Overview
Pathophysiology
Varicella‑zoster virus (VZV) lies dormant in cranial nerve VII sensory ganglia after primary chickenpox.
Varicella‑zoster virus (VZV) lies dormant in cranial nerve VII sensory ganglia after primary chickenpox. Age‑related immunosenescence, chemotherapy, HIV, or acute stress can weaken cell‑mediated immunity, allowing the virus to reactivate in the geniculate ganglion. The virus travels anterograde along the facial nerve, producing a vesicular eruption in its sensory distribution (external auditory canal, auricle, and nasopharynx) while inflammatory edema within the narrow bony fallopian canal compresses the motor fibers, yielding a peripheral facial palsy. Close proximity of the geniculate ganglion to the vestibulocochlear nerve explains the frequent hearing loss and vertigo that accompany the syndrome.
