ABSTRACT
Herpes zoster (HZ), also known as shingles, results from reactivation of varicella zoster virus, an a herpes virus, which has been persistent in a clinically latent state in spinal and cranial sensory ganglia since primary infection with varicella, often several decades earlier. Varicella is usually a childhood disease in temperate climates, but more often affects adolescents and adults in tropical areas. Clinical observation and mathematical modeling suggest that HZ pain may be divided into an acute phase lasting 30 days, subacute (30–120 days) and chronic phases (PHN) from three months after rash healing or four months from onset of prodrome. Both peripheral and central processes contribute to PHN and their contributions vary widely between patients from minimal deafferentation and severe allodynia to severe sensory loss but no allodynia. Patients with prominent allodynia often have minimal sensory loss and gain pain relief following local application of some analgesic agents.
