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Viral Meningitis inChildren andHearing
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Loss
BülentKara, MesutGüngör, EminSamiArısoy,
andGailJ.Demmler-Harrison
24.1 Introduction
Hearing loss (HL) is a common cause of speech, language, and cognition delays.
Hearing loss occurs in 1–3 newborns per 1000 births, with clinically signicant or
permanent HL in 1–2 per 1000 newborns and 2 per 1000 children [1, 2]. Early diagnosis of HL is critical, as improvement in speech and cognitive functions can be
achieved with early intervention [3]. Pediatric HL can be categorized as congenital
(genetic and non-genetic), acquired or sensorineural, conductive, and mixed [4].
Viral central nervous system (CNS) infections can lead to congenital and acquired
HL, mainly sensorineural. This chapter will focus on acquired HL associated with
viral meningitis and vaccines against viruses in children.
24
B. Kara (*)
Division of Pediatric Neurology, Department of Pediatrics, Faculty of Medicine, Kocaeli
University, Kocaeli, Türkiye
e-mail: bkuskudar@gmail.com
M. Güngör
Division of Pediatric Neurology, Department of Pediatrics, Faculty of Medicine, Selçuk
University, Konya, Türkiye
e-mail: mesutgungor@gmail.com
E. S. Arısoy
Division of Pediatric Infectious Diseases, Department of Pediatrics, Faculty of Medicine,
Kocaeli University, Kocaeli, Türkiye
e-mail: emin.sami.arisoy@gmail.com
G. J. Demmler-Harrison
Division of Infectious Diseases, Department of Pediatrics, Baylor College of Medicine,
Houston, TX, USA
Infectious Disease Service, Texas Children’s Hospital, Houston, TX, USA
e-mail: gdemmler@bcm.edu
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
A. E. Arısoy et al. (eds.), Hearing Loss in Congenital, Neonatal and Childhood
Infections, Comprehensive ENT, https://doi.org/10.1007/978-3-031-38495-0_24
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Meningitis is inammation of the meningeal membranes surrounding the brain
and the spinal cord [5]. It is characterized by pleocytosis, dened as an increased
leukocyte count in the cerebrospinal uid (CSF). Meningitis can be broadly divided
into two general classes, bacterial (septic) and aseptic meningitis. There are many
infectious and non-infectious causes of aseptic meningitis. Because viruses are the
most common cause of aseptic meningitis, the terms aseptic meningitis and viral
meningitis (VM) are commonly used synonymously [6]. More than 100 virus strains
have been directly or indirectly associated with human central or peripheral nervous
system disorders [7]. Viral meningitis is the most common neurological disorder
due to viruses [8].
B. Kara et al.
24.2 Definition
Viral meningitis can be dened as a febrile illness accompanied by clinical signs
and symptoms due to meningeal irritation without other neurological dysfunction,
no evidence of bacterial pathogen in CSF examination in a patient who did not
receive antibiotics before lumbar puncture (LP), and detection of viral deoxyribonucleic acid (DNA) or ribonucleic acid (RNA) in the patient’s CSF [9].
24.3 Epidemiology
The annual incidence of VM is estimated to be between 10 and 20 per 100,000 children [10]. This incidence peaks in children under the age of 1 and over the age of
5years. A Denmark study showed that the incidence of aseptic meningitis decreases
with age; 58.7 per 100,000 after birth, 38.7 per 100,000in 6-month infants, and 15.6
per 100,000in 5-year-old children [11]. In temperate climates, most cases occur in
summer and autumn, reecting the highest activity of enteroviral and arthropod
infections [11]. In a study from Palestine, 58% of patients with enteroviral meningitis were detected in spring and summer [12]. The incidence of VM due to enteroviruses (EVs) and human parechovirus was twice of bacterial meningitis in the
United Kingdom (UK) [13]. In many studies, viruses were found more frequently
than bacteria among causative agents of meningitis. In Lebanon, 250 cases with
conrmed meningitis were evaluated; 82.7% of cases were diagnosed with VM and
only 17.3% with bacterial meningitis [14]. The widespread application of vaccines
covering bacterial meningitis pathogens has led to an increase in the difference in
favor of viruses in the etiology of meningitis.
