The ulnar nerve is subject to compression as it pierces the medial intermuscular septum (MIS); at the arcade of Struthers; within the cubital tunnel; and between the humeral and ulnar heads of the flexor carpi ulnaris (FCU).
Pressure can be imparted to the ulnar nerve about the elbow in three ways: compression, stretch, and friction.
The capacity of the cubital tunnel is greatest when the elbow is in extension.
Pressure within the cubital tunnel is increased with elbow flexion and is further increased with contraction of the FCU.
Patients with intermittent symptoms, no atrophy, and mild electrodiagnostic findings may respond well to nonoperative treatment.
Surgical management options include endoscopic release, in situ decompression, medial epicondylectomy, and anterior transpositions.
Postoperative therapy depends on the surgical procedure performed.
The potential for full motor recovery after surgery is greatly reduced in those patients in whom preoperative symptoms have been present for more than 1 year or who have intrinsic muscle atrophy before surgery.
The term cubital tunnel syndrome was defined in 1958 by Feindel and Stratford , although the ability of the anatomic structures near the elbow joint to exert pressure on the ulnar nerve was known more than a century ago. In 1898, Curtis performed the first published case of management of ulnar neuropathy at the elbow, which consisted of a subcutaneous anterior transposition.
The ulnar nerve is the terminal branch of the medial cord of the brachial plexus containing fibers from C8, T1, and, occasionally, C7. Figure 50-1 illustrates the potential sites of compression of the ulnar nerve in the region of the elbow. At the level of the insertion of the coracobrachialis muscle in the middle third of the arm, the ulnar nerve pierces the MIS, a site of potential compression, to enter the posterior compartment of the arm. Here, the ulnar nerve lies on the anterior aspect of the medial head of the triceps, where it is joined by the superior ulnar collateral artery. The MIS extends from the coracobrachialis muscle proximally, where it is a thin and weak structure, to the medial humeral epicondyle, where it is a thick, distinct structure and lies medial to the brachial artery as far as the middle third of the arm.
Another potential site of compression is the arcade of Struthers. This structure is found in 70% of patients, 8 cm proximal to the medial epicondyle, and extends from the MIS to the medial head of the triceps. The arcade of Struthers is formed by the attachments of the internal brachial ligament (a fascial extension of the coracobrachialis tendon), the fascia and superficial muscular fibers of the medial head of the triceps, and the MIS.
Next, the ulnar nerve passes through the cubital tunnel. The cubital tunnel begins at the condylar groove between the medial epicondyle of the humerus and the olecranon of the ulna. The floor of the cubital tunnel is the elbow capsule and medial collateral ligament of the elbow joint. The roof is formed by the deep forearm investing fascia of the FCU and the arcuate ligament of Osborne, also know as the cubital tunnel retinaculum (CTR). This retinaculum is a 4 mm wide fibrous band that bridges from the medial epicondyle of the humerus to the medial aspect of the olecranon. Its fibers are oriented perpendicularly to the fibers of the FCU aponeurosis, which blends with its distal margin. The medial epicondyle and olecranon form the walls.
The capacity of the cubital tunnel is greatest when the elbow is in extension because the arcuate ligament is slack. Cadaveric measurements demonstrate that as the elbow moves from extension to flexion the distance between the medial epicondyle and the olecranon increases 5 mm for every 45 degrees of elbow flexion. The shape of the tunnel changes from a round to an oval tunnel, with a 2.5-mm loss of height. The shape change with flexion results in a 55% volume decrease in the epicondylar canal. Once through the cubital tunnel, the ulnar nerve passes between the humeral and ulnar heads of the FCU muscle. Fibrous bands have been described that compress the ulnar nerve distal to the cubital tunnel.
Sunderland described the internal topography of the ulnar nerve at the medial epicondyle ( Fig. 50-2 ). Sensory and intrinsic muscle fibers were found to be located superficially with the motor fibers to the FCU and flexor digitorum profundus deep within the nerve. The central location of these motor fibers provides protection from external forces.
