Intratemporal Bone Trauma

Updated: May 31, 2018
Author: Noah Massa, MD, FRCSC; Chief Editor: Arlen D Meyers, MD, MBA 



Of all the cranial nerves, the facial nerve is the most susceptible to injury. This nerve travels a complex course through the temporal bone, confined within a prolonged bony canal that is, in some cases, not much greater in diameter than the nerve itself. The susceptibility of the nerve to paralysis can be attributed to these anatomic factors. Facial nerve paralysis can result in devastating social consequences for the patient.

The seventh, ie, facial, nerve contains motor, sensory, and parasympathetic fibers. Among its functions are the vital control of facial expression, taste to the anterior two thirds of the tongue, and salivary-gland and lacrimal-gland secretion.

More than 40 causes of facial paralysis are known. Trauma is a distant second to idiopathic or Bell palsy as a cause of facial nerve paralysis. In an overview of 1322 patients with facial paralysis, May (1983) reported that 16% were caused by trauma.[1]

Although the facial nerve is susceptible to trauma along its entire length, the temporal bone is the most common site of trauma resulting in facial paralysis. The objective of this article is to review facial paralysis resulting from trauma to the intratemporal bone.



Approximately 5% of people who have trauma have temporal bone fractures. These fractures are traditionally classified with respect to the axis of the petrous ridge and include longitudinal, transverse, and mixed (or oblique) types. Longitudinal fractures are most common (70-80%), followed by transverse (10-20%) and mixed (10%) fractures. Facial paralysis most commonly occurs after transverse fractures of the temporal bone (50%). However, paralysis also occurs after longitudinal fractures (25%).

This traditional classification system was based on impact studies on cadaveric skulls.[2] Better visualization of temporal bone fractures using modern CT scan imaging has highlighted the limitations of this classification scheme. Recommendations for alternative classifications have been made, particularly with reference to whether the fracture is otic capsule sparing or otic capsule violating (2-6%).[3, 4] The clinical relevance of this classification system is emphasized by the observation that facial paralysis is twice as likely to occur in patients with otic capsule–violating fractures. However, 14% of patients with otic capsule sparing fractures still have facial paralysis.[3]

Given the propensity in the literature to reference fractures as longitudinal, transverse, and oblique, this traditional classification system is used for discussion purposes.


Temporal bone fracture caused by blunt closed-head trauma is by far the most common cause of traumatic facial paralysis. Motor vehicle accidents are the most common mechanism of injury (31%), followed by assaults, falls, and motorcycle accidents. Blunt extratemporal trauma to the face is a rare cause of paralysis and can be delineated from intratemporal bone trauma because it often involves only specific branches of the facial nerve.

Penetrating injuries (eg, lacerations, stab wounds) generally result in lesions to the facial nerve distal to the stylomastoid foramen. However, penetrating injuries from gunshot wounds can injure both the intratemporal and extratemporal portions of the facial nerve.

Iatrogenic injury during otologic or parotid surgery and injury caused by birth trauma represent rare but important causes of traumatic facial paralysis.


In a comprehensive review of the literature, Chang and Cass (1999) reported surgical findings of 4 types of facial nerve pathology after temporal bone trauma.[5] The authors' review of 67 longitudinal fractures from 3 studies revealed that 76% of fractures had bony impingement or intraneural hematoma, and 15% had transection. The remainder had no visible pathology except neural edema. In contrast, of 11 transverse fractures reviewed, 92% were transected, and 8% had bony impingement.

A study by Choi et al found pneumolabyrinth in 8% of ears with temporal bone fracture, including in 48.4% of otic capsule–violating fractures.[6]



Patients with multisystemic trauma require thorough evaluation for possible facial nerve injury. This examination is often relegated an inferior priority given the frequency of injuries more serious than this or life-threatening injuries (eg, intracranial-hemorrhage).

The mechanism and details of the traumatic forces involved are important historical factors. Substantial blows to the head are necessary to injure the temporal bone. The region of the head that received the blow is also important. Frontal and occipital blows are most likely to result in transverse temporal bone fractures, whereas lateral blows are most likely to produce longitudinal fractures.

