Surgical Treatment of Cubital Tunnel Syndrome

Reimer Hoffmann, MD

John D. Lubahn, MD

Dr. Lubahn or an immediate family member has received research or institutional support from Auxillium – Xiaflex. Neither Dr. Hoffman nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter.

The authors would like to thank Hand Fellows John P. Dupaix, MD and Wayne A. Chen, MD, for the revisions and preparation of this manuscript.

INTRODUCTION

Cubital tunnel syndrome is characterized by sensory and/or motor deficiencies of the ulnar nerve at the level of the elbow. It is the second most common compression syndrome affecting a peripheral nerve, exceeded in prevalence only by carpal tunnel syndrome. The pathology associated with cubital tunnel syndrome occurs at the elbow, where the ulnar nerve passes posterior to the medial epicondyle and beneath the arcuate or Osborne ligament and distal and proximal to the retrocondylar fossa. The syndrome is assumed to be caused by compression that may have one or multiple foci, but the exact cause of the pathology remains unknown. The cause may be traction on the nerve from repetitive or prolonged flexion of the elbow or a combination of traction and compression.

According to the literature, the annual incidence of cubital tunnel syndrome is about one tenth that of carpal tunnel syndrome.¹^,² Males are affected more often than females, and the left side is affected more often than the right, in contrast to carpal tunnel syndrome. Frequently, cubital tunnel syndrome occurs bilaterally.

FIGURE 1 Illustrations depict the anatomy of the cubital tunnel. A, The most common sites of ulnar nerve compression are labeled. B, Additional potential sites of compression of the ulnar nerve located in the submuscular membrane of the flexor-pronator muscle. Panel (B) copyright Joe Kanasz, the Cleveland Clinic Foundation, Cleveland, OH.

The cubital tunnel is composed of three parts: (1) The retrocondylar groove, which is partially covered by the humeroulnar arcade; (2) the humeroulnar arcade or Osborne ligament (also known as the arcuate ligament or the epitrochlear anconeus ligament), which passes into the aponeurosis between the two heads of the flexor carpi ulnaris (FCU) muscle and which is also called the cubital tunnel retinaculum; and (3) the deep flexor aponeurosis or flexor-pronator aponeurosis, which contains submuscular bands that may be located at variable distances from the medial epicondyle³ (Figure 1, A). This aponeurosis spreads from 5 to 12 cm distal to the medial epicondyle. The submuscular membrane, described by Matsuzaki et al⁴ and Hoffmann and Siemionow,³^,⁵ covers the nerve in the distal part of the cubital tunnel and is characterized by fibrous bands that may cause or add to compression as far as 9 cm distal to the retrocondylar fossa (Figure 1, B). The prevalence of compression distal to the retrocondylar area can only be estimated. According to MRI investigations by Vucic et al,⁶ the compression site was in the retrocondylar area in only 38% of their cases.

The role of the arcade of Struthers in compression of the ulnar nerve in the distal part of the humerus proximal to the cubital tunnel is controversial, but it may cause compression on the nerve proximally when the nerve is transposed anterior to the medial epicondyle.

PATIENT SELECTION

The initial office visit should focus on findings consistent with ulnar nerve palsy using sound anatomic principles to narrow the diagnosis to the cubital tunnel. Diminished sensation in the small finger, ulnar side of the ring finger, and dorsum of the ulnar side of the hand combined with ulnar-innervated muscle weakness in the hand and forearm and a positive elbow flexion test and/or positive Tinel sign over the ulnar nerve at the elbow localize the site of compression to the cubital tunnel. M4 muscle strength in the FDP to the small finger is an early finding in cubital tunnel syndrome and converts to M5 strength immediately following surgery. Sensory deficit should be measured by changes in two-point discrimination or Semmes-Weinstein monofilament testing. Weakness in the hand is measured by Jamar dynamometer or direct observation noting the presence or absence of a Froments or Wartenburg sign and the patient’s ability to cross the long finger over the index. It is also important to document whether the ulnar nerve subluxes anteriorly with elbow flexion at the time of the initial visit.

Physical Examination

The clinical examination includes inspection for muscle atrophy; examination for sensory deficits, including two-point discrimination; examination of ulnar nerve innervated muscles, including assessment for Froment and Wartenberg signs and the crossed-finger test (long over index); measurement of muscle power (M0-M5), particularly in the flexor digitorum profundus of the small finger; measurement of grip strength (Jamar dynamometer); testing for the presence and location of the Tinel sign; palpation of the course of the ulnar nerve for possible complete or partial subluxation of the ulnar nerve from the retrocondylar groove; examination of mobility and stability of the elbow joint; and the elbow flexion test.

Electrodiagnostic Testing

Although ulnar compression at the elbow can be diagnosed clinically, preoperative electrodiagnostic testing is often recommended to confirm the diagnosis and exclude the possibility of compression at other anatomic sites, quantify the degree of compression, and provide baseline numbers against which to compare subsequent studies to document progression or improvement of the condition.

