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HIGH MEDIAN NERVE ENTRAPMENTS
An Obscure Cause of Upper-Extremity Pain
A. Marc Tetro, MD, FRCSC, and David R. Pichora, MD, FRCSC
What is a high median nerve entrapment and how frequently does it occur? Why is it important but difficult to recognize? Hopefully, at the conclusion of this
article the reader will have an appreciation for this increasingly important entity that is becoming recognized as a significant cause of the painful upper extremity.
The median nerve is formed along the lateral
wall of the axilla by the confluence of the medial and lateral cords of the brachial plexus. It then travels a well-described path through the arm, across the elbow, and through the forearm to reach the carpal tunnel
and the hand. For our purposes, "high median nerve entrapment" is a compression occurring between its origin and the carpal tunnel.
Entrapment of the median nerve has become a very commonly diagnosed
entity over the past 20 years. In fact, carpal tunnel release (CTR) has become one of the most frequently performed surgical procedures in North America. Along with the dramatic advances in scientific knowledge of
carpal tunnel syndrome (CTS), a public awareness campaign has led to a virtual "epidemic" of median nerve entrapment. 12
With both the public and the medical community keenly aware of CTS, other less common sites of median nerve compression may be overlooked.
As said by Urbaniak,77
". . . although CTS is the most frequently encountered and best understood compression neuropathy, it is often overdiagnosed, misdiagnosed, or incompletely diagnosed." Dellon12
noted that ". . . many patients with CTS have been found to have a nerve compression at a higher, more proximal level, such as the elbow." The complications of CTR most commonly reported in the literature include injury to the palmar cutaneous nerve and incomplete release of the transverse carpal ligament.
33, 43 There is increasing speculation, although not quantitated, that failure of carpal tunnel surgery is often caused by an incorrect or incomplete diagnosis of the location of the median nerve entrapment.
51, 77 This often leads to inappropriate procedure but more importantly, often leaves the patient with a persistently symptomatic extremity.
Lister4l
noted that "The significance of the pronator syndrome is that it can easily be mistaken for carpal tunnel compression and the wrong treatment undertaken." The frequency of occurrence of proximal median nerve compression is still unknown but believed to be uncommon, but its importance in the management of chronic pain syndromes is becoming more recognized.
Although high median nerve entrapments have been reported for many years, there is still a general lack of awareness on the part of many physicians compared with CTS; because it occurs much less frequently, its
presentation and physical findings are not as "classic," and electrophysiologic investigations are often equivocal. In short, the diagnosis is elusive, the localization of compression is a challenge, and it is
often overlooked in the differential diagnosis.
SURGICAL ANATOMY OF THE MEDIAN NERVE AND ITS COMMONLY ASSOCIATED ANOMALIES
There are a few general patterns of high median nerve entrapment to consider
when discussing the pertinent anatomy. Compression of the median nerve in the arm is often caused by vascular structures because the nerve has an intimate relationship with brachial vessels. In the region of the elbow
and proximal forearm, the nerve may be compressed, often in a dynamic nature, by various musculoskeletal structures. Moreover, the presentation and diagnosis of a peripheral nerve compression may be confusing because of
the commonly associated anomalies of the nerve itself (e.g., Martin-Gruber anastomosis).
The median nerve is formed in the axilla by equal contributions of the medial (C5-C7) and lateral (C8-Tl) cords of the
brachial plexus. It therefore receives contributions from the anterior divisions of the roots of C5 through T1, being formed anterior to the distal one third of the axillary artery. As the nerve passes down the arm to
the elbow, it has an intimate relationship to the brachial artery crossing it from anterior to medial.
At the elbow, it has a consistent relationship with the surrounding structures. The biceps tendon, brachial
artery, and median nerve are arranged from lateral to medial respectively. The nerve consistently resides anterior to the brachialis muscle and deep to the lacertus fibrosus. Although the brachialis adds a level of
protection from the deeper osseous structures, the bulk of the muscle varies considerably and may contribute to compression against the lacertus. The median nerve then passes between the superficial (humeral) head and
deep (uInar) head of the pronator teres muscle, crossing to the lateral side of the ulnar artery as the artery passes posterior to the deep head of the pronator teres. The median nerve subsequently passes through the
arch formed by the two heads of the flexor digitorum. superficialis (FDS). It continues distal on the deep (or posterior) surface of the FDS through the mid portion of the forearm. At the distal third of the forearm,
the median nerve emerges from the lateral (radial) aspect of the FDS to enter the carpal tunnel.
Knowledge of the branching patterns of the median nerve is very important to understanding the various
presentations of median nerve entrapment. There are rarely any branches proximal to the elbow region. The first branch, off the medial aspect approximately 1 cm to 4 cm proximal to the elbow, penetrates and innervates
the pronator teres muscle. Soon after this, the median nerve gives off branches to the flexor carpi radialis (FCR), palmaris longus, and FDS. In the pronator teres muscle, at approximately 5 to 8 cm distal to the medial
epicondyle, an important branch, the anterior interosseous nerve (AIN), arises from the posterolateral surface of the nerve. Typically, the AIN branches immediately distal to the proximal border of the superficial head
of pronator teres and accompanies the median nerve through the fibrous arch of the FDS. The AIN then comes to lie on the interosseous membrane, coursing distally with the anterior interosseous artery (branch of the
uInar artery) to the level of the wrist. The AIN supplies motor branches to the flexor pollicis longus (FPL), flexor digitorum profundus (FDP) of the index and long fingers, and pronator quadratus (PQ).30
The branches to the FPL and FDP arise at the tendinous origin of the FDS (approximately 4 cm. distal to AIN origin). The AIN terminates in the PQ with small sensory branches to the carpus.
