Background
Temporal bone trauma accounts for 5% of all facial palsy cases , and 3% of all bilateral facial palsy. Only 7% of temporal bone fractures result in facial palsy and 25% of those result in complete facial paralysis. Historically, temporal bone fractures have been classified as either longitudinal or transverse, a classification scheme that refers to the direction of the fracture with respect to the long axis of the petrous temporal bone. Another classification scheme differentiates a fracture based on whether it involves or spares the otic capsule. Approximately 30%–50% of patients with a transverse fracture pattern have facial nerve injury resulting in paralysis. , The transverse fracture pattern is associated with more severe facial nerve injury and portends a poorer prognosis when compared with the longitudinal fracture pattern. Facial nerve injury occurs in only 10%–20% of patients with longitudinal fractures in comparison. , , Otic capsule violating fractures are quite rare (less than 6%) compared with otic capsule sparing fractures (>94%), and facial nerve injury is twice as common in otic capsule violating fractures than in its counterpart. ,
Evaluation
It is estimated that close to 1900 lbs of force is necessary to fracture a temporal bone. As such, patients presenting with facial palsy following a temporal bone fracture often present with other injuries. A CT temporal bone protocol with 0.625-mm-thick slices is best suited to evaluate the fracture pattern. Multiplanar formats can be created to enable fracture pattern interpretation that may be difficult to see on routine axial and coronal planes.
In an awake and cooperative patient, a careful history and physical exam should be performed. Patients lucid enough to provide an accurate history should be asked about the mechanism of injury, any lapses in memory or loss of consciousness, vision changes, presence of hearing loss or vertigo, or clear rhinorrhea or otorrhea. A full head and neck examination should be performed. One of many findings may be visible on otoscopic exam including a fracture extending into the EAC with disruption of the canal skin, rupture of the tympanic membrane, ossicular dislocation, clear otorrhea, and hemotympanum. A tuning fork exam may demonstrate sensorineural hearing loss, particularly for fractures violating the otic capsule. Conductive hearing loss may be present for patients with ossicular disruption or middle ear fluid or blood. A full cranial nerve examination should be performed. Documenting the initial facial nerve function is important in predicting nerve recovery, determining need for further electrodiagnostic studies, and deciding on the candidacy for surgical decompression.
In light of the degree of force necessary to cause a temporal bone fracture, many patients present with other concomitant injuries that necessitate intubation and sedation. In an intubated and sedated patient, a physical examination may be very limited. A sternal rub may stimulate the patient enough so that a grimace can be elicited. However, until the sedation can be held and the patient’s medical condition is stabilized, it may not be possible to obtain an accurate facial nerve examination in the acute setting.
Timing and extent of facial paralysis
Traumatic facial nerve injury can be classified into immediate-onset complete paralysis or delayed-onset or incomplete paralysis. , Patients with immediate-onset complete facial nerve paralysis have a poor prognosis of achieving full recovery. A systematic review of 35 studies showed that only 36% of patients with immediate-onset paralysis recovered fully without intervention, while 80% of patients with delayed-onset paralysis recovered fully. Similarly, only 57% patients with complete facial nerve paralysis achieved full facial nerve recovery without intervention compared with 82% of patients with partial facial nerve paralysis. Some studies cite recovery rates of delayed-onset incomplete paralysis as >90%. ,
Patients with incomplete paralysis have excellent long-term outcomes, and patients with <90% degeneration on electroneurography (ENOG) testing expected to regain close to or normal facial function. , As such, while patients with immediate-onset complete paralysis should undergo electrodiagnostic studies to determine if they are operative candidates, patients with delayed-onset or incomplete paralysis may be observed since there is a high likelihood of full facial nerve recovery.
It is often not possible to determine the nature and onset of the paralysis due to a patient’s intubation status or other coexisting injuries. In patients whose history and exam are unreliable, electrodiagnostic studies are important to determine whether surgical decompression would be beneficial.