The onset and progression of facial paralysis are opined to be important, although these are difficult to determine unless thorough assessment is performed at initial presentation. Patients with nerve transection present with immediate-onset of paralysis and have a poor functional outcome. Hematoma and impingement injuries may have a delayed manifestation and often indicate an improved prognosis.

Hearing loss or vertigo suggest temporal bone trauma and can be associated with facial nerve injuries.

Physical examination

After the patient's condition is hemodynamically secured and the acute injuries are stabilized, he or she should be evaluated early for signs of facial nerve injury. The examination should include assessment of facial nerve function and hearing status, including otoscopy to evaluate the middle ear.

Initial evaluation of a patient with trauma is often delayed because emergency and life-threatening injuries are treated. However, even in an unconscious patient, gross facial function can be elicited as a grimace in response to painful stimuli. Particular attention should be paid to any facial nerve function at presentation.

Otoscopic examination of the external auditory canal (EAC) may reveal a step deformity or bleeding from a lacerated canal wall. Examination of the tympanic membrane and middle ear for hemotympanum and perforation is essential. If a perforation of the tympanic membrane is present, the ear may have bloody and/or clear (CSF) discharge. Any of the above otoscopic findings suggests a longitudinal fracture of the temporal bone and potential for facial nerve injury. Nystagmus secondary to vestibular system injury is another sign of temporal bone fracture.

In a patient who is conscious and stable, thorough examination of facial nerve function, including topography, can be performed to indicate the location of the lesion. This examination may involve tympanometry with testing of the stapedial reflex, Schirmer to evaluate tear production, and chemical gustometry to test taste. In practice, these tests are not readily available on an urgent basis, they are difficult to perform in an acutely injured patient, and their results may not be predictive of the site of injury. Therefore, their usefulness is questionable.

Tuning-fork tests (eg, Weber or Rinne tests) can be performed easily in an emergency department, and its findings may substantiate conductive hearing loss. Conductive hearing loss is most commonly associated with longitudinal temporal bone fractures, whereas transverse fractures are most commonly associated with sensorineural loss.


Surgical indications for posttraumatic intratemporal facial paralysis remain controversial and poorly defined. Most patients with intratemporal trauma causing facial paralysis recover fully without intervention. The authors know of no randomized controlled studies of surgical versus nonsurgical treatments for facial paralysis. In general, recommendations for exploration of the facial nerve are contentious and based on personal opinion and data from case series to identify poor prognostic factors and define the population most likely to benefit from surgery.

Paralysis versus partial paresis is probably predictive of the degree of recovery. If a patient has incomplete paralysis, the likelihood of full recovery of normal facial function is excellent.

No data suggest that surgical intervention increases the likelihood of full recovery when facial paralysis is delayed in onset. The vast majority of patients with delayed-onset facial paralysis have recovery of normal facial function. Patients with immediate onset of a complete facial paralysis have a relatively poor prognosis, often due to transection of the facial nerve and the time of injury. The difficulty arises in that approximately 50% of patients with immediate-onset, complete paralysis recover normal or near-normal facial function.

Electrodiagnostic testing, primarily electroneuronography (ENoG) as Fisch (1981) popularized, has been used to determine which patients will not have full recovery.[7] Scientific data to justify the use of ENoG criteria to define which patients should be offered surgery is limited. Extensive data from nonrandomized studies are available to support use of ENoG to treat Bell palsy. Data on its use to treat traumatic facial paralysis is only emerging and confined to case series. Similar to the data for Bell palsy, findings in this setting suggest a favorable prognosis in patients with degeneration of less than 90% within 6 days or less than 95% within 14 days after their injury. More than 90% of individuals without poor prognostic factors are likely to recover normal facial function.

Traditional electromyography (EMG) performed by using intramuscular recording electrodes is probably most useful if more than 2 weeks has passed after the paralysis.

A management algorithm has been developed to integrate these prognostic factors to determine when surgery is warranted, as depicted in the image below.

Proposed algorithm for the management of intratemp Proposed algorithm for the management of intratemporal injury to the facial nerve.

