The patient is a 44-year-old right-hand dominant woman who presented with a 12-month history of paresthesias and numbness in the ring and small fingers of the left hand. She also noticed some clumsiness in her left hand and reported dropping objects occasionally over the past 3 months. She had tried conservative measures, including activity modifications, nonsteroidal anti-inflammatory drugs (NSAIDs), and elbow braces at night, with no appreciable improvement.
On examination, the patient’s symptoms were reproduced by holding the elbow in flexion for 1 minute, and Tinel’s signs were elicited over the cubital tunnel both proximal and distal to the medial epicondyle. No intrinsic wasting was apparent, and abduction strength of the first dorsal interosseous muscle was symmetric to the unaffected hand. Froment’s sign was negative, and static 2-point discrimination was 5/7 mm in the ring finger and 9/9 mm in the small finger. Strength of the flexor digitorum profundus (FDP) to the ring and small fingers and flexor carpi ulnaris (FCU) were 5/5, and there was diminished sensation to light touch on the dorsal–ulnar aspect of her hand. No ulnar nerve subluxation was appreciated with passive flexion and extension of the elbow.
Based on these findings, a diagnosis of cubital tunnel syndrome was made, which was confirmed with electrodiagnostic testing. Although we consider cubital tunnel syndrome a primarily clinical diagnosis, we routinely obtain either electrodiagnostic testing or ultrasound studies to confirm the diagnosis. Results of electrodiagnostic studies can frequently be negative in symptomatic patients, particularly those with less chronic compressive symptoms for which dynamic ischemia occurs, but there has not been extensive demyelination or axonal loss. Electrodiagnostic testing is especially helpful for patients with an atypical presentation and equivocal diagnosis, or those patients with a history of known cervical pathology that may be contributing to a double-crush phenomenon. While these patients may still benefit from cubital tunnel release, knowledge of cervical compression helps set expectations and referral for management of cervical pathology. Ultrasound provides the additional benefit of assessing static and dynamic views of the ulnar nerve within the cubital tunnel in elbow extension versus flexion.
We discussed treatment options with the patient, including continued conservative measures and close follow-up or surgical decompression, and the patient opted for surgery, as she felt the symptoms significantly affected her quality of life.
The patient had no external stigmata of injury over the course of the ulnar nerve and no appreciable wasting of ulnar-innervated musculature. On clinical examination, there was no appreciable ulnar nerve instability or subluxation out of the epicondylar groove. However, based on the patient’s clinical examination, we could deduce that the ulnar nerve was being compressed within the cubital tunnel, especially when the elbow was flexed.
The anatomic borders of the cubital tunnel are the medial condyle anteriorly, epicondylar groove of the ulna and medial collateral ligament of the elbow on the deep surface of the nerve, the olecranon posteriorly, and a roof consisting of aponeurotic fascia connecting the humeral head of the FCU muscle, which arises from the medial epicondyle anterior to the nerve, and the ulnar head of the FCU, which arises from the olecranon and dorsal–ulnar border posterior to the nerve. The proximal fibers of this aponeurotic connection between the two heads of the FCU is known as Osborne’s ligament, while more distally into the proximal forearm this aponeurosis is known as the arcuate ligament. Proximal to the elbow, the arcade of Struthers is a fascial band spanning from the medial intermuscular septum anterior to the nerve to the fascia of the medial head of the triceps muscle posterior to the nerve. The arcade of Struthers is located approximately 6 to 8 cm proximal to the medial epicondyle. An additional potential cause of ulnar nerve compression is the anconeus epitrochlearis (▶Fig. 22.1), a congenital accessory muscle spanning the medial epicondyle to the olecranon that is present in approximately 34% of the population.
