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- •Preface
- •Contents
- •1.3.4 The Eustachian Tube
- •1.3.5 Muscles
- •1.3.6 Innervation
- •1.3.7 Vascular Supply
- •1.4 The Inner Ear (Labyrinthine Cavity)
- •1.4.1 The Vestibule
- •1.4.2 Semicircular Canals
- •1.4.4 The Cochlea
- •1.4.5 Innervation
- •1.1 Introduction
- •1.2 The External Ear
- •1.2.1 The Auricle
- •1.2.3 The Eternal Auditory Canal/External Acoustic Meatus
- •1.3 The Middle Ear (Tympanic Cavity)
- •1.3.1 The Tympanic Membrane
- •1.3.3 Ossicles
- •1.4.6 Cochlea Nerve Anatomy
- •1.4.7 Vestibular Nerves
- •1.4.8 The Vestibulocochlear Nerve
- •1.5 The Central Hearing System
- •1.5.3 Auditory Input
- •1.5.4 The Auditory Nerve’s Descending Routes
- •References
- •2: Outer–Middle–Inner Ear Embryology
- •2.1 Introduction
- •2.2 Embryology
- •2.3.1 First Week
- •2.3.3 Third Week
- •2.3.4 Fourth Week
- •2.3.5 Sixth Week
- •References
- •3.1 Introduction
- •3.3 The Outer Ear
- •3.3.1 Anatomy
- •3.3.3 Localization
- •3.4 The Middle Ear
- •3.4.3 Middle Ear Muscles
- •3.4.4 The Eustachian Tube
- •3.4.5 Impedance Matching
- •3.5 The Inner Ear
- •3.5.1.1 Lateral Wall
- •3.5.1.2 Reissner’s Membrane
- •3.5.1.3 The Basilar Membrane
- •3.5.2.1 Hair Cells
- •Inner Hair Cells
- •Outer Hair Cells
- •3.5.3 The Tectorial Membrane
- •3.5.4 The Osseous Spiral Lamina
- •3.5.5 Cochlear Mechanics
- •3.5.5.1 Passive Mechanics
- •3.5.5.2 Active Mechanics
- •3.6.1 Auditory Nerve Fibers
- •3.6.2 The Subcortical Auditory Nuclei
- •3.6.2.1 The Cochlear Nucleus
- •3.6.2.2 The Superior Olivary Complex
- •3.6.2.3 The Lateral Lemniscus
- •3.6.2.4 Inferior Colliculus
- •3.6.2.5 The Medial Geniculate Body
- •3.6.3 The Auditory Cortex
- •3.7 Conclusion
- •References
- •4.1 Introduction
- •4.2 Eustachian Tube Anatomy
- •4.4 Eustachian Tube Dysfunction
- •References
- •5: Temporal Bone Radiology
- •5.1.1 Introduction
- •5.1.2 Computed Tomography (CT)
- •5.1.3 Temporal Bone CT Angiography
- •5.1.4 Magnetic Resonance Imaging (MRI)
- •5.1.5 Diffusion-Weighted Imaging (DWI)
- •5.1.6 Conclusion
- •5.2.1 Introduction
- •5.2.2.1 The External Auditory Canal (EAC)
- •5.2.3 Temporal Bone Fractures
- •5.2.4 Conclusion
- •5.3.1 Introduction
- •5.3.2 Necrotizing Otitis Externa
- •5.3.3 Middle Ear
- •5.3.3.2 Chronic Otitis Media
- •5.3.3.3 Cholesteatomas
- •5.3.3.4 Cholesterol Granulomas
- •5.3.4 Inner Ear
- •5.3.4.1 Labyrinthitis
- •5.3.4.2 Petrous Apicitis
- •5.3.5 Conclusion
- •5.4.1 Introduction
- •5.4.2.1 Cerebellopontine Angle Tumors
- •Vestibular Schwannomas
- •Arachnoid Cysts
- •Meningiomas
- •5.5.2 External Auditory Canal Aplasia
- •5.5.4 Inner Ear Malformations
- •5.5.4.1 Complete Labyrinthine Aplasia/Michel Anomaly
- •5.5.4.2 Rudimentary Otocysts
- •5.5.4.3 Common Cavity Malformation
- •5.5.4.4 Incomplete Partition (IP) Type I
- •5.5.4.5 Incomplete Partition Type II/Mondini Malformation
- •5.5.4.6 Incomplete Partition Type III
- •5.5.4.7 Cochlear Anomalies
- •5.5.4.8 Semicircular Canal Anomalies
- •5.5.6 Conclusion
- •5.6.1 Introduction
- •5.6.2 Otospongiosis/Otosclerosis
- •Epidermoids
- •5.4.2.2 The Middle Ear
- •5.4.2.4 Petrous Bone
- •5.4.2.5 Metastatic Tumors
- •5.4.3 Conclusion
- •5.5.1 Introduction
- •5.6.3 Third Window Lesions
- •5.6.4 Conclusion
- •References
- •6.1 Introduction
- •6.3.1 What Is Sound?