As CT scan resolution technology has improved, more recent studies take into account CT scan findings when considering surgical exploration.[8, 9] Although ENoG remains the most accurate test for guiding treatment, it is often unfeasible to perform in the multiply injured patient or is not readily available.

Iatrogenic paralysis is unique among the causes of traumatic facial paralysis. When paralysis occurs after temporal bone surgery (mastoidectomy), repeat exploration of the surgical site is indicated. Nerve decompression and/or repair of the nerve are performed as the findings dictate.

Relevant Anatomy

The facial nerve is a complex nerve with motor, sensory, and parasympathetic contributions. Motor fibers originate in the facial nucleus and innervate the posterior belly of the digastric muscle, stylohyoid muscle, stapedius muscle, and muscles of facial expression. The facial nerve carries cutaneous sensory fibers from the EAC, tympanic membrane, and areas of the external ear and postauricular region are carried to the fasciculus solitarius. The geniculate ganglion represents the nucleus of the sensory root of the facial nerve. Parasympathetic fibers originating in the superior salivatory nucleus and entering the facial nerve as the nervus intermedius innervate the lacrimal, submandibular, and sublingual glands, as well as glands of the nose, sinuses, and palate. Also included in this portion of the facial nerve are special sensory fibers carrying taste from the tongue.

Given the different fibers carried in the facial nerve, some authors advocate a complete topodiagnostic assessment of extrafacial branches of the facial nerve to identify the site of lesion. With this in mind, the facial nerve can be divided into 6 segments. From proximal to distal, they include the intracranial, meatal, labyrinthine, tympanic, mastoid (ie, vertical), and extratemporal segments. Two of these segments are outside the temporal bone. In the proximal portion, the intracranial segment extends from the brainstem to the internal auditory canal (IAC). In the distal portion, the extratemporal segment extends from the stylomastoid foramen to the muscles of the face.

The intratemporal segments are of particular relevance in temporal bone trauma. The meatal segment extends from the porus of the IAC to the meatal foramen. The meatal foramen represents the narrowest (0.68 mm) portion of the facial canal. The nerve runs superior to the transverse crest and anterior to the vertical crest (Bill bar) of bone at the distal IAC before entering the facial canal. The shortest segment, the labyrinthine segment (3-5 mm), extends from the meatal foramen to the geniculate ganglion. Its initial lateral course is followed by an anterior curve between the basal turn of the cochlea and the vestibule.

The end of the labyrinthine segment is marked by the formation of the geniculate ganglion. In this region, the greater superficial petrosal nerve carrying fibers to the lacrimal gland leaves anteriorly from the ganglion by means of the hiatus of the facial canal. The greater superficial petrosal nerve travels anteriorly, carrying parasympathetic fibers, for instance, to the lacrimal gland.

The Schirmer test for tear secretion is purportedly useful to assess the function of this branch. Adequate tear secretion implies a site of lesion distal to the geniculate ganglion.

The tympanic segment courses in a posterior direction following a 40-80° turn of the first genu at the geniculate ganglion. The facial nerve then enters the medial tympanic cavity, running in the facial canal and curving around the oval window niche. At this point, the nerve runs superior to the oval window niche where the bone of the facial canal can be thin and where it may be dehiscent in as many as 55% of individuals. The distal tympanic segment lies just anterior and inferior to the lateral semicircular canal, where the nerve curves through its second genu and begins its vertical descent. Most intratemporal traumatic injuries occur in the perigeniculate region and labyrinthine segment.

The mastoid (ie, vertical) segment of the facial canal is the longest of all segments (10-14 mm). It extends from the pyramidal process to the stylomastoid foramen. The stapedius muscle lies medial to the facial nerve and receives its motor branch in this segment. Tympanometry with stapedial-reflex measurement is performed to assess the function of the facial nerve at this level. Lastly, the chorda tympani nerve, which carries efferent fibers to the submandibular and submaxillary glands and special afferent (taste) fibers from the tongue branches from the facial nerve in this segment. Chemical and/or electrical gustometry can be used to assess the sense of taste on the anterior two thirds of the ipsilateral tongue.

