Nobumitsu Honda

Valacyclovir and prednisolone treatment for Bell's palsy: a multicenter, randomized, placebo-controlled study.

Objective: To investigate the effects of valacyclovir and prednisolone in comparison with those of placebo and prednisolone for the treatment of Bells palsy, excluding zoster sine herpete. Study Design: Prospective, multicenter, randomized placebo-controlled study. Setting: Six academic tertiary referral centers. Patients: Ultimately, 221 patients with Bells palsy who were treated within 7 days of the onset. Serological and polymerase chain reaction examinations were performed to distinguish Bells palsy from zoster sine herpete. Intervention: The patients were treated with either valacyclovir (dosage, 1,000 mg/d for 5 days) plus prednisolone (VP [n = 114]) or placebo plus prednisolone (PP [n = 107]) administered orally. Main Outcome Measure: Recovery from the palsy was defined as a score higher than 36 using Yanagihara 40-point scoring system without facial contracture or synkinesis. The patients were followed up until complete recovery occurred or for more than 6 months in cases with a poor prognosis. Results: The overall rate of patient recovery among those treated with VP (96.5%) was significantly better (p < 0.05) than the rate among those treated with PP (89.7%). The rate of patient recovery was also analyzed by classifying the initial severity of facial palsy. In cases of complete or severe palsy, the rates of patients treated with VP and PP who recovered were 95.7% (n = 92) and 86.6% (n = 82), respectively; the recovery rate for treatment with VP was significantly better than that with PP (p < 0.05). Conclusion: The valacyclovir and prednisolone therapy was more effective in treating Bells palsy, excluding zoster sine herpete, than the conventional prednisolone therapy. To our knowledge, this is the first controlled study of an antiviral agent in the treatment of a sufficient number of Bells palsy cases based on an etiologic background.

Efficacy of early treatment of Bell's palsy with oral acyclovir and prednisolone

Objective To investigate the therapeutic effects of acyclovir and prednisolone in relation to the timing of treatment in Bells palsy. Study Design This was a retrospective study of 480 Bells palsy patients who were treated with oral acyclovir and prednisolone (94 cases) or prednisolone alone (386 cases). Patients Patients met the after criteria: (1) severe or complete Bells palsy with a score lower than 20 on the 40-point Yanagihara facial score and (2) treatment started within 7 days after onset. The patients were treated with oral prednisolone (60–40 mg/day) with or without oral acyclovir (2,000 mg/day). Main Outcome Measure Rate of recovery, which was defined as a facial score of 36 or more, and the absence of contracture with synkinesis. Results The overall recovery rate of patients treated with acyclovir and prednisolone was 95.7 percent, which was better than that of patients treated with prednisolone alone (88.6%). The recovery rate in patients who began the combined therapy within 3 days of the onset of palsy was 100 percent and early treatment resulted in early remission. In contrast, the recovery rate in patients who started the combined therapy more than 4 days after onset was 86.2 percent. Conclusion These results suggest that early diagnosis and treatment within 3 days of the onset of paralysis are necessary for maximal efficacy of combined acyclovir and prednisolone therapy for Bells palsy.

Ramsay Hunt syndrome in children

In a retrospective study, 52 children were diagnosed with Ramsay Hunt syndrome. The facial palsy was milder and complete recovery of the function was achieved in 78.6% of patients. Associated cranial neuropathies were less common in children than in adults. The timing of vesicle appearance tended to be delayed in children. In preschool children, Ramsay Hunt syndrome was rare, although the frequency has recently increased. The syndrome is relatively common in older children. This study suggested that vaccination can prevent or reduce the occurrence of Ramsay Hunt syndrome. Ann Neurol 2000;48:254–256

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.

Varicella-Zoster Virus Distribution in Ramsay Hunt Syndrome Revealed by Polymerase Chain Reaction

The pathogenesis of facial nerve paralysis and vestibulo-cochlear dysfunction of Ramsay Hunt syndrome remains unclear as varicella-zoster virus (VZV) has not been demonstrated in the lesions. Using the polymerase chain reaction, we detected VZV genomes not only in the vesicles on the auricles or oral cavity but also in the facial nerve sheath, middle ear mucosa and cerebrospinal fluid from patients with Ramsay Hunt syndrome. The VZV genome was undetectable in the same kinds of clinical samples obtained from control patients with facial nerve paralysis of other etiologies. The results indicated that VZV spreads widely in the neural components, mucocutaneous tissue and cerebrospinal fluid. The present study will facilitate better understanding of the pathogenesis of facial nerve paralysis, vertigo, hearing impairment and other cranial nerve dysfunction of Ramsay Hunt syndrome.

