The pathogenesis and clinical manifestations of
herpes zoster and
postherpetic neuralgia and the use of nontraditional
analgesics in the management of
postherpetic neuralgia are reviewed.
Herpes zoster represents the reactivation in an immunocompromised host of dormant varicella-zoster virus (Herpesvirus varicellae) contracted during a previous episode of
chickenpox.
Fever,
neuralgia, and
paresthesia occur four to five days before skin lesions develop. Acute
herpes zoster pain usually does not last more than two weeks after all skin lesions have healed.
Postherpetic neuralgia is defined as
pain that persists in the affected dermatomes after the disappearance of all skin crusts. The
neuralgia can vary from "lightninglike" stabbing
pain to constant,
burning pain with
hyperesthesia; it can persist for years and is often refractory to traditional
analgesic therapy. A number of nontraditional
analgesic agents have been used in the management of
postherpetic neuralgia.
Tricyclic antidepressants, especially
amitriptyline, have been used alone and in combination with
phenothiazines or
anticonvulsants (
carbamazepine,
phenytoin,
valproate sodium), with good results. The effectiveness of
phenothiazines or
anticonvulsants as sole therapeutic agents has not been demonstrated. Although the intralesional administration of
corticosteroids appears to be beneficial, considerable fear about the potential for these agents to precipitate widespread viral dissemination exists. Positive results have been reported with
levodopa,
amantadine, and
interferon, but the role of these agents in the prevention of
postherpetic neuralgia remains unclear. Nontraditional
analgesic agents are useful in the management of
postherpetic neuralgia, but patients must be selected and monitored appropriately. A
tricyclic antidepressant (especially
amitriptyline) is a reasonable first choice.