Classic longitudinal fractures extend from the temporal squamosa along the roof of the EAC and petrous apex to the foramen lacerum, as depicted in the 1st image below. The fracture injures the tympanic membrane, facial canal, and middle ear, resulting in ossicular disruption and conductive hearing loss, as depicted in the 2nd image below. Because the otic capsule is made of dense bone, the fracture line often courses around this structure.

Fracture pattern of longitudinal temporal bone fra Fracture pattern of longitudinal temporal bone fractures. The axis of fracture is parallel to the petrous ridge after a person receives lateral blows to the skull (arrow).
Potential fracture plane and structures involved i Potential fracture plane and structures involved in longitudinal temporal bone fractures.

In contrast, transverse fractures extend from the jugular foramen in an anterolateral direction across the petrous pyramid ending at the foramen spinosum or foramen lacerum, as depicted in the 1st image below. In its course, the fracture line may traverse the otic capsule, resulting in sensorineural hearing loss, as depicted in the 2nd image below.

Fracture pattern of transverse temporal bone fract Fracture pattern of transverse temporal bone fractures. The axis of fracture is perpendicular to the petrous ridge extending to the foramen magnum after a person receives frontal or occipital blows to the skull (arrow).
Potential fracture plane and structures involved i Potential fracture plane and structures involved in transverse temporal bone fractures.


Attention must be paid to other life-threatening complications of trauma before intervention for facial nerve injury is started.

Patients without the poor prognostic factors (see Indications) have an excellent probability for good recovery. No data suggest that surgical intervention increases the likelihood of full recovery when the facial paralysis is delayed. Normal or near-normal facial function (ie, House-Brackmann grade I or II) can generally be expected in more than 90% of patients undergoing conservative treatment.

Moreover, a prospective study by Thakar et al found that even in the presence of unfavorable electrophysiologic characteristics, conservative treatment can successfully restore facial nerve function in patients with nondisplaced temporal bone fractures. Patients in the study, 26 out of 28 of whom had documented nondisplaced fractures and all of whom had a response to electroneurography [ENoG] of less than 5%, underwent 3 weeks of treatment with prednisolone, 1 mg/kg. Initial signs of clinical recovery were seen in all but one patient by 12 weeks and in 100% of patients by 20 weeks. By 40 weeks, House-Brackmann grade I/II facial nerve function had been achieved in 27 patients.[10]

Surgical intervention is not indicated in facial paralysis secondary to birth trauma or extracranial blunt trauma to the face. In both these instances, spontaneous and complete recovery is typical.



Imaging Studies

See the list below:

  • CT scanning

    • A high-resolution CT scan of the temporal bone can reveal findings diagnostic of temporal bone fracture, as depicted in the images below.

      High-resolution CT scan of the temporal bone demon High-resolution CT scan of the temporal bone demonstrates a longitudinal temporal bone fracture. Number sign marks the lateral extent of the fracture.
      High-resolution CT scan of the temporal bone demon High-resolution CT scan of the temporal bone demonstrates a transverse temporal bone fracture. Number sign marks the lateral extent of the fracture.
    • Scans reveal multiple fracture lines in most cases, and they may reveal bony impingement of the facial canal.

    • Whenever possible, direct axial and coronal scanning should be performed with 0.6 mm sections and with bone-algorithm views.

    • The integrity of the ossicular chain may also be evaluated with an optimal CT scan.

  • Magnetic resonance imaging

    • Gadolinium-enhanced MRI has been used to study facial nerve injuries after trauma.

    • MRI is often warranted to evaluate concomitant intracranial injuries.

    • The usefulness of MRI is limited because global signal enhancement makes interpretation of images difficult.

Other Tests

See the list below:

  • Audiometric testing: When the patient's condition permits, formal audiologic testing should be performed to characterize the extent of hearing loss. The findings help in determining the surgical approach if and when surgery is necessary.

  • Electrophysiologic assessment of the facial nerve: The most common electrodiagnostic tests used are ENoG and EMG.

