Herpesvirus infections due to varicella zoster are the cause for shingles. The pain that develops with a shingles infection is due to the residence of the herpesvirus within the neuron. The immune-mediated inflammation causes the neuritis. While the pain is usually self-limiting, the persistence of post-herpetic neuralgia is the most feared complication.

All of the current oral antiviral agents are found to be optimal if initiated within 48 hours of the prodrome or onset of the visible rash. The effectiveness is diminished if they’re used beyond that time. They aren’t, however, completely ineffective. I’ve found that they do have some benefit, especially in patients with extensive blistering, and in the more elderly population, who are more vulnerable to postherpetic neuralgia. I’ve found that the antiviral agents (acyclovir, valacyclovir, famcyclovir) are equivalent in managing herpes zoster.

The prevention of postherpetic neuralgia is more controversial. A variety of interventions have been reported, and the literature isn’t clear on superiority. Intralesional or systemic corticosteroids have been reported to be helpful, but there are negative studies. Neuromodulation by tricyclic antidepressants, antiepileptics such as carbamazepine, gabapentin, or pregabalin have assisted in blunting the severity of neuritic pain. The best way to treat zoster, though, is to prevent it. The zoster vaccine has demonstrated benefit in reducing the frequency and severity of zoster in elderly patients. It’s an attenuated vaccine, so should be used with caution in patients who have immunosuppression.

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