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5 Temporal Bone Radiology
95
diffuse and continuous cochlear involvement [56, 57]. There is a correlation between
grading and treatment success (Fig.5.31).
Fenestral otospongiosis usually begins in the ssure ante fenestra. Other anatomical sites of involvement include the cochlear promontory, the round window
niche, and the facial nerve canal [57]. Rarely are the stapes footplate and annular
ligament involved when the stapediovestibular joint becomes xed, resulting in conductive hearing loss. In early disease, the area of the affected demineralized bone is
limited to the ssure ante fenestra; in advanced disease, the width and anatomical
distribution of the demineralized bone areas increase. However, even in early disease, sclerotic lesions with a hyperdense, patchy appearance in the cochlea should
be carefully evaluated. Demineralized bone may cause a narrowing of the oval window, in which case the success of stapes surgery is reduced due to xed stapes [56].
In inactive advanced disease, the affected areas may have a density similar to the
rest of the otic capsule. In this case, indirect signs such as irregularity and scalloping
of the otic capsule support the diagnosis. Inactive advanced disease involving the
oval window and stapes footplate area is easier to differentiate. Contrast-enhanced
MRI is useful in the diagnosis of active disease, otherwise MRI is not part of the
routine imaging protocol [52].
Cochlear otosclerosis is less common and is almost always associated with
fenestral disease. There is a relationship between the location of the sensorineural
hearing loss and the location of the cochlea, and between the severity of the disease
and the severity of the hearing loss [58]. Because demineralization has the appearance of a ring surrounding the cochlea, the cochlea on CT takes on the appearance
of a “double ring;” this appearance is also known as the “fourth ring of Valvassori.”
As the disease progresses to the sclerotic phase, the spongiotic ndings disappear
and the otic capsule may be completely normal due to newly developing sclerosis.
Similar ndings may be seen around the affected vestibular SCCs and in the IAC
(Fig.5.32) [59]. The disadvantage of CT imaging is partial volume averaging in the
SCCs and the lateral labyrinth wall. MRI involvement is intermediate in signal
intensity on both T1A and T2A images in the spongiotic phase, and demineralized
areas on CT also show enhancement on contrast-enhanced MRI [59]. In addition,
abc
Fig. 5.31 Examples of otosclerosis at different stages in three different patients. (a) An axial CT
image showing a small lucent lesion in the ssula ante fenestram (arrow). This is an early stage
disease, and the lesion does not extend to the cochlea: grade 1 disease. (b) In a slightly more
advanced stage, it is observed that the lesion (arrow) is in contact with the middle turn of the
cochlea: grade 2a disease. (c) The lesion (arrow) completely surrounds the cochlea and extends to
the retrofenestral level (black arrow): grade 3 disease
96
ab
cd
M. B. Eser et al.
Fig. 5.32 Labyrinthitis ossicans. (a and b) A decrease in cochlear diameter, irregularity of con-
tours, and an increase in density are all indicated by arrows on axial CT images. (c and d) In
another patient, in addition to similar ndings in the cochlea (c), a signicant decrease in the
semicircular canal calibrations is observed; even the semicircular canals are so dense that they
cannot be visualized (d)
MRI is a more reliable method for visualizing the membranous labyrinth and areas
where partial volume averaging may occur on CT.
Osteogenesis imperfecta has similar radiologic ndings to fenestral otospongiosis and is therefore included in the radiologic differential diagnosis. Although some
rheumatologic diseases, Paget’s disease, and otosyphilis mimic radiologic ndings,
5 Temporal Bone Radiology
97
the differential diagnosis can be made with the presence of other systematic ndings
[59, 60].
5.6.3 Third Window Lesions
In the physiology of hearing, the sound signal is amplied in the air between the TM
and the oval window. Wide, short, and low-impedance channels responsible for
sound transmission are connected to the oval and round windows. Long, and highimpedance channels not involved in sound transmission are also included in the
system as the normal third window; normal-sized VA, normal-sized cochlear duct,
and neurovascular foramina [61, 62].
The third window phenomenon has been described relatively recently [63]. The
amplied signal throughout the ME is attenuated in pathologic third window, resulting in an air–bone gap on the audiogram at low frequencies. The most common
cause of pathologic third window is superior semicircular canal dehiscence (SSCD).
Other common causes include an enlarged VA, a stapes gusher, carotid-cochlear
dehiscence, and otosclerosis [61].
In SSCD, a bony defect at the top of the superior SCC causes communication
between the canal and the middle cranial fossa. While it is common for the canal to
be thin (<0.1mm) and defective (0.5–2%), only 13.6% of these individuals show
symptoms. A thin-slice (0.5mm or less) bone algorithm is essential for CT imaging.
Examinations perpendicular and parallel to the SCC are believed to increase lesion
detection, but there are insufcient data to support their routine use [61, 64].
