Both varicella and zoster may result in an array of neurological complications. The most common neurological complication of zoster is the development of a neuropathic pain syndrome either acutely or chronically, as postherpetic neuralgia (PHN). Many approaches have been proposed to treat the pain of acute zoster, to proactively prevent the development of PHN, and to treat PHN. This chapter reviews the options for analgesia and prevention of zoster-associated pain.

Neuropathic pain and other neurologic complications of herpes zoster

Viral invasion of nervous system structures, in skin, peripheral nerve, dorsal root ganglion, and more rostral CNS structures, probably underlies the development of the VZV neuropathic pain syndromes (see Table 20.1). Cerebrospinal fluid (CSF) from 40–50% of patients with uncomplicated herpes zoster may manifest pleocytosis (Applebaum et al., 1962; Gold, 1966). Direct meningeal spread of virus may explain the more uncommon neurological complications of zoster including multiple cranial neuropathies, polyneuropathy, meningitis, meningoencephalitis/meningoradicultis, encephalitis, and myelitis (Elliott, 1994b). The syndrome of zoster sine herpete, or zoster without rash, and associated development of persistent neuropathic pain with this phenomenon in some individuals, further confirms the capability of viral invasion at multiple levels of the neural axis (Elliott, 1994b).

Pain is the most common symptom of acute zoster and may precede the skin eruption by hours, days or weeks, and may rarely be the only presentation (Gilden et al., 1991, 1992). Spontaneous symptoms of both acute zoster and PHN include aching pain or a more superficial burning pain in the dermatomal distribution of the affected skin, and provoked symptoms of severe discomfort that accompany the syndrome of neuropathic pain.