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Bell's palsy is the most frequent type of peripheral facial paresis. Its cause is unknown. The prognosis is good in 85% of patients. Based on theories about its pathogenesis, antivirals and corticosteroids have been tried. In 6 studies with antivirals and 9 with corticosteroids (most ofthe studies were methodologically flawed), the efficacy of these treatments was not demonstrated.
OBJECTIVE: To detect the role of the plasma endothelin in the process of Bell palsy and its relationship to prognosis. METHOD: The plasma endothelin were respectively determined with radioimmunoassay in 21 patients with Bell palsy and 20 normal control subjects. RESULT: The patients who were suffering from Bell palsy exhibited a statistically significant (P < 0.01) increase in the endothelin level compared with that in the 20 normal control subjects. A significantly higher level of the plasma endothelin was found in unsatisfactory recovery group compared with that in satisfactory recovery group. CONCLUSION: Endothelin may play an important role in the process of Bell palsy, and may be a useful marker for the assessment of prognosis to the patients.
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Idiopathic facial palsy (IFP) (Bell's palsy) is the commonest cause of acute facial paralysis. Perhaps because of its unknown origin, a wide range of treatments are used. Controversy exists as to whether the disorder should be left to run its natural course or treated with steroids. The effect of early steroid treatment on the evolution of IFP was evaluated in the Ear, Nose, and Throat Service of the University Hospital of Alicante (Spain) with a prospective protocol from September 1991 to January 1992. The therapeutic protocol for all patients (47 patients) was an intramuscular injection of 60 mg prednisone in the Emergency Room followed by a course of oral steroids (deflazacort) that was gradually tape-red-off. The average duration of IFP before presentation in the Emergency Department was 1.30.9 days. Clinical improvement was observed on day 149 and a complete cure by day 3026. Full recovery of facial motor function without sequelae occurred in 95.6% of patients. Age, the intensity of paralysis, and a history of hypertension and diabetes had a negative influence on the course of IFP. These results support early steroid treatment for IFP.
Bell palsy is a condition resulting from a peripheral edematous compression on the nervous fibers of the facial nerve. This pathological condition often has clinical characteristics of no importance and spontaneously disappears in a short time in a high percentage of cases. Facial palsy concerning cranial nerve VII can also be caused by other conditions such as mastoid fracture, acoustic neurinoma, tumor spread to the temporal lobe (e.g., cholesteatoma), neoformation of the parotid gland, Melkersson-Rosenthal syndrome, and Ramsay-Hunt syndrome. Therefore, it is important to adopt an accurate diagnostic technique allowing the rapid detection of Bell palsy and the exclusion of causes of facial paralysis requiring surgical treatment. Magnetic resonance imaging (MRI) with medium contrast of the skull shows a marked increase in revealing lesions, even of small dimensions, inside the temporal bone and at the cerebellopontine angle. The authors present a clinical case to show the important role played by gadolinium MRI in reaching a diagnosis of Bell palsy in the differential diagnosis of the various conditions that determine paralysis of the facial nerve and in selecting the most suitable treatment or surgery to be adopted.
Bell palsy is largely a diagnosis of exclusion, but certain features in the history and physical examination help distinguish it from facial paralysis due to other conditions: eg, abrupt onset with complete, unilateral facial weakness at 24 to 72 hours, and, on the affected side, numbness or pain around the ear, a reduction in taste, and hypersensitivity to sounds. Corticosteroids and antivirals given within 10 days of onset have been shown to help. But Bell palsy resolves spontaneously without treatment in most patients within 6 months.
OBJECTIVE: To determine the plasma endothelin level in the acute stage in patients with Bell palsy (based on the hypothesis that endothelin, which is a potent vasoconstrictor, may play a role in the mechanism of the onset of facial nerve paralysis and in view of the fact that the etiology of Bell palsy is still a maze of unknowns). DESIGN: The study involved 62 patients with the acute stage (tested within 10 days of onset) of Bell palsy (i.e., idiopathic acute peripheral facial paralysis) and an additional 36 healthy persons who served as control subjects. To determine the content of endothelin, 2 ml of plasma samples was collected from each subject. Endothelin-1 was extracted and analyzed by a radioimmunoassay by using anti-endothelin-1 antibody. SETTING: Nihon University Itabashi Hospital, a referral and institutional center in Tokyo, Japan. RESULTS: The patients who were suffering from Bell palsy exhibited a statistically significant (P < .01) increase in the endothelin level compared with that in the 36 normal control subjects. An age-matched comparison (ranges, 20-29 years and 30-39 years) of patients with Bell palsy with normal control subjects revealed a significant difference between the normal group and the group with Bell palsy in the plasma endothelin level for both age groups that were tested (P < .01). The mean value of the endothelin level in patients with Bell palsy was maximal on day 5, and the percentage of patients with abnormally elevated endothelin levels was 100% from days 6 to 9. CONCLUSION: Endothelin, which has potent vasoconstrictive effects, may contribute to the pathogenesis of the microcirculatory impairment that occurs in patients with Bell palsy, mainly by promoting secondary ischemia.
