Unusual Compression Neuropathies of the Forearm, Part I: Radial Nerve

Unusual Compression Neuropathies of the Forearm,
Part I: Radial Nerve
Alan C. Dang, MD, Craig M. Rodner, MD
Peripheral compression neuropathies are familiar to the hand surgeon. Although compression
neuropathies of the forearm are far less common than those of the wrist (namely, carpal
tunnel syndrome), for the patient suffering from one of these neuropathies, a missed
diagnosis has far-reaching consequences. In this 2-part review (I: Radial Nerve; II: Median
Nerve), several compression neuropathies of the forearm are examined. We will first discuss
compression neuropathies affecting the radial nerve: (1) posterior interosseous nerve syndrome, (2) radial tunnel syndrome, and (3) superficial radial nerve compression (Wartenberg’s syndrome). (J Hand Surg 2009;34A:1906–1914. © 2009 Published by Elsevier Inc.
on behalf of the American Society for Surgery of the Hand.)
Key words Posterior interosseous nerve syndrome, radial tunnel syndrome, superficial
radial nerve compression, Wartenberg’s syndrome.
ATIENTS WITH PERIPHERAL compression neuropathies are ubiquitous in a hand surgeon’s practice.
Carpal tunnel syndrome is the most common of
these neuropathies, with an annual incidence between
0.1% and 0.35% in the general population, representing
more than twice the incidence of the second most common peripheral compression neuropathy.1–3 Compression of the ulnar nerve, such as at the cubital tunnel or
Guyon’s canal, is seen considerably less frequently,
with an annual incidence of 0.03%.1 Rarer still are
compressive neuropathies of the posterior interosseous
nerve (PIN) and superficial radial nerve (SRN), with an
annual incidence of 0.003%.1 The purpose of this 2-part
review is to discuss several of the more unusual compressive neuropathies of the forearm, such as those of
the radial nerve (Part I of this series), as well as those of
Current Concepts
From the Department of Orthopaedic Surgery, University of Connecticut Health Center, Farmington, CT.
Received for publication September 22, 2009; accepted in revised form October 17, 2009.
No benefits in any form have been received or will be received related directly or indirectly to the
subject of this article.
Corresponding author: Craig M. Rodner, MD, Department of Orthopaedic Surgery, University of
Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06034-4037; e-mail:
[email protected]
1906 䉬 ©  Published by Elsevier, Inc. on behalf of the ASSH.
the proximal median nerve, before its entry through the
carpal tunnel (Part II of this series).
The effects of compression on peripheral nerves can
be attributed to alterations of blood circulation to and
from the nerve as well as direct injury to the axonal
transport systems. Venous blood flow from the peripheral nerves is shown to be reduced at 20 to 30 mm Hg,
whereas frank ischemia can occur at pressures of 60 to
80 mm Hg.4 Blockade of axonal transport can occur at
pressures as low as 50 mm Hg and loss of nerve
impulse conduction occurs at pressures of 130 to 150
mm Hg.5,6
A compression neuropathy may begin as a mild
injury to epineural vessels under mild pressure. The
subsequent edema can lead to fibrosis, which increases
further pressure on the nerve, leading to a progressive
deterioration of the nerve.7 In addition to the mechanical effects, an increase in connective tissue has been
hypothesized to cause secondary changes in the mechanical sensitivity of the thin afferent fibers responsible for pain.8,9 Finally, compression may also produce
local intraneural sprouting and neuroma formation.10
Early on, compressive neuropathies can initially be
treated through nonsurgical methods. These include
rest, activity modification, nonsteroidal anti-inflammatory drugs, splinting, and corticosteroid injections.
FIGURE 1: Schematic of the radial nerve as it bifurcates into
the PIN, coursing under the supinator and the SRN, which
runs along the undersurface of the brachioradialis.
