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Fig. 29.1 Schematic
representation of the main
brainstem nuclei of the
auditory pathway, their main
connections, and
neurotransmitters. MSO
medial superior olivary
nucleus, LSO lateral superior
olivary nucleus, MNTB
medial nucleus of the
trapezoid body, IC inferior
colliculus, and the three
nuclei of the lateral
lemniscus: DNLL dorsal
nucleus of the lateral
lemniscus, INLL intermediate
nucleus of the lateral
lemniscus, VNLL ventral
nucleus of the lateral
lemniscus [48]
B. D. Ramos
inhibitory, likely mediated by gamma-amino-butyric acid
(GABA) [50].
The IC provides the principal source of innervation to the
medial geniculate body (MGB) and, thus, indirectly to the
auditory cortex [48]. Therefore, the IC is the nexus of the
auditory system because it processes and integrates almost
all ascending acoustic information from lower centers and
determines the form in which information is conveyed to
higher regions in the forebrain [48]. The central auditory system has both parallel and hierarchical afferent architectures
[43]. In the frequency domain, it is tonotopically constrained,
and in the spatial domain, it is dominated by a representation
of the contralateral acoustic hemield [43]. The CHL at early
age can disrupt the binaural integration of interaural level
differences in the IC [38].
Medial Geniculate Body (MGB)
Neurons are arranged tonotopically, in sheet-like layers,
each receiving its input from a single cochlear place [46].
They are narrowly tuned to tone frequency, have short
response latencies, and show the familiar patterns of binaural
input and interactions [46].
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259
Auditory Cortex
Some of the elds are tonotopically organized, and these
typically receive thalamic input from MGB, with the densest
such projection serving the primary auditory cortex [46].
Tonotopic maps describe the spatial arrangement of neurons
according to their frequencies [46]. The thalamocortical connections in the auditory system are largely reciprocal [46].
The cortical representation of a stimulus resides in the distribution of responses in space (and time) across the cortex
[46].
The combined effect of CHL paired with a loss of temporal delity and disorganized binaural cues can substantially
degrade the quality of afferent signals transmitted to brain
areas that represent and shape our perceptions of the auditory
world [1]. This hypothesis is supported by thousands of studies that characterize the development of higher (i.e., midbrain, thalamic, and cortical) sensory brain areas and describe
signicant alterations in the response properties of individual
neurons, as well as their coordinated arrangement into functional circuits and topographic maps, based on the presence
and quality of sensory-evoked afferent input [1].
Neurotransmitters
All aspects of audition, from pure tone hearing to complex
spoken language processing, rely on the transmission of neural information across synapses [42]. Information about
sound representation at the cochlea must be transmitted to
the brain through a complex network of neural synapses
[42]. Synaptic transmission, from neurotransmitter (NT)
synthesis, through binding and activation of receptors, to
reuptake and degradation of NT, is dependent on chemical
processes [42].
NT is a molecule that is synthesized in neurons, which
can modify the functioning of another cell. This chemical
communication depends on the NT passing from one neuron
to another through spaces known as synapses. The most
important excitatory NTs in the auditory system are acetylcholine, dopamine, noradrenalin, and glutamate, and the
most important inhibitory NTs are GABA and glycine [48] .
Moderate hearing loss during development can alter the
temporal properties of synapses and spikes and prevent the
synaptic inhibitory plasticity development which was regulated by the GABA-B receptors [38]. Hearing loss can impair
sound tolerance by reducing GABA inhibition in the IC,
which may be related to hyperacusis seen in children with
OM [38]. Failure to receive proper excitatory input from the
cochlea is known to cause the functional impairment in the
central auditory system and various sound processing decits [48]. Early age sound deprivation caused by CHL may
cause an irreversible impairment in the central auditory system and increases the risk of developing hyperacusis [38].
Central Auditory Processing Disorder (CAPD)
Behaviors which are most indicative of auditory processing
difculties include difculty hearing in background noise,
difculty following instructions, poor listening skills, academic difculties, poor auditory association skills, distractibility, and inattention [51].
Recurrent acute OM and chronic OME, especially when
they occur in the rst 3 years of life, may be causes of central
auditory processing disorder (CAPD), even after the resolution of middle ear disease and return of auditory thresholds
to normal [45]. The degree of CHL (rather than the presence
of OM per se) is decisive for the occurrence of central auditory decits [1]. CHL attenuates and delays sound passing
through the middle ear [1, 52].
