Since the ischemic hypothesis was first proposed by Kettel in 1947 [1], ischemia has been widely accepted as having one of the most important roles in the pathogenesis of Bell palsy. However, direct evidence supporting this hypothesis was lacking. Dr. Devriese [2] was the first to clearly show that increasing pressure and subsequent ischemia of the facial nerve could produce facial palsy. The results apparently substantiated Kettel's hypothesis and were repeatedly presented as having a role in the pathogenesis of Bell palsy at the Third (Zurich, 1976) and Fourth (Los Angeles, 1980) International Symposium on the Facial Nerve. We thus believe it appropriate to have referred to his representative paper.

It is true that the incidence of Bell palsy is lower than that of other manifestations of herpes simplex virus. The difference in the incidences of herpes manifestations might depend on the differences in frequency of latent herpes simplex virus infection between the geniculate ganglion and trigeminal ganglia or on the tolerance or susceptibility of ganglion cells and facial nerve against HSV-1 infection. For example, Furuta and colleagues [3] showed latent HSV-1 in 71% of human geniculate ganglia and in 81% of trigeminal ganglia. Asymptomatic or subclinical involvement of the facial nerve might exist even if HSV-1 reactivates in the geniculate ganglion, as occurs in patients with auricle herpes without facial palsy. In an animal model, we found subclinical involvement of HSV-1 in the facial nerve [4]. We also found that HSV-1 infection in the facial nerve causes inflammatory edema of the nerve in the narrow bony facial canal in which the facial nerve is compressed. Thus, HSV-1 infection in the nerve is the primary cause of facial palsy and, following compression and ischemia, might be secondary factors leading to profound palsy.

In 1907, James Ramsay Hunt investigated classic herpes zoster oticus and classified it into four different types according to the presence of facial palsy or vestibulo-cochlear symptoms [5]. His name was attached because of his intensive studies. Although zoster involvement is not localized in the geniculate ganglion as Hunt explained but rather extends to the cephalic ganglia, the term "Ramsay Hunt syndrome" has been more commonly used and is widely accepted worldwide. Perhaps the Eighth International Symposium on Facial Nerve, to be held in Japan in 1997, will be a good place to discuss this topic.