CURRENT CONCEPTS
Unusual Compression Neuropathies of the Forearm,
Part II: Median Nerve
Alan C. Dang, MD, Craig M. Rodner, MD
is formed from the terminal
divisions of the medial and lateral cords of the
brachial plexus, receiving contributions from
the roots of the 5th, 6th, 7th, and 8th cervical nerves
and the 1st thoracic nerve. It travels through the upper
arm medial to the brachial artery, giving off no
branches to muscles above the elbow, with the possible
exception of a distinct fascicular bundle that may leave
the parent nerve to innervate the pronator teres. In the
distal aspect of the upper arm proximal and medial to
the medial epicondyle, a supracondylar process, with its
attached ligament of Struthers, represents a possible site
of median nerve compression. The brachial artery may
accompany the median nerve deep to the ligament of
Struthers, or be superficial to it (Fig. 1). In marsupials,
the median nerve actually travels through a supracondylar foramen in this area of the distal humerus. Although no such foramen exists in humans, approximately 0.6% to 2.7% of us have a residual
supracondylar process with a vestigial fibrous band
connected to it that inserts into the medial epicondyle.1–3 This fibrous band, known today as the ligament
of Struthers, was interestingly first recognized by Tiede-
T
HE MEDIAN NERVE
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:
rodner@uchc.edu.
0363-5023/09/34A10-0028$36.00/0
doi:10.1016/j.jhsa.2009.10.017
mann in 18223; Struthers was the first person to describe
median nerve entrapment by this structure in 1848.4
As it travels across the elbow and enters the forearm,
the median nerve passes under the bicipital aponeurosis
or lacertus fibrosus into the antecubital region, medial to
both the biceps tendon and brachial artery, and volar to
the brachialis (Fig. 2). The median nerve then passes
between the 2 heads of the pronator teres, deep to the
humeral head and superficial to the ulnar head; although
rarely the ulnar head may be absent.5 After this, the
nerve travels deep to the proximal fibrous arch of the
flexor digitorum superficialis (FDS) (Fig. 3) before continuing its course through the forearm between the FDS
and the flexor digitorum profundus (FDP). In this area,
approximately 4 cm distal to the medial epicondyle or 5
to 8 cm distal to the lateral epicondyle, the anterior
interosseous nerve (AIN) courses off of the main trunk
of the median nerve to innervate the flexor pollicis
longus (FPL), FDP to the index and middle fingers, and
the pronator quadratus (Fig. 4).6 At approximately 4 to
5 cm proximal to the wrist crease, the palmar cutaneous
branch of the median nerve branches off to supply
sensory innervation to the radial palm.7 The median
nerve ultimately continues through the carpal tunnel,
where, of course, it is at greatest risk for compression.
Although there are several possible areas for median
nerve compression proximal to the carpal tunnel, including by the ligament of Struthers, the bicipital bursa,
anomalous arteries, and anomalous muscles (such as
Gantzer’s muscle, an accessory FPL muscle),8,9 pronator syndrome and AIN syndrome remain the 2 most
frequently referenced compression neuropathies of the
median nerve in the forearm.
©  Published by Elsevier, Inc. on behalf of the ASSH. 䉬 1915
Current Concepts
We have previously discussed compression neuropathies of the radial nerve in the forearm. In the
second half of this 2-part review, we will now turn our attention to 2 compression neuropathies
affecting the proximal median nerve, before its entry through the carpal tunnel: (1) pronator
syndrome and (2) anterior interosseous nerve syndrome. (J Hand Surg 2009;34A:1915–1920. ©
2009 Published by Elsevier Inc. on behalf of the American Society for Surgery of the Hand.)
Key words Pronator syndrome, anterior interosseous syndrome.
1916
RADIAL NERVE COMPRESSION
FIGURE 3: Schematic of the median the nerve as it passes
beneath the proximal fibrous arch of the flexor digitorum
superficialis in the forearm.