- •6.3.2 Sound Intensity
- •6.4 Psychoacoustics
- •6.4.1 Signal Detection Theory
- •References
- •7.1 Introduction
- •7.1.1 What Is Sound?
- •7.2 Fundamental Acoustic Concepts
- •7.2.3 Period
- •7.2.4 Frequency
- •7.2.5 Wavelength
- •7.3 Psychoacoustics
- •7.3.1 Loudness
- •7.3.2 Auditory Masking
- •7.3.2.1 Simultaneous Masking
- •7.3.2.2 Temporal Masking
- •7.4.2 Spatial Hearing
- •References
- •8.1 Introduction
- •8.2 Case History
- •8.3 The Audiology Test Room
- •8.4.1 Pure-Tone Audiometry
- •8.4.1.1 Masking
- •8.4.2 Speech Audiometry
- •8.4.3 Pediatric Assessment
- •8.5.1 Acoustic Immittance Audiometry
- •8.5.1.1 Tympanometry
- •Tympanogram Interpretation
- •8.5.1.2 Multifrequency Tympanometry
- •8.5.1.3 Wideband Tympanometry
- •8.5.1.4 Acoustic Reflex Test
- •8.5.1.5 The Reflex Decay Test
- •8.5.1.6 Eustachian Tube Evaluation
- •8.5.2 Otoacoustic Emissions
- •8.5.2.2 Performing Otoacoustic Emission Tests
- •8.5.3 Auditory Evoked Potentials
- •8.5.3.2 Auditory Evoked Brainstem Response
- •Stimulus Types
- •Stimulus Polarity
- •Stimulus Presentation Rate
- •Stimulus Intensity
- •Analysis Time (Recording Epoch)
- •Filters
- •Artifact Rejection Level
- •Electrodes
- •8.5.3.3 Auditory Steady-State Responses
- •8.5.3.4 Electrocochleography
- •Electrocochleography Analysis
- •8.5.3.5 Cortical Auditory Evoked Potentials
- •8.5.3.6 Event-Related Auditory Potentials
- •P300
- •Mismatch Negativity
- •Acoustic Change Complex
- •8.6 Conclusion
- •References
- •9.1 Introduction
- •9.2.3 Conductive Hearing Loss
- •9.2.4 Sensorineural Hearing Loss
- •9.2.4.1 Internal Acoustic Canal Tumors
- •9.2.4.2 Auditory Neuropathy Spectrum Disorder
- •9.2.4.3 Third Window Syndrome
- •9.2.4.4 Dead Region
- •9.2.5 Mixed Hearing Loss
- •9.3 Hearing Loss Configuration
- •9.3.3 Unilateral or Bilateral Hearing Loss
- •9.3.4 Symmetric or Asymmetric Hearing Loss
- •9.3.5 Fluctuating or Stable Hearing Loss
- •9.4 Diagnostic Tests
- •9.4.1 Pure Tone Threshold Testing
- •9.4.2 Speech Recognition Tests
- •9.4.3 Tympanometric Tests
- •9.4.4 Stapedial Reflex
- •9.4.5 Otoacoustic Emission Test
- •9.4.6 Auditory Brainstem Responses
- •9.6 Reporting Audiological Findings
- •9.7 Conclusion
- •References
- •10.1 Introduction
- •10.2.1 Anamnesis
- •10.2.2 Hearing Loss
- •10.2.3 Ear Pain (Otalgia)
- •10.2.4 Ear Discharge (Otorrhea)
- •10.2.5 Itchy Ear
- •10.2.8 Physical Examination
- •10.2.8.1 Inspection
- •10.2.8.2 Palpation
- •10.2.8.3 Otoscopy
- •10.2.12 Hearing Examination
- •10.2.13 Hearing Assessment
- •10.2.13.1 Whisper Test
- •10.2.13.2 Tuning Fork Tests
- •Rinne Test
- •Weber Test
- •Schwabach Test
- •Gelle Test
- •10.3 Conclusion
- •References
- •11.1 Introduction
- •11.2.1 Microphone
- •11.2.2 Amplifier
- •11.2.3 Receiver
- •11.2.4 Batteries
- •11.2.5 Earmolds/Domes
- •11.4 Hearing Aid Types
- •11.5.1 Directional Microphone Technologies
- •11.5.2 Digital Noise Reduction
- •11.5.3 Frequency Lowering
- •11.5.4 Feedback Canceller
- •11.5.5 Bluetooth
- •11.6 Other Hearing Aid Technologies
- •11.7 Pediatric Hearing Aid Application
- •11.7.3.7 Hearing Aid Fitting
- •Prescription Formula Preference
- •Objective Verification Tools
- •Subjective Verification Tools
- •Fine-Tuning
- •11.8 Adult Hearing Aid Application
- •11.8.1.1 Medical Evaluation
- •11.8.1.2 Audiological Evaluation