Edematous Swelling of the Facial Nerve in Bell's Palsy

Surgical decompression of the intratemporal facial nerve from the geniculate ganglion to the stylomastoid foramen was carried out in 91 patients with Bells palsy. All of the patients had denervation exceeding 95%, and a suprastapedial lesion. Edematous swelling of the nerve was assessed using the following three grades: + +, nerve swells beyond the bony facial canal; +, nerve swells beyond the nerve sheath, but within the bony canal, and -, no notable swelling observed. Varying degrees of swelling of the nerve were noted in all of the patients from onset to the end of the ninth week. The incidence of + + swelling was highest within 3 weeks of onset and then declined. + + swelling was most often noted in the vicinity of the geniculate ganglion, and was thought to be a manifestation of inflammation due to herpes simplex virus infection. There was a clear time dependency of the swelling in the horizontal and pyramidal segments, but not in the mastoid segment. After the ninth week, the incidence of swelling decreased sharply and no swelling of the nerve was observed in about one-third of the patients. Considering the etiology and the analysis of edematous swelling, we propose that the course of Bells palsy be differentiated into an acute phase (the first 3 weeks after onset), a subacute phase (from the fourth to ninth weeks) and a chronic phase (after the tenth week).Surgical decompression of the intratemporal facial nerve from the geniculate ganglion to the stylomastoid foramen was carried out in 91 patients with Bell’s palsy. All of the patients had denervation exceeding 95% and a suprastapedial lesion. Edematous swelling of the nerve was assessed using the following three grades: + + , nerve swells beyond the bony facial canal; + , nerve swells beyond the nerve sheath, but within the bony canal, and − , no notable swelling observed. Varying degrees of swelling of the nerve were noted in all of the patients from onset to the end of the ninth week. The incidence of + + swelling was highest within 3 weeks of onset and then declined. + + swelling was most often noted in the vicinity of the geniculate ganglion, and was thought to be a manifestation of inflammation due to herpes simplex virus infection. There was a clear time dependency of the swelling in the horizontal and pyramidal segments, but not in the mastoid segment. After the ninth week, the incidence of swelling decreased sharply and no swelling of the nerve was observed in about one-third of the patients. Considering the etiology and the analysis of edematous swelling, we propose that the course of Bell’s palsy be differentiated into an acute phase (the first 3 weeks after onset), a subacute phase (from the fourth to ninth weeks) and a chronic phase (after the tenth week).

Demyelination Associated with HSV-1-Induced Facial Paralysis

In 1995, we developed an animal model of transient homolateral facial nerve paralysis by inoculating Herpes simplex virus type 1 (HSV-1) into the auricle of mice. This study examined the mechanism of facial nerve paralysis in this model histopathologically. Using the immunofluorescence technique with anti-HSV-1 antibody, the time course of viral spread and the site of viral replication were investigated over the entire course of the facial nerve. Furthermore, viral replication and nerve degeneration at the site of viral replication were observed by electron microscopy. On the 7th day after inoculation, facial paralysis was observed in more than 60% of mice. Immunofluorescence study revealed HSV-1 in the geniculate ganglion, the descending root, and the facial nucleus at this stage. On the 9th day, the descending root in the sections stained with osmium looked pale, because prominent demyelination had occurred in this region; electron micrographs showed many degenerated oligodendrocytes and large naked axons. In contrast, the facial nucleus neurons showed no remarkable degeneration, despite HSV-1 particles in their cytoplasm. From these findings, we concluded that facial nerve paralysis in this model is caused mainly by facial nerve demyelination in the descending root.

Delayed facial palsy after middle-ear surgery due to reactivation of varicella-zoster virus

Viral reactivation is thought to be an important cause of post-operative facial palsy of delayed onset. We present an unusual case of Ramsay-Hunt syndrome that occurred as a consequence of middle-ear surgery by triggering varicella-zoster virus reactivation. As a pathognomonic auricular eruption was not seen, the patient was initially misdiagnosed as iatrogenic facial palsy. Clinical features, diagnosis and management are discussed.

Resection of peripheral branches of the posterior nasal nerve compared to conventional posterior neurectomy in severe allergic rhinitis

OBJECTIVE Transnasal resection of the posterior nasal nerve (TRPN) is the surgical procedure for drug therapy-resistant, intractable allergic rhinitis (AR). Submucous inferior turbinectomy also improves nasal symptoms in severe AR. Surgical injury to this peripheral nerve fibre may be the major cause of the decrease in allergic symptoms. During submucous turbinectomy, we have identified the peripheral branches of the posterior nasal nerve in the inferior turbinate and resected them (SRPN). The aim of this study was to evaluate the therapeutic effects of turbinoplasty with SRPN in severe AR. METHODS Improvements in subjective symptoms were compared between 13 patients who underwent SRPN with turbinoplasty (Group 1) and 11 who underwent TRPN combined with turbinoplasty and SRPN (Group 2) by retrospective chart review. Pre- and postoperative sneezing, rhinorrhea, and nasal obstruction were evaluated with questionnaires. Postoperative complications and drug therapy before and after surgery were investigated. RESULTS All symptoms improved postoperatively in both groups, with no significant differences in the improvements in nasal symptom scores between the groups. CONCLUSIONS SRPN combined with submucosal turbinectomy was shown to be a safe, useful, and efficient approach to patients with AR unresponsive to medical therapy. Although this is a short-term study, the results of this study suggest that SRPN represents one of the treatment options for intractable AR.

Salivary gland choristoma of the middle ear in a child: A case report

Salivary gland choristoma is a heterotopic rest of histologically normal salivary gland tissue. According to Ha et al,1 only 24 cases have been reported in the literature since the first description by Taylor and Martin in 1961.2 Because most of these ectopic rests occur in the middle ear, they should be distinguished from other mass lesions in the middle ear cavity, such as middle ear cholesteatoma, facial neuroma, and glomus tumor. This lesion does not require total removal because there is no potential for further growth or malignant change.3 We present the case of a 1-year-old girl with a salivary gland choristoma in the middle ear. Because the right middle ear mass appeared whitish and located behind the intact tympanic membrane, we first suspected it to be congenital middle ear cholesteatoma. Exploratory tympanotomy, however, revealed a salivary gland choristoma that adhered tightly to the facial nerve. Differential diagnosis and treatment of this rare condition are discussed.