cme current approach to radial nerve paralysis · identify all potential points of radial nerve...

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CME Current Approach to Radial Nerve Paralysis James B. Lowe, III, M.D., Subhro K. Sen, M.D., and Susan E. Mackinnon, M.D. St. Louis, Mo. Learning Objectives: After studying this article, the participant should be able to: 1. Identify all potential points of radial nerve compression and other likely causes of radial nerve injury. 2. Accurately diagnose both surgical and nonsurgical causes of radial nerve paralysis. 3. Define a safe and effective approach to the surgical release and reconstruction of the radial nerve. Radial nerve paralysis, which can result from a complex humerus fracture, direct nerve trauma, compressive neu- ropathies, neuritis, or (rarely) from malignant tumor for- mation, has been reported throughout the literature, with some controversy regarding its diagnosis and manage- ment. The appropriate management of any radial nerve palsy depends primarily on an accurate determination of its cause, severity, duration, and level of involvement. The radial nerve can be injured as proximally as the brachial plexus or as distally as the posterior interosseous or radial sensory nerve. This article reviews the etiology, prognosis, and various treatments available for radial nerve paralysis. It also provides a new classification system and treatment algorithm to assist in the management of patients with radial nerve palsies, and it offers a simple, five-step ap- proach to radial nerve release in the forearm. (Plast. Reconstr. Surg. 110: 1099, 2002.) The radial nerve is the most frequently in- jured major nerve in the upper extremity. 1 Ra- dial nerve paralysis generally can be divided into either open or closed injuries. All open injuries require exploration, whereas most closed injuries can usually be observed. The most common associated cause of radial nerve injury is a fracture to the shaft of the humerus. Iatrogenic injuries to the radial nerve may oc- cur during complex and routine procedures of the upper extremity. Acute trauma from lacer- ations, missiles, injections, or traction can also result in radial nerve paralysis. Chronic or acute radial nerve compression can initiate a wide range of clinical symptoms, from weak- ness in wrist extension to complete radial nerve paralysis. Rarely, a neuritis or tumor of the radial nerve at levels as high as the brachial plexus will present with radial nerve palsy. Treatment options for radial nerve paralysis are dependent upon the primary cause and level of injury. A radial nerve paralysis without an associated laceration or penetration is con- sidered “closed.” Fractures of the humerus may result in a closed radial nerve injury that is typically observed for a period of 3 months before surgical exploration. Idiopathic causes of radial nerve paralysis can be treated conser- vatively after treatable causes such as tumors have been excluded. The surgical options for open radial nerve injuries that result in a loss of nerve continuity include primary repair, nerve grafts, or tendon transfers. Recently, nerve transfer has been reported as a potential alter- native to tendon transfer after the complete loss of radial nerve function or a significant delay in treatment. 2 RELEVANT ANATOMY The radial nerve exits the brachial plexus from the posterior cord with contributions from C5, C6, C7, C8, and T1, traveling dorsal to the axillary artery and vein and closely abut- ting the shaft of the humerus near the spiral groove. Whitson 3 has shown that the nerve ac- tually lies several centimeters distal to the spiral groove, separated from the bone by a thin layer of the medial head of the triceps. It then runs posterolaterally, in proximity to the deep bra- chial artery beneath the lateral head of the From the Division of Plastic and Reconstructive Surgery, Washington University School of Medicine. Received for publication October 1, 2001; revised February 12, 2002. DOI: 10.1097/01.PRS.0000020996.11823.3F 1099

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Page 1: CME Current Approach to Radial Nerve Paralysis · Identify all potential points of radial nerve compression and other likely causes of radial nerve injury. 2. Accurately diagnose

CME

Current Approach to Radial Nerve ParalysisJames B. Lowe, III, M.D., Subhro K. Sen, M.D., and Susan E. Mackinnon, M.D.St. Louis, Mo.

Learning Objectives: After studying this article, the participant should be able to: 1. Identify all potential points of radialnerve compression and other likely causes of radial nerve injury. 2. Accurately diagnose both surgical and nonsurgicalcauses of radial nerve paralysis. 3. Define a safe and effective approach to the surgical release and reconstruction of theradial nerve.

Radial nerve paralysis, which can result from a complexhumerus fracture, direct nerve trauma, compressive neu-ropathies, neuritis, or (rarely) from malignant tumor for-mation, has been reported throughout the literature, withsome controversy regarding its diagnosis and manage-ment. The appropriate management of any radial nervepalsy depends primarily on an accurate determination ofits cause, severity, duration, and level of involvement. Theradial nerve can be injured as proximally as the brachialplexus or as distally as the posterior interosseous or radialsensory nerve. This article reviews the etiology, prognosis,and various treatments available for radial nerve paralysis.It also provides a new classification system and treatmentalgorithm to assist in the management of patients withradial nerve palsies, and it offers a simple, five-step ap-proach to radial nerve release in the forearm. (Plast.Reconstr. Surg. 110: 1099, 2002.)

The radial nerve is the most frequently in-jured major nerve in the upper extremity.1 Ra-dial nerve paralysis generally can be dividedinto either open or closed injuries. All openinjuries require exploration, whereas mostclosed injuries can usually be observed. Themost common associated cause of radial nerveinjury is a fracture to the shaft of the humerus.Iatrogenic injuries to the radial nerve may oc-cur during complex and routine procedures ofthe upper extremity. Acute trauma from lacer-ations, missiles, injections, or traction can alsoresult in radial nerve paralysis. Chronic oracute radial nerve compression can initiate awide range of clinical symptoms, from weak-ness in wrist extension to complete radial nerveparalysis. Rarely, a neuritis or tumor of the

radial nerve at levels as high as the brachialplexus will present with radial nerve palsy.

