Post-traumatic bilateral longitudinal temporal bone fracture with bilateral facial nerve palsy: a rare case

Abstract

Facial paralysis is a potentially disabling complication of temporal bone fractures. Although unilateral palsy is commonly encountered, bilateral facial nerve palsy is rare, especially in post-traumatic situations. Other recognised causes of bilateral facial palsy are neurologic, infectious, neoplastic, idiopathic or metabolic disorders. A 25-year-old male patient presented with difficulty in talking, eating and closing eyes for 15 days since a post-vehicular accident. CT of skull showed bilateral longitudinal temporal bone fractures. Bilateral facial palsy was confirmed by clinical and topodiagnostic tests. Patient was given a course of steroids which led to an early improvement on left side followed by a delayed right-sided improvement at 6 months.

Background

Idiopathic facial palsy, commonly referred to as ‘Bell’s palsy’ is the foremost cause of facial paralysis in unilateral cases, whereas bilateral palsy may result from infections, tumours, trauma, vascular disease and idiopathic causes. Unilateral facial nerve paralysis is also a familiar complication of temporal bone fractures. However, bilateral facial palsy is comparatively unusual with trauma; with an incidence of one case every year for 5 million populations, in comparison with unilateral facial palsy cases of 1000–1250 for same figures.¹

Temporal bone fractures are of two types, transverse and longitudinal depending on the direction of the fracture line in relation to axis of the petrous ridge.² Majority (70%–90%) of temporal bone fractures are longitudinal with only 10%–30% identified as transverse.² Only 7% temporal bone fractures cause facial paralysis and 25% of such cases have a complete facial palsy.³ They can also be divided into otic capsule sparing or otic capsule disrupting fractures based on the structures involved in the fracture line; only 2.5%–5.8% of fractures disrupt the otic capsule.⁴ Bilateral facial nerve palsy is as such uncommon, representing less than 2% of all facial palsies and moreover only 1% of bilateral facial palsy cases are post-traumatic.⁵

Facial nerve should be examined immediately after head trauma and before administration of any muscle relaxants. In post-traumatic cases, 27% have immediate onset of facial paralysis, while 73% have a normal initial examination and palsy may manifest later.³ The absence of facial asymmetry often makes bilateral facial palsy difficult to recognise. Thorough clinical history and physical examination coupled with high resolution CT imaging may assist in ascertaining bilateral facial nerve palsy.

The prognosis of facial palsy depends on the onset and the degree of injury and plays a crucial role in further management. Delayed onset facial paralysis has better prognosis and a higher degree of injury reduces the chances of recovery.

Case presentation

A 25-year-old male patient presented to our out-patient department with difficulty in talking, eating and closing eyes for 15 days. He had met with a road traffic accident with closed head injury 18 days back and started to notice the symptoms 3 days later (delayed onset). Patient had no history of loss of consciousness, vomiting, seizures ear or nasal bleed during head injury. At presentation, he was conscious, oriented and had normal vitals. On local examination, patient had an expressionless face, forehead wrinkling was absent and he was unable to close both eyes with maximal effort (figure 1). In addition bilateral nasolabial folds were flattened out and patient was unable to show his teeth and blow his cheeks. Neurological examination revealed bilateral lower motor neuron type facial palsy with House-Brackman Grade IV. There was no haemotympanum, temporal contusion and ecchymosis over mastoid (battle sign), on either side.

Figure 1.

Clinical picture of patient with inability to close eyes on maximal effort.

Investigations

High resolution computed tomogram (HRCT) temporal bone showed bilateral longitudinal temporal bone fracture involving squamous and petrous temporal bone, external auditory canal (EAC), without involvement of fallopian canal (figure 2). Pure tone audiometry revealed bilateral mild conductive hearing loss. Impedence audiometry showed bilateral ‘A’ type graph with absent Stapedial reflex. Schirmer’s test showed 5 mm on right side and 6 mm on left side. Patient also showed taste disturbances on anterior two-third of his tongue. Electrodiagnostic testing confirmed the diagnosis of bilateral facial nerve injury.

Figure 2.

Axial section of high resolution computed tomogram temporal bone, showing both right (black solid arrows) and left side longitudinal fracture (red solid arrows).

Differential diagnosis

Trauma is usually responsible for 5% of all cases of facial paralysis.⁶ Temporal bone fractures are a common cause of unilateral facial paralysis; however, only close to 3% cases of bilateral facial palsies result from temporal bone fractures.⁷ Other common causes of bilateral facial palsy are neurological, infectious, neoplastic, metabolic disorders or idiopathic.⁸

Treatment

Patient was managed conservatively and started on injectable methyl prednisolone 1 gram intravenously twice daily for 3 days and shifted to oral prednisolone at a dose of 1 mg/kg body weight/day. The steroid was gradually tapered off over a period of 18 days. Simultaneously, he was underwent physiotherapy (massage, electrical stimulation and facial exercises), applied lubricating eye drops and bilateral eye patch with Neosporin-H ointment during night. After 3 days of treatment patient started showing deviation of angle of mouth to left and closure of left eye (figure 3) indicating improvement on left side.

Figure 3.

