[Therapy of post-herpetic neuralgia. Pain therapy using an anti-varicella zoster immunoglobulin].

After remission of the dermatological symptoms of herpes zoster infection, post-zoster neuralgia (PZN) can persist or recur for months and years. Most frequently, satisfactory therapy of PZN is not possible. During recent years the persistence of viruses on the surface of neuronal cells has been discussed as the possible reason for chronic pain. Virostatic therapy as well as polyvalent 7s-IgG-immunoglobulins exerted a minimal effect on the pain level. In an open trial we therefore used a specific anti-varicella zoster immunoglobulin (VZI) for treatment of PZN. METHODS. In our study ten patients (six female, four male; age 55-87 years) with latencies between the acute infection and onset of immunoglobulin therapy between 10 months and 3 years were included. PZN was located according to the dermatomes involved: one trigeminal nerve, one cervical, four thoracic and four lumbal segments. All patients had received more than two different drugs or had had therapeutic procedures without success. On the visual analogue scale (VAS: 0-100%) all patients rated their subjective pain with at least 49%. Before starting the study the preexisting specific drug therapy was discontinued in all patients. VZI infusion was given i.v. at a dose of 2 ml/kg body weight within 120 min. All patients had to rate their pain at the VAS every 10 min during the 120 min infusion time, at day 1, 2, 7, 14, 30 and than every month after therapy with VZI. RESULTS. Even during the infusion all ten patients reported a sharp decrease in pain of at least 47% (average 87%) on the VAS. Fourteen days later the remaining pain level averaged 6% VAS. Only the first of the 10 patients reported twice a recurring increase of pain. He therefore received the standard dosage of VZI again at day 2 and day 214, respectively. Thereafter until day 566 the pain level of this patient was lower than 10% VAS. The maximum surveillance interval has so far been 600 days. No side-effects due to the infusion of VZI have been encountered. CONCLUSIONS. Treating pain in persistent PZN is extremely difficult and mostly results in a small diminution of the pain level. Persistence of viruses on the neuronal cell surface and resulting reduction of "luxury functions" of those cells may explain algogenesis by PZN and resistance to therapeutic efforts. We used VZI for the first time for therapy of PZN and observed a striking analgesic effect in all patients for the entire surveillance time.