Nobumitsu Honda

The Australian Society of Otolaryngology Head & Neck Surgery, Evans Head, New South Wales, Australia

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Publications (32)64.39 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The anatomical configuration of the facial nerve differs greatly between the intratemporal and extratemporal portions. The purpose of this study was to investigate the incidence of facial synkinesis and misdirection on clamping the facial nerve at the intratemporal or extratemporal portion of the facial nerve in guinea pigs. Experimental study. In 16 guinea pigs, the facial nerve was clamped with microsurgical needle forceps at either the extratemporal (group A) or intratemporal (group B) segment. Facial nerve function was evaluated 1 week postoperatively using electroneurography (ENoG), and the incidence of facial synkinesis was evaluated 15 weeks postoperatively using an evoked blink reflex test. Fifteen weeks postoperatively, two retrograde fluorescent tracers (Dil [1-1'-dioctodecyl-3,3,3',3'-tetramethyl-indocarbocyanine perchlorate] and True Blue) were injected into the facial muscles to observe reorganization of the facial nucleus. No significant difference in the ENoG threshold was observed between groups A and B. In group A, none of the animals developed facial synkinesis and the somatotopic organization of the facial nucleus was not disturbed. In contrast, synkinesis occurred and the somatotopic organization was disturbed in group B. A lack of funicular structure within the intratemporal facial nerve increases the possibility of misdirected regenerating axons and synkinesis.
    The Laryngoscope 03/2010; 120(5):1022-7. · 1.98 Impact Factor
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    ABSTRACT: To investigate the effects of valacyclovir and prednisolone in comparison with those of placebo and prednisolone for the treatment of Bell's palsy, excluding zoster sine herpete. Prospective, multicenter, randomized placebo-controlled study. Six academic tertiary referral centers. Ultimately, 221 patients with Bell's palsy who were treated within 7 days of the onset. Serological and polymerase chain reaction examinations were performed to distinguish Bell's palsy from zoster sine herpete. 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. 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. 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). The valacyclovir and prednisolone therapy was more effective in treating Bell's 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 Bell's palsy cases based on an etiologic background.
    Ontology & Neurotology 05/2007; 28(3):408-13. · 2.01 Impact Factor
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    ABSTRACT: Although both T-cell subsets are essential for inhibiting HSV-1 reactivation in the GG, CD4 + T cells play a more important role in host defense against virus replication. To elucidate the host immunological factors that participate in herpes simplex virus type 1 (HSV-1) reactivation in the geniculate ganglia (GG) and lead to facial paralysis, we developed a mouse model of facial paralysis that involved the reactivation of HSV-1 following general immune suppression. Eight weeks after recovery from primary facial paralysis caused by inoculating the auricle with HSV-1 the auricle was scratched and mice (n = 69) were given an i.p. injection of either anti-CD4 (n = 46) or anti-CD8 (n = 23) monoclonal antibody to deplete specific T-lymphocyte subsets. Following this reactivation procedure, the rate of recurrent facial paralysis was compared between the two models. The GG were examined histopathologically and using polymerase chain reaction to detect HSV-1 DNA. Facial paralysis developed in 42% of mice in the anti-CD4 model and in 13% in the anti-CD8 model. HSV-1 DNA was detected in 50% of the mice in both models. Histopathologically, neurons were destroyed in parts of the GG and numerous virus particles were seen in the surviving neurons.
    Acta Oto-Laryngologica 04/2005; 125(3):316-21. · 1.11 Impact Factor
  • Otolaryngology Head and Neck Surgery 04/2004; 130(3):378-80. · 1.73 Impact Factor
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    ABSTRACT: We present a rare case of bilateral cerebrospinal fluid (CSF) otorrhea via multiple bony defects in the left tegmen and a single defect with the herniated brain tissue on the right side. Initially, the patient complained of left hearing loss and fullness and was diagnosed with serous otitis media. After myringotomy, the pulsating watery discharge suggested CSF otorrhea. Five months after surgical repair of the left side, right-side CSF leakage occurred. The right side was repaired surgically, and the patient recovered without incident. From our findings and a review of the literature, we postulate that bilateral CSF otorrhea resulted mainly from the thinness of the tegmen because of well-pneumatized mastoid air cells and the weakness of the dura after chronic inflammatory changes. In case of spontaneous CSF otorrhea, the roof of tegmen should be assessed bilaterally with care using radiologic examinations so as not to overlook a subclinical condition on the contralateral side.
    American Journal of Otolaryngology 01/2004; 25(1):68-72. · 1.23 Impact Factor
