Dual spinal accessory nerve: an anatomical anomaly during neck dissection

Background

The XI cranial nerve, spinal accessory nerve (SAN), is an anatomical structure that is encountered during neck dissection. Preservation of this nerve from iatrogenic injury is an important consideration; this was widely recorded as a consequence of radical neck dissection (RND). Following the 1950s, the RND was revisited and modified approaches to neck dissection were employed, achieving reduction in overall morbidity, including improved function of the SAN postoperatively.1

Iatrogenic damage (75%–90%) is known to be the most common aetiology of SAN injury, which is clinically encountered postoperatively in neck dissections and rarely in lymph node needle biopsies.2 3 A spectrum of clinical presentations arise from damage to the SAN, commonly known as SAN palsy, which may present as drooping of the shoulder secondary to trapezius paralysis, shoulder weakness (in abduction), winging of the scapula and trapezius muscle atrophy. Anatomical variations of the SAN towards the skull base and its course in the posterior triangle are recognised to be potential causes of increasing rates of iatrogenic damage.4

Identification of the SAN has been a challenge for surgeons as great anatomical variation has been described throughout the literature. Therefore, a thorough understanding of the topographical anatomy is of utmost importance in neck dissection in order to avoid debilitating postoperative consequences.5 Although selective and modified techniques of neck dissection are now common practice, it has been shown that the incidence of shoulder injury remains high.6

We present a case of a patient undergoing parotidectomy with selective neck dissection for a primary parotid squamous cell carcinoma (SCC). We aim to discuss the surgical and clinical implications of a dual SAN and its rare relationship to the internal jugular vein (IJV).

Case presentation

The male described in this case report, who was in his 80s, was referred to the otolaryngology department with an enlarging left parotid mass. Examination revealed a mobile parotid tumour, no evidence of facial nerve involvement and the remaining head and neck was unremarkable, including skin survey. The patient had a medical history of surgically resected right shin basal cell carcinoma (BCC), hiatus hernia, osteoarthritis and gastritis. There were no known drug allergies. He had good functional capacity and was fully independent with all activities of daily living.

Following clinical review, a neck ultrasound scan and subsequent CT revealed a 15 mm tumour of the superficial lobe of the parotid gland (figure 1). Initial fine-needle aspiration was suspicious of malignancy and subsequent core biopsy confirmed SCC. There was no evidence of cervical lymphadenopathy or metastatic disease on CT staging. Positron emission tomography (PET) CT was undertaken given the rarity of primary parotid SCC to exclude an alternative primary site; however, the PET CT showed no increased avidity elsewhere in the head and neck. Although the dual SAN was present and visible on the preoperative scans, it was not reported by the radiologists or noted by the parent team.

The patient subsequently consented for the undertaking of a left superficial parotidectomy and level Ib-III selective neck dissection. Intraoperatively, a dual SAN was encountered (figure 2). Moreover, the dominant of the dual nerves was traversing the IJV.

The dual accessory nerves we identified followed two different courses to their final position, supplying the sternocleidomastoid (SCM) and trapezius muscles. The nerve following the anomalous course was the dominant nerve and the nerve following the usual course was the non-dominant accessory nerve, in terms of size; these definitions will be subsequently used to refer to each nerve.

Following its exit at the jugular foramen, the non-dominant nerve travelled medial to the IJV and then coursed laterally over the vein to run obliquely, inferior and lateral, to reach the deep surface of the SCM. After supplying the muscle at this point, it ran 1–2 cm superior to Erb’s point and crossed into the posterior triangle, embedded in loose connective tissue (the full nerve course was not dissected, as there was no clinical rationale to dissect level V).

The dominant nerve descended on the posterior surface of the IJV traversing through the vein, dividing the IJV into two, to emerge anteriorly at the junction of upper and middle third of the vein (figure 3). The anomalous course continued inferiorly on the anterior surface of the IJV to level III of the neck, finally coursing inferiorly and laterally (figure 4) without supplying SCM, into level 5 towards the trapezius muscle; again complete nerve dissection was not justified clinically.

Postoperatively, the patient had mild signs of SAN dysfunction reporting left shoulder girdle pain in the immediate days following the operation. The patient required input from the physiotherapy team for rehabilitation and movement exercises. Subsequently, the patient made a complete recovery with regard to left shoulder function. On follow-up since the parotidectomy and neck dissection, the patient displayed no signs of local or regional recurrence of cancer.