Acute Peripheral Facial Palsy Research Articles

Quantitative analysis of MRI intensity in of the major petrosal nerve in patients with idiopathic facial paralysis

The objective of this study was to evaluate signal intensity increases in the greater petrosal nerve after contrast agent administration to gather information on the etiology of idiopathic peripheral facial paralysis. Magnetic resonance images were obtained from 18 patients who received inpatient medical treatment for acute peripheral facial nerve palsy. Images of intratemporal segments of the facial nerve were taken with a slice thickness of 0.75 mm. After multiplanar reconstruction, regions of interest (ROI) were defined in the proximal segment of the greater petrosal nerve. After multiplanar reconstruction, it was possible to visualize the greater petrosal nerves of all 18 patients. The nerve's average diameter was found to be 0.68 mm (range 0.5-0.9). Signal intensity increased by an average of 50.3% (range -10-146%) after contrast agent administration. Whereas this intensity was slightly reduced in two patients, it was increased in 16. No correlation could be established between greater signal intensity and medical history, clinical condition, laboratory findings, or electrophysiological data. In contrast to quantitative measurements in the facial nerve, ROI measurements in the greater petrosal nerve do not correlate with medical history, clinical condition, or laboratory findings. For this reason, MRI of this nerve does not enable us to draw conclusions on the etiology of idiopathic peripheral facial paralysis.

Evaluation of Greater Petrosal Nerve Function in Patients with Acute Peripheral Facial Paralysis: Comparison of Soft Palate Electrogustometry and Schirmer's Tear Test

We tested sensory and secretomotor function of the greater petrosal nerve (GPN) by means of electrogustometry (EGM) of the soft palate and Schirmer's tear test in 115 patients (59 males, 56 females) with acute peripheral facial paralysis. Facial paralysis was caused by Bell's palsy in 78 cases, Ramsay Hunt syndrome in 27 cases and zoster sine herpetic lesions in 10. All patients had dysfunction of the stapedial nerve. An electrogustometer was used to test taste (GPN sensory function), and elevation of the threshold by > 6 dB on the affected side was considered abnormal. Schirmer's test was used to evaluate lacrimal (GPN secretomotor) function, which was considered abnormal when tear secretion on the affected side was < 50% of secretion on the non-affected side. Of the 78 patients with Bell's palsy, 28.2% had altered taste on the soft palate (sensory dysfunction) and 10.3% had lacrimal dysfunction, indicating that EGM of the soft palate is more sensitive than Schirmer's test for identifying dysfunction of the GPN in patients with facial paralysis due to Bell's palsy. Of the total of 115 patients, 32 (28%) had taste dysfunction and 9 (28.1%) of these 32 patients also had lacrimal dysfunction. This finding indicates that facial paralysis has different effects on the sensory and secretory nerve fibers of the GPN. The results of Schirmer's test were more closely related to the severity of, and prognosis for, facial paralysis than the results of EGM.

Secretory Function of the Salivary Gland in Patients with Taste Disorders or Xerostomia: Correlation with Zinc Deficiency

A notable proportion of patients with taste disorders complain of xerostomia and when zinc is prescribed the xerostomia is often improved in conjunction with the taste disorder. To study the relationship between taste disorders, zinc deficiency and xerostomia, we measured salivary gland function and zinc levels in 93 patients with hypogeusia and/or xerostomia and 60 patients with unilateral acute peripheral facial palsy who served as controls. We then prescribed zinc for patients with low serum zinc levels and evaluated xerostomia and taste sensation after 6 months of this treatment. The salivary gland secretory ratio (SGSR), determined by dynamic salivary 99mTc scintigraphy, was found to be an objective measure of salivary gland function and was reduced in patients with xerostomia. Patients with salivary gland dysfunction also had abnormal morphology of the papillae of the tongue. No significant relation was found between the severity of taste disorders and SGSR values, but low SGSR values were found in patients with zinc deficiency. Patients with taste disorders and/or xerostomia who were treated with zinc had relief of symptoms at 6 months, indicating that both taste disorders and xerostomia are among the symptoms of zinc deficiency.

Herpes virus reactivation and gadolinium-enhanced magnetic resonance imaging in patients with facial palsy.

