The radial nerve is a peripheral nerve originating from the ventral roots of the spinal nerves C5-T1. An extension of the posterior cord of the brachial plexus, it supplies both sensory and motor function to the upper extremity. Motor functions include innervation to the triceps brachii, posterior forearm compartment, and the extrinsic extensor muscles of the wrist and fingers. Sensory function includes cutaneous innervation of segments of the anterolateral arm, distal posterior arm, posterior forearm, and dorsal surface of the first three digits of the hand and the lateral half of the ring finger.[1, 2]
Due to the close proximity of the radial nerve to the humerus shaft, radial neuropathies most commonly result from fractures of the arm; other causes include penetrating wounds, compression, and ischemia.[3] Radial neuropathies can occur from surgical procedures such as humeral nailing performed to stabilize an acute humeral fracture.[4] Saturday night palsy, a radial nerve compression injury, commonly results from placing one’s arm over the backrest of a chair.
The pattern of clinical involvement is dependent on the mechanism, severity, and the level of injury. The most commonly reported symptom is loss of wrist extension (“wrist drop”).[5] However, affected patients can also present with sensory symptoms including pain, paresthesia, and numbness as well as motor symptoms of weakness involving extension of the elbow and fingers.
Management depends on the severity and mechanism of injury. Closed humerus fractures are often managed with conservative nonsurgical treatment, with failure of spontaneous recovery warranting surgical exploration. However, the appropriate timing of surgical exploration for radial nerve injuries remains controversial. Radial nerve injuries resulting from open humerus fractures are managed with surgical exploration and, if necessary, repair including primary neurorrhaphy and neural grafting.[6]
An introduction to radial nerve anatomy is essential for understanding the common mechanisms and locations of its injury. The radial nerve receives root innervation from C5-T1 spinal roots. It branches from the posterior cord of the brachial plexus, exiting the axilla posterior to the brachial axilla . In the upper arm, the radial nerve gives off motor branches to the triceps and anconeus muscles before it wraps around the humerus at the spiral groove (also known as the radial groove). Three sensory branches, which supply the skin over the triceps and posterior forearm, also are given off at this level. Here, its proximity to the humerus makes it susceptible to compression and/or trauma.
After exiting the spiral groove, the radial nerve supplies the brachioradialis muscle before passing over the lateral epicondyle and into the cubital fossa and forearm. Here, the radial nerve divides into the deep posterior interosseous branch and a sensory branch. The posterior interosseous branch is a pure motor nerve that supplies the supinator and then dives into the supinator through the fascia to supply the muscles of the wrist and finger extension. Known as the radial tunnel, this fascia is another common site for nerve damage to occur. The sensory branch arises near the elbow and travels down the forearm with the radial artery, inferiorly to the anterolateral portion of the radius deep to the brachioradialis. It becomes superficial at the wrist as it courses over the distal radius and over the anatomical snuffbox before it supplies the lateral aspect of the dorsum of the hand and the lateral three and a half digits (thumb, index finger, middle finger, and lateral half of the ring finger).[2] See the image below.
View Image
The Radial Nerve from Gray's Anatomy (published 1918, public domain, copyright expired).
Mechanisms of radial mononeuropathies
Crutch palsy
A compressive neuropathy that results from prolonged, direct pressure on the axilla, such as from a crutch. Patients often present with triceps weakness along with wrist and finger extensor weakness and paresthesia in the posterior forearm, posterior hand, and posterolateral portion of the last three and a half digits. Management is conservative with wrist splinting and the removal of external compression, including discontinuation of axillary crutches.
Saturday night palsy
A compressive neuropathy resulting from prolonged direct pressure against a firm object on the upper medial arm or axilla such as draping one’s arm over furniture. This injury often occurs in the setting of alcohol intoxication and deep sleep on the affected arm. Patients may present with motor symptoms including wrist drop and weakness in arm extension and sensory symptoms including numbness, tingling, and pain in the radial nerve distribution. Treatment is supportive with NSAIDs, steroids, and rest along with wrist splinting.
