Traumatic Facial Paralysis

Intracranial Injury To The Facial Nerve

The intracranial facial nerve, extending from the brainstem to the fundus of the internal auditory canal, is rarely damaged by penetrating trauma because of the excellent protection afforded by the petrous bone and cranial vault. However, severe trauma, as in stretch and shock wave–type injuries, may still occur. Penetrating trauma to this region is likely to be accompanied by extensive central nervous system injury, which must be evaluated and treated first. The evaluation of the injured nerve begins with a careful examination of motor function as soon as possible after the injury is sustained. If the nerve is functional at presentation and becomes progressively paretic, a complete transection injury is unlikely. If the nerve manifests any motion, periodic clinical observation can be used to monitor the status of the nerve. After the onset of complete paralysis, surgery is considered if the nerve shows electrical signs of near-total degeneration.

Intratemporal Injury To The Facial Nerve

The intratemporal facial nerve, extending from the fundus of the internal auditory canal to the stylomastoid foramen, is frequently injured from blunt trauma to the skull that leads to a temporal bone fracture. The intratemporal course of the facial nerve is tightly enclosed by the fallopian canal, leading to increased susceptibility to paralysis from direct trauma. Lack of any space to accommodate edema, which inevitably accompanies soft tissue trauma, leads to further neural injury. An injured nerve may not manifest significant clinical dysfunction initially, but later, once sufficient edema has occurred to prevent axoplasmic flow, the injury manifests. Fisch and others have shown that the area of the fallopian canal with the least expansion room for neural swelling is in the region of the meatal foramen. As most injuries to the facial nerve occur in the perigeniculate area just distal to the meatal foramen, edema in these tight quarters is a critical factor in the pathophysiology of this disorder.

Fractures as a result of blunt trauma have traditionally been grouped into longitudinal and transverse varieties, although fractures are not limited to these two patterns. Fractures with the main fracture line parallel to the long axis of the petrous pyramid are classified as longitudinal ( Fig. 27.2 ), whereas fracture lines perpendicular to the long axis (see Fig. 27.3 ) are considered transverse fractures. Longitudinal fractures are produced by trauma to the lateral aspects of the skull in the temporoparietal region and comprise 80% of fractures in most series. Transverse fractures are produced by trauma to the occipital or frontal regions of the skull and comprise approximately 20% of fractures. ^, Many fractures are oblique or combine elements of longitudinal and transverse fractures. Severely comminuted and complex fractures of the temporal bone are commonly produced by penetrating gunshot wounds of the temporal bone.

A longitudinal fracture (see Figs. 27.2B and 27.4 ) is suspected when a step-off is present in the external auditory canal and is frequently accompanied by blood in the external auditory canal. A perforation or tear of the tympanic membrane may be present, and cerebrospinal fluid (CSF) otorrhea is occasionally seen. Sterile instruments should be used during the examination of the external auditory canal to avoid introducing contamination into the area and producing retrograde meningitis. Conductive hearing loss will usually be present and can have numerous causes. Perforation of the eardrum, hematoma in the middle ear cleft, disruption of ligaments supporting the ossicles in the attic region, and disruption of the ossicular joints all can lead to varying degrees of conductive hearing loss.

A longitudinal fracture often extends through the temporal bone to the foramen ovale. Facial paralysis is seen in only 20% of longitudinal fractures but is the most common cause of facial paralysis in blunt trauma of the temporal bone because of the relative infrequency of transverse fractures. ^, The facial nerve is involved in the perigeniculate region in 90% of cases ^, and less commonly in the mastoid segment by fractures of the posterior external auditory canal ( Fig. 27.5 ). Causes of facial nerve injury in blunt temporal bone trauma, in decreasing order of occurrence, are intraneural hemorrhage, bony fragment impingement, and nerve transection. ^{, ,}

A transverse temporal bone fracture is suspected when a patient presents with sensorineural hearing loss and vertigo accompanied by facial paralysis. The external canal is frequently intact, and no evidence of canal wall discontinuity and hemotympanum may be present ( Figs. 27.3B and 27.6 ). Transverse fractures may also extend into the foramen spinosum or lacerum. These patients have a 50% incidence of facial paralysis, which occurs from damage to the geniculate ganglion region ( Fig. 27.7 ). The primary mechanisms of injury are the same as those for longitudinal fractures, with intraneural hemorrhage being the most common.