The course of the
median nerve and its branches have common variations relevant to proximal median nerve entrapment. In the arm, the most common variation relates to the "delayed" contribution of the lateral cord. In 24% of
cadaver dissections, the lateral cord has a very small proximal contribution but the musculocutaneous nerve sends a branch to the median nerve in the proximal arm. The medial and lateral cords can pass posteriorly to
the axillary artery to form the median nerve, which subsequently takes a posterior course to reach the medial aspect of the brachial artery. These anomalies, however, are not as pertinent to compressive neuropathies as
those at the level of the elbow and proximal forearm.
In 1848, Struthers71 noted a supracondylar "spur" in 3% of his cadaver dissections. "The osseous portion of the arch arose at
a distance from the internal condyle . . . then arrived downward inwards . . . gave attachment to the ligament which . . . joined the line close above the condyle and thus completed the arch . . . and transmitted the
median nerve and undivided humeral artery (brachial)." The continuity of this arch is variable and often not complete, but may still have the potential to compress the median nerve along with the
artery."Recent anatomic dissections suggest that this occurs in approximately 1% to 2% of the population."
The relationship of the median nerve to the pronator teres muscle is extremely variable.
Typically, the nerve gives off medial branches to the pronator teres as it penetrates the muscle. In 82% of people, the nerve courses between the superficial (humeral) and deep (ulnar) heads of pronator teres .2
In 9% of cadaver dissections, the deep head is absent; in 7%, the nerve lies deep to both heads; and in 2%, it passes through the superficial head. Dellon11
also noted significant abnormalities in the origin of the superficial head of pronator teres. In 20% of his cadaver dissections, the superficial head was noted to originate 2 cm proximal to the medial humeral epicondyle, and became confluent with the lacertus fibrosus. This has been postulated to compress the median nerve directly against the trochlea when the elbow is in extension and the forearm is in pronation. Dellon and MacKinnon
13 reported that 11 of 31 cadavers had a fibrous arch beneath the superficial head of pronator teres. In addition, 15 of 31 had a distinct fibrous band on the u1nar side of the deep head of the pronator teres.
13
The FDS is commonly reported to have two heads (humeral and interosseous membrane) with a tendinous arch linking them together. Ten of 31 cadavers had a third origin from the radius, with only four having a single origin of the FDS. Eleven of 31 specimens had a tough fibrous arch linking the two heads of the FDS, through which the median nerve passed and potentially could be compressed.
13
Internal anomalous anatomic features of the nerve proper are also important in proximal median nerve entrapment. Recall that more superficially positioned fascicles within a nerve are at increased
risk of compressive injury.66 For 2.5 cm prior to its origin, the AIN is situated posterolaterally within the median nerve.72
AIthough the AIN is often depicted to branch posteriorly off the median nerve, up to 60% of cadaver dissections have shown that the origin, in fact, is from the radial aspect. This variation may possibly play a role in AIN syndrome and posttraurnatic palsies.
44
External anomalies of the nerves are also extremely important with respect to compressive neuropathies of the upper extremity. There are two main types of presentation: (1) communication between
nerves (i.e., MartinGruber [M-G] anastomosis) and (2) unusual branching patterns of nerves.
These are significant sources of misdiagnosis; for instance, a proximal injury may cause weakness of a muscle that it
does not usually innervate. Or one may only see "partial" nerve lesions of muscles supplied by another "uninjured" nerve.39, 70, 76
The MG anastomosis is of particular interest in high median neuropathies. This communication between median and ulnar nerves is very common, occurring in approximately 17% of the population.39
Fortunately, as electrophysiologic skills and techniques improve, we are increasingly able to diagnose M-G communications by nerve conduction studies (NCS).76
COMPRESSION OF THE MEDIAN NERVE AND ITS BRANCHES
We will discuss the known and common areas of entrapment and the commonly described syndromes-the so-called pronator syndrome and the
anterior interosseous nerve syndrome. Moreover, high median nerve compression may involve either static or dynamic factors. Repetitive trauma disorders are a controversial cause of nerve compression. One must also
consider the possibility of double crush syndromes.5, 54,78
Compression of the Median Nerve in the Arm
Chronic pain arising from the proximal median nerve in the arm is predominantly caused
by trauma, typically direct damage caused by penetrating or crushing injuries.44
In this situation, the diagnosis and location of the lesion or site of entrapment are often straightforward. Nontraurnatic compression is predominantly caused by slowly expanding lesions, often vascular in nature. Arterial aneurysms, arteriovenous malformations, and expanding arteriovenous fistulas for hemodialysis are reported causes.
16, 58 Omer and Spinner53
reported on occult median neuropathy in six patients secondary to various vascular malformations in the arm. The increasing use of interventional investigations, arteriograms, and vascular access often is responsible for acute or subacute proximal median nerve injury or compression.
Compression of the Nerve in the Elbow Region
There are four commonly described sites of compression of the median nerve in the elbow and proximal forearm region. These include the common locations for
both pronator syndrome and anterior interosseous nerve syndrome. Pronator syndrome occurs with compression prior to branching of the median nerve. After branching of the AIN (level of pronator teres), however, the
presentation or syndrome varies depending on the degree of injury or compression to each nerve or its branches.
Trauma plays a role in compression of . the median nerve at the elbow region. Much has been written
in relation to supracondylar humeral fractures and, less frequently, elbow dislocations. Supracondylar humeral fractures have been associated with a 5% to 19% incidence of median nerve injury9; there is
evidence suggesting a higher incidence of anterior interosseous nerve injury associated with this fracture. In general, proximal median nerve injury is not a common cause of the painful upper extremity.