Honeymooner’s palsy
Another compressive neuropathy involving an individual falling asleep on the arm of another and resulting in compression of the person’s radial nerve. Similar to the presentation of Saturday night palsy, symptoms include wrist drop and sensory deficits affecting portions of the posterior forearm, hand, and fingers. Treatment involves supportive therapy with removal of external compression.
Humeral shaft fractures
Humeral shaft fractures account for 1–3% of all fractures.[7] Given the proximity of the radial nerve to the humerus bone, humeral shaft fractures are the most common cause of radial nerve mononeuropathy, with a metanalysis of 25 studies showing an overall prevalence of 11.8%. Transverse spiral fractures between the middle and distal parts of the humerus are more likely to be associated with radial nerve injury.[3] Clinical presentations vary depending on the location of the fracture and nerve injury. Patients with spiral groove fractures typically present with loss of wrist and finger extension but spare the triceps and arm extension. Patients also present with sensory deficits including loss of sensation to portions of the posterior forearm and dorsum of the hand.[8] Treatment of radial mononeuropathies related to open fractures involves early surgical exploration, while those injuries due to closed fractures are initially managed with conservative therapy followed by surgical exploration if spontaneous recovery does not occur.
Supinator syndrome is an entrapment neuropathy at the level of the supinator muscle in the arcade of Frohse (proximal border of the supinator muscle) caused by compression of the deep branch of the radial nerve passes between the heads of the supinator muscle before it becomes the posterior interosseous nerve. Supinator syndrome results from excessive supinator or pronation and commonly occurs in tennis players. Patients can present with elbow and lateral upper forearm pain and weakness in finger extension. Sensory function is preserved, as the superficial radial nerve branches off above the arcade of Frohse. Treatment involves non-surgical management with splinting, NSAIDs, and activity modification. Surgical decompression may be indicated if conservative management fails.
Radial tunnel syndrome
This is a compressive neuropathy of the posterior interosseous nerve in the proximal forearm that presents with pain over the radial tunnel, which is located along the lateral aspect of the forearm. Although similar to supinator syndrome, radial tunnel syndrome lacks motor weakness. Treatment is similar to supinator syndrome.
This is a compression or entrapment neuropathy of the superficial radial nerve over the lateral wrist characterized by sensory disturbances including pain, numbness, and/or tingling in the dorsal and radial aspect of the wrist and hand. Also known as handcuff neuropathy, the superficial radial neuropathy can result from tightened handcuffs or watchbands. Treatment is mainly conservative along with removal of sources of external compression.
The exact prevalence of radial mononeuropathy is unknown, as there are currently no recent epidemiologic studies in the literature. Their reporting in the scientific literature consists mainly of case reports.
Despite the lack of recent studies, one study using a closed claims database in the 1990s investigated nerve injury associated with anesthesia in the United States and found 15 cases of radial nerve injury out of 670 (2%) nerve injury claims as opposed to 190 ulnar nerve injuries (28%).[9]
Demographics
No racial preponderance is known. No gender predilection has been observed. Radial neuropahty is reported in all age groups.
However, mononeuropathies are rare among children and account for less than 10% of pediatric referrals for electromyographic testing[10] with ulnar mononeuropathy being the more frequently seen pediatric mononeuropathy.[11, 12]
In adults, radial mononeuropathy most commonly occurs at the spiral groove of the humerus. In contrast, a retrospective analysis of 19 children and adolescents ages one month to 19 years showed predominant localization to the posterior interosseous nerve or at the distal main radial trunk.[13]
Prognosis is dependent on the degree and type of radial nerve injury.
In most cases, in which the cause is successfully treated, patients will fully recover. However, in some cases, there may be residual partial or complete loss of movement or sensation
Most neuropathies usually representing neurapraxia and axonotmesis and caused by external compression will recover spontaneously or with conservative therapy within 2–4 months.
