Herpes Zoster Oticus Varicella Zoster Chicken

The varicella-zoster virus is a neurotropic DNA virus. Initial infection with the varicella-zoster virus is commonly known as chicken pox and displays a very characteristic vesicular cutaneous eruption. The virus can remain dormant in ganglion cells for many years, with subsequent reactivation of the dormant virus resulting in shingles. Neurologic involvement has been found in chicken pox and includes encephalitis, myelitis, and cerebellar ataxia. Chicken pox has very rarely been associated with facial nerve involvement. As of 1999, only 12 cases of facial palsy in association with an initial varicella-zoster infection were reported in the English literature (27). In contrast, reactivation of the latent virus has a high incidence of facial nerve involvement. Herpes zoster oticus, also termed Ramsay Hunt syndrome, is a specific subset of varicella-zoster reactivation. Patients with herpes zoster oticus present with the classic triad of otalgia, auricular vesicles, and facial paralysis. Patients may also develop other cranial neuropathies, as well as hyperacusis and sensorineural hearing loss. In fact, facial nerve involvement is so common with varicella-zoster reactivation that it remains second only to Bell's palsy as the most common cause of acute peripheral facial paralysis in the United States.

The mechanism of neuropathy appears to be from the neurotropic virus, which causes a diffuse lymphocytic and plasma cell infiltrate of the neural tissue with perivascular and perilymphatic cuffing. This has been demonstrated along the entire length of the facial nerve with some cases undergoing substantial demyelination (28). Alternatively, the viral infection could lead to compressive ischemia as the nerve swells along its tight bony canal.

Diagnosis is often clinical but can be confirmed by direct fluorescence antibody staining for varicella-zoster virus using Tzank preparations as well as serum titers. Magnetic resonance imaging demonstrates facial nerve enhancement with gadolinium in roughly 50% of patients (29).

Treatment is with valacyclovir 1000 mg t.i.d. for seven days, as well as prednisone 1 mg/kg/day (divided) tapered over 7 to 10 days. Sensorineural hearing loss and vertigo may be present with herpes zoster oticus but not with Bell's palsy. The prognosis is poorer than for Bell's palsy, with only 50% demonstrating satisfactory improvement. The course of facial nerve paralysis evolves more slowly, over three weeks. Surgical decompression has remained an extremely controversial issue. Investigators arguing against decompression claim that facial paralysis is unaltered by surgical intervention (30,31). Others have been strong advocates for decompression of the facial nerve, although a lack of consensus as to the areas of decompression remains. May performed a prospective study and concluded that transmastoid decompression of the facial nerve to the labyrinthine segment favorably alters the natural history in patients with herpes zoster oticus when they have a poor prognosis for spontaneous recovery based on electrophysiologic testing (32). Herpes and related viral diseases are discussed in detail in Chapter 10.

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