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| CASE REPORT |
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| Year : 2022 | Volume
: 28
| Issue : 1 | Page : 69-73 |
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Bilateral traumatic delayed facial nerve palsies: Challenges in management
Siti Nazira Abdullah, Azliana Aziz, Nik Adilah Nik Othman
Department of Otorhinolaryngology-Head and Neck Surgery, School of Medical Sciences, Universiti Sains Malaysia Health Campus, Kota Bharu, Kelantan, Malaysia
| Date of Submission | 04-Nov-2021 |
| Date of Acceptance | 03-Dec-2021 |
| Date of Web Publication | 25-Apr-2022 |
Correspondence Address:
Dr. Azliana Aziz
Department of Otorhinolaryngology-Head and Neck Surgery, School of Medical Sciences, Universiti Sains Malaysia Health Campus, 16150 Kota Bharu, Kelantan
Malaysia
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/indianjotol.indianjotol_241_20
Trauma causing bilateral temporal bone fracture has a unique mechanism. The type of fracture can predict the probability of facial nerve palsy. Commonly facial nerve palsy is managed by surgery or conservative management, depending on the onset, grading, and value of the objective electrodiagnostic test. The dilemma arises in our case when the young patient presented with delayed onset, bilateral incomplete facial nerve palsy, whereby the symmetrical monotonous looking can be misleading at initial diagnosis. We discussed several options of test available to give the prognostic value in the case if there is no normal side to be compared to.
Keywords: Abducens nerve palsy, bilateral facial palsy, electrodiagnostic test, temporal bone fracture
How to cite this article:
Abdullah SN, Aziz A, Nik Othman NA. Bilateral traumatic delayed facial nerve palsies: Challenges in management. Indian J Otol 2022;28:69-73 |
| Introduction | |  |
Temporal bone fracture frequently occurred, as high as two-thirds out of all skull base fractures.[1] While bilateral temporal bone fractures involvement is uncommon. A study reported bilateral involvement of temporal bone fracture in 10% of their patient, and 29% out of it presented with bilateral traumatic facial nerve palsies.[2] A temporal bone fracture can result from motor vehicle accident (29%), fall from height (31%), assault (11%), or gunshot wound (6%). The mechanism of insult for bilateral temporal bone fracture can either be unilateral trauma to one side of the head or bilateral trauma to the side of the head (e.g., head crushed in between ground and heavy object).[2] Longitudinal fracture is caused by blows coming from the lateral side of the head, where the impact is resultant on temporal or parietal areas.[3] The transverse fractures resulted from blows coming from the anterior or anterolateral side of the head, which impelled onto frontal or parietal areas.[3]
| Case Report | | |
A 39-year-old Malay gentleman, without comorbidity, was involved in a motor vehicle accident between a car and a motorbike. He was a motorbike rider and was unsure about the mechanism of injury. Posttrauma, he sustained loss of consciousness and bilateral ear bleeding. There was no rhinorrhea or otorrhea. Because of poor glasgow comma scale (GCS) level, he was intubated for airway protection. Upon review, he was still ventilated, whereby the facial nerve function was unable to be assessed. The ear bleeding resolved spontaneously. He was extubated 2 days later. On posttrauma day 4, he complained of inability to close both eyes fully and reduce hearing over the left ear. Upon further assessment, he was diagnosed to have delayed bilateral facial nerve palsy on posttrauma day 6, and therefore was started on a course of oral prednisolone.
On examination, the face showed masked-like facies. There were bilateral facial nerve palsies of Grade IV House-Brackmann, evidenced by the absence of forehead frown, incomplete eyelid closure, loss of nasolabial fold, inability to blow the cheek, poor oral competence, and loss of superficial muscle tension of the neck. Other cranial nerves examination was unremarkable. On otoscopy, the right membrane (tympanic membrane [TM]) was intact but dull looking, with a minimal clot on the roof of the ear canal. There was a small central perforation on the left TM with blood clot seen at the posterior wall of the ear canal. No Battle's sign or raccoon eye sign is seen. There was no bony facial tenderness elicited.
The tympanometry showed Type “B” on the left ear with a large ear canal volume (ECV) of 2.69 ml, while the right ear tympanometry was unable to present any result. The pure tone audiometry (PTA) showed bilateral moderate-to-severe mixed hearing loss.