24.4 Pathogenesis
Most viral pathogens affecting the CNS enter the host through respiratory secretions and the fecal–oral route and infect the mucosal surfaces of the respiratory and
gastrointestinal tracts [15]. This is followed by viral replication in regional lymph
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nodes. The primary viremia phase follows replication. In the primary viremia phase,
the initial symptoms of the disease and spread to other organs occur. Central nervous system involvement develops in the secondary viremia phase following viral
replication in other organs, particularly the liver and the spleen [16, 17]. The mecha-
nisms related to viral transport from the circulatory system to the brain are unknown.
When the virus reaches the vessels in the CNS, the transendothelial passage from
the choroid plexus, meninges, or cerebral vessels occurs through different mechanisms, such as transport within migrating leukocytes, pinocytosis or colloidal transport, passage through the damaged endothelial barrier, and direct infection of
endothelial cells [18, 19]. After entering the CNS, a strong inammatory immune
response is evoked and plays an important role in the clinical ndings of the disease [20].
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24.5 Etiology
Non-polio EVs are the most common causative agents of VM in children, accounting for 85% of cases [20]. Mumps, human parechoviruses, arboviruses such as West
Nile virus (WNV), herpesviruses, including herpes simplex virus (HSV), varicellazoster virus (VZV), cytomegalovirus (CMV), Epstein–Barr virus (EBV), human
herpesvirus (HHV) 6 and 7, lymphocytic choriomeningitis virus (LCMV), inuenza, and rabies viruses are other important causes of VM.
24.6 Clinical Features
Clinical ndings of VM include meningeal irritation signs and agent-specic systemic manifestations. Meningeal irritation signs are not specic to any virus and
have no value for the differential diagnosis of other CNS infections such as bacterial
meningitis, encephalitis, or brain abscesses [21]. There are no reliable clinical distinctions between viral and bacterial meningitis. Patients with bacterial meningitis
tend to be more severely ill and may experience cognitive impairment, seizures,
focal neurological decits, and/or hypotension more than VM.Brudzinski’s and
Kernig’s signs and nuchal rigidity are classical bedside tests to assess meningeal
irritation, but their diagnostic accuracy is limited and difcult to evaluate in newborns and infants [22, 23]. Bulging fontanelle may be a valuable nding in newborns and infants, but sensitivity and specicity for VM are too low. Jolt accentuation
of headache is a recently recognized physical examination technique to evaluate
meningeal irritation. This test is interpreted as positive if the headache is exacerbated by rotating the head horizontally 2–3 times/s. The sensitivity and specicity
of this test are found to be 65.3% and 70.4%, respectively, and considered low to use
in emergency settings to exclude meningitis [24].
Neurologic manifestations of VM vary according to age. Newborns may have
no neurologic symptoms or have irritability and lethargy [25]. Infants present
with non-specic symptoms such as irritability, poor feeding, vomiting, diarrhea,
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and short and fast breathing, accompanying acute-onset fever. Nuchal rigidity
and bulging fontanelle can be detectable in newborns and infants. The appearance of seizures and focal neurological signs suggests the progression of encephalitis. Older children typically present with fever, chills, headache, nausea,
vomiting, nuchal rigidity, difculty concentrating, double vision, and photophobia [26–28].
Newborns with viral meningoencephalitis are at increased risk for severe systemic disease. Systemic manifestations may include pneumonia, necrotizing hepatitis, myocarditis, necrotizing enterocolitis, and a sepsis-like picture [16]. Severe
systemic manifestations are rare in infants and older children unless there is an
additional risk factor. They usually suffer from non-specic systemic symptoms
such as loss of appetite, upper and lower respiratory problems, abdominal pain,
myalgias, and manifestations of viral illness such as rash, conjunctivitis, herpangina, and pharyngitis [26–28]. Some clinical ndings may be specic to the virus.
For example, EV-A71 (EV-71) usually causes hand-foot-mouth disease and rhombencephalitis, EV-D68 (EV-68) causes acute accid myelitis, and parechovirus
causes a clinical spectrum, including neonatal sepsis, meningitis, encephalitis, and
paralysis in neonates [29–32].
B. Kara et al.
24.7 Complications
Most patients with VM recover without complications. A small proportion may
experience chronic headaches [6]. Serious complications, such as hepatic necrosis,
necrotizing enterocolitis, and myocarditis, may develop in the neonatal period due
to multi-organ involvement [5]. Enteroviral meningitis typically has a benign
course, while enteroviral encephalitis can cause long-term neurological sequelae
[33]. It progresses with signicant morbidity and mortality in newborns and immunocompromised patients. In immunocompromised patients, especially with agammaglobulinemia or hypogammaglobulinemia, EV infection may become chronic
and persists for months [34].