Treatment options for radial nerve paralysisare dependent upon the primary cause andlevel of injury. A radial nerve paralysis withoutan associated laceration or penetration is con-sidered “closed.” Fractures of the humerus mayresult in a closed radial nerve injury that istypically observed for a period of 3 monthsbefore surgical exploration. Idiopathic causesof radial nerve paralysis can be treated conser-vatively after treatable causes such as tumorshave been excluded. The surgical options foropen radial nerve injuries that result in a loss ofnerve continuity include primary repair, nervegrafts, or tendon transfers. Recently, nervetransfer has been reported as a potential alter-native to tendon transfer after the completeloss of radial nerve function or a significantdelay in treatment.2

RELEVANT ANATOMY

The radial nerve exits the brachial plexusfrom the posterior cord with contributionsfrom C5, C6, C7, C8, and T1, traveling dorsalto the axillary artery and vein and closely abut-ting the shaft of the humerus near the spiralgroove. Whitson3 has shown that the nerve ac-tually lies several centimeters distal to the spiralgroove, separated from the bone by a thin layerof the medial head of the triceps. It then runsposterolaterally, in proximity to the deep bra-chial artery beneath the lateral head of the

From the Division of Plastic and Reconstructive Surgery, Washington University School of Medicine. Received for publication October 1, 2001;revised February 12, 2002.

DOI: 10.1097/01.PRS.0000020996.11823.3F

1099

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triceps, traveling along the anterior surface ofthe lateral intermuscular septum.

The radial nerve gives off branches to theextensor carpi radialis longus and brachiora-dialis as it enters the antebrachial fossa be-tween the biceps and brachialis medially andthe brachioradialis laterally. As it passes overthe elbow joint, it divides into a terminal motorand sensory branch at the level of the radio-capitellar joint, but the exact site may vary by asmuch as 5 cm.4,5 The motor branch is theposterior interosseous (or deep radial) nerve,and the sensory branch is the superficial radialnerve.

The superficial branch of the radial nerveruns into the forearm under the brachioradia-lis before innervating the radial aspects of thedorsal wrist and hand. The posterior interosse-ous nerve travels a short distance over the ra-diohumeral joint, passing dorsolaterallyaround the radial head before entering thesubstance of the supinator.6 The nerve thenwinds around the neck of the radius to travelon the dorsal surface of the interosseousmembrane.

The posterior interosseous nerve suppliesthe majority of forearm and hand extensors(including the extensor carpi radialis brevis,supinator, extensor digitorum communis, ex-tensor digiti quinti, extensor carpi ulnaris, ab-ductor pollicis longus, extensor pollicis longusand brevis, and extensor indicis proprius), withthe exception of the extensor carpi radialislongus and brachioradialis. The normal courseof the posterior interosseous nerve is throughthe supinator brevis muscle. Two anomalouscourses of the nerve have been described byWoltman and Learmonth.7 One anomaly oc-curs in substance of the supinator, and theother involves a branch traveling superficial tothe supinator brevis.

HISTORICAL PERSPECTIVE

In 1863, Agnew8 explored the forearm of apatient with flexor and extensor weakness andfound a mass compressing the posterior in-terosseous and median nerves. The patient re-portedly recovered after removal of the solidmass. Weinberger quoted Nancrede’s observa-tion of a patient with a bursa between thecommon extensor muscles and the extensorcarpi ulnaris compressing the posterior in-terosseous nerve.9 –11 In 1905, Guillain andCourtellemont12 reported a case of radial nervepalsy that they believed to be related to re-

peated pronation and supination in a musicalconductor. Grigoresco and Iordanesco13 re-ported a case of posterior interosseous nervepalsy after a minor injury was made worse bythe patient sleeping with his head on hisforearm.

At the Mayo Clinic in 1934, Woltman andLearmonth7 reported five cases of idiopathicposterior interosseous nerve paralysis that didnot improve with observation or surgery. Theexploration of one patient demonstrated ananatomic abnormality, with the radial nervelying entirely superficial to the supinator mus-cle. Hobhouse and Heald14 reported an iso-lated case of idiopathic posterior interosseousparalysis in 1936, and Otenasek15 reported acase of posterior interosseous nerve palsy in1947 that seemed to result from swellingaround the nerve at exploration.

Various authors throughout the early 1900sreported injury to the radial nerve after elbowtrauma.16,17 Richmond18 and Hustead et al.19

reported a case of radial nerve paralysis relatedto soft-tissue masses, and Kruse20 reported acase of radial nerve palsy in a swimmer thatresolved within 3 months without surgical in-tervention. By the middle of the 20th century,the symptoms associated with radial nerve palsyhad been fully described, but its specific patho-genesis remained unclear.

PATHOGENESIS OF RADIAL NERVE PALSY

Radial nerve paralysis may not always have aclear origin. The radial nerve may be paralyzedat any point along its course from the brachialplexus to the hand, resulting in a similar clin-ical presentation regardless of the cause. De-termining the level of injury often assists thephysician in identifying the origin of the disor-der. Several distinct causes of radial nerve pa-ralysis have been clearly identified in the liter-ature. A review of these potential causes willassist the physician in determining the mostappropriate surgical option.

Orthopedic Injury

The radial nerve is injured through orthope-dic trauma more than any other majornerve.21,22 It is estimated that over 237,000 hu-meral fractures occur each year in the UnitedStates, with 75 percent of these fractures involv-ing the humeral shaft.21 Approximately 12 per-cent of humeral shaft fractures are compli-cated by a radial nerve paralysis.1,23,24

Spontaneous recovery within 8 to 16 weeks has

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been reported in over 70 percent of thecases.21,23

Rarely, the radial nerve can become en-trapped in the bony fragments or callous afterhumeral fractures. In particular, spiral frac-tures of the distal shaft of the humerus withradial angulations have been associated withradial nerve paralysis.25 Bateman26 reportedthat radial nerve paralysis occurred more com-monly after open reduction of humeral frac-tures. Radial nerve paralysis associated with dis-location of the radial head is believed to resultfrom traction on the nerve within the sub-stance of the supinator, but the paralysis isusually transient.26 It is important to under-stand the vulnerability of the posterior in-terosseous nerve during surgical exploration ofthe elbow and its susceptibility to compressionin this area.

There is a prognostic difference between pri-mary (occurring after trauma) and secondary(occurring after treatment) radial nerve paral-ysis following humeral fractures. Shaw andSakellarides27 reported spontaneous recoveryin only 40 percent of patients with primaryparalysis, but in all patients with secondary pa-ralysis after closed or open reduction internalfixation. Garcia and Maeck28 reviewed over 226patients with fractures of the humeral shaft.They found that immediate radial nerve palsiesoccurred in 11.7 percent of patients with hu-meral shaft fractures. Twenty-three percent ofthe patients explored developed secondary ra-dial nerve paralysis, with 10 percent of thesepatients experiencing persistent symptoms.