The high-resolution computed tomography (HRCT) of the temporal bone showed a longitudinal fracture of both temporal bones [Figure 1] and [Figure 2]. The fracture line in the left temporal bone crossed the posterior and anterior wall of the left external auditory canal and extends through the left foramen spinosum and foramen ovale into the sphenoid sinus. While the fracture line seen in the right temporal bone traversed to the mastoid antrum and posterior wall of the right auditory canal. The bilateral incudomalleolar joint was intact; however, bilateral footplates of stapes showed obliteration by soft-tissue densities within. The mastoid air cells were well pneumatized, but there were soft-tissue densities within it, likely representing blood or fluid. The bony wall of meatal, labyrinthine, tympanic, and mastoid segment of the facial canal was intact bilaterally without any fracture line, bony spicules, or dehiscence seen. The magnetic resonance imaging (MRI) of the brain and internal auditory meatus revealed no abnormality of the trigeminal, abducens, facial, and vestibulocochlear nerves bilaterally. | Figure 1: Right longitudinal temporal bone fracture with hemosinus within the mastoid air cells
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 | Figure 2: Left longitudinal temporal bone fracture with hemosinus within mastoid air cells
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Repeated tympanogram 2-month posttrauma showed Type A for the right ear and Type Ad for the left ear with normal ECV bilaterally. Repeated PTA showed improvement over the right ear where it showed mild-to-severe mixed hearing loss, while there was a worsening hearing threshold for the left ear where it showed mild to profound mixed hearing loss. The stapedial reflexes were absent in all ipsilateral and contralateral testing. The electromyography (EMG) test was conducted for him at 3-month posttrauma, which shown some minimal regeneration on the right side of the face, but none on the left side.
Upon follow-up, the patient also complained of bilateral tinnitus which was worst on the left. He started to hear some clicking sound in the right ear during movement. He underwent left ear examination under anesthesia and ossiculoplasty at 3-month posttrauma, where intraoperatively revealed multiple layers of fibrosis encasing the ossicles with the incudomalleolar joint disruption. The facial canal was identified, and no dehiscence was seen. Upon direct stimulation, there was no signal shown in the facial nerve monitor. There was a fracture line seen at the posterosuperior part of the external ear canal, and it was not extending to the facial canal.
Up to the date this case was reported, he was seen at 6-month posttrauma, and the aggressive facial physiotherapy was continuous since earlier on. His facial palsy bilaterally was improved where the right side of the face showed Grade I and left was Grade II. The hearing was improved for the right ear and similar in the left ear. Other than bilateral facial palsy, he also demonstrated bilateral abducens nerve palsy, whereby the right was more severe than the left [Figure 3],[Figure 4],[Figure 5]. In view of the eye deviation persisted more than 6 months with unacceptable degree of deviations and unaidable with prisms, he was subjected to surgery to correct the strabismus. | Figure 3: At rest: Noted the face was symmetry, but there is a loss of bilateral nasolabial fold and monotonous-looking face. There was also bilateral abducens nerve palsy which right was more severe than the left. (picture was captured at 3-month posttrauma)
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 | Figure 4: At the active movement of the face: There was incomplete eye closure bilaterally, at his maximal effort, with the presence of doll's eye phenomenon. (picture was captured at 3-month posttrauma)
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 | Figure 5: At the active movement of the face: Inability to frown the forehead and inability to smile and blow the cheek. (picture was captured at 3-month posttrauma)
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| Discussion | | |
Clinically, temporal bone fracture is suspected when a trauma patient presented with ear bleeding, the cerebrospinal fluid (CSF) leak from the ear, hemotympanum, facial weakness, hearing loss, and Battle's sign.[2],[4] In CT brain showing the base of skull fracture or hemotympanum, HRCT scan of the temporal bone can be performed to delineate fracture of the temporal bone complete structure.[3] HRCT scan can be done as early as few hours for the freshly traumatic patient (provided the patient did not require immediate treatment for the intracranial complication and as late as 21 months after the onset of head injury.[3]
