Platysma Motor Nerve Transfer for Restoring Marginal Mandibular Nerve Function

BACKGROUND: Injuries of the marginal mandibular nerve (MMN) of the facial nerve result in paralysis of the lower lip muscle depressors and an asymmetrical smile. Nerve reconstruction, when possible, is the method of choice; however, in cases of long nerve gaps or delayed nerve reconstruction, conventional nerve repairs may be difficult to perform or may provide suboptimal outcomes. Herein, we investigate the anatomical technical feasibility of transfer of the platysma motor nerve (PMN) to the MMN for restoration of lower lip function, and we present a clinical case where this nerve transfer was successfully performed. METHODS: Ten adult fresh cadavers were dissected. Measurements included the number of MMN and PMN branches, the maximal length of dissection of the PMN from the parotid, and the distance from the anterior border of the parotid to the facial artery. The PMN reach for direct coaptation to the MMN at the level of the crossing with the facial artery was assessed. We performed histomorphometric analysis of the MMN and PMN branches. RESULTS: The anatomy of the MMN and PMN was consistent in all dissections, with an average number of subbranches of 1.5 for the MMN and 1.2 for the PMN. The average maximal length of dissection of the PMN was 46.5 mm, and in every case, tension-free coaptation with the MMN was possible. Histomorphometric analysis demonstrated that the MMN contained an average of 3,866 myelinated fiber counts per millimeter, and the PMN contained 5,025. After a 3-year follow-up of the clinical case, complete recovery of MMN function was observed, without the need of central relearning and without functional or aesthetic impairment resulting from denervation of the platysma muscle. CONCLUSIONS: PMN to MMN transfer is an anatomically feasible procedure for reconstruction of isolated MMN injuries. In our patient, by direct nerve coaptation, a faster and full recovery of lower lip muscle depressors was achieved without the need of central relearning because of the synergistic functions of the PMN and MMN functions and minimal donor-site morbidity.