Monteggia fractures involve dislocation ofthe radial head and fracture of the ulna. Thesefractures may be complicated by a radial nervepalsy at the level of the posterior interosseousnerve.29–31 A radial nerve injury is more com-mon in humeral fractures that are associatedwith a radial head dislocation because of theintimate anatomic relationship between thenerve and the radial head.29,32,33 In this type ofinjury, the radial nerve may be stretched, com-pressed, or lacerated. Lichter and Jacobsen34

reported a delayed posterior interosseousnerve palsy that occurred over 30 years after aMonteggia fracture.

The radial nerve may be inadvertently di-vided during any surgical procedures per-formed in proximity to the nerve. Most post-operative radial nerve paralysis results fromtraction during exposure. Forearm pronationcauses the posterior interosseous nerve to

move medially, thereby protecting it duringradial head exposure.1,35 Special care must betaken when using a posterolateral approach tothe proximal radial shaft because of the prox-imity of the radial nerve to this area. Of course,the superficial branch of the radial nerve isespecially susceptible to injury with transverseincision of the dorsoradial wrist and hand.

Tumor and Inflammation

Radial nerve compression can occur as theresult of either a benign tumor or a malig-nancy. The radial nerve is more susceptible toexternal compression near bones or jointswhere ganglions can form. Benign tumors aris-ing from the elbow or at the upper end of theradius have been reported to cause posteriorinterosseous nerve paralysis.36,37 Lipomas arethe most common tumors reported in the lit-erature to cause radial nerve palsy.18,38

Sharrard39 reported a case of posterior in-terosseous nerve palsy related to a fibroma,Bowen and Stone40 a case of radial nerve pa-ralysis caused by a ganglion at the level of theelbow, and Dharapak and Nimberg41 a case ofposterior interosseous nerve compression re-sulting from a mass effect of a traumaticaneurysm.

In 1966, Capener38 published a case reportand anatomic study of the vulnerability of theposterior interosseous nerve in the forearm.Although the case involved a posterior in-terosseous nerve paralysis related to a tumor,in his discussion the author referred to anassociation between radial nerve symptoms andtennis elbow. The decompression of the radialnerve with a release of the septum of the ex-tensor digitorum communis and supinator in10 patients with tennis elbow resulted in com-plete resolution of clinical symptoms. Rolesand Maudsley42 also reported significant im-provement in clinical symptoms in patientswith resistant tennis elbow who underwent si-multaneous release of the radial nerve.

Weinberger9 described a case of posteriorinterosseous nerve palsy believed to result frominflammation of the bicipitoradial and in-terosseous bursa of the forearm. Posterior in-terosseous nerve palsy has also been reportedin patients with a history of rheumatoid arthri-tis involving the elbow.43 Marmor et al.44 re-ported a case of radial nerve paralysis caused byrheumatoid arthritis that resulted in disloca-tion of the radial head.

Radial nerve palsy may also result from nerve

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tumors. Peripheral nerve tumors can be classi-fied into neoplasms of the nerve sheath, neo-plasms nerve cell origin, metastatic tumors,neoplasms of nonneural origin, and neuro-mas.45 Unless they are associated with signifi-cant compression, benign nerve tumors such asschwannomas, neurofibromas, or intraneurallipomas rarely result in complete nerve paraly-sis. Nerve tumors that do result in paralysisshould be fully evaluated because, althoughrare, they are more likely to be malignant (aswith malignant schwannomas or nerve sheathfibrosarcomas). An unusual benign surgical en-tity of the nerve also worth noting is hypertro-phic neuropathy (or “onion whorl disease”),which is characterized as a localized enlarge-ment of the nerve resulting in the progressiveloss of nerve function.46

Anatomic Compressions

Nontraumatic radial nerve palsy is rare com-pared with paralysis resulting from orthopedictrauma. The cause of spontaneous paralysis ofthe posterior interosseous nerve or the radialnerve is often unknown. Nevertheless, acutenerve paralysis requires investigation to ruleout treatable causes of the disease such as neu-ritis, tumors, or compression. Neuritis, for ex-ample, is usually associated with several weeksof severe pain.

Many authors have sought an explanationfor radial nerve paralysis without discovering aclear etiology.40,44 In 1905, Gullain and Cour-tellemont12 reported a case of posterior in-terosseous nerve paralysis in a patient who de-nied any history of trauma, and Whitely andAlpers47 presented a case of posterior interosse-ous nerve palsy associated with a spontaneousneuroma. Sharrard39reported the improve-ment of an idiopathic posterior interosseusneuritis after the release of a crossing fibrousband, and Capener38 likened radial nerve com-pression to carpal tunnel syndrome. Recently,there has been increased interest in the asso-ciation of this disease with idiopathic compres-sive neuropathies and the entity of hereditaryneuropathy, in which some individuals mayhave a particular sensitivity to the developmentof compressive neuropathies.48,49

The radial nerve can be compressed at mul-tiple points along its course. At the elbow, forexample, it can be compressed by the fibrousbands proximal to the radial tunnel, the vascu-lar leash of Henry (the radial recurrent artery),the tendinous margin of the extensor carpi

radialis brevis, and the arcade of Frohse (thetendinous superficial head of the supinator).50

Posterior interosseous nerve syndrome is a ra-dial nerve paralysis that is believed to resultfrom compression of the deep branch of theradial nerve at the level of the arcade ofFrohse.

Arcade of Frohse. Spinner’s classic descrip-tion of the arcade of Frohse as a mechanism toposterior interosseous nerve paralysis suc-ceeded in providing a reasonable explanationfor the syndrome.6 Spinner noted that radialnerve paralysis resulted from a narrowing at theleading edge of the superficial head of the su-pinator caused by adjacent structures, neo-plasms, or inflammation. The arcade of Frohsewas noted in approximately 30 percent ofadults, but was not identified in any fetal dis-sections. Spinner theorized that repeated rotarymovement of the forearm resulted in a thick-ening of the superficial head of the supinator.