This study investigated whether magnetic resonance imaging (MRI) patterns were different between patients with Bell's palsy and those with herpetic facial palsy in whom varicella-zoster virus (VZV) or herpes simplex virus type 1 (HSV-1) reactivation had been confirmed by polymerase chain reaction (PCR) or serologic assay. A retrospective study of 15 patients with acute peripheral facial palsy was performed to compare virologic tests and gadolinium (Gd)-enhanced MRI findings. Ramsay Hunt syndrome was diagnosed in one patient. By use of virologic tests, zoster sine herpete (VZV reactivation without zoster) was diagnosed in four patients and HSV-1 reactivation in three. Bell's palsy was diagnosed in the remaining seven patients. No significant difference in the frequency of Gd-enhanced MRI was observed between herpetic facial palsy and Bell's palsy. However, in those patients who underwent MRI on the day viral reactivation was confirmed by PCR, Gd enhancement of the meatal fundus was observed infrequently. In addition, when MRI was performed within 10 days of the onset of palsy, Gd enhancement was not detected at the geniculate ganglion in any patients with herpetic facial palsy. By contrast, both the meatal fundus and the geniculate ganglion were enhanced in all patients with Bell's palsy, regardless of when MRI was performed with respect to the onset of palsy. This study shows a difference in the pattern of Gd enhancement at the meatal fundus and the geniculate ganglion between patients with Bell's palsy and those with herpetic facial palsy. The results suggest that the meatal fundus or the geniculate ganglion may be affected first by virus reactivation in patients with herpetic facial palsy.

Herpes virus reactivation and serum tumor necrosis factor-α levels in patients with acute peripheral facial palsy

Recent studies have shown that tumor necrosis factor-α (TNF-α) plays an important regulatory role in several inflammatory and infectious diseases. In the present study, we evaluated serum TNF-α levels of patients with acute peripheral facial palsy using an ELISA method. We examined sera from each group ( n=25 per group) of patients with herpes simplex virus type 1 reactivation (HSV-1), varicella-zoster virus (VZV) reactivation, and with no HSV or VZV reactivation. We also tested the sera of 25 normal controls. No significant difference was found between the serum TNF-α levels in facial palsy and controls. No correlation was found between serum TNF-α levels in cases with HSV-1 or VZV reactivation and with no HSV-1 or VZV reactivation. These results indicate that serum TNF-α levels are not affected by HSV-1 or VZV reactivation in patients with facial palsy.

Herpes simplex virus type 1 reactivation and antiviral therapy in patients with acute peripheral facial palsy

Objective: Recent studies provide compelling data for the hypothesis that herpes simplex virus type 1 (HSV-1) is implicated in the pathogenesis of idiopathic peripheral facial palsy (Bell's palsy). The present study analyzed the severity of facial palsy in patients with HSV-1 reactivation and sought to determine the efficacy of acyclovir–prednisone therapy for these patients. Materials and methods: In total, 176 patients, clinically diagnosed with Bell's palsy, were divided into three groups by polymerase chain reaction (PCR) and serological tests — 31 patients with HSV-1 reactivation, 45 patients with VZV reactivation (zoster sine herpete) and 100 patients without HSV-1 or VZV reactivation (Bell's palsy). Results: The difference in the worst grade of facial palsy between patients with zoster sine herpete and Bell's palsy was significant ( P=0.01 10, Mann–Whitney U-test). In contrast, no difference in the severity of palsy was observed between patients with HSV-1 reactivation and Bell's palsy. Twelve patients received acyclovir–prednisone treatment within 7 days of onset based on positive PCR results and ten of the 12 (83%) recovered completely. In contrast, 14 patients with HSV-1 reactivation received prednisone treatment because their PCR tests were performed at a later date; ten of these 14 (71%) recovered completely. The difference in the cure rate between the two treatment groups was not significant ( P>0.05, Fisher exact test). Conclusions: The results indicate that the severity of palsy in patients with HSV-1 reactivation is similar to that in patients with Bell's palsy and suggest that early diagnosis of HSV-1 reactivation by PCR and subsequent acyclovir–prednisone therapy do not improve recovery from facial palsy.

Prognostic value of electromyography in acute peripheral facial nerve palsy.

