American Society for Peripheral Nerve

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Anatomical Course of the Greater Auricular Nerve: Implications of Surgical Decompression in Symptomatic Allodynia Following Rhytidectomy
John R. Barbour, MD; Gil Gontre, MD; David E. Halpern, MD
Barnes-Jewish Hospital, Saint Louis, MO, USA

Goal: Nerve injury in head and neck aesthetic surgery is a well-described phenomenon and may range from temporary neurapraxia to iatrogenic compression to complete transection. The great auricular nerve (GAN) is most frequently injured in the course of rhytidectomy, due to its anatomical location and superficial course. In complete or persistent GAN injury, the proximal end of the irritated nerve may become attached to the scar or anterior skin flap. Neuroma or stitch impingement will cause a trigger point on the lateral neck, which may lead to migraine-like pain on the side of the face. We review the anatomy of the GAN and present a case series in which this nerve was found to be compressed by scar tissue or suture material at re-operation.

Methods: Anatomic dissections were performed on cadaveric specimens to delineate normal course of the GAN and its relationship to dissection for minimally invasive rhytidectomy. In four patients with persistent allodynia symptoms following rhytidectomy, exploration was performed with identification of the GAN at its normal anatomical location. Compression and suture impingement was confirmed and extensive decompression was performed to protect the nerve from post-operative scar formation.

Results: The GAN leaves the cervical plexus at the posterior border of the sternocleidomastoid muscle (Erb's point) and courses anteriorly over its lateral surface. It continues superiorly, dividing into anterior and posterior branches. The expected course of the GAN is deep to the sternocleidomastoid muscle for the proximal aspect. More distally, the GAN should be lateral to the sternocleidomastoid, with superiorly diverging routes of the anterior and posterior branches. Four patients presented with suture impingement of the GAN and extensive peri-neural scarring. All four patients were successfully treated with exploration and decompression. Cosmetic appearance of re-exploration was acceptable in all four patients, and all patients exhibited improved sensibility post-operatively.

Conclusion: This demonstrates the potential for symptomatic compression of the GAN following minimally invasive rhytidectomy. Because successful treatment requires identification of this compression, the peripheral nerve surgeon should be familiar with the anatomy of the GAN and its cutaneous branches, as well as with the potential for iatrogenic compression along these nerves. In this series, a provocable Tinel’s sign in the distribution of the GAN alerted the surgeon to possible GAN compression. Re-exploration and surgical decompression may represent an excellent adjunct for sensory defects following rhytidectomy. Knowledge of anatomical relationships, nerve decompression techniques, and close patient follow-up allow for appropriate operative planning.


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