A central auditory test battery should include measures
that examine four different central processes: auditory pattern/temporal ordering; monoaural separation/closures; binaural integration/binaural separation; and binaural interaction
(BI) [42]. Tests generally should include both nonverbal
(e.g., tones, clicks, and complex waveforms) and verbal
stimuli to examine different aspects of auditory processing
and different levels of the auditory nervous system [42].
Unless tests incorporating verbal stimuli are available in the
individual’s native language, evaluation may require reliance
on nonverbal stimuli [42]. We will discuss below the most
performed tests in children with suspected CAPD secondary
to OM.
Binaural Interaction (BI)
The 2005 American Speech-Language-Hearing Association
technical report on CAPD identied BI as one of the main
central processes that may need to be assessed as part of the
evaluation for a CAPD, particularly if the referring complaint or clinical information indicates that there may be a
decit in this domain, e.g., difculty with sound localization
or hearing in a background noise [42]. There are several tests
that have been designed to assess BI, and they are thought to
be sensitive to brainstem pathology [45].
The neural connections subserving binaural processing
are present at birth, but they are immature [53, 54]. The neural circuitry that underpins binaural hearing undergoes a
structural reorganization after hearing onset [53, 54].
Postnatal maturation is experience-dependent, and reduced
or altered cochlear output during the early postnatal period
may change the normal development of the central auditory
system [53, 54].
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Several studies have investigated the effects of CHL
caused by OM during early childhood on binaural processing abilities [1, 25, 55–57]. Studies have consistently shown
disrupted binaural processing for years following reinstatement of hearing through either spontaneous resolution of
effusion or placement of tympanostomy tubes [1, 55, 56].
This impairs binaural hearing and other central auditory
functions dependent on high delity sound transmission
[52]. For example, children who have had multiple episodes
of OME in the rst few years of life may have poor detection
of sounds in noisy environments, evidenced by reduced binaural unmasking (BU) [52]. Recent research shows that a
“threshold” level of OME is required to produce impaired
BU [52]. Children who had OME in one or both ears for
more than about 50% of the rst 5 years had reduced BU
[52]. Animal research, using long-term ear plugging, suggests that total OME duration, rather than age at the time of
having the disease, determines its effect on BU [52]. Animals
reared with bilateral (but not unilateral) ear plugs also have
poor auditory temporal resolution, and reduced sensitivity to
short tones in the presence of background noise, after plug
removal [52]. However, given time (6–24months) and training, all animals regained normal temporal resolution [52].
Impaired spatial processing and BI could underpin symptoms of listening difculties, for example, impaired temporal
processing, increased auditory lter width, or enhanced
masking may lead to poor speech perception [58–60].
Children with BI decit are at greater risk of difculty in
hearing and processing the teacher’s speech when there is
environmental noise, which may affect negatively in the
learning process [1, 45].
Binaural Interaction Test: Masking Level
Dierence (MLD) Test
The binaural masking level difference (MLD) test is a measure of the ability to take advantage of interaural phase differences between the target and masker when detecting a
tone in background noise [45]. Measures of BI are sensitive
to low brainstem dysfunctions/lesions [42, 45]. BI tests
involve the dichotic stimulation, i.e., the concurrent delivery
of separate and different acoustic stimuli to the two ears [45].
The behavioral MLD may provide a measure of our ability to
segregate sounds based on their location in space and is
underpinned by early processing of spatial cues in the brainstem and subsequent gating of this information in the thalamus, although contributions by later processing stages are
also involved [45]. The localization and the lateralization of
auditory stimuli, the detection of acoustic signals in noisy
environments, and the binaural fusion depend on this ability
[45]. It is a perceptual test that affords researchers with an
objective and parametric assessment of perceptual acuity
that also relates to the real-world experience of hearing in
noisy environments, such as classrooms or gymnasiums, by
measuring a participant’s sensitivity to interaural time and
amplitude cues [1].
