Peripheral compressive neuropathies, also known as entrapment neuropathies, may result from mechanical compression of the nerve by an anatomic structure, extrinsic mass, fluid imbalance, or inflammatory process. Beyond a critical threshold of pressure, this compression may result in subsequent sensory and/or motor changes that initially can be aggravating but later can be debilitating if neglected. Axonal function is dependent on factors manufactured in the nerve’s cell body. Blockage of axonal transport at one point makes the entire axon more susceptible to compression. This “double crush” phenomenon is important to understand and is the reason why compromised nerves must be released from all points of compression if they are to recover maximally.
In general, entrapment neuropathies may be characterized by the phases of the disease. In the early phase the nerve is edematous with symptoms that can be clinically silent or, at most, mild and intermittent. Treatment is often conservative with rest and splinting, and symptom resolution is common. In the intermediate phase, symptoms become constant and more intense. Surgical treatment is typically pursued to prevent permanent nerve damage. In the late phase, sensory and motor deficits start to become clinically apparent and potentially disabling. In these late-presenting patients, surgical intervention provides less predictable outcomes. Incomplete recovery is expected in the majority of these cases, especially for persons of advanced age.
Compressive neuropathies can occur at any point along the course of a nerve. This chapter covers some of the more common areas of entrapment. For the median nerve, pronator and anterior interosseous nerve syndromes are reviewed. For the ulnar nerve, cubital tunnel syndrome is addressed. Finally, for the radial nerve, radial tunnel and posterior interosseous nerve syndromes are reviewed.
History
Anterior interosseous nerve (AIN) and posterior interosseous nerve (PIN) syndromes solely affect motor nerves, and thus the symptom presentation involves motor dysfunction of the respective innervated muscle groups. Cubital tunnel syndrome involves both motor and sensory fibers of the ulnar nerve, but the initial presentation is usually sensory changes due to the lower threshold for injury of the sensory fibers. Long-standing ulnar nerve compression subsequently affects motor function. For reasons that are unclear, pronator syndrome involves the median nerve at a level where both motor and sensory fibers are present, but patients mostly report pain with possibly minor motor complaints. Similarly, radial tunnel syndrome may affect the radial nerve proper or the PIN, but the presentation manifests mostly as pain.
Physical Examination
Physical examination findings for motor-only neuropathies are consistent with motor weakness or paralysis of the affected muscle groups. We will review these findings in the respective section for each syndrome. Sensory findings in persons with cubital tunnel syndrome can be detected most subtly with use of Semmes-Weinstein monofilament testing and can also be documented in a quantifiable way by noting the distance at which two-point discrimination is maintained. Advanced cubital tunnel syndrome may present with intrinsic muscle compromise or atrophy and may be detected with some well-described maneuvers. For the syndromes that only involve pain (i.e., pronator and radial tunnel syndromes), several provocative maneuvers can be used to compress the respective nerve and elicit pain. Persons with radial tunnel syndrome also have point tenderness at the dorsal part of the supinator muscle.
Testing and Imaging
Electrophysiologic Testing
Nerve conduction velocity (NCV) and electromyography (EMG) studies may provide pivotal information in some cases of entrapment neuropathy. Demyelination interrupts the normal conduction along a nerve, resulting in increased latency (slowing) of NCVs. Sensory nerves have less myelin and thus demonstrate increased latency of NCVs earlier in the disease process. Also, the number of axons carrying a signal is roughly proportional to the amplitude of the action potential. As axons stop functioning, the amplitude decreases. These studies objectify the severity of injury and clarify etiology, especially when a nerve is being compressed in multiple locations along its course.
Nerve studies are not infallible, and multiple variables may affect the data generated. The tests are generally performed with the limb in a static and neutral posture rather than, for instance, in a provocative flexed position, which may exacerbate a compressive neuropathy at the elbow. Additionally, the tests are performed when the patient is rested, not after strenuous activity when muscle swelling may dynamically affect the nerve in question. Finally, variations in room temperature may also affect results.
Entrapment neuropathies may result in only focal demyelination that can be missed on a conventional electrodiagnostic study. “Inching” studies have been used in persons with carpal or cubital tunnel syndrome to document focal slowing in sensory conduction across short segments; stimulation is provided at 1- to 2-cm intervals. “Inching” can be used to provide better localization of a lesion and to gain a rough estimate of the length of compression.
