Cubital tunnel syndrome results from compression and traction on the ulnar nerve about the elbow. It is the second most common upper extremity compressive neuropathy,1,2 with an incidence of 25 cases per 100,000 person-years in men and 19 cases per 100,000 person-years in women.3 Patients with cubital tunnel syndrome are more likely to have advanced disease when they seek treatment than patients with carpal tunnel syndrome are.4 Chronic ulnar nerve dysfunction can result in permanent loss of sensation, muscle weakness, and joint contractures. Therefore, timely surgical treatment is important in patients with ulnar nerve dysfunction that is worsening or producing constant symptoms despite nonsurgical treatment. In recent decades, the rate of surgical management of cubital tunnel syndrome has increased in the United States,1 and the rate of surgical management has increased from 31% to 67% in England.2
The ulnar nerve can be compressed at multiple sites about the elbow (Figure 1). Most proximally, the arcade of Struthers is a thickened connective tissue between the medial triceps and the intermuscular septum 6 to 10 cm proximal to the medial epicondyle. Although Tubbs et al5 identified the arcade of Struthers in 86.7% of cadavers, other authors have questioned its existence as a defined structure.6 Posterior to the medial epicondyle and covered by the Osborne ligament, the cubital tunnel proper is the most common site of ulnar nerve compression. The Osborne ligament originates at the medial epicondyle and humeral head of the flexor carpi ulnaris (FCU) and inserts onto the olecranon and the ulnar head of the FCU. The average thickness of the ligament is 0.14 mm, and the average length is 2.2 cm.7 It consists of three layers formed by an elastic myofascial laminar retinaculum.8 Pathologic fusion of these layers may reduce gliding of the ulnar nerve throughout the flexion-extension arc of the elbow.8 The cross-sectional area of the tunnel diminishes by 30% to 41% during elbow flexion as its shape changes from ovoid to trapezoidal.9 The ulnar nerve demonstrates up to 2.2 cm excursion and a maximal strain of 15% during elbow flexion within the cubital tunnel.10 Intraneural pressure is lowest at 40° to 50° of elbow flexion and sharply increases as the elbow flexes >90°.9 An anomalous muscle, the anconeus epitrochlearis, may also compress the ulnar nerve over the cubital tunnel when present. More distally in the forearm, the ulnar nerve can be entrapped on the deep fascia of the FCU, between the two heads of the FCU, and on the fascia of the flexor digitorum superficialis (FDS).
Posttraumatic cubital tunnel syndrome occurs after 1% to 10% of elbow dislocations and after an estimated 12% of distal humerus fractures.11-14 Symptoms may occur at the time of the initial injury, appear immediately after surgery, or develop in a delayed fashion as a result of deformity, swelling, scarring, and thickening of the cubital tunnel.
Paresthesia of the ulnar hand can also result from C8/T1 radicular compression, thoracic outlet syndrome, or ulnar nerve compression within the Guyon canal at the wrist. Medial epicondylitis and ulnohumeral osteoarthritis must be considered in patients with medial elbow pain. Ulnar wrist pain, while often attributable to cubital tunnel syndrome, may result from FCU tendinitis, pisotriquetral arthritis, nonunion of the hook of the hamate, or hypothenar hammer syndrome.
Cubital tunnel syndrome is diagnosed clinically on the basis of patient history and physical examination. Patients experience altered sensation about the volar and dorsal little finger and ring finger that is characteristically exacerbated by prolonged elbow flexion. They may also report hand weakness, difficulty clipping their fingernails, or a loss of coordination during other fine manipulation. Occasionally, pain is experienced along the course of the ulnar nerve from the posteromedial elbow into the ulnar forearm or hand.
Physical examination reveals impaired sensation (quantified by two-point discrimination, vibratory stimulation, or Semmes-Weinstein monofilament testing) in the little and ring fingers. Muscular atrophy is most readily appreciated in the first dorsal interosseous muscle, which normally provides bulk in the first web space (Figure 2). The Wartenberg sign is produced when the little finger cannot be actively adducted as a result of weakness in the ulnar innervated third palmar interosseous muscle and abducts as a result of the ulnar insertion of the extensor digiti quinti (Figure 3). The Froment sign is observed when the patient attempts a key pinch and exhibits obligate thumb interphalangeal joint flexion as the flexor pollicis longus attempts to compensate for weakness of the adductor pollicis. The Jeanne sign occurs when the extensor pollicis longus hyperextends the metacarpophalangeal joint while the patient attempts to adduct the thumb during a key pinch. In patients with more severe ulnar neuropathy, clawhand deformity occurs in the presence of intact extrinsic flexors, loss of lumbrical and interosseous muscles, and passive hyperextensibility of the metacarpophalangeal joints with the wrist in neutral position.
