Proximal median neuropathy is distinctly uncommon compared with median entrapment at the carpal tunnel. Differentiating between median neuropathy at the wrist and more proximal entrapments can be difficult based on clinical grounds alone, especially in mild cases. Electrodiagnostic (EDX) testing plays a key role in localizing the lesion in these unusual cases, especially if the lesion results from trauma or compression.
Detailed Anatomy at the Antecubital Fossa
As the median nerve descends in the upper arm, it runs medial to the humerus and anterior to the medial epicondyle. In a minority of individuals, a bony spur originates from the shaft of the medial humerus just cephalad to the medial epicondyle. A tendinous band known as the ligament of Struthers stretches between the spur and the medial humeral epicondyle. In the antecubital fossa, the median nerve travels adjacent to the brachial artery ( Figure 18–1 ). As it enters the forearm, it runs first beneath the lacertus fibrosus , a thick fibrous band that runs from the medial aspect of the biceps tendon to the proximal forearm flexor musculature. In most individuals, the median nerve then runs between the two heads of the pronator teres (PT) muscle to provide innervation to that muscle. In many individuals, there are fibrous bands within the two heads of the PT muscle. The anterior interosseous nerve then is given off posteriorly, approximately 5 to 8 cm distal to the medial epicondyle, after the median nerve passes between the two heads of the PT. As the median nerve runs distally, it passes deep to the flexor digitorum sublimis (FDS) muscle and its proximal aponeurotic tendinous edge, known as the sublimis bridge .
Etiology
Median neuropathy in the region of the antecubital fossa has been described as a consequence of external compression from casting, trauma, venipuncture, and compressive mass lesions, including tumor or hematoma. Rare cases of brachial artery puncture and subsequent hematoma formation have led to compartment syndromes and subsequent injury of the proximal median nerve.
In addition, several sites of proximal median entrapment have been reported ( Figure 18–1 ). All are uncommon, and some remain controversial. The four major potential sites of entrapment are as follows:
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Median nerve entrapment may occur at the ligament of Struthers in the distal upper arm, where both the median nerve and brachial artery pass between this ligament and the humerus.
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More distally in the region of the antecubital fossa, the median nerve may become entrapped beneath a hypertrophied lacertus fibrosus.
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Further distally, the median nerve may become entrapped in the substance of the PT muscle, especially in individuals who have additional fibrous bands running through that muscle.
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More distally, the median nerve may become entrapped beneath the sublimis bridge of the FDS muscle.
Traumatic Lesions
In patients with traumatic lesions, there usually is an obvious, acute disturbance of median motor and sensory function. Significantly, sensory disturbance in proximal median neuropathy is noted in the entire median territory, including the thenar eminence, as well as the thumb, index, middle, and lateral ring fingers. This feature clearly distinguishes proximal median neuropathy from carpal tunnel syndrome (CTS), in which sensation over the thenar eminence is spared. Sensory loss over the thenar eminence occurs as the palmar cutaneous branch, which innervates the thenar eminence, leaves the median nerve proximal to the carpal tunnel. Depending on the site of the lesion, weakness may affect some or all of the proximal median-innervated forearm muscles, including the PT, FDS, flexor digitorum profundus (FDP) to digits 2 and 3, flexor carpi radialis (FCR), flexor pollicis longus (FPL), and pronator quadratus (PQ), as well as the distal median-innervated muscles, including the abductor pollicis brevis (APB), opponens pollicis (OP), and first and second lumbricals. Weakness of the FDP to digits 2 and 3, FDS and FPL often leads to a characteristic high median neuropathy posture, whereby the individual is unable to flex the thumb, index, and middle fingers ( Figure 18–2 ).
Entrapment Syndromes
The symptoms and signs in the proximal median nerve entrapment syndromes are fairly nonspecific. Typically, there is pain or discomfort in the region of the entrapment. Unlike CTS, the symptoms are not exacerbated at night. The two major syndromes include (1) proximal entrapment of the median nerve at the ligament of Struthers and (2) median nerve entrapment more distally, either beneath the lacertus fibrosus, in the substance of the PT, or beneath the sublimis bridge ( Figure 18–1 ). The latter three entrapment sites usually are referred to collectively as the pronator syndrome . Strictly speaking, the term may be reserved for nerve entrapment within the substance of the PT muscle proper. However, entrapment at any of these last three locations usually produces a similar clinical syndrome.
Ligament of Struthers Entrapment
Entrapment at the ligament of Struthers is a very rare syndrome whereby the median nerve is entrapped by a tendinous band running from the medial epicondyle to a bony spur on the distal medial humerus ( Figure 18–3 ). The prevalence of such a supracondylar bony spur is approximated at 1 to 2% of the population. The syndrome is characterized by pain in the volar forearm and paresthesias in the median-innervated digits, which are exacerbated by supination of the forearm and extension of the elbow. The radial pulse also may be attenuated with these maneuvers, as the brachial artery also runs with the median nerve under the ligament of Struthers. A bony spur may be palpable at the distal humerus. Weakness of the PT and other median-innervated muscles may occur, and subtle sensory loss may be noted in the median distribution, including the thenar eminence.