The
presence of a fibrous or thickened tendinous arch of either the pronator teres or IDS places the nerve at risk of compression. If the patient's work requires a significant amount of repetitive use of the arm,
particularly pronation of the forearm or flexion of the fingers, then muscle hypertrophy increases the risk to the nerve. If, in addition, the AIN arises from the radial instead of the posterior aspect of the median
nerve, it may be particularly vulnerable to compression beneath this fibrous arch. Cumulative trauma disorders are an increasing concern in our society. Some cases of the painful upper extremity may be caused by
exertional compartment syndromes.24
Repetitive use of the arm with an associated anatomic anomaly, hypertrophy of muscle, and swelling could cause an exertional compartment syndrome. Chronic forearm pain, similar to pronator syndrome, may be caused by this entity.
24, 36, 57 Pedowitz55
reported a patient with exertionally produced pronator syndrome, increased compartment pressures during exercise, and complete relief of symptoms following fasciotomy. Some therefore believe that the benefit of surgical exploration in pronator syndrome, in fact, is attributable to the fasciotomy.
The prevalence and morphology of the ligament of Struthers and the associated supracondylar process are extremely variable. The spurs are of variable length, the fibrous band is not always present, and sometimes
the band occurs without the bone spur.20, 73 With 1% to 2% of the population having this anatomic arrangement, it is interesting that it only rarely appears to be a source of median nerve entrapment.1, 44
PRONATOR SYNDROME
The pronator syndrome was first described in 1951 by Seyffarth.62
He reported 17 patients whom he proposed were suffering from median nerve entrapment as the nerve passed through the pronator teres muscle or the FDS arch. This illustrates that from the time of the initial description, there has been ambiguity about the name because it includes more than just compression by the pronator teres. It is now often referred to as the so-called pronator syndrome because it has a common clinical presentation but a "spectrum" of locations of compression. Since 1951, there have been numerous reports of patients presenting with pronator syndrome who have gone on to surgical decompression with complete recovery. There are four more commonly described locations of compression:
1. Ligament of Struthers-an uncommon structure that is rarely believed to cause pronator syndrome 38, 77
2. Tight or thickened lacertus fibrosus-often associated with brachialis hypertrophy
25,46,66
3. Fibrous band within the pronator teres -particularly worsened by repeated pro-supination
4. Proximal edge of FDS- "sublimis arch"--a tight fibrous arch between the heads of the FDS
The most common areas of compression are at the level of the FDS arch 51 or by the nerve passing through the pronator teres muscle.21,30
Clinical Presentation
The pronator syndrome
is much less common than CTS. It usually presents in the fifth decade and is four times more common in women.31 The symptoms are insidious in onset, with a delay in diagnosis ranging from 9 months to 2 years.
25, 30, 1
The patient most Commonly complains of aching pain in the proximal volar forearm and the distal arm. Pain may radiate proximally, and is often aggravated by use of the upper limb, especially with resisted forceful pronation or repeated pronation/supination movements.
15, 35, 41, 62 As is the case in CTS, there is usually associated paresthesias and, possibly, altered sensibility in the radial three and a half digits,25, 62
but night awakenings and nocturnal pain are uncommon- a key symptom to help differentiate from CTS (see section on differential diagnosis).
Clinical examination is often very characteristic, with
tenderness and, frequently, firmness noted over the pronator teres muscle.25, 30,62
Atrophy of the forearm musculature is uncommon. Tinel's sign over the median nerve at the level of the pronator teres is frequently positive 25,49 but often takes 4 to 5 months to develop. 66
Paresthesias and altered sensibility may be noted, particularly upon provocative testing of the arm. Measurable sensory changes are extremely variable, with many reports not commenting on objective sensory testing. Motor weakness is also extremely variable and difficult to quantify: All seven patients in one study reported weakness,
49 compared to 0 of 71 patients in another study.30
Provocative testing of the median nerve for proximal entrapment is extremely useful because it is hypothesized that the compression of the
nerve relates to both the position of the forearm and muscular contraction. If pain or paresthesia is invoked by one of the following maneuvers, it suggests dynamic compression by the associated structure:
Pronator teres-resisted pronation of the forearm (in neutral position) with symptoms being reproduced as the elbow is gradually extended53 (Fig. 1)
 |
Figure 1. Test for compression of median nerve by pronator teres. Resisted pronation (forearm neutral) with symptoms reproduced as the elbow is gradually extended.
53
Arch of FDS-resisted contraction of the FDS to the long finger53 (Fig. 2)
Figure 2. Test for compression by arch of FDS. Resisted contraction of FDS of long finger.53
Lacertus fibrosus74-Symptoms with resisted flexion of the forearm in a position of greater than 120 degrees of elbow flexion, maximal
supination (Fig. 3)
Johnson and Spinner31 have attempted to delineate criteria for diagnosis of the pronator syndrome (Table 1). Unfortunately, there is
no objective method to use these criteria for a particular patient. We therefore must still rely on clinical skills, with some assistance from electrophysiologic investigations, to achieve a diagnosis.
