Because VZV becomes latent in cranial nerve, dorsal root, and autonomic ganglia along the entire neuroaxis, the virus can manifest anywhere on the body. Typically, the activated virus causes a prodrome consisting of skin sensitivity and mild-to-severe radicular pain, and after five days, a rash appears. The pain is associated with itching and dysesthesia. As with HSV-1, VZV infection decreases sensation in the affected dermatome, yet the affected skin is exquisitely sensitive to touch. The rash may continue to produce pustules that lead to crusting and ulceration. In many affected patients, healing is delayed beyond two weeks and is accompanied by increased skin pigmentation and scarring. Lesions can erupt outside the affected dermatome but rarely cross the midline and are not clinically significant. Distribution of 10 or more lesions outside a single dermatome suggests early evidence of viral dissemination. The term "zoster sine herpete" is used to describe VZV that is reactivated without the typical pattern of skin eruption.
Of the facial nerves, the ophthalmic division of the trigeminal nerve is most frequently affected in herpes zoster (Fig. 11), and this event can cause optic keratitis, a potential cause of blindness. The most visible sign of motor nerve involvement is facial paralysis as seen in Ramsay Hunt syndrome, a condition which is more properly described as herpes zoster cephalicus (Fig. 7). Patients affected with this condition also have palatal and laryngeal paralysis and hearing loss. Acute facial paralysis with pain and hearing loss is pathognomonic of herpes zoster infection. The diverse manifestations of VZV activation
are exemplified in Figure 12, which illustrates VZV affecting a left thoracic dermatome concomitantly with left-sided facial palsy. A diagnosis of zoster sine herpete should be considered for patients who have acute facial paralysis accompanied by moderate-to-severe pain and no vesicle formation (23).
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