Clinical presentations vary greatly, and thus a thorough history and physical examination should always be combined with any meaningful diagnostic testing. Positive results of a nerve study should be questioned when clinical signs are absent. The opposite situation of normal findings of nerve studies and a focal, reproducible examination for a compression neuropathy should still encourage a clinical response. Neurogenic pain is not measurable on nerve tests, and findings of nerve studies are often normal for persons with pronator or radial tunnel syndrome. EMG findings are often normal in the early phases of disease, whereas they become more pronounced and consistent in the intermediate and late phases.
Electrodiagnostic studies also may be used to compare responses of the nerve preoperatively versus postoperatively or to monitor spontaneous recovery of nerve conduction changes. Nerve studies are often used to monitor recovery during conservative treatment of persons with AIN or PIN syndrome.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) is a powerful and increasingly accurate tool for assessment of the soft tissue anatomy and may be used to identify either anomalous structures or neoplasms, which may directly affect neural structures as sources of extrinsic compression. Additionally, MRI is capable of mapping denervated skeletal muscles and can assist in identifying patterns or levels of nerve involvement.
Decision-Making Principles
For most compressive neuropathies, nonoperative treatment typically should be pursued for 3 to 6 months before surgical intervention is considered. The location and type of neuropathy, however, may alter the clinician’s comfort level with nonoperative treatment. In persons with cubital tunnel syndrome, the recommendation for operative nerve decompression is probably justified in all but the mildest of cases to prevent permanent nerve damage, given its proximal point of compression and long distance to intrinsic muscle innervation and sensory distribution.
Postoperative Management
Postoperative management includes gradual return to play once wound healing is complete, generally in 6 to 12 weeks depending on the specific condition and the surgical technique utilized. The athlete must prove that he or she has recovered enough joint motion and limb strength to safely compete at a high level.
Complications
Except for pronator and radial tunnel syndromes, when compressive neuropathies are not treated in a time-appropriate manner, eventual muscle atrophy and permanent disability may result. However, surgical intervention includes risks as well, including iatrogenic nerve injury and inadequate decompression or recurrence of compression as a result of the development of scar tissue. Finally, cases of complex regional pain syndrome sometimes develop in the setting of long-standing nerve compression, with or without surgical treatment, and are notoriously challenging to manage.
Median Nerve
Pronator Syndrome
Median nerve compression around the elbow tends to present after a person engages in high-load repetitive activities that require forceful forearm flexion and pronation. Athletes at risk include those in car racing and fast-pitch softball. Other sources of extrinsic compression include tumors, traumatic scarring, or anomalous muscles such as the Gantzer muscle, an accessory head of the flexor pollicis longus (FPL). Vascular anomalies, such as a persistent median artery, have also been reported to cause median nerve compression.
In the arm, the median nerve travels lateral to the brachial artery and medial to the short head of the biceps brachii muscle. It passes between the brachialis and the medial intermuscular septum, and then as it reaches the elbow, it crosses anterior to the brachial artery and eventually lies medial to it before reaching the antecubital space. A small population of patients (~1%) have an anomalous supracondylar process arising from the distal aspect of the humerus and located approximately 5 cm proximal to the medial epicondyle, which can be seen radiographically. In these patients, the supracondylar process may give origin to a fibrous band that extends to the medial epicondyle and is called the ligament of Struthers; if this ligament is present, the median nerve typically passes underneath it. Motor branches rarely leave the median nerve proximal to the elbow. The first motor branch to arise from the median nerve is usually the branch to the pronator teres, and the second branch is typically the flexor carpi radialis branch; both traverse in an ulnar direction. Other branches then arise to the palmaris longus and the flexor digitorum superficialis (FDS).
In the antecubital fossa, the median nerve is bordered laterally by the biceps tendon, anteriorly by the lacertus fibrosus (bicipital aponeurosis), medially by the pronator teres, and posteriorly by the brachialis. The nerve typically passes between the superficial (humeral) and deep (ulnar) heads of the pronator teres, although in 20% of persons, the deep head is absent or consists only of a small fibrous band. Additionally, the nerve can pass underneath both heads rather than between them, and rarely, it pierces the superficial head. Under the pronator teres, the AIN branches in a radial direction from the median nerve, and both pass underneath the fibrous arch of the FDS. The surgeon should also be aware of the Martin-Gruber anastomosis, which involves branches from either the median nerve or AIN to the ulnar nerve; this anastomosis occurs in 15% of the population. The most common site of compression of the median nerve is at the deep head of the pronator teres, followed by the FDS arch and finally the lacertus fibrosus.
