Mononeuropathies of the Upper Extremities

Long Thoracic Neuropathies

The long thoracic nerve originates directly from C5–C7 roots, before the formation of the brachial plexus. It innervates the serratus anterior muscle and has no cutaneous sensory representation ( Fig. 60.1 ). Weakness of the serratus anterior is debilitating because it stabilizes the scapula for pushing movements and elevates the arm above 90 degrees. This is the most common cause of scapular winging; it is best recognized by having the patient push against a wall. The inferior medial border is the most prominently projected away from the body wall. A dull shoulder ache may accompany this neuropathy. When severe acute pain occurs with the onset of scapular winging, brachial plexus neuritis should be considered.

The long thoracic nerve may be damaged by mechanical factors, including repetitive or particularly forceful injuries to the shoulder or lateral thoracic wall, and by surgical procedures including first rib resection, mastectomy, or thoracotomy. It is one of the most common nerves to be affected by acute brachial neuritis, solely or in combination with others.

Scapular winging also can be related to scapular fracture and avulsion. Because they are surgically correctable, it is important to distinguish them from a primary long thoracic nerve injury. Furthermore, scapular winging can be caused by weakness of the trapezius (resulting from injury of the spinal accessory nerve) or the rhomboid muscles (resulting from a dorsal scapular nerve lesion). Inspection of the posterior shoulder region can provide diagnostic clues. Although the scapula is typically displaced medially in long thoracic nerve lesions, lateral deviation points to weakness of the trapezius or rhomboids. Scapular winging is a predominant feature in patients with facioscapulohumeral muscular dystrophy, where its bilateral representation and the other associated clinical features distinguish it from long thoracic nerve palsy.

Dorsal Scapular Neuropathies

The dorsal scapular nerve receives fibers from the C5 nerve root. It innervates the levator scapulae and the rhomboideus major and minor muscles, which assist in the stabilization of the scapula, the rotation of the scapula in a medial-inferior direction, and the elevation of the arm ( Fig. 60.2 ). Rhomboid weakness can lead to scapular winging, which is most prominent when the patient raises the arm overhead. Possible etiologies of injury to this nerve include shoulder dislocation, weightlifting, and entrapment by the scalenus medius muscle.

Suprascapular Neuropathies

The suprascapular nerve emerges from the upper trunk of the brachial plexus, receiving fibers from C5 and C6 roots. It does not have any cutaneous innervation. The suprascapular nerve first provides innervation to the supraspinatus muscle, a shoulder abductor, and then to the infraspinatus, a shoulder external rotator (see Fig. 60.1 ). The suprascapular nerve may be injured at the suprascapular notch, before the innervation of the supraspinatus muscle, or distally at the spinoglenoid notch, affecting the infraspinatus alone. The most common site of entrapment is at the suprascapular notch, under the transverse scapular ligament. Acute-onset cases result from blunt shoulder trauma, with or without scapular fracture, or from forceful anterior rotation of the scapula. The suprascapular nerve may also be affected by brachial plexus neuritis in isolation or with other nerves. Suprascapular neuropathies of insidious onset often occur subsequent to callous formation after fractures, from entrapment at the suprascapular or spinoglenoid notch, by compression from a ganglion or other soft tissue mass, or by traction caused by repetitive overhead activities, such as volleyball or tennis.

Axillary Neuropathies

The axillary nerve, along with the radial nerve, is a terminal branch of the posterior cord of the brachial plexus. It innervates the deltoid and the teres minor and provides sensory innervation to the lateral upper part of the shoulder via the superior lateral brachial cutaneous nerve of the arm ( Fig. 60.3 , see also Fig. 60.2 ). In lesions of the axillary nerve, shoulder abduction is weakened and cutaneous sensibility of the lateral shoulder diminishes, overlapping the C5 dermatome. Because the teres minor is not the predominant external rotator of the shoulder, clinical isolation and testing are difficult. EMG may be necessary to define neurogenic injury to this muscle. Most axillary neuropathies are traumatic, related to anterior shoulder dislocations, humerus fractures, or both. Recognition of nerve injury may be delayed because of the shoulder injury. Acute axillary neuropathies can result from blunt trauma or as a component or sole manifestation of brachial plexus neuritis.

Musculocutaneous Neuropathies

The musculocutaneous nerve originates directly from the lateral cord of the brachial plexus. It innervates the coracobrachialis, biceps brachii, and brachialis muscles, and terminates in its cutaneous branch, the lateral antebrachial cutaneous nerve. Isolated musculocutaneous neuropathies are rare. They have been reported in weight lifters, after biceps tendon rupture, after surgery, and after prolonged pressure during sleep. Damage to the musculocutaneous nerve results in weakness of forearm flexion and supination and sensory loss of the lateral volar forearm (see Fig. 60.1 ). The biceps reflex is diminished, but the brachioradialis reflex (same myotome, different nerve) is preserved. More commonly, injury to this nerve occurs as part of a more widespread traumatic injury, usually involving the proximal humerus. The musculocutaneous nerve can also be preferentially involved in acute brachial plexus neuritis. Distal lesions of the lateral antebrachial cutaneous nerve may result from attempted cannulation of the basilic vein in the antecubital fossa. Rupture of the biceps tendon is a significant differential diagnostic consideration of musculocutaneous neuropathy.