Pronator Syndrome
Although rare, the pronator syndrome occurs more often than entrapment at the ligament of Struthers. The PT muscle may be enlarged or firm, with a Tinel’s sign over the site of entrapment. Pain may radiate proximally and often is aggravated by using the arm, especially with repeated pronation/supination movements. Specific maneuvers that may produce symptoms of pain in the forearm and paresthesias in the median-innervated digits depend on the site of entrapment ( Figure 18–4 ): resisted pronation with the elbow in extension (for the PT); resisted flexion of the proximal interphalangeal joint of the middle finger (for the sublimis bridge); and resisted flexion of the elbow with the forearm in supination (for the lacertus fibrosus). The sole finding of increased pain with these maneuvers is an unreliable sign, unless it is accompanied by median nerve territory paresthesias. Significant weakness or wasting of median-innervated muscles is rare, but mild weakness of the FPL and APB is not uncommon, with occasional involvement of the FDP to digits 2 and 3 and the OP. The pronator teres muscle is usually spared. There may be occasional paresthesias radiating into the median-innervated digits, with subtle impairment of sensation in the median nerve distribution, including the thenar eminence.
Anterior Interosseous Nerve Syndrome
The anterior interosseous nerve, the largest branch of the median nerve, leaves the main trunk of the median nerve just distal to the PT to innervate three muscles: FPL, FDP to digits 2 and 3, and PQ. It carries deep sensory fibers to the wrist and interosseous membrane, but it carries no cutaneous sensory fibers. Clinically, patients present with the inability to flex the distal phalanx of the thumb, index, and middle fingers, with weakness of pronation. Weakness of the PQ is best demonstrated with the elbow flexed to avoid the contribution of the PT, which is not involved in anterior interosseous syndrome. With the elbow flexed, the PQ is the primary muscle to pronate the arm; with the elbow extended, the PT is the primary muscle to pronate the arm. There is no sensory loss. A characteristic compensatory posture occurs when the patient attempts to make an “OK” sign and is unable to flex the distal thumb and index fingers. Compensatory hyperextension of the distal interphalangeal joint of the index finger and interphalangeal joint of the thumb then occurs ( Figure 18–5 ). Anterior interosseous neuropathy (AIN) has been reported to occur following fractures and crush injuries. In addition, it can rarely occur as an entrapment neuropathy, but more often it is a variant presentation of brachial neuritis, a full discussion of which is found in the section on brachial neuritis in Chapter 30 , including the electrophysiologic evaluation.
Occasionally, it may be difficult to recognize an AIN. In some patients, the slip of the FDP to digit 3 is supplied by the ulnar nerve, leaving middle finger flexion intact despite an AIN. The situation is more complicated when an AIN occurs in combination with a Martin–Gruber anastomosis (MGA). In MGA, there is an anomalous cross-over of median-to-ulnar fibers. Occasionally, the median fibers that cross over run in the anterior interosseous nerve. Thus, a patient with an AIN also can develop weakness of some ulnar-innervated intrinsic hand muscles, if an MGA is present and the cross-over fibers run in the anterior interosseous nerve.
Differential Diagnosis
In cases of acute trauma or injury, the clinical differential diagnosis is limited and usually straightforward. For the entrapment syndromes in the region of the antecubital fossa, however, the differential diagnosis is extensive because the symptoms often are vague. For example, local orthopedic problems may present in a similar fashion. Median neuropathy at the carpal tunnel also may give rise to diagnostic confusion. Patients with CTS can present with vague pain or heaviness in the forearm associated with median paresthesias, similar to symptoms in the proximal median entrapment syndromes. Additionally, patients with cervical radiculopathy may present with radiating pain associated with paresthesias into the hand. In cervical radiculopathy, however, there usually is a history of neck pain that radiates into the arm. Examination in cervical radiculopathy may reveal weakness outside the median territory, as well as decreased biceps, brachioradialis, or triceps reflexes.
Electrophysiologic Evaluation
The purpose of nerve conduction studies and electromyography (EMG) in suspected proximal median neuropathy is (1) to demonstrate that median nerve abnormalities are proximal to the wrist and (2) to exclude a lesion higher in the brachial plexus or cervical nerve roots. However, the EDX evaluation may be complicated by the fact that the electrophysiology in true cases of proximal median entrapment often is normal or nonspecific, despite what one might expect on theoretical grounds.
