Ultrasound study shows nerve atrophy in post herpetic neuralgia

Herpes zoster (HZ), or shingles, caused by reactivation of the latent varicella zoster virus (VZV) in the dorsal root or trigeminal ganglia, is most common after the sixth decade of life. It usually presents as a unilateral dermatomal vesicular rash, associated with severe pain. Painful rash eruption is usually localized to the thoracic nerves or to the ophthalmic division of the trigeminal nerve distribution. VZV usually persists asymptomatic in the sensory ganglia of anyone who has suffered from chickenpox. It reactivates in about 25% of people to travel along the sensory nerve fibers causing vesicular lesions in the dermatome supplied by the nerve. One of the most common and debilitating sequelae of HZ is post herpetic neuralgia (PHN), defined as pain persisting more than 3 months after the rash has healed. PHN is one of the most common causes of severe neuropathic pain. The diagnosis of both HZ and PHN is usually made clinically on the basis of the characteristic rash and patient's symptoms. We report the results of an ultrasonographic study of a patient with L5-S1 ganglionopathy due to VZV reactivation, followed by PHN.