Figure 3. Test for compression by lacertus fibrosus. Resisted flexion of elbow in
forearm in supination. 74
Electrodiagnostic Investigations
Electrophysiologic studies are rarely diagnostic for pronator
syndrome. Apart from Morris and Peters,49 who demonstrated positive studies in six of seven patients (slowed motor conduction) and Buchthal et al,7 who measured sensory conduction
abnormalities in three of seven patients, most series report few positive studies. 25, 30 Slowing of motor and sensory conduction between the wrist and elbow is neither specific nor diagnostic for
proximal median nerve entrapment. Patients with CTS may have slowing of median nerve conduction for a variable distance proximal to the wrist. 7, 8
The most valuable tool in the electrophysiologic studies is needle electromyography. The diagnosis of pronator syndrome is supported in some cases in which denervation potentials are noted
in median nerve-innervated- muscles. Even this can be variable, however, because of the relationship of the site of compression and the origin of a particular motor branch to a particular muscle.25
The value of electrophysiologic studies is primarily to help rule out other conditions that have similar clinical presentations, such as CTS, and to determine coexistent sites of compression (double
crush syndrome or multiple nerve entrapment)
Table 1.
CRITERIA PROPOSED BY JOHNSON AND SPINNER FOR DIAGNOSIS OF PRONATOR SYNDROME
Pronator teres tenderness / firmness to palpation
Positive Tinel's sign over pronator teres
increased paresthesias of radial three and a half digits with weak compression of pronator
Variable weakness of median nerve innervated muscles
Absence of night symptoms
Reproduction of symptoms with provocative test
Abnormal electrophysiological study
Muscle spasm / cramping with repetitive pinch-type exercise
Reproduction of symptoms with use of blood pressure cuff
Differential Diagnosis
The differential diagnosis of the pronator syndrome is extremely important because this entity is relatively uncommon compared with
CTS. In fact, as noted by Lister, 41 CTS are very similar to those of pronator syndrome.41 Table 2 lists the similarities and differences
between the two entities. Other important differentials include thoracic outlet syndrome, proximal brachial plexus neuropathies, cervical radiculopathy, and polyneuropathy. The diagnosis of these
conditions is assisted by the use of electrophysiologic investigations. These conditions are not mutually exclusive, however. The concept of double crush syndrome appears to be a
clinically relevant entity, with 50% of the cases of pronator syndrome reported by the Mayo clinic25 also having a positive Phalen's test at the wrist. In addition, 7 of 35 had undergone
previously unsuccessful carpal tunnel release and continued to experience chronic forearm pain.
Treatment of Pronator Syndrome
Nonoperative Treatment
The treatment of pronator syndrome involves the assessment of several factors, including the onset of symptoms, chronicity, degree of muscle weakness and sensory abnormalities, and the presence
of abnormal electrophysiologic studies. Many cases are mild, intermittent, and associated with strenuous repetitive activity; in those, pursuing a period of nonoperative therapy would be beneficial.
Avoidance of aggravating activities, rest of the extremity (including use of splints) and nonsteroidal anti-inflammatories are often beneficial. Morris and Peters49 reported seven patients treated
conservatively with corticosteroid injection in the region of the pronator teres. Five of the seven achieved complete relief of symptoms. Johnson30 had a 50% success rate with conservative treatment.
If the symptoms are progressive or resistant to nonoperative means, surgical exploration for release of offending structures must be considered. With an uncommon problem such as this, however,
there is no consensus as to how long to persist with conservative treatment. It is generally regarded that 8 to 12 weeks of conservative treatment are warranted before recommending surgery.66, 68
Surgical Treatment
The fact that the pathologic features seen at the time of surgery are often minimal seems to correlate with the vagueness of the
symptoms, lack of specific clinical findings, and, often, nonspecific electrophysiologic studies. Exploration of the entire proximal forearm region, examining all possible sites, therefore should be
done to rule out multiple or unusual compression sites.
The goal of the procedure is to relieve all constricting structures. As with many procedures, the surgical exposure is operator-dependent. Eversmann18
prefers to use a zig-zag type skin incision, whereas others prefer a longitudinal incision or a transverse skin incision, which recently was advocated by Tsai and Syed 75 but is
condemned by others because of the lack of exposure.44 Along with improved cosmesis, their cadaver dissections and clinical trial report that an adequate release is possible. Most, including Spinner and
Dellon,53 use a gentle lazy-S type incision, extending across the elbow while bemig careful to avoid crossing the flexion crease. The medial cutaneous nerve of the forearm crosses the elbow region
medially, and must be visualized and protected to prevent injury.44 Similarly, the terminal fibers of the lateral antebrachial cutaneous nerve are identified and protected.
The deep fascia of the arm is divided to expose the median nerve and brachial artery at the medial edge of the biceps. The lacertus fibrosus is completely divided along its length to continue the distal
exposure of the median nerve. If a supracondylar process or Struther's ligament is present, it is excised. The median nerve is identified entering the pronator teres. It must be recalled that the
"safe side" of the nerve is the radial/lateral side because the proximal motor branches to the flexor/pronator mass arise ulnarly/medially. The superficial head of the pronator usually is
taken down medially (protecting its motor branch) and the median nerve is identified. By doing this, any fibrous bands of the pronator are released and the uInar collateral artery is identified and divided,
if necessary. Infrequently, a Z-lengthening of the superficial head is required in severe cases of scarring (such as in Volkmann's contracture). If so, the superficial head is rerouted deep to the nerve.
More distal dissection is most often carried out by opening the interval between the pronator teres and FCR .66 The FDS tendinous arch, if present, is readily visible and divided. At this point, the
median nerve and anterior interosseous nerves should be well visualized and free of any constricting structures.
Perineural or intraneural fibrosis may cause significant wasting or
severe persistent sensory discomfort.44 Dellon advocated epineural and, possibly, intraneural neurolysis. This, in contrast to recurrent carpal tunnel or cubital tunnel syndrome, is not a particularly
common site for complications such as neuritis, neuropathy, or RDS of the multiply operated nerve. Here, the median nerve is well covered and insulated by muscle, as compared with the superficial
sites at the wrist, where scarred nerves or neuromas may become adherent to bone or dermis.
