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Radial Nerve Entrapment

  • Author: Mark Stern, MD; Chief Editor: Harris Gellman, MD  more...
 
Updated: Aug 21, 2015
 

Background

Radial nerve compression or injury may occur at any point along the anatomic course of the nerve and may have varied etiologies. Compression or scarring of the radial nerve at different points along its course may cause denervation of extensor or supinator muscles and numbness or paresthesias in the distribution of the radial sensory nerve (RSN). The result can be pain, weakness, and dysfunction.[1]

The most frequent site of compression is in the proximal forearm in the area of the supinator and involves the posterior interosseous branch. However, problems can occur proximally in relation to fractures of the humerus at the junction of the middle and proximal thirds, as well as distally on the radial aspect of the wrist.[2, 1, 3, 4, 5, 6, 7, 8]

Treatment may be conservative or surgical, depending on the pathology (see Treatment).[9]

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Anatomy

The radial nerve is the largest branch of the brachial plexus and is the continuation of the posterior cord, with nerve fibers from C6, C7, C8, and occasionally T1. It innervates the extensor and supinator musculature located in the arm and forearm and provides distal sensation.

The course of the radial nerve carries it across the latissimus dorsi deep to the axillary artery. It passes the inferior border of the teres major, winds around the medial side of the humerus, and enters the triceps muscle between the long and medial heads. It follows the spiral groove of the humerus, piercing the lateral intermuscular septum (10 cm proximal to the lateral epicondyle) from posterior to anterior, and runs between the brachialis and brachioradialis to lie anterior to the lateral condyle of the humerus.[5]

Branches to the brachioradialis and the extensor carpi radialis longus are given off just proximal to the elbow. The anconeus receives a branch from the radial nerve as well. The nerve then divides into a superficial branch and a deep branch. The extensor carpi radialis brevis may receive its innervation either from the radial nerve proper or from the posterior interosseous nerve.

The superficial branch, which is purely sensory, runs under cover of the brachioradialis in the forearm. Eight centimeters proximal to the tip of the radial styloid, the nerve pierces the fascia medial to the brachioradialis to lie dorsal to the extensor tendons. It divides into a medial branch and a lateral branch to innervate the radial wrist (with some variable overlap from the lateral antebrachial cutaneous nerve), dorsal radial hand, and dorsum of the radial three-and-a-half digits (to approximately the middle phalanx level).

The deep branch of the radial nerve, the posterior interosseous nerve, winds to the dorsum of the forearm, around the lateral side of the radius, and through the muscle fibers of the supinator. It then divides into medial and lateral branches, each of which supplies different extensor muscles.[10]

Clavert et al dissected 30 cadaveric upper limbs to define the radial nerve anatomic landmarks and to determine the relationship of the radial nerve main trunk and branches to the peripheral osseous and muscular structures in the anterior aspect of the elbow joint, so as to identify likely causes of compressive neuropathy.[11] No radial compressive neuropathy was found at the level of the supinator arch, and no adhesions were identified between the radial nerve and the joint capsule.

In four cases, Clavert et al noted dense fibrous tissue surrounding the radial nerve supply to the extensor carpi radialis brevis.[11] Neither fibrous structures nor adhesions of the deep branch of the radial nerve were observed along its course through the supinator. The fibrous arch of the supinator arose in a semicircular manner and was tendinous in 87% of extremities and membranous in 13%. The average length of the Frohse arcade was 25.9 mm, and the angle formed by the radial shaft and supinator arch was 23 degrees.

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Pathophysiology

Nerve injury secondary to compression or traction depends on intensity and duration.[4]

Seddon classified nerve injuries into the following three categories[12] :

  • Neurapraxia - This is a transient episode of motor paralysis with little or no sensory or autonomic dysfunction; no disruption of the nerve or its sheath occurs; with removal of the compressing force, recovery should be complete
  • Axonotmesis - This is a more severe nerve injury, in which the axon is disrupted but the Schwann sheath is maintained; motor, sensory, and autonomic paralysis results; recovery can occur if the compressing force is removed in a timely fashion and if the axon regenerates
  • Neurotmesis - This is the most serious injury, in which both the nerve and its sheath are disrupted; although recovery may occur, it is always incomplete, secondary to loss of nerve continuity

Sunderland classified nerve injury into five categories, as follows[4] :

  • The first is similar to neurapraxia
  • The second is similar to axonotmesis
  • The third, fourth, and fifth degrees correspond to varying degrees of neurotmesis
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Etiology

Radial nerve palsy

Radial nerve palsy in the arm most commonly is caused by fracture of the humerus, especially in the middle third (Holstein-Lewis fracture) or at the junction of the middle and distal thirds. The nerve may be compressed by the lateral intermuscular septum. This palsy may occur acutely at the time of the injury, secondary to fracture manipulation, or from a healing callus.

