Idiopathic facial nerve palsy (Bell's palsy): morphological changes in MRI.
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Adult↗
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A survey of idiopathic facial palsy (Bell's palsy) in southern Iran.
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Adolescent↗
[Early corticoid treatment of idiopathic facial palsy (Bell)].
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.
Adolescent↗
Diagnosis of Bell palsy with gadolinium magnetic resonance imaging.
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.
Adult↗
Plasma endothelin level in the acute stage of Bell palsy.
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.
Acute Disease↗
Impaired interferon production by leukocytes from patients with Bell palsy and lack of findings suggestive for a systemic viral involvement.
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.
Adolescent↗
Bell palsy complicating pregnancy: a review.
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.
Adrenal Cortex Hormones↗
Herpes simplex virus in idiopathic facial paralysis (Bell palsy).
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.
Adenoviridae↗
Bell palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle.
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.
Adult↗
Transmastoid decompression as a treatment of 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.
Adolescent↗
Acute peripheral facial palsy simulating Bell's palsy in a case of probable multiple sclerosis with a clinically correlated transient pontine lesion on magnetic resonance imaging.
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.
Acute Disease↗
Cranial polyneuritis and Bell 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.
Acute Disease↗
Polymerase chain reaction amplification of herpes simplex viral DNA from the geniculate ganglion of a patient with Bell's 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.
Aged↗
The use of nerve conduction studies in determining the short-term outcome of Bell's palsy.
Bell's palsy is a common neurological problem causing considerable loss of self-esteem among patients. A prospective observational study was conducted to determine the short-term outcome of Bell's palsy at 1 month and 2 months after the onset and the relationship between these outcomes with facial nerve degeneration. We also determined if gender, age, diabetes, systolic and diastolic blood pressure influence the severity of facial nerve degeneration and the clinical outcome at 2 months after the onset. After clinically grading the newly diagnosed unilateral Bell's palsy patients using the House-Brackmann facial nerve grading system, nerve conduction studies of the facial nerve were done to determine the severity of facial nerve degeneration. The recovery of the facial paralysis was clinically graded again at the end of 1 month and 2 months from the onset. A total of 37 patients were recruited. There was a strong positive correlation between facial nerve degeneration and the clinical outcome of Bell's palsy at 1 month (r = 0.794; p < 0.0005) and 2 months (r = 0.732; p < 0.0005) after the onset. There was no significant correlation between either the facial nerve degeneration or the clinical outcome at 2 months with the patients' age (p = 0.288 and p = 0.799 respectively), systolic blood pressure (p = 0.425 and p = 0.933 respectively) or diastolic blood pressure (p = 0.243 and p = 0.579 respectively). Neither the severity of facial nerve degeneration nor the clinical outcome at 2 months were significantly different between male and female patients (p = 0.460 and p = 0.725 respectively) or diabetic and non-diabetic patients (p = 0.655 and p = 0.655 respectively).
Adolescent↗
Recent-onset bell palsy complicated by diabetes: comparison of steroid and lipoprostaglandin E(1) therapy.
OBJECTIVE: To compare megadose steroid therapy (n = 17; group S) and lipoprostaglandin E(1) (lipo-PGE(1)) therapy (n = 14; group L) in patients with recent-onset Bell palsy complicated by diabetes. DESIGN: A nonrandomized controlled trial was performed. The 2 groups were almost identical in age, sex distribution, and laterality, and there was no difference in the average palsy scores in the 2 groups either at the time of the first visit or when the palsy was at its worst. RESULTS: There was no statistically significant difference in the cumulative rates of improvement in the 2 groups 4 weeks, 2 months, or 6 months after the first visit, revealing no difference in the therapeutic effects of the 2 agents. During the therapy, fasting blood glucose concentrations were increased in all patients in group S, whereas they were not increased in group L. Complicated diabetes was aggravated in group S, while it was not aggravated in group L. CONCLUSIONS: Lipo-PGE(1) therapy may have improved vascular flow in the facial nerves and accelerated recovery, resulting in a rate of improvement comparable with that obtained through megadose steroid therapy. Lipo-PGE(1) is a useful treatment method for patients with Bell palsy complicated by diabetes.
Adult↗
Magnetic resonance imaging findings in bilateral Bell's palsy.
Bell's palsy (idiopathic facial paralysis) is the most common cause of unilateral peripheral facial neuropathy. Bilateral involvement occurs in less than 10% of cases. The authors describe a 20-year-old man with bilateral idiopathic facial weakness. Brain magnetic resonance imaging (MRI) showed abnormal bilateral enhancement of the proximal intracanalicular segments of VII/VIII nerve complexes. The enhancement was most prominent in the leptomeningeal regions. There was no facial nerve swelling. Three months later he had improving residual bifacial weakness. To the authors' knowledge, this is the first report of abnormal MRI findings in bilateral Bell's palsy.
Adult↗
Practical management of Bell's palsy.
Bell's palsy is an acute unilateral weakness or paralysis of the face resulting from peripheral facial nerve dysfunction. While there is no readily identifiable cause, there is some recovery of function within 6 months. This article offers practical guidelines for diagnosing and treating Bell's palsy. These guidelines are based on the author's experience with 63 patients over the last 8 years. Physical examination should reveal diffuse nerve involvement, normal otoscopic findings, and no skin blebs or blisters and parotid masses. Other cranial nerve palsies may be present. Diagnostic testing should include basic audiometry if available, and computed tomography or magnetic resonance imaging scanning if paralysis is present. Facial photography is recommended. Topognostic testing is not helpful because it no longer guides the surgical approach, and prognostic tests are not necessary if the face is not paralyzed. The only sufficiently sensitive test to determine the need for possible surgery is electroneurography. Eye care is critical in all but the mildest cases, and steroids may also be helpful. Surgery is rarely needed and should consist only of middle fossa total decompression; simple decompression of the tympanic and mastoid segments is seldom helpful. The natural history of the disease and the limited role of surgery provide new guidelines for practical management of Bell's palsy.
Adolescent↗
Time course of Bell palsy.
This study was designed to quantitatively characterize the time course of facial palsy and the relationship between electroneurography and the facial nerve grading percentage as a function of onset time. Bilateral electroneurographic recordings during different stages in the course of the disease were repeated and compared with categorized videotaped facial movements using the House-Brackmann facial nerve grading system in 32 patients with Bell palsy. Preliminary results of this study demonstrate a time gap between the percentage of electroneurographic response and the category of the facial nerve grading system during the same period of disease progress. A theoretical model of the time course and specific patterns regarding the recovery of facial function is established. The theoretical time course of facial palsy is divided into 3 stages; preclinical, clinical, and postclinical. Based on the time course of electroneurographic and facial grading functions, the period between 10 and 14 days after onset was found to be most valuable for prediction of recovery. According to this theoretical model, a given time course pattern based on the results of serial electroneurographic recordings provides reliable prognostic information on recovery from Bell palsy.
Action Potentials↗