Radial Nerve Entrapment

Etiology

Radial nerve entrapment is often thought to result from overuse but can certainly occur secondary to other causes such as direct trauma, fractures, lacerations, compressive devices, or post-surgical changes. The radial nerve divides into the superficial radial and posterior interosseous nerves at the level of the radiocapitellar joint. The posterior interosseous nerve runs along the radial neck before piercing the supinator muscle, a common site of entrapment.  The nerve further divides into four terminal branches that can typically be compressed at one of four other sites as well. These four sites are the fibrous bands around the radial head, the recurrent radial vessels, the arcade of Frohse, and/or the tendinous margin of the extensor carpi radialis brevis. Overuse actions and exercises that can lead to this condition are often repetitive pronation and supination of the wrist and forearm and commonly occur in the locations discussed previously.[4][5]

Epidemiology

Radial nerve entrapment is uncommon and often under-recognized. The annual incidence rate of the posterior interosseous nerve compression is estimated to be 0.03%, while the rate for superficial radial nerve compression is 0.003%.[6][7]

Pathophysiology

This condition is typically a result of nerve injury secondary to compression, traction, or direct trauma, causing a process of local swelling, edema, or even partial or complete laceration. The compression and/or traction often occur secondary to repetitive motions causing inflammation or architectural changes to the surrounding tissue. There are varying degrees of nerve damage severity. In mild cases, the compression of the nerve causes no permanent damage to the nerve, and the nerve sheath fully recovers. More severe cases can cause permanent damage to the nerve and/or nerve sheath, causing persistent deficits.

Multiple classification systems exist to categorize nerve injury grading. A popular one is the Sunderland Classification which is detailed as follows:

• 1st degree
  • mild neurapraxia (traction/compression)
  • At most in early/low-grade nerve injuries, the myelin sheath is compromised
• 2nd degree
  • only the myelin sheath and axon are injured or disrupted
• 3rd degree 
  • injury with endoneurial scarring; all components of the peripheral nerve are injured except the perineurium and epineurium
  • most variable degree of ultimate recovery
• 4th degree
  • the nerve in continuity, but at the level of injury, there is complete scarring across the nerve; only the epineurium remains intact
• 5th degree
  • included within Seddon's neurotmesis

Correlating Sunderland and Seddon's classification systems with one another:

• Seddon first degree neurapraxia is the same as Sunderland 1st degree injury
• Seddon second degree axonotmesis is the same as Sunderland 2nd degree injury
• Seddon third-degree neurotmesis injuries span Sunderland 3rd, 4th, and 5th-degree injuries

History and Physical

The presentation can certainly vary, given multiple areas of possible entrapment. Symptoms usually develop very slowly. The duration of symptoms often averages multiple years before a definitive diagnosis is made. As mentioned previously, symptoms of this type of nerve entrapment include pain, sensory and motor changes, paresthesias, and/or paralysis. Physical exam and/or history often reveal symptoms limited to the dorsoradial aspect of the distal forearm and hand. Findings of decreased sensation over the dorsoradial aspect of the forearm or hand help establish the diagnosis. A positive Tinel sign along the radial aspect of the mid-forearm is suggestive of this process. Wrist flexion, ulnar deviation, and pronation place strain on the nerve and will often reproduce or exacerbate symptoms. Resisted extension of the middle finger with the elbow extended is another sign of nerve entrapment. This sign is often used to aid in the diagnosis of lateral epicondylitis, but it also often positive in cases of radial nerve entrapment.

Evaluation

• If entrapment is suspected, radiographs should be performed to detect or rule out a fracture, healing callus, or tumor as the cause of the entrapment.
• Ultrasonography can often provide reliable visualization of injured nerves. For example, axonal swelling, hypoechogenicity of the nerve, loss of continuity of a nerve bundle, formation of a neuroma, and/or partial laceration of a nerve can all be visualized, which may aid in diagnosis.
• Magnetic resonance imaging (MRI) can be useful in detecting more subtle causes not found on radiographs or ultrasound, such as small tumors, masses, aneurysms, or compressive synovitis. MRI can also, at times, detect nerve changes during acute entrapments.
• A diagnostic nerve block to help define the distribution of pathology and presentation is considered in some situations.
• EMG/nerve conduction studies can also be considered but are inconsistent and should only be considered if surgery is a possibility.
• No standard laboratory work is necessary for establishing the diagnosis.[8][9]

Treatment / Management

First and Second Degree Nerve Injuries

• Most patients respond and recover after several months -- recommended management consists of serial exams and serial EMG/NCS testing
• Most patients respond well to conservative therapy. Consider removing any restrictive or compressive devices that are routinely worn. Consider relative rest from offending activity such as limiting repetitive pronation, supination, wrist flexion, and ulnar deviation. Often nerve glide exercises as part of occupation/physical therapy are performed in conjunction with rest and activity modification. If symptoms do not resolve with cessation of activity and rest, then consider splinting.
• If an area of pathology indicates possible compression and can be visualized on ultrasound, providers can consider ultrasound-guided hydro-dissection to free the compressed portion of the nerve.
• Oral or topical NSAIDs can be used for pain. Corticosteroid and an anesthetic combination can be injected into the point of maximal tenderness for symptomatic relief. The steroid may help decrease any inflammation contributing to the process.
• In the setting of suspected mild degrees of nerve injury, but either prolonged, absent, or delayed evidence of recovery of nerve function both clinically and by serial EMG/NCS testing, surgery should be the last option if this process has become chronic and conservative treatment has failed after six to 12 months.[10][11]
(A1)

Third Degree Nerve Injuries (Neurotmesis)

• Acutely, direct surgical repair of the partial versus complete nerve laceration.
• Nerve grafting techniques are employed in the setting of lacerations with retractions; often, this can present in the subacute setting after injury.
• Residual defects or "injury gaps" measuring >2.5 cm are recommended for nerve grafting techniques.
  • Autograft options include the sural or saphenous nerves
    • There is no documented improved functional recovery or outcome when comparing autograft versus allograft or nerve conduits

Differential Diagnosis

• Median neuropathy
• Multifocal motor neuropathy
• Radial neuropathy
• Ulnar neuropathy

Prognosis

If radial nerve entrapment has resulted in only mild damage to the nerve (neurapraxia), recovery should be rapid and complete in a relatively short time period ranging from 2 to 8 weeks. However, more severe injuries (axonotmesis) will recover more slowly. Recovery time depends on how far the regenerating axon must grow to reinnervate affected muscles; this healing rate is typically 1 mm/day.  

Surgical recovery depends on the extent of preoperative damage. Following early release of neurapraxia, the result should be a return to normal function in 80 to 90% of cases. Even after early release, the results will be less favorable with axonotmesis than in cases of neurapraxia, with complete return of function being rare.[12]

Complications

Most complications are related to surgery and include:

• Stretching of the nerve
• Severing of the nerve
• Incomplete release
• Muscle atrophy