There is debate in the literature on the appropriate timing of surgical exploration of radial nerve injuries associated with closed humerus fractures. Most clinicians recommend surgical exploration if there is no recovery within 8–10 weeks. However, the opposing view advocates for early operative exploration, citing that nerve lacerations in up to 20% to 42% of cases associated with closed humeral shaft injuries show improved outcomes over delayed nerve repair.[6]
In a metanalysis of 23 articles looking at radial nerve palsies associated with humeral shaft fractures, spontaneous radial nerve recovery occurred in 77.2% of patients. Patients who failed conservative nonsurgical management and subsequently underwent nerve exploration more than 8 weeks after their injury had a 68.1% recovery rate compared to 89.8% of patients who underwent surgical exploration within 3 weeks of injury.[14]
In cases where recovery fails, tendon transfer surgery may provide adequate hand function.
Electromyographic testing may help not only to localize the lesion but also to provide prognostic information.
Discussing prognosis and possible complications in order to manage patient expectations and satisfaction is important. Patients should be educated on strategies and lifestyle modifications to prevent recurrence or worsening of injury. For example, in patients with posterior interosseous lesions, discuss the avoidance of activities involving repetitive pronation/supination of the forearm.
Symptoms are dependent on the site of the lesion. The onset of symptoms may be acute or insidious. Patients may present acutely with upper limb sensory and/or motor deficits depending on the site of injury and progress to more long-term complications including mild-to-severe hand deformities. The most common reported symptom is wrist drop.
Axilla lesions:
Weakness of all radial-innervated muscles (wrist drop and loss of triceps and brachioradialis reflexes)
Sensation loss in the dorsum of the arm
Arm lesions:
Weakness of radial-innervated muscles with sparing of arm extension if the lesion is at or distal to the spiral groove as the motor branch to the triceps branches off before the humerus midshaft
If the lesion is high above the elbow, then numbness of the forearm and hand may be an additional symptom
Forearm lesions
Sensation typically is spared despite the wrist drop
Pain in the forearm resembling tennis elbow may be prominent
This presentation is initially acute for several days to weeks
If the lesion is at the wrist, patients report isolated sensory changes and paresthesias over the back of the hand without motor weakness
Wrist lesions
If the lesion is at the wrist, patients report isolated sensory changes and paresthesias over the back of the hand without motor weakness
Radial neuropathy typically presents with weakness of wrist dorsiflexion (ie, wrist drop) and finger extension.
If the lesion is in the axilla, all radial-innervated muscles are involved.
The triceps and brachioradialis reflexes are decreased
Sensation is decreased occur over the triceps, the posterior part of the forearm, and dorsum of the hand
Acute compression of the radial nerve commonly occurs at the spiral groove. If the lesion is at this level, all radial-innervated muscles distal to the triceps are weak.
Triceps reflex is preserved, but brachioradialis is decreased
Sensory loss occurs over the radial dorsal part of the hand and the posterior part of the forearm
Numbness over the triceps area is variable
In isolated posterior interosseous lesions, sensation is spared and motor involvement occurs in radial muscles distal to the supinator.
Brachioradialis reflex is intact
The extensor carpi radialis sometimes is also spared, resulting in radial deviation with wrist extension
Pain may occur with palpation at the proximal forearm and with forceful supination
In distal radial sensory lesions at the wrist, no motor weakness occurs. Numbness of the dorsal hand is noted, sparing the fifth digit.
Penetrating trauma can cause injury anywhere along the nerve.
Compressive lesions high in the axilla can occur from improper use of crutches.
Compression injuries at the humeral spiral groove occur in patients with sustained compression of this area over a period of several hours.[15]
Reported in patients who fall asleep in a drunken or drug-induced stupor with an arm over a chair and in honeymooners.
Results from fracture of the humerus that leads to compression or secondary laceration of the nerve as it wraps around the humerus near the spiral groove.[16]
Reported in wheelchair users, when the spiral groove of the humerus is compressed on a hard wheelchair surface.[17]
Subluxation of the radius can produce radial nerve injury in the proximal forearm.
The posterior interosseous syndrome typically occurs from compression of this division of the radial nerve as it penetrates the supinator muscle within the proximal forearm.[18]
Associated with repetitive supination of the forearm and hypertrophy of the supinator muscle.
Can occur secondary to elbow synovitis, ganglion cysts[19] , enlarged bursa from the elbow, or tumors (especially lipomas at the entry of the radial nerve into the supinator muscle).