Fallopian canal fracture pattern
The course of the facial nerve can be anatomically divided into five segments: (1) intracranial, (2) internal auditory canal, (3) labyrinthine, (4) tympanic, and (5) mastoid. The facial nerve traverses through the bony fallopian canal, which can be variably dehiscent. Various fallopian canal fracture patterns have been described ( Fig. 11.1 ). The perigeniculate region between the labyrinthine and tympanic segment is the most common site of facial nerve injury in temporal bone fractures. It is affected in approximately 80%–90% of cases. The next most common site is the mastoid segment making up 10%–20% of cases. , Tympanic segment fractures are the least common, with a prevalence of around 5%. , The perigeniculate region is thought to the be the most prone area to facial nerve injury not only because the nerve is tethered by the greater superficial petrosal nerve as the labyrinthine segment turns into the tympanic segment, but also because the meatal foramen and labyrinthine segment are the narrowest portions of the fallopian canal that can predispose the nerve to ischemic injury from perineural edema. Facial nerve injury from temporal fractures can also result from extratemporal and internal auditory canal fractures.
Electrodiagnostic tests
Electrodiagnostic testing is indicated for patients with immediate-onset or unknown onset of facial paralysis as it can help determine the prognosis of nerve recovery and identify patients who may be candidates for surgical decompression. The utility of electrodiagnostic testing has been studied most extensively in acute facial paralysis resulting from Bell’s palsy . Many facial nerve injuries resulting from temporal bone trauma can have a similar pathophysiology and pathway of nerve degeneration as Bell’s palsy and can be managed similarly. These types of injuries are typically more subtle on imaging and likely result from perineural edema leading to a similar nerve degeneration cascade as that seen in Bell’s palsy. Electrodiagnostic testing could be helpful in these cases. In more severe injuries with obvious nerve displacement or transection on imaging, electrodiagnostic testing may be of limited utility since the extent of the injury may already indicate the need for surgical exploration and possible nerve repair. Electrodiagnostic testing is not indicated in patients with incomplete or delayed paralysis since those patients carry a favorable prognosis. ENOG and electromyography (EMG) are the two most useful electrophysiologic tests available.
Wallerian degeneration, wherein the axon distal to the site of injury degenerates, begins 72 h after injury and continues for about 2 weeks. ENOG estimates the proportion of nerve fibers that have degenerated and is useful between day 4–14 after the onset of injury. Electrodiagnostic testing is not performed before day 4 since it takes 72 h for Wallerian degeneration to begin. Moreover, testing is typically not performed after 14 days since if the ENOG continues to be favorable up to 14 days, the chance of recovery to HB 1 or 2 has been shown to be nearly 100%, and patients are not considered to be candidates for surgery. However, a recent study by Remenschneider et al. argues for longer serial electrodiagnostic testing of up to 2 months for facial palsy resulting from temporal bone trauma since some patients with initially favorable testing can develop degeneration beyond 2 weeks.
ENOG is performed by applying a supramaximal electrical current at the stylomastoid foramen and measuring the response as a compound muscle action potential (CMAP), while EMG measures voluntary motor activity by placing electrodes in the orbicularis oculi and oris muscles. The CMAP in ENOG estimates the number of remaining nerve fibers after Wallerian degeneration that remain viable. The CMAP on the affected side is compared with that of the unaffected side, and a percentage is calculated. If 90% or greater degeneration is reached within 14 days of the injury, an EMG is performed to determine the presence of “deblocking.” Deblocking refers to the process by which asynchronous discharge of actively regenerating nerve fibers and motor units can cause phase cancellation of the overall electrical output and thereby reduce the CMAP amplitude. The presence of deblocking suggests a favorable prognosis for nerve recovery. Patients with deblocking on EMG should be observed despite the degree of degeneration seen on ENOG.
Management
The management of facial palsy depends on the timing and degree of paralysis ( Fig. 11.2 ). Patients with delayed-onset or incomplete facial paralysis should be treated nonsurgically with high-dose corticosteroids. , , Patients can be started on 1 mg/kg per day of prednisone or an equivalent dose of steroid with a 1–3 week taper. As mentioned before, these patients have an excellent prognosis in achieving full recovery.