Spinner’s theory of radial nerve compressionby the arcade of Frohse has been confirmedover the years. Goldman et al.51 reported com-pression of the posterior interosseous nerve atthe arcade of Frohse, which was identified byelectromyographic examination. AlthoughNielsen52 described four cases of posterior in-terosseous nerve paralysis that were improvedby releasing the fibrous band at the supinatormuscle, Bryan et al.53 found no improvementin a patient with radial nerve paralysis 10months after the release of the arcade ofFroshe.

The size of the opening of the arcade ofFroshe is variable. The posterior interosseousnerve travels beneath the proximal edge of thesuperficial supinator and can be further nar-rowed by the tendinous medial border of theextensor carpi radialis brevis. A full release ofthe fascial edge of the extensor carpi radialisbrevis will not only improve exposure, it willalso help to decrease compression of the nerveat this level and relieve any associated symp-toms of lateral epicondylitis.

Triceps compression. Reports of transient pal-sies of the radial nerve after strenuous muscleactivity have been attributed to compression ofthe nerve by the lateral head of the triceps mus-cle.54,55 Lotem et al.54 were the first to describea radial nerve palsy resulting from a fibrous archformed by the lateral head of the triceps. Thisarch was reportedly located approximately 2 cmdistal to the deltoid insertion or the lateral bor-der of the humerus. Although the injury was

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thought to be a radial neuropraxia that did notrequire surgical intervention, Manske55 later re-ported a permanent paralysis of the radial nervein this area after strenuous activity, requiringsurgical exploration and release. As far back as1945, Sunderland56 reported radial nerve pa-ralysis that had resulted from nerve compres-sion at the edge of the latissimus dorsi tendonand long head of the triceps from usingcrutches.

Open Wounds

The radial nerve is seldom divided in trau-matic lacerations because of the deep positionof the motor component of the nerve.1 Never-theless, penetrating wounds associated with ra-dial nerve palsy require surgical exploration torule out axonotmesis. When the radial nerve issharply divided, the clinical results after pri-mary repair have been good to fair in mostinstances, if the nerve is explored early andrepaired without tension.1,57 It is of particularinterest that the radial nerve has been found tobe transected in up to 50 percent of patientsfollowing gunshot wounds associated with hu-meral fractures.5

The treatment of postoperative radial nervepalsy requires a great deal of consideration. Toidentify nerve injuries in advance and to avoidany questions of origin after surgery, it is im-portant to do a complete upper extremitynerve exam before any invasive procedure isperformed in proximity to major nerves. Theradial nerve can be injured inadvertently dur-ing orthopedic or vascular access proce-dures.58,59 A previous surgical scar or an explo-ration of the arm without the aid of atourniquet often prevents a clear identificationof nerves during dissections. Radial nerve pa-ralysis may occur as the result of a tractioninjury or compressive neuropraxia after sur-gery.60,61 A thorough and honest reflection bythe surgeon is required when a radial nerveparalysis is noted after surgery. If there is anychance that the nerve may have been severedor partially transected, immediate re-explora-tion is indicated to ensure the best clinicaloutcome.62–64

Other Causes

Radial nerve paralysis has been reported inassociation with the use of a tourniquet or withinjection injuries.45 The radial and sciaticnerves are those most commonly injured byinjections.65 The high percentage of injuries to

these nerves can be attributed to their proxim-ity to common intramuscular injection sites.Tourniquets are used routinely in the operat-ing room to provide a bloodless field, andnerve paralysis after tourniquet use is 2.5 timesmore common in the upper extremity than inthe lower extremity. Upper extremity nerveparalysis is estimated to occur in one out of13,000 applications. The radial nerve is thenerve most susceptible to tourniquet trauma,with its involvement present to some extent inup to 96 percent of upper extremity tourniquetinjuries.65

Postoperative radial nerve palsies can also berelated to patient positioning or to blood pres-sure cuffs. Radial nerve paralysis may developduring sleep, especially when the patient isintoxicated, such as in a “Saturday night pal-sy.”1 Sunderland56 described a variety of radialnerve injuries resulting from compressioncaused by local trauma and ischemia. He re-ported seven cases of radial nerve palsy, five ofwhich occurred during sleep with compressionnoted at the level of the lateral intermuscularseptum. All seven patients experienced com-plete resolution of paralysis with time. Tractioninjuries after motor vehicle accidents or otherblunt traumas may result in prolonged paraly-sis of the radial nerve. Most of these nervelesions can be treated conservatively if they are“closed” and if axonotmesis is not suspected.Patients who develop a spontaneous neuropa-thy may also have a susceptibility to othercompressive neuropathies (i.e., hereditaryneuropathy).

Radial nerve paralysis has been reported asthe result of pentazocine-induced fibrous my-opathy.66 Repeated pentazocine injections tothe deltoid region was noted to induce tricepsfibrosis, causing radial nerve compression. Thepatient developed a persistent wrist drop thatrequired surgical decompression. Radialmononeuritis has also been related to alcohol,lead, arsenic, typhoid, and serum sickness.5,67

Idiopathic radial neuritis has been describedthroughout the literature, but its specific causehas yet to be clearly defined.

CLINICAL EVALUATION

Clinical presentation of radial nerve paralysisis dependent upon the cause and level of nerveinvolvement. Some patients have symptoms ofchronic compression that progress to completeparalysis, whereas other patients experience

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the acute onset of paralysis. All lesions of theradial nerve must first be distinguished fromlesions affecting the nerve roots (C5 throughT1) or the brachial plexus. The clinical symp-toms of radial nerve paralysis are often straight-forward, with patients primarily demonstratinga motor deficit of wrist and finger extension.Radial nerve injuries usually result in a de-crease in power grip and pinch primarily re-lated to the loss of wrist extension.

The level of injury can often be determinedby physical examination of the motor and sen-sory components. Anesthesia after radial nervepalsy may vary to include the dorsal surface ofthe proximal half of the thumb, index, andmiddle fingers and is usually limited to a small,triangular area on the dorsum of the first andsecond metacarpal webspaces.1 Because thesensory deficit is not on the tactile surface ofthe hand, the sensory deficit is usually trivial,but can be painful.

