It is possible to predict the prognosis of facial paralysis on the basis of several clinical findings. NET response, severe initial paralysis, age 50 years or older, and, as a second-stage factor, severity of facial paralysis 1 month after the onset were found to be especially important factors for predicting the prognosis of facial paralysis.

The reactivation of herpes simplex virus-1 on the affected side is involved as a pathogenic factor of Bell's Palsy. A reactivation of herpes simplex virus-1 may be generated even on the unaffected side in the early phase of the disease. Herpes simplex virus deoxyribonucleic acid was not detected in any of the examined specimens collected from the remaining 11 cases. The need for constant study to clarify other causative factors of Bell's Palsy remains.

Evaluations with the two systems correlated significantly with self-evaluations by patients on the whole. These two methods of evaluation are considered appropriate not only for physicians but also for patients. In contrast, some discrepancies were observed. This point should be taken into account in routine patient care.

The possible involvement of depression on cellular immunity in reactivation of varicella-zoster virus (VZV) in herpes zoster oticus was investigated. The subjects comprised 59 cases of herpes zoster oticus, 33 cases of herpes zoster sine herpete (ZSH) with facial paralysis, and 205 cases of Bell's palsy. The transformation rate of lymphocytes to phytohaemagglutinin in herpes zoster oticus tended to be lower than that in Bell's palsy. In skin tests with purified protein derivatives of tuberculin, the positivity rate in herpes zoster oticus was significantly lower than that in Bell's palsy (p<0.015). In skin tests using VZV antigen, the positivity rate in herpes zoster oticus and ZSH were significantly lower than that of Bell's palsy (p<0.001 andp<0.015, respectively). Thus, it was noted that cellular immunity, especially specific cellular immunity against VZV, was significantly depressed in herpes zoster oticus and ZSH. We consider that depression of specific cellular immunity plays an important role in triggering reactivation of VZV and onset of these diseases.