Anatomy of the mandibular branches of the facial nerve.

In operative dissections of mandibular branches of the facial nerve, we identified certain branches below the inferior border of the mandible in all cases. These usually supplied the depressor labii inferioris and mentalis muscles, though infrequently the branch to the depressor anguli oris was also below the mandible. At least 3 nerve branches were identified in all dissections. The clinical applications of this include the necessity to identify and protect these nerve branches during operations in the submandibular triangle, as well as when incising the platysma muscle or removing fat from over the body of the mandible in a face-lift procedure.     

Cardiac asystole secondary to carotid sinus compression in the face-lift operation.

We present 3 cases of carotid sinus compression with cardiac asystole which occurred in healthy patients undergoing routine rhytidectomies. The mechanism is discussed and suggestions are made regarding preoperative evaluation and operative management.     

Diphenylpiperazines enhance regeneration after facial nerve injury

Immature rat facial motoneurons are very sensitive to injury with nearly 80% dying during the first week after axotomy. This motoneuron death is apoptotic, similar to that induced in neurons after tropic factor withdrawal. The diphenylpiperazines, flunarizine and cinnarizine, protect dorsal root ganglion neurons from death after withdrawal of trophic support, i.e., nerve growth factor withdrawal, in vitro. Similarly, the monoamine oxidase inhibitor, deprenyl, promotes survival of facial motoneurons after axotomy. These pharmacological agents were assessed both alone and in combination for their ability to prevent death in non-nerve growth factor dependent CNS motoneurons after facial nerve axotomy in newborn rats. Long-term experiments were done with the diphenylpiperazines to evaluate potential enhancement of regeneration. Facial nerve transection resulted in 78% neuronal loss in the injured compared with the contralateral, uninjured nucleus. Systemic administration of diphenylpiperazines for 1 week after facial nerve transection doubled the number of surviving motoneurons from 23% to 47%. Similar results were obtained with deprenyl. Combinations of diphenylpiperazines and deprenyl provide a similar degree of neuronal protection 1 week after injury as that obtained by either agent alone. We assessed the ability of diphenylpiperazines to protect facial motoneurons from death over a prolonged period and enhance subsequent regeneration. Motor neuron counts in rats treated with diphenylpiperazines for 1 month after injury and assessed 2 months later demonstrated long-term enhancement of neuronal protection with an increase of 45% in the number of horseradish peroxidase-labelled motoneurons. The diphenylpiperazines group had ～80% more regenerated myelinated axons in the distal facial nerve than the control group. Thus, diphenylpiperazine treatment during the first month after injury provides long-term protection of non-nerve growth factor dependent CNS motoneurons with subsequent potentiation of long-term facial nerve regeneration.     

Anatomy of the frontal branch of the facial nerve: the significance of the temporal fat pad

The anatomy of the temporal region, with reference to the frontal branch of the facial nerve, was examined in 12 fresh cadaver dissections. In all dissections, the frontal branch traveled in a constant plane along the undersurface of the temporoparietal fascia and was quite superficial as it crossed the zygomatic arch. The deep temporal fascia and superficial temporal fat pad are anatomically important structures which adjoin the periosteum of the zygomatic arch and lie deep to the frontal nerve. Based on these relationships, a safe method of dissection within the temporal region is formulated.     

Exacerbation of facial motoneuron loss after facial nerve axotomy in CCR3-deficient mice

We have previously demonstrated a neuroprotective mechanism of FMN (facial motoneuron) survival after facial nerve axotomy that is dependent on CD4⁺ Th2 cell interaction with peripheral antigen-presenting cells, as well as CNS (central nervous system)-resident microglia. PACAP (pituitary adenylate cyclase-activating polypeptide) is expressed by injured FMN and increases Th2-associated chemokine expression in cultured murine microglia. Collectively, these results suggest a model involving CD4⁺ Th2 cell migration to the facial motor nucleus after injury via microglial expression of Th2-associated chemokines. However, to respond to Th2-associated chemokines, Th2 cells must express the appropriate Th2-associated chemokine receptors. In the present study, we tested the hypothesis that Th2-associated chemokine receptors increase in the facial motor nucleus after facial nerve axotomy at timepoints consistent with significant T-cell infiltration. Microarray analysis of Th2-associated chemokine receptors was followed up with real-time PCR for CCR3, which indicated that facial nerve injury increases CCR3 mRNA levels in mouse facial motor nucleus. Unexpectedly, quantitative- and co-immunofluorescence revealed increased CCR3 expression localizing to FMN in the facial motor nucleus after facial nerve axotomy. Compared with WT (wild-type), a significant decrease in FMN survival 4 weeks after axotomy was observed in CCR3^−/− mice. Additionally, compared with WT, a significant decrease in FMN survival 4 weeks after axotomy was observed in Rag2^−/− (recombination activating gene-2-deficient) mice adoptively transferred CD4⁺ T-cells isolated from CCR3^−/− mice, but not in CCR3^−/− mice adoptively transferred CD4⁺ T-cells derived from WT mice. These results provide a basis for further investigation into the co-operation between CD4⁺ T-cell- and CCR3-mediated neuroprotection after FMN injury.     

Incidence of cervical branch injury with "marginal mandibular nerve pseudo-paralysis" in patients undergoing face lift

The anatomy of the cervical and marginal mandibular branches of the facial nerve is reviewed. In the senior author's practice, "pseudoparalysis of the marginal mandibular nerve" due to cervical branch injury occurred in 34 of 2002 superficial musculoaponeurotic system-platysma face lifts (1.7 percent) and was associated with a full recovery in 100 percent of cases within a time period ranging from 3 weeks to 6 months. Cervical branch injury can be distinguished from marginal mandibular nerve injury by the fact that the patient will be able to evert the lower lip because of a functioning mentalis muscle.     

Primary neoplasms of the facial nerve

A series of 30 primary facial nerve tumors is reviewed. Most of them were benign (n = 26); there were four malignant tumors. Neoplasms originating within the temporal bone were found to have preoperative facial paralysis in 84 percent of cases; the extracranial tumors had a 35 percent incidence of preoperative facial paralysis. All tumors in this series were treated surgically--by means of a middle fossa or transmastoid approach for the intratemporal group of tumors; the extracranial tumors were removed by the technique of parotid tumor surgery with complete facial nerve dissection. All the patients with preoperative facial weakness required facial nerve transection. Facial paralysis was rehabilitated with nerve grafts, hypoglossal crossover, or muscle transfers. Because "normal" facial expression is still not attainable following repair of complete facial nerve transection, an early diagnosis, hopefully prior to total neurotmesis, is essential. All patients with unexplained facial weakness, especially that which is progressive and persistent, should have the entire course of the facial nerve investigated for the possibility of treatable etiology.     

Endotemporal branching of the facial nerve

Out of 400 specimens of temporal bone the authors found two cases of branching of the facial nerve in the mastoid course, i.e., 0.5%. Knowledge of this anomaly has a certain practical value in surgical intervention of the middle ear.