Pathogenesis: Any individual previously infected with VZV in the form of chickenpox is predisposed to develop herpes zoster later in life. Most cases occur with advancing age, as cell-mediated immunity tends to wane with time. The virus remains latent in the nerve ganglia until it reactivates. The ability to reactivate and the exact signal for reactivation are unknown. Once the virus reactivates, it begins to replicate and to cause necrosis of the affected nerve cells. The virus travels along the cutaneous sensory nerves and eventually affects the skin that is innervated by the nerve root where the virus became reactivated.
Treatment: Treatment with antiviral medications from the acyclovir family should be instituted immediately. The sooner therapy is started, the better is the chance of decreasing the length of disease. Therapy may also decrease the incidence of postherpetic neuralgia. The use of oral corticosteroids in conjunction with the antiviral medication has been advocated to help decrease the risk of postherpetic neuralgia, but large studies have thus far shown inconclusive data to support this approach. The therapy has the best chance of changing the course of the disease if given within the first 72 hours after the onset of disease symptoms.
A live attenuated zoster vaccine for the prevention of herpes zoster is being given to patients older than 60 years of age. This vaccine has been shown to boost natural immunity against VZV and to decrease the number of cases of herpes zoster and the frequency of postherpetic neuralgia in those who do develop herpes zoster after vaccination. As with all live vaccines, its use in immunosuppressed patients is contraindicated.
Currently, the treatment of postherpetic neuralgia is not optimal. Amitriptyline, gabapentin, lidocaine patches, pregabalin, anticonvulsants, and opioids are all used with varying success.
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