Temporal bone fracture classification was developed following cadaveric observations, where the term of longitudinal, transverse, or mixed temporal bone fracture was established.[5] Another classification using otic capsule sparing or otic capsule violating type of temporal bone fracture was suggested to stratify the risk and sequelae of intracranial complication that might arise.[6] In otic capsule violating type, there is two times risk of developing facial nerve palsy, four times of CSF leak, seven times risk to get profound hearing loss, and more likelihood to have intracranial hematoma or hemorrhage.[6] In a patient with spared otic capsule, conservative treatment can be advocated in case facial nerve palsy and conductive hearing loss developed.[7] Temporal bone fracture also can be classify using petrous and nonpetrous involvement.[4] Petrous type is the fracture line involving otic capsule or petrous apex, where this anatomical region housing the vestibulocochlear organ, facial canal with facial nerve within, as well as carotid artery. For the nonpetrous type, the fracture line can involve the middle ear or mastoid region, which reflects possible injury toward ossicular chain and mastoid air cells. Petrous type of temporal fracture carries a higher risk of mortality or morbidity.[4] From a study, around 80% of cases where the facial canal was able to be delineated in HRCT of the patient with facial nerve palsy.[3] The most common site of involvement of facial canal injury is at the region of geniculate ganglion which showed the occurrence of 54% from the HRCT[3] and 100% in intraoperative findings.[2] At geniculate ganglion, the demonstration of injury is often not reliable in axial cut, as the canal for great superficial petrosal nerve might wrongly interpreted as fracture line.[3] Geniculate ganglion fracture is clearer when seen from coronal view, where distorted contour of geniculate ganglion fossa can be demonstrated.[3]
In our patient, despite having bilateral facial nerve palsies, the facial canal fracture bilaterally was not demonstrable in HRCT, and no soft-tissue lesion or injury was seen in MRI too. Theoretically, when there are no anatomical abnormalities if the facial nerve is seen on imaging, with the presentation of delayed incomplete facial nerve palsy, recovery should be expected. Therefore, time should be given to allow spontaneous recovery where the duration is up to 12 months[8] while awaiting the axonal sprout from the original nerve which is promoted by biochemical changes from the denervated muscle. The outcome of this biochemical activity is the regeneration of motor endplate which in return will activate neuromuscular junction.[9] The denervated muscle can sustain up to 18–24 months before it underwent atrophy and fibrosis.[9] The incidence of bilateral facial canal dehiscence was very low, reported as 5.5% in an operative study.[10] In our patient, there was no detectable dehiscence detected by HRCT temporal, as well as intraoperatively on the operated side during ossiculoplasty surgery. The ability of CT scan to detect facial canal dehiscence was quite low with sensitivity of 11% and specificity of 79%.[11] However, the chances of detection are higher in light microscopy histologic study[12] where the possibility of microdehicnce which cannot be picked up by imaging and direct vision.
There is scarce literature or case report regarding bilateral traumatic facial nerve palsy. Hartley reported a case where the patient had traumatic unilateral temporal lobe extradural hematoma with no abnormality seen on the contralateral side, presented with delayed bilateral lower motor neuron facial nerve palsy, which the HRCT temporal does not show any evidence of temporal bone fracture. However, given the bilateral presentation, they are still investigating the possibilities of nontraumatic cause by checking the other blood and CSF parameters to exclude infection or systemic cause.[8] The EMG done showed bilateral no spontaneous muscle activity bilaterally and dense motor unit interference pattern on both sides, where they concluded about the possibility of posttraumatic demyelinating neuropathy in the absence of temporal bone fracture or new brain injury. In this case, the patient's facial nerve condition was resolved at 3 months to follow-up.[8]
In cases of nontraumatic bilateral facial nerve palsies, other causes must be considered such as Guillain–Barre syndrome, multiple cranial neuropathies, benign intracranial hypertension, brain tumor, and syphilis.[13] Therefore, after performing clinical examination and MRI to visualize the course of the facial nerve, it is advocated to do CSF study and blood test to exclude syphilis, infectious mononucleosis, human immunodeficiency virus, leukemia, sarcoidosis, and Lyme disease.[13]
There are few electrodiagnostic tests that can be used to monitor the prognosis of bilateral facial nerve palsy. Electroneurography (ENoG) is a popular test, and it is most convenient to the otologist and audiologist. Normally, the value of affected side is compared to the healthy side and portrayed in the percentage of function left behind. However, when there is no normal side to be compared to the value of voltage collected at the distal probe can be used to estimate the facial nerve conductivity as a sole value in each side of the face.[14] The sequel of ENoG voltage value can be observed within 3-day posttrauma, up to 21 days, where the prognosis can be the gauge by seeing the pattern of improvement.
The value of the EMG test is higher compared to other tests as it shows a characteristic pattern of the facial muscle action potential in each side of the face without the need to compare to the other side of the face. The other value it showed is the excitability of the nerve, conduction latency, amplitude, duration of response, and the range of submaximal stimulation.[15] All of these parameters can be compared with normative data; therefore, it is the most suitable investigation to determine the prognosis of bilateral facial nerve palsy in our case.