Some EV subtypes, such as EV-71 and EV-68, are associated with more severe
neurological disease and a worse prognosis. Enteroviral infections’ most common
serious complications are meningoencephalitis, myocarditis, and pericarditis. Acute
accid paralysis and rhombencephalitis are also among the neurological complications of enteroviral infection in children.
Neuropsychiatric disorders may also occur after VM but are typically not as
severe as those that occur after bacterial meningitis [35]. Sleep disturbance may
become evident as a complication of VM [36]. Statistically, signicant retardation
was found in the development of perceptual language in the 3-year follow-up of
infants with a VM history in the rst 3months of life [37]. Another study showed an
increased risk of attention decit hyperactivity disorder in patients after EV-71
infection [38].
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24.8 Diagnosis
In children with suspected meningitis, an LP should be done to collect CSF regardless of the presence or absence of meningeal irritation signs [22]. Intracranial hypertension should be excluded before LP to avoid herniation syndromes. Cerebrospinal
uid should be evaluated for color, opening pressure, Gram stain and bacterial culture, cell count and differential, glucose, protein, and viral polymerase chain reaction (PCR) studies. In addition, CSF lactate level (≥4.2mmol/L) can be used for the
differential diagnosis of viral and bacterial meningitis with 100% specicity [39].
The CSF analysis mainly aims to differentiate VM from bacterial meningitis.
Cerebrospinal uid pleocytosis is an essential criterion for the diagnosis of meningitis. White blood cell (WBC) count ranging from 10 to 500/mm3 with mononuclear
cell predominance supports VM; however, CSF pleocytosis is not observed in a
group of infants (38%) and children (39%) in enteroviral meningitis, and 25% of
patients may have neutrophilic predominance [40–42]. Eosinophilic pleocytosis can
be seen in some EV types. The cloudy appearance of CSF is an excluding characteristic for VM.The CSF protein levels vary between normal and slightly elevated
(<150 mg/dL), and glucose levels are normal or slightly reduced (≥40% of the
serum value) in VM.The CSF protein levels can be inconsistently high in WNV
meningitis. Hypoglycorrhachia is a frequently reported feature in mumps meningitis. Bacterial meningitis has a higher CSF protein level, a lower glucose level, and a
higher CSF lactate level than VM [6]. Viral cultures are no longer used except in
exceptional cases. Serological testing for EVs has no value in the diagnosis [40].
However, detecting virus-specic antibodies is very important for diagnosis in cases
of meningitis due to arboviruses [43]. In cases of VM due to HSV, detecting immunoglobulin (Ig) M and IgG antibodies against HSV-1 and HSV-2in serum and CSF
may be helpful in the diagnosis.
The PCR is the gold standard test for diagnosing VM.The PCR test detects and
quanties viral RNA or DNA particles in CSF, and its sensitivity is 100% [44].
Targeted reverse transcriptase (RT)-PCR analysis can be used for EVs, but HSV or
WNV may also be warranted in suspected cases. Multiplex PCR analysis detects
many viral, bacterial, and fungal pathogens simultaneously, but its sensitivity may
be low for HSV-1 and HSV-2. The PCR tests allow rapid diagnosis, shorten hospital
stay, and reduce unnecessary antibiotic use [45]. In cases where CSF cannot be
obtained, specimens such as throat and nasal swabs, blood, urine, and stool may be
used, particularly in patients suspected of enteroviral meningitis.
The leukocyte count may be slightly increased in the complete blood count with
lymphocyte predominance in VM.Acute phase reactants are not expected to reach
very high levels unless complications develop [5]. Serum procalcitonin (PCT) levels above 1.20ng/mL and serum C-reactive protein (CRP) levels above 40mg/L
show a high risk for bacterial meningitis [46]. Elevated myocardial enzymes in
cases with pericarditis or myocarditis, hypertransaminasemia in cases of hepatitis,
or radiological ndings in patients with respiratory system infection may be seen as
the accompanying systemic manifestations of viral infection.
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Neuroimaging is not necessary for diagnosing VM.Severely depressed mental
status (coma), papilledema, focal neurologic decit (except sixth or seventh cranial
nerve palsy), history of hydrocephalus and/or presence of a CSF shunt, and a recent
history of CNS trauma or neurosurgery are indications for neuroimaging before
LP.These ndings are not expected in uncomplicated VM cases.
