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ORIGINAL ARTICLE
Muscle Activation Patterns in Snapping Triceps Syndrome Andrea J. Boon, MD, Robert J. Spinner, MD, Kathie A. Bernhardt, BS, Scott R. Ross, DO, DC, Kenton R. Kaufman, PhD ABSTRACT. Boon AJ, Spinner RJ, Bernhardt KA, Ross SR, Kaufman KR. Muscle activation patterns in snapping triceps syndrome. Arch Phys Med Rehabil 2007;88:239-42. Objective: To compare the muscle activation pattern in subjects with and without “snapping triceps syndrome” (dislocation of the medial head of the triceps and ulnar nerve over the medial epicondyle). Design: Controlled study. Setting: Biomechanics laboratory. Participants: Eight male subjects (9 elbows), with symptomatic snapping triceps and 9 male controls. Interventions: Not applicable. Main Outcome Measures: Activation pattern of the 3 triceps heads during active elbow extension at 0°, 45°, 70°, 90°, and 115° of flexion, recorded by fine-wire electromyography. Results: There were no significant differences between subjects and controls in the firing pattern of the triceps heads. The medial head fired first in 6 of 9 symptomatic elbows and in 7 of 9 controls at 90° of flexion, and in 6 of 9 elbows of both subjects and controls at 115° of flexion, positions where snapping typically occurs. There was no significant difference between the groups as to how often the medial head fired maximally. Conclusions: This study suggests the firing pattern of the triceps heads may not contribute to the pathogenesis of this syndrome. Rather, the authors believe the anatomic position of the medial head causes it to dislocate over the medial epicondyle, often resulting in ulnar neuritis. Key Words: Electromyography; Dislocations; Rehabilitation; Ulnar nerve. © 2007 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation NAPPING TRICEPS SYNDROME is a dynamic condition in which a portion of the medial head of the triceps S dislocates over the medial epicondyle, typically along with the ulnar nerve. It occurs as the elbow is either fully flexed from an extended position or extended from a fully flexed position. Symptomatic patients may complain of medial elbow pain, snapping, and/or ulnar neuritis. It most often is detected in men, many of whom participate in weight lifting, but also in those who perform pushups.1
From the Departments of Physical Medicine and Rehabilitation (Boon), Neurology (Boon), Neurosurgery (Spinner), Orthopedic Surgery (Spinner, Bernhardt, Kaufman), Mayo Clinic, Rochester, MN; and Springs Rehabilitation, Colorado Springs, CO (Ross). Supported by the Mayo Foundation. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated. Correspondence to Kenton R. Kaufman, PhD, Motion Analysis Laboratory, Mayo Clinic, Charlton North L-110L, 200 First St SW, Rochester, MN 55905, e-mail: [email protected]. Reprints are not available from the author. 0003-9993/07/8802-10655$32.00/0 doi:10.1016/j.apmr.2006.11.011
Snapping triceps was first described in 1970 by Rolfsen.2 A patient was found to have snapping of a portion of the medial triceps after 2 previous ulnar nerve transpositions had been done for symptomatic ulnar nerve dislocation; at the third operation persistent snapping was shown to be due to dislocation of the medial triceps over the medial epicondyle.2 Several case reports of snapping triceps were then reported, including early ones by Hayashi et al3 and Dreyfuss and Kessler4, followed by a relatively large series by Spinner and Goldner.1 Based on the incidental finding of snapping triceps in combination with dislocating ulnar nerves in asymptomatic persons, Spinner and Goldner postulated that an unknown subset of patients previously identified to have an “isolated” dislocating ulnar nerve (estimated to be approximately 4% by Childress5 in his examination of 1000 healthy subjects) may in fact have (a previously unrecognized) dislocation of the medial triceps as well as the ulnar nerve. Snapping triceps and a dislocating ulnar nerve may be suspected by history but is diagnosed on physical examination or radiographically. Two snapping structures may be shown to be snapping over the medial epicondyle with passive and active elbow flexion: the ulnar nerve typically dislocates at 90° and the medial head of the triceps occurs most frequently at about 115°.1 When the condition is suspected clinically but is not diagnosed, magnetic resonance imaging (MRI) performed with the elbow fully extended and fully flexed or dynamic ultrasonography may show the snapping structures.6 Although this condition is still not widely known or commonly recognized, snapping of the medial head of the triceps is becoming increasingly diagnosed, particularly by surgeons specializing in treatment of elbow disorders.1 Recognizing this condition is important because if ulnar nerve transposition is performed without correction of the snapping medial head of the triceps, the surgery is often unsuccessful.7 Several possible causes for the snapping have been proposed, including anatomic variation of the triceps muscle (congenital or developmental) and/or the bony structures around the elbow (posttraumatic).2-4,8 These causes may include a variant (ie, accessory) triceps muscle belly or tendon, hypertrophied muscle, or any condition in which the triceps line of pull is displaced medially (eg, cubitus varus deformity). We wondered whether an abnormal firing pattern of the different components of the triceps muscle may exist. What has not been well defined is the electromyographic firing pattern of the major muscles of the elbow during activities, and how the firing pattern of these muscles might differ between people who dislocate their triceps and those who do not. It is possible that early firing of the medial head of the triceps could result in an imbalance of forces at the elbow, with medial dislocation of that portion of the muscle, dislocating the ulnar nerve with it. This would be somewhat analogous to the knee, where inhibition of the vastus medialis obliquus results in a biomechanic disadvantage and has been implicated as a cause of patellofemoral pain.9-11 The goal of this study was to use fine-wire electrodes, which permit selective electromyographic recording during kinesiologic studies,12-14 to examine and quantify the electromyoArch Phys Med Rehabil Vol 88, February 2007
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graphic activity of the triceps during voluntary isometric elbow extension in subjects with and without known dislocation (snapping) of the medial portion of the triceps. The authors hypothesized that people with snapping triceps have a pattern of muscle firing during elbow motion that differs from that of the normative population. If proven, this information could then be used to determine if muscle retraining techniques could be employed to establish normal muscle firing patterns and restore muscle balance, in order to prevent muscle dislocation and snapping, and thereby avoid surgical intervention. METHODS The study was approved by the authors’ institutional internal review board. All subjects were informed of the goals of the study and signed a written informed consent before participating. Eight subjects with symptomatic snapping triceps (a total of 9 elbows) were enrolled. Some had presented for definitive surgical management and were studied prior to undergoing surgical correction; the others had elected not to pursue surgery at that point in time. Nine controls were recruited by advertising within the authors’ institution. All subjects received a nominal payment for participation. Inclusion criteria for the subjects with snapping triceps included a history of painful snapping at the medial aspect of the elbow with evidence of medial dislocation of both the ulnar nerve and a portion of the medial head of the triceps muscle with active or passive elbow flexion and extension. Exclusion criteria for both subjects and controls included history of corrective elbow surgery such as an ulnar nerve transposition or valgus osteotomy, and/or prior elbow or forearm trauma or surgery. Control subjects were also excluded if they had a history of elbow snapping, elbow pain, or tendonitis in the past year, congenital or acquired bony elbow deformities, history of ulnar nerve symptoms or neuropathy, or if they had evidence of snapping of soft tissue across the medial epicondyle on physical examination. A history and physical examination were performed at the time of study entry, including demographic data, joint range of motion, elbow varus and valgus angle, elbow stability, upper-extremity neurologic examination (sensory, motor, and reflex testing), and ulnar nerve and triceps muscle stability. Using standard techniques, we placed fine-wire indwelling 30mm, 27 gauge electromyography electrodesa in the medial, lateral, and long head of the triceps, and in the anconeus.12 Electrode placement was confirmed using electromyographic and muscle activation, and all leads were secured using adhesive tape. For data reduction, we determined the electromyographic activity of each muscle’s maximal voluntary contraction (MVC) by subtracting the resting signal (recorded with the subject seated) from the peak 3-second electromyographic activity recorded for that muscle during 3 voluntary 3-second maximal isometric contractions at 90° of elbow flexion.12,15 Subjects were tested in a seated position, and for added stabilization during elbow extension testing, an investigator provided added support to the chair. After confirmation of proper placement of the fine wires, the subject was seated at the testing table, and background resting muscle electromyographic activity was recorded for a 3-second period of relaxation. Next the maximal isometric muscle electromyographic activity (recorded as peak 3-second electromyographic signal) was elicited with a full effort elbow extension at 5 positions: 0° (which equates to full extension), 45°, 70°, 90°, and 115° of elbow flexion. We determined the angle of flexion for each testing position using a hand-held goniometer,b with the hinge of the goniometer placed over the lateral epiArch Phys Med Rehabil Vol 88, February 2007