FIGURE 1: Schematic of the median nerve above the elbow as
it travels medial to the brachial artery. The artery may be
superficial to the ligament of Struthers (as shown here) or
accompany the median nerve deep to it.
FIGURE 4: Schematic of the AIN as it branches off of the
main trunk of the median nerve deep to the flexor digitorum
superficialis.
Current Concepts
FIGURE 2: Schematic of the median nerve as it enters the
forearm, deep to the bicipital aponeurosis, and medial to both
the biceps tendon and brachial artery.
PRONATOR SYNDROME (PS)
Pronator syndrome commonly refers to compression of
the median nerve as it passes between the 2 heads of the
pronator teres muscle or under the proximal edge of the
proximal FDS arch. Symptoms usually have an insidious onset and typically are not diagnosed as part of an
overall clinical syndrome for months to years.10 –12 PS
typically presents with aching pain in the proximal,
volar forearm with paresthesias radiating into the
thumb, index finger, middle finger, and the radial half of
the ring finger, similar to the sensory alterations of
carpal tunnel syndrome (CTS). These symptoms are
often made worse by repetitive pronosupination movements. As originally described by Seyffarth in 1951,13
PS is actually a somewhat misleading term because it
actually refers to compression of the median nerve at
more anatomic sites than just the pronator teres.
Discriminating clinically between PS and CTS can
be difficult because of their shared symptoms in the
median nerve–innervated radial 3½ digits and pain in
the volar wrist and forearm. However, several discriminating factors can aid in the differential diagnosis.
Because the palmar cutaneous branch of the median
nerve arises 4 to 5 cm proximal to the transverse carpal
ligament,7 a patient presenting with CTS-like symp-
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RADIAL NERVE COMPRESSION
1917
toms in addition to decreased sensation over the thenar
eminence should be evaluated for a more proximal
lesion (ie, a cervical radiculopathy, brachial plexopathy,
or a more proximal compression of the median nerve).
Unlike patients with CTS, individuals with PS should
not have a Tinel sign over the wrist, nor should their
symptoms be provoked with wrist flexion. For this
reason, unlike CTS, PS does not characteristically produce nocturnal symptoms.10
In patients with PS, a helpful examination maneuver
is to resist the patient’s pronation of his or her forearm
in a neutral position. If pain or parasthesias are reproduced during this maneuver as the elbow is extended,
the clinician should suspect entrapment of the median
nerve at the level of pronator teres.14 If resisted contraction of the FDS to the middle finger reproduces
symptoms, median nerve compression at the level of
the fibrous arch between the heads of the FDS might be
suspected.14 If symptoms are elicited by resisted flexion
of the forearm in full supination, compression at the
more proximal level of the lacertus fibrosus might be
considered.15 Electrodiagnostic studies can be useful in
the diagnosis of PS in that they may exclude other sites
of nerve compression or help identify a double-crush
syndrome.16
AIN SYNDROME
The first description of an AIN neuropathy can be
attributed to Duchenne de Boulogne, who reported an
isolated palsy of the FPL in 1872.20 In 1952, Kiloh and
Nevin described in detail the clinical manifestations of
FIGURE 5: A characteristic physical examination finding in AIN
syndrome is that a patient will be unable to flex his thumb
interphalangeal joint and index finger distal interphalangeal joint to
make an “OK” sign, as this patient can.
an isolated compression of the AIN.21 Because the AIN
is a motor-only nerve innervating the deep muscles of
the forearm (FPL, FDP to the index and middle fingers,
and pronator quadratus), a patient with a complete AIN
palsy would present with no motor function to all 3 of
these muscles. Patients with incomplete palsies or with
Martin-Gruber anastomoses (in which axons of the AIN
may, for example, cross over to innervate the hypothenar muscles)22 may present differently. In addition, the
clinician must consider that the FDP to the middle
finger may not always be exclusively innervated by the
median nerve, so intact middle finger distal interphalangeal joint flexion does not unto itself exclude AIN
syndrome as a potential diagnosis.