Table 2. SIMILARITIES AND DIFFERENCES BETWEEN PRONATOR SYNDROME AND CARPAL TUNNELSYNDROME
Similarities Between Two Syndromes
Pain in wrist and forearm regions
Weakness of thenar muscles
Numbness/paresthesias of radial three and a half digits
Differences in Two Syndromes
No nocturnal pain in pronator syndrome
Negative Tinel's sign at wrist in pronator syndrome
Nerve conduction study-no delay at wrist in pronator syndrome
Dysesthesia in palmar cutaneous distribution in pronator syndrome
Results of Treatment
There have been a limited number of reported series of surgical treatment of pronator syndrome. In general, most series report approximately 85% to 90% good to excellent outcomes. 25, 30, 79
There is no consistency of objective criteria by which to compare the results, however. The Mayo Clinic series noted the best results occurring when a definite anatomic constriction was found. Despite
these results, the result for a given patient often relates to the cause and degree of compression and the duration of symptoms. In chronic cases of compression with associated significant nerve
deficits, the prognosis is less favorable.
ANTERIOR INTEROSSEOUS NERVE SYNDROME
AIN accounts for fewer than 1% of all upper extremity neuropathies,69
yet it remains an important entity when considering the painful hand. One of the earliest descriptions of AIN came from Kiloh and Nevin34 in 1952. Since that time, Spinner 65 and others
have clarified our knowledge regarding this entity.
There are three general categories of anterior interosseous nerve dysfunction 70: (1) direct trauma, (2) apparent AIN lesion but truly a
partial median nerve proper lesion (proximal), (3) neuropathies caused by either compression or inflammation of the AIN.
Apart from trauma, there is still much debate as to the causes of
the AIN syndrome, particularly the relative contribution of compression versus inflammation of the nerve.47,70 The surgical literature emphasizes the theory of compression, whereas the
neurologic literature favors the inflammatory 'neuritis' etiology.15,59 Surgical findings, including epineural artery thrombosis or grayish discoloration of the nerve caused by ischemia,47
do not help resolve the question of cause. Both compression and inflammation could theoretically cause such a picture.70 A more complete list of the possible causes appears in Table 3.
Presentation
The AIN syndrome is a pure motor palsy that classically presents with weakness or paralysis of the FPL, FDP of index or long fingers, and PQ. In addition, the AIN has a terminal sensory branch that
supplies the region of the wrist. Wrist and forearm pain therefore are also common features. The picture is often variable, with many reports of atypical (or incomplete) presentations of this syndrome.
Table 3.
CAUSES OF THE ANTERIOR INTEROSSEOUS NERVE SYNDROME
"Pseudo-anterior interosseous nerve syndrome"-a partial lesion of the median nerve proximally, involving primarily the fascicles of the AIN
Trauma
Fractures (supracondylar humeral fractures, forearm fractures)
Dislocations-of elbow Penetrating injuries-missile, stab wounds Crush injuries
latrogenic
Arterial or venous access (cutdowns, catheterization, venipuncture)
Muscle release Open reduction/internal fixation of fractures
Spontaneous causes
Compression
By musculotendinous bands-pronator teres, FDS arch
Anomalous course deep to pronator teres
Accessory muscles: Ganzter's muscle (aberrant head of FPQ, FCR, palmaris profundus, forearm mass
Enlarged bicipital bursa
Repetitive trauma with excess muscle use (?)
Vascular
Aberrant radial artery
Thrombosed uInar collateral artery
Inflammation
Neuralgic amyotrophy Infection-cytomegalovirus
Arteritis-polyarteritis nodosa
Complete Syndrome
There is a history of spontaneous pain in the proximal volar forearm
in the region of the pronator teres muscle and volar wrist. Symptoms tend to increase with activity, especially repetitive forearm motion. Weakness is usually preceded by pain,44 with the
pain often subsiding partially or completely over weeks to months.57 There is classically weakness of the FPL, FDP of the index and long fingers, and PQ. This often leaves the patient complaining of
difficulty with writing or picking up small objects.69 It is discriminated from pronator syndrome by the lack of paresthesias and altered sensibility.
On clinical examination, the most prominent feature is weakness of the thumb FPL, index and long finger FDP, and PQ muscle.61 Spinner was the first to describe the "classic attitude" of the weak
pinch with this syndrome (Fig. 4).
Interestingly, there are many reports of "incomplete" AIN syndromes. Essentially, the primary difference is the isolated paralysis of the FPL or the index FDP muscles.
26, 65 These atypical presentations may be caused by anatomic variations, such as:
1. The ulnar nerve may innervate the long finger (partial or complete
in 50%),61 therefore preserving the long finger FDP strength. The ftidex FDP is always supplied by the AIN.72
2. The Martin-Gruber anastomosis, present in 17% of people, has a
connection between the median and ulnar nerves.31 One of the common variants has a connection from the anterior interosseous nerve to the uInar nerve (i.e., connection supplies some intrinsic
muscles of hand), therefore resulting in AIN syndrome with the addition of intrinsic weakness.
3. The AIN may innervate the complete FDP muscle, therefore leaving weakness of all the fingers
4. The AIN may also supply part of the FDS (30% of people)72
Diagnosis
The differential diagnosis of AIN syndrome is extremely important.
