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. Whitson3 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
1100
triceps, traveling along the anterior surface of
the lateral intermuscular septum.
The radial nerve gives off branches to the
extensor carpi radialis longus and brachiora-
dialis as it enters the antebrachial fossa be-
tween the biceps and brachialis medially and
the brachioradialis laterally. As it passes over
the elbow joint, it divides into a terminal motor
and sensory branch at the level of the radio-
capitellar joint, but the exact site may vary by as
much as 5 cm.4,5 The motor branch is the
posterior interosseous (or deep radial) nerve,
and the sensory branch is the superficial radial
nerve.
The superficial branch of the radial nerve
runs into the forearm under the brachioradia-
lis before innervating the radial aspects of the
dorsal wrist and hand. The posterior interosse-
ous nerve travels a short distance over the ra-
diohumeral joint, passing dorsolaterally
around the radial head before entering the
substance of the supinator.6 The nerve then
winds around the neck of the radius to travel
on the dorsal surface of the interosseous
membrane.
The posterior interosseous nerve supplies
the 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 longus
and brevis, and extensor indicis proprius), with
the exception of the extensor carpi radialis
longus and brachioradialis. The normal course
of the posterior interosseous nerve is through
the supinator brevis muscle. Two anomalous
courses of the nerve have been described by
Woltman and Learmonth.7 One anomaly oc-
curs in substance of the supinator, and the
other involves a branch traveling superficial to
the supinator brevis.
HISTORICAL PERSPECTIVE
In 1863, Agnew8 explored the forearm of a
patient with flexor and extensor weakness and
found a mass compressing the posterior in-
terosseous and median nerves. The patient re-
portedly recovered after removal of the solid
mass. Weinberger quoted Nancrede’s observa-
tion of a patient with a bursa between the
common extensor muscles and the extensor
carpi ulnaris compressing the posterior in-
terosseous nerve.9 –11 In 1905, Guillain and
Courtellemont12 reported a case of radial nerve
palsy that they believed to be related to re-
PLASTIC AND RECONSTRUCTIVE SURGERY, September 15, 2002
peated pronation and supination in a musical
conductor. Grigoresco and Iordanesco13 re-
ported a case of posterior interosseous nerve
palsy after a minor injury was made worse by
the patient sleeping with his head on his
forearm.
At the Mayo Clinic in 1934, Woltman and
Learmonth7 reported five cases of idiopathic
posterior interosseous nerve paralysis that did
not improve with observation or surgery. The
exploration of one patient demonstrated an
anatomic abnormality, with the radial nerve
lying entirely superficial to the supinator mus-
cle. Hobhouse and Heald14 reported an iso-
lated case of idiopathic posterior interosseous
paralysis in 1936, and Otenasek15 reported a
case of posterior interosseous nerve palsy in
1947 that seemed to result from swelling
around the nerve at exploration.
Various authors throughout the early 1900s
reported injury to the radial nerve after elbow
trauma.16,17 Richmond18 and Hustead et al.19
reported a case of radial nerve paralysis related
to soft-tissue masses, and Kruse20 reported a
case of radial nerve palsy in a swimmer that
resolved within 3 months without surgical in-
tervention. By the middle of the 20th century,
the symptoms associated with radial nerve palsy
had been fully described, but its specific patho-
genesis remained unclear.
PATHOGENESIS OF RADIAL NERVE PALSY
Radial nerve paralysis may not always have a
clear origin. The radial nerve may be paralyzed
at any point along its course from the brachial
plexus to the hand, resulting in a similar clin-
ical presentation regardless of the cause. De-
termining the level of injury often assists the
physician 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 will
assist the physician in determining the most
appropriate surgical option.
Orthopedic Injury
The radial nerve is injured through orthope-
dic trauma more than any other major
nerve.21,22 It is estimated that over 237,000 hu-
meral fractures occur each year in the United
States, 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
Vol. 110, No. 4 / RADIAL NERVE PARALYSIS
been reported in over 70 percent of the
cases.21,23
Rarely, the radial nerve can become en-
trapped in the bony fragments or callous after
humeral fractures. In particular, spiral frac-
tures of the distal shaft of the humerus with
radial angulations have been associated with
radial nerve paralysis.25 Bateman26 reported
that 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 result
from traction on the nerve within the sub-
stance of the supinator, but the paralysis is
usually transient.26 It is important to under-
stand the vulnerability of the posterior in-
terosseous nerve during surgical exploration of
the elbow and its susceptibility to compression
in 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 and
Sakellarides27 reported spontaneous recovery
in only 40 percent of patients with primary
paralysis, but in all patients with secondary pa-
ralysis after closed or open reduction internal
fixation. Garcia and Maeck28 reviewed over 226
patients with fractures of the humeral shaft.
They found that immediate radial nerve palsies
occurred in 11.7 percent of patients with hu-
meral shaft fractures. Twenty-three percent of
the patients explored developed secondary ra-
dial nerve paralysis, with 10 percent of these
patients experiencing persistent symptoms.