Isolated distal sensory radial neuropathy is associated with compression from handcuffs and tight bracelets.
Bilateral radial palsies suggest lead intoxication. Lead exposure may be occupational.[20]
A study showed that ultrasound examination can localize radial neuropathy more rapidly than standard electrophysiological testing.[21, 22] Visualization of the superficial radial nerve with high-resolution sonography has recently been reported.[23, 24]
Occasionally, imaging of the elbow region or the humeral area is indicated to determine if any mass or bony lesions are compressing the nerve. Plain radiographs may show bony causes of compression, such as fractures, dislocations, callus formations, or osteophytes. MRI is particularly helpful for soft tissue evaluation and more direct imaging of the nerve.[18]
Nerve conduction studies and needle electromyography (EMG) are essential for specific localization and to rule out a more generalized process. Nerve conduction studies of both the superficial radial sensory and radial motor nerves should be performed. For the radial motor study, stimulation sites include the forearm, the elbow, below the spiral groove, and above the spiral groove.
Needle EMG is used to differentiate among posterior interosseus neuropathy, radial neuropathy at the spiral groove, radial neuropathy in the axilla, a posterior cord lesion, C7 radiculopathy, and a central lesion. Muscle selection often includes the triceps, brachioradialis, extensor carpi radialis, extensor digitorum communis, extensor carpi ulnaris, and extensor indicis proprius.
Nerve and skin biopsies to evaluate nerve damage are rarely needed.
Various grading systems have been used by physicians for classifying peripheral nerve injuries including the Seddon classification (1972) and the Sunderland classification (1978).
The Seddon classification groups nerve injuries into three categories.[25]
1. Neuropraxia
Transient complete motor paralysis with minimal sensory involvement that commonly results from mechanical pressure. Spontaneous recovery often occurs when the offending pressure is removed.
2. Axonotmesis
More severe than neurapraxia and results from the disruption and loss of continuity of the axon with preservation of the supporting connective tissue structures including the endoneurium, perineurium, and epineurium. It is characterized by loss of both motor and sensory function. Complete recovery depends on removal of the insult and axon regeneration.
3. Neurotmesis
This is the most severe level of injury characterized by complete transection of the peripheral nerve leading to complete loss of sensory and motor function. Spontaneous recovery of function is unlikely and suboptimal without surgical intervention.
The Sunderland classification groups nerve injuries into five degrees. Grade 1 and grade 2 correspond to neurapraxia and axonotmesis, respectively. Grades 3, 4, and 5 correspond to increasing levels of neurotmesis severity. Grade 3 refers to loss of axonal and endoneurial continuity. Grade 4 involves loss of axonal, endoneural, and perineurial continuity. Grade 5 corresponds to loss of axonal, endoneurial, perineural, and epineural continuity.[26]
Therapy is dependent on the site and cause of the lesion.
When the lesion is due to external compression at the spiral groove, removing the source of the compression and conservative management is indicated.
Physical therapy, occupational (hand) therapy, and wrist splinting helps in reestablishing functional use of the hand.
If the lesion is due to a humeral fracture, the fracture must be carefully reduced and set to avoid further injury. This may require external fixation.
If no recovery is noted within several months, then exploration for the site of compression or transection with possible surgical re-anastomosis may be indicated.[27]
With posterior interosseous neuropathies, repetitive supination of the forearm should be avoided.
In distal radial sensory nerve lesions, management is typically conservative.
Oral or topical NSAIDs along with corticosteroid injections may be used for pain relief.
Surgical exploration may be considered for a chronic compressive lesion or transection.
Surgical exploration frequently is indicated for release of the nerve from tethered points in the forearm.
Localizing the lesion prior to surgery via EMG is important to assist the surgeon in identifying which section of the nerve is most likely involved.
When transection is suspected as the mechanism of injury, conservative management for several months is indicated to assure that no nerve regrowth has occurred either clinically or by electrodiagnostic measures.
If no regeneration or inadequate regeneration is confirmed, surgical exploration with possible re-anastomosis may be indicated.