The most commonly misdiagnosed problem is that of a tendon rupture, usually of the FPL and also of the FDP. Hill26 reported that 10 of 33 patients with AIN were initially diagnosed as having a
tendon rupture (three had FPL exploration unnecessarily), with other reports of FPL rupture misdiagnosed as AIN syndrome. The examiner should look for the tenodesis effect produced by intact flexor tendons. 11,61
Mody48 described dorsiflexion of the wrist and hyperextension of the carpornetacarpal and metacarpophalangeal joints, looking for passive flexion of the interphalangeal joints (i.e.,
intact tendon). Electrical stimulation of the FPL or FDP muscle will also identify the presence of an intact tendon.29 Other common diagnoses in the differential include acute brachial plexus
neuropathy neuritis, partial proximal median nerve injury, (pseudoanterior interosseous syndrome), 1, 65 thoracic outlet syndrome, and cervical radiculopathy. History, clinical examination,
and electrophysiologic studies help rule out these entities, which are also potentially vague, nonspecific problems that can cause chronic pain of the upper extremity.
Electrophysiologic studies are much more useful in anterior interosseous nerve syndrome than in pronator syndrome. Electromyography has a high success rate in localizing the
muscles affected and therefore confirming the diagnosis of AIN syndrome.26
Treatment of the Anterior Interosseous Nerve Syndrome
The management of the patient with AIN syndrome depends
primarily on the cause of the injury. If the injury is a closed crush injury or is associated with musculoskeletal trauma, treatment is usually expectant. Patients are followed closely with clinical
examination and electromyograms; if, after 3 to 4 months, there is no recovery, surgery is considered. Immediate exploration is usually indicated for penetrating trauma. Most insidious or spontaneous
cases areinitially treated nonoperatively.
 |
Figure 4. "Classic attitude" of the weak pinch of anterior interosseous nerve syndrome. 65
Nonoperative Treatment
The initial treatment is rest, avoidance of aggravating factors,
splinting, and nonsteroidal anti-inflammatory medication. Some have advocated corticosteroid injections into the region of the pronator teres .47, 65 Controversy arises as to the duration of conservative
treatment. The surgical literature still espouses nortoperative treatment for 8 to 12 weeks. If there is no improvement, surgical exploration is considered .57, 65 In cases in which the deficit is
partial or slowly improving, the nonoperative period is longer.
The neurologic literature indicates that inflammation is the primary cause, and has questioned the need for surgical intervention. There
are reports of improvement beyond 18 months50 and even 2.5 years26 after conservative treatment. All of England and Sumners 15
patients experienced full recovery when treated conservatively.
In spontaneous or unexplained cases, treatment depends upon whether compression or inflammation is the suspected cause.
Features suggestive of an entrapment phenomenon include slow development, "mild" pain (forearm pain, primarily), or neurologic deficits isolated to the AIN. Inflammation may be suspected if the
pain is severe, extends beyond the elbow into the shoulder region, precedes neurologic deficit by a few days or if neurologic deficits reach a maximum rapidly (in a matter of days), or if there is an
associated ipsi- or contralateral brachial plexopathy.72 If inflammation is suspected, therefore, Millender 65,69 suggests that conservative treatment be carried out for 6 months. The surgical
literature suggests exploration at 12 weeks if entrapment is the suspected cause.
Because the pathogenesis, natural history, and clinical presentation
are still not clarified, it is difficult to make any valid, firm conclusions regarding the relative roles of conservative and surgical management in this condition.
Operative Treatment
The operative treatment for anterior interosseous syndrome is essentially the same as for pronator syndrome. The surgical approach is identical, with complete release of Struther's ligament,
excision of lacertus fibrosus, and decompression of the median nerve through the pronator teres. At the level of the pronator, the anterior interosseous nerve arises from the median nerve and they
both descend through the sublimis arch, which is released. The anterior interosseous nerve is then followed to ensure there is no entrapment from other anomalous muscle origins (i.e., Gantzer's
muscle, flexor carpi radialis brevis, and palmaris profundus).
Postoperative treatment is the same as for pronator syndrome, with a soft dressing for approximately 5 to 7 days then beginning gentle
physiotherapy with active and active assisted exercises.
SUMMARY
Compression of the median nerve at the wrist is the most common nerve entrapment syndrome but may be over- or misdiagnosed.
With high (proximal) median nerve entrapment being uncommon and having an elusive diagnosis, proximal compression may be overlooked as a cause of the painful upper extremity. Recognition
and diagnosis of this problem will help ensure timely and effective management of the more common pain syndromes.
