Bell's palsy, which is defined as idiopathic peripheral facial paralysis of sudden onset, accounts for >50% of all cases of facial paralysis. Different theories on the etiology of Bell's palsy have been proposed and investigated. Various clinical studies have suggested an etiological link between Bell's palsy and herpes simplex virus (HSV). In addition, animal experiments have shown the ability of HSV to induce facial paralysis. In our opinion, the possible link between Bell's palsy and HSV can only be explored properly by studying the human facial nerve, and especially the geniculate ganglion itself. Different groups have tried to detect hypothetically reactivated and hypothetically latent HSV in the facial nerves of Bell's palsy patients and control patients, respectively. The isolation of infectious HSV from facial nerve tissue by conventional cell culture methods appeared to be very difficult, also when Bell's palsy patients were tested. Instead, modern molecular methods, such as in situ hybridization and the polymerase chain reaction (PCR) could easily detect HSV DNA in geniculate ganglia. The detection of HSV‐specific latency‐associated transcripts in the ganglia of control patients provided further evidence for the hypothetically latent state of HSV in the geniculate ganglia in these patients. Recent PCR experiments performed by a Japanese group strongly suggest that the area adjacent to the geniculate ganglia does not usually contain any HSV at all, except in patients with Bell's palsy. This well‐controlled study provides conclusive evidence that reactivation of HSV genomes from the geniculate ganglia is the most important cause of Bell's palsy. Consequently, it has been suggested that “Bell's palsy” be renamed as “herpetic facial paralysis”.

A serological study using the complement fixation reaction for herpes zoster virus (HZV) and herpes simplex virus (HSV) was carried out on 120 patients with Bell's palsy and 5 with Ramsay-Hunt syndrome. Three Bell's palsy patients (2.5%) showed a significant HZV antibody titre rise. In no case was a rise of HSV antibody titre observed. Two Ramsay-Hunt patients showed a significant rise of HZV antibody titre. Rise of HSV antibody titre was not observed in this group either. The Monosticon test to exclude infectious mononucleosis, proved to be negative in all cases of Bell's palsy. In 2 cases of Bell's palsy, a biopsy specimen for virus isolation was obtained during a decompression operation. No virus could be cultured from the epineurium of the first patient. That of the second patient was found to contain HSV type I. There was no serological evidence of a HSV antibody titre rise.

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A serological study using the complement fixation reaction for herpes zoster virus (HZV) and herpes simplex virus (HSV) was carried out on 120 patients with Bell's palsy and 5 with Ramsay‐Hunt syndrome. Three Bell's palsy patients (2.5%) showed a significant HZV antibody titre rise. In no case was a rise of HSV antibody titre observed. Two Ramsay‐Hunt patients showed a significant rise of HZV antibody titre. Rise of HSV antibody titre was not observed in this group either. The Monosticon test to exclude infectious mononucleosis, proved to be negative in all cases of Bell's palsy. In 2 cases of Bell's palsy, a biopsy specimen for virus isolation was obtained during a decompression operation. No virus could be cultured from the epineurium of the first patient. That of the second patient was found to contain HSV type I. There was no serological evidence of a HSV antibody titre rise.