Loss of motor function depends on the levelof the radial nerve lesion. Although loss of theanconeus muscle is not clinically noticeableafter proximal radial nerve paralysis, the othermuscles in the upper arm can be more clearlyidentified on physical examination. These mus-cles include the triceps, brachioradialis, andextensor carpi radialis longus and brevis. Lossof triceps function reflects an injury at the levelof the brachial plexus. If the brachioradialis orextensor carpi radialis longus are not func-tional, then the injury is most likely at the levelof the humeral shaft. Proximal radial nerveinjuries result in a complete loss of extension atthe wrist and metacarpophalangeal jointsalong with a loss in extension and abduction ofthe thumb.

Posterior interosseous nerve paralysis typi-cally involves a more distal injury to the radialnerve. Patients with classic posterior interosse-ous nerve palsy experience radial deviation ofthe wrist with dorsiflexion because of the pres-ervation of the extensor carpi radialis longus.These patients are usually unable to extendtheir fingers or thumb at the metacarpopha-langeal joints, and they have no sensory deficitbecause the superficial radial nerve is pre-served. The presence of active contractions ofthe brachioradialis and wrist extension in ra-dial deviation allows for localization of the ra-dial nerve injury to a point distal to the originof the posterior interosseous nerve.

DIAGNOSTIC STUDIES

A complete patient history and a physicalexamination are often all that is needed todetermine the level of injury and the suspectedcause of radial nerve paralysis. A plain film ofthe involved area should be obtained if a frac-ture, dislocation, or foreign body is suspected.Plain x-rays of the elbow can be especially use-ful in ruling out more complicated orthopedicinjuries or disorders of the radial head. Mag-netic resonance imaging should be obtained ifa mass is suspected at any level along thecourse of the radial nerve. Nevertheless, stud-ies such as magnetic resonance imaging thatare used for diagnostic purposes in patientswith radial nerve paralysis may also be mislead-ing without clinical confirmation.

All patients experiencing neural compro-mise after penetrating injury in proximity tonerves should be explored without the needfor preoperative electrodiagnostic studies.Plain films, magnetic resonance imaging, orarteriograms may be indicated before explora-tion in some situations, but electrodiagnosticstudies are rarely helpful within the first severalweeks after nerve injury because these studiescannot differentiate between nerve injuriesthat will or will not recover spontaneously withthat time. Standard electrodiagnostic studieswill, however, help to determine the level ofinjury or its distribution if the physical exami-nation is unclear. Patients with nerve paralysisthat persists beyond 6 to 8 weeks should beexamined with electrodiagnostic studies. By 12weeks, motor unit potentials will be presentand will help to differentiate between recover-able injures and those that will require surgery.

Intraoperative nerve-to-nerve studies are anexcellent adjunct in the care of patients withperipheral nerve injuries.68,69 The results ofthese studies can assist the surgeon in the op-erative plan as long as the injury has beenallowed to fully mature. The level and extent ofa radial nerve lesion can be determined in theoperating room using this technology. Intraop-erative nerve-to-nerve studies can be used toexamine the nerve proximal and distal to asuspected lesion. If the radial nerve demon-strates conduction across a lesion, spontaneousrecovery is possible. If conduction is absentproximal to a lesion, a nerve repair or graftmay not be indicated because either a moreproximal injury must be present or the nerve iswithout function.

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CLASSIFICATION

A conservative approach to the restoration ofhand function after radial nerve paralysis haslong been advocated in the literature. In themiddle of the 20th century, many authors per-formed operations to remove offending factorscausing radial nerve paralysis, but no one re-ported functional improvement after sur-gery.7,11,15 Sharrard39 reported one case of ra-dial nerve palsy that required up to 4 years torecover. Clearly, there were no establishedguidelines at this time for the treatment ofidiopathic radial nerve palsy. In 1968, however,Spinner6 began to advocate surgical explora-tion of patients with radial nerve palsy 6 to 8weeks after clinical presentation of the disease.

Currently, most surgeons agree that oncethe diagnosis of radial nerve palsy is made,close observation is indicated. All patients re-quire a wrist splint and hand therapy to pre-vent joint stiffness or permanent loss of func-tion; however, controversy still exists as to thelength of time a patient should be observedbefore surgical intervention.4,37,45 The confu-sion surrounding the appropriate clinical treat-ment of radial nerve palsy often stems from thelack of a clear and relevant classification sys-tem. Clearly, it is important categorize all ra-dial nerve lesions based on the type of injuryand the level of involvement. A complete his-tory and physical are often all that is requiredfor complete classification, but electrodiagnos-tic or other studies may be needed in somesituations. Once the radial nerve injury is clas-sified, the appropriate treatment options canbe applied based on the information available.

In general, all nerve injuries can be classifiedas first- through sixth-degree injury.45,70 First-degree injury is a neurapraxia that results froma segmental demylination without loss of nervecontinuity or Wallerian degeneration. Second-degree injury is axonotmesis with injury to theaxon, but intact endoneurial tissue andSchwann cell tubes. Third-degree injury in-volves additional injury to the endoneurium,but the perineurium remains intact. Fourth-degree injury involves a neuroma in continuitywith complete scar block of nerve function.Fifth-degree injury is a transected nerve. Sixth-degree injury has been described and popular-ized by Mackinnon and Dellon45 as a combina-tion of any of the above injuries.

After determining the degree of nerve in-jury, we developed a classification system for

radial nerve paralysis to further assist with itsclinical diagnosis and intervention (Table I).This new classification system takes into ac-count other relevant factors critical to the suc-cessful management of patients with radialnerve palsies. All radial nerve injuries must firstbe classified as either open or closed. It isimportant to make a distinction between openand closed injuries because the management isquite different based on the degree of nerveinjury most likely associated with each disor-der. Closed injuries include radial nerve paral-ysis associated with orthopedic trauma, com-pression, neuritis, or idiopathic causes. Openinjuries include lesions associated with pene-trating wounds, lacerations, or surgical explo-rations in proximity to the radial nerve. If thereis even the slightest concern that the nerve maybe lacerated by bone fragments or surgicaltrauma, then the nerve should be explored.