Provocative maneuvers used in the physical examination of patients with irritation of the ulnar nerve include nerve percussion at the retrocondylar groove and the elbow flexion test (the elbow is held in full flexion and the wrist is extended; a positive test reproduces paresthesia and pain).15 The flexion-compression test is performed by means of manual compression over the ulnar nerve posterior to the medial epicondyle during elbow flexion. In the scratch collapse test, the examiner lightly scratches a patient’s skin over the presumed area of nerve compression while the patient sustains resisted external rotation. Allodynia caused by compression neuropathy is thought to impart a brief loss of muscle resistance after the stimulation, resulting in the subsequent collapse of the extremity under resistance. Cheng et al16 found higher sensitivity when using the scratch collapse test than when using both nerve percussion and the flexion-compression test for cubital tunnel syndrome. However, Makanji et al17 found less sensitivity and more variability among examiners in detecting patients with cubital tunnel syndrome using the scratch collapse test, compared with other examination maneuvers. In our practice, we do not rely on the scratch collapse test to diagnose nerve compression.
Ulnar nerve stability is assessed by placing a finger posterior to the medial epicondyle to determine whether the nerve subluxates, perches, or remains stable throughout elbow flexion.18 Ulnar nerve hypermobility has been found in 37% of elbows in adults.18 Although nerve hypermobility was not found to be associated with symptomatic cubital tunnel syndrome, it should be assessed before surgery because the presence of a hypermobile nerve in a patient with cubital tunnel symptoms may lead the surgeon to consider an alternative to simple in situ decompression.18
Electrodiagnostic studies may inform but do not establish the diagnosis of cubital tunnel syndrome. Electrodiagnostic criteria for ulnar neuropathy are a decrease in absolute conduction velocity to <50 m/s or a relative drop in conduction velocity of ≥10 m/s across a measured interval around the elbow. False-negative electrodiagnostic data can result from variable compression of ulnar nerve fascicles and near normal conduction of unaffected large nerve fibers during testing.19 Diagnostic error is also attributable to variable elbow position, skin temperature, and soft-tissue bulk about the elbow.
Dellon20 and McGowan21 each developed classifications of cubital tunnel syndrome severity that are commonly referenced. According to the modified McGowan and Dellon system, type 1 or mild disease produces subjective sensory symptoms without objective loss of two-point sensibility or muscular atrophy. Patients with weakness on pinch and grip without atrophy are classified as having Dellon type 2 or McGowan type 2A disease. Patients with McGowan type 2B disease demonstrate atrophy and intrinsic muscle strength ≤3 on a five-point scale. Severe cubital tunnel syndrome is marked by profound muscular atrophy and sensory disturbance (McGowan type 3) and weakness that prohibits active finger crossing (Dellon type 3).
Initial nonsurgical management is indicated in patients with mild and possibly moderate cubital tunnel syndrome.22 Splint options range from rolled towels placed in the antecubital fossa and secured with an elastic bandage to rigid thermoplastic custom-fit orthoses that reduce compressive and tensile pressure on the ulnar nerve by limiting elbow flexion.9 Patients are instructed to avoid direct pressure over the medial aspect of the elbow, repetitive triceps strengthening exercises, and prolonged rest in elbow flexion.
Shah et al23 reported that 88% of patients with mild or moderate (Dellon type 1 or 2) cubital tunnel syndrome responded to activity modification and the use of rigid night splints. Svernlöv et al24 found that 90% of patients with mild to moderate cubital tunnel symptoms (most patients had normal electrodiagnostic testing) improved with nonsurgical treatment. In that study, 10% of patients had proceeded to surgical intervention at 6 months. The addition of nighttime splinting or nerve glide exercises to patient education alone did not change outcomes in this randomized trial. Dellon et al22 calculated that patients with mild cubital tunnel syndrome had a 21% probability of requiring surgery, patients with moderate disease had a 33% probability of requiring surgery, and patients with severe disease had a 66% probability of requiring surgery. The authors of that study recommended that nonsurgical treatment be reserved only for patients with mild cubital tunnel syndrome. We routinely offer surgical treatment to patients with impaired two-point sensibility and/or muscle atrophy because we think that ongoing nerve compression results in intrinsic nerve damage and loss of muscle that gradually becomes increasingly recalcitrant to treatment.