To analyze the value of electromyography in predicting recovery from acute idiopathic facial nerve paralysis. Retrospective case-series review. University-based hospital department of otorhinolaryngology/head neck surgery. Three hundred fifty-five patients with sudden facial paralysis of unknown cause (Bell's palsy). Treatment consisted uniformly of high-dose prednisolone, dextran, and pentoxifylline. Prognostication was based on electromyography performed not earlier than 10 to 14 days after the onset of palsy. The findings were classified according to Seddon into neurapraxia and axonotmesis/ neurotmesis. There is an inherent statement on prognosis in this classification because neurapraxia is presumed to recover completely within 8 to 12 weeks, whereas axonotmesis is most likely to be followed by sequelae. Facial nerve function after 6 months. Complete recovery was predicted correctly in 92.4% of cases. For the relatively rare and therefore principally more difficult predictable event defective recovery prognosis was still accurate in 80.8%. The detection of spontaneous fibrillation in needle electromyography is a reliable sign predicting unfavorable outcome. An accuracy of 80.8% for predicting unfavorable outcome may be sufficient to advise patients what to expect in the course of their facial nerve disorder. However, it seems dubious to build a decision about surgical intervention on such a test, because in the process, unnecessary surgery would be accepted for as much as one fifth of the patient population.

抗ウイルス剤アシクロビルが奏効したＢｅｌｌ麻ひの２例

The most common cause of acute idiopathic peripheral facial nerve paralysis (Bell's palsy) remains unknown. Recent studies have shown that herpes simplex virus type 1 (HSV-1) is one of the most common causes of Bell's palsy. We describe two cases of Bell's palsy that responded to treatment with the antiviral agent acyclovir. Although infectious HSV and HSV-DNA could not be detected in saliva samples obtained from either patient, serological studies indicated that the paralysis was attributed to reactivation of HSV-1. The patients were given acyclovir and prednisolone for 2 weeks. Neural symptoms resolved gradually, and facial nerve paralysis disappeared after 3 weeks.These two cases suggest that early treatment with acyclovir and prednisolone is effective in patients with Bell's palsy.

Reactivation of varicella‐zoster virus in delayed facial palsy after dental treatment and oro‐facial surgery

In rare cases, acute peripheral facial palsy occurs several days after dental treatment and oro-facial surgery. Surgical procedures have been known to trigger reactivation of varicella-zoster virus (VZV) and herpes simplex virus type 1 (HSV-1). The present study examined eight patients who exhibited delayed facial palsy after dental treatment or oro-facial surgery. Ramsay Hunt syndrome was diagnosed in three patients and varicella-zoster virus (VZV) reactivation without zoster lesions (zoster sine herpete) was diagnosed in three patients either by PCR or serological assay. Therefore, VZV reactivation was detected in 75% (6 of 8) of patients who exhibited delayed facial palsy after dental or oro-facial treatment. The results suggest that VZV reactivation is a major cause of delayed facial palsy after dental treatment or oro-facial surgery. J. Med. Virol. 62:42–45, 2000. © 2000 Wiley-Liss, Inc.

High prevalence of varicella-zoster virus reactivation in herpes simplex virus-seronegative patients with acute peripheral facial palsy.

Varicella-zoster virus (VZV) and herpes simplex virus (HSV) are considered to be the major causes of acute peripheral facial palsy (APFP). One hundred and forty-two patients with APFP were analyzed by serological assays and polymerase chain reaction analysis. Ramsay Hunt syndrome was diagnosed in 21 patients. Of the remaining 121 patients clinically diagnosed with Bell's palsy, VZV reactivation without zoster (zoster sine herpete) was detected in 35 patients (29%). The prevalence of antibodies to HSV among patients with Bell's palsy was significantly higher than the prevalence among those with VZV reactivation (Ramsay Hunt syndrome or zoster sine herpete). In contrast, a high incidence (88%) of VZV reactivation among HSV-seronegative patients with APFP was observed. Our data indicate that VZV is one of the major etiologic agents of clinically diagnosed Bell's palsy and that VZV reactivation causes APFP in most patients who lack antibodies to HSV.

Bell palsy complicating pregnancy: a review.

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. Obstetricians & Gynecologists, Family Physicians 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.

Rapid strip assay for detection of anti-herpes simplex virus antibodies: application to prediction of varicella-zoster virus reactivation in patients with acute peripheral facial palsy.

