Facial nerve trauma can be a devastating injury resulting in functional deficits and psychological distress. Deciding on the optimal course of treatment for patients with traumatic facial nerve injuries can be challenging, as there are many critical factors to be considered for each patient. Choosing from the great array of therapeutic options available can become overwhelming to both patients and physicians, and in this article, the authors present a systematic approach to help organize the physician’s thought process.
Key points
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If the facial nerve is anatomically intact, or if the injury is limited to the medial portion of a peripheral branch, treatment is usually medical with close observation and possible electrophysiologic testing for monitoring of progression.
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If the nerve is transected, immediate exploration with direct anastamosis provides the best chance of recovery.
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If a large segment of nerve is injured, an interposition graft should be placed immediately. If the injured segment is not easily accessible for repair, nerve transposition is the treatment of choice.
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For facial muscles with irreparable damage or extensive disuse atrophy, muscle transfer procedures are the best option for dynamic facial reanimation.
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Regardless of the type of injury or treatment, ocular protection is of primary concern to prevent avoidable complications.
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Treatment of traumatic facial nerve injuries can be a variable and dynamic process, but having a clear understanding of the diagnostic and treatment algorithms can help of a meaningful recovery for these patients.
Introduction
Trauma to the facial nerve is the second most common cause of facial paralysis and can result in devastating consequences including ocular complications, impaired speech, feeding difficulties, and inability to convey emotion through facial expression. It is critical that otolaryngologists and facial plastic surgeons have a thorough understanding of the principles of facial nerve trauma management because timing of treatment can have a significant impact on a patient’s chances and extent of recovery. The number of possible treatment options can be overwhelming to both patient and physician, including whether or not surgery is indicated and, if so, which operation should be chosen and at what point in time should it be performed.
Introduction
Trauma to the facial nerve is the second most common cause of facial paralysis and can result in devastating consequences including ocular complications, impaired speech, feeding difficulties, and inability to convey emotion through facial expression. It is critical that otolaryngologists and facial plastic surgeons have a thorough understanding of the principles of facial nerve trauma management because timing of treatment can have a significant impact on a patient’s chances and extent of recovery. The number of possible treatment options can be overwhelming to both patient and physician, including whether or not surgery is indicated and, if so, which operation should be chosen and at what point in time should it be performed.
Evaluation
Management of traumatic facial nerve injuries depends on the timing of facial paralysis after trauma (immediate vs delayed), the extent of paralysis (complete vs incomplete), the type of trauma (blunt, penetrating, or iatrogenic), the condition of the nerve, the duration of facial paralysis, and the status of the motor end plates of the facial muscles.
One key factor that should be assessed in all cases is the potential for recovery of facial function. Reversibility of facial function depends on both the integrity of the nerve and the status of the end-organ facial muscles. In general, if the motor end plates of the facial muscles are still functional, treatment should be aimed at restoring innervation to the facial muscle. If the motor end plates are not functional, then treatment should be focused on transferring an alternate muscle to restore dynamic facial movement.
Details from the history, pertinent clinical examination, neuroimaging, and facial nerve testing can provide the necessary data to guide the decision-making process. A treatment algorithm is presented to help physicians simplify the management strategy and maximize the chances of optimal facial nerve recovery ( Fig. 1 ).
Critical questions in the decision tree include
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Is the facial muscle function reversible (ie, are the motor end plates intact)?
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Is the facial nerve interrupted or anatomically intact?
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Is the facial weakness complete or incomplete?
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Was the onset of paralysis immediate or delayed?
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Is the injury medial or lateral to the lateral canthus?
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Is the location of facial nerve injury surgically accessible?
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Are the facial muscles irreparably damaged, either through direct trauma or atrophy from chronic denervation?
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Is electrophysiologic testing useful given the time frame?
Anatomy
The injured segment of the facial nerve can be classified according to its location: intracranial, intratemporal, or extratemporal. The intracranial component of the nerve runs from its origin at the ventral aspect of the pontomedullary junction of the brain stem to the porus acousticus of the internal auditory canal (IAC). The intratemporal component includes the portion of the nerve from within the IAC to the stylomastoid foramen and is subdivided to include the meatal, labyrinthine, tympanic (horizontal), and mastoid (vertical) segments. The tympanic segment is dehiscent in 40% to 50% of people, and is therefore the most commonly injured segment during middle ear and mastoid surgery. The extratemporal nerve then begins at the level of the stylomastoid foramen and ends at the motor end plates of the muscles of facial expression. After exiting the stylomastoid foramen, the extratemporal facial nerve divides at the main pes anserine into the temporofacial and cervicofacial branches. These 2 branches then further divide into the temporal, zygomatic, buccal, marginal mandibular, and cervical branches. All muscles of facial expression are innervated on their deep surface except for the mentalis, levator anguli oris, and buccinator muscles.