- •11.8.1.3 Physical Evaluation
- •11.8.1.4 Psychological Evaluation
- •11.8.2 Hearing Aid Application Process
- •11.8.2.1 Anamnesis
- •11.8.2.6 Hearing Aid Fitting
- •Fine-Tuning
- •11.9 Conclusion
- •11.10 Case Studies
- •11.10.1 Case 1
- •11.10.2 Case 2
- •11.10.3 Case 3
- •11.10.4 Case 4
- •References
- •12.1 Introduction
- •12.3.1 Pathophysiology
- •12.3.2 Management
- •12.3.3 Etiology
- •12.3.4 Epidemiology
- •12.3.5 Assessing
- •12.3.6 Treatment
- •References
- •13: Otoplasty
- •13.1 Introduction
- •13.2 General Information
- •13.2.1 Auricular Anthropometry
- •13.3 History
- •13.8.1 Conservative Treatment
- •13.8.2 Surgical Treatment
- •13.11 Patient Follow-Up
- •13.12 Case Examples
- •13.13 Complications
- •13.13.1 Early Complications
- •13.13.2 Late Complications
- •13.13.3.1 Telephone Ear Deformity
- •13.13.3.2 Reverse Telephone Ear Deformity
- •13.13.3.5 Antihelical Malposition
- •13.13.3.6 Tragal Prominence
- •13.13.3.7 Auricular Lines
- •13.14 Revision Otoplasty
- •References
- •14: External Ear Tract Diseases
- •14.1 Introduction
- •14.2.1 Atopic Dermatitis
- •14.2.2 Allergic Contact Dermatitis
- •14.2.3 Photoallergic Dermatitis
- •14.2.4 Psoriasis
- •14.2.5 Relapsing Polychondritis
- •14.2.6 Gout
- •14.3 Traumatic Disorders
- •14.3.1 Irritant Contact Dermatitis
- •14.3.2 Phototoxic Dermatitis
- •14.3.3 Phototrauma
- •14.4 Infectious Diseases
- •14.4.1 Otitis Externa
- •14.4.1.1 Background
- •14.4.1.2 Anatomy
- •14.4.1.3 Classification
- •14.4.1.5 Diagnosis
- •14.4.1.6 Management
- •References
- •15: Auricula Tumors
- •15.1 Introduction
- •15.2 Benign Tumors
- •15.2.1 Chondrodermatitis Nodularis Chronica Helicis
- •15.2.2 Cystic Chondromalacia
- •15.2.3 Ceruminous Gland Adenoma
- •15.3 Malign Tumors
- •15.3.1 Basal Cell Carcinoma (BCC)
- •15.3.2 Squamous Cell Carcinoma
- •15.3.3 Ceruminous Gland Adenocarcinoma
- •15.4 Conclusion
- •References
- •16: Acute Suppurative Otitis Media
- •16.1 Introduction
- •16.2 Pathophysiology
- •16.3 Etiology
- •16.3.1 Host Factors
- •16.3.1.1 Immune System
- •16.3.1.2 Hereditary Susceptibility
- •16.3.1.3 Mucins
- •16.3.1.4 Anatomic Abnormalities
- •16.3.1.5 Physiologic Dysfunction
- •16.3.2 Infectious Factors
- •16.3.2.1 Bacterial Pathogens
- •16.3.2.2 Viral Pathogens
- •16.3.3 Environmental Factors
- •16.3.3.1 Infant Feeding Methods
- •16.4 Classification
- •16.6 Diagnosis
- •16.7 Treatment
- •16.7.1 Antibiotic Therapy Versus Observation
- •16.7.2 Initial Antibiotic Therapy
- •16.7.3 Supplemental Programs
- •References
- •17.1 Introduction
- •17.2 Definition
- •17.4 Pathophysiology
- •17.5 Diagnosis
- •17.5.1 Clinical Evaluation
- •17.6 Treatment
- •17.6.1 Medical Treatment
- •17.6.2 Surgical Treatment
- •17.7 Conclusion
- •References
- •18: Chronic Suppurative Otitis Media
- •18.1 Introduction
- •18.2 Epidemiology
- •18.3 Pathophysiology
- •18.4 Microbiology
- •18.5 Histopathology
- •18.6 Clinical Manifestations
- •18.6.1 Tubotympanic Type
- •18.6.2 Atticoantral Type
- •18.7 Diagnosis
- •18.7.1 Anamnesis
- •18.7.2 Otoscopic Examination
- •18.7.3 Audiological Evaluation
- •18.7.4 Imaging
- •18.8 Treatment
- •18.8.1 Medical Treatment
- •18.8.2 Surgical Treatment
- •18.9 Complications
- •18.10 Future Directions
- •18.11 Conclusion
- •References
- •19: Cholesteatoma
- •19.1 Introduction
- •19.2 Definition