Varicella-zoster virus (VZV) reactivation causes acute peripheral facial palsy in the majority (88%) of patients who lack anti-herpes simplex virus (HSV) antibodies, suggesting that an absence of anti-HSV antibodies is a reliable serological marker for the diagnosis of VZV reactivation in patients who are diagnosed initially as idiopathic peripheral facial palsy (Bell's palsy) [Furuta et al., 2000] Clinical Infectious Diseases]. A simple and rapid immunoassay for detection of anti-HSV antibodies based on HSV type 1 glycoprotein D was developed by modifying the conventional Western blot technique. The assay was evaluated by comparing the results with those of conventional Western blot. In total, 100 sera obtained from patients with acute peripheral facial palsy were tested and judged blindly by two investigators. Twenty-four of 26 HSV-seronegative sera were obtained from patients with VZV reactivation (Ramsay Hunt syndrome or zoster sine herpete). The sensitivity of the assay was over 95% and the specificity was 100%. The two investigators agreed on the diagnosis in 99 of the 100 sera. These results indicate that the rapid strip assay is applicable to prediction of VZV reactivation in patients diagnosed clinically with Bell's palsy before zoster lesions appear or PCR using saliva samples indicates VZV reactivation.

Reactivation of varicella-zoster virus in delayed facial palsy after dental treatment and oro-facial surgery

In rare cases, acute peripheral facial palsy occurs several days after dental treatment and oro-facial surgery. Surgical procedures have been known to trigger reactivation of varicella-zoster virus (VZV) and herpes simplex virus type 1 (HSV-1). The present study examined eight patients who exhibited delayed facial palsy after dental treatment or oro-facial surgery. Ramsay Hunt syndrome was diagnosed in three patients and varicella-zoster virus (VZV) reactivation without zoster lesions (zoster sine herpete) was diagnosed in three patients either by PCR or serological assay. Therefore, VZV reactivation was detected in 75% (6 of 8) of patients who exhibited delayed facial palsy after dental or oro-facial treatment. The results suggest that VZV reactivation is a major cause of delayed facial palsy after dental treatment or oro-facial surgery.

Determining the Pathway of the Blink Reflex through Transcutaneous Electrical Stimulation of the Facial Nerve over the Stylomastoid Foramen

The afferent pathway of the late response (R2 component) of the blink reflex in response to transcutaneous electrical stimulation of the facial nerve over the stylomastoid foramen remains uncertain. The two major hypotheses regarding the afferent pathway of R2 are that it may consist of either the trigemino-facial or the facio-facial reflex. This study was performed to determine the afferent pathway of R2. Ninety-one patients with acute unilateral peripheral facial palsy and 21 controls were studied. The degree of facial nerve damage was classified into three groups: mild, moderate, and severe according to their electroneurographic value. In each group, the appearance rate, latency, and area under the curve of contralateral R2 elicited by electrical stimulation of the injured facial nerve over the stylomastoid foramen were measured and compared with those of controls. The contralateral R2 parameters did not differ between the patient groups and the controls. The results indicate that the afferent pathway of R2 is mediated not only through the facial nerve. We conclude that the auriculotemporal nerve (V3) and the great auricular nerve (C2, C3) may also contribute to the afferent pathway of R2.

IgG index in acute idiopathic peripheral facial palsy.

Etiologic hypotheses in acute idiopathic peripheral facial palsy (AIPFP) mostly point to an immunologic dysfunction, probably virus-induced. Though various immunologic abnormalities are reported, the problem is still unsolved. We investigated intrathecal immunoglobulin synthesis in AIPFP as a clue for central nervous system (CNS) immunopathology. We studied IgG index in 24 patients with AIPFP, 10 with other neurological diseases (OND) and 17 with multiple sclerosis (MS). CSF and serum IgG were measured by radial immunodiffusion technique. IgG index is calculated according to Tibbling's formula. IgG indexes were abnormal in 6 patients with AIPFP, 3 with OND and 10 with MS patients. There was no statistical difference between AIPFP and OND groups, while marked difference existed between AIPFP and MS groups. Though IgG indexes were high in 25% of AIPFP patients, statistical analyses did not show any significance of this finding. Lack of a positive result might reflect non-existence of an extensive immunologic pathology within CNS, excluding a very limited one.

