An entirely different type of delayed vasculitis that affects small vessels, with which we have had limited experience, is being reported in patients with HIV and other forms of immunosuppression. In this condition, weeks or months after one or more attacks of zoster, a subacute encephalitis ensues, including fever and focal signs. Some cases apparently arise without a rash, but viral DNA and antibodies to VZV are found in the CSF. The MRI shows multiple cortical and white matter lesions, the latter being smaller and less confluent than in progressive multifocal leukoencephalopathy. There is usually a mild pleocytosis. Almost all cases have ended fatally. The vasculitic and other neurologic complications of zoster have been reviewed by Gilden and colleagues (2002). Nagel and coworkers from Gilden’s laboratory have also found cases in which the temporal arteries contain VZV particles and they have suggested that the vascular changes caused by the virus may be the cause of temporal arteritis.
An important inception for shingles has been a live, attenuated vaccine that can be administered to adults over age 60. It has been shown to reduce the emergence of shingles and to decrease the incidence of postherpetic complications by two-thirds (Oxman et al).
During the acute stage of shingles, analgesics and drying and soothing lotions, such as calamine, help to blunt the pain. Nerve root blocks may provide temporary relief but are not often used. After the lesions have dried, the repeated application of capsaicin ointment (derived from hot peppers) may relieve the pain in some cases by inducing a cutaneous anesthesia. When applied too soon after the acute stage, however, capsaicin is highly irritating and should be used cautiously.
Acyclovir shortens the duration of acute pain and speeds the healing of vesicles, provided that treatment is begun within approximately 48 h (some authorities say 72 h) of the appearance of the rash (McKendrick et al, 1986). Several studies have suggested that the duration of postherpetic neuralgia is reduced by treatment during the acute phase with famciclovir or valacyclovir, but the incidence of this complication is not markedly affected. Famciclovir (500 mg tid for 7 days) or the better absorbed valacyclovir (2 g orally qid) are possibly better alternatives than the previously favored acyclovir (see below on the subject of postherpetic neuralgia). Other studies have shown favorable results in preventing postherpetic pain by starting a tricyclic antidepressant during the acute phase.
All patients with ophthalmic zoster should receive acyclovir or valacyclovir orally; in addition, acyclovir applied topically to the eye, in either a 0.1 percent solution every hour or a 0.5 percent ointment 4 or 5 times a day, is recommended by some ophthalmologists. Patients who are immunocompromised or have disseminated zoster (lesions in more than 3 dermatomes) should generally receive intravenous acyclovir for 10 days. There is now available (from state health agencies) a VZV immune globulin (VZIG) that may protect against dissemination in immunosuppressed patients but is not indicated for established disease. Although it may reduce the incidence of postherpetic neuralgia (Hugler et al), this is not its main purpose and it does not appear to prevent or ameliorate CNS complications.
The treatments of zoster myelitis and encephalitis are uncertain but intravenous valaciclovir, with or without corticosteroids has been used.
Postherpetic Neuralgia (See Also Chaps. 7 and 9)
This severely painful syndrome follows shingles in 5 to 10 percent of patients but occurs almost three times more often among individuals older than age 60 years. The possible effect of acute treatment on the severity of postherpetic neuralgia is mentioned above but potential prevention with the vaccine is even more appealing.