Monteggia fractures involve dislocation of
the radial head and fracture of the ulna. These
fractures may be complicated by a radial nerve
palsy at the level of the posterior interosseous
nerve.29 –31 A radial nerve injury is more com-
mon in humeral fractures that are associated
with a radial head dislocation because of the
intimate anatomic relationship between the
nerve and the radial head.29,32,33 In this type of
injury, the radial nerve may be stretched, com-
pressed, or lacerated. Lichter and Jacobsen34
reported a delayed posterior interosseous
nerve palsy that occurred over 30 years after a
Monteggia 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 from
traction during exposure. Forearm pronation
causes the posterior interosseous nerve to
1101
move medially, thereby protecting it during
radial head exposure.1,35 Special care must be
taken when using a posterolateral approach to
the proximal radial shaft because of the prox-
imity of the radial nerve to this area. Of course,
the superficial branch of the radial nerve is
especially susceptible to injury with transverse
incision of the dorsoradial wrist and hand.
Tumor and Inflammation
Radial nerve compression can occur as the
result of either a benign tumor or a malig-
nancy. The radial nerve is more susceptible to
external compression near bones or joints
where ganglions can form. Benign tumors aris-
ing from the elbow or at the upper end of the
radius have been reported to cause posterior
interosseous nerve paralysis.36,37 Lipomas are
the 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 the
elbow, and Dharapak and Nimberg41 a case of
posterior interosseous nerve compression re-
sulting from a mass effect of a traumatic
aneurysm.
In 1966, Capener38 published a case report
and anatomic study of the vulnerability of the
posterior 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 an
association between radial nerve symptoms and
tennis elbow. The decompression of the radial
nerve with a release of the septum of the ex-
tensor digitorum communis and supinator in
10 patients with tennis elbow resulted in com-
plete resolution of clinical symptoms. Roles
and Maudsley42 also reported significant im-
provement in clinical symptoms in patients
with resistant tennis elbow who underwent si-
multaneous release of the radial nerve.
Weinberger9 described a case of posterior
interosseous nerve palsy believed to result from
inflammation of the bicipitoradial and in-
terosseous bursa of the forearm. Posterior in-
terosseous nerve palsy has also been reported
in 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 by
rheumatoid arthritis that resulted in disloca-
tion of the radial head.
Radial nerve palsy may also result from nerve
1102 PLASTIC AND RECONSTRUCTIVE SURGERY,
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 as
schwannomas, neurofibromas, or intraneural
lipomas rarely result in complete nerve paraly-
sis. Nerve tumors that do result in paralysis
should be fully evaluated because, although
rare, they are more likely to be malignant (as
with malignant schwannomas or nerve sheath
fibrosarcomas). 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 progressive
loss of nerve function.46
Anatomic Compressions
Nontraumatic radial nerve palsy is rare com-
pared with paralysis resulting from orthopedic
trauma. The cause of spontaneous paralysis of
the posterior interosseous nerve or the radial
nerve is often unknown. Nevertheless, acute
nerve paralysis requires investigation to rule
out treatable causes of the disease such as neu-
ritis, tumors, or compression. Neuritis, for ex-
ample, is usually associated with several weeks
of severe pain.
Many authors have sought an explanation
for radial nerve paralysis without discovering a
clear 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 and
Alpers47 presented a case of posterior interosse-
ous nerve palsy associated with a spontaneous
neuroma. Sharrard39reported the improve-
ment of an idiopathic posterior interosseus
neuritis after the release of a crossing fibrous
band, 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 hereditary
neuropathy, in which some individuals may
have a particular sensitivity to the development
of compressive neuropathies.48,49
The radial nerve can be compressed at mul-
tiple points along its course. At the elbow, for
example, it can be compressed by the fibrous
bands proximal to the radial tunnel, the vascu-
lar leash of Henry (the radial recurrent artery),
the tendinous margin of the extensor carpi
September 15, 2002
radialis brevis, and the arcade of Frohse (the
tendinous superficial head of the supinator).50
Posterior interosseous nerve syndrome is a ra-
dial nerve paralysis that is believed to result
from compression of the deep branch of the
radial nerve at the level of the arcade of
Frohse.
Arcade of Frohse. Spinner’s classic descrip-
tion of the arcade of Frohse as a mechanism to
posterior interosseous nerve paralysis suc-
ceeded in providing a reasonable explanation
for the syndrome.6 Spinner noted that radial
nerve paralysis resulted from a narrowing at the
leading edge of the superficial head of the su-
pinator caused by adjacent structures, neo-
plasms, or inflammation. The arcade of Frohse
was noted in approximately 30 percent of
adults, but was not identified in any fetal dis-
sections. Spinner theorized that repeated rotary
movement of the forearm resulted in a thick-
ening of the superficial head of the supinator.
