Proximal Nerves of the Upper Extremity: Spinal Accessory Nerve

The clinical demonstration of weakness and atrophy specific to one of these nerves provides important differential diagnostic clues. Typically, the patient with a primary orthopedic problem, such as a rotator cuff injury or calcific bicipital tendonitis, also usually has significant shoulder pain, but, in contrast to these proximal neuropathies, they lack weakness. The patient with one of these orthopedic problems may be a challenge to examine because his or her joint-related pain will initially lead them to report having weakness, because often it is initially “too painful” for them to cooperate. However, a skillful neurologic or orthopedic examination can often sort out these anatomic challenges by asking the patient to give full effort, for just a few seconds, to eliminate the pain component limitation. This becomes more confusing when there is major shoulder joint trauma because both the joint and its proximate nerves are affected. In this setting, the combination of careful electromyography and magnetic resonance imaging (MRI) will allow definition of the nature of the lesion.

The spinal accessory nerve is unique in that it is derived from two seemingly disparate motor neuron populations. However, in fact, these are in continuity. One set originates intracranially from bulbar fibers, originating in line with the nucleus ambiguous within the medulla. However, the primary source for the spinal accessory nerve lies within cervical spinal cord segments C1-5, 6. Here its cell bodies are found within the lateral anterior gray column’s posterolateral anterior horn. This nerve exits the skull via the jugular foramen, accompanying the vagus nerve. The cranial fibers innervate some of the laryngeal muscles, whereas the primary portion of the spinal accessory nerve fibers innervates the sternocleidomastoid and trapezius muscles. The spinal portion is joined by fibers from the third and fourth upper cervical rami; these innervate the caudal trapezius muscle. In contrast, the remainder of the trapezius and the entire sternocleidomastoid are supplied by the accessory portion of this nerve.

Injury to the spinal accessory nerve rarely occurs and usually is secondary to surgical procedures involving the posterior triangle of the neck, where it is particularly at risk with lymph node biopsies. Spinal accessory nerve injury can lead to scapular winging secondary to loss of some innervation of the trapezius muscle. This is characterized by one of the two forms of scapular winging that is recognized by lateral scapula deviation (see Plate 5-5). This needs to be differentiated from long thoracic nerve palsy.

The long thoracic nerve originates directly from C5 to C7 roots immediately before the formation of the brachial plexus. It primarily innervates the serratus anterior muscle that stabilizes the scapula for pushing movements and elevates the arm above 90 degrees. There is no cutaneous sensory innervation. Long thoracic neuropathy is the common cause for scapular winging. This is best recognized by having a patient extend the arms and then push against a wall; in this instance, the inferior medial scapular border is prominently projected away from the chest. Unilateral scapular winging can also be caused by weakness of the trapezius (spinal accessory neuropathy) or the rhomboid muscles (dorsal scapular neuropathy). These neuropathies produce a lateral scapula deviation, in contrast to the long thoracic medial scapula deviation. The long thoracic nerve may be damaged by acute brachial neuritis, mechanical factors, and surgical procedures, including mastectomy or thoracotomy. Occasionally, patients present with bilateral scapular winging. This is most commonly related to facioscapulohumeral muscular dystrophy because it is unusual to have bilateral long thoracic nerve palsies.

The dorsal scapular nerve (C5) arises from the uppermost root of the brachial plexus. It pierces the scalenus medius, runs deep to the levator scapulae, helping to innervate this muscle. It terminates by supplying the rhomboid muscles (C5). These muscles stabilize and rotate the scapula in a medial-inferior direction as well as elevate the arm (see Plate 5-6). Rhomboid weakness presents with scapular winging, most prominent when the patient raises the arm overhead. The patient typically notes difficulty reaching into a back pocket of his or her slacks or trying to scratch the back. These rare dorsal scapular neuropathies have varying pathophysiologic mechanisms, including shoulder dislocation, weightlifting, and entrapment by the scalenus medius muscle.

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