Decompression for Bell's palsy: why I don't do it.

All decompression surgery is based on the lack of understanding that Bell's palsy is a viral demyelinating disease that is longitudinal--not perpendicular--to the facial canal and that surgery cannot possibly help a viral disease. These findings exclude the etiologic possibility of an "ischemic paralysis" and are in accord with our logically derived belief that treatment directed to relieve neural entrapment is a wasted effort.

A preliminary study of cocaine absorption from the nasal mucosa.

Objective/hypothesis: To determine factors affecting the safe use of topical cocaine for anesthesia and vasoconstriction during rhinologic surgery.

Study Design: Prospective, randomized study of the kinetics of cocaine absorption through human nasal mucosa in 12 consecutive patients without nasal mucosal disease who were having septoplasty or septorhinoplasty.

Methods: With patients under general anesthesia, cocaine was applied topically to each nasal cavity by using cottonoid pledgets.

Bell's palsy treatment with acyclovir and prednisone compared with prednisone alone: a double-blind, randomized, controlled trial.

In a double-blind study, we compared the final outcome of 99 Bell's palsy patients treated with either acyclovir-prednisone (53 patients) or placebo-prednisone (46 patients). For patients receiving acyclovir, the dosage was 2,000 mg (400 mg 5 times daily) for 10 days. Electrical tests included electroneurography and the maximal stimulation test.

An analysis of the Adour-Swanson and House-Brackmann grading systems for facial nerve recovery.

Lack of uniformity in reporting facial nerve recovery in patients with facial nerve paralysis has been a major disadvantage in comparing treatment modalities. To remove subjectivity from the analysis, we devised a facial paralysis recovery profile as a system for measuring facial motion. This profile has been used since 1968 at Kaiser Permanente Medical Center, Oakland, California.

Otological complications of herpes zoster.

Otological complications of varicella-zoster virus (Ramsay Hunt syndrome) include facial paralysis, tinnitus, hearing loss, hyperacusis (dysacousis), vertigo, dysgeusia, and decreased tearing. Cranial nerves V, IX, and X are often affected. Gadolinium-enhanced magnetic resonance imaging demonstrates enhancement of the geniculate ganglion and facial nerve.

Audiometric comparison of Lassa fever hearing loss and idiopathic sudden hearing loss: evidence for viral cause.

A recently published prospective study on acute sensorineural deafness in Lassa fever among a West African population showed the audiometric pattern of a known virally induced hearing loss. Using the audiometric data from the patients with Lassa fever in that study, we analyzed and classified the initial hearing loss and final recovery into three groups by pure-tone average values and then did the same for 222 patients with idiopathic sudden hearing loss (SHL) in our study. Statistical analyses of the severity of initial hearing loss and the hearing recovery pattern indicate that the clinical course of our 222 patients with idiopathic SHL showed no statistically significant differences from the clinical course of the patients with Lassa fever.

Medical management of idiopathic (Bell's) palsy.

Experience with treating more than 400 cases of Antoni's palsy, the findings of autoimmune reaction, and recent gadolinium-enhanced magnetic resonance imaging reports in "idiopathic" Bell's palsy verify the hypothesis that the disease results from a viral geniculate ganglionitis. The diagnosis no longer needs to be one of exclusion. We now are capable of establishing a positive diagnosis, permitting the clinician to initiate treatment with corticosteroids and acyclovir confidently.

Endoscopic diverticulotomy for the treatment of Zenker's diverticulum.

First described by Mosher in 1916, endoscopic treatment of Zenker's diverticulum has since been reported infrequently in the surgical literature and continues to engender controversy. Between 1978 and 1989, we treated 11 unselected patients surgically for pharyngoesophageal diverticula. Endoscopic diverticulotomy was used in 11 patients and an external approach was used in the others.

Hilger facial nerve stimulator: a 25-year update.

Percutaneous nerve excitability testing using the Hilger facial nerve stimulator was introduced about 25 years ago. The test is reliable, easy to use, and inexpensive; it continues to be the most frequently used method for predicting prognosis of facial nerve disorders. Between 1966 and 1974, we recorded 10,243 nerve excitability tests on 865 patients with a mean of 3.

The beneficial effect of methylprednisolone in acute vestibular vertigo.

To assess the efficacy of corticosteroids in acute vestibular vertigo, we randomly selected 20 patients so that half took methylprednisolone and half took placebo. Extensive neurotologic examination confirmed the diagnosis. If no significant reduction of vertigo occurred within the first 24 hours of treatment, patients were instructed to switch medications.

Audiological manifestations of Ramsay Hunt syndrome.