condyle of the humerus, the proximal arm aligned with the lateral midline of the humerus, using the acromion process as reference, and the distal arm aligned with the lateral midline of the radius. All testing was carried out with the subject in a seated position, resting the testing hand on a securely mounted lever arm. Data collection was initiated and then the subject was told to start pushing as hard as possible, and to continue pushing until instructed to stop. Data were recorded for 3 seconds. Subjects completed one set of 3 consecutive repetitions of isometric elbow extension (with each repetition separated by 30 seconds of rest) at each of the 5 testing positions while electromyographic activity was recorded from the 3 heads of the triceps and the anconeus. We collected electromyographic signals at 2000Hz using an MA300 electromyography systemc and a custom software data acquisition program.d Signals were processed using a custom computer program.e All data were rectified and filtered using a 6Hz fourth-order Butterworth low-pass filter. All electrodes provided an alternating current-coupled, low-gain, high common mode rejection ratio (⫻20 gain, 110dB min) preamplifier with a double differential input and built-in filter and were connected to an amplifier providing 20 to 2000Hz bandwidth detection. The amplifier was connected to the computer by a single thin, flexible, 2.3mm (3/32in) diameter coaxial cable. For each test motion, the mean peak 3-second electromyographic activity in the 4 target muscles was generated by collecting electromyographic signals during each test motion, and normalizing as described above, to generate a percent MVC. The primary variables of interest were the peak electromyographic activity recorded separately for the anconeus and the 3 heads of the triceps, and the pattern of electromyographic muscle recruitment, during isometric elbow extension. The data were stripped of identifiers prior to data analysis to blind the primary investigator to the subject’s group. The 3 trials at each of the 5 positions of extension were averaged and the processed data was graphed for each muscle using an Excelf spreadsheet, with time on the x axis and percentage of MVC electromyographic activity on the y axis (fig 1). The muscle (or muscles) that fired first during active extension at each position was identified from the graph (see fig 1), and the peak activity of each muscle was quantified, as maximal (50%– 100% MVC), moderate (25%–50% MVC), or minimal (⬍25% MVC) activation. The Fisher exact test was used to evaluate differences in muscle firing between the symptomatic subject and control population, using a significance level of .05.
Fig 1. Fine-wire electromyographic recordings from the 3 heads of the triceps during active isometric elbow extension at 45° of flexion.
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index, and whether or not they performed weight lifting as a part of their usual daily routine. This was felt to decrease the chance that a difference in muscle firing pattern might be detected due to differences between muscle bulk in the symptomatic subjects and controls. Nonetheless, we did not specifically try to quantitate the size and anatomic position of the 3 heads of the triceps, using ultrasound or magnetic resonance imaging, and it is theoretically possible that the symptomatic subjects had significantly different triceps muscle bulk, thereby predisposing them to medial triceps dislocation.
Fig 2. Number of participants where each head of the triceps fired first during resisted elbow extension at 5 different positions of flexion, in symptomatic subjects (S) and controls (C) (nⴝ9 for each group).
RESULTS Eight otherwise healthy male subjects with symptomatic snapping of the medial head of the triceps and 9 healthy male controls were enrolled. One of the subjects had bilateral symptoms and therefore both elbows were studied. The subjects ranged in age from 23 to 41 years (mean, 29y) and the controls from 28 to 40 years (mean, 26y). Body mass index for the 8 subjects ranged from 22 to 35kg/m2 (mean, 26kg/m2) and for the 9 controls from 21 to 31kg/m2 (mean, 25kg/m2). Seven of the 8 subjects (8/9 symptomatic elbows) and 7 of the 9 controls lifted weights as part of their usual exercise routine. The data for each head of the triceps (with regard to initial firing and maximal firing) for the 5 different test positions are presented in figures 2 and 3. In this small group of subjects and controls, using the Fisher exact test to compare each group, there was no significant difference in the firing pattern of the 3 different heads of the triceps between subjects or controls at any of the 5 testing positions. Data from the anconeus were unreliable due to a flat line recording in several subjects; this was thought to be due to the subject’s elbow resting on the table and displacing the fine-wire electrodes. As a result, the anconeus data were not included in the final analysis due to insufficient numbers of subjects and controls with valid data. DISCUSSION The relative contribution of anatomic factors and abnormal firing patterns of the medial head to the other heads of the triceps in patients with snapping