References
1. Al-Qattan MM, Robertson GA: Pseudo-anterior interosseous nerve syndrome: A case report. J Hand Surg Am 18A:440-442,1993
2. Beaton LE, Anson BJ: The relation of the median nerve to the pronator teres
muscle. Anat Rec 75:2326, 1939
3. Boswick JA, Stromberg WB: Isolated injury to the median nerve above the elbow: A review of 13 cases. J Bone Joint Surg Am 49A:653-658, 1967
4. Braun RM, Spinner RJ: Spontaneous bilateral median nerve compressions in the distal arm. J Hand Surg Am 16A:244--247,1991
5. Breidenbach W, Tsai T, Manstean C: Ipsilateral pronator teres in carpal hinnel
compression of the median nerve. J Hand Surg Am 1OA:432,1985
6. Brumback RA, Bobele GB, Rayan GM: Electrodiagnosis of compressive nerve lesions. Hand Clin 8:241-254, 1992
7. Buchthal F, Rosenflack A, Trojaborg W: Electrophysiological findings in entrapment of the median nerve at wrist and elbow. J Neurol Neurosurg Psychiatry 37:340-360, 1974
8. Cho DS, MacLean IC: Pronator syndrome: Establishment of electrophysiological parameters. Arch Phys Med Rehabil 62:531, 1981
9. Culp RW, Osterman AL, Davidson RS, et al: Neural injuries associated with
supracondylar fractures of the humerus in children. J Bone Joint Surg Am 72A:1211-1215, 1990
10. Dahlin LB, Rydevik B: Pathophysiology of nerve compression. In Gelberman RH
(ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 847-866
11. Dellon AL: Musculotendinous variations about the medial humeral epicondyle. J Hand Surg Br 11B:175181,1986
12. Dellon AL: Patient evaluation and management considerations in nerve compression. Hand Clin 8:229239,1992
13. Dellon AL, MacKinnon SE: Musculoaponeurotic variations along the course of
the median nerve in the proximal forearm. J Hand Surg Br 12B:359-363, 1987
14. Dellon AL, MacKinnon SE, Danveshvar A: Terminal branch of the anterior
interosseous nerve as a source of wrist pain. J Hand Surg Br 913:316-322, 1984
15. England JD, Sumner AJ: Neuralgic amyotrophy: An increasingly diverse entity. Muscle Nerve 10:60, 1987
16. Ergungor MF, Kars HZ, Yalin R: Median neuralgia caused by brachial pseudoaneurysm. Neurosurgery 24:924-925, 1989
17. Eversmann WW: Proximal median nerve compression. Hand Clin 8:307-315, 1992
18. Eversmann WW: Entrapment and compression neuropathies. In Green DP, Hotchkiss RN (eds): Operative Hand Surgery, ed 3. New York, Churchill Livingstone, 1993, pp 1341-1386
19. Gainor BJ, Jeffries JT: Pronator syndrome associated with a persistent median artery: A case report. J Bone Joint Surg Am 69A:303-304, 1987
20. Gessini L, Jandolo B, Pietrangli A: Entrapment neuropathies of the median nerve at and above the elbow. Surg Neurol 19:112-116, 1983
21. Goldner JL: Median nerve compression lesions and clinical analysis. Bull J Dis 44:199-223, 1984
22. Greenberg BM, Pess GM, May JW: Macrodactyly and the epidennal nevus syndrome. J Hand Surg Am 12A:730-733, 1987
23. Hallett J: Entrapment of the median nerve after dislocation of the elbow: A case report. J Bone Joint Surg Br 63B:408-412, 1981
24. Halpern AA, Nagel DA: Compartment syndromes of the forearm: Early
recognition using tissue pressure measurements. J Hand Surg 4:258, 1979
25. Hartz CR, Linscheid RL, Gramse RR, et al: The pronator teres syndrome:
Compressive neuropathy of the median nerve. J Bone Joint Surg Am 63A:885 890,1981
26. Hill NA, Howard FM, Huffer BR: The incomplete antenor interosseous nerve syndrome. J Hand Surg Am 1OA:4-16,1985
27. Hollinshead WH: In Anatomy for Surgeons, the Back and Limbs, ed 3. Philadelphia, Harper & Row, 1982
28. Holtzman RNN, Patel MR, Mark MH: Median nerve neuralgia caused by a
fibrovascular band in the distal forearm. J Hand Surg Am 1 1A:894-895, 1986
29. Howard FM: Compression neuropathies in the anterior forearm. Hand Clin 2:737-745, 1986
30. Johnson RK, Spinner M, Shrewsbury MM: Median nerve entrapment syndrome in the proximal forearm. J Hand Surg 4:48-51, 1979
31. Johnson RK, Spinner M: Median nerve compression in the forearm: The
pronator tunnel syndrome. In Szabo RM: Nerve Compression Syndromes: Diagnosis and Treatment. Thorofare, NJ, Slack 1989, pp 137 151
32. Jones N, Ming N: Persistent median artery as a causeof pronator syndrome. J
Hand Surg Am 13A:728 732, 1988
33. Kessler FB: Complications of the management of carpal tunnel syndrome. Hand Clin 2:401-406, 1996
34. Kiloh LG, Nevin S: Isolated neuritis of the anterior interosseous nerve. Br Med J 1:250-252, 1952
35. Kopell HP, Thompson WAL: Pronator syndrome: A confirmed case and its diagnosis. N Engl J Med 259:713-715, 1958
36. Kutz JE, Singer R, Lindsay M: Chronic exertionalcompartment syndrome: A case report. J Hand Surg 60. 1OA:302
37. Lacey SH, SoIclatis JJ: Bilateral pronator syndrome associated with anomalous
heads of the pronator 61 teres muscle: A case report. J Hand Surg Am 18A:349-351, 1993
38. Laha RK, Lunsford LD, Dujovny M: Lacertus fibrosus compression of the median nerve: Case report. J Neurosurg 48:838-841, 1978
39. Leibovic SJ, Hastings H 11: Martin-Gruber revisite. J Hand Surg Am 17A:47-53,1992
40. Limb D, Hodkinson SL, Brown RF: Median nerve palsy after posterolateral elbow
dislocation. J Bone Joint Surg Br 76B:987-988, 1994
41. Lister G: The Hand: Diagnosis and Indications, ed 3. New York, Churchill Livingstone, 1993, pp 291-292