Spinner’s theory of radial nerve compression
by the arcade of Frohse has been confirmed
over the years. Goldman et al.51 reported com-
pression of the posterior interosseous nerve at
the arcade of Frohse, which was identified by
electromyographic examination. Although
Nielsen52 described four cases of posterior in-
terosseous nerve paralysis that were improved
by releasing the fibrous band at the supinator
muscle, Bryan et al.53 found no improvement
in a patient with radial nerve paralysis 10
months after the release of the arcade of
Froshe.
The size of the opening of the arcade of
Froshe is variable. The posterior interosseous
nerve travels beneath the proximal edge of the
superficial supinator and can be further nar-
rowed by the tendinous medial border of the
extensor carpi radialis brevis. A full release of
the fascial edge of the extensor carpi radialis
brevis will not only improve exposure, it will
also help to decrease compression of the nerve
at this level and relieve any associated symp-
toms of lateral epicondylitis.
Triceps compression. Reports of transient pal-
sies of the radial nerve after strenuous muscle
activity have been attributed to compression of
the nerve by the lateral head of the triceps mus-
cle.54,55 Lotem et al.54 were the first to describe
a radial nerve palsy resulting from a fibrous arch
formed by the lateral head of the triceps. This
arch was reportedly located approximately 2 cm
distal to the deltoid insertion or the lateral bor-
der of the humerus. Although the injury was
Vol. 110, No. 4 / RADIAL NERVE PARALYSIS
thought to be a radial neuropraxia that did not
require surgical intervention, Manske55 later re-
ported a permanent paralysis of the radial nerve
in this area after strenuous activity, requiring
surgical exploration and release. As far back as
1945, Sunderland56 reported radial nerve pa-
ralysis that had resulted from nerve compres-
sion at the edge of the latissimus dorsi tendon
and long head of the triceps from using
crutches.
Open Wounds
The radial nerve is seldom divided in trau-
matic lacerations because of the deep position
of the motor component of the nerve.1 Never-
theless, penetrating wounds associated with ra-
dial nerve palsy require surgical exploration to
rule out axonotmesis. When the radial nerve is
sharply divided, the clinical results after pri-
mary repair have been good to fair in most
instances, if the nerve is explored early and
repaired without tension.1,57 It is of particular
interest that the radial nerve has been found to
be transected in up to 50 percent of patients
following gunshot wounds associated with hu-
meral fractures.5
The treatment of postoperative radial nerve
palsy requires a great deal of consideration. To
identify nerve injuries in advance and to avoid
any questions of origin after surgery, it is im-
portant to do a complete upper extremity
nerve exam before any invasive procedure is
performed in proximity to major nerves. The
radial 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 a
tourniquet often prevents a clear identification
of nerves during dissections. Radial nerve pa-
ralysis may occur as the result of a traction
injury or compressive neuropraxia after sur-
gery.60,61 A thorough and honest reflection by
the surgeon is required when a radial nerve
paralysis is noted after surgery. If there is any
chance that the nerve may have been severed
or partially transected, immediate re-explora-
tion is indicated to ensure the best clinical
outcome.62– 64
Other Causes
Radial nerve paralysis has been reported in
association with the use of a tourniquet or with
injection injuries.45 The radial and sciatic
nerves are those most commonly injured by
injections.65 The high percentage of injuries to
1103
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, and
nerve paralysis after tourniquet use is 2.5 times
more common in the upper extremity than in
the lower extremity. Upper extremity nerve
paralysis is estimated to occur in one out of
13,000 applications. The radial nerve is the
nerve most susceptible to tourniquet trauma,
with its involvement present to some extent in
up to 96 percent of upper extremity tourniquet
injuries.65
Postoperative radial nerve palsies can also be
related to patient positioning or to blood pres-
sure cuffs. Radial nerve paralysis may develop
during sleep, especially when the patient is
intoxicated, such as in a “Saturday night pal-
sy.”1 Sunderland56 described a variety of radial
nerve injuries resulting from compression
caused by local trauma and ischemia. He re-
ported seven cases of radial nerve palsy, five of
which occurred during sleep with compression
noted at the level of the lateral intermuscular
septum. All seven patients experienced com-
plete resolution of paralysis with time. Traction
injuries after motor vehicle accidents or other
blunt traumas may result in prolonged paraly-
sis of the radial nerve. Most of these nerve
lesions 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 other
compressive neuropathies (i.e., hereditary
neuropathy).
Radial nerve paralysis has been reported as
the result of pentazocine-induced fibrous my-
opathy.66 Repeated pentazocine injections to
the deltoid region was noted to induce triceps
fibrosis, causing radial nerve compression. The
patient developed a persistent wrist drop that
required surgical decompression. Radial
mononeuritis has also been related to alcohol,
lead, arsenic, typhoid, and serum sickness.5,67
Idiopathic radial neuritis has been described
throughout the literature, but its specific cause
has yet to be clearly defined.