- •19.3 Epidemiology
- •19.4 Histopathology
- •19.7 Cholesteatoma Types
- •19.7.1 Congenital Cholesteatoma
- •19.7.2 Acquired Cholesteatoma
- •19.7.2.2 Epithelial Migration Theory
- •19.7.2.3 Basal Cell Hyperplasia Theory
- •Tos Staging
- •Sade Staging
- •19.7.3 Unclassified Cholesteatomas
- •19.7.4 Petrous Bone Cholesteatomas
- •19.8 Practical Classification
- •19.8.1 Attic Cholesteatomas
- •19.8.2 Sinus Cholesteatomas
- •19.8.3 Pars Tensa Cholesteatomas
- •19.9 Clinical Presentations
- •19.9.1 Cholesteatoma Microbiology
- •19.10 Diagnosis
- •19.10.2 Computed Tomography
- •19.10.3 Magnetic Resonance Imaging
- •19.10.4 Audiometric Evaluation
- •19.11.1 Closed Techniques
- •19.11.2 Open Techniques
- •19.12 Conclusion
- •References
- •20.1 Introduction
- •20.2 Physiology
- •20.2.4 Tympanic Isthmus
- •20.4 Pathophysiology
- •20.5 Clinical Picture
- •20.6 Management
- •20.6.1 Surgical Management
- •20.6.1.2 Tympanoplasty
- •20.6.1.3 Mastoid Surgery
- •20.7 Adhesive Otitis Media
- •20.7.1 Pathogenesis
- •20.7.2 Clinical Findings
- •20.7.3 Imaging
- •20.7.4 Treatment
- •20.8 Conclusion
- •References
- •21.1 Introduction
- •21.2 Intratemporal Complications
- •21.2.1 Acute Mastoiditis
- •21.2.2 Facial Nerve Paralysis
- •21.2.3 Labyrinthitis
- •21.2.4 Labyrinthine Fistula
- •21.2.5 Petrositis
- •21.3 Intracranial Complications
- •21.3.1 Meningitis
- •21.3.2 Lateral Sinus Thrombosis
- •21.3.3 Brain Abscess
- •21.3.4 Otitic Hydrocephalus
- •21.3.5 Epidural Abscess
- •21.3.6 Subdural Empyema
- •21.4 Conclusion
- •References
- •22: Basic Otological Surgical Techniques
- •22.1 Introduction
- •22.3 Atticotomy
- •22.4 Mastoidectomy
- •22.4.1 Simple (Cortical) Mastoidectomy
- •22.4.2 Canal Wall-Up Mastoidectomy
- •22.4.3 Canal Wall-Down Mastoidectomy
- •22.4.4 Retrograde Mastoidectomy
- •22.4.5 Modified Radical Mastoidectomy
- •22.4.6 Radical Mastoidectomy
- •22.4.7 Mastoid Obliteration
- •22.5 Petrosectomy
- •22.6 Conclusion
- •References
- •23: Tympanoplasty
- •23.1 Introduction
- •23.2.1 Chronic Otitis Media
- •23.2.2 Traumatic Perforations
- •23.5 Tympanoplasty Types
- •23.7 Graft Materials
- •23.8 Graft Techniques
- •23.8.1 The Perichondrium/Cartilage Island Graft
- •23.8.2 The Palisade Graft
- •23.8.3 The Temporalis Fascia Graft
- •23.9 Surgical Approaches
- •23.9.1 Microscopic Approach
- •23.9.2 Endoscopic Approach
- •23.10.1 Transmeatal Incisions
- •23.10.1.1 The Rosen Incision
- •23.10.1.3 Anterior Tympanomeatal Flap
- •23.10.2 Endaural Incision
- •23.10.3 Postauricular Incision
- •23.11 Pediatric Tympanoplasty
- •23.12 Prognostic Factors
- •23.14 Conclusion
- •References
- •24: Ossiculoplasty
- •24.1 Introduction
- •24.4 Indications/Contraindications
- •24.5 Reconstruction Materials
- •24.7 Surgical Preparation
- •24.8 Surgical Technique
- •24.9 Ossiculoplasty Results
- •24.10 Complications
- •24.11 Postoperative Care
- •24.12 Follow-Up
- •24.13 Conclusion
- •References
- •25: Tympanomastoidectomy
- •25.1 Introduction
- •25.2 Surgical Anatomy
- •25.4 Indications
- •25.5 Technique
- •25.5.1 Patient’s Preparation
- •25.5.3 Simple Mastoidectomy
- •25.5.4 Posterior Tympanostomy or Facial Recess Approach
- •25.5.5 Epitympanectomy
- •25.5.6 Endolymphatic Sac Procedures
- •25.5.8 Atticotomy-Atticoantrotomy

3 Physiology ofthePeripheral andCentral Hearing System
53
