[Downloaded free from http://www.mamcjms.in on Friday, April 7, 2023, IP: 202.67.40.

238]

MAMC Journal of Medical Sciences

Review Article

Herpes Zoster Oticus: A Morbid Clinical Entity

Santosh Kumar Swain1, Roshna Rose Paul2
1
Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University, Bhubaneswar, Odisha, 2Department of Otorhinolaryngology,
Christian Medical College, Vellore, Tamil Nadu, India

Abstract
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

INTRODUCTION published in the medical literature. The purpose of this

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
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
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
Address for correspondence: Prof. Santosh Kumar Swain, Department of
Otorhinolaryngology, IMS & SUM Hospital, Siksha “O” Anusandhan University,
Kalinga Nagar, Bhubaneswar-751003, Odisha, India.
E-mail: santoshvoltaire@yahoo.co.in
Received: 14 July 2020 Revised: 8 September 2020
Accepted: 30 December 2020 Published: 25 June 2021

Access this article online This is an open access journal, and articles are distributed under the terms of the
Quick Response Code: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows
Website: others to remix, tweak, and build upon the work non-commercially, as long as
www.mamcjms.in appropriate credit is given and the new creations are licensed under the identical
terms.

For reprints contact: reprints@medknow.com

DOI:
10.4103/mamcjms.mamcjms_80_20 How to cite this article: Swain SK, Paul RR. Herpes Zoster Oticus: A
Morbid Clinical Entity. MAMC J Med Sci 2021;7:99-103.

© 2021 MAMC Journal of Medical Sciences | Published by Wolters Kluwer - Medknow 99

