[Prevention of wound complications after salvage total laryngectomy following chemoradiotherapy with a pectoralis major muscle interposition flap].

There is an increased risk of wound complications in patients undergoing salvage laryngectomy following chemoradiotherapy. To reduce the rate of wound complications after a salvage total laryngectomy, a fresh tissue reinforcement of the pharyngeal suture line (pharyngeal interposition graft) has been reported to be useful. In the present study, wound complications after a salvage total laryngectomy with a pectoralis major muscle flap as a pharyngeal interposition graft were analyzed. Four patients with recurrent laryngeal cancer (three with supraglottic, and one with glottic cancer) after chemoradiotherapy underwent salvage total laryngectomy using a pectoralis major muscle interposition flap. Minor wound complications were observed in three of the four patients, with an infection around the tracheostoma, a minor subcutaneous abscess, and a superficial skin necrosis in one patient each. These complications were managed with local wound care. No patients had major wound complications such as pharyngocutaneous fistulas. There were no necroses or wound complications of the pectoralis major muscle flap. This study has suggested that the pectoralis major muscle flap as a pharyngeal interposition graft is safe and useful for prevention of wound complications in salvage total laryngectomy following chemoradiotherapy.

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 Bell's palsy, excluding zoster sine herpete. STUDY DESIGN: Prospective, multicenter, randomized placebo-controlled study. SETTING: Six academic tertiary referral centers. PATIENTS: 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. 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 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.

Varicella-zoster virus load and cochleovestibular symptoms in Ramsay Hunt syndrome.

OBJECTIVES: The mechanism by which varicella-zoster virus (VZV) reactivation causes cochleovestibular symptoms (CVSs) in patients with Ramsay Hunt syndrome (RHS) remains to be elucidated. The present study analyzed the relationship between VZV load and the onset of CVSs in RHS. METHODS: The subjects consisted of 56 patients with RHS; 29 exhibited CVSs and facial paralysis (FP; group 1), and 27 exhibited FP without CVSs (group 2). The VZV DNA copy number in the saliva was measured with a quantitative polymerase chain reaction. Anti-VZV antibodies were assayed by an enzyme-linked immunosorbent assay with paired sera. RESULTS: There was no significant difference in maximum viral copy number between the two groups. In group 1, CVSs occurred at various times between the early phase and the regression phase of VZV reactivation. In some patients, CVSs occurred in the early phase of VZV reactivation, before the onset of zoster lesions and FP. CONCLUSIONS: There are various different patterns in the development of eighth cranial nerve dysfunction, which is caused by progression of neuritis or labyrinthitis following VZV reactivation. Our data suggest that CVSs in RHS may also be caused by reactivation of VZV in the spiral and/or vestibular ganglia.

Varicella-zoster virus reactivation is an important cause of acute peripheral facial paralysis in children.

BACKGROUND: Reactivation of herpes simplex virus type 1 is thought to be a major cause of adult idiopathic peripheral facial paralysis or Bell's palsy. However, few studies have examined the pathogenesis of this condition in children. Serologic assays and polymerase chain reaction (PCR) analysis of paired sera and saliva samples were used here to investigate the causes of acute peripheral facial paralysis in pediatric patients. METHODS: A total of 30 children with acute peripheral facial paralysis were recruited. Paired sera were assayed for evidence of herpesvirus, mumps virus or Borrelia infection. PCR was used to detect herpes simplex virus type 1 and varicella-zoster virus (VZV) DNA in saliva samples. RESULTS: Ramsay Hunt syndrome with accompanying zoster lesions was diagnosed clinically in 2 patients, and VZV reactivation was confirmed serologically. VZV reactivation in the absence of zoster (zoster sine herpete) was diagnosed in 9 patients with either serologic assays or PCR. Thus VZV reactivation was demonstrated in 11 of 30 (37%) patients. The prevalence of VZV reactivation among patients between 6 and 15 years of age was significantly higher than in those younger than 5 years of age (53% versus 9%, P = 0.023). CONCLUSIONS: Our data indicate that VZV reactivation is an important cause of acute peripheral facial paralysis in children, especially those between 6 and 15 years of age.

Varicella-zoster virus DNA level and facial paralysis in Ramsay Hunt syndrome.

We have investigated whether the copy number of varicella-zoster virus (VZV) in saliva correlates with the clinical symptoms in patients with Ramsay Hunt syndrome. A real-time quantitative polymerase chain reaction assay was used to examine the VZV DNA copy number in saliva samples from 37 patients. We detected VZV DNA in 6 of the 7 patients with oropharyngeal zoster lesions (86%) and in 17 of the 30 patients who had zoster lesions only on the skin (57%). Patients with oropharyngeal zoster lesions had a high VZV load in their saliva, and the difference between the copy number in patients with oropharyngeal zoster lesions and those without was around 10,000 copies per 50 microL. In addition, patients with oropharyngeal zoster lesions showed worse recovery of facial function than those without. It seems that the VZV DNA level in saliva reflects the kinetics of viral reactivation in the facial nerve, as well as in the oropharyngeal epithelium, in patients with Ramsay Hunt syndrome.

Variable patterns of varicella-zoster virus reactivation in Ramsay Hunt syndrome.

The mechanism by which reactivation of varicella-zoster virus (VZV) causes facial paralysis in Ramsay Hunt syndrome remains unclear. The relationship between VZV load and the onset of facial paralysis was analyzed in 42 patients with Ramsay Hunt syndrome. The patients were divided into three groups according to the times of appearance of zoster and of facial paralysis; group I (zoster preceding, n = 13), group II (simultaneous, n = 22), group III (paralysis preceding, n = 7). A real-time quantitative PCR assay was used to measure VZV DNA copy number in saliva, and paired sera were assayed for anti-VZV IgG and IgM antibodies. In group I, the VZV DNA-positive rate was low and virus load decreased gradually after the initial hospital visit around the time of onset of paralysis. The level of anti-VZV antibodies had in most cases already increased at that time. In group III, viral load tended to increase after the onset of paralysis and peaked around the time of appearance of zoster. The level of anti-VZV antibodies was low at the onset of paralysis but showed a significant increase when paired sera were tested. In group II, virus load and changes in level of anti-VZV antibodies either resembled group I or group III behavior. These results indicate that facial paralysis in Ramsay Hunt syndrome can occur at various times between the early and the regression phase of VZV reactivation, suggesting that there are variable patterns of development of facial nerve dysfunction caused by VZV reactivation and the progression of neuritis.