Other, less common causes of radial nerve palsy in the arm include compression at the fibrous arch of the lateral head of the triceps and compression by an accessory subscapularis-teres-latissimus muscle.[13, 14, 15, 16, 17]

Radial tunnel syndrome

This diagnosis is highly controversial and is thought to be a result of overuse. Some authors believe that radial tunnel syndrome may represent an early posterior interosseous nerve syndrome.[3] Sites of compression include the fibrous bands attached to the radiocapitellar joint, radial recurrent vessels, the tendinous origin of the extensor carpi radialis brevis, the tendinous origin of the supinator (ie, arcade of Frohse), and fibrous thickenings within and at the distal margin of the supinator.[18, 19, 20]

Posterior interosseous nerve syndrome

The etiology of posterior interosseous nerve syndrome is similar to that of radial tunnel syndrome. Compression is thought to occur after takeoff of the branches to the radial wrist extensors and the RSN. After emerging from the supinator, the nerve may be compressed before it bifurcates into medial and lateral branches, causing a complete paralysis of the digital extensors and dorsoradial deviation of the wrist secondary to paralysis of the extensor carpi ulnaris.

If compression occurs after the nerve bifurcates, selective paralysis of muscles occurs, depending on which branch is involved. Compression of the medial branch causes paralysis of the extensor carpi ulnaris, extensor digiti quinti, and extensor digitorum communis. Compression of the lateral branch causes paralysis of the abductor pollicis longus, extensor pollicis brevis, extensor pollicis longus, and extensor indicis proprius. Most commonly, entrapment occurs at the proximal edge of the supinator.

Other possible etiologies for posterior interosseous nerve dysfunction include trauma (Monteggia fractures[21] ), synovitis (rheumatoid), tumors, and iatrogenic injuries.

Wartenberg syndrome, described in 1932, is essentially entrapment of the superficial sensory branch of the radial nerve. Many factors may contribute to the development of Wartenberg syndrome. In patients with de Quervain tenosynovitis, secondary irritation of the RSN is frequent. Other common causes include postoperative injury, external compression, and trauma.

The anatomic site of compression corresponds to the transit of the nerve from its submuscular position beneath the brachioradialis to its subcutaneous position on the extensor carpi radialis longus. Especially with pronation, these two muscles can create a scissorlike effect, compressing the RSN.

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Epidemiology

Among the problems associated with the three major nerves in the upper extremity, radial nerve entrapment is the least common. Carpal tunnel syndrome (median nerve compression at the wrist) and cubital tunnel syndrome (ulnar nerve compression at the elbow) are much more frequent.[22, 23]

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Prognosis

Outcome and prognosis depend on the type of injury to the affected nerve, as follows:

  • With a neurapraxic lesion, whether it is in the arm, elbow, or wrist, return to normal function is rapid and complete in at least 90% of cases
  • With axonotmesis, the results after early release are not as good, and complete return of function is less reliable; recovery will probably be complete, but it will take longer, depending on the distance the nerve must travel to reach the denervated muscle
  • Neurotmesis rarely occurs in an entrapment syndrome, but if the nerve continuity has been completely disrupted, complete recovery will not occur, and the degree of recovery can only be estimated; the results of treating neurotmesis, even with surgical repair, are generally unsatisfactory

Noaman et el studied 36 patients who underwent early surgical exploration of radial nerve injury associated with fracture of the shaft of the humerus.[24] A narrow dynamic compression plate was generally used for fixation. Compression at the lateral intermuscular septum was present in 19 cases, entrapment in the fracture site in nine, and loss of continuity in eight.

In this study, neurolysis was required in 20 cases, epineurorrhaphy in nine, interfascicular nerve grafts in five, and first-intention tendon transfer in two.[24] Mean follow-up was 8.2 years. Outcome was rated good to excellent in 28 patients, fair in one, and poor (failure) in three. First-intention tendon transfers were performed in two patients, and two patients were lost to follow-up. Mean delay to recovery was 7 months after neurolysis and nerve repair and 15 months after nerve grafts. Fracture was united in all cases, and the mean time of union was 5 months.

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Contributor Information and Disclosures
Author

Mark Stern, MD Former Chief, Department of Orthopedic Surgery, Cedars-Sinai Medical Center

Mark Stern, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Medical Association, California Medical Association, Western Orthopaedic Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

N Ake Nystrom, MD, PhD Associate Professor of Orthopedic Surgery and Plastic Surgery, University of Nebraska Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Harris Gellman, MD Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine, Clinical Professor, Surgery, Nova Southeastern School of Medicine

Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, Arkansas Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

A Lee Osterman, MD Director of Hand Surgery Fellowship, Director, Philadelphia Hand Center; Director, Professor, Department of Orthopedic Surgery, Division of Hand Surgery, University Hospital, Thomas Jefferson University

Disclosure: Nothing to disclose.

References
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