Surgical management is appropriate when nonsurgical intervention is unsuccessful or in patients with advanced cubital tunnel syndrome. The most common surgical interventions are simple decompression, medial epicondylectomy, and anterior transposition (subcutaneous, intramuscular, or submuscular). In the past two decades, a growing preference for simple decompression has emerged.1
In Situ Decompression
In situ decompression consists of releasing the fascial structures superficial to the ulnar nerve along the medial aspect of the elbow. In the open technique, a 4-cm incision is made midway between the olecranon and medial epicondyle, whereas endoscopic decompression can be accomplished through an incision as small as 2 cm25 (Figure 4). The Osborne ligament and the superficial and deep fascia of the FCU are released distally while the fascia between the medial triceps and medial intermuscular septum is released proximally. This technique typically results in decompression approximately 6 cm proximal and distal to the medial epicondyle. Circumferential dissection of the nerve is avoided to minimize devascularization and to avoid creating hypermobility of the nerve. Early motion is allowed after open and endoscopic decompression.
The endoscopic technique for ulnar nerve decompression, first described in 1995 by Tsai et al,26 continues to evolve. Current instrumentation allows total decompression of ≤30 cm.25 Nonrandomized studies have demonstrated similar ultimate neurologic recovery and satisfaction rates between open and endoscopic decompression.27 In those studies, the potential advantages of endoscopic release included reduced early postoperative pain, earlier return to work, and diminished peri-incisional paresthesia.
In situ decompression is associated with concern for persistent symptoms secondary to continued tension and instability of the nerve.28,29 However, numerous randomized controlled trials have demonstrated outcomes equivalent to those of ulnar nerve transposition.30,31 Whether to perform simple decompression of the hypermobile ulnar nerve (a nerve that moves onto or over the medial epicondyle during flexion of the elbow) is unclear. Most surgeons recommend transposition or epicondylectomy in patients with a hypermobile nerve, and the authors of most published randomized controlled series have performed transposition in patients with a hypermobile nerve, considering it a contraindication to in situ decompression. In two trials in which patients with hypermobile nerves were explicitly treated with decompression alone, nerve stability did not influence surgical outcomes.30,32 In our practice, patients with a hypermobile ulnar nerve are treated with epicondylectomy or transposition and not with in situ decompression.
In our experience, open in situ decompression has been a successful intervention in patients with a stable ulnar nerve but is associated with a higher percentage of early recurrence requiring revision, compared with anterior transposition or medial epicondylectomy. At our institution, 19% of patients (44 of 231) who have undergone in situ decompression have required revision for either persistent or recurrent symptoms.33 This revision rate contrasts with data published by Song et al,34 who reported only one revision transposition after 39 primary decompressions. Despite a low revision rate, patients in the study by Song et al34 frequently experienced persistent symptoms. Nearly half the patients showed either no change in two-point discrimination or slight worsening at 1 year, with patient-reported outcomes indicating mild improvement and persistent symptoms (preoperative carpal tunnel questionnaire symptom score of 2.7 compared with 1.9 at 1 year postoperatively).