Pillsbury et al.(1991) found reduced binaural MLDs in
children with OM (and associated CHL) during the disease
as well as 1 and 3months after ventilation tube surgery compared to normal hearing controls [61]. Furthermore, they
reported a (nonsignicant) trend for the binaural MLDs of
the OM children to increase over time [61]. Moore et al.
(1991) observed signicantly smaller binaural MLDs in children with more than ve OM episodes (as assessed using
parental reports) compared to normal hearing controls [62].
Hall etal. (1995) measured binaural MLDs in OM children
3months, 1, 2, 3, and 4years after the CHL had disappeared
[58]. They observed reduced MLDs that persisted for up to
2 years, leading them to propose that binaural function in
OM children recovers slowly [58]. Hogan and Moore (2003)
studied the effects of OM history on the binaural MLD in
6-year-old children [56]. The middle ear status and the
degree of CHL associated with OM of the children were prospectively documented from birth to the time of testing [56].
They found long-term negative effects of OM-related CHL
on the binaural MLD, which was related to the number of
experienced OM episodes [56]. Using a prospective study
design, Gravel etal. (2006) investigated the long-term effects
of CHL associated with OM in the rst 3years of life on the
binaural MLD [25]. In contrast to the aforementioned studies, these authors did not nd a signicant effect on the binaural MLD at school age [25]. A possible explanation for the
contrary outcomes of these studies might be the age at which
these children were tested [25]. The auditory system may
have recovered by the age of 8 years [25].
Monaural Low-Redundancy Speech Test:
Speech-in-Noise Test
The main complaint of the patient with auditory processing
disorder is the difculty in understanding speech with background noise. The type of noise used in speech-in-noise tests
can vary considerably [63]. White noise, multitalker babble,
and even competing discourse have been used in various
speech-in-noise tests [63]. These tests have moderate sensitivity for brainstem and cortical dysfunction [63].
Since performance on monoaural low-redundancy speech
tests is not affected by interhemispheric involvement (i.e.,
corpus callosum), they are especially useful when used
alongside dichotic tests or pattern tests that are sensitive to
hemispheric as well as interhemispheric involvement [63].
The tests used are the Synthetic Sentence Identication (SSI)
and the Pediatric Speech Intelligibility (PSI) [63]. The SSI
test consists of the presentation of synthetic sentences (sig-
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261
nal) in the presence of competitive noise, in the same ear
[63]. The task is to listen to the sentence and point it in the
frame [63]. The ability analyzed in this test is gure-ground
[63]. The PSI test, for children who are not yet reading, consists of gures description (signal) in the presence of competitive noise, in the same ear [63]. The child is asked to
point to the picture that is heard [63]. Patients with low to
mid-brainstem involvement, as well as cortical lesions typically perform poorly on speech-in-noise tests [63].
Children with a history of OM and subsequent bilateral
tubes placement surgery presented a lower performance than
children with no history of OM in the mean responses for the
SSI test of approximately 8% [33]. There is a causality
between OM in early life and its accompanied hearing loss
and lower performance on higher-order auditory skills, such
as speech perception in noise, even up to the age of 7years
[10]. Poor speech perception in noise can have negative consequences in daily situations and impair communicative situations with background noise [10]. Especially in educational
settings with background noise in the classroom, important
information can be missed which consequently also affects
other academic skills [10].
Gravel and Wallace (1992) demonstrated in a prospective
study that 4-year-olds with a history of OM needed a signicantly higher signal/noise ratio than children with a negative
OM history [64]. Gravel etal. (2006) have used the PSI test
to test 8-year-old children with a prospectively followed history of OM [25]. The authors found that functional auditory
processes, evaluated by psychoacoustic measures, were not
associated with early conductive hearing loss or experience
with OM [25]. Also, the PSI test was not correlated to earlier
OM, in contrast to the study by Gravel and Wallace (1992)
[25, 64]. A possible explanation for the contrary outcomes of
these two studies might be the age at which these children
were tested [25, 64]. Consequences of OM on speech recognition in noise might still be present at the age of 4 years,
while the auditory system may have recovered by the age of
8 years [25, 64].