CLINICAL EVALUATION
Clinical presentation of radial nerve paralysis
is dependent upon the cause and level of nerve
involvement. Some patients have symptoms of
chronic compression that progress to complete
paralysis, whereas other patients experience
1104
the acute onset of paralysis. All lesions of the
radial nerve must first be distinguished from
lesions affecting the nerve roots (C5 through
T1) or the brachial plexus. The clinical symp-
toms of radial nerve paralysis are often straight-
forward, with patients primarily demonstrating
a 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 determined
by physical examination of the motor and sen-
sory components. Anesthesia after radial nerve
palsy may vary to include the dorsal surface of
the proximal half of the thumb, index, and
middle fingers and is usually limited to a small,
triangular area on the dorsum of the first and
second metacarpal webspaces.1 Because the
sensory deficit is not on the tactile surface of
the hand, the sensory deficit is usually trivial,
but can be painful.
Loss of motor function depends on the level
of the radial nerve lesion. Although loss of the
anconeus muscle is not clinically noticeable
after proximal radial nerve paralysis, the other
muscles in the upper arm can be more clearly
identified on physical examination. These mus-
cles include the triceps, brachioradialis, and
extensor carpi radialis longus and brevis. Loss
of triceps function reflects an injury at the level
of the brachial plexus. If the brachioradialis or
extensor carpi radialis longus are not func-
tional, then the injury is most likely at the level
of the humeral shaft. Proximal radial nerve
injuries result in a complete loss of extension at
the wrist and metacarpophalangeal joints
along with a loss in extension and abduction of
the thumb.
Posterior interosseous nerve paralysis typi-
cally involves a more distal injury to the radial
nerve. Patients with classic posterior interosse-
ous nerve palsy experience radial deviation of
the wrist with dorsiflexion because of the pres-
ervation of the extensor carpi radialis longus.
These patients are usually unable to extend
their fingers or thumb at the metacarpopha-
langeal joints, and they have no sensory deficit
because the superficial radial nerve is pre-
served. The presence of active contractions of
the brachioradialis and wrist extension in ra-
dial deviation allows for localization of the ra-
dial nerve injury to a point distal to the origin
of the posterior interosseous nerve.
PLASTIC AND RECONSTRUCTIVE SURGERY, September 15, 2002
DIAGNOSTIC STUDIES
A complete patient history and a physical
examination are often all that is needed to
determine the level of injury and the suspected
cause of radial nerve paralysis. A plain film of
the 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 orthopedic
injuries or disorders of the radial head. Mag-
netic resonance imaging should be obtained if
a mass is suspected at any level along the
course of the radial nerve. Nevertheless, stud-
ies such as magnetic resonance imaging that
are used for diagnostic purposes in patients
with radial nerve paralysis may also be mislead-
ing without clinical confirmation.
All patients experiencing neural compro-
mise after penetrating injury in proximity to
nerves should be explored without the need
for preoperative electrodiagnostic studies.
Plain films, magnetic resonance imaging, or
arteriograms may be indicated before explora-
tion in some situations, but electrodiagnostic
studies are rarely helpful within the first several
weeks after nerve injury because these studies
cannot differentiate between nerve injuries
that will or will not recover spontaneously with
that time. Standard electrodiagnostic studies
will, however, help to determine the level of
injury or its distribution if the physical exami-
nation is unclear. Patients with nerve paralysis
that persists beyond 6 to 8 weeks should be
examined with electrodiagnostic studies. By 12
weeks, motor unit potentials will be present
and will help to differentiate between recover-
able injures and those that will require surgery.
Intraoperative nerve-to-nerve studies are an
excellent adjunct in the care of patients with
peripheral nerve injuries.68,69 The results of
these studies can assist the surgeon in the op-
erative plan as long as the injury has been
allowed to fully mature. The level and extent of
a radial nerve lesion can be determined in the
operating room using this technology. Intraop-
erative nerve-to-nerve studies can be used to
examine the nerve proximal and distal to a
suspected lesion. If the radial nerve demon-
strates conduction across a lesion, spontaneous
recovery is possible. If conduction is absent
proximal to a lesion, a nerve repair or graft
may not be indicated because either a more
proximal injury must be present or the nerve is
without function.
Vol. 110, No. 4 / RADIAL NERVE PARALYSIS
CLASSIFICATION
A conservative approach to the restoration of
hand function after radial nerve paralysis has
long been advocated in the literature. In the
middle of the 20th century, many authors per-
formed operations to remove offending factors
causing 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 to
recover. Clearly, there were no established
guidelines at this time for the treatment of
idiopathic radial nerve palsy. In 1968, however,
Spinner6 began to advocate surgical explora-
tion of patients with radial nerve palsy 6 to 8
weeks after clinical presentation of the disease.