Bell's palsy is named after Sir Charles Bell (1774-1842), who has long been considered to be the first to describe idiopathic facial paralysis in the early 19th century. However, it was discovered that Nicolaus Anton Friedreich (1761-1836) and James Douglas (1675-1742) preceded him in the 18th century. Recently, an even earlier account of Bell's palsy was found, as observed by Cornelis Stalpart van der Wiel (1620-1702) from The Hague, The Netherlands in 1683. Because our current knowledge of the history of Bell's palsy before Bell is limited to a few documents, it is interesting to discuss Stalpart van der Wiel's description and determine its additional value for the history of Bell's palsy. It is concluded that Cornelis Stalpart van der Wiel was the first to record Bell's palsy in 1683. His manuscript provides clues for future historical research.
OBJECTIVE: To find out a method for increasing clinical therapeutic effect on Bell palsy at acute stage. METHODS: Ninety cases of Bell palsy were randomly divided into an observation group, a control group I and a control group II, 30 cases in each group. They were treated respectively with acupuncture plus exercise therapy, simple acupuncture therapy, and simple exercise therapy, and their therapeutic effects were observed. RESULTS: The cured rate was 66.7% in the observation group, 53.3% in the control group I and 46.70% in the control group II, the observation group being better than the two control groups (P<0.05). CONCLUSION: Acupuncture by stage combined with exercise therapy can increase the therapeutic effect on Bell palsy at acute stage, and it is a better therapy for Bell palsy.
HYPOTHESIS: This study aimed to test the hypothesis that viral and other microbial infections cause Bell palsy and to use the interferon (IFN) alpha/beta-induced MxA protein as an indicator of systemic viral infection. BACKGROUND: Bell palsy has been previously associated with several viral infections. Recently, after this study was completed, herpes simplex virus DNA was detected in the endoneurial fluid of some patients with Bell palsy. METHODS: Serum and blood mononuclear cells were obtained from 30 patients with Bell palsy and 12 control subjects. The sera were tested for antibodies to 21 microbes. Mononuclear cells were assayed for (a) MxA protein using immunoblotting and (b) capacity to produce IFN in short-term culture after stimulation with influenza A virus. RESULTS: No significant differences were seen in serum antibodies or MxA protein between the patients and controls. The geometric mean of leukocyte IFN production in the convalescent phase of Bell palsy patients was higher than in the acute phase but remained still at significantly lower levels as compared with the control group (p < 0.05). In three patients there was no detectable IFN production. CONCLUSIONS: These results provide no evidence for a systemic viral involvement in Bell palsy, but the observed decreased IFN-producing capacity at the onset of Bell palsy could be a sign of transient immunosuppression or of an abnormal frequency of leukocyte subpopulations in the disease.
UNLABELLED: The aim of the present work was to review the published evidence on the association of Bell palsy (BP), an acute idiopathic peripheral facial paralysis of unknown etiology, with pregnancy. Reports have shown that women of reproductive age are affected two to four times more often than men of the same age, and pregnant women 3.3 times more often than nonpregnant women. The apparent predisposition of pregnant women to Bell palsy has been attributed to the high extracellular fluid content, viral inflammation, and immunosuppression characteristic of pregnancy, but findings are controversial. Most cases of Bell palsy occur in the third trimester or the puerperium. Onset is acute and painful. Some authors suggest that Bell palsy increases the risk of hypertension and toxemia of pregnancy, whereas the pregnant state, in turn, may affect the course and severity of disease. Recovery is usually good; poor prognostic markers are recurrence in subsequent pregnancy and bilateral disease, both of which are rare. Neonatal outcome is apparently unaffected, although this has been studied rarely. The preferred mode of management remains undecided; it is usually confined to supportive care. Corticosteroids in pregnancy are controversial. We think clinicians should be aware of these findings to avoid unnecessary testing and treatment and to help the patient cope with this acute, painful disease. TARGET AUDIENCE: Obstetricians & Gynecologists, Family Physicians LEARNING OBJECTIVES: After completion of this article, the reader will be able to identify the potential etiologies of Bell palsy associated with pregnancy and to describe the clinical presentation of this condition in pregnancy and its likelihood for recovery.
