The most common causes of acute unilateral facial paralysis include Bell’s palsy and trauma to the temporal bone. The physical as well as emotional liability it produces can be devastating. Accurate evaluation and proper management can reduce the sequelae the patient may sustain. Because most facial palsies are associated with some spontaneous resolution, the evaluation of various treatment modalities has been problematic.

Important prognostic and management implications can be determined by means of accurate observation at the time of initial physical examination, with documentation of any degree of facial function that subsequently deteriorates. The House–Brackmann classification grading facial paralysis has been widely accepted and is recommended by the American Academy of Otolaryngology—Head and Neck Surgery (AAO-HNS).1

By definition, patients with Bell’s palsy have idiopathic facial paralysis with no other identifiable cause. Fortunately, most patients with Bell’s palsy have a satisfactory recovery, but 15 to 20% will have significant sequelae. Facial paralysis associated with the unilateral auditory or vestibular symptoms should be evaluated to rule out retrocochlear pathology. In addition, recurrent ipsilateral Bell’s palsy, or one that has a poor outcome after 6 months, should be imaged. Whether all patients with Bell’s palsy require an imaging procedure is debatable.

Patients with facial paralysis secondary to temporal bone trauma frequently have other life-threatening injuries, making facial nerve evaluation a low priority, and simply not possible in other cases. Frequently, the otolaryngologist is consulted several days after the initial trauma, confounding the important assessment of whether the facial paralysis was complete, of immediate onset, or a partial delayed progressive paralysis. The timing of this assessment is critical, especially in extratemporal facial nerve injuries, because surgical exploration is facilitated substantially by intraoperative electrical stimulation, which can only be done up to approximately 3 days after injury.

Temporal bone imaging after traumatic facial paralysis, especially for intratemporal injuries, provides important information required for subsequent decision making. Although axial computed tomography (CT) scan of the head has usually already been performed, it is usually inadequate for evaluation of the temporal bone. CT scan of the temporal bone should be done in 1-mm-thin cuts in axial and coronal planes. The full course of the nerve should be evaluated. Cervical spine injury may prevent coronal CT scanning of the temporal bone. Magnetic resonance imaging (MRI) for evaluation of facial nerve trauma has not been helpful in our experience.

Electrodiagnostic Testing

Electrodiagnostic testing has been advocated as an important element in diagnostic evaluation of facial paralysis. It is used to determine the extent of facial nerve injury and to provide prognostic information for the use of treatment planning. The electrical tests that we have found the most helpful include electroneuronography (ENOG), volitional motor unit potentials on electromyelogram (EMG), spontaneous EMG responses, and Hilger nerve stimulation minimum nerve excitability test (NET). ENOG is used to document the extent of facial nerve degeneration in comparison with the contralateral side. It should not be performed until approximately 3 to 4 days after the development of a complete unilateral paralysis. ENOG provides valuable information up to 21 days after injury. Degeneration to less than 10% function compared with the contralateral side is considered significant and is considered to be the threshold for possible surgical exploration.² Sources of error do occur in ENOG, including electrode placement, skin impedance, masseter muscle artifact, equipment variability, and lack of standardization. Consequently, ENOG results alone should not be considered sufficient in selecting patients for surgery.

In NET, a 2–3 1/2mA difference between sides of stimulation threshold is considered significant. Hilger NET testing is used to collaborate findings on ENOG as well as a possible substitute for ENOG in good prognostic situations. Hilger stimulation is usually quicker, easier to perform, and more economical to the patient than is ENOG testing. The test, however, introduces subjectivity in that it relies on visual detection of response.

EMG responses reflect postsynaptic membrane potentials that may be either initiated at the neuromuscular junction voluntarily or spontaneously across the membrane potential. The presence of voluntary EMG facial motoring unit potentials early on after an acute facial paralysis was noted by Granger³ to be associated with ultimate recovery from a facial paralysis. Motor unit potentials in four or five muscle groups during the first 3 days after onset of an acute facial paralysis was associated with satisfactory outcome in more than 90% of the patients. Thus, the presence of EMG voluntary facial motor unit potentials despite clinically absent motion has important prognostic implications. Spontaneous EMG activity has prognostic implications at 6 months after a major intratemporal facial nerve injury. Fibrillation potentials in the muscle are considered evidence of continuing complete denervation. Polyphasic potentials are considered evidence of regeneration, as well as a good prognostic finding. Reevaluation with EMG at the 6-month point has been selected because this provides adequate time for an intratemporal facial nerve injury to regenerate at the expected 1-mm day growth rate to the facial periphery.

The pathogenesis of Bell’s palsy is obscure. Histologic and clinical data exist to establish that injury to the nerve and loss of impulse conduction result from edema and constriction in an unexpandable bony canal. Prolonged or increased constriction leads to Wallerian degeneration. Viral etiology has been proposed as a cause for Bell’s palsy. In 1975, Adour et al.4 found elevated viral antibody titers in 40 patients with Bell’s palsy and deduced that reactivated herpes simplex virus (HSV) was the probable cause of Bell’s palsy. Subsequent information has also added to the validity that viral etiology is a cause of Bell’s palsy. Animal studies have shown that herpes virus inoculation can produce facial paralysis in animals.⁵ Other studies have shown viral DNA in endoneural fluid and muscle in patients with Bell’s palsy and HSV.

The use of corticosteroids to treat the patients with Bell’s palsy has been widely accepted.⁶ Several studies show more favorable outcome with steroid therapy. It may reduce the risk of denervation if initiated early on. It may prevent synkinesis and progression of incomplete to complete paralysis; it may also hasten recovery. Patients presenting within the first week of facial paralysis are administered corticosteroid therapy consisting of prednisone, 1 mg kg over three equal divided doses for the first week. Patients are then reevaluated during the second week after onset of facial paralysis. If their symptoms are resolving, the prednisone is tapered over the following week. The side effects of steroids are well documented, including hyperglycemia, emotional changes, fluid and electrolyte disturbances, gastrointestinal tract hemorrhage, and aseptic necrosis of the hip.

Adour et al.⁷

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