The traditional classification scheme, based on anatomical cadaveric studies performed over half a century ago, has been criticized for its lack of ability to predict complications of temporal bone fractures. The traditional classification scheme of temporal bone fractures provides a way to communicate the course and location of a temporal bone fracture but has not been found to be predictive of sequelae. Several authors have proposed new classification schemes with predictive ability. These similar schemes are based on violation of the otic capsule and/or petrous apex. Fractures involving the otic capsule were more likely to result in the complications of facial nerve injury, sensorineural hearing loss, and CSF leak than those that did not. The new classification systems appear to have significant predictive ability for these serious sequelae of temporal bone fractures. Table 27.1 lists the typical features of temporal bone fractures by classification.

Gunshot wounds to the temporal bone region typically produce extensive damage, the degree of which is determined by the velocity of the projectile. Low-velocity civilian projectiles have relatively low energy and produce mainly locally destructive manifestations. In contrast, high-velocity, large-caliber weapons are capable of widespread destruction, with extensive local and regional manifestations produced by the concomitant shock wave. Severe life-threatening injuries, including vascular and intracranial damage, are seen in one-third to one-half of patients and must be stabilized first. Angiography and computed tomography (CT) scans of the head are needed as part of the initial evaluation.

In gunshot wounds to the temporal bone, the incidence of facial nerve injury is approximately 50%, with the vertical segment being the most frequently damaged. ^, The less frequent sites of injury include the tympanic segment, the main trunk just distal to the stylomastoid foramen, and the labyrinthine segment. At the time of surgery, two-thirds to three-fourths of patients were found to have complete transection of the facial nerve ^, ; interposition grafts and transmastoid decompression have been the primary modalities of treatment. Because residual bullet fragments can remain lodged in the temporal bone and become a nidus for infection, a canal wall-down or radical mastoidectomy has been advocated as the approach of choice. Gunshot wounds of the temporal bone frequently result in loss of a segment of the nerve, usually in the vertical portion, requiring interposition grafting for repair. There is also a high incidence of concomitant vascular and central nervous system injuries.

Extratemporal Injury To The Facial Nerve

Facial paralysis after a laceration or iatrogenic injury to the parotid region is best repaired primarily and as soon as the patient’s condition permits. If no loss of nerve substance has occurred, the nerve should be repaired by direct anastomosis. When nerve substance loss has occurred, an interpositional graft should be used. In cases where direct anastomosis or interpositional grafting is not possible, such as after the loss of motor end plates in chronic paralysis, numerous options for reanimation exist ( Chapter 56, Chapter 57 ). The reader is referred to comprehensive articles on the topic.

Patient Evaluation

Cases of trauma to the head and neck should begin with a primary survey assessing the airway, breathing, and circulation. Open wounds should be cleaned, and antibiotic and tetanus prophylaxis should be administered. Once the patient is stabilized, a thorough assessment of facial nerve function can be performed.

The findings elicited from a careful history and physical examination upon the patient’s presentation to the emergency department provide prognostic data and determine appropriate management. Eyewitness accounts of facial nerve function immediately after the injury and of any progression during transport to the emergency department are often unreliable and likely to be fraught with inaccuracy. However, they can still provide important information, especially if an initial examination is not possible due to other life-threatening injuries. An accurate analysis of the facial nerve function might be impossible if the patient has been intubated and sedated as part of the primary survey, but every effort should be made to elicit some sort of facial movement, even a grimace in a comatose patient. Patients with any facial movement after the injury and before the onset of paralysis rarely need surgical intervention. A nerve with diffuse weakness in all branches can be observed clinically and, if some function persists, expectant management can be used. If this situation deteriorates to total paralysis, electrical testing should be used to follow up the nerve to ensure that total degeneration does not occur.

Audiometric evaluation should also be performed as soon as the patient’s condition permits. The type of hearing loss can corroborate the CT scan findings. In one recent retrospective study, it was noted that patients with incomplete facial nerve palsy and conductive hearing loss were more likely to demonstrate improvement in both their hearing and facial nerve function. Additionally, it was noted that the presence of sensorineural loss at presentation did not portend a poor prognosis for facial nerve recovery. If surgical exploration is warranted, the severity of the hearing loss in the affected ear guides the surgeon in determining the best approach and serves as a baseline with which to compare the postoperative results.