Dichotic Digits (DD) Test
The dichotic digits (DD) test analyzes the ability of binaural
integration performed by the corpus callosum [65]. Dichotic
listening means simultaneous stimulation of both ears, but
with different stimulus in each ear [65]. When asking
patients to make a verbal response in a dichotic test, the primary auditory cortex and related areas are recruited [65]. In
a majority of patients, this neural center is located in the left
hemisphere [65]. As such, both left and right ear signals
must reach the left hemisphere in order to be repeated back
verbally. The right ear signal has a direct route to this region,
as it ascends contralaterally to the left hemisphere [65]. The
left ear signal, however, ascends to the right hemisphere and
then must be transmitted across the corpus callosum to
reach the left hemisphere [65]. The corpus callosum is a
heavily myelinated structure, and rapid transmission of
interhemispheric signals is dependent on the integrity of this
myelin [65]. Neuroanatomic studies have shown that children do not have adultlike levels of myelin at birth, and the
normal time course of myelin development is approximately
10–12 years of age [65]. Because right ear performance
typically matures before left ear performance, most children
will show normal interaural asymmetries on dichotic tests
throughout the development process, with better results in
the right ear [65].
The DD test consists of a list of digits, in which four different digits are presented simultaneously, two in each ear
[65]. The participants are instructed to repeat all the numbers
they have heard [65]. The order did not matter [65].
Children with a history of OM did not show as much
improve in left ear performance as normal hearing controls
when attending to the left ear on binaural separation tasks
[65]. Children with a history of OM and subsequent bilateral
tubes placement surgery presented a lower performance than
children with no history of OM in the mean responses for the
DD test of approximately 5% in both ears [33].
This suggests that a persistence of deprivation induced
dichotic decits [65].
Auditory Temporal Processing andPatterning
Tests: Frequency Pattern Test (FPT)
Temporal ordering, or sequencing, refers to the processing of
two or more auditory stimuli in their order of occurrence in
time [66]. Accurate temporal ordering requires that both the
left and the right hemispheres be anatomically and physiologically intact. It also requires integration of information
from both hemispheres across the corpus callosum [66].
Pattern tests are sensitive to hemispheric lesions, as well as
interhemispheric dysfunction [66].
The frequency pattern test (FPT) veries temporal ordering ability [66]. The ability of the brain to decode incoming
speech is dependent on the accurate perception of rapid
acoustic changes [9].
It is composed of three tones that are either high frequency (H—1122Hz) or low frequency (L—880Hz) [66].
Each tone is 150ms in duration and an intertone interval of
200 ms [66]. There are six possible combinations of the
three-tone sequence (LLH, LHL, LHH, HLH, HLL, and
HHL) [66]. The subjects were instructed that they would
hear sets of three consecutive tones that varied in pitch [66].
The task of the subject was to repeat by humming and
verbalizing the tonal pattern with the frequency patterns
(e.g., high-low-high, low-low-high) [66].
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Children with a history of OM and subsequent bilateral
tubes placement surgery presented a lower performance than
children with no history of OM in the mean responses for the
FPT of 9.6% for humming and 30% for naming [33].
Auditory Temporal Processing andPatterning
Tests: Gaps-in-Noise Test (GIN)
The gaps-in-noise (GIN) test measures temporal resolution
ability [66]. The temporal processing is primarily mediated
in the cerebrum [66]. Children aged 7 years demonstrate the
same performance as adults, and no ear asymmetry is
observed [66].
It consists of a series of sixsegments of broadband noise
[66]. Each segment contains zero to three silent intervals or
gaps per noise segment [66]. The gap durations presented 2,
3, 4, 5, 6, 8, 10, 12, 15, and 20ms [66]. The approximate gap
detection threshold is dened as the shortest gap duration
which is correctly identied at least four out of six times
[66]. The participants were instructed to indicate each time
they perceived a gap [66].
Children with a history of OM and subsequent bilateral
tubes placement surgery showed signicantly poorer performance (p<0.001) than children with no history of OM in the
GIN test [33].
The ability of the brain to decode incoming speech is
dependent on the accurate perception of rapid acoustic
changes [9]. The higher the threshold obtained, the worse the
test performance [66].
Note that no time gaps or explicit boundaries segment the
ongoing speech stream into distinct phonemes or syllables
[7]. For example, in the syllables /ba/ and /da/, the only differentiating cues occur within the initial 40-ms formant transition [7].
development [69], selective attention [70], social use of language [71], and literacy [72].
