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After Bell’s palsy (a viral infection), facial nerve trauma is the second most common cause of facial paralysis. The nerve can be injured anywhere along its course from its origin in the brain to its termination in the muscles of facial expression.  

Frequent causes of facial nerve injury include skull base fractures, gun shot wounds, sharp penetrating injuries such as stab wounds and disruption during surgical procedures.  The location of the injury, initial presentation and mechanism of injury all play a significant role in determining treatment and long-term prognosis.  

Blunt trauma to the head and neck often sustained in automobile accidents and aggravated assaults is a common cause of temporal bone fractures.  Temporal bone fractures with a transverse orientation can breach the otic capsule producing facial nerve injury and hearing loss.  
If the onset of the paralysis occurs immediately at the time of injury, surgical treatment in the form of facial nerve decompression is often warranted.  Individuals with temporal bone fractures who experience a more delayed onset of facial weakness are often treated with steroids and careful observation.  

Electrical testing (ENoG) can also be beneficial in guiding therapy especially in the management of gun shot wounds.  A decrease of facial nerve conduction to 90 % of baseline is an additional indication for surgical exploration in some centers.  At the time of exploration compressive bone fragments may be identified and removed.  Alternately, a transected or severely damaged nerve segment may be encountered requiring the placement of an interposition nerve graft.

Clean, sharp transection of the facial nerve in the region of the ear and cheek usually warrant surgical exploration and repair.  This is often performed in a very timely fashion as the down stream end of the nerve will continue to conduct electricity for 48-72 hours facilitating identification.  If the nerves cannot be coapted without tension then a nerve graft can be utilized.  If the associated wound is heavily contaminated then the nerve ends may be tagged to facilitate delayed repair once initial wound healing has been achieved. 

Medial facial lacerations with associated weakness may be sutured closed without nerve repair as the nerve branches are tiny in these regions and enough branching has occurred to allow recovery. Injuries to the facial nerve can also be sustained during surgical procedures. At times, segments of the facial nerve or higher centers in the brain are necessarily sacrificed to manage tumors (i.e. cerebellopontine angle tumors) and other disease states (i.e. cavernous malformations). In this situation, immediate nerve reconstruction is often included as part of the surgical plan.

Inadvertent injury to the facial nerve can also occur during parotid surgery, mastoidectomy and reconstruction of the eardrum. The use of intraoperative facial nerve monitoring has significantly reduced the rate of facial paralysis following acoustic neuroma excision; however, the frequency of facial nerve injury is still significant when managing large tumors. If the facial nerve remains grossly intact following schwannoma excision then reconstruction is often delayed for 10-12 months providing an opportunity for spontaneous regeneration to occur.

Injuries to the facial nerve can also occur during cosmetic surgical procedures including face lifts. If a facial nerve is accidentally divided during face lift surgery it should be immediately repaired. Alternately, segmental facial nerve weakness suggests incomplete nerve injury and a meaningful improvement develops on its own over the following year. In these situations electrical testing (EMG) can also help guide management. Rarely, facial paralysis is encountered after wisdom tooth extraction although the mechanism of action is poorly understood.