Blink test can be conducted in patient with bilateral facial nerve palsy. The concept of blink test is the same as stapedial reflex where the effector needs intact facial nerve function to complete the response arc. The value of this study is true for a subtle orbicularis oculi weakness when it is difficult to be seen subjectively. The stimulus is given by gently tapping the glabella, and the amplitude and velocity of eyelid blinking are recorded using electronystagmography.[16] In the cases of unilateral facial nerve palsy, the ratio between both two is called blink index. There is the role of this test in our patient as the value of ENoG on each eye can be recorded objectively to monitor the facial nerve function during follow-up without acquiring the blink index itself.
The tests that need a normal side as a guide are nerve excitability test (NET) and maximal stimulation test (MST), and therefore, these investigations are not suitable for our patient. NET measures the minimum voltages required to produce visible muscle contractions both in the normal and affected sides. The difference in excitabilities is compared, and it is considered unimpaired if there is no difference in both values.[15] MST is conducted by determining the greatest threshold of electric that can produce the highest amplitude of action potential of facial muscle on the healthy side. Then, the same value of electrical current is tested on the contralateral same muscle and branch of the facial nerve, whereby the amplitude difference between affected and healthy side is compared.[17]
In a study of the role of stapedial reflex in determining the facial palsy prognosis, positive response within 2 weeks of the paralysis onset showed the recovery of the palsy within 12 weeks, while positive response within 4 weeks showed return of facial recovery within 24 weeks.[18] In this patient with bilateral mixed hearing loss, the stimulus (sound above the hearing threshold to elicit stapedial reflex) can affect the result; therefore, it is not suitable to be carried out. Besides, stapedial reflex is one of the topodiagnostic tests to locate the lesion of the facial nerve, and in our case, since all reflexes were absent, the lesion was located proximal to the stapedius nerve in both ears.
Most of the authors agreed that decompressive surgery is indicated if electroneuronography shows a rapid evolution of degeneration,[3] specifically when the value of ENoG is <10% of the healthy side.[14] Based on another literature review with the clinical diagnosis was comparable to our case, their patient with bilateral traumatic delayed facial nerve palsy, who have been treated conservatively, achieved near-complete recovery by 10 months after the trauma.[19]
Intensive physiotherapy is crucial to maintain the partially denervated muscle bulk to prevent disuse atrophy. However, facial reanimation treatment can be offered to him when the return of facial function is not that tremendous while he is still young and needs to come back to work with the concern of facial cosmesis and its function, especially eye and lip closure. The facial reanimation has been described in the literature for incomplete facial nerve palsy using free gracilis muscle transfer to the predetected bucco-zygomatic residual movement in a single-stage procedure.[20] The other investigation to know the prognosis is facial muscle biopsy where it can show the histologic changes of denervated and regeneration in the muscle.[9] However, the histologic changes must be correlated with the electroneurophysiological testing on the facial muscle so it can guide the surgeon about the choice of facial reanimation depending on the viability of the muscle.[9]
From the literature, there was a 26% occurrence of both sixth and seventh nerve palsy developed in temporal bone fracture.[21] Due to its anatomical course where abducens nerve took a long pathway intracranially, exposed itself to the vast majority of pathology including trauma.[22] Most of the time, abducens palsy showed excellent prognosis where it will achieve recovery with conservative measure, as high as 73% within 6-month posttrauma.[23] Spontaneous recovery was reported more commonly in unilateral cases (84%) than in bilateral cases (38%).[23] Abducens palsy recovery is defined as the presence of complete abduction of the affected eye with an absence of diplopia.[24] In the setting of immediate management of unilateral abducens palsy, occlusion of one (either) eye can be done to alleviate the double vision experienced by the patient, as well as usage of prism lenses.[22] However, after failed conservative treatment, strabismus surgery or Botox injection can be offered to the patient.[22]
| Conclusion | | |
Bilateral delayed traumatic facial palsy renders challenge in determining the prognosis with a wide knowledge of available electrodiagnostic test is crucial, so that the surgeon can select which test can help to decide further management for the patient. The rare occurrence of this condition which is deviant from the common unilateral facial palsy needs more than a subjective facial nerve evaluation whereby it aids in intervention in timely manners, or conservative waiting with reassurance can be issued to the patient by serial correct objective tests results.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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