Histologic Findings

On a histopathologic level, most injuries to the facial nerve occur in the labyrinthine segment and perigeniculate region, resulting in anterograde and retrograde axonal degeneration. This area includes the narrowest portion of the facial canal, or the meatal foramen, which measures 0.68 mm in diameter. Edema or hematoma in this confined space may result in ischemic injury to the facial nerve secondary to compression of its vascular supply. In some patients, formation of intraneural fibrosis at the site of injury impedes distal regeneration of axons, resulting in poor functional recovery though proximal regeneration seems to occur.

Ulug et al described surgical findings in 11 patients with complete facial paralysis after temporal bone fracture treated with surgical exploration.[8] Fibrosis at the geniculate ganglion was seen in 5 fractures, impingement of the facial nerve by bone spicules at the geniculate ganglion in 2 fractures, disruption or laceration at the origin of the greater superficial petrosal nerve in 2 fractures, and perigeniculate ganglion edema in the remaining 2 fractures.



Medical Therapy

Patients with traumatic facial paralysis are often treated empirically with a short course of oral steroids. In contrast to idiopathic facial paralysis or Bell palsy, no studies confirm or dispute the utility of steroid treatment after traumatic facial paralysis. The potential risks of using corticosteroids in a patient with multiple trauma and possible risk of infectious complications must be weighed against the unknown probability for benefit in decreasing the risk of permanent facial paralysis. A typical course of high-dose prednisone is 1 mg/kg for up to 10 days followed by a tapering regimen.

Proper eye care with use of artificial tears and night patching should be implemented as long as eye closure is impaired.

Preoperative Details

Because multiple injuries are possible at any point along the course of the facial nerve, it may have to be entirely decompressed from the IAC to the stylomastoid foramen. Localization of the site of injury should be attempted preoperatively.

The choice of surgical approach is primarily based on whether the patient has a loss of auditory or vestibular function allowing sacrifice of the labyrinth. Needle EMG may be used intraoperatively early after an injury has occurred to test integrity of the facial nerve.[11, 12, 13]

Intraoperative Details

Patients with intact auditory and vestibular function should undergo exploration of the facial nerve by means of a combined approach involving the mastoid, middle ear, and middle cranial fossa under general anesthesia. Minor variations in technique are used. The following discussion provides a general overview.

After a standard postauricular incision is made, complete mastoidectomy is performed. The nerve is exposed throughout its vertical segment to the stylomastoid foramen. General surgical principles involve the use of diamond-tipped burrs of various sizes and copious irrigation to remove bone and prevent additional thermal trauma to the facial nerve. The final thin layer of bone overlying the nerve is removed with blunt elevators. The benefit of performance of neurolysis of the nerve sheath to decompress the nerve is debatable.

The tympanic cavity is approached by means of the facial recess, and assessment of the integrity of the ossicles is then possible. Visualization of the tympanic course of the facial canal is also undertaken. Bone overlying the tympanic segment is removed to the cochleaform process. Because the canal bone is thin, only the smallest diamond burr is used. Removal of the incus and amputation of the head of the malleus is likely necessary to expose the tympanic segment of the nerve.

A middle cranial fossa approach is undertaken to expose the labyrinthine portion of the facial nerve. A posteriorly based trap-door incision is made above the ear as a separate cut or as an extension of a postauricular incision. The skin is elevated to expose temporal muscle fascia, which is harvested for later closure of dural defects. The muscle and underlying periosteum are then elevated.

A temporal bone flap is then elevated. A properly positioned flap is one in which the base parallel to the middle cranial fossa floor, with two thirds of the square anterior and one third posterior to a line drawn vertically through the EAC. Great care must be exercised when the flap is elevated to avoid injury to branches of the middle meningeal artery, which are often embedded in the inner table. Dural elevation from the floor of the middle cranial fossa proceeds from posterior to anterior to avoid avulsion injury to the geniculate ganglion. Elevation continues until the petrous ridge is reached and until the arcuate eminence and greater superficial petrosal nerve are identified.