Patients with AIN syndrome most commonly recognize weakness or absence of FPL function. Although no
sensory loss occurs, pain may be present in the forearm
along the course of the nerve. A characteristic physical
examination finding is a patient’s inability to make an
“OK” sign when asked by the examiner to flex his
thumb interphalangeal joint and index finger distal interphalangeal joint (Fig. 5). In patients with mild AIN
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Current Concepts
Management
Surgery is usually not necessary to treat PS. Not surprisingly, first-line treatments such as the avoidance of
aggravating activities, rest of the extremity, and nonsteroidal anti-inflammatory medication are frequently successful in alleviating symptoms. Conservative management has been shown to be effective in 50% to 70% of
patients.11,17 Corticosteroids have also been shown to
be efficacious.18 When a space-occupying lesion is
present or a several-month course of nonsurgical treatment fails, surgery may be indicated.19 The surgical
approach used for decompression of the median nerve
in the forearm will be discussed in more detail in the
next section on AIN syndrome. The success rate with
surgery in the treatment of PS approaches 90% in the
literature,10,11,17 although there remains no consensus
on how long to pursue nonsurgical treatment before
surgical intervention; and yet again, no randomized
clinical trials exist comparing surgery with conservative
management.
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RADIAL NERVE COMPRESSION
FIGURE 6: A patient with AIN syndrome may be unable to
pinch a sheet of paper between his thumb interphalangeal joint and index finger distal interphalangeal joint, and may
compensate by using a more adaptive grip in which these
joints remain extended.
Current Concepts
compression, subtle weakness of these muscles may be
the only clinical finding. Such weakness of the FPL and
index finger FDP may be uncovered by asking the
patient to pinch a sheet of paper between his thumb and
index finger using only the fingertips and then trying to
pull the paper away. A patient with AIN syndrome may
be unable to hold on to the sheet of paper with just his
fingertips and may compensate by using a more adaptive grip in which the interphalangeal joint of the thumb
and distal interphalangeal joint of the index finger remain extended (Fig. 6).
A noncompressive neuropathy, such as a brachial
neuritis,23 may mimic the clinical manifestations of an
AIN neuropathy and must be considered in the differential diagnosis. A sudden onset of symptoms associated with a viral prodrome suggests the diagnosis of
such a viral neuritis (Parsonage-Turner syndrome)23
instead of a compression neuropathy. It is also important to consider rupture of the FPL tendon in the differential diagnosis, which may occur in patients with
rheumatoid arthritis. To exclude this diagnosis, the
wrist should be passively flexed and extended to confirm that the patient has an intact tenodesis effect. If the
tendons are intact, passive wrist extension brings the
thumb interphalangeal joint and index finger distal interphalangeal joint into a relatively flexed position compared with when the wrist is passively flexed.
Electrodiagnostic studies are an important element in
the workup of AIN syndrome because they confirm the
diagnosis and objectively assess the severity of the
neuropathy. Electromyography is often helpful in ruling
out more proximal lesions as a cause of the symptoms,
as well as distinguishing AIN syndrome from a flexor
tendon rupture in patients with severe rheumatoid disease who have such limited wrist motion that determination of an intact tenodesis effect is impossible. Imaging studies, such as magnetic resonance imaging (MRI),
are not commonly used in the diagnosis of AIN syndrome, although there is literature describing the MRI
findings associated with AIN syndrome in which increased signal intensity can be seen in the AINinnervated muscles on T2-weighted, fat-saturated images or short inversion time inversion recovery
sequences.24,25 MRI may actually provide a theoretical
advantage of increased sensitivity over electrodiagnostic studies in that abnormal findings after nerve injury
are detectable earlier with MRI (alterations in signal
intensity can be seen as early as 4 days after injury) than
they are with electromyography (which requires 2 to 3
weeks).26 In clinical practice, this theoretical advantage
is unlikely to affect the treatment course.