Current Concepts
Splinting prevents the patient from moving the extrem(Fig. 1).11,12 The PIN is a motor nerve that courses
ity into positions that result in additional compression to
deep beneath the supinator muscle; the SRN is a
the nerve, and therefore reduces inflammation that
sensory nerve that travels anteriorly on the undercan lead to progressive worsening of symptoms. In
surface of the brachioradialis and, in the distal
instances when conservative management has
one-third of the forearm, travels subcutaneously to
failed, surgical decompression may be warranted
provide sensation to the dorsoradial hand (Fig. 2).
to eliminate the anatomical structures responsible
Compression neuropathies involving the PIN and
for compression.
the SRN have been sepaThe radial nerve begins as EDUCATIONAL OBJECTIVES
rately described. We will
Describe the anatomy of the radial nerve in the arm and forearm
the terminal branch of the
discuss compression neuposterior cord of the brachial ● List the various potential compression sites of the radial nerve in the fore- ropathies involving the
plexus. The nerve begins
PIN and the SRN as 3 separm
posterior to the axillary ar- ● Explain the differences between posterior interosseous nerve syndrome arate entities: PIN comtery and travels through the
pression syndrome, radial
and radial tunnel syndrome
triangular interval and then ● State the surgical indications for posterior interosseous nerve syndrome tunnel syndrome (RTS),
continues along the spiral
and SRN compression
and radial tunnel syndrome
groove of the humerus. The
(Wartenberg’s syndrome).
Earn up to 2 hours of CME credit per JHS issue when you read the related
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ment as it penetrates the latINTEROSSEOUS
eral intermuscular septum approximately 10 to 12 cm
proximal to the elbow. The radial nerve continues to
The PIN is thought of as a “motor-only” nerve that
travel distally and ultimately bifurcates into deep (PIN)
travels through the radial tunnel. The radial tunnel is a
and superficial (SRN) branches approximately 6.0 to
potential space 3 to 4 finger breadths long, lying along
10.5 cm distal to the lateral intermuscular septum and 3
the anterior aspect of the proximal radius through which
to 4 cm proximal to the leading edge of the supinator
the PIN travels. The floor of the radial tunnel is created
by the capsule of the radiocapitellar joint, which continues as the deep head of the supinator muscle. Anatomically, there are 5 potential sites of compression of
the PIN in the area of the radial tunnel: (1) fibrous bands
of tissue anterior to the radiocapitellar joint between the
FIGURE 2: Schematic of the SRN in the dorsoradial forearm.
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brachialis and brachioradialis; (2) the recurrent radial
vessels that fan out across the PIN at the level of the
radial neck as the so-called “leash of Henry”; (3) the
leading (medial proximal) edge of the extensor carpi
radialis brevis (ECRB); (4) the proximal edge of the
superficial portion of the supinator, commonly referred
to as the arcade of Fröhse; and (5) the distal edge of the
supinator muscle.
The proximal border of the superficial head of the
supinator muscle, or arcade of Fröhse, lies approximately 1 cm distal to the leading edge of the ECRB and
is thought to cause most PIN neuropathies. The lateral
portion of the supinator is tendinous and originates on
the lateral portion of the lateral epicondyle. These tendinous fibers course distally before joining the supinator’s medial fibers, which originate from the medial
portion of the lateral epicondyle, and can be membranous or tendinous.13 In individuals with a tendinous
arcade, the PIN experiences pressures of 46 mm Hg
during passive pronation of the forearm and peak pressures of 190 mm Hg during maximal active muscle
Interestingly, RTS and PIN syndrome describe compression of the same nerve and therefore can be approached with identical surgical interventions. Although in each syndrome the same nerve is affected, the
clinical presentations are divergent. Whereas patients
with PIN syndrome have a loss of motor function,
patients with RTS typically present with mobile wad
and lateral forearm pain without motor involvement.
The difference in clinical presentation may well be
attributed to a difference in the degree of compression
of the nerve.