Sera from all 41 adult patients with idiopathic facil paralysis (Bell palsy) and 35 (85%) of 41 matched controls who had never had Bell palsy contained antibodies to herpes simplex virus (P smaller than.05). The frequency of antibodies to herpes zoster virus did not differ in patients and controls. A rise in antibody titer, indicating primary herpes simplex virus infection, was not found in these patients. That Bell palsy may be caused by reactivation of herpes simplex virus is suggested by (1) clinical, neurologic, laboratory, and immunologic similarities between idiopathic facial paralysis and known manifestations of reactivated herpes simplex virus infection, and (2) the known neurotropism of herpes simplex virus, including its presence in latent form in the trigeminal ganglia, and parallels with known facial paralysis due to varicella zoster virus, a closely related agent. The presence of antibodies to herpes simplex virus is the only common factor among the patients tested in this study.
OBJECTIVE: To determine whether herpes simplex virus type 1 (HSV-1) causes Bell palsy. DESIGN: Prospective study. SETTING: University inpatient service. PATIENTS: 14 patients with Bell palsy, 9 patients with the Ramsay-Hunt syndrome, and 12 other controls. MEASUREMENTS: Viral genomes of HSV-1, varicella-zoster virus, and Epstein-Barr virus were analyzed in clinical samples of facial nerve endoneurial fluid and posterior auricular muscle using polymerase chain reaction (PCR) followed by hybridization with Southern blot analysis. RESULTS: Herpes simplex virus type 1 genomes were detected in 11 of 14 patients (79%) with Bell palsy but not in patients with the Ramsay-Hunt syndrome or in other controls. The nucleotide sequences of the PCR fragments were identical to those of the HSV-1 genome. CONCLUSIONS: Herpes simplex virus type 1 is the major etiologic agent in Bell palsy.
OBJECTIVE: We sought to assess the efficacy of transmastoid decompression after steroid treatment. STUDY DESIGN: One hundred one adults with Bell palsy having denervation exceeding 95% after steroid treatment were divided into 2 groups. In 58 patients decompression from the labyrinthine segment to the stylomastoid foramen was performed, and the remaining 43 patients were only followed up. Using the Yanagihara score and House Brackmann grading system, the recovery from the palsy was assessed. RESULTS: There was a statistically significant difference in the final facial score of the 2 groups. Within 60 days after the onset, the chance of better recovery from the palsy was higher in the patients with decompression. CONCLUSION: In the era of steroid treatment, we cannot discard the transmastoid decompression of the facial nerve in the treatment of severe Bell palsy with profound denervation, although further effort is needed to obtain definitive evidence to show the benefit of the operation.
A transient pontine lesion was demonstrated in a young adult male who had a complete acute peripheral facial nerve palsy due probably to multiple sclerosis. In the acute stage of the palsy. T2-weighted magnetic resonance imaging (MRI) revealed a high signal intensity in the ipsilateral pons in the region of the nucleus and pontine part of the facial nerve. The patient recovered completely 5 weeks after the onset of the palsy, and at this stage, the lesion in the brainstem was no longer demonstrable on MRI. The onset and course of the disease resembled the idiopathic form of facial palsy (Bell's palsy): the present findings along with recent MRI and topodiagnostic studies may indicate that in some cases of Bell's palsy the primary lesion is located centrally. By improved MRI techniques and intravenous contrast agents it may be possible to visualize and follow the disease process and ascertain more of the pathogenesis of Bell's palsy.
In view of the specific nature of the clinical and neurologic findings in Bell palsy and other acute benign cranial neuritides, the neural component of cutaneous herpes simplex, the predilection of the herpesvirus for sensory nerves, and intrinsic behavior and immunologic interreactions of the herpesvirus within ganglion cells, it is suggested that (1) the entity that has been termed "idiopathic facial paralysis" be recognized as an acute benign cranial polyneuritis; and (2) other acute benign cranial neuritides be recognized as formes frustes of Bell palsy.
Bell's palsy is the most common cause of facial paralysis. In this study, we demonstrate the presence of herpes simplex viral type 1 (HSV-1) genomic DNA in the geniculate ganglion of a patient who had Bell's palsy. This association suggests that in this patient, HSV-1 may have caused Bell's palsy. If HSV-1 is a cause of Bell's palsy, treatment with acyclovir may be beneficial. Additional studies should be done to establish the prevalence of HSV-1 as an etiologic agent of Bell's palsy.