History
Compression of the median nerve at the pronator teres will result in a pain syndrome with minimal complaints of numbness or weakness. The pain is located in the proximal anterior forearm. As with the other compressive neuropathies in athletes, symptoms generally worsen with activity and improve with rest. In contrast to carpal tunnel syndrome, pronator syndrome could result in sensory disturbances in the palmar cutaneous branch distribution (proximal radial palm) and most often a lack of nocturnal symptoms and awakening.
Physical Examination
Physical examination should include provocative tests for specific potential sites of compression. Proximally, if the median nerve is compressed under the ligament of Struthers, pain can be elicited with resisted elbow flexion at 120 to 130 degrees. Compression under the lacertus fibrosus is likely to cause pain with resisted elbow flexion with the forearm in pronation. Pain with resisted forearm pronation with the elbow extended and the wrist flexed points to the two heads of the pronator teres as the site of compression. Finally, compression at the FDS origin can be assessed with resisted middle finger proximal interphalangeal joint flexion.
Decision-Making Principles
Pronator syndrome often responds to conservative management over a 3- to 6-month period. Antiinflammatory medications, splinting, and activity modification should be used initially. Imaging is performed to evaluate for concurrent pathology, such as distal biceps tendinopathy, or a source of extrinsic compression. If the condition has not improved by 6 months, surgical intervention should be considered.
Treatment Options
The skin incision begins in the distal arm about 5 cm above the elbow and along the medial aspect of the biceps muscle. The incision curves toward the lacertus fibrosus at the elbow crease and then continues distally over the flexor-pronator mass. Care should be taken to preserve cutaneous nerve branches. If a supracondylar process was identified radiographically, exploration should start proximally to seek and release the accompanying ligament of Struthers. The median nerve should then be traced distally to the lacertus fibrosus, which should either be divided or partially excised. Dissection then proceeds through the two heads of the pronator teres, keeping in mind that the median nerve is often adherent to this muscle. Antegrade dissection with magnification can aid in protecting the motor branches emanating from the median nerve in this region. The superficial head of the pronator teres is elevated, and its insertion is separated from the deeper ulnar head. If scarring is present as a result of trauma, it may be necessary to perform a Z-lengthening of the pronator teres tendon. The median nerve is then followed as it descends under the FDS arch, and the arch is released to complete the decompression. Throughout its course in the surgical field, the median nerve is inspected for signs of compressive pathology, such as focal narrowing or enlargement.
Postoperative Management (Return to Play)
Postoperatively, mobilization should begin within 1 week. Sport-specific reconditioning progresses according to patient tolerance and is often prolonged, with some patients taking up to 6 months to regain full upper extremity strength.
Results
Global decompression of all sites gives good to excellent relief of symptoms in approximately 80% of patients. In a study by Olehnik et al., however, 25% of patients experienced no change in symptoms at all. It is difficult to know whether this lack of symptom relief may be a result of concomitant untreated pathology or incomplete surgical decompression.
Complications
Causes of operative treatment failure include inadequate decompression or misdiagnosis. Additionally, iatrogenic injury to cutaneous nerve branches or the median nerve itself could lead to continued postoperative discomfort or could even escalate to complex regional pain syndrome. Finally, postoperative scarring of the pronator teres muscle may result in recurrent compression.
AIN Syndrome
AIN syndrome involves selective median nerve motor loss without sensory involvement. AIN innervated muscles include the index and long flexor digitorum profundus (FDP), FPL, and pronator quadratus. Patients often have no accompanying injury, and the cause is most often deemed idiopathic.
At the level of the pronator teres muscle, the AIN branches off the median nerve in a radial direction before both pass under the FDS arch. The AIN then continues along the volar aspect of the interosseous membrane in the interval between the FPL and FDP, ending distally with branches to the pronator quadratus and wrist joint.
The most common site for AIN compression is the FDS arch. Other possible sources of compression are similar to pronator syndrome and include fibrous bands within the pronator teres, the edge of the lacertus fibrosus, an enlarged bicipitoradial bursa, or the Gantzer muscle if it is present.
History
With compression of the AIN, patients typically describe a dull, deep ache in the volar forearm with general loss of dexterity, including weakness of the radial-sided digit and thumb flexion. It is important to distinguish AIN syndrome caused by Parsonage-Turner syndrome, or brachial neuritis. Persons with Parsonage-Turner syndrome often experience a prodromal viral-like illness and significant shoulder pain for days to weeks before the onset of any AIN-innervated muscle weakness. Although the recovery period may be extensive, persons with Parsonage-Turner syndrome typically improve without surgical intervention.