The approximate level of radial nerve injuryshould be determined next. The radial nervemay be injured or paralyzed at different pointsalong its course, but there are several specificpoints at which it is more susceptible to injury.The nerve may be injured along the spiralgroove, near the radial head, or at the arcadeof Frohse.71 We have defined the level of radialnerve injury to be a high injury when it occursabove the level of insertion of the pectoralismajor muscle to the humerus, an intermediateinjury when it occurs between the insertion ofthe pectoralis muscle and the terminalbranches of the radial nerve, and a low injurywhen it involves the posterior interosseousnerve. The level of involvement can usually bedetermined by physical examination or elect-rodiagnostic studies.

Radial nerve paralysis can also be classified as

TABLE IClassification of Radial Nerve Palsy

Injury Classification Explanation of Classification

Open versus closed Injury is distinguished as either penetratingor nonpenetrating

High Injury occurs above the distal insertion ofthe pectoralis major

Intermediate Injury occurs between the insertion of thepectoralis major and the posteriorinterosseous nerve

Low Injury involves the posterior interosseous orradial sensory nerve

Compressive Injury involves chronic or acute anatomiccompression

Delayed presentation Injury involves a delay in presentation thatsignificantly limits the availabletreatment options

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either acute or chronic compression injuries.There are several important areas in which theradial nerve is particularly susceptible to eitheracute or chronic compressive neuropathy. Forinstance, the posterior interosseous nerve canbe compressed by the fascia of the radiocapi-tellar joint, the leash of Henry, the fascia of theextensor carpi radialis brevis, the arcade ofFrohse, or the distal edge of the supinator.72

The radial nerve can be compressed above theelbow by the lateral head of the triceps orhumeral exostosis.72 Radial nerve palsy may re-sult from invasion by a malignant tumor orcompression from a benign mass. If there isevidence of persistent compression at any ana-tomic point or by a nonanatomic mass, thenimmediate exploration may be indicated.

Finally, radial nerve paralysis should also beclassified based on the time of presentation. Ifa patient presents a long time after the originalinjury, the clinical management will signifi-cantly alter based on the situation. The recon-structive options for a symptomatic patient pre-senting 1 year after a high radial nerve injuryare limited. It is also extremely difficult to ex-plore open radial nerve lesions more than 10days after the injury because of significant in-flammation and scarring. The time of presen-tation after radial nerve paralysis is particularlyimportant because the motor endplates mustbe reinnervated within 1 year if motor functionis to be restored.45 Electrodiagnostic studiesshould be obtained on all patients who fail todemonstrate improvement within 3 months ofinjury. The level and duration of the injury will

ultimately be the primary factors that deter-mine the reconstructive options available.Therefore, it is extremely important to involvea peripheral nerve surgeon early in the man-agement of all patients presenting with radialnerve palsy to optimize care and recovery.

MANAGEMENT OPTIONS

An algorithm for the treatment of radialnerve palsy was developed to determine theneed for surgical reconstruction based on aconcise and clinically relevant classification sys-tem (Fig. 1). The first step in determining atreatment is to classify the lesion as either openor closed. All radial nerve palsies associatedwith open wounds should be explored surgi-cally. If the nerve is found to be in continuity atthe time of the exploration, it is treated as aclosed injury. If the radial nerve has beensharply transected, but there is adequate nervelength and minimal soft-tissue injury, then itshould be repaired primarily.

A primary nerve repair should be performedwithout tension by mobilizing the nerve bothproximally and distally. To ensure completeremoval of the lesion or zone of injury, onlysurgeons familiar with the technique shouldperform acute nerve grafting in this situation.The proximal and distal extent of thetransected or injured nerve can be moreclearly delineated if the surgery is delayed for 3weeks. Nevertheless, it may be quite difficult toexplore a nerve safely after a delay because ofthe progression of the surgical scar. Before 3weeks, the extent of nerve injury can be deter-

FIG. 1. Radial nerve palsy algorithm.

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mined with intraoperative electrodiagnosticstudies and microscopic examination.

The management of closed radial nerve pal-sies is far less straightforward. Closed radialnerve injuries can be associated with a widerange of underlying pathology. Surgical explo-ration is indicated only when transection of theradial nerve is suspected, as might be the caseafter a comminuted humeral fracture. If a ra-dial nerve transection is not suspected, thenthe patient should be observed closely for aperiod of 3 months.6,45 The clinical outcome isdependent upon an accurate determination ofthe degree of nerve injury based on a completepatient history and physical and a well-timedelectrodiagnostic study (when indicated). For-tunately, most closed radial nerve palsies areassociated with either a neurapraxia or a sec-ond- or third-degree injury that usually recov-ers spontaneously with time. A Tinel sign canbe used to follow the progressive recovery ofthe nerve along its anatomic course in bothsecond- and third-degree injuries.

A physical examination of the upper extrem-ity will help to determine a clinically obviousmass causing radial nerve compression. How-ever, magnetic resonance imaging may beneeded in some situations to rule out a lessobvious soft-tissue mass, although both false-negative and false-positive magnetic resonanceimaging reports may be seen in this situation. Itis important to prevent joint contractures witha wrist splint and aggressive hand therapy dur-ing the 3 months of observation. Patients whodo not demonstrate clinical evidence of recov-ery within 2 to 3 months of observation or aftera negative surgical exploration should undergo

electrodiagnostic evaluation. Surgical interven-tion is indicated if no clinical or electrical evi-dence of reinnervation is seen within 3months.

Electrodiagnostic studies will help to deter-mine the level and extent of the radial nerveinjury. High, intermediate, or low radial nerveinjuries should be explored, compressionpoints should be released, and the nerveshould be repaired or reconstructed when con-servative management fails. The level of thenerve injury can be further delineated by anintraoperative, nerve-to-nerve study, as men-tioned earlier. Because the motor endplatesare not out of reach for regenerating axons,patients with low and intermediate radial nerveinjuries repaired primarily or grafted at 3 to 4months have an excellent prognosis.4,73 Con-versely, the axons have a long distance to travelafter a high radial nerve injury. This has re-sulted in the recommendation for tendon ornerve transfer after high injuries that fail torecover within 3 months. Also, patients withcomplete loss of radial nerve function follow-ing neuritis or whose treatment has been sig-nificantly delayed should be considered fortendon or nerve transfer (Table II).