Pressure can be applied to the ulnar nerve about the elbow in three ways: compression, stretch, and friction. Small pressures applied to a nerve initially affect the endoneural microcirculation. The nocturnal paresthesias reported by patients stem from the increased tissue pressure and edema that occur during sleep. A critical pressure level has been reported to be 30 mm Hg within the tunnel. Functional loss caused by acute compression is a result of ischemia and not of mechanical deformation. Pechan and Julis have measured intraneural pressure in the ulnar nerve at the cubital tunnel in cadaver experiments: The pressure was 7 mm Hg with full elbow extension and 11 to 24 mm Hg at 90 degrees of flexion. Werner and colleagues noted that, during elbow flexion, pressure within the tunnel increases sevenfold and can increase more than 20-fold with contraction of the flexor carpi ulnaris.
Experimental studies have demonstrated a progressive thickening of the external and internal epineurium as well as thickening of the perineurium. Persistent paresthesias are related to chronic alterations in the blood flow resulting from intraneural fibrosis. , The muscle wasting and loss of two-point discrimination found in advanced nerve compression are related to loss of nerve fiber function.
Extraneural compression of longer durations (28 days) has been studied. As with the short-term studies, subperineurial edema may persist even after the removal of the extraneural compression. Inflammatory and fibrin deposits occur within hours, followed by proliferation of endoneurial fibroblasts and capillary endothelial cells. Fibrous tissue from endoneurial fibroblasts proliferates within several days, followed by invasion of mast cells and macrophages into the endoneurial space. Axonal degeneration is noted in nerves subjected to compression for 4 weeks.
Histologic examination of nerves at the site of compression injury reveals proliferation of the endoneurial and perineurial microvasculature, edema in the epineurial space, and fibrotic changes. Initial changes occur in the nerve–blood barrier, followed by edema and epineurial fibrosis. Thinning of the myelin sheath then occurs at the periphery of the nerve. Axonal degeneration follows prolonged compression ( Fig. 50-3 ). The rate and severity of these changes differ throughout the nerve, possibly because of variations in the amount of connective tissue. These pathologic changes appear to be dose-dependent, based on the duration and force of compression.
Potential points of nerve compression or irritation include the arcade of Struthers, MIS cubital tunnel at the level of the medial epicondylar groove, and Osborne’s fascia, which is part of the fibrous origin and connects the two heads of the FCU ( Fig. 50-4 ). Additional causes include subluxation of the ulnar nerve over the medial epicondyle, cubitus valgus, bony spurs, hypertrophied synovium, muscle anomalies, ganglia, and direct trauma.
Laxity of the fibroaponeurotic band can result in subluxation or dislocation of the ulnar nerve from the epicondylar groove. This occurs during elbow flexion. Asymptomatic hypermobility of the nerve is found in approximately 16% of the population and is often bilateral.
One muscle anomaly, the anconeus epitrochlearis ( Fig. 50-5 ) was identified as occurring in 3.2% of symptomatic patients treated surgically. The anconeus epitrochlearis muscle was first described by Wood in 1868 and later by LeDouble in 1897 in their works about anomalous muscles in humans. The presence of this muscle is frequently associated with a prominence of the medial head of the triceps; that is, the ulnar nerve is completely covered by the triceps up to the medial humeral epicondyle, at the level of the ulnar canal, and near the olecranon notch. This configuration peculiarity exacerbates the clinical syndrome and the consequent surgical difficulties. In 1986, Dellon demonstrated the presence of the anconeus epitrochlearis in 11% of 64 cadaver dissections and of the ulnar nerve beneath the medial head of the triceps in 24% of the dissections. Clinical history of intense muscular activity (in work or sports) in young patients with cubital tunnel syndrome without other risk factors may sometimes be present.
Axial MRI is used to identify the anconeus epitrochlearis muscle extending from the medial epicondyle to the medial aspect of the olecranon and permits measurement of the diameter and recognition of the size and shape of the muscle. Coronal and sagittal slices allow for the identification of muscle position and the measurement in craniocaudal length. Short-time inversion recovery images reveal the features of muscle edema, if present. The relationships among the ulnar nerve, the muscle, and the adjacent soft tissue may be demonstrated with the use of MRI.
