Abstract
Herpes zoster (HZ), usually painful dermatomal rash, is caused by reactivation of varicella-zoster virus, and postherpetic neuralgia (PHN) refers to prolonged pain after HZ. In addition to ganglionitis and peripheral neuritis, subclinical inflammation in the central nervous system is common in HZ. In quantitative sensory testing, abnormal findings are common in HZ, but they are not associated with the development of PHN, whereas mechanical allodynia and pinprick hypoesthesia predict PHN. In acute zoster, skin inflammation excites nociceptors, and inflammation and direct viral damage can affect neurons. Transition from acute zoster pain to PHN involves both peripheral and central changes. Mechanical allodynia and sensory changes are typical of PHN. Three pathophysiological subtypes of PHN are suggested: the irritable nociceptor subtype, the deafferented allodynic subtype, and the deafferented nonallodynic subtype. Underlying pathophysiology may vary from patient to patient and with the duration of PHN.
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