In the 1950s, King and Morgan35 described medial epicondylectomy as an option for the management of cubital tunnel syndrome. Complete epicondylectomy has resulted in persistent elbow pain and iatrogenic elbow instability. Therefore, the contemporary surgical technique involves decompressing the ulnar nerve and then performing an oblique osteotomy between the sagittal and coronal planes of the medial epicondyle, taking care to preserve the insertion of the medial collateral ligament and repair the periosteum to prevent perineural scarring.36 This technique promotes anterior translation of the ulnar nerve over the smooth osteotomized medial aspect of the elbow, thus reducing neural strain more than in situ decompression does.35 O’Driscoll et al37 determined that removal of >19% of the medial epicondyle compromises the anterior band of the medial collateral ligament. They reported acceptable outcomes in a series of 52 patients treated with limited oblique epicondylectomy; 1 patient had postoperative flexion contracture, and 3 patients had residual medial elbow pain. We see postoperative elbow pain as the primary concern with modern epicondylectomy. However, patients at our institution have experienced largely positive results with this technique (59% excellent, 34% good).36 In our practice, this technique is most advantageous for the management of a hypermobile ulnar nerve in thin patients, in whom we would otherwise perform submuscular transposition because of the limited subcutaneous fat. Additionally, epicondylectomy can be performed in patients with vascular pathology and a subluxating ulnar nerve because it avoids the potential for iatrogenic devascularization of the ulnar nerve that is associated with transposition surgery.
Submuscular, Intramuscular, or Subcutaneous Transposition
Anterior transposition of the ulnar nerve relieves both nerve compression and strain by moving the ulnar nerve anterior to the ulnohumeral axis. The procedure begins with decompression of the nerve and includes circumferential dissection of the nerve to allow for transposition. We preserve the inferior ulnar collateral artery and maintain longitudinal vessels with the nerve in the arm (Figure 5). After the nerve is fully mobilized and the medial intermuscular septum is excised, the nerve is transposed anteriorly and secured with subcutaneous tissue, placed anterior to a fascial sling, or placed within or beneath the flexor pronator mass (Figure 6). Submuscular transposition requires release of the entire flexor pronator mass and subsequent repair over the nerve to create a direct, well-vascularized course for the ulnar nerve (Figure 7). Generally, submuscular transposition is reserved for either very thin patients, in whom a subcutaneously transposed ulnar nerve would remain prominent, or patients with advanced disease, in whom the technique offers the opportunity to address the ulnar nerve as definitively as possible in one procedure. In practice, submuscular transposition is a highly effective procedure for patients with advanced disease.38 However, it increases surgical time and involves greater surgical morbidity. Surgical wound complications are more likely after transposition surgery than after in situ decompression. Several series have identified increased rates of deep infection (9% to 14% versus zero to 3%) and more frequent loss of sensation around the incision (19% versus 3%)30,37 after transposition, compared with in situ decompression. Furthermore, circumferential dissection of the ulnar nerve can, in rare instances, result in a catastrophic loss of nerve function in patients with vascular pathology.
Comparison of Surgical Techniques
Over the last decade, several randomized controlled trials have compared outcomes of popular surgical techniques. Biggs and Curtis31 compared in situ decompression to submuscular transposition in a randomized controlled trial in which 44 patients were enrolled. Both procedures were equally effective in providing clinical improvement at 1 year. Only one patient did not improve clinically, and no patients had worse neurologic scores postoperatively. In this study, 45% of the patients who underwent transposition and 57% of the patients who underwent decompression improved by one McGowan grade. The two groups did not differ with regard to neurologic recovery.
Bartels et al30 compared in situ decompression to subcutaneous transposition by randomizing 152 patients in whom cubital tunnel syndrome was identified and confirmed electrodiagnostically to undergo one of these two procedures. Outcomes were assessed at 1 year. No patients with traumatic cubital tunnel syndrome were included in the study. In this study, unlike the other randomized controlled trials, hypermobility of the nerve was not an exclusion criterion for in situ decompression. The outcomes were assessed by clinical examination and by patient-reported scores on the Medical Outcomes Study 36-Item Short Form and the McGill Pain Questionnaire. At 1 year, 48% of patients who underwent simple decompression and 60% of patients who underwent anterior transposition were free of signs and symptoms of cubital tunnel syndrome. The data indicated ongoing improvement from the 6-week follow-up, when 16% and 22% of patients, respectively, were symptom-free. Surgical time was longer in the anterior transposition group (31 minutes versus 14 minutes), and complications (primarily loss of sensibility around the surgical incision) were more frequent after transposition, compared with decompression (31% versus 10%). Of the 75 patients who underwent decompression, 20 patients had hypermobile ulnar nerves, with the nerve fully dislocating over the epicondyle in 8 patients. Although ulnar nerve hypermobility did not affect the outcome of decompression, 18 surgical procedures overall were unsuccessful in this trial.
