.
At the most recent follow-up examination four years later, the patient had no snapping or sensory disturbance and he had regained a full range of motion and strength.
Snapping of the medial head of the triceps with so-called ulnar neuritis was apparently first described21 in a patient in 1970. We are aware of subsequent reports by others on only five additional patients (six limbs) with this condition7,11,12,20. The six patients were eighteen to forty-five years old (average, twenty-six years old); five were men. The medial head of the triceps muscle dislocated in six limbs, and an accessory triceps tendon dislocated in one limb. The ulnar nerve dislocated in four limbs, dislocation was prevented by a tendinous arch of the flexor carpi ulnaris in one limb12, and the mobility of the ulnar nerve in the two remaining limbs was not reported. The ulnar neuropathy was believed to be due to friction in three limbs and to compression in one. Two of the seven limbs had post-traumatic cubitus varus deformity. The diagnosis was inaccurate for four patients (five limbs), and the misdiagnosis led to at least two operative procedures in three patients (four limbs).
The findings in the present study suggest that snapping of the medial head of the triceps may have a spectrum of clinical presentations. Although all patients described in the previous reports7,11,12,20,21 had snapping and ulnar neuropathy, we found that patients may have pain in the medial aspect of the elbow, snapping, or ulnar neuropathy, or a combination of the three. Painless snapping and the incidental finding of snapping in asymptomatic patients on routine screening suggest that this entity may be more prevalent than has been recognized in the past. Furthermore, not all dislocating triceps snap16,24.
Analysis of the activities that exacerbated the symptoms was helpful in determining the diagnosis and in understanding the mechanism of the disorder. For example, symptoms were produced by overhead pitching of a baseball, which involves flexion of the elbow beyond 90 degrees during windup and increased valgus stress on the medial aspect of the elbow during cocking and early acceleration. Similarly, symptoms were provoked by lifting weights (especially curling or bench-pressing) or performing push-ups, activities that require a phase of resisted flexion of the elbow beyond 90 degrees as well as resisted extension.
Variations in the anatomy of the triceps have been reported in patients who have recurrent dislocation of the triceps or ulnar neuropathy, or both14,15,19. Once thought to be fairly rare26, localized structural variation in the triceps muscle9 is becoming more widely recognized. However, the anatomy of the musculotendinous insertion of the triceps has not been well defined. In one study, a prominent medial head of the triceps was reported in sixteen (25 per cent) of sixty-four cadavera5. In fourteen of eighteen cadavera that had a subluxating or dislocating ulnar nerve, the medial head of the triceps entered the floor of the cubital tunnel (p < 0.001)5. However, no snapping of the medial head of the triceps was identified in that study. Normally, with flexion of the elbow, the medial head of the triceps4,14 moves the ulnar nerve anteromedially 7.5 millimeters3. We believe that an abnormal medial head of the triceps or an accessory triceps tendon may increase the normal anteromedial displacement of the ulnar nerve or increase compression or irritation of the nerve, or both.
A prominent medial head of the triceps can be congenital or acquired, whereas an accessory tendon suggests a congenital etiology. In the present series, one patient (two limbs; Cases 5L and 5R) was a member of a family with bilateral dislocation of the triceps and ulnar neuropathy in three generations, as previously reported23. This patient was included to emphasize the possibility of an inheritable predisposition. In contrast, several of our patients had well defined muscles and became symptomatic only after they began bodybuilding. Their symptoms could have been related to repetitive flexion and extension of the elbow during weight lifting in combination with increased bulk of the triceps.
Osseous abnormalities on the medial side of the elbow, whether post-traumatic1,7,12,16,18,27 or developmental22,25, also have been associated with dislocation of the triceps, dislocation of the ulnar nerve, or ulnar neuropathy2,10,17. Three of our patients had a cubitus varus deformity as a result of a previous supracondylar fracture. In fact, the medial head of the triceps appeared to be of normal size in the two limbs with cubitus varus that were treated operatively, which highlights the importance of the osseous malalignment. We believe that cubitus varus alters the line of pull of the triceps and may contribute to dislocation of the medial head of the triceps with dislocation of the ulnar nerve.
Although the natural history of snapping of the triceps is not known, our current treatment of this clinical entity depends on the severity of the symptoms. Snapping that is detected incidentally and painless snapping without symptoms related to the ulnar nerve do not warrant treatment. Patients who have only mild, intermittent, or positional symptoms can usually be managed effectively with non-operative measures, such as avoidance of activities that involve repetitive flexion and extension of the elbow. While non-operative treatment may decrease symptoms, it usually does not eliminate the underlying snapping. Patients who have persistent painful snapping or symptoms related to the ulnar nerve despite a trial of non-operative therapy should be considered for operative management. Although we do not have an adequate population sample to determine the prevalence of snapping of the triceps, the frequency with which this entity was found incidentally suggests that it is not uncommon. As demonstrated by the present study, most patients are not sufficiently symptomatic to necessitate operative intervention.
In conclusion, our operative procedures addressed the specific underlying pathoanatomy; all six patients (seven limbs) who were managed operatively were doing well at the time of follow-up. The elbow should be flexed and extended intraoperatively to document dislocating structures and to understand the dynamic nature of the snapping with regard to the medial head of the triceps, the ulnar nerve, and the medial epicondyle. The operation should be directed at correction of the snapping and elimination of the compression or irritation of the nerve, if present.
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