Currently, most surgeons agree that once
the 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 the
length of time a patient should be observed
before surgical intervention.4,37,45 The confu-
sion surrounding the appropriate clinical treat-
ment of radial nerve palsy often stems from the
lack of a clear and relevant classification sys-
tem. Clearly, it is important categorize all ra-
dial nerve lesions based on the type of injury
and the level of involvement. A complete his-
tory and physical are often all that is required
for complete classification, but electrodiagnos-
tic or other studies may be needed in some
situations. Once the radial nerve injury is clas-
sified, the appropriate treatment options can
be applied based on the information available.
In general, all nerve injuries can be classified
as first- through sixth-degree injury.45,70 First-
degree injury is a neurapraxia that results from
a segmental demylination without loss of nerve
continuity or Wallerian degeneration. Second-
degree injury is axonotmesis with injury to the
axon, but intact endoneurial tissue and
Schwann cell tubes. Third-degree injury in-
volves additional injury to the endoneurium,
but the perineurium remains intact. Fourth-
degree injury involves a neuroma in continuity
with 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
1105
TABLE I
Classification of Radial Nerve Palsy
Injury Classification Explanation of Classification
Open versus closed Injury is distinguished as either penetrating
or nonpenetrating
High Injury occurs above the distal insertion of
the pectoralis major
Intermediate Injury occurs between the insertion of the
pectoralis major and the posterior
interosseous nerve
Low Injury involves the posterior interosseous or
radial sensory nerve
Compressive Injury involves chronic or acute anatomic
compression
Delayed presentation Injury involves a delay in presentation that
significantly limits the available
treatment options
radial nerve paralysis to further assist with its
clinical 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 radial
nerve palsies. All radial nerve injuries must first
be classified as either open or closed. It is
important to make a distinction between open
and closed injuries because the management is
quite different based on the degree of nerve
injury most likely associated with each disor-
der. Closed injuries include radial nerve paral-
ysis associated with orthopedic trauma, com-
pression, neuritis, or idiopathic causes. Open
injuries include lesions associated with pene-
trating wounds, lacerations, or surgical explo-
rations in proximity to the radial nerve. If there
is even the slightest concern that the nerve may
be lacerated by bone fragments or surgical
trauma, then the nerve should be explored.
The approximate level of radial nerve injury
should be determined next. The radial nerve
may be injured or paralyzed at different points
along its course, but there are several specific
points at which it is more susceptible to injury.
The nerve may be injured along the spiral
groove, near the radial head, or at the arcade
of Frohse.71 We have defined the level of radial
nerve injury to be a high injury when it occurs
above the level of insertion of the pectoralis
major muscle to the humerus, an intermediate
injury when it occurs between the insertion of
the pectoralis muscle and the terminal
branches of the radial nerve, and a low injury
when it involves the posterior interosseous
nerve. The level of involvement can usually be
determined by physical examination or elect-
rodiagnostic studies.
Radial nerve paralysis can also be classified as
1106
either acute or chronic compression injuries.
There are several important areas in which the
radial nerve is particularly susceptible to either
acute or chronic compressive neuropathy. For
instance, the posterior interosseous nerve can
be compressed by the fascia of the radiocapi-
tellar joint, the leash of Henry, the fascia of the
extensor carpi radialis brevis, the arcade of
Frohse, or the distal edge of the supinator.72
The radial nerve can be compressed above the
elbow by the lateral head of the triceps or
humeral exostosis.72 Radial nerve palsy may re-
sult from invasion by a malignant tumor or
compression from a benign mass. If there is
evidence of persistent compression at any ana-
tomic point or by a nonanatomic mass, then
immediate exploration may be indicated.
Finally, radial nerve paralysis should also be
classified based on the time of presentation. If
a patient presents a long time after the original
injury, 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 injury
are limited. It is also extremely difficult to ex-
plore open radial nerve lesions more than 10
days after the injury because of significant in-
flammation and scarring. The time of presen-
tation after radial nerve paralysis is particularly
important because the motor endplates must
be reinnervated within 1 year if motor function
is to be restored.45 Electrodiagnostic studies
should be obtained on all patients who fail to
demonstrate improvement within 3 months of
injury. The level and duration of the injury will
FIG. 1. Radial nerve palsy algorithm.
PLASTIC AND RECONSTRUCTIVE SURGERY, September 15, 2002
ultimately be the primary factors that deter-
mine the reconstructive options available.
Therefore, it is extremely important to involve
a peripheral nerve surgeon early in the man-
agement of all patients presenting with radial
nerve palsy to optimize care and recovery.
MANAGEMENT OPTIONS
An algorithm for the treatment of radial
nerve palsy was developed to determine the
need for surgical reconstruction based on a
concise and clinically relevant classification sys-
tem (Fig. 1). The first step in determining a
treatment is to classify the lesion as either open
or closed. All radial nerve palsies associated
with open wounds should be explored surgi-
cally. If the nerve is found to be in continuity at
the time of the exploration, it is treated as a
closed injury. If the radial nerve has been
sharply transected, but there is adequate nerve
length and minimal soft-tissue injury, then it
should be repaired primarily.