42. Lundborg G, Dahlin LB: The Pathophysiology of Nerve Compression. Hand Clin 8:215-227, 1992
43. MacDonald RI, Lichtman DM, Hanlon JJ, et al: Complications of surgical
release for carpal tunnel syndrome. J Hand Surg 3:70-77,1978
44. MacKinnon SE, Dellon AL: Surgery of the peripheral nerve. New York, Thierne, 1988
45. MacKinnon SE, Novak CB: Clinical commentary: Pathogenesis of cumulative trauma disorder. J Hand Surg Am 19A:873-883, 1994
46. Martinelli P, Gabollini AS, Poppi N, et al: Pronator syndrome due to thickened
bicipital aponeurosis. J Neurol Neurosurg Psychiatry 45:181-182, 1982
47. Miller-Breslow A, Terrono A, Millender LH: Nonoperative treatment of anterior interosseous nerve paralysis. J Hand Surg Am 15A:493-496,1990
48. Mody BS: A simple clinical test to differentiate rupture of the flexor pollicus longus and incomplete anterior interosseous paralysis. J Hand Surg Br 17B:513-514, 1992
49. Morris HH, Peters BH: Pronator syndrome: Clinical and electrophysiological features in seven cases. J Neurol Neurosurg Psychiatry 39:461-464, 1976
50. Nakano KK, Lundergan C, Okihiro MM: Anterior interosseous nerve syndromes: Diagnostic methods and alternative treatments. Arch Neurol 34:477-480, 1977
51. Olehnik WK, Manske PR, Szerzinski J: Median nerve compression in the proximal forearm. J Hand Surg Am 19A: 121-126, 1994
52. Omer GE Jr: Injuries to nerves of the upper extremity. J Bone Joint Surg Am
56A:1615-1624, 1974
53. Omer GE Jr, Spinner M: Management of Peripheral Nerve Problems. Philadelphia, WB Saunders, 1980
54. Osterman AL: Double crush and multiple compression neuropathy. In
Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 1215-1221
55. Pedowitz RA, Toutounghi F: Chronic exertional compartment syndrome of the
forearm muscles. J Hand Surg 13A:694, 1988
56. Posner MA: Compressive neuropathies of the median and radial nerves at the elbow. Clin Sports Med 9:343-363, 1990
57. Rask MR: The anterior interosseous nerve entrapment: Kiloh-Nevin syndrome. Clin Orthop Re] Res 142:176-181, 1979
58. Reinstein L, Reid WP, Sadler JH: Peripheral nerve compression by brachial
artery-basilic vein vascular access in long-term hemodialysis. Arch Phys Med Rehab 65:142-144, 1984
59. Rennels GD, Ochoa J: Neuralgic amyotrophy manifesting as an anterior
interosseous nerve palsy. Muscle Nerve 3:160, 1987
60. St Clair Strange FG: Entrapment of the median nerve after dislocation of the elbow. J Bone Joint Surg Br 64B:224-245, 1982
61. Schantz K, Riegels-Nielsen P: The anterior interosseous nerve syndrome. J Hand Surg 17B:510-512, 1992
62. Seyffarth H: Primary myoses in the M. Pronator Teres as a cause of lesions of
the N. Medianus (the pronator syndrome). Acta Psychiatrica Neurologica 74(suppl):251-254, 1951
63. Siegel DB, Gelberman RH: Median nerve: Applied anatomy and operative
exposure. In Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 365-377
64. Smith RV, Fisher RG: Struthers ligament-a source of median nerve compression
above the elbow (case report). J Neurosurg 38:778-779, 1973
65. Spinner M: The anterior interosseous nerve syndrome: With special attention to its variations. J Bone Joint Surg Am 52A:84-94, 1970
66. Spinner M, Spencer PS: Nerve compression lesions of the upper extremity: A clinical and experimental review. Clin Orthop 104:46-65,1974
67. Spinner RJ, Carmichael SW, Spinner M: Partial median nerve entrapment in
the distal arm because of an accessory bicipital aponeurosis. J Hand Surg Am 16A:236-244, 1991
68. Stem PJ, Fassler PR: Pronator syndrome. In Gelberman RH (ed): Operative
nerve repair and reconstruction. Philadelphia, JB Lippincott, 1991, pp 995-1002
69. Stem PJ, Fassler PR: Axiterior interosseous nerve compression syndrome. In
Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 983-994
70. Stewart JD: Focal Peripheral Neuropathies, ed 2. New York, Raven Press, 1993, pp 157-195
71. Struthers J: On a peculiarity of the humerus and humeral artery. Monthly J Med Sci 28:264-267, 1848
72. Sunderland SS: Nerves and Nerve Injuries, ed 2. New York, Churchill Livingstone, 1978
73. Suranyi L: Median nerve compression by Struthers 79. ligament. J Neurol Neurosurg Psychiatry 46:1047 1049,1983
74. Swiggett R, Ruby LK: Median nerve compression 80. neuropathy by the lacertus
fibrosis: Report of three cases. J Hand Surg Am 11A:700-703,1986
75. Tsai TM, Syed SA: A transverse skin incision for decompression of pronator teres syndrome. J Hand Surg Br 1913:40-42, 1994
76. Uchida Y, Sugioka Y: Electrodiagnosis of MartinGruber connection and its clinical importance in peripheral nerve surgery. J Hand Surg Am 17A:54-59, 1992
77. Urbaniak JR: Complications of treatment of carpal tunnel syndrome. In Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 967-979
78. Upton ARM, McComas AJ: The double crush in nerve-entrapment syndrome. Lancet 2:359-361, 1973
79. Werner CO, Rosen 1, Thomgren KG: Clinical and neurophysiologic
characteristics of the pronator syndrome. Clin Orthop 197:231-236,1985
80. Wertsch JJ, Melvin J: Median nerve anatomy and entrapment syndromes: A review. Arch Phys Med Rehab 63:623-627, 1982
Address reprint requests to
David R. Pichora, MD, FRCSC
Queen's University Kingston General Hospital 76 Stuart Street Kingston, Ontario, Canada K7L 2V7
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