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Post-herpetic neuralgia: The painful aftermath of shingles

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Figure 1: The vesicles following reactivation of t Figure 1: The vesicles following reactivation of the virus are initially clear, but eventually cloud, rupture, crust and involute

Shingles — also known as herpes zoster (HZ) — is a painful, blister-filled rash caused by the reactivation of the varicella-zoster virus (VZV); the same virus that causes the primary infection varicella or chickenpox1. The virus affects an individual nerve and the skin surface that is served by that nerve; this is called a dermatome.1 The virus lies dormant in the dorsal root ganglia, reactivating when the immune system is weakened. This can occur at any age, but usually in older patients over 60 years, as the immune system declines in efficiency, or those who are immunocompromised, for example by chemotherapy, especially for blood cancers, solid-organ transplant, or to a lesser extent following treatment for HIV.2

In the UK, the annual incidence is estimated to be around 2 cases per 1,000 people; rising to 11 cases per 1,000 people in individuals over 80 years,3 consequently the incidence nationally is increasing due to the change in demographics; with individuals having a 20–30% risk of developing shingles during their lifetime.4 Most people only have one lifetime incidence of shingles; however, risk factors can increase this incidence. Patients presenting with shingles will almost always have had chickenpox, typically in childhood, or have been vaccinated against it1.

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