Gervasio et al38 randomized patients with severe cubital tunnel syndrome (Dellon type 3) to undergo in situ decompression or submuscular transposition. Patients with hypermobile ulnar nerves were excluded from the study. No difference in clinical or electrophysiologic outcomes was noted at 4-year follow-up for the 70 enrolled patients; 54% of the simple decompression group and 51% of the transposition group had excellent outcomes.
Nabhan et al39 randomized 66 patients to either subcutaneous anterior transposition or in situ decompression. Final clinical and electrophysiological outcomes revealed no substantial differences between the two treatment groups. The report of this trial is limited by a lack of detailed description of the methodologies used and clinical outcomes obtained.
Geutjens et al40 randomized patients to either medial epicondylectomy or anterior transposition (25 and 22 elbows, respectively). Clinical measures and nerve conduction velocity studies demonstrated no difference between these treatments at a minimum of 1 year postoperatively. In the medial epicondylectomy group, 23 of 25 patients stated they would undergo the procedure again, compared with 15 of 22 patients in the anterior transposition group. On the basis of the data, the authors concluded that patients who underwent medial epicondylectomy were more satisfied than those who underwent anterior transposition.
Brauer and Graham41 performed a decision analysis in which they compared cubital tunnel surgery techniques using the previously mentioned randomized controlled studies. They recommended in situ decompression as a primary surgical procedure for patients with moderate to severe ulnar nerve compression at the cubital tunnel. Submuscular transposition was recommended as a salvage procedure for patients with persistent symptoms. Using this model, if 60% of patients who underwent in situ decompressions required revision surgery, the authors of the study would still recommend in situ decompression as an index procedure because of the difference between the utility (expected positive outcomes) of the procedures and their disutility (possible complications). This model did not take into account recent data suggesting inferior outcomes after revision surgery.32
Management of Posttraumatic Cubital Tunnel Syndrome
Shin and Ring42 suggested that patients with posttraumatic cubital tunnel symptoms do not respond well to nonsurgical treatment. Surgery in patients with posttraumatic cubital tunnel syndrome has been associated with less chance of complete symptom resolution and higher rates of revision surgery, compared with atraumatic cubital tunnel syndrome.33,42 McKee et al43 reported on anterior transposition in 20 patients (21 elbows) with posttraumatic cubital tunnel syndrome after distal humerus fracture, olecranon fracture, or elbow dislocation. The patients had varied degrees of preoperative ulnar nerve dysfunction, with 4 elbows classified as McGowan type 1, 7 elbows classified as McGowan type 2, and 10 elbows classified as McGowan type 3. For 16 of 21 elbows (76%), the patients reported being highly satisfied with the return of intrinsic muscle strength after undergoing treatment of moderate or severe cubital tunnel syndrome. Although highly satisfied, 95% of patients still reported experiencing limitation in the use of their arm. In our practice, we counsel patients with posttraumatic cubital tunnel syndrome about the increased chance of persistent symptoms after treatment, and we prefer to perform transposition of the ulnar nerve instead of in situ decompression in these patients.
Revision and Salvage Procedures
Revision Cubital Tunnel Surgery
In some patients, cubital tunnel surgery will inadequately alleviate symptoms. Possible causes of unsuccessful surgical treatment that could be improved by revision surgery include persistent nerve tension and incomplete decompression. Alternatively, a poor response to primary surgery may be attributable to chronic compression resulting in recalcitrant nerve damage or more general neuropathic changes, both of which are unlikely to be improved by secondary surgery. Revision surgery is technically demanding because of perineural scarring. Regardless of the index procedure, submuscular transposition is the most commonly recommended revision technique.44 However, some surgeons will not change the position of the ulnar nerve during revision surgery if an obvious area of compression can be identified and relieved.
Our approach to revision surgery includes extending the incisions proximal and distal to the prior incisions. After the skin incisions are made, our first goal is to identify the ulnar nerve proximal to the area of prior dissection. The nerve is carefully dissected from the surrounding scar from proximal to distal. In patients with severe scarring, we will combine this dissection with meticulous dissection from distal to proximal, ending in the area of maximal adhesions. The key is to avoid blind dissection through a scarred surgical bed without visualization of the nerve because doing so would increase the risk of iatrogenic nerve injury.
