Ramsay Hunt syndrome: pathophysiology of cochleovestibular symptoms

Abstract

Ramsay Hunt’s hypothesis that herpes zoster oticus results from reactivation of the varicella zoster virus (VZV) in the geniculate ganglion is supported by the detection of viral genome in archival temporal bones of normals and Ramsay Hunt patients by the polymerase chain reaction. Ramsay Hunt syndrome is characterized by the presence of cochleovestibular symptoms in association with facial paralysis. VZV has also been demonstrated in the spiral and/or vestibular ganglion. Two cases are reported in which cochleovestibular symptoms outweighed the facial nerve symptoms, presumably representing VZV reactivation in the spiral and/or vestibular ganglion. From these observations and the known dormancy of VZV in non-neuronal satellite cells, it is argued that the cochleovestibular symptoms in Ramsay Hunt syndrome may result from VZV transmission across the nerves inside the internal auditory canal and that prompt treatment with an antiviral-corticosteroid combination might be justified in the management of any acute non-hydropic cochleovestibular syndrome.