triceps is unknown. This study tried to address this lack of information. The finding that the firing pattern of subjects with and without symptomatic snapping of the triceps are similar suggests that abnormal muscle activation may not be the underlying cause for this syndrome. Because this condition is commonly found in weight lifters, who are predominantly male, we believe that the increased bulk of the medial head of the triceps results in relative displacement of the longitudinal axis of the hypertrophied muscle, more medially, predisposing to dislocation of that portion of the muscle over the medial epicondyle during elbow flexion. Our findings suggest there may be little role for neuromuscular re-education as a means of conservative treatment. We chose to study only male subjects, because this clinical problem is typically seen in men, and due to the low number of subjects, it was felt that the population would be more homogeneous if men only were included. The symptomatic subjects and controls were fairly well matched for age, body mass
Study Limitations This study is significantly limited by the small numbers of subjects and controls—snapping triceps syndrome is a relatively rare disorder and the authors wished to obtain preliminary data on the muscle firing patterns of subjects and controls to help determine whether more extensive research in this area should be pursued. Although the Fisher exact test is a valid statistical test to compare the 2 groups, obviously a significant difference in muscle firing patterns could have potentially been overlooked due to the small number of subjects and controls. There was not even a trend, however, toward a difference in firing patterns between the 2 groups at any of the 5 positions tested, with the exception of (1) the terminal position (0° of elbow flexion, ie, full extension—which is furthest from the point where snapping typically occurs1), where all 9 patients with snapping triceps but only 6 controls fired the medial head first, and (2) the position of 45° of flexion, where 5 controls but only 3 subjects fired the long head first, suggesting that muscle firing patterns are not the primary problem in this syndrome. It may be significant that testing was performed during isometric contraction of the triceps, albeit at 5 different elbow positions, and therefore, the dynamic component of the muscle firing pattern could not be captured; furthermore, it is possible that the muscle firing pattern may differ during eccentric and concentric muscle activation. One other limitation to this study is the inability to evaluate the anconeus due to problems with maintaining the fine-wire electrodes in position during testing. The anconeus has not been well studied with regard to pattern of activation in relation to the triceps muscle, either in subjects without pathology (no neuromusculoskeletal pathology) or in subjects with elbow disorders. Being a small, primarily slowtwitch fiber, uniarticular muscle, with a short lever arm, its most likely primary role is to act as an elbow stabilizer. It is also quite possible that early activation of the anconeus is important in muscular control around the elbow.
Fig 3. Number of participants where each head of the triceps fired maximally during resisted elbow extension at 5 different positions of flexion, in symptomatic subjects (S) and controls (C) (nⴝ9 for each group; in some cases more than 1 head fired maximally at each position).
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CONCLUSIONS This study does not support early or asynchronous firing of 1 head of the triceps as a factor in the development of snapping triceps. We believe that snapping triceps syndrome may be explained by pathoanatomic relationships of the triceps and the ulnar nerve to the medial epicondyle with elbow flexion and extension. Further research in this area may be better directed at the evaluation of firing patterns during dynamic extension and flexion of the elbow, and/or anatomic studies using dynamic imaging, such as ultrasound or functional MRI. References 1. Spinner RJ, Goldner RD. Snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve. Anatomical and dynamic factors. J Bone Joint Surg Am 1998;80:239-47. 2. Rolfsen L. Snapping triceps tendon with ulnar neuritis. Report on a case. Acta Orthop Scand 1970;41:74-6. 3. Hayashi Y, Kojima T, Kohno T. A case of cubital tunnel syndrome caused by the snapping of the medial head of the triceps brachii muscle. J Hand Surg [Am] 1984;9:96-9. 4. Dreyfuss U, Kessler I. Snapping elbow due to dislocation of the medial head of the triceps. A report of two cases. J Bone Joint Surg Br 1978;60:56-7. 5. Childress H. Recurrent ulnar-nerve dislocation at the elbow. J Bone Joint Surg Am 1956;38:978-84. 6. Spinner RJ, Hayden FR Jr, Hipps CT, Goldner RD. Imaging the snapping triceps [published erratum in: AJR Am J Roentgenol 1997;168:133]. AJR Am J Roentgenol 1996;167:1550-1. 7. Spinner RJ, O’Driscoll SW, Jupiter JB, Goldner RD. Unrecognized dislocation of the medial portion of the triceps: another cause of failed ulnar nerve transposition. J Neurosurg 2000; 92:52-7.