Current Concepts
Posterior Interosseous Nerve (PIN) syndrome
The PIN is thought of as a “motor-only” nerve innervating the ECRB, supinator, extensor carpi ulnaris, extensor digitorum communis, extensor digiti minimi,
abductor pollicis longus, extensor pollicis longus,
extensor pollicis brevis, and extensor indicis proprius. It does not innervate the extensor carpi radialis
longus (ECRL). PIN syndrome occurs when there is
sufficient compression on the PIN—presumably of
its large myelinated fibers—to produce a motor loss,
which can result from benign tumors (most commonly lipomas or ganglia) or peri-elbow synovitis
associated with rheumatoid arthritis.15
Although in 1863 Agnew16 described a compressive
neuropathy of the PIN in a woman with a “hickory
nut”–sized lesion that compressed both the PIN and the
median nerve, the first report of an isolated PIN palsy
was made by Guillain and Courtellemont in 1905.17
They wrote about an orchestral conductor whose palsy
was attributed to the repetitive trauma of alternating
forearm pronation and supination. As a result of this
first description, occupations with repetitive pronosupination were considered to be a risk factor for injury to
the PIN, although, owing to the relative infrequency of
this condition, no data exist to confirm the magnitude of
this risk. Nonetheless, subsequent reports of PIN syndrome have included a bartender,18 a violinist,19 a
corsetiere,20 a dairyman,20 a swimmer,21 and even an
infantryman after prolonged carrying of an M60 machine gun.22
Patients with PIN syndrome typically present with
dropped fingers and thumb resulting from compression
of the PIN at the proximal aspect of the supinator
muscle.23 Even in situations where there is a complete
PIN palsy, the function of the ECRL is always preserved, and thus the wrist is able to extend and radially
deviate even in cases of severe neuropathy. Partial
lesions are seen when there is compression not of the
PIN in its entirety, but rather of isolated PIN branches.
For example, compression of the medial branch would
cause weakness of the extensor carpi ulnaris, extensor
digiti minimi, and extensor digitorum communis,
whereas compression of the lateral branch would cause
weakness of the abductor pollicis longus, extensor pollicis brevis, extensor pollicis longus, and extensor indicis proprius.15 Imaging studies are not commonly used
in the diagnosis of PIN syndrome, although magnetic
resonance imaging may, of course, be helpful to delineate a soft tissue mass responsible for compression.
Once a PIN palsy has been diagnosed, lipomas should
be considered as a causative factor, because they
are the most commonly reported tumor to cause
PIN syndrome.24 –32 Other sources of compression
that have been described include ganglia arising
from the anterior capsule of the proximal radioulnar joint and in the supinator muscle,33– 40 rheumatoid pannus,41 septic arthritis of the elbow,42
synovial chondromatosis,43– 45 and vasculitis.46
One case report described the use of sonography to
detect fibrous bands that compress the PIN,47 although this imaging modality is not commonly
employed in the workup of PIN syndrome.
Although clinical examination is the key in making
the diagnosis of PIN syndrome, electrodiagnostic studies should be used for additional confirmation. Because
loss of motor function is the hallmark of PIN syndrome,
electromyographic evaluation is usually positive (in
contrast to RTS). Other more proximal etiologies
should be ruled out, including lesions of the cervical
spine, brachial plexus, and radial nerve proper at the
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Radial Tunnel Syndrome (RTS)
Although it is the same PIN that is being compressed in
both RTS and PIN syndrome, patients with these 2
conditions present altogether differently. Rather than
weakness or paralysis as their chief report, patients with
RTS typically present with lateral proximal forearm
pain, which must be distinguished from lateral epicondylitis. Typical reports include mobile wad area tenderness that worsens with activity. Although RTS was
introduced as an entity unto itself in 1972, earlier descriptions of “resistant tennis below” refractory to conventional therapy had been described as early as 1883
and may be referring to the same entity.48 Today, the
existence of RTS remains a source of controversy owing to limited objective tools that can be used to define
its diagnosis, in that it is a pain-only phenomenon with
no significant findings on imaging nor electrodiagnostic
The clinical diagnosis of RTS must be distinguished
from that of lateral epicondylitis by the location of
tenderness on physical examination. In lateral epicondylitis, the focal point of tenderness is on the lateral
epicondyle at the insertion of the ECRB. In contrast, the
characteristic pain of RTS is located 3 to 4 cm distal to
the lateral epicondyle in the area of the mobile wad and
radial tunnel.48 Compression of the PIN is made greater
by placing maximal traction on the radial nerve, by
extending the elbow, pronating the forearm, and flexing
the wrist. Additional physical examination tests that
have been described include pain with resisted active
supination or wrist extension, pain with resisted middle
finger extension at the metacarpophalangeal joint,48,49
and localized tenderness along the path of the PIN.50
The practitioner should remember, of course, that several of these clinical maneuvers would also provoke
pain in the patient with lateral epicondylitis.