Physical Examination
Various clinical manifestations are possible, with the most common being complete loss of the FPL and index FDP, although some patients exhibit isolated loss of one or the other. It is important to rule out tendon disruption if only one digit is weak (such as in Mannerfelt-Norman syndrome with isolated FPL rupture). Spontaneous tendon ruptures occur most frequently in patients with inflammatory arthropathy. The FDP and FPL are tested with the “O” sign or precision tip-to-tip pinch ( Fig. 67-1 ). Patients with AIN syndrome are unable to form the letter “O” and will instead assume an extended posture at the thumb interphalangeal joint and the index finger distal interphalangeal joint. The pronator quadratus can be assessed with resisted pronation with the elbow maximally flexed.
Decision-Making Principles
Rest, immobilization, and avoidance of aggravating activities such as repetitive pronation and heavy gripping are the mainstay of conservative management. The elbow can be splinted in 90 degrees of flexion for up to 8 to 12 weeks. The vast majority of patients will recover without surgery, but for those whose symptoms persist after 3 to 6 months, surgical decompression may be indicated.
Treatment Options
The recommended surgical technique is similar to the one described for pronator syndrome but without the more proximal distal arm dissection. The humeral head of the pronator teres is reflected in an ulnar direction to give good visualization of the AIN. After the FDS arch is released, the muscle fibers can be gently retracted to allow visualization of the AIN distally. It is important to protect the motor branches to the FPL and FDP during the decompression ( Fig. 67-2 ).
Postoperative Management (Return to Play)
Splinting or casting should be avoided postoperatively, and early range of motion should be encouraged. Sport activities can be resumed as tolerated in a 1- to 3-week period in most cases, depending on recovery of hand function and its role in competing effectively.
Results
Reported operative series are small but generally report up to 70% to 90% recovery. The definitive role of operative management, however, remains in question. In one small study performed by Sood and Burke, no differences in outcome were found between nonoperative and operative management.
Complications
Complications are similar to those seen in pronator syndrome and include injury to cutaneous nerve branches, injury or scarring of the AIN, or scarring of the forearm musculature.
Ulnar Nerve
Cubital Tunnel Syndrome
Cubital tunnel syndrome is the most common entrapment neuropathy at the elbow. Most cases of idiopathic compression occur at the anatomic cubital tunnel under the arcuate ligament of Osborne or between the two heads of the flexor carpi ulnaris (FCU). Compression also may be due to hypertrophied muscle origins whose passageways no longer allow smooth nerve gliding, which results in both compressive and traction mechanisms of neural injury. As with other compressive neuropathies, soft tissue tumors such as lipomas or synovial ganglia may cause cubital tunnel syndrome, as can the anconeus epitrochlearis, an anomalous, thin, straplike muscle extending from the triceps or olecranon to the medial epicondyle. Additionally, the nerve is vulnerable in its superficial location and subject to irritation and compromise from direct trauma to the medial elbow. Any posttraumatic deformity (classically a lateral condyle malunion) that results in a cubitus valgus position may secondarily lead to tardy ulnar nerve palsy. Similarly, after any elbow fracture or dislocation, the ulnar nerve may lose its smooth gliding path as a result of adhesion formation.
Repetitive throwing activities may be a source of cubital tunnel syndrome. The act of throwing creates tensile loads on the ulnar (medial) collateral ligament (UCL), which is located adjacent to the ulnar nerve in the cubital tunnel. Changes in the UCL may generate an inflammatory reaction and impingement of the ulnar nerve ( Fig. 67-3 ). Elbow flexion in the cocking phase of throwing requires the ulnar nerve to elongate approximately 5 mm. In the late cocking phase of the overhead throwing motion, the combination of elbow flexion and wrist extension results in a sixfold increase in the pressure seen within the cubital tunnel, a situation analogous to an exertional compartment syndrome in the lower extremity. In fact, one cadaveric study demonstrated that strain on the ulnar nerve was increased in all phases of throwing and that in the acceleration phase, the maximal strain approached the elastic and circulatory limits of the nerve. In baseball pitchers, the chronic valgus extension overload forces applied to the elbow eventually lead to UCL instability medially and compressive forces laterally. More than 50% of professional pitchers have some degree of acquired valgus elbow deformity, which itself can result in an ulnar nerve palsy. Additionally, there is a slight loss of terminal elbow extension in pitchers because of posterior humeroulnar osteophyte formation that may predispose pitchers to ulnar neuritis. Arcuate ligament tears in association with ulnar nerve subluxation have also been documented in baseball pitchers.
