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Year : 2021  |  Volume : 7  |  Issue : 2  |  Page : 99-103

Herpes Zoster Oticus: A Morbid Clinical Entity

1 Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University, Bhubaneswar, Odisha, India
2 Department of Otorhinolaryngology, Christian Medical College, Vellore, Tamil Nadu, India

Date of Submission14-Jul-2020
Date of Decision08-Sep-2020
Date of Acceptance30-Dec-2020
Date of Web Publication25-Jun-2021

Correspondence Address:
Prof. Santosh Kumar Swain
Department of Otorhinolaryngology, IMS & SUM Hospital, Siksha “O” Anusandhan University, Kalinga Nagar, Bhubaneswar-751003, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mamcjms.mamcjms_80_20

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The reactivation of varicella zoster virus (VZV) at the geniculate ganglion of the facial nerve results in herpes zoster virus. Patients of herpes zoster oticus (HZO) often present with symptoms related to the cochleovestibular dysfunction along with otalgia and vesicular eruption at the pinna and external auditory canal. Patients of HZO usually present with hearing loss, vertigo, and facial nerve paralysis. When it is associated with facial nerve paralysis, HZO is called Ramsay Hunt syndrome (RHS). In the majority of cases, patients with vertigo have hearing loss, whereas patients without hearing loss have no vertigo. It is a self-limiting viral disease and the morbidity is often caused due to facial nerve paralysis. If HZO is not diagnosed immediately and treated timely often it progress to RHS. Clinician education is vital for detecting the HZO/RHS at an early stage so that facial nerve paralysis can be prevented along with associated morbidity. In this review article, we discuss the current concept and recent advances in the etiopathology, diagnosis, and treatment of HZO.

Keywords: Acyclovir, facial nerve paralysis, herpes zoster oticus, Ramsay Hunt syndrome

How to cite this article:
Swain SK, Paul RR. Herpes Zoster Oticus: A Morbid Clinical Entity. MAMC J Med Sci 2021;7:99-103

How to cite this URL:
Swain SK, Paul RR. Herpes Zoster Oticus: A Morbid Clinical Entity. MAMC J Med Sci [serial online] 2021 [cited 2023 Feb 4];7:99-103. Available from: https://www.mamcjms.in/text.asp?2021/7/2/99/319363

  Introduction Top

Herpes zoster oticus (HZO) is an infectious disease characterized by erythematous vesicular eruptions or rashes in the pinna and external auditory canal along with severe otalgia. When it is accompanied by ipsilateral facial nerve paralysis, it is called Ramsay Hunt syndrome (RHS).[1] The peripheral facial nerve paralysis occurs due to the inflammation of the facial nerve by reactivation of the varicella zoster virus (VZV). The vestibulocochlear symptoms like vertigo, tinnitus, and hearing loss are common among patients with HZO. There are few neurological complications such as alterations in cerebrospinal fluids, peripheral motor neuropathy, aseptic meningitis, and cranial neuropathy encountered.[2] Although HZO is rarely found in clinical practice, it is more often found in immunocompromised patients. It is very important for clinicians or otorhinolaryngologists to suspect, diagnose, and manage HZO among elderly or pediatric patients. However, there have been, to our best of knowledge, not many articles that emphasized on HZO published in the medical literature. The purpose of this review article is to discuss the etiopathology, clinical manifestations, and management of the HZO, although these are rarely found in day to day clinical practice.

  Methods of literature search Top

Research articles regarding HZO were searched through a multiple approach. First, we conducted an online search of the PubMed, Scopus, and Medline databases with the words “herpes zoster oticus,” “Ramsay Hunt syndrome,” “etiopathology of herpes zoster oticus,” clinical presentations, diagnosis, and treatment of HZO. The abstracts of the published articles were identified by this search method and other articles were identified manually from the citations. This review article reviews the etiopathology, clinical presentations, diagnosis, and treatment of HZO. This review article presents a baseline from where further prospective trials can be designed and helps as a spur for further research in this clinical entity where not many studies are done.


James Ramsay Hunt first described the etiology for HZO where he described the reactivation of the VZV at the geniculate ganglion.[3] James Ramsay Hunt described the different clinical manifestations of this syndrome, which was finally named after him. Although he described the HZO, but the syndrome which was named after him, RHS, is defined as HZO plus ipsilateral facial nerve paralysis. He described that the additional clinical presentations are because of the close proximity of the geniculate ganglion to the vestibulocochlear nerve within the bony facial canal.[3],[4] In 1972, the VZV antigens were identified by immunofluorescence and electromicroscopy of the trigeminal ganglion of the patients who had ophthalmic zoster and the patients died.[5] Later on, Wackym demonstrated that VZV genomic DNA was found at the geniculate ganglion. James Ramsay Hunt classified the RHS into four types according to the pathological process of the disease at the geniculate ganglion.[6] These were as follows: (1) disease involving the sensory part of the seventh cranial nerve, (2) disease involving both sensory and motor part of the seventh cranial nerve, (3) disease involving sensory and motor parts of the seventh cranial nerve along with auditory symptoms, and (4) disease involving sensory and motor parts of the seventh cranial nerve along with auditory and vestibular symptoms.


