There is probably no benign ailment that causes patients more physical and emotional suffering than facial palsy.1–4 The curse of permanent facial disfigurement is a burden to patients who sustain it and, for most, it is difficult to accept. Bell’s palsy can result in a lifetime of facial disfigurement if not treated promptly and properly. The sudden development of facial paralysis constitutes a medical and surgical emergency. The patient must consult an otologist immediately so that medical treatment is initiated within the first few hours after the onset of palsy. Thorough diagnostic evaluation must be completed within a few days and surgical decompression of the nerve accomplished before the 6th day of complete paralysis. In the year 2000, management in this manner of acute facial palsy, one type of which is Bell’s palsy, is the only way that normal facial function can be routinely restored in almost every patient.3 Once irreparable damage to the facial nerve has occurred because of delayed or inadequate treatment, normal facial expression is seldom attained. Unfortunately, few physicians are knowledgeable about Bell’s palsy, and fewer still are trained to perform surgery of the nerve. In addition, most physicians minimize the significance of facial disfigurement to the patient. Although the facts regarding Bell’s palsy have been known and published for several decades, they have been ignored and obscured by unsubstantiated, unscientific misleading opinions. This chapter reviews the known facts, the author’s analysis of the implications of these facts, and the best treatment of acute facial palsy.
Established Facts about Acute Facial (Bell’s) Palsy
- No test is available to determine prognosis before it is too late to avoid risk of a poor result.5
- Without treatment, 29% of patients with acute facial palsy have permanent disfigurement.1
- The cause of acute facial palsy is edema of the facial nerve in the fallopian canal.3, 5
- Recovery beginning within 5 days of the onset results in 100% recovery.1
- Surgery performed while nerve excitability tests are normal results in 100% recovery.5
- In Bell’s palsy, edema involves only the mastoid and tym-panic portions of the nerve in 85%; the labyrinthine portion is also involved in 15%. Herpes zoster oticus involves the labyrinthine segment in 66% of cases.
- Facial nerve decompression surgery can be performed:3, 5–8
a. To reach the entire facial nerve
b. With no injury to the facial nerve
c. Without making a mastoid cavity
d. Without causing hearing loss nor vestibular loss
- In 15% of patients with acute facial palsy, the cause is a neoplasm, and not Bell’s palsy.9–11
* This investigation was supported in part by Ear International, Los Angeles, California
Real Examples of Results
RESULTS WITH ADEQUATE TREATMENT
A 24-year-old woman awoke one morning with a complete right facial palsy and right ear pressure. She had had a cold 1 week before for which she was taking tetracycline, 250 mg qid. She immediately consulted an otologist, who treated her with prednisone, 20 mg tid, and told her that recovery would be good. On the 9th day of palsy, another physician obtained an electromyelogram (EMG), which demonstrated facial nerve degeneration. At the direction of her uncle, a neurosurgeon, she was referred to the author. She was found to have a complete right facial palsy. Hilger nerve excitability test showed no activity on the right. The Schirmer tear test had 1.5-cm saturation of paper on the right. The electric taste test showed no reaction on the right. Audiogram for pure tones and speech discrimination was normal bilaterally.
Electronystagmography (ENG) showed a second-degree left-beating spontaneous nystagmus with normal caloric reactions. Impedance audiometry demonstrated absent stapedius reflexes on her right. Petrous pyramid imaging was within normal limits. The diagnosis of right Bell’s palsy was made. On the 13th day postpalsy, a right facial nerve decompression from the stylomastoid foramen to the cochleariform process was performed. Edema 3+++ of the facial nerve was found extending from the tympanic segment near the midpoint of the footplate to the stylomastoid foramen. Facial motion began to return 7 weeks later. The face moved normally with no evidence of synkinesis when she was examined 14 weeks after surgery. Follow-up examination 9 months later indicated a perfect result, and she was very happy. This patient was very fortunate to have a good result despite delaying surgical decompression until nerve excitability had been lost.
The window of opportunity between the stage of neuropraxia and the development of degeneration and scarring is fleeting and of uncertain length. The availability of a prognostic test to determine which patient will develop axon degeneration before it occurs would be ideal. As much as everyone would like to have such a test, unfortunately none exists. Surgical decompression performed when nerve excitability is normal will eliminate the risk of residual facial deformity. Decompression performed after loss of nerve excitability has occurred will minimize, but not always avoid, permanent poor results. The earlier surgery is done, the better the result, even in cases where the delay is months or years from the onset of complete palsy.
RESULTS WITHOUT EFFECTIVE TREATMENT
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