Herpes zoster (shingles) is reactivation of varicella-zoster virus infection. Risk factors for reactivation include immunodeficiency secondary to cancer, chemotherapy, radiation therapy, and HIV infection. Typically, the virus remains latent in a dorsal root ganglion, and reactivation manifests as painful skin lesions following a dermatomal distribution. However, rarely the virus remains latent in the geniculate ganglion and upon reactivation causes symptoms involving the 7th and 8th cranial nerves.
Symptoms of herpes zoster oticus include
Vesicles occur on the pinna and in the external auditory canal along the distribution of the sensory branch of the facial nerve. Symptoms of meningoencephalitis (eg, headache, confusion, stiff neck) are uncommon. Sometimes other cranial nerves are involved.
Although there is no reliable evidence that corticosteroids, antiviral drugs, or surgical decompression make a difference in herpes zoster oticus, they are the only possibly useful treatments. When used, corticosteroids are started with prednisone 60 mg orally once/day for 4 days, followed by gradual tapering of the dose over the next 2 weeks. Either acyclovir 800 mg orally 5 times/day or valacyclovir 1 g orally 2 times a day for 10 days may shorten the clinical course and is routinely prescribed for immunocompromised patients.
Vertigo is effectively suppressed with diazepam 2 to 5 mg orally every 4 to 6 hours. Pain may require oral opioids. Postherpetic neuralgia may be treated with amitriptyline.
Surgical decompression of the fallopian canal may be indicated if the facial palsy is complete (no visible facial movement), but must be performed within 2 weeks of onset of the facial paralysis to be effective. Before surgery, however, electroneurography is done and should show a >90% decrement.