Herpes simplex and herpes zoster are ubiquitous in the population. It remains in a latent state at the nerve ganglia. During the time of stress, there will be reactivation of the viruses. The reactivation of the viruses occurs by surgical intervention that leads to symptomatic HZO. RHS occurs due to reactivation of the latent VZV at the geniculate ganglion of the facial nerve. RHS is responsible for 2% to 10% of all cases of acute peripheral facial nerve palsy.[1] One study reported that RHS that the prevalence of facial nerve palsies induced by VZV reactivation in 6 to 15 years old was higher than among children younger than age of the 5 years (53% versus 9%).[7] The incidence of RHS among children is around 3/100,000 and so it should be considered as a differential diagnosis of the atraumatic facial palsy.[8],[9]


HZO is an infectious condition that occurs due to VZV. VZV is a herpes virus that causes two distinct syndromes such as the primary infection, called varicella (chickenpox virus) that is common and highly contagious. Reactivation of the VZV causes herpes zoster (shingles), which can involve cranial nerves and spinal cords. HZO occurs due to the reactivation of the latent VZV at the geniculate ganglion, which affects the facial nerve and vestibulocochlear nerve. The histopathological picture shows perivascular, intra-neural, and perineural aggregation of the round cells in the facial nerve of the patients with RHS.[10] The auditory function depends on the basis of the cochlear and retro-cochlear structures. Cochlear type of hearing loss occurs due to dysfunction of the hair cells of the organ of corti, whereas retro-cochlear type of hearing loss occurs due to defect in auditory nerve and or lesion in the central auditory system. Involvement of the inner ear and Cranial Nerve (CN) VIII may show inflammatory cell infiltration found in the cochlear and vestibular nerve ganglia and degeneration of the inner ear end-organ in RHS. The involvement of the CN VII and VIII are caused by reactivation of the VZV at the ganglion of CN VII and spread of infection from CN VII to CN VIII through vestibulofacial or vestibulocochlear anastomosis.[10] This is supported by the presence of VZV DNA in the geniculate ganglion of CN VII and the vestibular and cochlear nerves.[4],[10] Although the way of transmission of the VZV from CN VII to CN VIII or labyrinth and end organs is still not clear, the transmission of the VZV infection from the dehiscent part of the facial canal to the inner ear via the round or oval window has been thought as a potential route for the involvement of the inner ear.[4] For interneural transmission, the spread of VZV via perineural tissues inside the internal auditory canal has been suggested as a possible route of infection. Involvement of the CN VIII and inner ear was demonstrated by the presence of the inflammatory cells in presence of the RHS. Therefore, widespread inflammation by VZV infection from CN VIII through inner ear end organs in patients of RHS is responsible for vestibulocochlear dysfunction.

The involvement of the inner ear by VZV infection causes sensorineural hearing loss as per part of the labyrinth. Concerning the cranial nerves, there are two cranial nerves that are affected, that is, ophthalmic division of the trigeminal nerve and facial nerve. Involvement of the facial nerve along with HZO is more common in clinical practice.

Clinical presentations

Patients of HZO often present with clinical manifestations due to dysfunctions of the eighth cranial nerve. It is usually associated with a viral prodrome and severe pain in and around the ear. Patients of HZO typically presents varicelliform rash with blisters [Figure 1] that may be found at the ipsilateral pinna and external auditory canal or at the soft palate. Patients usually present with mild to moderate hearing loss that is due to cochlear and/or retro-cochlear involvement.[11] The vestibular symptoms such as vertigo are sometimes severe and the study showed that both the superior and inferior divisions of the vestibular part of the eighth cranial nerve are widely involved.[12] Postmortem examination of the patients shows inflammation within the vestibular and auditory nerves and the labyrinth.[13] The most common vestibulocochlear symptoms are hearing loss, vertigo, and tinnitus. A severe type of HZO can involve the whole of the vestibule-cochlear nerve bundle along in its entire course producing symptoms such as that of Ménière syndrome in which patients present with sensorineural hearing loss, tinnitus, and vertigo. Hearing impairment may be more severe and include high- and low-frequency involvement. The hearing loss is usually more severe in patients with vertigo than without vertigo; however, the degree of hearing loss is not significantly different between RHS patients with and without facial nerve paralysis.[14] As the superior vestibular nerve is often connected with the facial nerve, vertigo may be due to the transmission of virus via anastomosis that reflects severe degeneration of the facial nerve. If the viral infection spreads from the internal auditory canal to the cochlea via CSF and perilymphatic fluid, the basal turn of the cochlea can be damaged earlier than the apical turn of the cochlea.
Figure 1 Patients of herpes zoster oticus typically present varicelliform rash with blisters in the pinna and surrounding area.

