Proximal Median Neuropathies

PRIMARY MEDIAN TRUNK

All median nerve function is potentially compromised with very proximal lesions. In contrast to the patient with carpal tunnel syndrome (CTS) experiencing finger paresthesias, median trunk lesions present with combined sensory/motor dysfunction not only affecting the classic 3.5 lateral digits but also diminished palmar sensation because of median palmar cutaneous branch involvement, something not characteristic of CTS. All median-innervated muscles may be affected. Often, these very proximal median lesions are idiopathic, although some may represent another brachial neuritis variant.

Supracondylar humerus fractures leading to nerve compression, entrapment, or total laceration are common causes of proximal median nerve lesions. The primary median nerve trunk is usually damaged; however, occasionally, because of the fascicular characteristics of peripheral nerves, the anterior interosseous nerve may be traumatized in isolation at a proximal site. Elbow dislocations, hyperextension of the arm, shoulder falls, lacerations, blunt nerve trauma, arterial or venous puncture, and repetitive pronation/supination are other mechanisms.

Median nerve entrapment rarely occurs just above the elbow at the ligament of Struthers. This is a fibrous band extending from a small supracondylar spur on the humerus to its medial epicondyle. Here it forms the roof of a tunnel, radiographically identifiable in about 2% of the population. Median entrapment has occurred with a distal humeral osteoid osteoma and congenital fibromuscular bands. Lipofibromas, hamartomas, neurofibromas, hemangiomas, juvenile cutaneous mucinosis, calcified flexor digitorum superficialis tendons, and abscess have also led to proximal median nerve lesions.

ANTERIOR INTEROSSEOUS NERVE (AIN)

Sometimes clinical involvement of the AIN is referred to as the pronator syndrome; however, this is not a well-accepted terminology because multiple other mechanisms, besides entrapment within the pronator teres, may be operative at this level. These patients present with a characteristic clinical picture, wherein they initially report difficulty with handwriting or placing a key in a lock. This symptom is related to an inability to pinch because concomitant damage to the flexor pollicis longus (FPL) and flexor digitorum profundus (FDP; C8, T1) muscles limit the patient’s ability to flex the distal interphalangeal joints of both the index finger and thumb. The third muscle innervated by the AIN, the pronator quadratus (PQ, C8, T1) is clinically silent but provides localizing value with needle electromyography (EMG).

Some instances of idiopathic anterior interosseous neuropathies, having an acute onset and possibly representing an autoimmune process, have also been likened to a partial brachial neuritis variant. One interesting modification is a syndrome of acute median nerve compression by the bicipital aponeurosis at the elbow. Here an acute elbow pain develops during a maximal and vigorous contraction of the biceps brachii muscle. Examination demonstrates severe pain on median nerve palpation at the elbow as well as with triceps contraction when extending the elbow, but there is no neurologic compromise.

EVALUATION

EMG is the primary means for identifying these proximal median nerve lesions as discussed above. The role of ultrasound and magnetic resonance imaging (MRI) await prospective analysis, but it is expected that these modalities will be particularly useful for both localization and sometimes identification of the pathology.

THERAPY AND PROGNOSIS

The decision to pursue surgical exploration for diagnosis and therapeutic potential is a difficult one. At times, this is indicated for the syndrome of acute painful median nerve compression at the elbow, as previously noted. In this instance, exploratory surgery sometimes defines an acute median nerve entrapment at the ligament of Struthers, lacertus fibrosis, pronator teres, or flexor digitorum superficialis, requiring decompression. In more chronic settings, good results occur variously with local corticosteroid injection, surgical explorations, as well as conservative management. However, in the last instance, if signs of a progressive median deficit develop, surgical exploration is definitely in order. Although the region of the pronator teres may be a prime site from which to start, unless a well-defined lesion is identified there, the incision needs to be extended to avoid missing an adjacent occult site of entrapment. If an entrapment site is identified and the nerve decompressed, the prognosis will depend on the degree of axonal damage and the chronicity of the lesion. The spontaneously occurring, possibly autoimmune, AIN lesions often resolve on their own.

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