Differential Diagnosis of Shoulder Mononeuropathies

The most common etiologies of shoulder pain are injuries to glenohumeral, subacromial, and acromioclavicular regions. Pain often may be reproduced by local pressure or provocative movements and positions. Rotator cuff tears can mimic nerve injury because of apparent weakness of shoulder abduction (supraspinatus) and external rotation (teres minor and infraspinatus). Motor neuron disease may begin in the shoulder region. It must be considered in the differential diagnosis of weakness without associated pain or sensory signs and symptoms. C5 radiculopathy also enters the differential diagnosis in patients reporting shoulder pain, sometimes extending into the upper arm with weakness and numbness. This pain might originate within the scapular region and not the neck. Having patients flex their neck laterally in the direction of the symptomatic limb may reproduce the pain. Patients with C5 weakness have problems with shoulder abduction (deltoid and supraspinatus muscles), external rotation (infraspinatus), and arm flexion (biceps brachii). The biceps stretch reflex is often diminished. Paresthesias or sensory loss occurs in a discrete patch on the lateral proximal arm overlying the deltoid muscle.

Diagnostic Approach

EMG is the primary diagnostic tool in the evaluation of suspected shoulder mononeuropathies. It is particularly helpful to identify mononeuropathies affecting the shoulder girdle for several reasons. Neurogenic injury may go unsuspected, because pain is the predominant symptom. Weakness may be hidden by the observation of normal strength within unaffected muscles performing similar functions; for example, supraspinatus weakness obscured by normal deltoid function. Conversely, nerve injury may be suspected because of apparent weakness caused by tendon rupture, only to be refuted by the absence of denervation on needle EMG. Although theoretically nerve conduction studies can be performed on the musculocutaneous and axillary nerves, their value is limited by technical factors. These nerves are typically accessible at only one stimulation site, precluding the determination of conduction velocities and accurate identification of conduction block. However, demyelination with conduction block may be suspected when a normal compound muscle action potential is obtained from a weak muscle; often, this finding portends an excellent prognosis. This conclusion should be reached cautiously because the same pattern may result from axon loss when the study is performed within the first week after injury, before wallerian degeneration has taken place.

Needle EMG can identify even subtle axon loss by the detection of fibrillation potentials. The evaluating physician and the electromyographer should always examine the patient and consider every potential neuropathic cause of shoulder pain. Otherwise, uncommon neuropathies can easily be overlooked.

A common clinical dilemma occurs with patients who have nontraumatic shoulder girdle mononeuropathies. It is difficult to differentiate a primary idiopathic lesion from a limited form of brachial plexus neuritis and to determine whether entrapment or a related process necessitating surgical exploration is involved. A thorough clinical and electrodiagnostic examination is thus required. Subtle clinical or electrodiagnostic evidence of involvement of muscles innervated by a different nerve usually suggests that a conservative approach is indicated, as this constellation of findings speaks against compression of a single nerve.

Routine radiographs are useful to detect scapular fractures secondary to acute injuries, which sometimes predispose patients to suprascapular neuropathies or serratus anterior dehiscence from the scapula. MRI can define insidious-onset neuropathies that may be caused by expanding masses, for example a ganglion cyst in the spinoglenoid notch.

Management and Prognosis

Unfortunately, shoulder bracing provides little benefit to patients with shoulder girdle weakness. Exercises to strengthen other shoulder girdle muscles may provide partial functional compensation. If nerve transection from acute penetrating injury is suspected, surgical exploration and primary anastomosis should be considered, although results are mixed. In acute nonpenetrating injury, exploration can be considered after 3–6 months, provided no clinical or electrodiagnostic evidence of reinnervation exists. Nerve grafting is an option if unanticipated nerve transection is found. For insidious-onset neuropathies without a defined cause, imaging can exclude ganglion cysts or other masses. If no mass is demonstrable and the patient shows no evidence of improvement, exploration may be considered, particularly at potential sites of entrapment such as the suprascapular or spinoglenoid notches.

Despite apparent axonal injury in brachial plexus neuritis, the prognosis is good for functional recovery, which may take 6 months to 2 years. The prognosis for direct compressive injury is less predictable and probably depends on reinnervating distance, patient age, and comorbidities. Stretch injuries and entrapment have the highest likelihood of a significant demyelinating component, with excellent outcome being the rule, particularly if entrapment is recognized and removed before significant axon loss occurs.