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The sites of the lesion are responsible for vestibulocochlear symptoms in patients of HZO. Audiological symptoms are cochlear and retro-cochlear hearing loss. Labyrinth, vestibular nerve, or both are possible sites for pathogenesis.[14] The incidence of hearing loss in HZO is 6.5% to 85%.[15] In addition to the same side facial nerve palsy, it may present with polycranial neuropathy that includes symptoms such as hearing loss, vertigo, speech disturbances, and swallowing problem. HZO accounts for 2% to 10% of all the facial nerve paralysis.[16] Ipsilateral lower motor neuron facial nerve palsy with same side face drop or weakness may be obvious. There may be hyperacusis due to palsy of the stapedius muscle and tensor tympani. The other clinical presentations are vertigo and same-side hearing loss, and tinnitus along with same-side acute peripheral facial nerve paralysis.[17] In children, HZO by reactivation of VZV can result in RHS. If children with HZO are not diagnosed early and timely treated, they can be vulnerable to RHS. Although it is a rare cause for facial nerve palsy in children, physicians should be educated for early detection of HZO or RHS so that the associated morbidity can be prevented. The differential diagnosis of HZO includes Bell’s palsy along with certain diseases such as autoimmune, granulomatous, and demyelinating diseases. [18]


The diagnosis of HZO is usually done on the basis of history and physical findings. The diagnosis of HZO is often made without any difficulty when the characteristic clinical presentations are there. The classical clinical presentations are usually deep ear pain that is paroxysmal at first but after 1 to 2 days, the pain radiates outward into the pinna and then becomes constant in nature. The patients also complain about rash or blisters at the distribution of the nervus intermedius that may include anterior two-thirds of the tongue, external auditory canal, soft palate, and pinna. Isolation of VZV in conventional cell culture provides a definite diagnosis. Its specificity is 100% but is not always feasible in routine clinical practice. Tzanck test is done for identification of the VZV.[19] Detection of VZV antigen by direct immunofluorescence assay has a sensitivity of 90% and specificity of 99%.[20] The severity of the facial nerve paralysis is assessed by House-Brackmann grading. Hearing loss is assessed by pure tone audiometry. Hearing impairment is more severe in patients with vertigo than those without vertigo in both low and high frequency ranges. Facial nerve electroneuronography (ENoG) is an important electrophysiological test for measuring the nerve degeneration and evaluation of the disease progression. ENoG is useful for predating the prognosis of the facial nerve recovery and decide for facial nerve decompression. Patient of HZO with facial nerve palsy, showing reduction in ENoG amplitude to lower than 10% of the normal side may be predictive for incomplete recovery.[21] Patients with facial nerve weakness showing less than 90% degeneration in ENoG within 2 weeks were documented to recover to House-Brackmann grade I or II at seventh month after development of the facial weakness,[22] and those having 95% degeneration within 2 weeks were found to show 50% chance of very poor recovery.[22] Histopathological examination show inflammatory cell infiltration in cochlear and vestibular nerve along with degeneration of the inner ear end organs are often observed in patients of HZO or RHS. The VZV DNA is studied from the tear and saliva of the parotid and submandibular glands.[23] The DNA of the VZV was identified in 72% of the saliva samples of submandibular salivary glands, 57% of the parotid gland saliva, and 27% of the tear fluid samples of the patients with HZO.[23] Serological confirmation for HZO virus is often (not always) possible either by a positive IgM antibody titer or by raised IgG response within 2 weeks after the development of facial nerve paralysis. Other investigation method is the detection of VZV DNA in blood mononuclear cells or cerebrospinal fluid by PCR method.[24]