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    ABSTRACT: Problem: The facial nerve synkinesis is one of the common complaints after facial palsy. However, the precise mechanism of synkinesis is still unknown. In this study we tried to establish an animal model of synkinesis.Methods: Extratemporal portion of the facial nerve (group 1, n = 6) and the intratemporal portion (group 2, n = 6) were compressed by using a micro needle holder. After the compression, the grade of facial nerve injury was evaluated by electroneurography. The existence of synkinesis was judged by the presence of R1 in the orbicularis oris muscle by the electrophysiolgical blink reflex. For evaluating the misdirection of nerve fibers, double labeling was performed by injecting retrograde fluorescence tracer in the orbicularis oculi muscle and the orbicularis oris muscle, and then facial nucleus was investigated for the presence of the neurons with aberrant fluorescence.Results: In both groups, all animals showed the ENoG threshold under 10%. In group 1, none of animals developed synkinesis. On the other hand, in group 2, all animal developed synkinesis. Furthermore, disrupted neurons in the facial nucleus, representing the existence of misdirection, were observed in all animals of group 2.Conclusion: In this study we succeeded in making a synkinesis model only in group 2 and reported the existence of misdirection in these animals. Sunderland found that the facial nerve consisted of a single bundle in the intratemporal portion, even though it had a mulitifuniculated plexiform structure in the extratemporal portion. Because of this anatomical feature, when the facial nerve was injured in the intra- and extra-temporal portions, the misdirection may occur only in the intra-temporal portion. This is thought as a reason for the appearance of synkinesis only in group 2.Significance: It is important to know the pathogenesis of synkinesis for diagnosing and treating facial nerve disorders.Support: None reported.
    Otolaryngology-head and Neck Surgery - OTOLARYNGOL HEAD NECK SURG. 01/2004; 131(2).
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    ABSTRACT: Problem: The middle ear mechanism involves the conduction of mechanical vibrations along the ossicular chain. Although the functional mechanism and ossicular motion of the middle ear have been revealed in many papers, the acoustic role of ossicular joints is still unclear in human temporal bones.Methods: Eleven fresh human temporal bones with intact middle and inner ear were measured for the peak-to-peak displacement and phase on umbo and stapes footplate using a laser Doppler vibrometer system. Sound was generated and controlled by a SYSid 6.5 audio analysis system and the stimulus was a sound input of 80 to 120 dB SPL at the tympanic membrane over the 0.1 to 10 kHz frequency range. After the baseline measurements, incus was carefully removed and replaced to ordinary position with cyanoacrylate glue. Measurements of umbo and stapes footplate motion were repeated.Results: The average time lag between umbo and footplate in the middle ear was 89 μs, which was constant at a measured frequency range from 0.1 to 10 kHz. After the fixation of ossicular joints, the delay was reduced to 35 μs for sound transmission between umbo and stapes footplate. With the incus removed and reglued, the footplate displacement was about 7 dB lower than for the intact middle ear at frequencies below 1 kHz.Conclusion: The time lag in the middle ear seems to be caused by the slippage of the ossicular joints, not only the I-S joint but also the M-I joint. The 89 μs delay means that when malleus moves inward, stapes footplate moves outward at 5.6 kHz.Significance: In middle ear surgery, the surgical exposure could be improved by resection of incus, because the acoustic damage of the incus reposition was less than 6 dB.Support: None reported.
    Otolaryngology-head and Neck Surgery - OTOLARYNGOL HEAD NECK SURG. 01/2004; 131(2).
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    ABSTRACT: To investigate the therapeutic effects of acyclovir and prednisolone in relation to the timing of treatment in Bell's palsy. This was a retrospective study of 480 Bell's palsy patients who were treated with oral acyclovir and prednisolone (94 cases) or prednisolone alone (386 cases). Patients met the after criteria: (1) severe or complete Bell's 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). Rate of recovery, which was defined as a facial score of 36 or more, and the absence of contracture with synkinesis. 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. 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 Bell's palsy.
    Ontology & Neurotology 12/2003; 24(6):948-51. · 2.01 Impact Factor