A primary nerve repair should be performed
without tension by mobilizing the nerve both
proximally and distally. To ensure complete
removal of the lesion or zone of injury, only
surgeons familiar with the technique should
perform acute nerve grafting in this situation.
The proximal and distal extent of the
transected or injured nerve can be more
clearly delineated if the surgery is delayed for 3
weeks. Nevertheless, it may be quite difficult to
explore a nerve safely after a delay because of
the progression of the surgical scar. Before 3
weeks, the extent of nerve injury can be deter-
Vol. 110, No. 4 / RADIAL NERVE PARALYSIS
mined with intraoperative electrodiagnostic
studies and microscopic examination.
The management of closed radial nerve pal-
sies is far less straightforward. Closed radial
nerve injuries can be associated with a wide
range of underlying pathology. Surgical explo-
ration is indicated only when transection of the
radial nerve is suspected, as might be the case
after a comminuted humeral fracture. If a ra-
dial nerve transection is not suspected, then
the patient should be observed closely for a
period of 3 months.6,45 The clinical outcome is
dependent upon an accurate determination of
the degree of nerve injury based on a complete
patient history and physical and a well-timed
electrodiagnostic study (when indicated). For-
tunately, most closed radial nerve palsies are
associated with either a neurapraxia or a sec-
ond- or third-degree injury that usually recov-
ers spontaneously with time. A Tinel sign can
be used to follow the progressive recovery of
the nerve along its anatomic course in both
second- and third-degree injuries.
A physical examination of the upper extrem-
ity will help to determine a clinically obvious
mass causing radial nerve compression. How-
ever, magnetic resonance imaging may be
needed in some situations to rule out a less
obvious soft-tissue mass, although both false-
negative and false-positive magnetic resonance
imaging reports may be seen in this situation. It
is important to prevent joint contractures with
a wrist splint and aggressive hand therapy dur-
ing the 3 months of observation. Patients who
do not demonstrate clinical evidence of recov-
ery within 2 to 3 months of observation or after
a negative surgical exploration should undergo
Treatment Recommendations for Radial Nerve Palsy
Level of Injury
Low
Intermediate
High
* I, first-degree injury or neuropraxia; II, second-degree injury with axonotmesis involving the axon and myelin but intact endoneurium; III, third-degree injury
with axonotmesis involving the axon, myelin, and endoneurium but intact perineurium; IV, fourth-degree injury is a neuroma in-continuity; V, fifth-degree injury is
a 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.
1107
electrodiagnostic evaluation. Surgical interven-
tion is indicated if no clinical or electrical evi-
dence of reinnervation is seen within 3
months.
Electrodiagnostic studies will help to deter-
mine the level and extent of the radial nerve
injury. High, intermediate, or low radial nerve
injuries should be explored, compression
points should be released, and the nerve
should be repaired or reconstructed when con-
servative management fails. The level of the
nerve injury can be further delineated by an
intraoperative, nerve-to-nerve study, as men-
tioned earlier. Because the motor endplates
are not out of reach for regenerating axons,
patients with low and intermediate radial nerve
injuries repaired primarily or grafted at 3 to 4
months have an excellent prognosis.4,73 Con-
versely, the axons have a long distance to travel
after a high radial nerve injury. This has re-
sulted in the recommendation for tendon or
nerve transfer after high injuries that fail to
recover within 3 months. Also, patients with
complete loss of radial nerve function follow-
ing neuritis or whose treatment has been sig-
nificantly delayed should be considered for
tendon or nerve transfer (Table II).
Five-Step Radial Nerve Release
The general approach to the posterior in-
terosseous nerve has been described previously
in the literature.74 The radial nerve at the fore-
arm is approached using a standard, five-step
approach in which: 1) The interval between
the extensor carpi radialis longus and the bra-
chioradialis muscle is palpated preoperatively
by having the patient extend his or her wrist
TABLE II
Type of Injury* Treatment Recommendation(s)
Neurapraxia Observation for 3 months
Axonotmesis (I, II, III, VI) Observation for 3 months
Axonotmesis (IV) Nerve graft
Neurotmesis Primary repair, nerve graft
Neurapraxia Observation for 3 months
Axonotmesis (I, II, III, VI) Observation for 3 months
Axonotmesis (IV) Nerve graft
Neurotmesis Primary repair, nerve graft
Neurapraxia Observation for 3 months
Axonotmesis (I, II, III, VI) Observation for 3 months
Axonotmesis (IV) Tendon transfer, nerve transfer
Neurotmesis Tendon transfer, nerve transfer
1108
against resistance; 2) a longitudinal incision is
made, and the interval between the two mus-
cles is identified by a slight color difference
and the intervening posterior cutaneous nerve
of the forearm; 3) the nerve is protected, and
the avascular plain between the two muscles is
carefully dissected; 4) the fascial edge of the
extensor carpi radialis brevis is identified and
released, exposing the underlying supinator;
and 5) the edge of the supinator is identified
and released, exposing the underlying
branches of the radial nerve.