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8. Dellon AL. Musculotendinous variations about the medial humeral epicondyle. J Hand Surg [Br] 1986;11:175-81. 9. Cowan SM, Bennell KL, Crossley KM, Hodges PW, McConnell J. Physical therapy alters recruitment of the vasti in patellofemoral pain syndrome. Med Sci Sports Exerc 2002;34:1879-85. 10. Crossley K, Bennell K, Green S, Cowan S, McConnell J. Physical therapy for patellofemoral pain: a randomized, double-blinded, placebo-controlled trial. Am J Sports Med 2002;30:857-65. 11. McConnell J. The physical therapist’s approach to patellofemoral disorders. Clin Sports Med 2002;21:363-87. 12. Basmajian J. A new bipolar indwelling electrode for electromyography. J Appl Physiol 1962;17:849-9. 13. Inman VT, Ralston HJ, Saunders JB, Feinstein B, Wright EW Jr. Relation of human electromyogram to muscular tension. Electroencephalogr Clin Neurophysiol Suppl 1952;4:187-94. 14. Sisto DJ, Jobe FW, Moynes DR, Antonelli DJ. An electromyographic analysis of the elbow in pitching. Am J Sports Med 1987;15:260-3. 15. Kendall FP, McCreary EK, Provance PG. Muscles: testing and function. 4th ed. Baltimore: Lippincott Williams & Wilkins; 1993. Suppliers a. Nicolet Biomedical Inc, 5225 Verona Rd, Madison, WI 53711. b. Lafayette Instrument Co, 3700 Sagamore Pkwy N, Lafayette, IN 47903. c. Motion Lab Systems, 3617 Westwind Blvd, Santa Rosa, CA 95403. d. LabView 6.1; National Instruments, 11500 N Mopac Expwy, Austin, TX 78759-3504. e. Matlab 6.0 software; The MathWorks, 3 Apple Hill Dr, Natick, MA 01760-2098. f. Microsoft Corp, One Microsoft Way, Redmond, WA 98052.
ORIGINAL ARTICLE
Muscle Activation Patterns in Snapping Triceps Syndrome Andrea J. Boon, MD, Robert J. Spinner, MD, Kathie A. Bernhardt, BS, Scott R. Ross, DO, DC, Kenton R. Kaufman, PhD ABSTRACT. Boon AJ, Spinner RJ, Bernhardt KA, Ross SR, Kaufman KR. Muscle activation patterns in snapping triceps syndrome. Arch Phys Med Rehabil 2007;88:239-42. Objective: To compare the muscle activation pattern in subjects with and without “snapping triceps syndrome” (dislocation of the medial head of the triceps and ulnar nerve over the medial epicondyle). Design: Controlled study. Setting: Biomechanics laboratory. Participants: Eight male subjects (9 elbows), with symptomatic snapping triceps and 9 male controls. Interventions: Not applicable. Main Outcome Measures: Activation pattern of the 3 triceps heads during active elbow extension at 0°, 45°, 70°, 90°, and 115° of flexion, recorded by fine-wire electromyography. Results: There were no significant differences between subjects and controls in the firing pattern of the triceps heads. The medial head fired first in 6 of 9 symptomatic elbows and in 7 of 9 controls at 90° of flexion, and in 6 of 9 elbows of both subjects and controls at 115° of flexion, positions where snapping typically occurs. There was no significant difference between the groups as to how often the medial head fired maximally. Conclusions: This study suggests the firing pattern of the triceps heads may not contribute to the pathogenesis of this syndrome. Rather, the authors believe the anatomic position of the medial head causes it to dislocate over the medial epicondyle, often resulting in ulnar neuritis. Key Words: Electromyography; Dislocations; Rehabilitation; Ulnar nerve. © 2007 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation NAPPING TRICEPS SYNDROME is a dynamic condition in which a portion of the medial head of the triceps S dislocates over the medial epicondyle, typically along with the ulnar nerve. It occurs as the elbow is either fully flexed from an extended position or extended from a fully flexed position. Symptomatic patients may complain of medial elbow pain, snapping, and/or ulnar neuritis. It most often is detected in men, many of whom participate in weight lifting, but also in those who perform pushups.1
From the Departments of Physical Medicine and Rehabilitation (Boon), Neurology (Boon), Neurosurgery (Spinner), Orthopedic Surgery (Spinner, Bernhardt, Kaufman), Mayo Clinic, Rochester, MN; and Springs Rehabilitation, Colorado Springs, CO (Ross). Supported by the Mayo Foundation. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated. Correspondence to Kenton R. Kaufman, PhD, Motion Analysis Laboratory, Mayo Clinic, Charlton North L-110L, 200 First St SW, Rochester, MN 55905, e-mail: [email protected]. Reprints are not available from the author. 0003-9993/07/8802-10655$32.00/0 doi:10.1016/j.apmr.2006.11.011