Electrodiagnostic studies in the diagnosis of RTS
have been described, although they are almost always
unrevealing in the absence of a PIN syndrome. Forearm
rotation can produce differential latencies in nerve conduction studies under laboratory conditions, but the vast
majority of patients with RTS have normal electrodiagnostic testing.51,52 Because there is a paucity of objective tests to confirm the presence of RTS, pain relief
after the administration of a local corticosteroid injection adjacent to the PIN at the level of the proximal
radius has a useful role in diagnosis.53 Injecting the
corticosteroid with a short-acting local anesthetic is
wise, because temporarily producing a PIN palsy confirms accurate placement of the cortisone. Unlike PIN
syndrome, imaging does not have a key role in the
workup of RTS, although one study reported muscle
edema and atrophy as characteristic magnetic resonance
imaging findings in RTS.54
Nonsurgical management of both PIN syndrome and
RTS is recommended initially and may include a trial of
rest, activity modification, splinting, stretching, and antiinflammatory medications.55 In managing RTS, nonsurgical treatment is standard and the patient should
make every attempt to eliminate frequent provocative
positioning of the arm, which would include avoiding long periods of elbow extension, forearm pronation, and wrist flexion. Because no randomized controlled trials have been done to compare nonsurgical
and surgical treatments, the optimal duration and
efficacy of conservative regimens have not yet been
After activity modification is attempted, an injection
of local anesthetic and corticosteroid is frequently used
to confirm the diagnosis of RTS and may additionally
serve a therapeutic purpose. In 1 study of 25 patients
with RTS, 18 patients (72%) had resolution of their
symptoms with a single injection of 2 mL 1% lidocaine
and 40 mg of triamcinolone in 1 mL of carrier at 6
weeks of follow-up and 16 patients continued to have
long-term pain relief at greater than 2 years.57 Injection
may also have a role in the management of PIN syndrome, but if there is an underlying cause detected, such
as a lipoma or ganglion occupying the radial tunnel and
producing motor weakness, early surgical excision of
the mass is more appropriate. If there is no cause
identifiable on imaging studies, initial nonsurgical management of PIN syndrome is appropriate.
If there is no improvement in the motor dysfunction
by approximately 3 months, spontaneous recovery is
not likely and surgery is recommended. In a 1996 study
by Hashizume et al.,58 94% of patients (16 of 17) had a
full recovery of motor function at a mean of 4.5 months
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Current Concepts
level of the humeral shaft. Finally, it is important to
consider peripheral neuropathy or mechanical limitations to finger extension in the differential diagnosis.
Extensor tendon rupture or extensor digitorum communis tendon subluxation may mimic a PIN palsy clinically at first glance but can be ruled out with a more
thorough physical examination. The characteristic feature of extensor tendon subluxation is the ability to
maintain but not obtain metacarpophalangeal extension,
whereas tendon rupture can be evaluated by passively
bringing the wrist from a position of extension to flexion and determining whether there is an appropriate
tenodesis effect.
Current Concepts
after surgery. Vrieling et al. showed 75% good to excellent results after a mean of 5 years in a smaller study
of 8 patients with nontraumatic PIN syndrome.59 What
may account for the difference in success is that Hashizume et al.’s patients underwent surgery after 2.2
months after the onset of symptoms, whereas the Vrieling et al. patients underwent surgery an average of 4.7
months after the onset of symptoms. If PIN syndrome is
neglected for approximately 18 months, muscle fibrosis
of PIN-innervated muscles will occur, leaving only
tendon transfers as a viable surgical option.