[Downloaded free from http://www.mamcjms.in on Friday, April 7, 2023, IP: 202.67.40.238]
Swain and Paul: Herpes zoster oticus
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.
History
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.
Epidemiology
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]
Etiopathology
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
100 MAMC Journal of Medical Sciences ¦ Volume 7 ¦ Issue 2 ¦ May-August 2021
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
[Downloaded free from http://www.mamcjms.in on Friday, April 7, 2023, IP: 202.67.40.238]
Swain and Paul: Herpes zoster oticus
Figure 1: Patients of herpes zoster oticus typically present varicelliform
rash with blisters in the pinna and surrounding area.
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.
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
MAMC Journal of Medical Sciences ¦ Volume 7 ¦ Issue 2 ¦ May-August 2021
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]
Diagnosis
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
101
[Downloaded free from http://www.mamcjms.in on Friday, April 7, 2023, IP: 202.67.40.238]
Swain and Paul: Herpes zoster oticus
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]
Treatment
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
102
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]
Prognosis
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
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.
Financial support and sponsorship
Nil.
MAMC Journal of Medical Sciences ¦ Volume 7 ¦ Issue 2 ¦ May-August 2021
[Downloaded free from http://www.mamcjms.in on Friday, April 7, 2023, IP: 202.67.40.238]
Swain and Paul: Herpes zoster oticus
Conflicts of interest
There are no conflicts of interest.
REFERENCES
1. Psillas G, Dova S, Ieridou F, Kyrgidis A, Constantinidis J. Ramsay
Hunt syndrome: clinical presentation and prognostic factors. B-ENT
2019;15:297-302.
2. Arya D, Bajaj T, Gonzalez J, Elkin R. Ramsay Hunt syndrome with
multiple cranial neuropathy in an human immunodeficiency virus
(HIV) patient. Am J Case Rep 2018;19:68-71.
3. Elshereye A, Erdinc B, Sahni S. Disseminated varicella-zoster virus
infection complicated by encephalitis and Ramsay Hunt syndrome in
an HIV patient. Cureus 2020;12:1-7.
4. Kanerva M, Jones S, Pitkaranta A. Ramsay Hunt syndrome:
characteristics and patient self-assessed long-term facial palsy
outcome. Eur Arch Otorhinolaryngol 2020;277:1235-45.
5. Kanamori K, Shoji K, Kinoshita N, Ishiguro A, Miyairi I. Complications
of herpes zoster in children. Pediatr Int 2019;61:1216-20.
6. Jeon Y, Lee H. Ramsay Hunt syndrome. J Dent Anesth Pain Med
2018;18:333-7.
7. Furuta Y, Ohtani F, Aizawa H, Fukuda S, Kawabata H, Bergstro¨m T.
Varicella zoster virus reactivation is an important cause of acute peripheral
facial paralysis in children, Pediatr Infect Dis J 2005;24:97-101.
8. Inagaki A, Minakata T, Katsumi S, Murakami S. Data for temporal
facial nerve recovery in Ramsay Hunt syndrome following
intratympanic steroid therapy. Data Brief 2020;410:1-6.
9. Swain SK, Behera IC, Sahu MC. Head injury with sudden onset
bilateral facial palsy − can happen without temporal bone fractures
and brain injury! Egypt J Ear Nose Throat Allied Sci 2016;17:23-25.
10. Pitton Rissardo J, Fornari Caprara AL. Herpes zoster oticus,
ophthalmicus, and cutaneous disseminated: case report and literature
review. Neuroophthalmol 2019;43:407-10.
11. Tsau PW, Liao MF, Hsu JL, et al. Clinical presentations and outcome
studies of cranial nerve involvement in herpes zoster infection: a
retrospective single-center analysis. J Clin Med 2020;9:946-55.
12. Júnior NC, Brooks JB. Ramsay Hunt syndrome. A case report. J Clin
Case Rep Images 2020;2:1.
13. Lee YH, Young YH, Lin YT. Visualizing Affected Nerve Bundles of
Cranial Nerves VII and VIII in Herpes Zoster Oticus. Otol Neurotol
2020;41:1174-6.
14. Kim CH, Choi H, Shin JE. Characteristics of hearing loss in patients
with herpes zoster oticus. Medicine 2016;95:1-5.
15. Shin DH, Kim BR, Shin JE, Kim CH. Clinical manifestations in
patients with herpes zoster oticus. Eur Arch Otorhinolaryngol
2016;273:1739-43.
16. Engström M, Berg T, Stjernquist-Desatnik A, et al. Prednisolone and
valaciclovir in Bell’s palsy: a randomised, double-blind, placebo-
controlled, multicentre trial. Lancet Neurol 2008;7:993-1000.
17. Yawn BP, Saddier P, Wollan PC, St Sauver JL, Kurland MJ, Sy LS. A
population-based study of the incidence and complication rates of
herpes zoster. Mayo Clin Proc 2007;82:1341-9.
MAMC Journal of Medical Sciences ¦ Volume 7 ¦ Issue 2 ¦ May-August 2021
18. Swain SK, Behera IC, Sahu MC. Bell’s palsy among infants-Our
experiences in a tertiary care hospital of eastern India. Asian J
Pharm Clin Res 2017;10:85-87.
19. Durdu M, Baba M, Seçkin D. The value of Tzanck smear test in
diagnosis of erosive, vesicular, bullous, and pustular skin lesions. J Am
Acad Dermatol 2008;59:958.
20. Coffin SE, Hodinka RL. Utility of direct immunofluorescence and
virus culture for detection of varicella-zoster virus in skin lesions. J
Clin Microbiol 1995;33:2792-5.
21. Swain SK, Choudhury J, Acharya S. Herpes zoster oticus among
pediatric patients: Our experiences at a tertiary care teaching
hospital. Indian J Health Sci Biomed Res 2020;13:215-20.
22. Gantz BJ, Rubinstein JT, Gidley P, Woodworth GG. Surgical
management of Bell’s palsy. Laryngoscope 1999;109:1177-88.
23. Swain SK, Acharya S, Shajahan N, Agrawala R. Herpes zoster
laryngitis. J Sci Soci 2020;47:45-7.
24. Gilden D, Cohrs RJ, Mahalingam R, Nagel MA. Neurological disease
produced by varicella zoster virus reactivation without rash. Curr Top
Microbiol Immunol. 2010;342:243-53.
25. Balatsouras DG, Rallis E, Homsioglou E, Fiska A, Korres SG.
Ramsay Hunt syndrome in a 3-month-old infant, Pediatr Dermatol
2007;24:34-37.
26. Choi JW, Nahm H, Shin JE, Kim CH. Atypical clinical manifestations
of herpes zoster oticus: diagnostic usefulness of magnetic resonance
imaging. J Neurovirol 2019;25:874-82.
27. Kang BH, Lee YW, Kim JI. Atypical presentation of acute vestibular
syndrome with Ramsay Hunt syndrome. Res Vestib Sci 2020;19:16-21.
28. Koshy E, Mengting L, Kumar H, Jianbo W. Epidemiology, treatment
and prevention of herpes zoster: a comprehensive review. Indian J
Dermatol Venereol Leprol 2018;84:251-62.
29. Galluzzi KE. Management strategies for herpes zoster and postherpetic
neuralgia. J Am Osteopath Assoc 2007;107:8-13.
30. Kunitomo K. Ramsay Hunt syndrome. Postgrad Med J 2020;96:168.
31. Dai S, Huang X, Chen Y, et al. Bilateral asymmetrical herpes-zoster
with Ramsay Hunt syndrome in an immunocompetent adult. Virol J
2020;17:1-5.
32. Gross GE, Eisert L, Doerr HW, et al. S2k guidelines for the diagnosis
and treatment of herpes zoster and postherpetic neuralgia. J Dtsch
Dermatol Ges 2020;18:55-78.
33. Kansu L, Yilmaz I. Herpes zoster oticus (Ramsay Hunt syndrome) in
children: case report and literature review. Int J Pediatr
Otorhinolaryngol 2012;76:772-6.
34. Motswaledi MH. Herpes zoster (shingles). South Afr Family Pract
2018;60:28-30.
35. Swain SK, Sahu MC, Behera IC. Management of Ramsay Hunt
syndrome among HIV patients: Our experience in a tertiary care
hospital of eastern India. Polish Ann Med 2016;23:92-96.
36. Coulson S, Croxson GR, Adams R, Oey V. Prognostic factors in
herpes zoster oticus (Ramsay Hunt syndrome). Otol Neurotol
2011;32:1025-30.
37. Kim SH, Jung J, Jung SY, et al. Comparative prognosis in patients with
Ramsay-Hunt syndrome and Bell’s palsy. Eur Arch Otorhinolaryngol
2019;276:1011-6.
103