Serial gadolinium-enhanced magnetic resonance imaging and assessment of facial nerve function in Bell's Palsy

Eleven patients with mild or moderate acute idiopathic peripheral facial palsy, so-called Bell’s palsy, were serially examined by gadolinium-DTPA–enhanced MRI on mean days 11, 40, and 97 (third examination, n = 10) after the onset of palsy. Results of the clinical and neurophysiologic assessment of facial nerve function were compared with the gadolinium-enhanced MRI findings. Eight of the 11 patients demonstrated contrast enhancement of the facial nerve at the initial examination, but in 7 of them, the enhancement had disappeared by the time of the serial follow-up gadolinium-enhanced MRI scans. The disappearance of facial nerve enhancement was found to be related to clinical and neurophysiologic improvements in facial nerve function during recovery from Bell’s palsy. The three patients whose scans were negative at the initial gadolinium-enhanced MRI examination had the same clinical severity of palsy, but initially they had milder neurophysiologic involvement than those who demonstrated enhancement; these three patients did not exhibit enhancement at serial follow-up scans. These findings indicate that the presence of enhancement at the initial MRI scan is not necessarily indicative of a poor prognosis for recovery. (Otolaryngol Head Neck Surg 1997;117:559-66.)

Detection of varicella-zoster virus DNA in patients with acute peripheral facial palsy by the polymerase chain reaction, and its use for early diagnosis of zoster sine herpete

Varicella-zoster virus (VZV) reactivation without cutaneous vesicles (zoster sine herpete) has been demonstrated in 8 to 25% of patients with acute peripheral facial palsy (APFP) by serological methods. To make an early diagnosis of zoster sine herpete, VZV DNA in oropharyngeal swabs from patients with APFP was examined by the polymerase chain reaction (PCR). VZV DNA was detected in oropharyngeal swabs from 6 of 36 (17%) patients with APFP by PCR. VZV DNA was detected in the oropharyngeal swabs from the six patients at their initial visit (2 to 4 days after the onset of APFP), while the anti-VZV IgM and IgG antibody titers were not increased significantly. In contrast, VZV DNA was undetectable in the oropharyngeal swabs at the time when the VZV specific antibody response appeared. These results indicate that detection of VZV DNA in oropharyngeal swabs by PCR is more useful than currently available serological assays for the early diagnosis of zoster sine herpete in patients with APFP.

Detection of varicella‐zoster virus DNA in patients with acute peripheral facial palsy by the polymerase chain reaction, and its use for early diagnosis of zoster sine herpete

Varicella-zoster virus (VZV) reactivation without cutaneous vesicles (zoster sine herpete) has been demonstrated in 8 to 25% of patients with acute peripheral facial palsy (APFP) by serological methods. To make an early diagnosis of zoster sine herpete, VZV DNA in oropharyngeal swabs from patients with APFP was examined by the polymerase chain reaction (PCR). VZV DNA was detected in oropharyngeal swabs from 6 of 36 (17%) patients with APFP by PCR. VZV DNA was detected in the oropharyngeal swabs from the six patients at their initial visit (2 to 4 days after the onset of APFP), while the anti-VZV IgM and IgG antibody titers were not increased significantly. In contrast, VZV DNA was undetectable in the oropharyngeal swabs at the time when the VZV specific antibody response appeared. These results indicate that detection of VZV DNA in oropharyngeal swabs by PCR is more useful than currently available serological assays for the early diagnosis of zoster sine herpete in patients with APFP. J. Med. Virol. 52:316–319, 1997. © 1997 Wiley-Liss, Inc.

Reinfection in Lyme borreliosis

Two patients with reinfection of Borrelia burgdorferi are presented. An 11-year-old girl developed recurrent acute peripheral facial palsy at an interval of five years. A 64-year-old woman showed paraesthesia in the leg and effusion in the knee. Three years later, an erythema migrans developed at the thigh. In both patients tick bites, corresponding clinical manifestations, and detection of specific antibodies proved the reinfections. The course of the humoral immune responses showed basic differences between the patients. At the interval between the first and second infection, the specific antibodies of the girl decreased beyond the cut-off level. On the other hand, the titer of specific IgG antibodies of the other patient remained at a constant level. Reasons for the failure of immune protection are discussed.

Plasma Endothelin Level in the Acute Stage of Bell Palsy

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). 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. Nihon University Itabashi Hospital, a referral and institutional center in Tokyo, Japan. 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. 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.