Detailed history and physical examination play an essential role in diagnosing
VM.In addition to a thorough neurological examination, a careful systemic examination should also be performed. Acute bacterial meningitis must be excluded
before the diagnosis of VM.Therefore, a CSF sample should be taken without
delay. Clinical and CSF ndings of VM and bacterial meningitis can sometimes
overlap. Empirical antibiotic therapy should be started if CSF PCR analysis is negative and acute bacterial meningitis cannot be excluded. Bacterial meningitis is
excluded mainly by the absence of microorganisms in CSF gram staining and lymphocytic pleocytosis in cell count [5–8]. The denitive diagnosis of VM is made by
negative bacterial cultures and demonstrating the viral agent in CSF.
B. Kara et al.
24.9 Treatment
Patients with conrmed VM usually do not need hospitalization. Children under
1year of age, immunocompromised patients, and patients requiring empirical antibiotic therapy or intravenous uid therapy should be hospitalized [47]. Care and
treatment of patients should be carried out in a quiet, calm, and dim room, regardless of whether the patient is at home or in the hospital. Antipyretics, analgesics, and
antiemetics can be used when needed [7]. The efcacy of corticosteroids against
VM is not well-studied. Intravenous uid therapy should be administered in cases
where oral intake is poor, or uid loss occurs due to vomiting, etc. [47]. Various
algorithms have been developed to assess the likelihood of bacterial meningitis.
However, the application of these algorithms may be misleading in children younger
than 3months, immunocompromised patients, patients in poor general condition,
patients who received antibiotic treatment for another reason within 72h before LP,
and those who had a traumatic LP.Empirical antibiotic therapy should be given to
these patients until the diagnosis of bacterial meningitis is denitively excluded [48].
Most children with uncomplicated VM do not require empirical antiviral therapy.
However, in immunocompromised children, cases of acute encephalitis, or cases
suspected of neonatal HSV infection, initiation of empirical antiviral therapy with
acyclovir would be an appropriate approach. In clinically recovered patients, acyclovir treatment may be discontinued when CSF HSV PCR is negative or another
diagnosis, such as EV PCR positivity, is established. Conrmed HSV meningitis is
treated with acyclovir [49]. Acyclovir also can be used for VZV meningitis [50].
Psoromic acid is a new antiviral drug that inhibits the replication of HSV-1 and
HSV-2 and can be an alternative to acyclovir in the future for treating HSV meningitis [51]. Enterovirus and parechovirus infections are mostly self-limited and
require only symptomatic and supportive treatments. Experimental antiviral drugs
can be used only for life-threatening conditions such as neonatal infections, severe
myocarditis, or disseminated infections in immunocompromised patients. Using
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intravenous immunoglobulin (IVIG) for complicated cases is controversial.
Pleconaril inhibits enteroviral replication and has high CNS concentrations. It may
alleviate clinical manifestations in selected patients with enteroviral meningitis [52].
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24.10 Prognosis
Most patients with VM recover fully [5, 53]. The prognosis depends on the age of
the child and the etiologic agent. In children, the duration of symptoms and clinical
improvement is usually less than 1week. The recovery phase is usually longer in
adolescents and young adults, and some may complain of fatigue, irritability,
decreased concentration, muscle weakness, and poor coordination for several weeks
after the acute illness [20]. Enteroviral meningitis typically has a benign clinical
course [53, 54]. The morbidity and mortality of enteroviral meningitis are not
known precisely because it is common, and there is no obligation for notication.
Mortality has been reported in up to 10% of immunocompromised individuals and
newborn infants. Death is usually due to hepatic failure in echovirus infection and
myocarditis in coxsackievirus infection [55, 56].
24.11 Prevention
Cesarean delivery decreases vertical transmission of HSV in women with active
genital skin lesions when performed before the rupture of membranes. American
College of Obstetricians and Gynecologists (ACOG) suggests oral acyclovir treatment before delivery [57]. Hand washing is a simple method to prevent the spread
of EVs [33]. Personal protection measures to avoid mosquito and tick exposure are
the mainstay of preventing the transmission of many viruses. In children hospitalized with the diagnosis of VM, contact precautions should be observed during the
hospitalization.