The ulnar nerve arises from the C8 and T1 roots and is the terminal branch of the medial cord of the brachial plexus. In the arm, it may contribute a motor branch to the medial triceps muscle belly. The nerve passes from the anterior to the posterior compartment and then travels deep to a thick aponeurotic band between the medial head of the triceps and the medial intermuscular septum called the arcade of Struthers, which is found approximately 8 cm proximal to the medial epicondyle. The nerve continues distally and medially on the anterior surface of the medial head of the triceps muscle and then descends posterior to the medial epicondyle, entering the cubital tunnel ( Fig. 67-4 ). The lateral wall of the cubital tunnel consists of the medial trochlea, the medial epicondylar groove, and the posterior portion of the UCL. The arcuate ligament of Osborne extends from the olecranon to the medial epicondyle, forms the roof of the tunnel, and blends distally with the aponeurosis between the two heads of the FCU. Distal to the cubital tunnel, the ulnar nerve travels between the ulnar and humeral heads of the FCU. Further distally, it passes between the FCU and the FDP muscle bellies, providing motor branches to these muscles before continuing into the forearm and hand.
The five classic major anatomic sites of compression in persons with cubital tunnel syndrome are the arcade of Struthers, the medial intermuscular septum, the medial epicondyle, the cubital tunnel (the arcuate ligament of Osborne), and the deep flexor pronator aponeurosis. Still, the most common site remains at or near the cubital tunnel. Other alternative sites of compression in a minority of cases include the anconeus epitrochlearis, triceps hypertrophy, and the ligament of Spinner, which is a distinct aponeurosis between the ring finger FDS and the humeral head of the FCU. Lastly, specific to athletes, distinct muscular hypertrophy of the FCU may be a primary source of ulnar nerve compression.
History
Patients typically report paresthesias in the early stages of cubital tunnel syndrome. The involved areas usually include the ulnar forearm and hand, the small finger, and the ulnar half of the ring finger. These sensory changes can be tolerated for a lengthy period despite obvious progression of frequency and intensity. Nocturnal symptoms are common, especially in persons who sleep in the fetal position, with the elbows hyperflexed. Further neglect may result in complaints of hand weakness and dysfunction.
In athletes, ulnar neuropathy may elicit pain along the medial upper extremity both proximal and distal to the elbow, and this pain is exacerbated by the action of throwing. The cause of any localizing pain to the medial elbow must be carefully differentiated between valgus extension overload syndrome, medial epicondylitis, flexor pronator mass strain, UCL injury, or ulnar neuropathy. Furthermore, ulnar nerve subluxation during forceful elbow flexion and extension as a result of an incompetent Osborne ligament can create a painful snapping or popping sensation. It is important to distinguish between this phenomenon and medial triceps subluxation, because both are possible and may even coexist.
Physical Examination
A positive Tinel sign at the cubital tunnel is confirmatory, but it is not always present. The elbow flexion test is more useful; it is performed by fully flexing the elbow with the wrist fully extended for 1 minute ( Fig. 67-5 ). Tingling or numbness in the ulnar nerve distribution indicates a positive test. Severe ulnar neuropathies result in muscle weakness with atrophy of the intrinsic musculature and a potential claw hand deformity with weak pinch and grasp ( Fig. 67-6 ). The classic Froment sign may be elicited by having the patient pinch an object between the thumb and index finger; a weak adductor pollicis leads to compensatory firing of the FPL (flexing the interphalangeal joint of the thumb) to hold the object. During this test, it is possible that concurrent volar plate laxity of the metacarpophalangeal joint could lead to a hyperextended posture, termed a positive Jeanne sign. The examiner can also test resistance to small finger abduction as a way to localize weakness to the ulnar nerve innervated abductor digiti minimi. Ulnar-supplied extrinsic muscles including the FCU and the ring and small FDP are typically unaffected because of the protected central location of the extrinsic motor fibers within the nerve microanatomy and topography. Weak intrinsic musculature may decrease overall grip strength substantially and should be compared with the contralateral hand. Decreased sensation of the dorsal ulnar part of the hand (dorsal cutaneous branch) will help differentiate the location of the ulnar neuropathy to the elbow rather than to the wrist within the Guyon canal.
