Postherpetic neuralgia (PHN) is a common and often devastatingly painf
ul condition. It is also one of the most extensively investigated of t
he neuropathic pains. Patients with PHN have been studied using quanti
tative testing of primary afferent function, skin biopsies, and contro
lled treatment trials. Together with insights drawn from an extensive
and growing literature on experimental models of neuropathic pain thes
e patient studies have provided a preliminary glimpse of the pain-gene
rating mechanisms in PHN. It is clear that both peripheral and central
pathophysiological mechanisms contribute to PHN pain. Some PHN patien
ts have abnormal sensitization of unmyelinated cutaneous nociceptors (
irritable nociceptors). Such patients characteristically have minimal
sensory loss. Other patients have pain associated with small fiber dea
fferentation. In such patients pain and temperature sensation are prof
oundly impaired but light moving mechanical stimuli can often produce
severe pain (allodynia). In these patients, allodynia may be due to th
e formation of new connections between nonnociceptive large diameter p
rimary afferents and central pain transmission neurons. Other deaffere
ntation patients have severe spontaneous pain without hyperalgesia or
allodynia and presumably have lost both large and small diameter fiber
s. In this group the pain is likely due to increased spontaneous activ
ity in deafferented central neurons and/or reorganization of central c
onnections. These three types of mechanism may coexist in individual p
atients and each offers the possibility for developing new therapeutic
interventions. (C) 1998 Academic Press.