Indications

This procedure is used for a patient with loss of shoulder abduction secondary to nerve injury, generally from injury to upper roots or superior trunk of the brachial plexus. Less commonly, this procedure can be used in patients with isolated nerve injuries to the SSN. The ideal candidate for the technique is a young person with a recent focal brachial plexus injury. Though there is no absolute upper age limit, nerve regeneration potential declines with age, and this must be considered when considering the functional risks and benefits in an older patient.

Timing

As with all nerve injuries, timing is important. As a rule, the sooner the nerve is repaired, the better the functional outcome. However, a neurapraxia or axonotmesis may result in spontaneous recovery, and for these patients no surgery is required. The type of injury can help guide the decision of when to proceed with operative exploration. A high-energy injury is more likely to result in nerve ruptures or avulsions and should be explored as early as possible. A lower-velocity injury may have resulted in neurapraxia or axonotmesis, and these should be monitored for several months prior to exploration. An injury greater than a year old is much less likely to get useful recovery. These patients can be evaluated with electromyography (EMG) to see if there is still some activity in the muscle. If no fibrillations are seen, the muscles are unlikely to recover and salvage procedures, such as shoulder fusion, should be considered.

Contraindications

One clear contraindication for SAN to SSN nerve transfer is a patient with injury to the accessory nerve. When assessing the patient, palpate the trapezius to ensure the patient′s ability to generate a firm contraction. Also an elderly, frail patient may have a poor risk-to-benefit ratio and represents a relative contraindication. Finally, ensure that there is no other shoulder pathology, such as limited or painful passive shoulder motion. After transfer, the newly reinnervated muscles will not be able to overcome much inherent shoulder derangement.

Examination/Imaging

It is important to know the type of accident and any associated injuries. For example, if a person had a high-velocity motorcycle accident, there should be concern that beyond the upper plexus lesion there may also be a secondary injury of the SSN at the scapular notch. In this setting, surgery from a posterior approach is preferable to ensure that the transfer will not be futile, as would be the case if the SAN were coapted via an anterior approach to a nerve with a second, distal injury.

Physical exam includes a thorough evaluation of the neck and upper extremity. The shoulder exam should ensure that the patient has nearly full passive and painless range of motion of the shoulder. If movement is limited or there is pain with loading the joint, further exploration for concomitant shoulder pathology is warranted. There is typically visible atrophy of the deltoid muscle and above the scapular spine. The patient should not be able to abduct the shoulder away from the body. Subluxation of the glenoid is not uncommon after a C5–C6 injury, as the deltoid muscle is also paralyzed, and with time the weight of the arm pulls the humeral head downward. This will improve with recovery of muscle function, and subluxation is not a contraindication to surgery. Finally, assess the SAN by assessing the strength of the sternocleidomastoid and trapezius muscles. If these are weak, then the SAN has likely also been injured and is unsuitable for transfer.

Imaging is generally not required, but electrodiagnostic studies can be useful. Myography will give some insight into whether the nerve is recovering.

Relevant Anatomy

Injury to the SSN is often the result of a brachial plexus injury. The SSN originates from the C5 and C6 roots. These roots join together and form the upper trunk at the Erb point, located on the surface of the scalenus medius ~ 2–3 cm above the clavicle. The SSN exits off the superolateral border of the upper trunk and travels posteriorly, running anterior to the trapezius muscle. The SSN then passes from anterior to posterior through the scapular notch. The notch is crossed cephalad by the superior transverse scapular ligament, and the suprascapular artery typically runs above the ligament and the SSN runs below. The nerve continues deep to the supraspinatus and rounds the notch of the scapular neck into the infraspinous fossa, innervating both supraspinatus and infraspinatus ( Fig. 19.1 ).

The spinal accessory nerve (SAN) is a cranial nerve that exits the skull through the jugular foramen. It courses under the sternocleidomastoid (SCM) and innervates it. The SAN exits beneath the posterior border of the SCM ~ 5–6 cm below the mastoid process, at the same level as the emergence of the greater auricular nerve. After it exits from the SCM muscle, the SAN continues obliquely through the posterior triangle, toward the anterior border of the trapezius muscle. The average length of the SAN between the SCM and trapezius muscles is 6 to 8 cm. The point of entry into the anterior border of the trapezius is roughly 5 cm above the midpoint of the clavicle. The SAN innervates the trapezius muscle, and the two to three branches that supply the upper part of the muscle come off the SAN before it enters the muscle.

The SAN travels on the deep surface of the trapezius muscle after it exits the posterior triangle of the neck. At the anterior border of the trapezius it pierces the fascia covering the deep surface of the muscle. Proximal to its entry into the fascia, the accessory nerve lies in fatty tissues, allowing the nerve to move with neck and shoulder movement. It then runs between the muscle and the fascia ~ 2 cm from the anterior border of the muscle. It then turns medially and inferiorly. At a distance of ~ 7 cm below the scapular spine, it divides into terminal muscular branches. Beyond this point, however, the nerve is tethered to the fascia and immobile ( Fig. 19.2 ).

The SAN and SSN are of similar caliber, but the mean number of myelinated axons is different, with the distal SAN having 1,600 and the SSN 6,000 axons. This difference in number of axons translates into decreased strength of the ultimate reconstruction even if every axon regenerates across the repair site.1