[SURGICAL TREATMENT OF CANCER OF THE FACIAL SKIN].
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Perineural invasion of cranial nerves, including the facial nerve by squamous cell carcinoma of the skin, is a poor prognostic factor for recurrent disease and disease-specific mortality. We discuss 2 patients who presented to the Otolaryngology/Head and Neck Surgery service with complete facial nerve paralysis and a history of skin cancer. Based on our experience with these patients, we recommend that patients who present with facial nerve paralysis and a history of cutaneous malignancy undergo aggressive management including early intervention and complete exploration of the facial nerve from the geniculate ganglion out to the periphery. Such rigorous care achieves the best possible oncologic outcomes for a proven aggressive disease.
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BACKGROUND: Sentinel lymph node biopsy (SLNB) for primary cutaneous head and neck melanoma (CHNM) has been shown to be successful and is the current standard of care for intermediate-thickness melanoma. We evaluated our experience with CHNM associated with SLNB mapping to the region of the parotid gland. METHODS: Retrospective review of a prospectively collected melanoma database identified 1014 CHNMs. Two-hundred twenty-three patients underwent SLNB, and 72 (32%) had mapping in the region of the parotid gland between May 1995 and June 2003. RESULTS: The mean number of SLNs per patient was 2.5. A sentinel lymph node (SLN) was successfully identified in 94% of patients, and in 12%, the SLN was positive for metastatic disease. Biopsy of intraparotid SLNs was performed in 51.4% and of periparotid SLNs in 26.4%, and a superficial parotidectomy was performed in 22.2%. Ten patients were found to have lymph nodes in the parotid region with metastatic disease (eight identified by SLNB), and two (20%) patients developed intraparotid lymph node recurrence in the setting of a negative SLNB. Same-basin recurrence in SLN-negative patients was 3.3% with a median follow-up of 26 months. Facial nerve dysfunction was identified in seven (10%) patients. Facial nerve function returned to preoperative status in all patients. CONCLUSIONS: SLNB for patients with primary CHNM mapping to the parotid gland can be performed with a high degree of accuracy and a low morbidity consisting of temporary facial nerve paresis.
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Two patients with intracranial dissemination of squamous carcinoma along the trigeminal nerve had facial dysesthesias mistakenly diagnosed as tic douloureux. In one case, tumor originated in the skin of the lateral canthus and spread along an orbital nerve to involve the cavernous sinus and Gasserian ganglion. In the other, the primary site was the retromolar trigone, with preponderantly deep intraosseous growth. Perineural spread occurred along the inferior alveolar nerve to eventually involve the facial and the ocular motor nerves. Such neurotropic spread of tumors is unfamiliar to many clinicians, yet early diagnosis may be life-saving. If intracranial foramina have not been transgressed, surgery and radiotherapy have been curative; otherwise, treatment is largely palliative. Adequate initial treatment of the primary lesion would seem to be the best preventive measure. Treatment of recurrent lesions should include consideration of neural invasion.
Neurogenic neoplasms of the intraparotid facial nerve are uncommon and are usually diagnosed intraoperatively by tissue biopsy. Fifty-six cases of primary neurogenic neoplasms involving the facial nerve have been reported. The majority of these have been schwannomas. A case of a solitary neurofibroma involving the main trunk of the facial nerve is presented. Schwannomas and neurofibromas have distinct histological features which must be considered prior to the management of these tumors. The management of neurogenic tumors associated with normal facial function is a particularly difficult problem. A new approach for the diagnosis and management of neurogenic neoplasms is described utilizing electroneurography.
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