Nerve Conduction Studies
Nerve conduction studies should include routine median motor studies stimulating the median nerve at the wrist and antecubital fossa, recording at the APB ( Box 18–1 ). If there is a question of entrapment at the ligament of Struthers, proximal stimulation should also be performed at the axilla. Routine ulnar motor and sensory studies should also be performed to exclude a coexistent polyneuropathy. Sensory nerve conductions of median-innervated digits should always be performed, recording the most symptomatic digit(s), especially if numbness or paresthesias have been observed on clinical examination. If values are borderline or just slightly above the upper limits of normal, comparison with the contralateral side should be done. Finally, in all suspected median neuropathies, it is imperative to perform at least one of the median-versus-ulnar comparison studies across the wrist to exclude median neuropathy at the wrist . If values are borderline or just slightly above the upper limits of normal, a second median-versus-ulnar comparison study should be done to look for median neuropathy at the wrist.
Routine studies:
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Median motor study recording abductor pollicis brevis, stimulating wrist, antecubital fossa, and axilla
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Ulnar motor study recording abductor digiti minimi, stimulating wrist, below groove, and above groove
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Median and ulnar F responses
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Median sensory response, recording digit 2 or 3, stimulating wrist (bilateral studies suggested)
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Ulnar sensory response, recording digit 5, stimulating wrist
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Median and ulnar palm-to-wrist mixed nerve studies using identical distances of 8 cm
The following patterns suggest possible proximal median neuropathy:
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Reduced median compound muscle action potential and/or sensory nerve action potential amplitudes with distal latencies that are either normal or only slightly prolonged (never in the demyelinating range) and no significant slowing of the median palm-to-wrist latency compared with the ulnar
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Either conduction block/temporal dispersion or marked conduction velocity slowing between the wrist and antecubital fossa, or between antecubital fossa and axilla, with normal or only slightly prolonged distal latencies on median motor studies
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Prolonged median F responses despite a relatively normal distal compound muscle action potential amplitude and distal latency
A lesion of the median nerve that results in wallerian degeneration, regardless of the lesion site, will result in decreased compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) amplitudes distal to the lesion. Often the distal latencies will be slightly prolonged, and conduction velocity will be mildly slowed because of dropout of the fastest-conducting axons. However, although such findings are abnormal and indicate a median nerve lesion, they do not localize the lesion. If there is focal demyelination at the ligament of Struthers, one might expect to see either focal slowing or a drop in CMAP amplitude (i.e., conduction block or temporal dispersion) between the antecubital fossa and the axilla sites. If there is a focal lesion in the region of the antecubital fossa, there may be a conduction block between the wrist and antecubital fossa sites. Although such findings can be expected on theoretical grounds, in fact they rarely occur.
Electromyographic Approach
The EMG usually is more gratifying than the nerve conduction studies in patients with a suspected proximal median neuropathy ( Box 18–2 ). The distal median muscles (APB) should always be studied. However, the critical part of the study consists of careful examination of several median-innervated muscles proximal to the carpal tunnel. These muscles include the PT, FCR, FDS, FDP to digits 2 and 3, FPL, and PQ. If any of these muscles are abnormal (evidence of denervation or reinnervation), the problem must be proximal to the wrist. If the lesion is at the level of the ligament of Struthers, EMG abnormalities may be noted in all the median-innervated muscles, including the PT. In the pronator syndrome, EMG abnormalities have been reported most often in the FPL and FDP to digits 2 and 3, less often in the FDS and APB, and only rarely in the PT, because the compression site most often occurs distal to its innervation. If any of the proximal median-innervated muscles are abnormal, other muscles innervated by the same myotomes as the proximal median muscles, but supplied by different nerves, should be sampled to exclude a more proximal lesion of the brachial plexus or cervical nerve roots. At a minimum, one non-median C6–C7 innervated muscle (e.g., triceps) and one non-median C8–T1 innervated muscle (e.g., first dorsal interosseous) must be checked.
Needle examination of:
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Median muscle distal to the carpal tunnel (abductor pollicis brevis)
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At least two median muscles proximal to the carpal tunnel, including the pronator teres and one of the following: flexor pollicis longus, flexor carpi radialis, flexor digitorum sublimis
If the abductor pollicis brevis is abnormal:
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Test at least two other non-median, lower trunk/C8–T1 innervated muscles (e.g., first dorsal interosseous, extensor indicis proprius, flexor digitorum profundus to digits 4 and 5) to exclude a lower brachial plexopathy, polyneuropathy, or C8–T1 radiculopathy
If the proximal median muscles are abnormal:
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Test at least one non-median C6–C7 and C7–C8 innervated muscle (e.g., triceps, extensor digitorum communis, extensor indicis proprius) to exclude a more proximal brachial plexopathy or cervical radiculopathy
Note : If nerve conduction studies show a non-localizing median neuropathy, electromyography can only localize the lesion to at or above the take-off to the most proximally affected median-innervated muscle. For example, an abnormal flexor carpi radialis with a normal pronator teres does not necessarily localize the lesion to the median nerve between those two muscles, but only to at or proximal to the take-off to the flexor carpi radialis muscle. Although this may seem counterintuitive, remember that there are proximal lesions that spare some of the muscles distal to the lesion while affecting others.
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