Patients who undergo revision cubital tunnel surgery typically do not achieve outcomes comparable to those of patients undergoing primary surgery. In a recent study, Aleem et al32 retrospectively assessed 28 patients requiring revision cubital tunnel surgery and compared outcomes with those of matched control patients undergoing primary cubital tunnel surgery. The two groups were matched by demographic data, results of electrodiagnostic studies, and McGowan grading at the time of index surgery. At the time of follow-up, the revision group experienced more residual symptoms and poorer Levine-Katz and Patient-Rated Elbow Evaluation scores. After revision surgery, patients more frequently demonstrated loss of elbow extension, residual ulnar nerve tenderness, weaker key pinch, increased two-point discrimination, and persistent Wartenberg signs, compared with control patients. Although 79% of patients who underwent revision surgery reported subjective symptomatic relief, only 25% improved by at least one McGowan grade, compared with 64% in the control group. In series from separate institutions, 21% to 25% of patients had either no change in McGowan grade or a worsened McGowan grade after revision ulnar nerve surgery.32,45 A described adjunct to revision cubital tunnel surgery has included wrapping the nerve in vein or collagen matrix. In a study of 17 patients, saphenous vein wrapping produced positive functional improvement and limited donor morbidity in patients undergoing revision cubital tunnel surgery; however, widespread adoption of this technique has not yet occurred.46 Currently, when discussing revision cubital tunnel surgery, we explain to patients that complete resolution of symptoms is unlikely. We cautiously note that many patients report subjective improvement but counsel patients that increased symptoms may be experienced after the additional surgery.
Salvage Procedures for the Management of Ulnar Nerve Dysfunction
In patients with persistent ulnar nerve dysfunction after adequate surgical treatment and in patients with end-stage disease in whom nerve recovery is unlikely to occur, salvage options are considered. Tendon and nerve transfers can correct flexible claw deformity and improve pinch strength. Claw correction is obtained by performing a tendon transfer using FDS slips harvested 2 cm proximal to their insertion site, routed through the lumbrical canal, and attached to the lateral bands. Alternatively, FDS tendon slips can be harvested at the same site, routed proximal to the A1 pulley, and sewn back on each other (Figure 8). One FDS slip is harvested per finger. This transfer reliably produces a mild flexion contracture of the metacarpophalangeal joints that both improves appearance and gives the extensor digitorum communis and extensor digiti minimi tendons the mechanical advantage to actively extend the proximal interphalangeal joints. Pinch strength is lost when the ulnar innervated adductor pollicis weakens. An extensor carpi radialis brevis tendon or FDS tendon can be used to perform an adductorplasty. Finally, flexor digitorum profundus tendons can be sutured side-to-side, allowing for composite function to improve little finger distal interphalangeal flexion weakness.
Nerve transfer can also be considered as a salvage method. The transfer of the pronator quadratus branch of the anterior interosseous nerve to the deep motor branch of the ulnar nerve was developed in the early 1990s.47 Although only preliminary results are available, one retrospective chart review found ulnar motor regeneration in all eight patients studied.47
Cubital tunnel syndrome is a common entrapment neuropathy of the upper extremity. Most patients with mild and moderate symptoms should undergo a trial of nonsurgical treatment. Surgical intervention produces good, yet imperfect, outcomes independent of technique. The effects of nerve hypermobility and cubital tunnel syndrome etiology (posttraumatic versus idiopathic) on the outcomes of surgical treatment remain to be determined. Although no consensus has been reached on the preferred technique for the surgical management of cubital tunnel syndrome, we consider both the rate of revision surgery and the relative surgical morbidity of each procedure when discussing surgical management with patients. Revision cubital tunnel surgery offers the possibility of improvement in patients with a correctable reason for failure of the index surgical procedure; however, revision surgery should be undertaken only after careful consideration of the risks and benefits in light of tempered expectations for ultimate nerve recovery.
Evidence-based Medicine: Levels of evidence are described in the table of contents. In this article, references 30, 31, and 38-40 are level I studies. References 1, 6, 16-20, 22-24, 29, and 41 are level II studies. References 27, 32, and 33 are level III studies. References 2-4, 12-15, 28, 34, 36, and 43-47 are level IV studies. References 25 and 26 are level V expert opinion.
References printed in bold type are those published within the past 5 years.
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