Prospective studies with documented OM episodes and
hearing thresholds are recommended for future research.
Prevention ofCAPD
Delay theStart ofDaycare at Least Until
12Months
The common cold or upper respiratory infection (URI), a
disease caused by a variety of viruses, is a universal illness.
Particularly susceptible to URI are young children, especially those who attend day care centers. More than 60% of
episodes of symptomatic URI among young children were
complicated by acute OM (37%) and/or OME (24%) [67].
The strategy to prevent OM should involve prevention of
viral URI, by delaying school starting age [67].
Insert Tympanostomy Tubes
For children with chronic OME, tube insertion reduces the
prevalence of MEE by 32% in the rst year and improves
average hearing levels by 5–12dB [73–75].
Motherese
The linguistically simplied and acoustically exaggerated
speech that adults universally use when speaking to infants
makes phonetic units more distinct from one another [8].
Talk slightly louder, slightly slower, clearly, and looking at
the child’s eyes [8].
Recruitment Bias
Overall, recruitment bias in retrospective studies cannot be
ruled out completely, and therefore a prospective study
design is preferable. During an episode of upper respiratory
infection (URI), at least a quarter of young children would
have asymptomatic OM, without their parents realizing it
[67]. Furthermore, retrospective studies can generally not
provide information about the hearing threshold during an
OM episode. The possibility of missing information regarding OM episodes in retrospective studies cannot be completely ruled out [67].
Several studies correlate mild peripheral hearing loss in
early childhood with speech-in-noise hearing and various
aspects of cognition [68], including speech and language
Decrease Environment Noise
Children may have mild to moderate hearing loss for several
weeks or months, during and possibly for some time after the
middle ear effusion resolves. These children may experience
considerable difculties in perceiving the speech of teachers
and peers in noisy classrooms, which can lead to increased
listening effort, fatigue, and suboptimal quality of life [76]. It
is important to assess this type of difculty, improve the
management of OME-related CHL, and advise educators on
ways to improve disadvantageous classroom acoustic conditions and optimize the listening and learning environment for
children with OME-related hearing loss [16]. Avoiding permanent background noise should also occur at home, as
hearing sound stimuli clearly with interaction is necessary
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for the child to develop cortical auditory maps responsible
for the perception of auditory-verbal language [8]. If the
television, radio, or stereo system are always on, these maps
will not develop properly [77].
Intervention
Listening Strategies
The simplest way to improve speech perception is to teach
the child to look directly at the speaker and ask the speaker
to direct speech toward the listener and ensure that their face
is uncovered [42, 78].
Modifying theListening Environment
More evidence-based than other strategies [78]. Increasing
the signal (speech) level relative to that of the background
noise will usually result in enhanced perception [42, 78].
This may be achieved by sitting or standing closer to a
speaker (preferential seating) [42, 78]. Reducing the noise
level of a listening environment may also be feasible and
has been shown to be helpful [42, 78]. FM and Bluetooth
wireless listening devices are becoming simpler to use,
more affordable, and smaller [78]. Such systems can
improve learning outcomes, auditory perception, and the
delity with which the auditory brainstem encodes speech
signals [42, 78].
Auditory Training
assume that the benets of those interventions will persist
[78]. After 1 year of music training, the children who actively
engaged with sound through instrumental music training had
faster and more robust neural processing of speech than the
children who stayed in the music appreciation class, observed
in neural responses to a speech sound /d/ [79]. The neurophysiological measures found to be enhanced in the instrumentally trained children have been previously linked to
reading ability, suggesting a gain in neural processes important for literacy stemming from active auditory learning [79].
Aerobic exercise is the activity for which there is the best
evidence of retention and enhancement of cognitive function, underpinning all aspects of hearing and listening [80].
Conclusions
Often, when caring for a child with OM, we do not know if
this is the rst episode, if there was already a MEE before the
onset of symptoms, or if there is hearing loss. Therefore, we
must monitor OM episodes and auditory thresholds.
The baby makes a brain map of all the phonemes of the
native language until the end of the rst year of life, but for
this map to be perfect, it is necessary to ensure perfect hearing. The guidelines for talking while looking into the eyes,
slower, a little louder, with higher intonation, and avoiding
permanent background noise are very important at this age.