Whereas patients with motor weakness or palsy (ie,
those with PIN syndrome) might be diagnosed and
surgically treated relatively early, those with RTS might
not be diagnosed for many months. Once a patient is
diagnosed with RTS, nonsurgical treatments should be
attempted. If activity modification is not helpful and if
multiple cortisone injections are only temporarily efficacious, surgical intervention should be considered. Because of a lack of high-level evidence, the optimal
duration of such nonsurgical treatments is unknown. In
a recent review of observational studies on various
interventions for treating RTS, Huisstede et al.56 identified 6 articles9,48,49,60 – 62 of an eligible 21 over the
past few decades that met their standards for methodological quality (although 5 used a retrospective study
design). Together, those reports show a tendency for the
efficacy of surgical decompression of the radial tunnel
in patients with RTS, but say almost nothing about the
natural history of untreated RTS or the effectiveness of
conservative treatment. An evaluation of the literature
reveals that no randomized controlled trials examine the
precise role of surgical decompression versus conservative treatment in the management of patients with
Of the 6 higher-quality RTS studies cited by Huisstede et al., the efficacy of surgical decompression of
the radial tunnel ranged from 67%62 to 92%48 when the
criteria put forth by Roles and Maudsley48 or Hagert et
al.61 were used. Werner described an 81% success rate
after 90 procedures9 and Lister et al. documented pain
relief in 95% of their patients.49 However, not all data
are so promising. Despite having 75% effectiveness
using the above-mentioned criteria, patients in the De
Smet et al. study60 only had a 40% patient satisfaction
rate. Similarly, in a lower-quality study (using the Huisstede et al. methodological assessment), Atroshi and
colleagues reported 41% patient satisfaction after surgical decompression in 37 patients at an average of 3.5
years of follow-up.63
When one reviews the RTS literature, it is important
to recognize when a study does not exclude patients
with concomitant lateral epicondylitis. Jalovaara and
Lindholm, for example, published a large series of 111
procedures in 1989.64 However, their findings cannot
be extrapolated to patients with a single diagnosis of
RTS, because the authors did not clearly distinguish
between the 2 entities. A more recent study examined
the relationship between radial tunnel release and coexisting lateral epicondylitis.65 In that 2007 study by
Lee et al., surgical decompression had good results in
86% of patients with a lone diagnosis of RTS, but was
only 40% successful in patients with concomitant tennis elbow. Furthermore, surgery was only 57% successful in patients with multiple compression syndromes.
Because RTS is a pain-only phenomenon without abundant objective criteria to aid in diagnosis, strict patient
selection becomes essential to achieving reasonably
good outcomes. Not surprisingly, patients who receive
workers’ compensation or who are in litigation have
been shown to have relatively poor outcomes after
radial tunnel decompression.65,66 Lee et al. reported a
success rate of 58% in patients receiving workers’ compensation (compared with 73% not receiving it).65 Similarly, Sotereanos et al. demonstrated a dramatically low
32% success rate after surgery in patients involved with
workers’ compensation.66 Only 1 study showed no statistically significant difference between work-related
and work-unrelated claims; however, it is unclear
whether the study had adequate statistical power to
determine such a difference, because it was comparing
14 patients with workers’ compensation and 9 patients
who did not receive such benefits.67
The method of radial tunnel decompression in the
treatment of both PIN syndrome and RTS may vary
from surgeon to surgeon, but should share the common
theme of releasing the 5 potential sites of PIN compression that we have outlined previously. The preferred
method of the senior author (C.M.R.) was taught by his
mentors Weiss and Akelman,68 and is performed
through a longitudinal or 6-cm lazy-S-type incision that
is centered over the mobile wad starting just distal
(approximately 1 cm) to the radial aspect of the elbow
flexion crease. The brachioradialis-ECRL interval is
identified by a fascial stripe. Dissection is continued
bluntly with a probing finger down to the fatty tissue
surrounding the radial nerve. We use bipolar electrocautery to maintain meticulous hemostasis during the
surgery to aid in visualization and avoid a postoperative
hematoma. The SRN can be seen coursing along the
undersurface of the brachioradialis and is protected
throughout the surgery. The arcade of Fröhse and supinator muscle proper are identified, as is the PIN,
which is dissected distally until it disappears, passing
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beneath the arcade of Fröhse. If traversing vessels compromise visualization, they may have to be bipolar
electrocauterized or suture ligated, depending on their
caliber. Once the PIN is identified as coursing deep to
the supinator muscle, the surgery is performed by either
excising the soft tissue mass encroaching upon it (as in
PIN syndrome, for example) or freeing it up from all the
potential sites of compression (as in RTS). The decompression should begin with the release of any proximal