sounds presented from the ipsilateral side of the head are dominant in the lateral
efferent and send excitatory projections to the contralateral inferior colliculus. On
the contrary, MOC sends excitatory projections from the contralateral side of the
head to the inferior colliculus on the same side. These results show that the contralateral side of the brain dominates the sound source to the inferior colliculus [9, 18].
3.6.2.4 Inferior Colliculus
This is the main receiving station of the pathway originating from the auditory
nuclei in the brainstem. It is the primary place where sound identication and localization information is collected. It is organized tonotopically, and the frequency
mapping of bers with the same characteristic frequency, but from different nuclei
in the same tonotopic order, is managed here in the auditory pathway. Although the
medial geniculate is the obligatory transition zone for all auditory inputs entering
the body, the projection of some neurons may bypass the inferior colliculus.
Inhibition of inferior colliculus cells ensures sustained responses to complex signals
over a wide range of stimulus intensities. This inhibition reduces transmembrane
resistance, increases temporal accuracy in rapid temporal uctuations, and may provide frequency selectivity [9, 61–64].
3.6.2.5 The Medial Geniculate Body
Specically, this is a thalamic relay within the auditory system. It receives afferent
input from the inferior colliculus and transmits it to the cerebral cortex. It has very
dense reciprocal connections with the cortex. It is divided into three parts: ventral,
dorsal, and medial. It projects to the center of the auditory cortex. The ventral part
sharpens frequency resolution and is a specialized region for advanced analysis in
hearing. It has very dense reciprocal connections with the auditory cortex, making
it a functional unit of the cortex. The dorsal and medial parts receive a lot of input
(except for the auditory system), but it has the characteristic of being a seldom used
pathway that projects widely to the primary auditory cortex [9, 11, 13].
Apart from the auditory response, the somatosensory has multimodal interactions in visual stimuli, which allows us to have responses that can change as a result
of learning. While the dorsal part is particularly involved in novel stimuli, the ventral part, due to its close relationship with the amygdala, allows responses to dangerous stimuli that evoke fear [9, 18].
3.6.3 The Auditory Cortex
Located bilaterally in the superior temporal gyrus of the right and left temporal
lobes, extending to the lateral sulcus and transverse temporal gyrus (Heschl’s gyrus),
the auditory cortex is the region where the basic and highest-level processes related
to hearing take place. The tonotopically organized auditory cortex, which includes
Brodmann areas 41 and 42, receives direct input from the contralateral ear via the
medial geniculate body and enables recognition of basic elements such as pitch and
loudness [9, 11, 13]. It is responsible for the analysis of heard sounds and their

54
M. Baran et al.
adaptation according to the characteristics of the incoming auditory stimuli. When
recognizing speech features, neurons in the cerebral cortex use ipsilateral and contralateral spectral information [11].