When we know that the child has had OM for a long time,
there is no need to wait for the child to present complaints
such as hyperacusis, difculty understanding speech in noisy
environment, or learning difculties. We must recommend
musical training, to strengthen the auditory system, the attention, and the memory.
Mixed results [78]. Current software auditory training provides robust “on-task” learning of the exact skill trained,
but little or no transfer of learning to untrained tasks or
skills [78].
Compensatory Strategies
Not well validated [78]. Training in metacognitive and metalinguistic strategies can also be considered [78]. These strategies include self-regulation and problem-solving, by
identifying individual listening strengths and weaknesses
and listening situations that are more challenging [78].
Long-Term Benet: Music andExercise
To the extent that good listening strategies and acoustic
enhancement may be lifelong changes in behavior, we can
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Balance andOtitis Media
https://t.me/medicina_free
Rafaelda CostaMonsanto, JoséCarlosConventoJúnior,
JoséVicenteBoleliScardiniAlves,
andNormade OliveiraPenido
30
Introduction
The term “otitis media” (OM) refers to a group of inammatory and infectious diseases that affect the middle ear [1].
Many different types of otitis media have been described in
the past, most of which are variations of the three following
groups: (1) otitis media with effusion (OME), characterized
by the presence of chronic middle ear effusion (>3months)
[2]; (2) acute otitis media (AOM), dened as an acute onset
of symptoms of middle ear inammation [3]; and (3) chronic
otitis media (COM), dened as the presence of a chronic
inammation inf the middle ear cleft associated with clinically intractable tissue changes (such as tympanic membrane
perforation, cholesterol granuloma, brosis, and ossicular
erosion) [1].
Otitis media is considered by the World Health
Organization (WHO) a public health problem for several reasons [4]. The lofty burden of disease caused by otitis media
has been recently described by Monasta etal. [5]. In their
study, the authors showed that the different types of otitis
media associate with high worldwide incidence rates, which
reects in the fact that it one the most frequent causes for
antibiotic prescription yearly. Furthermore, otitis media
associates with excessive healthcare costs and can cause a
severe impact on the quality of life of patients. Concerning
the incidence of acute otitis media (AOM), it has been dem-
R. da CostaMonsanto (*)
Department of Otolaryngology, Head and Neck Surgery,
University of Minnesota, Minneapolis, MN, USA
Department of Otolaryngology, Head and Neck Surgery,
Universidade Federal de São Paulo/Escola Paulista de Medicina
(UNIFESP/EPM), São Paulo, Brazil
e-mail: rdacosta@umn.edu
J. C. C. Júnior · J. V. B. S. Alves
Department of Otolaryngology, Banco de Olhos de Sorocaba
Hospital, Sorocaba, Brazil
N. de OliveiraPenido
Department of Otolaryngology, Head and Neck Surgery,
Universidade Federal de São Paulo/Escola Paulista de Medicina
(UNIFESP/EPM), São Paulo, Brazil
onstrated that 80% of children worldwide will have one episode of AOM before the age of 3 years [6], and over 40% will
have six or more recurrences before the age of 7 years [7, 8].
The yearly global incidence of AOM is 10.85%, accounting
for more than 700 million new cases [5]. Otitis media with
effusion (OME) is even more common: it was estimated that
virtually 100% of children will experience at least one episode of transitory effusion in the middle ear—these observations led authors to dene OME as an “occupational hazard
of the childhood” [2]. Finally, the yearly incidence of new
cases of chronic otitis media (COM) is 4.76 per thousand
people, resulting in ~31 million cases. Otitis media may also
culminate in intracranial and extracranial complications in
8–12% of all cases, and these are associated with high mortality rates (5–26%) [9].
The association of otitis media and inner ear decits (such
as hearing loss, tinnitus, and vestibular impairment) has been
demonstrated in the past [10]. Data from the WHO demonstrated that otitis media is the third leading cause of hearing
impairment among all causes, ranking behind genetic hearing loss and presbycusis [4]. The estimated prevalence of
permanent hearing loss (>25dB in the best-hearing ear) was
30.82 per 10,000 cases [5]. Although otitis media leads to
conductive hearing loss in most cases, studies demonstrated
that it can also result in sensorineural hearing loss. The pioneer study in this regard was published by Paparella etal.