fascial bands connecting the brachialis to the brachioradialis, and then continue through the leash of Henry, the
fibrous edge of the ECRB, and all the way through the
radial tunnel with a complete release of the arcade of
Fröhse and distal supinator muscle (Fig. 3). Current
opinion suggests that release of the arcade of Fröhse
may be the most important element in decompressing
the radial tunnel.69,70 The wound is closed in layers and
early active range of motion is allowed, although many
surgeons favor a short course of a postoperative
Although RTS is classically described as a nerve compression and entrapment syndrome, there is dispute
over its etiology. Skeptics note that the signs and symptoms of RTS contrast from other well-described entrapment neuropathies such as carpal tunnel syndrome and
cubital tunnel syndrome in that there is: (1) prominent
focal tenderness, (2) normal neurologic function, and
(3) no confirmatory electrodiagnostic evidence of nerve
Prominent focal tenderness in the area of the radial
tunnel remains one of the principal diagnostic criteria
for RTS. However, focal tenderness at the radial tunnel
in RTS differs from a positive Phalen’s test in carpal
tunnel syndrome in that the symptoms do not occur in
the distribution of the purportedly affected nerve. Finally, although there are several reports supporting the
efficacy of surgery in RTS, there has been no randomized controlled trial that compares surgical with nonsurgical treatment or with a placebo.56 Skeptics of RTS
point to the great variability of surgical results reported
in the literature as one of the characteristics of placebo
Randomized controlled studies will certainly be
needed to definitively settle this issue, but a review of
basic science principles provides 1 hypothesis for RTS
as a viable entrapment neuropathy. Although the PIN is
classically thought of as being a “motor-only” nerve,
the PIN also carries unmyelinated (group IV) afferent
fibers from the wrist capsule as well as small myelinated (group IIA) afferent fibers from the muscles along
its distribution.73 Unmyelinated group IV fibers from
muscles (designated as C-fibers when of cutaneous origin) have long been associated with nociception and
pain. Whereas many group IV fibers respond to
noxious stimuli, others have been shown to be
excited by relatively innocuous mechanical stimuli. Small myelinated group IIA afferent fibers
have been associated with temperature sensation.
Importantly, unmyelinated and small myelinated
fibers are not assessed by nerve conduction studies. Under mild to moderate compression, it is
possible that the unmyelinated and small myelinated fibers of the PIN are affected, thereby producing the painful clinical picture of RTS, whereas the
large myelinated fibers of the PIN remain completely unfazed, accounting for a normal motor
examination and nerve study. If the degree of
compression is notable enough to cause damage to
these larger myelinated fibers, as may be the case
with a large soft tissue mass in the radial tunnel,
the motor-palsy presentation of PIN syndrome
might be seen. The absence of pain in PIN syndrome might be consistent with a complete dys-
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Current Concepts
FIGURE 3: Intraoperative photographs of a left elbow A during and B after release of the arcade of Fröhse and supinator muscle.
After release, the PIN is well visualized at the superior aspect of the photograph (with an hourglass-type compression deformity
appreciated at the former location of the arcade of Fröhse) and the SRN is well visualized at the inferior aspect of the photograph,
as it courses deep to the brachioradialis.
function of the unmyelinated group IV and small
myelinated group IIA fibers.
Current Concepts
The SRN is the superficial sensory branch of the radial
nerve. After the radial nerve bifurcates into the SRN
and PIN, the SRN courses distally into the forearm deep
to the brachioradialis. Approximately 9 cm proximal to
the radial styloid, the SRN becomes a subcutaneous
structure by traveling between the brachioradialis and
ECRL tendons (Fig. 2).74 The SRN continues to travel
in the subcutaneous tissues and branches out into dorsal
digital nerves responsible for afferent sensory input
from the dorsum of the thumb, index, and middle fingers proximal to the proximal interphalangeal joints.
In 1932, Wartenberg published a series of 5 adult
patients describing an isolated neuropathy of the
SRN.75 Given its clinical similarity to isolated neuropathy of the lateral femoral cutaneous nerve in the lower
extremity (also known as meralgia paresthetica),
Wartenberg coined the term “cheiralgia paresthetica”
for this syndrome. Although compression neuropathy
of the SRN had been described a decade earlier by other
authors,76,77 Wartenberg syndrome and cheiralgia paresthetica have since become synonymous with a compression neuropathy of the SRN.
The SRN can be compressed at any point along its
course in the forearm, but it is believed to be at greatest
risk at the posterior border of the brachioradialis as the
nerve transitions from a deep to a subcutaneous structure. Trauma is also a common etiology for SRN compression, which can occur from direct pressure on the
nerve (ie, by a wristband75–78 or handcuffs79 – 81) or
from a stretch injury to the nerve (ie, during a closed
reduction of a forearm fracture82).
