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

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Abstract

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.

Introduction

The cause of idiopathic peripheral facial palsy, or Bell's palsy, is still controversial. Recent reports, however, suggest that reactivation of herpes simplex virus type 1 (HSV-1) is one of its major causes [1], [2]. On the basis of this hypothesis, Adour et al. [3] conducted a double-blind controlled study evaluating the effects of an antiviral agent in combination with conventional steroid therapy in patients with Bell's palsy. They reported that a favorable response to the acyclovir–prednisone therapy was obtained when the agents were administered within 3 days of onset of palsy. In addition, de Diego et al. [4] reported that acyclovir therapy alone resulted in a worse recovery than prednisone therapy alone. These reports, however, did not determine whether or not the patients actually had HSV-1 reactivation. Furthermore, varicella-zoster virus (VZV) is known to cause acute peripheral facial palsy (APFP) without skin lesions; such cases are termed zoster sine herpete (ZSH) and are initially diagnosed as Bell's palsy. As such, it would be beneficial to distinguish ZSH from Bell's palsy by employing appropriate virological tests.

We previously reported that polymerase chain reaction (PCR) is a useful tool for the early diagnosis of HSV-1 reactivation in patients with Bell's palsy [2]. In a recent study, we distinguished cases of ZSH from Bell's palsy using PCR and serological assays and reported that 30% of patients clinically diagnosed with Bell's palsy had HSV-1 reactivation within 5 days of onset of facial palsy [5].

The facial palsy associated with Ramsay Hunt syndrome is more severe and has a lower recovery rate than that of Bell's palsy [6]. Acyclovir–prednisone treatment yielded a beneficial response in patients with Ramsay Hunt syndrome when the treatment began within 3 days of onset of palsy [7]. No report, however, has described the severity of facial palsy in patients who have HSV-1 reactivation upon the onset of facial palsy. Furthermore, because HSV-1 reactivation is difficult to diagnose early after onset, the effect of antiviral agents on the recovery of palsy in patients with HSV-1 reactivation has not been evaluated.

Based on a PCR diagnosis of HSV-1 reactivation, the present study analyzed the severity of facial palsy in patients with HSV-1 reactivation and sought to determine whether acyclovir–prednisone therapy is more efficacious than conventional steroid therapy for the treatment of facial palsy in patients with HSV-1 reactivation.

Section snippets

Patients

Between September 1994 and January 2000, 185 patients over 10 years of age with APFP were diagnosed with Bell's palsy at the first visit (within 5 days of onset) after careful clinical examination. After the first visit, zoster lesions appeared in nine of the 185 patients and Ramsay Hunt syndrome was diagnosed in these nine patients. Therefore, 176 patients were clinically diagnosed with Bell's palsy.

Diagnosis of HSV-1 reactivation

At every visit, saliva samples were collected from each patient. DNA was extracted from 100 μl

Diagnosis of HSV-1 reactivation

HSV-1 DNA was detected by PCR in 16 of the 90 (18%) patients who were tested immediately upon admission. Twelve of the 16 patients were given acyclovir–prednisone treatment within 7 days of onset (acyclovir–prednisone group). Two PCR-positive patients did not receive acyclovir–prednisone therapy because their palsy was judged as Grade III. One PCR-positive patient, who had hepatitis, received acyclovir alone and one patient received prednisone alone due to the delay of the second visit (Table 1

Discussion

On the basis of virological analyses, the present study shows that the grade of facial palsy in patients with zoster sine herpete is more severe than that in patients without HSV-1 or VZV reactivation (Bell's palsy). These results concur with previous reports that the grade of palsy associated with Ramsay Hunt syndrome is more severe than that associated with Bell's palsy [6]. In contrast, no difference in the severity of palsy was observed between patients with HSV-1 reactivation and those

Acknowledgements

We thank Izumi Satoh and Erina Katoh for their excellent technical assistance. This study was supported by grant-in-aid for Scientific Research, Ministry of Education, Science and Culture (Japan) and The Akiyama Foundation.

References (9)

  • S. Murakami et al.

    Bell's palsy and herpes simplex virus: Identification of viral DNA in endoneurial fluid and muscle

    Ann. Intern. Med.

    (1996)
  • Y. Furuta et al.

    Reactivation of herpes simplex virus type 1 in patients with Bell's palsy

    J. Med. Virol.

    (1998)
  • K. Adour et al.

    Bell's palsy treatment with acyclovir and prednisone compared with prednisone alone: A double-blind, randomized, controlled trial

    Ann. Otol. Rhinol. Laryngol.

    (1996)
  • J.I. de Diego et al.

    Idiopathic facial paralysis: A randomized, prospective, and controlled study using single-dose prednisone versus acyclovir three times daily

    Laryngoscope

    (1998)
There are more references available in the full text version of this article.

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