The primary auditory cortex (PAC) or core area, Brodmann area 41, is located in
the posteromedial part of Heschl’s gyrus. The PAC is surrounded by areas embedded in the sulci called the belt and parabelt. The auditory stimulus is rst analyzed
in this central region and then directed to the belt and parabelt areas. The PAC and
some belt areas are tonotopically organized. The area surrounding the PAC is called
the secondary auditory cortex or the auditory association area. While unilateral
destruction of the PAC results in mild hearing loss in the contralateral ear, destruction of both cortices greatly reduces hearing sensitivity. Destruction of the secondary auditory cortex (belt and parabelt areas) results in an inability to interpret the
meaning of sounds [9, 11, 13, 18].
3.7 Conclusion
In summary, the perception of sound stimuli involves a nely tuned sequence of
events, beginning with the capture and conduction of sound waves by the outer and
middle ear, followed by the conversion of these waves into electrical signals by the
inner ear. This process underscores the complexity of the auditory system and the
importance of each component in the overall function of hearing. Disorders at any
stage can lead to hearing loss, underscoring the need for a thorough understanding
of the system for effective diagnosis and treatment.
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57

Eustachian Tube: AnOverview
ZeynelÖztürk, NurayBayar Muluk,
andGabrielaKopacheva-Barsova
4.1 Introduction
As a complicated anatomical structure, the Eustachian tube (ET) (also called the
pharyngotympanic or auditory tube) plays a critical role in maintaining homeostasis
in the middle ear. It begins in the middle ear and continues medially before opening
just behind the inferior turbinate; the bony lateral third passes through the squamous
and petrous parts of the temporal bone. Two-thirds of the medial brocartilage
forms the torus tubarius, a mucosal elevation that opens into the nasopharynx. When
one yawns, sneezes, swallows, or performs the Valsalva maneuver—all of which
apply positive pressure—the levator and tensor veli palatine muscles contract, opening the tube [1].
When the ET is unable to perform any of the above three functions, the condition
is called Eustachian tube dysfunction (ETD). It can be classied as acute if it occurs
within 3months or as chronic if it occurs after that time. Fullness or “popping” in
the ear, decreased hearing, tinnitus, autophony, otalgia, and imbalance are symptoms of ETD, which affect 1% of the population. Dilatative ETD, patulous ETD,
and barotrauma-induced ETD are the three main types [2–4].
4
Gabriela Kopacheva-Barsova was deceased at the time of publication.
Z. Öztürk
Faculty of Medicine, Department of Otorhinolaryngology, Nişantaşı University,
Istanbul, Turkey
Baypark Hospital, Istanbul, Turkey
N. Bayar Muluk (*)
Faculty of Medicine, Department of Otorhinolaryngology, Kirikkale University,
Kirikkale, Turkey
G. Kopacheva-Barsova (Deceased)
Faculty of Medicine, Department of Otorhinolaryngology, Cyril and Methodius University
of Skopje, Skopje, Republic of North Macedonia
© 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_4
59

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Z. Öztürk et al.
4.2 Eustachian Tube Anatomy
The ET is composed of cartilage and bone. The adult ET extends inferiorly, anteriorly,
and medially from the middle ear and measures approximately 36mm. The lateral onethird, which is 12mm in length, is bony and originates from the anterior wall of the
middle ear cavity; the medial two-thirds, which is 24mm in length, is brocartilaginous and enters the posterolateral wall of the nasopharynx. The tube opens near the
posterior end of the inferior turbinate, approximately 1.25cm behind and just below it.
The bony portion is broad at the tympanic orice. The narrowest part of the ET
is the isthmus; it gradually narrows as it passes through the temporal bone at the
juncture of the squamous and petrous parts [5].
A posteromedially oriented cartilaginous plate forms the cartilaginous portion.
The cartilage forms the anterior curvature of a short ange at the nasopharyngeal
orice. Fibrous tissue constitutes the remainder of the anterolateral wall. At the
isthmus, the brocartilaginous portion of the tube ends laterally as the apex and
continues with the bony portion, whereas the torus, where the brocartilaginous
tube broadens and ends medially, lies below and elevates the nasopharyngeal mucosal surface. The Rosenmüller fossa is a recess just behind this elevation; it is often
the site of nasopharyngeal carcinoma and occult primary tumors [5].
A potential slit-like space between the greater wing (ala major) of the sphenoid
bone and the petrous portion of the temporal bone secures the cartilaginous ET to
the skull base [5].
The ET has a nearly triangular lumen with a vertical diameter of 2–3mm and a
horizontal diameter of 3–4mm. Unlike the bony portion, which is continuously
open, the brocartilaginous portion remains closed until swallowing, yawning, or
vigorous ination causes it to open.