Snapping triceps was first described in 1970 by Rolfsen.2 A patient was found to have snapping of a portion of the medial triceps after 2 previous ulnar nerve transpositions had been done for symptomatic ulnar nerve dislocation; at the third operation persistent snapping was shown to be due to dislocation of the medial triceps over the medial epicondyle.2 Several case reports of snapping triceps were then reported, including early ones by Hayashi et al3 and Dreyfuss and Kessler4, followed by a relatively large series by Spinner and Goldner.1 Based on the incidental finding of snapping triceps in combination with dislocating ulnar nerves in asymptomatic persons, Spinner and Goldner postulated that an unknown subset of patients previously identified to have an “isolated” dislocating ulnar nerve (estimated to be approximately 4% by Childress5 in his examination of 1000 healthy subjects) may in fact have (a previously unrecognized) dislocation of the medial triceps as well as the ulnar nerve. Snapping triceps and a dislocating ulnar nerve may be suspected by history but is diagnosed on physical examination or radiographically. Two snapping structures may be shown to be snapping over the medial epicondyle with passive and active elbow flexion: the ulnar nerve typically dislocates at 90° and the medial head of the triceps occurs most frequently at about 115°.1 When the condition is suspected clinically but is not diagnosed, magnetic resonance imaging (MRI) performed with the elbow fully extended and fully flexed or dynamic ultrasonography may show the snapping structures.6 Although this condition is still not widely known or commonly recognized, snapping of the medial head of the triceps is becoming increasingly diagnosed, particularly by surgeons specializing in treatment of elbow disorders.1 Recognizing this condition is important because if ulnar nerve transposition is performed without correction of the snapping medial head of the triceps, the surgery is often unsuccessful.7 Several possible causes for the snapping have been proposed, including anatomic variation of the triceps muscle (congenital or developmental) and/or the bony structures around the elbow (posttraumatic).2-4,8 These causes may include a variant (ie, accessory) triceps muscle belly or tendon, hypertrophied muscle, or any condition in which the triceps line of pull is displaced medially (eg, cubitus varus deformity). We wondered whether an abnormal firing pattern of the different components of the triceps muscle may exist. What has not been well defined is the electromyographic firing pattern of the major muscles of the elbow during activities, and how the firing pattern of these muscles might differ between people who dislocate their triceps and those who do not. It is possible that early firing of the medial head of the triceps could result in an imbalance of forces at the elbow, with medial dislocation of that portion of the muscle, dislocating the ulnar nerve with it. This would be somewhat analogous to the knee, where inhibition of the vastus medialis obliquus results in a biomechanic disadvantage and has been implicated as a cause of patellofemoral pain.9-11 The goal of this study was to use fine-wire electrodes, which permit selective electromyographic recording during kinesiologic studies,12-14 to examine and quantify the electromyoArch Phys Med Rehabil Vol 88, February 2007
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graphic activity of the triceps during voluntary isometric elbow extension in subjects with and without known dislocation (snapping) of the medial portion of the triceps. The authors hypothesized that people with snapping triceps have a pattern of muscle firing during elbow motion that differs from that of the normative population. If proven, this information could then be used to determine if muscle retraining techniques could be employed to establish normal muscle firing patterns and restore muscle balance, in order to prevent muscle dislocation and snapping, and thereby avoid surgical intervention. METHODS The study was approved by the authors’ institutional internal review board. All subjects were informed of the goals of the study and signed a written informed consent before participating. Eight subjects with symptomatic snapping triceps (a total of 9 elbows) were enrolled. Some had presented for definitive surgical management and were studied prior to undergoing surgical correction; the others had elected not to pursue surgery at that point in time. Nine controls were recruited by advertising within the authors’ institution. All subjects received a nominal payment for participation. Inclusion criteria for the subjects with snapping triceps included a history of painful snapping at the medial aspect of the elbow with evidence of medial dislocation of both the ulnar nerve and a portion of the medial head of the triceps muscle with active or passive elbow flexion and extension. Exclusion criteria for both subjects and controls included history of corrective elbow surgery such as an ulnar nerve transposition or valgus osteotomy, and/or prior elbow or forearm trauma or surgery. Control subjects were also excluded if they had a history of elbow snapping, elbow pain, or tendonitis in the past year, congenital or acquired bony elbow deformities, history of ulnar nerve symptoms or neuropathy, or if they had evidence of snapping of soft tissue across the medial epicondyle on physical examination. A history and physical examination were performed at the time of study entry, including demographic data, joint range of motion, elbow varus and valgus angle, elbow stability, upper-extremity neurologic examination (sensory, motor, and reflex testing), and ulnar nerve and triceps muscle stability. Using standard techniques, we