Clinical picture of same patient showing left facial recovery with deviation of mouth to left.

Outcome and follow-up

At 1-month of follow-up, the patient showed complete improvement on left side, but showed minimal improvement on right side. The patient was explained prognosis and oral treatment stopped; however, physiotherapy was continued. At 6-month follow-up, the right side also had improved, with minimal perceptible paresis and no complaints.

Discussion

Fractures of the petrous bone are categorised as transverse and longitudinal type, in relation to their direction with respect to the long axis of the temporal bone. In transverse fractures of temporal bones, fracture line runs vertically through the squamous petrous bone generally proceed from the foramen magnum across the petrous pyramid and the otic capsule. The fracture mostly passes through the jugular foramen, internal auditory canal and foramen lacerum; thus sparing ossicular chain and EAC and is seen in 10% of all temporal bone fractures.^{9 10} These occur from blows to the occipital region. Roughly 30%–50% of patients suffering a transverse fracture of the temporal bone develop facial paralysis and concomitant sensori-neural hearing loss and are eight times more likely to develop cerebrospinal fluid otorrhea.^{11 12} Facial paralysis is severe and prognosis worse in transverse fractures as compared with longitudinal. In addition, meningitis may supervene because of failure of the otic capsule enchondral bone to remodel and heal.¹³

In longitudinal fractures of temporal bone, the fracture line runs horizontally along the long axis of the temporal bone through the squamous portion of the temporal bone, the postero-superior wall of the EAC, involving the mastoid air cells, middle ear and the tegmen mastoideum, tegmen tympani. These longitudinal fractures usually result from a blow to the temporoparietal region. This type of fracture accounts for 90% of all temporal bone fractures, with facial paralysis occurring in 10%–25% of cases.¹⁴ Bilateral traumatic facial nerve paralysis usually occurs in longitudinal temporal bone fractures across the skull base.¹⁵ The longitudinal fracture may cause backward displacement of petrous apex and coronal splitting of sphenoid body, leading to mirror image fracture in opposite side temporal bone.¹⁶

Diamond and Frew divided traumatic facial nerve injury into two broad groups: those with immediate onset of facial paralysis and delayed onset.¹⁷ In immediate onset cases, the facial nerve is directly affected either by laceration or contusion or is transected at the site of fracture consequent to bone splinters, crush or traction to the facial nerve. Nerve decompression is indicated in these types of cases.

Delayed onset facial paralysis manifests itself generally after 4–5 days or longer following injury.¹⁷ The cause of facial paralysis in these cases can be localised oedema, arterial vasospasm, arterial or venous thrombosis or haematoma causing external compression. Here, the nerve is initially intact; however, the prolonged compression leads to partial or complete nerve degeneration. There is a role of steroids in these cases, which act by reducing oedema, swelling and avoiding scar formation. Our case with bilateral facial palsy is explained by this mechanism.

Topodiagnostic tests give an idea of the site of lesion, as branch proximal to the site of injury will be spared. They are lacrimal flow test for greater superficial petrosal nerve, salivary flow test and salivary pH test for chorda tympani and stapedial reflex for nerve to stapedius.

Electro-diagnostic studies can be used in patients with traumatic facial palsy primarily to determine the prognosis.¹⁸ It helps in delineating if there is neuropraxia, axonotmesis, neurotmesis or nerve transection. Neuropraxia is the mildest form and characterised by conduction block due to myelin damage alone and axonal sparing; hence the recovery too is rapid and adequate. Axonotmesis however entails axonal transection with sparing of myelin sheath; wallerian degeneration in the distal axon occurs in next 7 days. Recovery is often reasonable as axon regeneration occurs. Neurotmesis means that the nerve is severed with disruption of axonal and myelin sheath continuity. In facial palsy subsequent to complete nerve transection, surgical intervention with nerve grafting is the only option. Based on these, retrospectively we may consider our patient to be suffering from axonotmesis on right side with neuropraxia on left. There are variety of electrodiagnostic tests for facial nerve, which rely on stimulation of nerve percutaneously adjacent to the stylomastoid foramen.¹⁸ In both nerve excitability test and electroneurography, the comparison of paralysed side is done with normal side in terms of threshold and response, respectively. Thus, it was not possible in our case as ours was bilateral paralysis. The electromyography done on 15th day confirmed the presence of bilateral facial nerve paralysis, with the presence of fibrillation potentials.

HRCT temporal bone aids in localisation of the fracture line and its proximity to the fallopian canal.¹⁶ Immediate onset facial palsy with imaging confirming temporal bone fracture line traversing the canal indicates an imminent surgical intervention. Ours was delayed onset, hence conservative protocol was followed.

Patient’s perspective.

I am very much satisfied and relieved almost completely, after many months of injury.

Learning points.

• Facial nerve is a functionally and psychologically debilitating condition for the patient. Early diagnosis and prompt treatment of the condition is essential.

• Bilateral facial palsy can be difficult to diagnose, especially when associated intracranial injury. For optimal recovery of facial function after injury, it is essential to have early detection, evaluation and intervention.

• In a case with temporal bone fracture, it is important to rule out unilateral or bilateral, facial nerve injury. Delayed onset facial paralysis has favourable prognosis.