Causes of facial nerve trauma
Facial nerve injury can be a result of blunt or penetrating trauma. The most common cause of facial nerve injury is blunt trauma from a fracture of the temporal bone. Motor vehicle accidents are also common sources of blunt trauma that can damage the facial nerve. Typical examples of penetrating trauma that may produce facial nerve injury include animal bites to the face, laceration from knife trauma, or blast injuries from gunshot wounds, explosives, or slag injury.
Injuries to the facial nerve can also occur iatrogenically and arise most frequently during salivary gland and otologic surgeries. Traumatic forceps delivery during birth can result in injury to the facial nerve of the newborn.
Classification of nerve damage
The severity of gross damage to the nerve varies and can include simple traction injury with an anatomically intact nerve, crush injury, partial or full transection, or loss of a segment of nerve. The extent of nerve damage can help predict recovery. In general, nerve injuries that result in disruption of the neural tube require surgical intervention for recovery. In 1943, Seddon classified nerve damage into 3 levels ( Table 1 ).
| I. Neuropraxia | Conduction block only |
| II. Axonotmesis | Wallerian degeneration occurs but axonal contents are intact |
| III. Neurotmesis | Axon is disrupted Surgical intervention likely required for recovery Synkinesis likely to develop |
In 1951, Sunderland then further divided the Seddon III Neurotmesis category based on the level of the neural tube affected ( Table 2 ).
| Conduction block only No Wallerian degeneration Full spontaneous recovery expected |
| Wallerian degeneration occurs but axonal contents are intact Full spontaneous recovery expected (neural regeneration rate of ∼1 mm/d) |
| Surgical intervention likely required for recovery |
| Surgical intervention likely required for recovery |
| Surgical intervention likely required for recovery |
Initial assessment
Cases of trauma to the face, head, and neck, as with all cases of significant trauma, should begin with a primary survey assessing the patient’s airway, breathing, and circulation. Wounds should be cleaned and copiously irrigated, and antibiotic therapy and any necessary tetanus prophylaxis should be administered. Detailed examination of facial movement can then be performed, including eyebrow movement, eye closure with gentle and full effort, midface movement, and capacity to smile and pucker. If possible, any sedation should be lightened for the facial nerve examination. If the patient is unable to cooperate, a transient noxious stimuli can be used to assess for a grimace.
If facial paralysis is noted to be incomplete or segmental, a thorough description of the involved branches and the severity of paresis/paralysis is helpful to accompany a grade from an established facial nerve grading system. A video or a series of photographs can be helpful to document the baseline clinical examination. If the patient is noted to have complete facial paralysis, an effort should be made to determine whether this paralysis is of immediate or delayed onset.
Electrophysiologic testing
Electroneuronography (ENOG) and electromyography (EMG) are 2 electrodiagnostic tests that can aid in the clinical decision making when considering whether to intervene in a traumatic facial nerve injury. If the facial nerve is believed to be anatomically intact, these tests can help determine whether the injury is a Sunderland I or II, or whether the injury is more severe. Electrophysiologic testing is not needed in incomplete facial paralysis or in segmental paralysis. In cases of complete paralysis, these tests are not helpful in the first 3 days after injury, because, even in a fully transected nerve, Wallerian degeneration has not had time to occur and the nerve continues to transmit distal impulses and potentially provide a false-positive result. ENOG uses a surface electrode to provide stimulation to the main trunk of the facial nerve and records any action potentials at the level of the distal facial muscles. The response on the paretic side is compared with the normal side. ENOG can be tested in a serial fashion, and if more than 90% degeneration is seen compared with the normal side, surgical intervention can be considered.
In practice, it is logistically difficult to see patients with traumatic facial paralysis in the early period and perform serial ENOG in the critical 6 days after facial paralysis. This may partly be due to limited availability of electrodiagnostic resources or the presence of other more serious injuries. At 2 to 3 weeks after an injury resulting in complete facial paralysis, EMG is the most helpful electrophysiologic test to determine whether the nerve is in the process of recovery. Myogenic electrical activity is recorded with a needle inserted into the end-organ facial muscle. The presence of fibrillation potentials indicates nerve degeneration, whereas polyphasic action potentials indicate neural regeneration.