Magnetic resonance imaging (MRI) with gadolinium contrast is useful for identifying the facial nerve status. The normal facial nerve shows minimal enhancement of the geniculate ganglion whereas, in RHS, there is an intense enhancement of the facial nerve from the meatal segment to the mastoid segment. In addition to the facial nerve, there is an enhancement of the eighth cranial nerve can also be found.[25] MRI with contrast (Gadolinium) shows enhancement of both cochlear and vestibular nerves that indicates (in contrast to Bell’s palsy) polyneuronitis.[26] MRI can identify the exact site of the injury in the facial nerve. Gadolinium enhancement does not correlate with the severity of the disease and can be used as for prognostic factor. A severe form of Herpes zoster can involve the whole of the vestibule-cochlear nerve bundle along in its entire course producing symptoms such as that of Ménière syndrome. Diagnosis in such cases can be made clinically supplemented by pure tone audiometry that shows sensorineural hearing loss and MRI revealing enhancement of the nerves.[27] MRI with gadolinium contrast is the most recent method for identifying the damaged part of the facial nerve and vestibulocochlear nerve bundle. Normally the facial nerve shows minimal enhancement at the geniculate ganglion. However, in RHS, it shows intense enhancement of the facial nerve from the meatal segment to the mastoid segment and also enhancement of the CN VIII.[27]


The early treatment of the HZO is often similar to the Bell palsy as HZ and herpes simplex type 1 are both DNA viruses of the herpes group. It is often accepted that patients with acute facial nerve paralysis should receive prednisone (70–100 mg daily for 5–10 days) as well as antiviral drugs against herpesvirus (acyclovir or valaciclovir). The treatment of HZO was highly improved after the advent of the new virostatic drugs such as acyclovir or valaciclovir. Acyclovir is a good virostatic drug that is effective against replicating herpes group viruses. To act against the virus, the acyclovir must be phosphorylated within the herpes virus. Acyclovir is usually metabolized into monophosphate in the infected cells possessing the virus-specific thymidine kinase. The monophosphate is then changed into acyclovir triphosphate with help of the host cell enzymes that terminate the DNA of the VZV. Antiviral drugs are highly effective for decreasing the severity and duration of HZO when the treatment started within 72 hours of the onset of the rash. HZO with facial nerve paralysis treated with prednisone has an improvement of facial grading at recovery and decrease denervation in comparison to placebo-treated patients.[28] Patients who underwent treatment with prednisone are less likely to develop complete facial nerve paralysis. Incomplete eye closure should be addressed immediately by using artificial tear drops, ointment, and specially designed eye-tapes at night time. Relief of the pain can be achieved by anticonvulsants, opioids, tricyclic antidepressants, and topical treatments such as lidocaine containing patches and certain creams such as capsaicin cream.[29] Retrospective studies revealed that early administration with steroids and antiviral drugs within 3 days of the onset of the clinical symptoms has 75% rate for a full recovery of the disease, whereas 30% if combined treatment is started after 1 week from the onset of symptoms. The combined treatment includes a 7 to 10 days course of acyclovir (60–80 mg/kg/day, 8th to 6th hourly) or famciclovir (500 mg, 3 times daily) along with oral steroid such as prednisone (60 mg daily for 3 to 5 days).[30] Surgical facial nerve decompression has no role in this disease.[31] Antibiotics can be given for the treatment of the secondary infection. Supportive care can be given to patients such as eye/corneal care. The zoster (shingles) vaccine is often an effective way to decrease the incidence of HZO and postherpetic neuralgia and minimize the outbreak.[28] The treatment of the HZO will provide maximum benefit if it is started within 72 hours of onset clinical presentations.[32]


The prognosis of HZO in pediatric patient is better than adult patients.[33] Advanced audiovestibular finding, facial nerve paralysis, and late treatment leads to bad prognosis.[32] Elderly patients with diabetes mellitus and Bell palsy and patients of HZO have worse prognosis of their palsy than patients of Bell palsy only.[34] Hearing loss in patients of HZO often recovers well. Co-existing illness of the patient and age has poor prognosis.[35] The prognosis of the facial nerve paralysis in HZO has bad prognosis than patient with Bell palsy. Around 10% of the complete facial nerve paralysis in HZO recovers completely.[1],[35] No single symptom affects the recovery of this disease. However, presence of the swallowing difficulty or diplopia suggest toward worse outcome.[36],[37]

  Conclusion Top

HZO occurs due to VZV reactivation that may lead to RHS. If not diagnosed immediately and not timely treated, HZO usually progresses to RHS. Patients of HZO often have cochleovestibular symptoms. Proper evaluation of the hearing loss and vertigo is important for managing the patients with HZO even without presence of the facial nerve weakness. Education to clinicians is vital for detecting HZO at very early stage as it can be a rare cause for facial nerve paralysis in pediatric patients and thereby prevent the associated morbidity. Therefore, adequate awareness is required among clinicians for early detection and management of HZO for preventing morbidity.

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Conflicts of interest

There are no conflicts of interest.

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