Michael J. LaRouere, M.D.
Michigan Ear Institute
Bell's Palsy, the acute onset of facial paralysis, is a devastating disorder to both the patient and their family. Most often however this paralysis is short lived and recovery occurs back to normal in the majority of patients. A study by Peitersen looked at 1,011 patients studying the natural history of Bell's Palsy. Without any treatment 84% of patients had facial function recover to either normal or near normal function. It is the remaining 16% of patients who demonstrate a poor outcome that treatment has been directed towards.
The etiology of Bell's Palsy appears to be the herpes simplex virus type I. This has been demonstrated in several studies. The virus affects the nerve and causes swelling. The facial nerve itself is within the fallopian canal, the narrowest point being the area of the meatal foramen which is the entrance to the facial nerve canal just distal to the internal auditory canal. This area is approximately .68 mm in diameter and is where the nerve is believed to be compressed in Bell's Palsy. Both anatomical and electro physiological studies have demonstrated this.
The treatment of Bell's Palsy thus centers around the reduction of swelling of the facial nerve as well as an attack on the herpes simplex one virus. Currently medical treatment consists of high dose steroids and Acyclovir. Our current approach includes Prednisone 60 mg per day (20 mg t.i.d.) for at least one week followed by a rapid taper. Famvir in a dose of 500 mg b.i.d. is used for Bell's Palsy and 500 mg t.i.d. of Famvir is utilized for herpes zoster oticus. All patients with Bell's Palsy are treated in the above manner. Those patients with a partial facial paralysis are treated in order to prevent them from going to complete facial paralysis. Patients with a complete facial paralysis are also treated in this manner. In addition however further testing is needed on those patients with clinically apparent complete facial nerve paralysis as these patients may present with a much poorer prognosis.
Those patients with complete facial paralysis or grade VI on the House-Brackmann scale are evaluated somewhat differently than those patients with incomplete paralysis. Patients with complete facial paralysis undergo electrical testing. Two electrical tests are currently used. The first is that of electroneurography or ENOG. Electroneurography uses a maximally evoked electrical potential at the stylomastoid foramen and measures the amplitude of the facial muscle compound action potential near the nasolabial groove. Using Esslen and Fisch's data, it has become apparent that those patients showing greater than 90% degeneration on ENOG have a poor long term facial outcome. In addition voluntary EMG recording is also used. This is used when electroneurography testing shows 100% neural degeneration. If motor unit potentials are observed with voluntary contractions during the first two weeks after the onset of paralysis a good outcome can be expected even if electroneurography testing shows 100% degeneration. This is due to a phenomenon called early deblocking or asynchronous firing of the nerve which leads to subclinical motion that can be detected with the EMG recordings.
Those patients with greater than 90% degeneration on ENOG and no voluntary potentials noted on EMG recordings demonstrate a low likelihood of returning to near normal facial function. These candidates would be patients for facial nerve decompression.
A recent study by Bruce Gantz, M.D. and others outlines the role of surgical decompression in Bell's Palsy. Those patients with complete clinical facial paralysis, greater than 90% degeneration on ENOG and no evidence of voluntary action muscle potentials on EMG testing were candidates for surgical decompression. Those patients under going decompression within the first two weeks of the onset of paralysis showed a 91% chance of a good outcome vs a 42% chance of obtaining a House-Brackmann scale grade I or II if treated with steroids only. Facial nerve decompression should be performed by the middle cranial fossa technique in order to achieve decompression of the meatal foramen area. The risk of surgical decompression including a 2-5% incidence of sensorineural hearing loss and dizziness must be explained to the patient. In addition it should be noted that 42% of patients with ENOG features of a poor prognosis did recover normal or near normal facial function, however this is compared to 91% who recovered normal or near normal facial function with decompression if performed within the first two weeks following the onset of the paralysis.
Our data on facial nerve decompression at the Michigan Ear Institute confirms Dr. Gantz study. We have found that early decompression, generally within the first three weeks leads to an overall better result compared to medically treated patients with complete facial paralysis and ENOG features of severe degeneration. It does appear that the middle cranial fossa approach, decompressing the area of the meatal foramen, offers these patients the most benefit.