Vaccines against some common VM pathogens are available, and others are
under development. The mumps vaccine signicantly reduced the incidence of
mumps-related meningitis. Three inactivated EV-71 vaccines have recently been
licensed in China [58]. Central nervous system infections due to inuenza and some
arboviruses, such as Japanese encephalitis and tick-borne encephalitis, can be prevented with vaccines. Vaccines for coronavirus disease 2019 (COVID-19) are
expected to decrease severe neurologic and other systemic complications in
adolescents.
24.12 Viral Meningitis inChildren andHearing Loss
Hearing loss is currently the second leading cause of years lived with a disability, and
viral infections contribute to this high burden. Many viruses can cause congenital or
acquired and unilateral or bilateral HL [59]. Direct or immune-mediated damage to
inner ear structures and reactivation of latent viral infection in the inner ear are the
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three main mechanisms of viral infection-triggered HL [59, 60]. Viral infectionrelated HL may occur in the late period of the disease, and it may be challenging to
establish a cause-effect relationship. The severity of HL varies from mild or severe to
profound [61, 62]. Hearing loss, especially in the rst years of life, has a serious
adverse effect on the patient’s speech, language, and cognitive development [63].
Viruses mainly cause sensorineural HL (SNHL), but conductive HL (CHL) can
be seen with opportunistic microorganisms in immunocompromised patients with
ear infections. Problems in the outer or middle ear that impair the transmission of
sound to the inner ear are called CHL.Conductive HL usually occurs acutely and is
mostly temporary. Damage, disease, or disorders of inner ear structures such as the
cochlea, inner ear hair cells, organ of Corti, or the eighth cranial nerve may
cause SNHL.
There are hereditary and acquired causes of SNHL.In childhood, the etiology of
acquired SNHL can be determined at around 10%. Bacterial meningitis is the most
common cause of acquired SNHL, and virus infections are less common [61]. In a
study conducted with a population of 220 infants with VM, delay or no response in
auditory evoked potentials was found in 92.5% of the patients in the initial evaluation, but SNHL was detected in only two patients (0.9%) at follow-up [64]. A study
conducted in China between 2015 and 2017 studying the etiology of HL showed
that 60% of bilateral SNHL are due to preventable acquired causes. Among the
acquired reasons, meningitis had a rate of 13.2% [65]. In a series of 200 patients
with SNHL candidates for cochlear implantation in the UK, it was reported that
meningitis was responsible for the etiology in 28% of the cases [62]. Neither study
investigated the viral or bacterial etiology of meningitis.
B. Kara et al.
24.13 Common Viruses Causing Intrauterine Infection-Related
Congenital Hearing Loss
Cytomegalovirus, rubella virus, LCMV, and Zika virus cause intrauterine infection
and congenital HL.However, HL related to congenital infections is out of the scope
of this chapter.
24.14 Common Viruses Causing Meningitis andAcquired
Hearing Loss inChildren
24.14.1 Mumps andHearing Loss
The mumps virus is a single-stranded RNA virus that belongs to the Paramyxovirus
family. It is transmitted through infected respiratory secretions and primarily infects
salivary glands. The central nervous system is the most common extra salivary
organ involved in mumps cases. Aseptic meningitis and encephalitis are potential
complications of mumps infection [59, 66, 67]. The risk of developing meningitis in
mumps is 1–10%, and the risk of encephalitis is 0.1% [68]. Meningitis occurs after
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about 5days of parotitis but may occur before or after 2weeks of parotid swelling
[69, 70]. There is no salivary gland involvement in approximately half of the meningitis cases due to mumps infection [71]. Mumps meningitis is usually benign, and
severe neurological sequelae and mortality are not expected. Encephalitis should be
considered in patients who develop seizures, focal neurological signs, or cognitive
abnormalities at follow-up.
Sensorineural HL is a well-known complication of mumps. Mumps virus can
invade auditory structures directly as the sole neurologic manifestation of the disease, but the HL complication usually accompanies meningitis or meningoencephalitis. The incidence of HL range from 1 per 1000 to 1 per 20,000in mumps cases
[72]. Transient high frequency-range HL is frequent in mumps, and in an adult male
(military) series, it was reported at 4% in frequency [73]. Although the risk of unilateral, prominent HL is reported as 1 per 20.000in an old study, in a recent epidemiological study from Japan, of 68,812 patients with mumps, mumps-related
deafness was reported in 102 patients (1in 668 patients) [74, 75]. The incidence of
mumps deafness was 7.2 times higher among 6- to 15-year-old children than among
0- to 5-year-old children with no sex difference [75].