The length of the ET in the newborn is about 18mm. Compared to the adult ET,
it is typically atter, less angular, and about half the size. While the cartilaginous
portion lies inferiorly, the bony portion is more elongated and larger in diameter [5].
The respiratory epithelium, consisting of mucosal glands, goblet cells, and columnar ciliated cells, lines the ET at its nasopharyngeal opening. The bony portion of the
tube is where the respiratory epithelium meets the mucosa of the middle ear.
The posterior wall of the ET has a more extensive mucosal surface and more
mucosal folds (microturbines) in pediatric specimens compared to adult specimens,
according to a study by Ozturk etal. In addition to contributing to the development
of ET dysfunction, these microturbines may play a critical clearing and protective
role in children, according to their ndings [3].
4.3 Eustachian Tube Function andPhysiology
Below are the physiological functions of the ET specied in three bullet points:
• Controls airow or pressure in the middle ear.
• Protects the middle ear from pressure and secretions from the nose and throat.
• Cleans the nasopharynx of middle ear secretions.

4 Eustachian Tube: AnOverview
61
4.3.1 Control ofAirflow or Pressure
At rest, the ET is compressed and there may be a slight negative pressure in the
middle ear. Routine air pressure is maintained by repeated opening of the ET [5].
When a person swallows or yawns, the tensor veli palatini muscle contracts and
opens the ET.ET dysfunction is a consequence of cleft palate, which is caused by a
defect in the function due to the anatomic defect in the tensor veli palatini muscles.
The role of the levator veli palatini muscle remains to be determined. Some have
questioned its role in opening the ET [5].
The effectiveness of ET ventilation is lower in children than in adults. Middle ear
disease is more common in children, and other contributing factors include oversized adenoids and recurrent upper respiratory tract infections. However, the
decreasing incidence of otitis media from infancy to adulthood shows that ET function improves as children develop.
Due to the regular opening of the ET, middle ear pressure typically remains stable in the range of +50mm to −50mm H2O.However, forces outside or above this
range are not always indicative of middle ear disease [5]. The middle ear can absorb
approximately 1mm of gas or air per day. The mastoid air cell system is accounted
as the gas source and reservoir of the middle ear [5]. At rest, the ET remains closed.
Thus, the nasopharynx serves to attenuate sudden loud sounds before they reach the
middle ear [5].
Patulous ET is a rare but serious condition characterized by an abnormally patent
Eustachian line. The patient often expresses dissatisfaction with ear fullness and
autophony, which are symptoms of hearing loss. Rapid weight loss, which can lead
to shrinkage of the ET, is believed to exacerbate the problem [5].
The ET conducts normal middle ear secretions to the nasopharynx via the mucociliary transport system and repeated active opening and closing of the tube passages [5]. Reux of nasopharyngeal secretions into the tube, which can cause
otorrhea, can occur when there is a disruption in the closed middle ear system,
including after mastoid surgery or a ruptured tympanic membrane [5].
In addition, blowing one’s nose too hard can cause pressure to build up in the
nasal airway and nasopharynx, causing secretions from the nose to get stuck in the
middle ear. Otitis media with effusion (OME) has now been linked to laryngopharyngeal reux (LPR). Pepsinogen was found in 84% of OME by Al-Saab etal., with
1.86–12.5 times higher concentrations than the serum [6].
It is believed that nasopharyngeal secretions that reach the middle ear cavity with
LPR through ET can sometimes result in otorrhea when the closed middle ear system is disrupted as in the perforation of the tympanic membrane or after a mastoidectomy procedure [5].
4.4 Eustachian Tube Dysfunction
Otitis media with effusion (OME), atelectasis of the middle ear, and chronic otitis
media with tympanic membrane perforation appear to be caused by persistent ET
dysfunction [1]. It is common practice for surgical procedures to address

62
Z. Öztürk et al.
complications resulting from ET dysfunction rather than the problem itself.
Sedlmaier etal. documented the results of laser ablation toward the posterior portion of the nasopharyngeal orice of the tubal ostium [7]. In the presence of pathological signs such as tubal tonsillar, restricted ET orice, or adenoids, ET function
was optimized in 70% of patients [5].
In 2011, Poe etal. presented the results of a pilot clinical study evaluating the
efcacy and safety of ET balloon dilatation. According to their ndings, patients
with long-term OME, who could not self-insufate their ET by Valsalva maneuver,
swallowing, or yawning, appeared to benet from cartilaginous ET dilatation and
there were no signicant side effects [8].