placed fine-wire indwelling 30mm, 27 gauge electromyography electrodesa in the medial, lateral, and long head of the triceps, and in the anconeus.12 Electrode placement was confirmed using electromyographic and muscle activation, and all leads were secured using adhesive tape. For data reduction, we determined the electromyographic activity of each muscle’s maximal voluntary contraction (MVC) by subtracting the resting signal (recorded with the subject seated) from the peak 3-second electromyographic activity recorded for that muscle during 3 voluntary 3-second maximal isometric contractions at 90° of elbow flexion.12,15 Subjects were tested in a seated position, and for added stabilization during elbow extension testing, an investigator provided added support to the chair. After confirmation of proper placement of the fine wires, the subject was seated at the testing table, and background resting muscle electromyographic activity was recorded for a 3-second period of relaxation. Next the maximal isometric muscle electromyographic activity (recorded as peak 3-second electromyographic signal) was elicited with a full effort elbow extension at 5 positions: 0° (which equates to full extension), 45°, 70°, 90°, and 115° of elbow flexion. We determined the angle of flexion for each testing position using a hand-held goniometer,b with the hinge of the goniometer placed over the lateral epiArch Phys Med Rehabil Vol 88, February 2007
condyle of the humerus, the proximal arm aligned with the lateral midline of the humerus, using the acromion process as reference, and the distal arm aligned with the lateral midline of the radius. All testing was carried out with the subject in a seated position, resting the testing hand on a securely mounted lever arm. Data collection was initiated and then the subject was told to start pushing as hard as possible, and to continue pushing until instructed to stop. Data were recorded for 3 seconds. Subjects completed one set of 3 consecutive repetitions of isometric elbow extension (with each repetition separated by 30 seconds of rest) at each of the 5 testing positions while electromyographic activity was recorded from the 3 heads of the triceps and the anconeus. We collected electromyographic signals at 2000Hz using an MA300 electromyography systemc and a custom software data acquisition program.d Signals were processed using a custom computer program.e All data were rectified and filtered using a 6Hz fourth-order Butterworth low-pass filter. All electrodes provided an alternating current-coupled, low-gain, high common mode rejection ratio (⫻20 gain, 110dB min) preamplifier with a double differential input and built-in filter and were connected to an amplifier providing 20 to 2000Hz bandwidth detection. The amplifier was connected to the computer by a single thin, flexible, 2.3mm (3/32in) diameter coaxial cable. For each test motion, the mean peak 3-second electromyographic activity in the 4 target muscles was generated by collecting electromyographic signals during each test motion, and normalizing as described above, to generate a percent MVC. The primary variables of interest were the peak electromyographic activity recorded separately for the anconeus and the 3 heads of the triceps, and the pattern of electromyographic muscle recruitment, during isometric elbow extension. The data were stripped of identifiers prior to data analysis to blind the primary investigator to the subject’s group. The 3 trials at each of the 5 positions of extension were averaged and the processed data was graphed for each muscle using an Excelf spreadsheet, with time on the x axis and percentage of MVC electromyographic activity on the y axis (fig 1). The muscle (or muscles) that fired first during active extension at each position was identified from the graph (see fig 1), and the peak activity of each muscle was quantified, as maximal (50%– 100% MVC), moderate (25%–50% MVC), or minimal (⬍25% MVC) activation. The Fisher exact test was used to evaluate differences in muscle firing between the symptomatic subject and control population, using a significance level of .05.
Fig 1. Fine-wire electromyographic recordings from the 3 heads of the triceps during active isometric elbow extension at 45° of flexion.
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index, and whether or not they performed weight lifting as a part of their usual daily routine. This was felt to decrease the chance that a difference in muscle firing pattern might be detected due to differences between muscle bulk in the symptomatic subjects and controls. Nonetheless, we did not specifically try to quantitate the size and anatomic position of the 3 heads of the triceps, using ultrasound or magnetic resonance imaging, and it is theoretically possible that the symptomatic subjects had significantly different triceps muscle bulk, thereby predisposing them to medial triceps dislocation.
Fig 2. Number of participants where each head of the triceps fired first during resisted elbow extension at 5 different positions of flexion, in symptomatic subjects (S) and controls (C) (nⴝ9 for each group).