Management
Once the diagnosis of AIN syndrome is made, treatment should begin nonsurgically with the typical regimen of rest, splinting, and observation. Because most
patients with AIN syndrome seem to improve without
any surgical intervention,27,28 observation for a period
of several months has been suggested before decompression.8 For those patients who have a space-occupying mass in the area, or who fail a several-month course
of nonsurgical treatment, surgical decompression has
been recommended. As we saw to be the case with
compression neuropathies of the radial nerve, there is a
paucity of high-quality literature supporting the appropriate duration of conservative treatment in this condition as well.
The surgical approach for patients with PS or AIN
syndrome is performed through a lazy-S–type incision
that begins with an exploration of the median nerve
proximal to the antecubital flexion crease, as this allows
for identification of the median nerve proper and exposure of the ligament of Struthers if need be. Of course,
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Controversy
There is controversy surrounding the treatment of PS
and AIN syndrome in that it is extremely difficult to
glean from the literature when surgical intervention is
appropriate. Because the natural history of PS and AIN
syndrome is not well delineated and no randomized,
controlled trials exist comparing conservative and surgical treatments, it is difficult to make evidence-based
recommendations on the timing of surgical intervention.
For AIN syndrome, Spinner recommended surgical
exploration after 12 weeks of persistent symptoms or a
persistent abnormality on electrodiagnostic studies.30
However, spontaneous recovery has been seen even as
long as 1 year after the onset of symptoms.27,31–34 In
Miller-Breslow et al.’s series of 10 patients with AIN
syndrome, 8 who were treated by observation alone had
signs of spontaneous recovery within 6 months and
went on to a full recovery by 1 year.27 Nakano and
colleagues reported on 2 patients with bilateral AIN
palsies, with separate times of onset for each side.28 The
first side was treated surgically, whereas the contralateral side was treated nonsugically. Interestingly, all 4
extremities recovered and surgery did not produce an
earlier return of function. Stern reported 3 cases of AIN
syndrome that failed to respond to nonsurgical treatment after 3 to 5 months, which then went on to a
complete resolution of symptoms 5 months after surgical decompression.35
Proponents of surgical decompression point to the
case series of Schantz and Riegels-Nielsen who re-
ported on 20 patients with AIN syndrome, 15 of whom
underwent surgical decompression.36 Satisfactory function after surgery was reported in 11 patients (73%),
whereas nonsurgical management had only a 40% rate
of recovery. Moreover, 3 of the 5 patients treated nonsurgically were noted as having a persistent palsy at
4-year follow-up.
Because a clinical AIN palsy may result from a
compression neuropathy of the AIN proper, a compression of the median nerve more proximally, an AIN
neuritis, or some combination of the 3, the studies in the
literature may in fact be reporting upon patients with
different etiologies of AIN dysfunction. Antecedent
pain or systemic prodromic symptoms such as fever,
malaise, or myalgias are suggestive of more an inflammatory etiology than a compressive one. Since all of
Miller- Breslow et al.’s patients reported a prodome of
forearm pain, it is possible that at least several of the
patients in their study may not have had a true compression neuropathy.27 In cases of AIN neuritis, an
extended course of conservative therapy is warranted,
as a spontaneous resolution of symptoms seems to be
the norm. In the absence of evidence suggesting a
neuritis, most authors still recommend a trial of conservative management of at least 12 weeks,34 although the
prognosis for spontaneous recovery in such patients
seems to be more guarded.
Although compression neuropathies of the forearm,
such as those of the median nerve, present far less
frequently than those of the wrist, it is essential that
clinicians consider these less common entities when
evaluating their patients. Once a diagnosis is made,
conservative management, including avoidance of aggravating activities, rest, and anti-inflammatory medication, is recommended. If symptoms persist despite
these measures, surgery is appropriate and has been
shown to be effective. Randomized, controlled trials
examining the ideal duration of nonsurgical management and the timing of surgical intervention for PS and
AIN syndrome (as well as for compression neuropathies of the radial nerve in the forearm) are warranted.
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Current Concepts
the surgical approach and extent of proximal exploration can be tailored to the surgeon’s specific areas of
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1919
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Current Concepts
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