The VA is a physiologic canal located between the bony vestibule and the middle
cranial fossa. The normal canal is short and long; when the canal is wide, it functions as a pathologic third window. According to the Cincinnati criteria, the VA is
considered wide if it is >2mm at the operculum and/or 1mm at the midpoint in the
axial plane (Fig.5.33). The 45° oblique plane (Pöschl) allows the entire VA to be
viewed, and measurements in this plane have been shown to be more reliable [64].
ab
Fig. 5.33 An enlarged vestibular aqueduct. (a) An axial thin-section CT image showing a right-
sided enlarged vestibular aqueduct. (b) An axial thin-section MR image showing a left-sided
enlarged vestibular aqueduct in a different patient
98
M. B. Eser et al.
5.6.4 Conclusion
HRCT has a pivotal role in the diagnosis of both otosclerosis and pathologic third
window. In otospongiosis, contrast-enhanced MRI is helpful in the diagnosis.
Although there are typical ndings in the diagnosis of third window phenomena,
image quality is important in diagnosing the lesions.
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101
Part II
Hearing and Management of Hearing Loss
Sound andAcoustics: AnOverview
NeslihanSarı, İbrahimÇukurova, CemalCingi,
andNurayBayar Muluk
6.1 Introduction
The middle ear is primarily responsible for preventing the loss of acoustic energy
that would result from direct contact between the low-impedance air in the ear canal
and the high-impedance cochlear uid [1]. Much of the acoustic energy that would
otherwise travel through a medium with low impedance (like air) is reected off the
liquid and never reaches its destination (like water). Without the middle ear, the
cochlea would only receive 0.1% of the acoustic wave energy that travels through
the air, while 99.9% would be reected [2, 3].
To compensate for the difference in impedance between water and air, a cochlear
amplication system is required for physiological hearing. A well-functioning middle and external ear with a healthy tympanic membrane, an ossicular chain, and an
adequately ventilated tympanic cavity are necessary for accurate impedance matching. A person’s clinical inability to hear sounds correctly, known as conductive hearing loss, is the outcome of any malfunction or illness of these components [2].
6
N. Sarı
Faculty of Medicine, Department of Otorhinolaryngology, Mardin Artuklu University,
Mardin, Turkey
İ. Çukurova
Department of Otorhinolaryngology, University of Health Sciences, Tepecik Training and
Research Hospital, Izmir, Turkey
C. Cingi
Faculty of Medicine, Department of Otorhinolaryngology, Eskisehir Osmangazi University,
Eskisehir, Turkey
N. Bayar Muluk (*)
Faculty of Medicine, Department of Otorhinolaryngology, Kırıkkale University,
Kırıkkale, Turkey
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
M. T. Kalcioglu et al. (eds.), Otology Updates, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-76173-7_6
105
106
N. Sarı et al.
6.2 Hearing andAcoustic Noise
To put it simply, the ear functions like a wideband receiver. It has an extensive frequency range (of about 103Hz) and can detect sound intensities across a vast range
(~1012 Hz); for human hearing, it is 20Hz–20kHz. On the other hand, the human
eye is only sensitive to light with a twofold frequency range [4].
There are three parts to our auditory system: the cochlea, which is mechanical
and stimulates hairs there; the auditory nerves, which are sensors that generate
action potentials; and the auditory cortex, a part of the brain that decodes these signals [4].
The human ear has a peak sensitivity between 2 and 5kHz, although this sensitivity does not extend across the audible spectrum [5]. Sensitivity varies with age as
well. Most people’s highest audible frequency drops with age, while the decibel
level required to hear it rises. Exposure to loud noises over long periods accelerates
the natural decline of hearing [4].
The mental reaction to the physical intensity of a sound is its loudness. The relationship between loudness and the logarithm of intensity is almost linear to narrow
the enormous dynamic range that the human ear perceives. Resonance also has a
signicant impact on loudness. Because of this logarithmic relationship, the decibel
(dB) scale is used to measure the strength of sound. This decibel scale can be
adjusted to weight values for the ear’s sensitivity since there is a frequency dependence on hearing. Therefore, dB(A) and dB(C) are standard units of measurement [4].
In addition to the environment around the sound source and detector, the detector
itself (and its weighting) will determine the measured sound levels. Since good
sound pressure level (SPL) considers environmental factors, it is a standard metric
for reporting sound levels [4].
A standard denition of audible noise is “unwanted” sound. Qualities like mode,
duration, intensity, and frequency range dene it. When we talk about the way of
noise, we are referring to how it is made [4].
Hearing loss can occur after prolonged exposure to quite loud sounds. A transient shift in the hearing threshold (transient threshold shift [TTS]) is a possible
symptom of short injury to the auditory nerve. After being exposed to acoustic
noise, the average hearing recovery rate is fast and exponential. Of the patients
evaluated without earplugs, 43% reported having TTSs, according to an early study
by Brummett et al. [6]. Recovery time increases with increasing noise levels. In
extreme cases, permanent threshold shifts (PTSs) can develop, leading to irreversible hearing loss within a narrow frequency range [4–6].
The concept of “hidden hearing loss” (HHL) has gained more and more attention
and worry in the last several years. As indicated earlier, typical audiological testing
can identify supercial damage to the outer hair cells, which frequently causes variations in the threshold, either temporarily or permanently. However, regular audiometric testing can miss signs of damage to the auditory nerve and inner hair cells,
which can happen due to exposure to acoustic noise [7, 8]. Although hearing