Patients with SRN compression typically report pain
or dysesthesias on the dorsal radial forearm radiating to
the thumb and index finger, although the distribution of
symptoms may vary owing to differences in anatomy.
When such sensory disturbances present concomitantly
with weakness of the PIN-innervated muscles, the clinician should consider alternative diagnoses, such as a
more proximal lesion (of the cervical spine, posterior
cord of the brachial plexus, or radial nerve proper) or
perhaps a mass in the radial tunnel large enough to
affect both the PIN and SRN. Because irritation of the
SRN often occurs in the region of the first dorsal compartment, SRN compression symptoms may be confused with the symptoms of de Quervain’s stenosing
tenosynovitis owing to pain with ulnar deviation of the
wrist. One principal difference between the 2 conditions
is that patients with SRN tend to have symptoms at rest,
independent of the position of the wrist and thumb.
SRN compression and de Quervain’s tenosynovitis may
in fact both be present simultaneously.83,84 A Tinel’s
sign over the course of the SRN is the most common
physical examination finding, although the clinician
should be mindful that this may also be positive in
patients with more proximal pain generators, such as a
lateral antebrachial cutaneous neuritis. Although electrodiagnostic testing is often negative in cases of SRN, it
is part of a thorough workup and may be helpful if
Patience is the cornerstone of therapy in patients with
SRN compression symptomatology because spontaneous resolution is common. As external compression is a
common underlying etiology, removal of the inciting
element such as a wristwatch or bracelet is an essential
component of nonsurgical management. In addition,
rest, splinting, and nonsteroidal anti-inflammatory
drugs are, of course, appropriate first-line treatments.
The role of corticosteroid injection is less clear. Lanzetta and Foucher reported a 71% success rate in 29
patients who underwent conservative management
alone, which was defined as removal of a tight watch
strap, splinting, and, in 3 cases, a corticosteroid injection.83 Surgical decompression, which was offered only
to patients who failed conservative therapy or whose
symptoms were longstanding and had no distal progression of a Tinel’s sign, had a 74% success rate in 23
patients. Surgical decompression may also be indicated
in posttraumatic situations in which scar tissue may be
the critical compressive factor. As was the case with the
PIN syndrome/RTS literature, there are no randomized
controlled trials to our knowledge examining the efficacy of different types of conservative regimens (compared with one another or with surgical decompression)
in the management of Wartenberg’s syndrome.
Owing to the subcutaneous location of the SRN, a
number of noninvasive therapeutic modalities centered
around peripheral nerve stimulation (PNS) have been
studied for the treatment of nerve pain, including pulsed
low-intensity infrared laser, as well as direct electrical
stimulation.85– 89 The use of PNS to treat neuropathic
pain is based on the gate control theory of pain originally described by Melzack and Wall in 1965.90 The
theory suggests that pain is not the result of simple
on-and-off signals from nociceptive fibers, but is instead subject to neuromodulation, and may perhaps
JHS 䉬 Vol A, December 
even be inhibited by simultaneous activation of tactile
afferents mediating touch (which may explain why a
child’s pain may be alleviated by a mother’s touch).
Although this theory has found support in the medical
literature and is certainly intriguing,91 there is mixed
evidence supporting the use of PNS. Although some
studies have shown no measurable effect from laser
stimulation,86,87,89 others have shown alterations in the
cortical evoked potential latency and amplitude, suggesting that stimulation of peripheral nerves suppresses
nociceptive processing.85,88 Certainly, more clinical research is warranted to determine the precise role of PNS
in the treatment of SRN compression and other subcutaneous peripheral neuropathies.
Compression neuropathies of the radial nerve include PIN syndrome, RTS, and SRN compression.
When the clinician encounters a patient with digital
extension weakness or palsy, mobile wad pain, or
numbness and tingling in the dorsoradial forearm and
wrist, he or she must consider these diagnoses. Initial
treatment is usually nonsurgical; however, surgical decompression has been shown to yield good results after
failure of conservative management. No consensus exists in the literature regarding the optimal duration of
conservative management and the timing of surgical
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