Bell's palsy is the most common etiology of facial paralysis. This unilateral facial disorder is also known as idiopathic facial palsy, since its etiology has not yet been rigorously proved.
"Aided by developments in molecular biology techniques, an increasing number of investigators have reported evidence for a viral etiology in many cases of 'idiopathic' facial paralysis," according to C.A. Bauer and N.J. Coker ("Update on Facial Nerve Disorders," Otolaryngology Clinics of North America, 29: 445-454).
"Sufficient clinical, laboratory, magnetic resonance imaging, and pathology data have accumulated to add veracity to the hypothesis that herpes simplex causes Bell's palsy," concluded K.K. Adour and his associates.1
Their study concludes that a combination of acyclovir (anti-viral) and prednisone (steroid) medicine is superior to prednisone alone in treating Bell's palsy. Perhaps then the best advice we can give the acute patient with Bell's palsy is to seek a prescription from their physician for these two drugs immediately in order to mitigate any long-term sequelae as much as possible.
In an interesting epidemiological study, J.N. Bleicher et al. divided facial paralysis etiologies into five major classifications: idiopathic, infectious, neurologic, neoplastic, and traumatic.2 This gives credence to the contention that all facial palsy is not necessarily Bell's. Etiologies include as vestibular schwannoma (acoustic neuroma), Ramsay-Hunt syndrome (herpes zoster oticus), pregnancy, sarcoidosis, temporal bone fracture (trauma), and Lyme disease.
Bell's palsy is a single event causing damage to the facial nerve (CN VII) inside the temporal bone, not an ongoing disease process.
The degree of compression and the length of time that compression is sustained determines the degree of damage to the facial nerve.
In a natural history study published in 1982, D. Peitersen investigated spontaneous recovery in 1,011 patients with Bell's palsy over a 15-year period who were given no specific medical treatment. All of the patients were followed until normal function was restored or one year had passed. His results indicated that "71 percent recovered normal mimical function of the face, 13 percent had insignificant sequelae, and the last 16 percent had permanently diminished function."3
Because such a high percentage will recover spontaneously, it makes sense to focus our efforts on educating the acute patient but actually treating only that last 16 percent following the acute phase of peripheral nerve damage to CN VII.
An evoked electromyography diagnostic test, if done within three to 21 days of the period of onset, can provide an accurate prediction of expected recovery in Bell's palsy.4 Most primary care physicians appear ignorant of this test, much to the disservice of the patient.
If all patients with Bell's palsy received this test in a timely manner, we would have a clearer idea of prognosis.
In J. Moldaver's chapter in The Facial Palsies, he states that the facial muscles "generally survive much longer than the other skeletal muscles after denervation. Some of them have survived up to 15 to 20 years after being deprived of their motor nerve supply."5
Surgeons who do facial reanimation surgery know this.6
They may wait 12 to 18 months before performing a nerve graft procedure following acoustic neuroma surgery, in which the facial nerve was said to have been left intact but complete palsy resulted anyway. This is in hope that spontaneous recovery will occur. If it does not, a nerve graft procedure can restore some "power" to that side of the face.
1. Adour, K.K., Ruboyianes, J.M., VonDoersten, P.G., et al. (May 1996). Bell's palsy treatment with acyclovir and prednisone compared with prednisone alond: A double-blind, randomized, controlled trial. Ann Otol Rhin & Laryngol, 105: 371-378.
2. Bleicher, J.N., Hamiel, S., Gengler, J.S., et al. (June 1996). A survey of facial paralysis: Etiology and incidence. Ear Nose & Throat, 75: 355-358.
3. Peitersen, D. (October 1982). The natural history of Bell's palsy. American Journal of Otolaryngology, 4: 107-111.
4. Beck, D.L. & Benecke, J.E. (1993). Electroneurography: Electrical evaluation of the facial nerve. Journal of the American Academy of Audiology, 4: 109-115.
5. Moldaver, J. (1980). Anatomical and functional characteristics of the muscles supplied by the facial nerve. In J. Moldaver, J. Conley (Eds.). The Facial Palsies, pp. 16-19. Springfield, IL: Thomas.
6. Schaitkin, B. (1997). Personal communication.
Todd Henkelmann is clinical director of the Facial Rehabilitation Center, Eagle Physical Therapy/Theraphysics Partners of West, PA, Mars, PA. He was a consultant in the clinic of Pittsburgh area otolaryngologists Barry Schaitkin, MD, and Mark May, MD, now retired, specialists in facial nerve disorders. Dr. May's book, The Facial Nerve (New York: Thieme, 1986) is considered a standard reference on this subject. He and Dr. Schaitkin are co-editing a second edition, due out later this year.
Classifications and Incidence Of Facial Paralysis Etiologies
Idiopathic, 49.5 percent
Infectious, 15.3 percent
Neurologic, 13.5 percent
Neoplastic, 13.5 percent
Traumatic, 8.2 percent