Five-Step Radial Nerve Release

The general approach to the posterior in-terosseous nerve has been described previouslyin the literature.74 The radial nerve at the fore-arm is approached using a standard, five-stepapproach in which: 1) The interval betweenthe extensor carpi radialis longus and the bra-chioradialis muscle is palpated preoperativelyby having the patient extend his or her wrist

TABLE IITreatment Recommendations for Radial Nerve Palsy

Level of Injury Type of Injury* Treatment Recommendation(s)

Low Neurapraxia Observation for 3 monthsAxonotmesis (I, II, III, VI) Observation for 3 monthsAxonotmesis (IV) Nerve graftNeurotmesis Primary repair, nerve graft

Intermediate Neurapraxia Observation for 3 monthsAxonotmesis (I, II, III, VI) Observation for 3 monthsAxonotmesis (IV) Nerve graftNeurotmesis Primary repair, nerve graft

High Neurapraxia Observation for 3 monthsAxonotmesis (I, II, III, VI) Observation for 3 monthsAxonotmesis (IV) Tendon transfer, nerve transferNeurotmesis Tendon transfer, nerve transfer

* I, first-degree injury or neuropraxia; II, second-degree injury with axonotmesis involving the axon and myelin but intact endoneurium; III, third-degree injurywith axonotmesis involving the axon, myelin, and endoneurium but intact perineurium; IV, fourth-degree injury is a neuroma in-continuity; V, fifth-degree injury isa transected nerve or neurotmesis; VI, sixth-degree injury is a combination of any of the above injuries (Mackinnon, S. and Dellon, A. L. Surgery of the Peripheral Nerve.New York: Thieme, 1988.

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against resistance; 2) a longitudinal incision ismade, and the interval between the two mus-cles is identified by a slight color differenceand the intervening posterior cutaneous nerveof the forearm; 3) the nerve is protected, andthe avascular plain between the two muscles iscarefully dissected; 4) the fascial edge of theextensor carpi radialis brevis is identified andreleased, exposing the underlying supinator;and 5) the edge of the supinator is identifiedand released, exposing the underlyingbranches of the radial nerve.

The radial sensory nerve, the nerve to theextensor carpi radialis brevis, and the posteriorinterosseous nerve can be fully distinguishedthrough the above-described approach. Spe-cific areas of compression can now be ad-dressed, such as the vascular leash of Henry,the arcade of Frohse, the superficial head ofthe supinator, and the fascia around the radio-capitellar joint. The posterior interosseousnerve can be approached in several differentways, depending on the surgeon’s preferenceor familiarity with the procedure.75 We havefound the approach to the radial nervethrough the brachioradialis-extensor carpi lon-gus interval to be particularly useful in ensur-ing a complete release of all potential points ofcompression at this level.

Neurorrhaphy and Nerve Grafting

The radial nerve is the most suitable forneurorrhaphy of all major nerves because thefascicles are largely motor and the most com-mon site of injury is close to motor endplates.76

Several factors, such as age, level of injury,length of defect, associated injuries, and inter-val to surgery, have been noted to influencethe recovery from nerve injury.63,77,78 Better re-sults in children probably stem from bettercentral adaptation to altered profiles afternerve repair.79 Excellent results ranging be-tween 78 and 90 percent have been reportedafter primary radial nerve repair.57,80,81

The results of radial nerve repair using nervegrafts have been comparable with primary re-pairs. Millesi et al.82,83 reported that 77 percentof patients with interfascicular radial nervegrafting obtained four out of five motorstrength. Dolenc84 reported 14 cases of radialnerve transections that required nerve grafts ofvarying lengths. He determined that the timefrom injury to surgery and the surgical condi-tion were more important than the length ofthe nerve graft. In other studies, good results

have been noted in 80 percent of patients thatrequired radial nerve grafts.85,86 Nerve graftingis indicated if the nerve defect is large or thereis significant tension on the repair.

Tendon Transfers

Most authors agree that tendon transfersprovide good results if nerve reconstructionfails in patients with radial nerve palsy. Sunder-land56 recommended a tendon transfer if therewere no signs of radial nerve recovery within 1year. In 1916, Jones87 described a tendon trans-fer for radial nerve palsy that included thepronator teres to the wrist radial extensors, theflexor carpi radialis to the extensors comminis,and the flexor carpi ulnaris to extensor indicisand pollicis longus. The transfer of both wristflexors has since been abandoned by most sur-geons because of the excess morbidity from theloss in wrist flexion.

Currently, there is continued disagreementon the best combination of tendon transfers touse in treating patients with radial nerve paral-ysis. The level of the radial nerve injury and apatient’s overall function and anatomy oftendictate the best surgical option available. Mostauthors agree that the extensor carpi radialisbrevis and longus should be reconstructed us-ing the pronator teres tendon.75,88,89 The exten-sor digitorum communis can be reconstructedusing the flexor digitorum superficialis (III),the flexor carpi ulnaris, or the flexor carpiradialis.75,88,89 The rerouted extensor pollicislongus can be reconstructed using the palmarislongus or the flexor digitorum superficialis(IV), and, in some cases, the abductor pollicislongus and extensor pollicis brevis can be re-constructed with the flexor carpi radialis.75,88,89

We prefer to use the pronator teres to theextensor carpi radialis brevis, the flexor carpiulnaris to the extensor digitorum communis,and the palmaris longus rerouted to the exten-sor pollicis longus (when available); otherwise,we use the flexor digitorum superficialis.

In the 1970s, Bevin80 advocated early tendontransfer in radial nerve transection. He re-ported an average recovery time from nerverepair to be 7.5 months, with 66 percent ofpatients achieving good or excellent function.In the tendon transfer group, all patientsnoted good to excellent results in 8 weeks. Thepronator teres was transferred to the extensorcarpi radialis longus and brevis, the palmarislongus was transferred to the thumb extensorsand long abductor (when present), and the

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flexor carpi ulnaris was transferred to the com-mon digital extensors. When the palmaris lon-gus was not present, the thumb extensors andabductor were motored by the flexor carpi ul-naris as well. However, it was difficult to fullydetermine from Bevin’s article the approxi-mate level of the radial nerve injury in thepatients reviewed.