[11]—in this translational study, the authors demonstrated
the presence of high-frequency sensorineural hearing loss in
patients with COM. The authors later demonstrated otopathological correlates of these ndings, showing a signicant decrease in number of inner and outer cochlear hair
cells in temporal bone specimens with COM.These studies
were later corroborated by several of experimental and clinical studies.
More recently, it has been hypothesized that otitis media
may also cause vestibular damage in addition to the cochlear/
auditory impairment [12]. Studies dedicated to evaluating
vestibular dysfunction secondary to otitis media are scarce in
the literature. The hypothesis of a direct vestibular damage
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. V. Goycoolea et al. (eds.), Textbook of Otitis Media, https://doi.org/10.1007/978-3-031-40949-3_30
267
268
ab
https://t.me/medicina_free
R. da CostaMonsanto et al.
caused by otitis media in the absence of perilymphatic stula
has been subject of an intense debate [13]. Although no study
has yet peremptorily demonstrated that AOM and OME
cause vestibular impairment, recent evidence showed that
COM associates with a high prevalence of vestibular symptoms (40–60%) and abnormalities in several vestibular function tests (including caloric tests and cervical vestibular
myogenic potentials). A meta-analysis [10] revealed that
most of these studies have several potential biases and methodological problems that undermine the validity of their
data. However, recent histological and clinical evidence have
shed additional light in the subject, revealing that otitis media
(more specically COM) may result in direct vestibular
impairment.
In this chapter, we explore the clinical and experimental
evidence available in the literature showing the association
between otitis media and vestibular impairment.
Pathophysiology
The rst description of an inner ear sequelae of otitis media
was published by Adam Politzer, in 1894 [14]. In this study,
the author investigated the hearing of patients with chronic
OME—although there was no objective way to test the hearing at the time, it was observed that these patients had worse
hearing than controls. The hypothesis was later explored in
the decade of 1920: Mackenzie [15], Turner and Fraser [16],
and Druss [17] described potential pathways from which otitis media could progress to the inner ear, including through
the oval and round windows, or through and hematogenic
route.
It was only in the 1960s and 1970s that these theories
were evaluated in an experimental setting: rst, Arslan [18],
in a study evaluating a potential osmotic mechanism leading
to Meniere’s disease, observed an outow of perilymph
through the round window membrane after placement of
NaCl over this structure. This observation was later explored
in a series of studies by Schachern and Goycoolea [19–22]:
these studies revealed that the round window membrane is
permeable to albumin, inammatory mediators and genes,
bacterial toxins, and even whole bacteria. The translational
study published by Paparella et al. [11] observed that the
most critical inner ear lesions in patients with COM occurred
in the cochlear hair cells in the basal turn of the cochlea
(Fig.30.1). The lesion site in the inner ear in these patients
with otitis media, together with the observation that the
round window membrane is semi-permeable, has corroborated that the inner ear is susceptible to lesion in cases of
otitis media, in a process called by Paparella as “middle ear/
inner ear interactive disease” [13].
Recently, the group at the University of Pittsburgh evaluated
the inner ear environment in otitis media models [23–26]. In
these studies, it was shown that both acute and chronic otitis
media impact on the expression of hundreds of middle and
inner ear genes. It was demonstrated that otitis media associated with an upregulation in the concentration of proinammatory cytokines and mediators (such as tumor necrosis
factor TNF-alpha and interleukins) and downregulation of antiinammatory mediators in the middle and inner ears. Moreover,
the elevation of these inammatory mediators in the inner ear
seemed to occur by two distinct mechanisms: (1) direct passage through the round window membrane; and (2) through an
active immunological mechanism mediated by the spiral ligament, which amplify the inammatory response in the inner ear
following otitis media. Although such amplication would—
hypothetically—aim to suppress an inammatory issue in the
inner ear, it could increase the risks of cochlear damage.
Fig. 30.1 Two representative human temporal bone sections, one from
a healthy donor (a) and other from a donor with chronic otitis media (b)
seen in optic microscopy (hematoxylin & eosin). In (a), the organ of
Corti is normal, with normal number of inner (black arrow) and outer
(*) hair cells. In (b), the inner hair cell (black arrow) is present, but
there is a complete loss of outer hair cells (white arrow)
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