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    ABSTRACT: Objective: To investigate the therapeutic effects of acyclovir and prednisolone in relation to the timing of treatment in Bell's palsy. Study Design: This was a retrospective study of 480 Bell's 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 Bell's 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 Bell's palsy. Bell's palsy is defined as an idiopathic peripheral facial nerve paralysis of sudden onset and is considered the most common cause of facial nerve paralysis. Theories on a viral etiology for Bell's palsy have been proposed (1) and investigated (2,3), and herpes simplex virus (HSV) has been implicated as a causative pathogen in recent molecular biological investigations (4). In 1996, we detected HSV genomes in the facial nerve fluid of 79 percent of patients with Bell's palsy (5). That study provided conclusive evidence that the reactivation of HSV genomes from the geniculate ganglia is the most important cause of Bell's palsy. In addition, animal experiments performed in our laboratory have demonstrated the ability of HSV to induce facial paralysis (6-8). Conversely, varicella zoster virus (VZV) reactivation was detected in 29 percent of Bell's palsy patients as zoster sine herpes (ZSH) (9). We believe that HSV and VZV are both major etiologic agents of Bell's palsy. Unfortunately, more than 10 percent of Bell's palsy patients are unable to recover normal facial movement after conventional, conservative corticosteroid treatment. In this study, we used acyclovir to improve the rate of complete recovery; acyclovir interferes with the DNA polymerase of herpes virus and inhibits DNA replication. Some trials of acyclovir therapy have already been evaluated in patients with Bell's palsy (10,11). However, the correlation between the timing of treatment and the recovery of facial nerve function has not been analyzed in sufficient numbers of patients. In this study, we retrospectively compared the outcomes of 480 Bell's palsy patients who were treated with both acyclovir and prednisolone or with prednisolone alone. Treatment was begun within 7 days of onset of paralysis to determine the period during which acyclovir was effective in treating Bell's palsy. We also investigated the significance of early remission after these therapies.
    Ontology & Neurotology 10/2003; 24(6):948-951. · 2.01 Impact Factor
  • Yoshihisa Ookouchi, Nobumitsu Honda, Kiyofumi Gyo
    Otolaryngology Head and Neck Surgery 02/2003; 128(1):160-2. · 1.73 Impact Factor
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    ABSTRACT: 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.
    Experimental Neurology 12/2002; 178(1):68-79. · 4.65 Impact Factor
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    ABSTRACT: Although Ramsay Hunt syndrome is one of the most important diseases causing peripheral facial palsy, the detailed pathology of the disease in the intratemporal facial nerve remains unclear. The purpose of this study was to increase knowledge of the pathogenesis of the syndrome by means of surgical findings. Between April 1976 and March 1997 we performed subtotal decompression of the facial nerve in 74 patients with severe Ramsay Hunt syndrome. The grade of nerve swelling was assessed using a microscope and recorded in a standardized form. The relationships between nerve swelling, the timing of surgery and the swelling of each segment were analyzed. Pronounced neural swelling, involving the geniculate ganglion and the horizontal segment, was consistent finding in the acute phase. Although the incidence of pronounced swelling of the horizontal segment gradually declined with time after onset, in most cases nerve swelling persisted even beyond the 16th week after onset. These data suggest that diffuse viral neuritis occurs throughout the intratemporal facial nerve. We assume that the viral inflammatory swelling involving the geniculate ganglion and horizontal segment is mostly responsible for the acute facial palsy in the acute phase.
    Acta Oto-Laryngologica 05/2002; 122(3):348-52. · 1.11 Impact Factor
  • Otology & Neurotology - OTOL NEUROTOL. 01/2002; 23.
  • Otology & Neurotology - OTOL NEUROTOL. 01/2002; 23.
  • Otology & Neurotology - OTOL NEUROTOL. 01/2002; 23.
  • Otology & Neurotology - OTOL NEUROTOL. 01/2002; 23.
  • Otology & Neurotology - OTOL NEUROTOL. 01/2002; 23.
  • Otology & Neurotology - OTOL NEUROTOL. 01/2002; 23.
  • Otology & Neurotology - OTOL NEUROTOL. 01/2002; 23.
  • [Show abstract] [Hide abstract]
    ABSTRACT: In order to investigate the mechanism of Bell's palsy, we developed an animal model of facial nerve paralysis induced by the reactivation of herpes simplex virus type 1 (HSV-1). Eight weeks after recovery from facial nerve paralysis caused by inoculation with HSV-1, the mice were treated with auricular skin scratch at the site of the previous inoculation, or with intraperitoneal injection of anti-CD3 monoclonal antibody (mAb), or combination of both procedures. No mice developed facial nerve paralysis when they were treated with either auricular scratch or mAb injection alone. In contrast, 20% of mice developed facial nerve paralysis with the combined treatment. With one exception, no mouse treated with either auricular scratch or mAb injection showed HSV-I DNA in their facial nerve tissue, whereas 4 out of 6 mice receiving both treatments showed HSV-1 DNA on day 10 after treatment. Histopathological findings showed neuronal degeneration in the geniculate ganglion and demyelination of the facial motor nerve in paralyzed mice. These findings suggest that a combination of stimuli, local skin irritation, and general immunosuppression is essential for successfully inducing facial nerve paralysis in mice with latent HSV-1 infection.
    Journal of Neuropathology and Experimental Neurology 07/2001; 60(6):621-7. · 4.35 Impact Factor

Publication Stats

390 Citations
64.39 Total Impact Points

Institutions

  • 2004
    • The Australian Society of Otolaryngology Head & Neck Surgery
      Evans Head, New South Wales, Australia
  • 2002–2004
    • Ehime University
      • Department of Otolaryngology
      Matuyama, Ehime, Japan