Is Bell's palsy a reactivation of varicella zoster virus?

  • Michael Morgan* (Corresponding Author)
  • , Margaret Moffat
  • , Lewis Ritchie
  • , Ian Collacott
  • , Thomas Brown
  • *Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

53 Citations (Scopus)

Abstract

Despite various pointers to an infectious aetiology, the cause of Bell's palsy remains obscure. We examined paired sera from 62 patients with facial palsy and 50 age and sex matched contemporaneous controls. Significantly more patients than controls had IgM antibodies by ELISA to varicella zoster virus (56.5% vs. 20%, P=0.0001) and herpes simplex virus (47.9% vs. 18%, P=0.006). Additionally, significantly more patients than controls were positive for CF antibody to varicella zoster virus (14.5% vs. 0%, P=0.004) but not to herpes simplex or cytomegalovirus. Significantly more controls than patients (54% vs. 25.8%, P=0.002) had no evidence of antigenic stimulation by any member of the herpesvirus group. No significant difference between patients and controls in seropositivity by IgM ELISA to cytomegalovirus, Epstein-Barr virus and IFA for human herpes virus 6 was found. Furthermore, there was no significant difference between the two groups as to evidence of recent infection by the following agents: rubella virus and Borrelia burgdorferi by IgM ELISA, influenza A, influenza B, adenovirus, respiratory syncytial virus, mumps and measles, Mycoplasma pneumoniae, Coxiella burnetii and chlamydia spp. by complement fixation text. The first reported case of clinically and serologically proven Mycoplasma pneumoniae pneumonia associated with Bell's palsy is described. The rate of complete recovery at 6-8 weeks after onset was not significally different in patients who were given steroids compared to those who were not. Ear related symptoms were the most common, occurring in 12 ot 65 cases, but only three (4.6%) had clinical shingles (vesicles in ear). The above data suggest that as in Ramsay Hunt syndrome, reactivation of varicella zoster virus may constitute the 'final common pathway' in the pathogenesis of Bell's palsy and that the latter is in effect a manifestation of zoster sine herpete. Further studies are needed to determine the pathogenesis of facial nerve damage as well as the benefit, if any, or early acyclovir therapy on the course and outcome of Bell's palsy.

Original languageEnglish
Pages (from-to)29-36
Number of pages8
JournalJournal of Infection
Volume30
Issue number1
DOIs
Publication statusPublished - Jan 1995

Bibliographical note

Funding Information:
This study was supported by financial grants from Grampian Health Board and Tenovus-Scofland. The authors are indebted to Grampian General Practitioners, the staff of the Virology Laboratory, Aberdeen Royal Hospitals and Liz Byrne for their assistance during the course of this study. We would also like to thank Daphne Russell for help with statistical analysis and Professor % H. Pennington and Dr H. McKenzie for their support.

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