Bone dissection begins with exposure of the greater petrosal nerve and geniculate ganglion until connection is made with the previous tympanic dissection. Drilling then continues posteriorly to the arcuate eminence to expose otic capsule bone and the blue line of the superior semicircular canal. The IAC is identified and exposed in the bifurcation of the angle between the superior semicircular canal and the greater superficial petrosal nerve. The labyrinthine segment of the facial nerve is followed to the geniculate ganglion. Careful dissection is essential to avoid the superior semicircular canal and the basal turn of the cochlea in this region.

Once entirely exposed, the nerve can be examined and tested for integrity or injury. Neurolysis and/or nerve repair may be performed at this stage, depending on the degree of injury to the facial nerve. If primary repair is not possible in the case of nerve transection, a rerouting procedure or interpositional grafting can be used.

A piece of bone flap is used to cover defects made in the tegmen tympani and IAC to prevent herniation of the temporal lobe into the middle ear. In addition, the previously harvested temporalis fascia is used to seal any dural defects that were created. Repositioning of the temporal bone flap and layered closure are then accomplished.

Exploration of the facial nerve by means of the translabyrinthine approach is performed when hearing and vestibular function is lost. This approach offers access to the entire intratemporal course of the facial nerve with substantially decreased morbidity.

After a postauricular incision is made, the mastoid and tympanic portions of the facial nerve are exposed as described above. Complete labyrinthectomy follows to expose the IAC.

Blunt removal of bone over the nerve begins at the IAC by extending along the labyrinthine segment to the geniculate ganglion. Distal dissection to the stylomastoid foramen is then performed. Lastly, fascia and muscle may be used to fill the middle ear by plugging the auditory tube orifice, and the mastoid is obliterated with harvested abdominal fat.


Patients and families must be counseled that improvement in function may not be realized for as long as a year after surgery. In the case of repaired transection injuries, initial recovery may occur at 6 months with continued recovery for as long as 24 months after surgery. Follow-up visits are periodically scheduled throughout the recovery period. Ongoing eye care is essential during the postoperative healing phase.


The main deterrence to decompression of the facial nerve is further injury to an already traumatized nerve that prolongs or possibly prevents nerve recovery. Only surgeons experienced with surgery in the temporal bone should perform facial nerve decompression.

Additional complications include dural tears, conductive or sensorineural hearing loss, vestibular function loss, persistent CSF leaks, and meningitis. These complications can also occur secondary to temporal bone fracture alone. Dural tears and subsequent CSF leaks are most likely incurred during elevation of the middle fossa dura. Repair should be performed intraoperatively by using temporalis fascia with or without augmentation with fibrin glue.

Meningitis is a rare complication of persistent CSF leaks, occurring in approximately 8% of patients. Prophylactic antibiotics may not be effective in lowering this rate. However, antibiotics are usually given perioperatively. Conductive hearing loss can result from ossicular disruption during dissection or from temporal-lobe herniation after surgery. Direct injury to the cochlea, vestibule, semicircular canals, or internal auditory vessels may produce permanent sensorineural hearing loss and/or vestibular function loss.

Outcome and Prognosis

Exploring the facial nerve after traumatic paralysis remains controversial. Further studies are necessary to resolve the issue over which patients should undergo decompressive surgery to recover facial nerve function.

With nonpenetrating trauma, the overall rate of good recovery (ie, House-Brackmann grade 1 or 2) after decompression of the facial nerve is traditionally 50%. Previous data suggested an equal probability of recovering good function with nonoperative management when all injuries and presentations are considered.

For example, McKennan and Chole (1992) questioned the benefit of surgery.[14] Exploratory surgery and repair was performed on 14 patients with immediate-onset complete facial paralysis. Nerve transection was found in 8 patients. However, only 4 were monitored longer than 1 year after surgery. Of the 4 patients, 2 improved to moderately severe dysfunction (ie, House-Brackmann grade 4), and the remaining 2 continued to have total paralysis (ie, House-Brackmann grade 6).

Authors of small case series such as these that lack adequate follow-up questioned the utility of surgery among patients with nerve transection. Severe injuries, such as nerve transection, were thought to carry a poor prognosis irrespective of surgical intervention and repair. With this possibility in mind, the merits of surgical decompression need further evaluation, especially when the clinically significant risks and complications of an intracranial procedure are considered.

