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