Burkhalter76 also advocated early tendontransfer because he believed the transfer actsboth as a substitute during regrowth of thenerve or when lesions are irreparable and alsoas a helper during reinnervation. In a recentarticle, Kruft et al.90 reported that irreversibleradial nerve paralysis should be treated withearly tendon transfer. They reported 43 pa-tients who underwent tendon transfer, with 38patients ultimately returning to their originaljobs. The authors qualified their results by stat-ing that tendon transfers “never fully replacean intact radial nerve for the purpose of con-trolling the hand.”

Elton and Omer91 observed that patientswith radial nerve paralysis treated by tendontransfer often experienced extensor tightness,which prevented simultaneous flexion of thewrist and fingers. Barton1 described this as a“rather unnatural movement, seldom neededin ordinary life.” Several authors have thoughtthat the greatest functional loss after radialnerve palsy was not the loss of finger extension,but instead the loss of power grip, which can-not be easily recreated with standard tendontransfers.76,92 As such, it is important to fullyexamine alternative approaches to treating ra-dial nerve palsy to decrease the long-term mor-bidity associated with tendon transfers thatclinically often appear “unnatural.”

Nerve Transfer

In 1948, Lurje93 described the use of nervetransfers for severe brachial plexus injurieswhen other options were not available. In the1960s, the popularity of nerve grafting tendedto overshadow such early pioneering work innerve transfers.94 Currently, nerve transfers aretypically performed under limited circum-stances such as brachial plexus avulsions, whenno other options are available.95–99 Although,we have had excellent experience with nervetransfers using nearby, expendable motor fi-bers for reconstruction,94 we believe that nervetransfers may have limited applications for cer-tain types of high radial nerve palsies or incases of radial neuritis.

The median nerve has a limited number ofanatomic variations in the forearm; therefore,it provides several dependable sources fornerve transfer to the distal radial nerve.100 Themedian nerve supplies several redundant nervebranches to the flexor digitorum superficialismuscle groups that can be transferred in cer-tain situations. The nerve branch to the pal-maris longus can also be sacrificed if it is notrequired for future tendon transfers. Intraop-erative sensorimotor topographical identifica-tion can be used to identify redundantbranches of the median nerve that can betransferred to the radial nerve. We have suc-cessfully transferred redundant branches ofthe median nerve to the posterior interosseousnerve in the forearm of several radial nerveparalysis patients, with good long-term results2;however, additional experience with this tech-nique is needed before definitive recommen-dations regarding its indications and use canbe made. Nevertheless, continued success withnerve transfers in patients with radial nerveparalysis may provide a useful alternative totendon transfers in patients with delayed pre-sentation or high proximal nerve injuries or insituations of complete loss of nerve function.

CONCLUSIONS

The optimal treatment of patients with ra-dial nerve paralysis requires a thorough un-derstanding of the specific anatomy, clinicalpresentations, and potential causes or ori-gins of the disorder. A systematic approachto the examination and diagnosis of the dis-ease is vital to ensure the appropriate treat-ment and future recovery of these patients. Aclinically relevant classification system for ra-dial nerve paralysis should encourage clini-cians to address specific diagnostic dilemmasand injury types. Our classification systemattempts to define both the key clinical issuesthat ultimately determine the need for surgi-cal intervention and the most appropriatesurgical reconstruction. Recommendationsfor the management of radial nerve paralysisare based on the level and degree of injuryconfirmed by history and physical and byelectrodiagnostic studies (when indicated).Finally, the algorithm provides a generalguide for both the surgical and nonsurgicaloptions available based on the time of pre-sentation and the type of injury. A full inte-gration of the above material on radial nerveparalysis should assist in the overall care and

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management of patients who present withthis often complex and challenging clinicalproblem.

James B. Lowe, M.D.Division of Plastic and Reconstructive SurgeryWashington University School of MedicineOne Barnes Hospital Plaza, Suite 17424St. Louis, Mo. 63110

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Self-Assessment Examination follows onthe next page.

1112 PLASTIC AND RECONSTRUCTIVE SURGERY, September 15, 2002

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Self-Assessment Examination

Current Approach to Radial Nerve Paralysisby James B. Lowe, III, M.D., Subhro K. Sen, M.D., and Susan E. Mackinnon, M.D.

1. THE POSTERIOR INTEROSSEOUS NERVE SUPPLIES ALL THE FOLLOWING MUSCLES OF THE UPPEREXTREMITY EXCEPT:A) Extensor carpi radialis brevisB) SupinatorC) Extensor carpi ulnarisD) Abductor pollicis longusE) Brachioradialis

2. RADIAL NERVE COMPRESSION HAS BEEN REPORTED AT ALL POINTS LISTED BELOW EXCEPT:A) Triceps tendonB) Vascular leash of HenryC) Arcade of FrohseD) Tendinous margin of the extensor carpi radialis brevisE) Tendinous margin of the extensor carpi radialis longus

3. UPPER EXTREMITY NERVE PARALYSIS FOLLOWING TOURNIQUET APPLICATION IS ESTIMATED TOOCCUR AT APPROXIMATELY WHAT RATIO?A) One out of 130B) One out of 1300C) One out of 13,000D) One out of 130,000E) One out of 1,300,000

4. DURING SURGICAL EXPLORATION OF THE RADIAL HEAD AT THE ELBOW, WHAT MANEUVER WOULDPROTECT THE RADIAL NERVE DURING A STANDARD EXPOSURE?A) Forearm supinationB) Forearm pronationC) Elbow distractionD) Elbow extensionE) Elbow flexion

5. COMPRESSION OF THE POSTERIOR INTEROSSEOUS NERVE BY THE ARCADE OF FROHSE IS CAUSED BY:A) Dislocation of the radial headB) Enlargement of the deep head of the supinatorC) Thickening of the superficial head of the supinatorD) Congenital deformity of the arcade of FrohseE) Malposition of the extensor radialis carpal tendon

6. NERVE TRANSFER IS MOST LIKELY INDICATED IN WHAT SITUATION?A) Closed injuryB) Acute sharp nerve transectionC) Injuries also involving the median nerveD) Delayed diagnosis with no identifiable healthy proximal nerve segmentE) Loss of range of motion at the elbow

To complete the examination for CME credit, turn to page 1210 for instructions and the response form.