During ulnar nerve dissections of nonhuman primates, Dellon demonstrated that in nonanthropoid apes such as the baboon, the ulnar nerve is within the triceps and the anconeus epitrochlearis muscle is present. In anthropoid apes, the ulnar nerve is more superficial, covered by a thin sheet of triceps medial head fibers blending into the MIS, the anconeus epitrochlearis muscle is present, and Osborne’s band is not well developed. , During evolution, the medial head of the triceps regressed in humans, leaving a thin layer of fascia from the medial head of the triceps to the MIS, with the ulnar nerve lying below this thin film of fascia. The anconeus epitrochlearis muscle became so thin that the fibrous band described by Osborne may be identified as the remnant of the muscle. , Comparative anatomy studies such as the treatise of Padoa clarified that the anconeus epitrochlearis muscle and the prominent medial head of the triceps strengthened elbow adduction and extension for brachiation in climbing. In humans, this function is not required; thus, the anconeus epitrochlearis became a potential compressive agent, as did the prominence of the medial head of the triceps.
McGowan provided the following classification system:
Grade I—Mild lesions with paresthesias in the ulnar nerve distribution and a feeling of clumsiness in the affected hand; no wasting or weakness of the intrinsic muscles
Grade II—Intermediate lesions with weak interossei and muscle wasting
Grade III—Severe lesions with paralysis of the interossei and a marked weakness of the hand
Wadsworth , classified the cubital tunnel syndrome on an etiologic basis: (1) acute and subacute external compression and (2) chronic internal compression caused by a space-occupying lesions or lateral shift of the ulna (injury of the capitelar physis in childhood).
Childress studied 2000 ulnar nerves in 1000 normal subjects and found an incidence of 16% with subluxation of the ulnar nerve from the humeral epicondylar groove during elbow flexion. Two types of subluxation were defined: (1) the nerve moves onto the tip of the epicondyle when the elbow is flexed to or beyond 90 degrees, and (2) the nerve passes completely across and anterior to the epicondyle when the elbow is completely flexed. Approximately 75% of ulnar nerves with recurring subluxation are the first type.
Patients with cubital tunnel syndrome often complain of sharp or aching pain on the medial aspect of the elbow, which may radiate proximally or distally. , These patients also typically report numbness and tingling radiating into their little finger and ulnar half of the ring finger. Additional complaints may include weakness with grip and small finger usage. Symptoms vary from a vague discomfort to hypersensitivity, which is initially intermittent in nature and gradually becomes more severe and constant. Many patients report an exacerbation of their symptoms during sleep, especially with elbow flexion. Patients with longstanding neuropathy note loss of grip and pinch strength as well as loss of fine dexterity. Lastly, those with prolonged compression present with intrinsic muscle wasting, clawing, and abduction of the little finger.
Physical examination findings include a positive percussion test (Tinel’s test) over the ulnar nerve at the elbow, abnormal mobility of the ulnar nerve at the medial epicondyle, or a positive cubital tunnel compression or elbow flexion test with increased symptoms with the elbow maximally flexed. The elbow flexion test, if positive, causes reproduction or exacerbation of pain or parasthesias (or both). Evaluation should also include muscle and sensory testing, including vibratory perception and light touch with Semmes–Weinstein monofilaments. See Chapter 6 , Chapter 11 , Chapter 52 for further discussion of clinical testing procedures.
Electrodiagnostic testing may further aid in diagnosis and treatment. The loss of evoked sensory potential is a very sensitive indicator of altered conduction. Ulnar nerve compression gives rise to reduced electrical velocities across the elbow of less than 50 m/sec. Electromyographic (EMG) studies may show denervation potentials in the ulnar-innervated muscles and are consistent with cubital tunnel syndrome when nerve conduction velocity is less than 41 m/sec.
Roentgenographic studies should be done to determine the degree of cubitus valgus or assess bony lesions that can potentially compromise the cubital tunnel.
More recently, ultrasound imaging of the ulnar nerve at the elbow has been used to help confirm the diagnosis of ulnar nerve entrapment. Ultrasound is the most commonly used imaging modality because it is inexpensive, provides high resolution, is readily available, and allows for dynamic imaging during elbow flexion. Most studies suggest that the key ultrasonographic finding is enlargement of the ulnar nerve at the site of entrapment. As with previous studies, the ulnar nerve was enlarged in those with entrapment compared with controls.