Recent authors profess the utility of surgery in specific situations, especially when a severance of a nerve is suspected. Although the overall incidence of transection is low, the outcome is undoubtedly poor without intervention.

For example, in a prospective case series of 10 patients with 11 temporal bone fractures, decision for surgical intervention was mainly based on high-resolution CT scan and lack of regeneration potentials on EMG. In this series, no nerve transections were encountered. After surgical exploration and decompression, 5 fractures recovered to House-Brackmann (HB) grade 1, 4 patients recovered HB grade 2, and 2 patients recovered HB grade 3.[8]

In a retrospective study, Darrouzet et al (2001) examined 115 patients with posttraumatic facial paralysis.[15] Patients with immediate and electrophysiologically severe facial paralyses with a clear fracture line on the fallopian canal on CT scans were treated with surgery as soon as possible. Patients with delayed or severe facial paralyses and a mixed electrophysiologic pattern were treated medically. Patients with severe facial paralyses without a clearly visible fracture line on CT underwent electrophysiologic and clinical monitoring with the option of late surgery if they did not recover. Of 65 patients who underwent surgery, 52 (80%) had immediate severe paralysis, 2 (3%) had delayed-onset paralysis, and 11 (17%) had unknown delay-associated paralysis. Nerve transection was found in 9 patients (14%). After 2 years of follow-up, 61 patients (94%) had a grade 1-3 recovery. A grade 4 recovery was observed in 4 patients; no patients recovered to a grade 5 or 6 level.

In what appears to be a related article to this study, the functional outcome of 64 cases of facial paralysis following temporal bone fracture was better described.[9] Based on a decision algorithm combining CT scan findings and electroneuronography, 38 patients were given medical treatment and 26 underwent surgery. Normal or near-normal facial nerve recovery (HB 1-2) were obtained in 63% of medically treated patients and 39% of surgically treated patients. Grades 3-4 were obtained in 13% of medically treated patients and 42% of surgically treated cases. In addition, the authors concluded that grade 3 is the best obtainable result after nerve anastomosis.

In addition, data have also challenged the timing of surgery. Initial beliefs held that surgery should be performed within 2-3 weeks after injury. However, because most patients have multisystemic trauma, surgery for facial nerve decompression within this window is not feasible.

Quaranta et al (2001) retrospectively reviewed outcomes after late facial nerve decompression.[16] All 9 patients satisfied traditional electrophysiologic criteria and were operated on 27-90 days after trauma. Normal or near-normal (HB 1-2) facial function was achieved in 7 (78%) after more than 1 year of follow-up. The remaining 2 patients, operated on 3 months after trauma, obtained grade 3 recoveries. The authors concluded that, in patients who cannot undergo surgery early and who present at 1-3 months with more than 95% denervation on ENoG, facial nerve decompression may still be beneficial. However, studies such as this lack a control group; therefore, knowledge about the potential for recovery of such patients when treated medically or untreated is lacking.

A study by Liu et al reported good outcomes from extended subtotal facial nerve decompression performed through the transmastoid approach in patients with facial palsy after temporal bone fracture, but indicated that such surgery should be performed within 8 weeks following the causative trauma. Of the 12 patients who underwent surgery within 8 weeks of trauma, 11 of them (91.7%) achieved complete or near-complete recovery from facial palsy, while of the six patients who underwent decompression between 9 and 14 weeks after injury, only four (66.7%) attained complete or near-complete recovery.[17]

Future and Controversies

Despite emerging studies, the management of intratemporal facial paralysis remains controversial. Data with regard to patient-selection criteria and the benefit of surgical intervention remain inconclusive.

Further controlled studies in which algorithm-based, as depicted in the image below, patient-selection criteria are used will help define the role of surgery.

Proposed algorithm for the management of intratemp Proposed algorithm for the management of intratemporal injury to the facial nerve.

Furthermore, with further improvement in CT scanning and MRI technology, imaging may allow for a noninvasive determination of the integrity of the facial nerve and/or the extent of injury. This ability might facilitate proper selection of patients who may benefit from exploration or repair of a transected facial nerve.