The radial sensory nerve, the nerve to the
extensor carpi radialis brevis, and the posterior
interosseous nerve can be fully distinguished
through 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 of
the supinator, and the fascia around the radio-
capitellar joint. The posterior interosseous
nerve can be approached in several different
ways, depending on the surgeon’s preference
or familiarity with the procedure.75 We have
found the approach to the radial nerve
through the brachioradialis-extensor carpi lon-
gus interval to be particularly useful in ensur-
ing a complete release of all potential points of
compression at this level.
Neurorrhaphy and Nerve Grafting
The radial nerve is the most suitable for
neurorrhaphy of all major nerves because the
fascicles 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 influence
the recovery from nerve injury.63,77,78 Better re-
sults in children probably stem from better
central adaptation to altered profiles after
nerve repair.79 Excellent results ranging be-
tween 78 and 90 percent have been reported
after primary radial nerve repair.57,80,81
The results of radial nerve repair using nerve
grafts have been comparable with primary re-
pairs. Millesi et al.82,83 reported that 77 percent
of patients with interfascicular radial nerve
grafting obtained four out of five motor
strength. Dolenc84 reported 14 cases of radial
nerve transections that required nerve grafts of
varying lengths. He determined that the time
from injury to surgery and the surgical condi-
tion were more important than the length of
the nerve graft. In other studies, good results
PLASTIC AND RECONSTRUCTIVE SURGERY, September 15, 2002
have been noted in 80 percent of patients that
required radial nerve grafts.85,86 Nerve grafting
is indicated if the nerve defect is large or there
is significant tension on the repair.
Tendon Transfers
Most authors agree that tendon transfers
provide good results if nerve reconstruction
fails in patients with radial nerve palsy. Sunder-
land56 recommended a tendon transfer if there
were no signs of radial nerve recovery within 1
year. In 1916, Jones87 described a tendon trans-
fer for radial nerve palsy that included the
pronator teres to the wrist radial extensors, the
flexor carpi radialis to the extensors comminis,
and the flexor carpi ulnaris to extensor indicis
and pollicis longus. The transfer of both wrist
flexors has since been abandoned by most sur-
geons because of the excess morbidity from the
loss in wrist flexion.
Currently, there is continued disagreement
on the best combination of tendon transfers to
use in treating patients with radial nerve paral-
ysis. The level of the radial nerve injury and a
patient’s overall function and anatomy often
dictate the best surgical option available. Most
authors agree that the extensor carpi radialis
brevis and longus should be reconstructed us-
ing the pronator teres tendon.75,88,89 The exten-
sor digitorum communis can be reconstructed
using the flexor digitorum superficialis (III),
the flexor carpi ulnaris, or the flexor carpi
radialis.75,88,89 The rerouted extensor pollicis
longus can be reconstructed using the palmaris
longus or the flexor digitorum superficialis
(IV), and, in some cases, the abductor pollicis
longus and extensor pollicis brevis can be re-
constructed with the flexor carpi radialis.75,88,89
We prefer to use the pronator teres to the
extensor carpi radialis brevis, the flexor carpi
ulnaris 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 tendon
transfer in radial nerve transection. He re-
ported an average recovery time from nerve
repair to be 7.5 months, with 66 percent of
patients achieving good or excellent function.
In the tendon transfer group, all patients
noted good to excellent results in 8 weeks. The
pronator teres was transferred to the extensor
carpi radialis longus and brevis, the palmaris
longus was transferred to the thumb extensors
and long abductor (when present), and the
Vol. 110, No. 4 / RADIAL NERVE PARALYSIS
flexor carpi ulnaris was transferred to the com-
mon digital extensors. When the palmaris lon-
gus was not present, the thumb extensors and
abductor were motored by the flexor carpi ul-
naris as well. However, it was difficult to fully
determine from Bevin’s article the approxi-
mate level of the radial nerve injury in the
patients reviewed.
Burkhalter76 also advocated early tendon
transfer because he believed the transfer acts
both as a substitute during regrowth of the
nerve or when lesions are irreparable and also
as a helper during reinnervation. In a recent
article, Kruft et al.90 reported that irreversible
radial nerve paralysis should be treated with
early tendon transfer. They reported 43 pa-
tients who underwent tendon transfer, with 38
patients ultimately returning to their original
jobs. The authors qualified their results by stat-
ing that tendon transfers “never fully replace
an intact radial nerve for the purpose of con-
trolling the hand.”
Elton and Omer91 observed that patients
with radial nerve paralysis treated by tendon
transfer often experienced extensor tightness,
which prevented simultaneous flexion of the
wrist and fingers. Barton1 described this as a
“rather unnatural movement, seldom needed
in ordinary life.” Several authors have thought
that the greatest functional loss after radial
nerve palsy was not the loss of finger extension,
but instead the loss of power grip, which can-
not be easily recreated with standard tendon
transfers.76,92 As such, it is important to fully
examine alternative approaches to treating ra-
dial nerve palsy to decrease the long-term mor-
bidity associated with tendon transfers that
clinically often appear “unnatural.”
