The radial nerve pierces the lateral intermuscular septum 10 to 12 cm above the lateral epicondlye. It travels along the lateral border of the brachialis muscle and is covered laterally and anteriorly by the brachioradialis (BR), extensor carpi radialis longus (ECRL), and extensor carpi radialis brevis (ECRB) muscles (see FIG 1B, Chap. 97).

It divides into the PIN and the superficial radial sensory nerve 3 to 5 cm distal to the lateral epicondyle.

The PIN then enters the “radial tunnel.”

Proximal to the supinator, the nerve often is crossed superficially by branches of the radial recurrent artery known as the vascular leash of Henry.

Roles and Maudsley⁹ described the concept of radial nerve compression in 1972, suggesting that it could result in a wide spectrum of symptoms. Both radial tunnel and posterior interosseous syndrome are thought to be due to compression of the PIN. It is thought that the different clinical presentations may be attributed to a difference in the degree of compression.

The compression may rarely be due to space-occupying lesions such as ganglion, neoplasm, or florid synovitis of the proximal radioulnar, radiocapitellar, or ulnotrochlear joints.

The sites of compression of the PIN most often cited are the fibrous proximal border of the supinator (arcade of Frohse), the medial border of the ECRB, fibrous bands passing volar to the radial head, and the vascular leash of Henry.

Werner et al¹³ recorded pressures from 40 to 50 mm Hg exerted on the nerve with passive stretch of the supinator muscle. Pressures exceeding 250 mm Hg have been recorded on the nerve with stimulated tetanic contraction of the supinator muscle. Ischemia of the nerve has been demonstrated at 60 to 80 mm Hg and blockade of axonal transport at 50 mm Hg.

The documented changes in pressure due to positioning of the forearm in conjunction with the observation that symptoms often are associated with repetitive pronation and supination have led to the theory that the clinical syndrome may be provoked by dynamic and intermittent compression on the radial nerve.

Although the PIN is considered a motor nerve, it has been well documented that afferent sensory fibers run within the nerve. The muscles innervated by the PIN contain nerve endings corresponding to group IIA fibers and unmyelinated group IV fibers from muscle fibers along its distribution. These fibers are commonly thought to be responsible for the pain from muscle cramps and, therefore, could likely be mediators of pain in radial tunnel syndrome. These small myelinated and unmyelinated fibers are not associated by nerve conduction studies.

Because of the common association with (or difficulty in distinguishing it from) lateral epicondylitis, some authors have suggested that referred pain from lateral epicondylitis or intraarticular pathology may contribute to radial tunnel syndrome.

The diagnosis of radial tunnel syndrome is based on clinical findings. Historically, it was described as a cause of treatment-resistant lateral epicondylitis. The two disorders may have similar and overlapping symptoms. The clinician should distinguish when possible between these two diagnoses.

Symptoms can be variable, but the classic history described by the patient with radial tunnel syndrome is of pain over the lateral forearm musculature distal to the lateral epicondyle (along the course of the radial nerve) that is exacerbated by activity.

The most specific finding on physical examination is pain with digital pressure placed on the radial nerve over the mobile wad at the radial neck or over the proximal edge of the supinator approximately 4 cm distal to the lateral epicondyle.

Two other pathognomonic signs (described by Lister et al⁶) are pain in the lateral forearm with resisted extension of the middle finger and pain with resisted supination.

The most sensitive examination for radial tunnel syndrome involves application of firm constant pressure over the mobile wad onto the radial neck to locate the point of maximum tenderness.

The middle finger test—extension of the middle finger against resistance with the elbow extended—transmits pressure to the third metacarpal, indirectly tensioning the ECRB and causing increased pressure on the PIN.

If pain is reproduced at the point of maximal tenderness with supination of the forearm against resistance, the supinator is implicated as the culprit in intermittently increasing pressure on PIN.

If the patient’s clinical examination is suggestive of elbow arthritis or cervical radiculopathy, radiographs of the elbow and a cervical spine series may be helpful in elucidating associated pathology that may contribute to a neuropathy of the radial nerve caused by an anterior osteophyte of the elbow or degenerative disc disease of the cervical spine.

Magnetic resonance imaging (MRI) can be helpful in identifying possible cervical degenerative disc disease or elbow ganglia.

Injection of lidocaine into the radial tunnel has been described as a diagnostic tool for radial tunnel syndrome.

Multiple studies using electromyography (EMG) and nerve conduction velocity have shown no consistent relation between symptoms of radial tunnel syndrome and the findings on these tests.

A course of nonoperative treatment should always be attempted.

Activity modification may be helpful, particularly in patients whose vocation or avocation involves frequent repetitive supination and pronation of the forearm.

The patient should attempt stretching exercises of the supinator and the ECRB, with pronation of the forearm and wrist flexion with the elbow in extension. Gentle strengthening exercise also may be helpful in improving symptoms.

An injection of local anesthetic and corticosteroid in the radial tunnel may provide relief in some patients.

Surgical management should be considered in the patient who has failed nonoperative treatment.

There is no consensus as to which anatomic structures should be released at the time of surgery. It is agreed, however, that this is typically a clinical decision. Electrodiagnostic studies do not reliably locate the area of pathology.