For patients presenting with early signs of compression and no motor weakness, conservative measures can be attempted initially for a period of at least 3 months. These efforts are directed primarily at avoiding excessive flexion of the elbow that elicits symptoms, as the area inside the cubital tunnel decreases up to 50% with elbow flexion, while pressure within the cubital tunnel increases. This includes orthotics for elbow extension at night and modification of workplace activities to avoid acute flexion of the elbow at rest. Positional modification can be supplemented with NSAIDs. However, corticosteroid injection into the cubital tunnel has not been proven to be efficacious. Surgery is indicated if conservative measures fail, if the patient’s symptoms have a significant negative impact on work and leisure activities, or if there is evidence of intrinsic muscle weakness indicating a more severe compression neuropathy.
When surgical intervention is indicated, our preferred solution to cubital tunnel syndrome is a minimally invasive in situ release of the ulnar nerve in the cubital tunnel. Advantages of in situ decompression compared to more invasive methods include reduced risk of iatrogenic nerve injury or transient devascularization of the ulnar nerve by sacrificing ulnar collateral arterial branches, decreased operative time, and expedited patient recovery without the need for postoperative immobilization. More invasive approaches, including anterior nerve transposition with subcutaneous, intramuscular, or submuscular placement, are better reserved for recalcitrant cubital tunnel symptoms following an in situ release. Medial epicondylectomy can be performed, but this is not recommended by the authors. Other contraindications to an in situ release include a failed prior in situ release, elbow arthritis, and ulnar nerve instability diagnosed either preoperatively or intraoperatively. In this case, a primary ulnar nerve transposition with subcutaneous or submuscular placement is indicated.
• In situ decompression of the ulnar nerve in the cubital tunnel, consisting of the following:
– Division of Osborne’s ligament over the cubital tunnel.
– Division of the aponeurosis between the humeral and ulnar heads of the FCU distally (the arcuate ligament).
– Division of the aponeurotic fascia overlying the epicondylar groove and arcade of Struthers proximally.
– Ensuring no subluxation of ulnar nerve following unroofing of the cubital tunnel.
– Allowing early active range of motion of the arm immediately with no splint immobilization.
The patient is taken to the operating room and placed supine on the operating table. For in situ cubital tunnel release, anesthesia can vary depending on surgeon, anesthesiologist, and patient. General, nerve block, intravenous regional, or local anesthesia with sedation are all options for this procedure. The arm is abducted 90 degrees and placed on a hand table. If a tourniquet is used, it can be placed in a nonsterile or sterile fashion. The arm is then prepped and draped with chlorhexidine in the standard fashion.
The surgeon sits medial to the patient’s arm with an assistant lateral to the arm. The assistant externally rotates the patient’s shoulder and flexes the elbow to expose the medial epicondyle of the humerus and olecranon process of the ulna. The skin incision is marked in a line halfway between the medial epicondyle and olecranon, extending from this interval to approximately 2 to 3 cm distal over the FCU muscle, directly over the course of the ulnar nerve (▶Fig. 22.2). If a tourniquet is used, then the arm is raised and exsanguinated using an Esmarch bandage. The tourniquet is then inflated to 250 mm Hg and the Esmarch bandage is removed.
An incision is made with a no. 15 blade through skin and superficial subcutaneous tissue (▶Fig. 22.3). Tenotomy scissors are then used to spread the subcutaneous tissue in a direction perpendicular to the incision in order to identify posterior branches of the medial antebrachial cutaneous (MABC) nerve that course through the plane of dissection. Dissection with scissors continues to the deep fascia overlying the flexor/pronator origin, and skin flaps are mobilized sufficiently to expose this fascia.
The ulnar nerve can be palpated posterior to the medial epicondyle and courses posterior to the medial intermuscular septum. The leading edge of the FCU (Osborne’s ligament) is visualized proximally along with the medial intermuscular septum distally. An incision is made carefully with a no. 15 blade in the fascia overlying the nerve. Release is then continued proximally above the medial epicondyle to include aponeurotic fascia overlying the epicondylar groove and the arcade of Struthers, ending at the medial border of the medial head of the triceps muscle (▶Fig. 22.4).