Ramsay Hunt syndrome is known to cause audiological signs and symptoms, including sudden, unexpected hearing loss. We carried out a retrospective review of the audiological manifestations of 186 patients with Ramsay Hunt syndrome, measuring their hearing loss patterns, hyperacusis, tinnitus, herpetic rash, facial paralysis, pain and vertigo. Statistical correlations of these parameters were equated with prognosis.

Mona Lisa syndrome: solving the enigma of the Gioconda smile.

The Mona Lisa smile is presented as a possible example of facial muscle contracture that develops after Bell's palsy when the facial nerve has undergone partial wallerian degeneration and has regenerated. The accompanying synkinesis would explain many of the known facts surrounding the painting and is a classic example of Leonardo da Vinci as the compulsive anatomist who combined art and science.

Recurrent Bell's palsy: analysis of 140 patients.

Of 1,700 patients with facial paralysis seen in a retrospective study from 1969 through 1977 and 280 patients seen prospectively from 1983 through 1986, 7.1% had recurrence of Bell's palsy. In this group, the frequency of ipsilateral recurrence was equal to that for contralateral recurrence.

Ramsay Hunt facial paralysis: clinical analyses of 185 patients.

In a prospective study of 1507 patients, evaluated consecutively for facial palsy in the Cranial Nerve Research Clinic at the Kaiser Permanente Medical Center, Oakland, California, between 1966 and 1976, 185 cases (12%) were diagnosed as Ramsay Hunt syndrome. In 46 cases (25%), the diagnosis of herpes zoster was confirmed by acute and convalescent serum titers for varicella-zoster virus. In 139 cases (75%), viral titers were not performed and the diagnosis was based on the characteristic clinical presentation of the Ramsay Hunt syndrome.

Facial paralysis and Bell's palsy: a protocol for differential diagnosis.

In the past, most cases of facial paralysis have been erroneously labeled Bell's palsy. Bell's palsy has been synonymous with and defined as idiopathic facial paralysis affecting only the facial nerve within the confines of the temporal bone. In the last ten years, Bell's palsy has been redefined as viral polyneuritis, probably caused by herpes simplex reactivation, and its diagnosis is no longer reached by exclusion.

Current medical treatment for facial palsy.

Medical treatment for facial palsy includes an accurate diagnosis and reliable estimate of prognosis as well as appropriate medication. Cranial polyneuritis (Bell's palsy and Ramsay Hunt syndrome), the most common cause of facial palsy, is an inflammatory, autoimmune, demyelinating disease best treated by parenteral steroids without surgical intervention. The antiviral agent acyclovir is now being tested as an adjunct to or replacement for steroid therapy.

Herpes simplex virus and acute temporomandibular joint pain-dysfunction syndrome.

Although the TMJ or myofascial pain-dysfunction syndrome is probably not brought about by any single etiologic agent, the findings discussed here offer strong evidence that the primary disease is a form of cranial polyneuritis similar in onset, duration, and natural course to acute facial paralysis. These findings of sensory neuritis with secondary neuromuscular dysfunction leave no question unanswered, whereas the classic concept that has evolved through the years into the pain-dysfunction syndrome cannot adequately explain the myriad of signs and symptoms found in this condition. By removing the psychophysiologic (functional) label and recognizing the organic nature of this self-limiting disease, we should now be able to consolidate the many different modes of therapy that are effective in treating patients with the acute TMJ pain-dysfunction syndrome.

The facial paralysis prognostic index.

The treatment of facial paralysis requires a reliable estimate of prognosis as well as an accurate diagnosis. Although the majority of patients recover, the degree of subsequent facial function varies. An estimation of the risk of nerve degeneration and subsequent disability is needed to guide therapy and to advise patients.

Acute cranial polyneuritis with vertigo after stapedectomy.

Acute vertigo occurring 48 hours after stapedectomy is assumed to be related to inner ear trauma. Similarly, acute vertigo occurring weeks after stapedectomy could be related to a fistula of the oval window. No one has tested the hypothesis that some of these cases could represent concomitant cranial polyneuritis.

Decompression of the facial nerve in Bell's palsy: a historical review.

This year, 1981, is the 50th anniversary of facial nerve decompression for Bell's palsy. The procedure was first suggested in 1923 but not performed until 1931. From the start, facial nerve decompression has generated disagreement regarding the indication and timing for surgical treatment and the anatomic extent of decompression.

Vestibular vertigo. A form of polyneuritis?

Vestibular vertigo traditionally has been considered to be of viral origin and some forms (acute vestibular neuronitis, acute labyrinthitis, acute vertigo) may be manifestations of a viral cranial polyneuritis. To test this hypothesis, otoneurologic signs and serum complement-fixation titers to herpes simplex and herpes zoster were determined in 16 patients with acute vertigo during their attack and several weeks later. One hundred unselected patients seen for nonotoneurologic problems served as control subjects.