Radiographic imaging
In cases of complete facial paralysis in patients with trauma to the skull, high-resolution computed tomography (CT) with fine cuts (1-mm slices) through the temporal bone can be useful to evaluate for disruption of the fallopian canal. Contrast is generally not needed unless there is concern about associated vascular injury. When gross fracture lines are not obvious, the region around the geniculate ganglion fossa (GGF) should be closely inspected. An enlarged GGF on temporal bone CT is an additional clue for the diagnosis of GGF fracture in patients with traumatic facial paralysis. This correlates with findings of edema, fibrosis, bony spicules impinging on the facial nerve often found in the GGF when decompressing the facial nerve in cases of trauma.
Management
An approach to treating trauma-related facial nerve injuries is to categorize the injuries into reversible and irreversible palsies. Patients with injuries that are considered reversible have viable and functional facial muscles, and treatment is aimed at reinnervation of these muscles through repair of the facial nerve or transposing another nerve to power the distal end of the facial nerve. Patients without viable facial muscles have irreversible injuries and typically require functional muscle transfers to restore facial movement. Static slings and suspension procedures can be considered as adjuvant interventions to further improve symmetry and function.
Reversible Facial Nerve Injury
The primary consideration in the initial management of a patient with a traumatic facial paralysis is the reversibility of facial muscle function. In cases of reversible injury, it is important to determine which cases will recover spontaneously with medical therapy and close observation and which warrant immediate surgical repair. Answering the following questions help to clarify the next step to take:
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Was the onset of facial weakness immediate or delayed?
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If the onset was immediate, is the facial weakness complete, incomplete?
- 3.
If the onset is immediate and the paralysis is complete, is the damaged segment located medially or laterally to the lateral canthus of the eye?
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In complete paralysis, is the nerve anatomically continuous or interrupted?
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When the nerve is interrupted, can the proximal segment be easily mobilized for nerve grafting?
Medical treatment and expectant observation
Medical therapy and close observation is appropriate for those patients with incomplete paralysis, delayed onset of paralysis, blunt trauma to the extratemporal nerve, and injury that occurs medial to the lateral canthus of the eye. In these categories of patients, recovery is usually spontaneous without the need for immediate surgical exploration or repair. Some traumatic birth injuries resolve spontaneously and without surgical intervention. If medical therapy is chosen, the patient should be closely observed to ensure that a meaningful and sufficient recovery is achieved in a timely manner. If sufficient recovery is not evident within 6 months after the trauma, surgical intervention should then be considered to prevent irreversible chronic atrophy of the facial muscles (typically with a nerve transposition procedure).
Cases of incomplete paralysis secondary to injury or edema are associated with a nerve that is anatomically continuous with neuropraxia or axonotmesis. Treatment should be aimed at minimizing edema and preventing viral infection. The use of steroids is supported in the treatment of incomplete paralysis, but there are mixed data on the benefit of antivirals.
Delayed onset of complete or incomplete paralysis suggests an anatomically intact nerve, with delayed neuropraxia or axonotmesis. This diagnosis requires certainty that facial function was transiently intact immediately after the injury, either from direct examination or by obtaining a clear history from the initial trauma team or family members. In cases of delayed complete paralysis, some investigators recommend serial electrophysiologic testing with ENOG between days 3 and 14, and consideration of surgical facial nerve decompression if there is greater than 95% loss of axonal function compared with the unaffected side. In cases of possible iatrogenic injury, it is important to determine if the nerve was noted to be anatomically intact and stimulated at the end of the procedure. Adequate time should also be allowed for the effect of local anesthetic to wear off to account for cases of temporary paresis from medication. Initial treatment with steroids to minimize inflammation and edema is reasonable.
Blunt trauma to the extratemporal nerve is usually managed conservatively with expectant observation. Surgery is considered if no recovery is seen after 6 months.
Injury that occurs medial to the lateral canthus of the eye rarely results in clinical paralysis. In the midface, there are rich cross-anastomotic connections of the nerve that allow spontaneous recovery of facial function. However, in the rare circumstance that an injury medial to the lateral canthus does cause clinical paralysis of that segment, then exploration of the nerve with repair should be considered.
Traumatic birth injuries are usually associated with emergency forceps delivery. Because the stylomastoid foramen is more lateralized in infants compared with adults, the main trunk of the nerve is at high risk for external trauma. Fortunately, more than 90% of traumatic birth injuries to the facial nerve resolve spontaneously without long-term sequelae.
Early surgical exploration and repair
When traumatic injury to the face and head results in immediate paralysis, it should be assumed that the facial nerve is interrupted or severely crushed to result in neurotmesis. Early surgical exploration and repair is indicated for such patients ( Fig. 2 ). The ease of exploration and the approach selected depends on the suspected site of injury. Exploration within 3 days of injuries allows the use of a nerve stimulator to identify distal segments of disrupted facial nerve branches. If there are contraindications to immediate repair, then efforts should be made to tag the nerve endings for easier identification during a subsequent staged repair.