The precision of nerve conduction velocity studies is highly dependent on the examiner and the technique used. Locating the exact point of stimulation distally at the postcondylar groove is difficult, especially in cases of strongly developed muscles in the lower arm or in obese patients. In patients with low skin temperature or gliding of the nerve when the elbow is flexed or in the setting of an electrodiagnostic test following a prior ulnar nerve transposition, inaccuracies in measurements may occur.

Preoperative Imaging

Imaging techniques including ultrasonography⁷ and MRI⁸ have recently increasingly gained acceptance and now are in some cases regarded as relevant examination studies that may be used in addition to electrodiagnostic testing in some cases. Unlike electrodiagnostic testing, these modalities may detect morphologic changes directly and localize them more precisely.

A radiographic examination of the elbow joint in at least two projections, including tangential imaging of the retrocondylar groove, can help to detect anatomic variations. A CT examination is recommended only in exceptional cases of skeletal deformity.

Indications

The goal of the surgical intervention, usually performed in an outpatient center, is the decompression of the ulnar nerve throughout the entire cubital tunnel. There are currently several generally well-accepted surgical procedures for the treatment of cubital tunnel syndrome: (1) in situ decompression; (2) endoscopic decompression (outside-in or inside-out); (3) decompression with subsequent subcutaneous transposition, intramuscular transposition, or submuscular transposition; and (4) in situ decompression in conjunction with medial epicondylectomy. Whichever technique is performed, a few principles are important and common for each technique. These include complete decompression of any compressive structures; assuring that the nerve is in a hospitable environment at the completion of the procedure, whether that is transposed or an in situ release (ie, avoiding placing the nerve directly over hardware or other potentially bothersome areas); avoiding iatrogenic injury to the medial antebrachial cutaneous nerve, which if injured, can result in a bothersome or painful numb patch; and assessment for possibly bothersome nerve instability following completion of the procedure. If the nerve is transposed, it is important to remove a portion of the intermuscular septum and to assure that no new areas of compression or impingement upon the nerve are created. Our preferred technique for the treatment of cubital tunnel syndrome is endoscopic in situ decompression.⁹^,¹⁰^,¹¹^,¹²^,¹³

Endoscopic cubital tunnel release has been recently demonstrated to favorably compare with open in situ release. Midterm to long-term follow-up demonstrates endoscopic cubital tunnel release is both safe and effective with 78 to 84.9% of patients had good or excellent results with similar complication rates to open release.¹⁴^,¹⁵ Similarly, in their systematic review, Toriac et al¹⁶ found that endoscopic cubital tunnel release was superior to open in
situ release in terms of patient satisfaction and complications. In contrast, the systematic review and meta-analysis by Buchannan et al found no significant superiority, however, did find lower scar tenderness/elbow pain with equivalent revision surgery rates to open in situ release.¹⁷

When considering treatment options for patients with cubital tunnel syndrome, a trial of nonsurgical management may be considered. In cases of a recent onset of intermittent paresthesia and pain that developed over a period of 14 days, it is acceptable to manage symptoms nonsurgically for up to 3 months (“wait and see”). Ongoing neurologic and electrophysiologic surveillance of the patient is recommended, however. If after this period of time the patient shows no signs of improvement or if physical findings such as two-point discrimination and grip strength worsen, surgical intervention should be considered. If electrodiagnostic and ultrasonographic testing remain negative, other neurologic causes have been ruled out, and the patient is unhappy, an operation may still be considered.

In situ decompression of the ulnar nerve performed open or endoscopically is now, in most cases, the treatment of choice for primary cubital tunnel syndrome.⁹^,¹⁰ In situ decompression is effective in patients with severe compression as well as in patients with milder forms of the syndrome.¹⁰ In situ decompression may also be recommended for cases of ulnar nerve subluxation, although this is one instance where transposition may be indicated if the nerve is snapping back and forth over the medial epicondyle with pain and instability preoperatively. In situ decompression is also effective in cases where the elbow joint is deformed secondary to other posttraumatic changes or where an epitrochlear anconeus muscle or prominent medial triceps are found.

In situ decompression, including endoscopic decompression, also may be chosen in posttraumatic cubital tunnel syndrome, as there is currently no evidence to suggest anterior transposition is better.

IN SITU DECOMPRESSION

Room Setup/Patient Positioning

In situ decompression is almost always performed in an outpatient setting. General anesthesia is preferred, although some patients may prefer local anesthesia with sedation. A bloodless field is an advantage. The patient is positioned supine on the operating table, and the arm is abducted 90° at the shoulder, flexed at the elbow, and supinated.

Special Instruments/Equipment/Implants

For the endoscopic decompression described below, a special endoscopy set (Karl Storz Endoscopy) is used. The set includes an illuminated speculum with a blade length of 9 to 11 cm; a 4-mm, 30° endoscope with a shaft length of 15 cm and a blunt dissector on its tip; and an endoscopic bipolar forceps.

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