Herpes Zoster (HZ), or Shingles, is a localized cutaneous disease, characterized by a unilateral, dermatomal, and often painful vesicular rash. After the infection of varicella zoster virus (VZV), the virus gains access and remains latent in the cranial nerve, dorsal root and sensory ganglia. The outbreak results from reactivation of latent VZV, years or decades after primary infection with VZV.1 HZ is primarily a disease in older adults or individuals with a weakened immune system. VZV is responsible for an estimated four cases of herpes zoster infection per one thousand people per year, with approximately 50% of these cases affecting patients at least 50 years old.1, 2 The ...view middle of the document...
3, 4 According to PHN article, pain is described as burning, throbbing, lancinating, or electric-shock-like.4 An erythematous maculo-papular rash starts in dermatomal distribution and later advances to clusters of clear vesicles. The areas of the body affected by the disease can be extremely sensitive and tender. Later on, rash continues to form for days and progresses in multiple stages of maculo-papular rash, pustulation and ultimately crusting.2,3 Eventually the crusts fall away, ultimately leaving behind flesh-colored scars. Gradually, scars become hypopigmented and atrophic, with some instances of clearing from any signs of infection. However, permanent changes to skin might occur. The progress of pain resolution and skin healing usually occurs within 3 to 4 weeks post first onset of symptoms.3-5 In cases of residual pain, post lesion healing, disease progresses to post-herpetic neuralgia (PHN).
Herpes Zoster begins with chickenpox, as primary manifestation of VZV. During VZV, the virus gains entry via the respiratory tract and spreads shortly after to the lymphoid system.4 The Infectious virus enters the endings of sensory nerves in the skin and travels up the sensory nerves to the dorsal root and cranial sensory ganglia.4, 5 Later, the virus travels to areas where the nerve cell bodies are clustered, and establishes a latent infection.4,5 Herpes zoster results from reactivation of VZV that has stayed in a latent state. The rash begins when virus escapes the nerve terminals and invades the skin. The latent virus reactivates in a ganglion and tracks down the sensory nerve to the area of the skin innervated by the accompanied nerve, producing a characteristic rash in dermatome distribution.4, 5 According to Post-Herpetic Neuralgia article, the associated inflammation of the peripheral nerve and skin damage is supposed to be responsible for the acute pain in patients with HZ.3-5 More than 99.5% of adults 40 years of age and older in the United States have serologic evidence of prior VZV infection.1,2
The most common complication of Herpes Zoster is Post Herpetic Neuralgia. In 1990, Dworking and Portenoy proposed a definition for PHN as pain at 3 months after healing. Later on, the definition was revised with further distinction, as pain present within 30 days from the onset of rash and is defined as acute herpetic neuralgia. Pain that is present between 30 and 120 days is defined as sub-acute herpetic neuralgia and pain persisting after 120 days from the onset of HZ is defined as PHN.4 Overall, it is the most feared complication of the HZ disease. HZ may also involve sensory branches of the facial nerve, causing Bell’s palsy. Also, occasional instances of geniculate ganglion involvement exist, causing Ramsay Hunt syndrome. Patients with Ramsay Hunt syndrome commonly present with involvement of vesicular eruptions, external auditory canal, and acute facial paralysis that is commonly...