Among children with intractable chronic obstructive ET dysfunction, a great
majority as high as 80% showed clinical symptom relief after balloon dilation therapy according to a study by Tisch etal. [9].
Adults with persistent dilatory ET dysfunction may nd temporary relief with
balloon dilatation, according to a retrospective study by Satmis and van der Torn.
There was a statistically signicant improvement in patients’ ET Dysfunction
Questionnaire (ETDQ-7) scores at 1 and 3months following surgery. The air–
bone gap also improved postoperatively. Approximately 43% and 48% of participants reported being satised at the rst and second follow-up visits,
respectively [10].
According to a literature review by Mehta etal., only 11–18% of patients with
chronic ET dysfunction showed clinical improvement after intranasal corticosteroid
monotherapy. Buteyko breathing and intranasal corticosteroid treatment relieved
symptoms in half of the chronic patients in one study [11].
With the utilization of tissue engineering in the regeneration of mastoid air cells
(MACs), Kanemaru etal. investigated the altered function of the ET [12]. They
found that the ET portion and middle ear gas exchange were improved by tissueengineered regeneration of MACs [5].
Using transnasal video endoscopy in a sample of 33 adults, Alper etal. found that
individuals with a history of middle ear disease but otherwise healthy middle ears
had less soft palate elevation during swallowing. This correlates with a wider ET
orice and rotation of the medial lamina, suggesting impaired ET function and an
increased risk of otitis media [5, 13].
ET dysfunction treatment is explained in detail in Chap. 29.
4.5 Epidemiology ofEustachian Tube Dysfunction
Recent research has shown that for every pediatric clinic visit for ET dysfunction,
there are 0.77 adult visits, indicating that the prevalence is higher in children than in
adults. As one of the known consequences of ET dysfunction, OME affects nearly
90% of children before they enter school [14]. ET dysfunction is diagnosed in
approximately 1% of adults. Men are typically diagnosed before the age of 20,
while women tend to be diagnosed later in life. To date, there is no evidence of a
statistically signicant seasonal variation [15].

4 Eustachian Tube: AnOverview
63
4.6 Etiology ofEustachian Tube Dysfunction
In barotrauma-induced ET dysfunction, middle ear pressure is not adequately regulated because the ET does not open in response to changes in ambient pressure.
Patients may have normal otoscopy and tympanometry results due to increased air
pressure in certain situations, such as deep sea diving or descending from a high
altitude. Repeated equalization efforts caused by elevated atmospheric pressure
cause local irritation and mucosal edema of the ET mucosa. This makes it difcult
to be open and transparent in the future. The goal of treating baro-challenge ET
dysfunction with oral or topical decongestants is to reduce mucosal edema and local
tissue hyperemia, which, in turn, shrinks the nasopharyngeal mucosa and improves
ET patency [1].
An overly patent ET causes patulous ET dysfunction because the tube does not
close properly at rest, allowing the nasopharynx and middle ear to communicate
continuously. Autophony, characterized by repetitive “snifng” to reduce selfvocalization, is a sign of this [1].
An episode of rhinitis, upper respiratory tract infection, or gastroesophageal
reux syndrome may cause inammation and mucosal edema, leading to orice
obstruction and dysfunction and resulting in dilatory ET dysfunction. It is important
to rule out malignancies such as nasopharyngeal cancer, when a patient presents
with unilateral obstruction. Benign causes of obstruction such as adenoid hypertrophy or complications following adenoidectomy should also be considered [1]. A
common symptom caused by harmful pressure buildup in the middle ear is ear fullness [16–18].
4.7 Evaluation oftheEustachian Tube
Tympanic insufation may demonstrate active negative pressure, and negative resting middle ear pressures may be inferred from a type C tympanogram. A complete
hearing evaluation must include tuning fork testing with Rinne’s and Weber’s tuning
forks and pure-tone audiometry [1].
Using a scoring system, the ETDQ-7 attempts to screen for the severity of ET
dysfunction as reported by the patient. The seven questions range from “no problem” (a score of 1) to “severe problem” (a score of 7). ET dysfunction is present if
the mean score is >2.0 [19].
4.8 How toApproach Eustachian Tube Malfunction
The most likely cause of ET dysfunction determines the course of treatment [1]:
Reducing acid production in the body and adopting a healthier lifestyle are the
mainstays of treatment for gastroesophageal reux disease. Possible options include
proton pump inhibitors and other anti-acid medications. If possible, try to make
lifestyle changes to eliminate allergens. Nasal corticosteroids and antihistamines
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