Decision-Making Principles
Initial treatment is conservative and consists of rest and activity modification, use of nonsteroidal antiinflammatory drugs, and use of local modalities. A padded elbow sleeve may be used to limit terminal elbow flexion and helps cushion the area over the nerve from impact against hard surfaces, and use of a splint fabricated at 45 degrees of elbow flexion at night may decrease nocturnal symptoms by blocking elbow hyperflexion in people who sleep in the fetal position. Approximately 50% of patients will improve with implementation of conservative measures. Patients with localized blunt trauma to the elbow with ulnar nerve irritation initially may also be treated conservatively, with many cases resolving over weeks to months. If symptoms do improve, a rehabilitation program including reconditioning will hasten a return to competitive sports. The practice of injecting corticosteroids at or around the cubital tunnel is controversial and unpredictable in its effectiveness. Surgical decompression should be considered in patients who have persistent symptoms that prevent a return to activity or progress to motor weakness. Most treating surgeons recommend operative treatment for all but the mildest of cases. A decrease of conduction velocity across the elbow to below 50 m/sec is considered the threshold for pathologic ulnar nerve compression; further decreases in measured conduction velocity typically correlate with increasingly severe disease and the constellation of subjective and objective findings.
Treatment Options
Many options are available for the operative management of cubital tunnel syndrome, and the optimal treatment in every case is largely uncertain. Options include in situ decompression alone (open vs. endoscopic), medial epicondylectomy, or anterior transposition (with subcutaneous, intramuscular, and submuscular variations). As long as no denervation has occurred and symptoms are intermittent, any technique gives approximately 80% to 90% relief of preoperative symptoms. For patients with moderate to severe disease, submuscular transposition may be the most effective technique. For persons with severe disease, medial epicondylectomy has actually resulted in overall poor outcomes and should be avoided.
In Situ Decompression
In situ decompression, which is the simplest and least invasive option, can be accomplished via an open procedure or endoscopically. Favorable results equivalent to those of anterior transposition have been shown in prospective studies. However, athletes with ulnar neuritis associated with UCL laxity and elbow instability may not benefit from an in situ release alone. In a cadaveric study, in situ decompression did not significantly reduce tensile strains on the ulnar nerve.
The most critical aspect of in situ decompression is that the nerve is not moved from its normal anatomic course. The size of incision and extent of dissection vary. A 14-cm incision may be made with nerve decompression from the arcade of Struthers to between the two FCU heads, with possible excision of the intermuscular septum and the brachial fascia. It is also possible to make a smaller incision over the area of suspected compression, typically directly over the cubital tunnel and/or the aponeurosis of the FCU heads. Obviously, the limited open approach does not permit inspection of the more proximal and distal potential sites of nerve compression or tethering. An important consideration is that when more of the ulnar nerve is released, the likelihood of nerve subluxation increases, which may necessitate transposition.
Endoscopically assisted cubital tunnel release has been described, and several outcomes studies have been published recently. This procedure permits a smaller skin incision (approximately 1.5 to 2 cm) with less soft tissue dissection, yet allows decompression of the nerve 10 cm proximal and 10 cm distal to the medial epicondyle. Patient satisfaction outcomes are similar to those for open procedures. Insufflation of carbon dioxide can be used to open up a safe working space. Severe elbow deformity, osteoarthritis, and recurrent cases are all contraindications for this procedure.
Anterior Subcutaneous Transposition
An incision starting 8 cm proximal and 6 cm distal to the medial epicondyle can be made at the medial elbow centered between the medial epicondyle and olecranon or in the perimedial epicondyle region ( Fig. 67-7 ). After skin incision, the subcutaneous tissue is divided to the level of the fascia, taking care to look for posterior branches of the medial antebrachial cutaneous nerve. The ulnar nerve is best located proximal to the cubital tunnel, and the fascia on top of the nerve is carefully divided. The division is carried distally, releasing the arcuate ligament of Osborne (the roof of the cubital tunnel) and the aponeurosis of the FCU heads. Articular branches to the elbow are sacrificed to facilitate transposition. Similarly, motor branches to the FCU may tether the transposed nerve. Preservation of these motor branches is preferred, but in our experience, sacrifice of one or two of these branches to allow for safe transposition has not engendered any obvious motor deficits after surgery.