RESULTS Eight otherwise healthy male subjects with symptomatic snapping of the medial head of the triceps and 9 healthy male controls were enrolled. One of the subjects had bilateral symptoms and therefore both elbows were studied. The subjects ranged in age from 23 to 41 years (mean, 29y) and the controls from 28 to 40 years (mean, 26y). Body mass index for the 8 subjects ranged from 22 to 35kg/m2 (mean, 26kg/m2) and for the 9 controls from 21 to 31kg/m2 (mean, 25kg/m2). Seven of the 8 subjects (8/9 symptomatic elbows) and 7 of the 9 controls lifted weights as part of their usual exercise routine. The data for each head of the triceps (with regard to initial firing and maximal firing) for the 5 different test positions are presented in figures 2 and 3. In this small group of subjects and controls, using the Fisher exact test to compare each group, there was no significant difference in the firing pattern of the 3 different heads of the triceps between subjects or controls at any of the 5 testing positions. Data from the anconeus were unreliable due to a flat line recording in several subjects; this was thought to be due to the subject’s elbow resting on the table and displacing the fine-wire electrodes. As a result, the anconeus data were not included in the final analysis due to insufficient numbers of subjects and controls with valid data. DISCUSSION The relative contribution of anatomic factors and abnormal firing patterns of the medial head to the other heads of the triceps in patients with snapping triceps is unknown. This study tried to address this lack of information. The finding that the firing pattern of subjects with and without symptomatic snapping of the triceps are similar suggests that abnormal muscle activation may not be the underlying cause for this syndrome. Because this condition is commonly found in weight lifters, who are predominantly male, we believe that the increased bulk of the medial head of the triceps results in relative displacement of the longitudinal axis of the hypertrophied muscle, more medially, predisposing to dislocation of that portion of the muscle over the medial epicondyle during elbow flexion. Our findings suggest there may be little role for neuromuscular re-education as a means of conservative treatment. We chose to study only male subjects, because this clinical problem is typically seen in men, and due to the low number of subjects, it was felt that the population would be more homogeneous if men only were included. The symptomatic subjects and controls were fairly well matched for age, body mass
Study Limitations This study is significantly limited by the small numbers of subjects and controls—snapping triceps syndrome is a relatively rare disorder and the authors wished to obtain preliminary data on the muscle firing patterns of subjects and controls to help determine whether more extensive research in this area should be pursued. Although the Fisher exact test is a valid statistical test to compare the 2 groups, obviously a significant difference in muscle firing patterns could have potentially been overlooked due to the small number of subjects and controls. There was not even a trend, however, toward a difference in firing patterns between the 2 groups at any of the 5 positions tested, with the exception of (1) the terminal position (0° of elbow flexion, ie, full extension—which is furthest from the point where snapping typically occurs1), where all 9 patients with snapping triceps but only 6 controls fired the medial head first, and (2) the position of 45° of flexion, where 5 controls but only 3 subjects fired the long head first, suggesting that muscle firing patterns are not the primary problem in this syndrome. It may be significant that testing was performed during isometric contraction of the triceps, albeit at 5 different elbow positions, and therefore, the dynamic component of the muscle firing pattern could not be captured; furthermore, it is possible that the muscle firing pattern may differ during eccentric and concentric muscle activation. One other limitation to this study is the inability to evaluate the anconeus due to problems with maintaining the fine-wire electrodes in position during testing. The anconeus has not been well studied with regard to pattern of activation in relation to the triceps muscle, either in subjects without pathology (no neuromusculoskeletal pathology) or in subjects with elbow disorders. Being a small, primarily slowtwitch fiber, uniarticular muscle, with a short lever arm, its most likely primary role is to act as an elbow stabilizer. It is also quite possible that early activation of the anconeus is important in muscular control around the elbow.
Fig 3. Number of participants where each head of the triceps fired maximally during resisted elbow extension at 5 different positions of flexion, in symptomatic subjects (S) and controls (C) (nⴝ9 for each group; in some cases more than 1 head fired maximally at each position).
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CONCLUSIONS This study does not support early or asynchronous firing of 1 head of the triceps as a factor in the development of snapping triceps. We believe that snapping triceps syndrome may be explained by pathoanatomic relationships of the triceps and the ulnar nerve to the medial epicondyle with elbow flexion and extension. Further research in this area may be better directed at the evaluation of firing patterns during dynamic extension and flexion of the elbow, and/or anatomic studies using dynamic imaging, such as ultrasound or functional MRI. References 1. Spinner RJ, Goldner RD. Snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve. Anatomical and dynamic factors. J Bone Joint Surg Am 1998;80:239-47. 2. Rolfsen L. Snapping triceps tendon with ulnar neuritis. Report on a case. Acta Orthop Scand 1970;41:74-6. 3. Hayashi Y, Kojima T, Kohno T. A case of cubital tunnel syndrome caused by the snapping of the medial head of the triceps brachii muscle. J Hand Surg [Am] 1984;9:96-9. 4. Dreyfuss U, Kessler I. Snapping elbow due to dislocation of the medial head of the triceps. A report of two cases. J Bone Joint Surg Br 1978;60:56-7. 5. Childress H. Recurrent ulnar-nerve dislocation at the elbow. J Bone Joint Surg Am 1956;38:978-84. 6. Spinner RJ, Hayden FR Jr, Hipps CT, Goldner RD. Imaging the snapping triceps [published erratum in: AJR Am J Roentgenol 1997;168:133]. AJR Am J Roentgenol 1996;167:1550-1. 7. Spinner RJ, O’Driscoll SW, Jupiter JB, Goldner RD. Unrecognized dislocation of the medial portion of the triceps: another cause of failed ulnar nerve transposition. J Neurosurg 2000; 92:52-7.
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