Characteristics of hearing loss in patients with herpes zoster oticus

Abstract

Patients with herpes zoster oticus (HZO) may commonly show symptoms associated with 7th and 8th cranial nerve (CN VII and CN VIII) dysfunction. The aim of this study is to investigate the characteristics of hearing loss in patients with HZO and discuss possible mechanisms.Ninety-five HZO patients who showed at least one of the symptoms of CN VII and CN VIII dysfunction between January 2007 and October 2014 were included in this study. Hearing loss was defined when the mean thresholds of pure tone audiometry (PTA) in speech frequency (0.5 kHz + 1 kHz + 2 kHz/3) or isolated high frequency (4 kHz + 8 kHz/2) were greater than 10 dB in the affected ear compared with the healthy ear, and a total of 72 patients were classified as the hearing loss group.The difference of mean PTA thresholds between affected and healthy ears was significantly greater in the high frequency range than in low range (20.0 ± 11.5 dB vs. 12.9 ± 15.7 dB, P = 0.0026) in patients with hearing loss (n = 72). The difference between affected and healthy ear was significantly greater in patients with vertigo (n = 34) than those without vertigo (n = 38) in both the high (P = 0.033) and low (P = 0.024) frequency ranges. In contrast, the differences between affected and healthy ears were not significantly different between patients with facial palsy (n = 50) and those without facial palsy (n = 22) in both the high (P = 0.921) and low (P = 0.382) frequency ranges.In patients with HZO, hearing loss is more severe in the high frequency range than in the low frequency range. Hearing impairment is more severe in patients with vertigo than in those without vertigo in both the high and low frequency ranges, even though the degree of hearing impairment is not significantly different between patients with and without facial palsy. These findings indicate that the mechanisms of viral spread from CN VII to CN VIII may differ between vestibular and audiologic deficits.

Case Study for treatment considerations for patients with Ramsay Hunt Syndrome

“…According to Sweeny et al [6] "RHS may initially be indistinguishable from Bell's Palsy…due to delayed development of vesicles after the onset of facial weakness." SC's symptoms were consistent with those of previous patients who have been diagnosed with RHS via research articles [4- 6,8,[11][12][13][14][15][16][17][18][19]. The severities and number of symptoms per patient varied, but were overall similar in nature.…”

Manifestaciones clínicas del síndrome de Ramsay-Hunt en una serie de 20 casos

“…A esta tríada sintomática patognomónica se asocian en un porcentaje variable del 10 al 85% síntomas cocleovestibulares [36], aunque la mayoría de los autores expresa esta incidencia entre un 25 y un 50% [7]. En los casos presentados se manifiesta en el 63%.…”

“…Por tanto, el déficit coclear puede deberse a la extensión viral desde el VII al líquido cefalorraquídeo (LCR) dentro del conducto auditivo interno (CAI), o a través de un canal de Falopio dehiscente, atravesando las ventanas redonda y oval, vía perilinfática [42]. Si la hipótesis de la transmisión vírica a la cóclea a través del LCR del CAI es correcta, la espira basal se lesionaría con mayor facilidad [36]. En algunos pacientes puede asociarse otitis media serosa e hipoacusia de transmisión o mixta, por afectación directa de la mucosa del oído medio [8] [7], los síntomas y signos característicos de este daño, son el vértigo con nistagmo espontáneo y el desequilibrio con desviación hacia el lado afecto [43].…”

Treatment of Ramsay–Hunt's syndrome with multiple cranial nerve involvement and severe dysphagia

“…Ramsay–Hunt's syndrome (RHS) is characterized by herpetic eruption in the external auditory canal, facial paralysis and otalgia. [ 1 – 4 ] The classical concept of RHS is the reactivation of the varicella zoster virus (VZV) of the alpha herpes family, involving the facial nerve and the vestibulocochlear nerve. [ 1 – 4 ] RHS has been reported to have an incidence of five per 100,000, and incidence and severity increases in immune-compromised persons.…”

“…[ 1 – 4 ] The classical concept of RHS is the reactivation of the varicella zoster virus (VZV) of the alpha herpes family, involving the facial nerve and the vestibulocochlear nerve. [ 1 – 4 ] RHS has been reported to have an incidence of five per 100,000, and incidence and severity increases in immune-compromised persons. [ 5 ] Once VZV infection occurs, the virus is never cleared from the body, and keeps itself hidden from the host's immune system.…”