Nerve Transfer
In 1948, Lurje93 described the use of nerve
transfers for severe brachial plexus injuries
when other options were not available. In the
1960s, the popularity of nerve grafting tended
to overshadow such early pioneering work in
nerve transfers.94 Currently, nerve transfers are
typically performed under limited circum-
stances such as brachial plexus avulsions, when
no other options are available.95–99 Although,
we have had excellent experience with nerve
transfers using nearby, expendable motor fi-
bers for reconstruction,94 we believe that nerve
transfers may have limited applications for cer-
tain types of high radial nerve palsies or in
cases of radial neuritis.
1109
The median nerve has a limited number of
anatomic variations in the forearm; therefore,
it provides several dependable sources for
nerve transfer to the distal radial nerve.100 The
median nerve supplies several redundant nerve
branches to the flexor digitorum superficialis
muscle groups that can be transferred in cer-
tain situations. The nerve branch to the pal-
maris longus can also be sacrificed if it is not
required for future tendon transfers. Intraop-
erative sensorimotor topographical identifica-
tion can be used to identify redundant
branches of the median nerve that can be
transferred to the radial nerve. We have suc-
cessfully transferred redundant branches of
the median nerve to the posterior interosseous
nerve in the forearm of several radial nerve
paralysis patients, with good long-term results2;
however, additional experience with this tech-
nique is needed before definitive recommen-
dations regarding its indications and use can
be made. Nevertheless, continued success with
nerve transfers in patients with radial nerve
paralysis may provide a useful alternative to
tendon transfers in patients with delayed pre-
sentation or high proximal nerve injuries or in
situations 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, clinical
presentations, and potential causes or ori-
gins of the disorder. A systematic approach
to the examination and diagnosis of the dis-
ease is vital to ensure the appropriate treat-
ment and future recovery of these patients. A
clinically relevant classification system for ra-
dial nerve paralysis should encourage clini-
cians to address specific diagnostic dilemmas
and injury types. Our classification system
attempts to define both the key clinical issues
that ultimately determine the need for surgi-
cal intervention and the most appropriate
surgical reconstruction. Recommendations
for the management of radial nerve paralysis
are based on the level and degree of injury
confirmed by history and physical and by
electrodiagnostic studies (when indicated).
Finally, the algorithm provides a general
guide for both the surgical and nonsurgical
options available based on the time of pre-
sentation and the type of injury. A full inte-
gration of the above material on radial nerve
paralysis should assist in the overall care and
1110
management of patients who present with
this often complex and challenging clinical
problem.
James B. Lowe, M.D.
Division of Plastic and Reconstructive Surgery
Washington University School of Medicine
One Barnes Hospital Plaza, Suite 17424
St. Louis, Mo. 63110
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Self-Assessment Examination follows on
the next page.
 Self-Assessment Examination

Current Approach to Radial Nerve Paralysis

by 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 UPPER
EXTREMITY EXCEPT:
A) Extensor carpi radialis brevis
B) Supinator
C) Extensor carpi ulnaris
D) Abductor pollicis longus
E) Brachioradialis

2. RADIAL NERVE COMPRESSION HAS BEEN REPORTED AT ALL POINTS LISTED BELOW EXCEPT:
A) Triceps tendon
B) Vascular leash of Henry
C) Arcade of Frohse
D) Tendinous margin of the extensor carpi radialis brevis
E) Tendinous margin of the extensor carpi radialis longus

3. UPPER EXTREMITY NERVE PARALYSIS FOLLOWING TOURNIQUET APPLICATION IS ESTIMATED TO

OCCUR AT APPROXIMATELY WHAT RATIO?
A) One out of 130
B) One out of 1300
C) One out of 13,000
D) One out of 130,000
E) One out of 1,300,000

4. DURING SURGICAL EXPLORATION OF THE RADIAL HEAD AT THE ELBOW, WHAT MANEUVER WOULD
PROTECT THE RADIAL NERVE DURING A STANDARD EXPOSURE?
A) Forearm supination
B) Forearm pronation
C) Elbow distraction
D) Elbow extension
E) Elbow flexion

5. COMPRESSION OF THE POSTERIOR INTEROSSEOUS NERVE BY THE ARCADE OF FROHSE IS CAUSED BY:
A) Dislocation of the radial head
B) Enlargement of the deep head of the supinator
C) Thickening of the superficial head of the supinator
D) Congenital deformity of the arcade of Frohse
E) Malposition of the extensor radialis carpal tendon

6. NERVE TRANSFER IS MOST LIKELY INDICATED IN WHAT SITUATION?

A) Closed injury
B) Acute sharp nerve transection
C) Injuries also involving the median nerve
D) Delayed diagnosis with no identifiable healthy proximal nerve segment
E) 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.