Hearing loss usually has a sudden onset, but gradual onset is possible. Vertigo
often accompanies HL [76]. Hearing loss mostly presents as unilateral and profound SNHL.Severe HL has a poor prognosis, but spontaneous recovery has been
reported in mild cases. Some patients with mild HL can be overlooked; therefore, it
is difcult to know the actual frequency of mumps deafness [77–80].
Acute Severe Hearing Loss Study Group, the Ministry of Health, Labor and
Welfare of Japan, proposed the diagnostic criteria for mumps deafness in 1987 and
revised it in 2013 (Table24.1) [79, 80].
Serological tests for patients with sudden SNHL are recommended to be screened
to detect mumps deafness, but it needs to be careful regarding false-positive results
[81]. Elevated anti-mumps IgM antibody levels were reported in 5.7–7.2% of
Japanese SNHL patients [82, 83]. The continuation of IgM positivity and IgMpositive cases in normal adults may have caused the rate to be high due to false positivity. After introducing the new enzyme immunoassay (EIA) test, anti-mumps IgM
positivity was found to be 1% in sudden SNHL patients, lower than previously
reported [84].
Table 24.1 Criteria for the diagnosis of mumps deafness
Denite diagnosis
1. Patients with evident clinical signs of mumps, such as swelling of the parotid and
submandibular glands and acute severe hearing loss during the period from 4days before
to 18days after the appearance of such swelling.
2. Patients without evident clinical signs of mumps but immunoglobulin (Ig) M antibodies
against the mumps virus are detected within 3months after the onset of acute severe
hearing loss.
Referent case: Patients in whom mumps deafness is suspected clinically.
1. Patients whose family members or friends have a mumps infection
2. Patients who have different periods to denite criterion 1
a
Adapted from Ref. [80]
a
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There is no effective treatment for mumps deafness. Most patients with mumps
are refractory to therapies such as corticosteroids, vitamin B12, vasodilators, and
hyperbaric oxygen therapy [79]. Therefore, vaccination against mumps has a priority. The incidence of mumps deafness has signicantly decreased in countries where
mumps vaccination is widely applied [85]. The rst dose of the mumps vaccine for
children is recommended at 12–18months of age, and to eliminate mumps infection, the second dose is at 4–6years of age.
Mumps occasionally causes bilateral HL.Cochlear implantation may be a good
choice for these patients because the labyrinth might be a site of lesions following
mumps in the majority of patients [86, 87]. Early cochlear implantation intervention
showed good speech sound perception in these patients, but the same effect was not
demonstrated in late implantation patients [88]. The low success rate of cochlear
implantation is also reported for patients with retrolabyrinthine HL due to CNS
damage caused by meningitis or meningoencephalitis [89].
B. Kara et al.
24.14.2 Measles (Rubeola) andHearing Loss
The measles virus (rubeola) is a single-stranded RNA virus belonging to the
Paramyxovirus family, including the mumps virus. Measles was frequently causing
epidemics in the pre-vaccine period with severe complications. Measles encephalitis occurs in approximately 1 in 1000 cases [90]. However, evidence of CNS
involvement, such as CSF pleocytosis and transient electroencephalogram (EEG)
abnormalities, can be observed in more than half of measles patients [90].
Sensorineural HL is one of the severe complications of measles [59]. Measles
accounted for 4–9% of all cases of bilateral deafness due to profound SNHL before
widespread vaccination [91]. Children are still at high risk for measles-associated
HL in countries where live measles vaccination is rare.
Additionally, immigrations create an obstacle to global measles eradication.
Hearing loss is typically bilateral, severe to profound, sensorineural, and may occur
after measles encephalitis [90]. Degeneration of the organ of Corti and stria vascularis and cellular inltration of the cochlea were shown in temporal bone studies on
patients with measles and animal models [90, 92]. Otitis media is a frequent complication of measles caused by bacterial superinfection and may also play a role in
the development of HL [93].
There is a theory that measles causes otosclerosis. Otosclerosis is an autoinammatory disorder that causes stapes xation and bone remodeling of the human otic
capsule. It is a frequent cause of CHL, constituting 18–22% of all CHL.The relationship between the persistent measles virus infection and otosclerosis is controversial and needs further investigation [93].
Cochlear implantation is effective for patients with severe to profound SNHL in
measles. Mild-to-moderate cases can be supported with hearing aids.
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