Selective tendon transfer may allow for finger extension and thumb extension in cases of long-standing, irreparable radial nerve lesions.[28, 29]
Consensus has not been reached regarding the need for and timing of surgical therapy to treat radial nerve palsy with accompanying humeral fracture.[30, 31, 32, 33]
Avoid activities that can exacerbate symptoms and worsen injury such as activities involving compression along the radial nerve including the axilla or humeral region.
Avoid repetitive activities involving wrist extension and forearm rotation.
Exercise and passive movement of the elbow, forearm, and wrist should be performed to maintain full range of joint motion.
Although no medications are specifically designed for radial mononeuropathy, in cases of neuropathic pain related to the neuropathy, various agents that may help reduce neuropathic pain should be considered.
Corticosteroid injections and oral steroids can be used to reduce inflammation, swelling, and pressure around the nerve.
What is radial mononeuropathy?What is the pathophysiology of radial mononeuropathy?What is the prevalence of radial mononeuropathy in the US?What are the racial predilections of radial mononeuropathy?What are the sexual predilections of radial mononeuropathy?How does the prevalence of radial mononeuropathy vary by age?What are the signs and symptoms of radial mononeuropathy?Which physical findings are characteristic of radial mononeuropathy?What causes radial mononeuropathy?What are the differential diagnoses for Radial Mononeuropathy?What is the role of imaging studies in the evaluation of radial mononeuropathy?What is the role of nerve conduction studies and needle electromyography (EMG) in the evaluation of radial mononeuropathy?How is radial mononeuropathy treated?What is the role of surgery in the treatment of radial mononeuropathy?Which specialist consultations are beneficial to patients with radial mononeuropathy?What is the role of medications in the treatment of radial mononeuropathy?
Nasheed I Jamal, MD, Assistant Clinical Professor, Department of Neurology, Director, UCLA Neuromuscular Medicine Fellowship Program, University of California, Los Angeles, David Geffen School of Medicine; Acting Chief, Neurology Service, Associate Chief of Neurology, Los Angeles Ambulatory Care Center, Director, Multidisciplinary Clinic, Co-Director, Tele-Polyneuropathy Clinic, Department of Neurology, VA Greater Los Angeles Healthcare System
Disclosure: Nothing to disclose.
Coauthor(s)
Charley Jang, BS, MD Candidate, University of California, Los Angeles, David Geffen School of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
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.
Neil A Busis, MD, Chief of Neurology and Director of Neurodiagnostic Laboratory, UPMC Shadyside; Clinical Professor of Neurology and Director of Community Neurology, Department of Neurology, University of Pittsburgh Physicians
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Academy of Neurology<br/>Serve(d) as a speaker or a member of a speakers bureau for: American Academy of Neurology<br/>Received income in an amount equal to or greater than $250 from: American Academy of Neurology.
Chief Editor
Nicholas Lorenzo, MD, CPE, MHCM, FAAPL, Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Former Chief Medical Officer, MeMD Inc
Disclosure: Nothing to disclose.
Additional Contributors
Aashit K Shah, MD, FAAN, FANA, Chief of Neurology, Carilion Clinic; Professor, Neurology, Virginia Tech Carilion School of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Carilion Clinic<br/>Received research grant from: Xenon.
Wayne E Anderson, DO, FAHS, FAAN, Assistant Professor of Internal Medicine/Neurology, College of Osteopathic Medicine of the Pacific Western University of Health Sciences; Clinical Faculty in Family Medicine, Touro University College of Osteopathic Medicine; Clinical Instructor, Departments of Neurology and Pain Management, California Pacific Medical Center
Disclosure: Nothing to disclose.
References
Palastanga N, Soames R. The upper limb: Nerve supply. Demetriou-Swanwick R, Davies S. Anatomy and human movement: Structure and function. 6th ed. Toronto: Elsevier Ltd.; 2012. 189-192.
Jones HR Jr, Ryan MM. Mononeuropathies. Darras B, Jones HR Jr, Ryan MM, De Vivo D. Neuromuscular Disorders of Infancy, Childhood, and Adolescence: A Clinician's Approach. 2nd ed. Academic Press; 2014 Nov 25. 243-273.
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