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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4507_Библиотеки_им_академика_М_И_Перельмана.pdf
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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

138
Table 8.4 Behavioral tests in infants and children
Age
0–5Months Behavioral
Test name
Observation
Audiometry
(BOA)
Technical
Reex responses to sudden and loud sounds presented in the
free eld include speech signals (e.g., “bah-bah-bah”),
warble tones, narrow-band noise, and various manually
generated noise-producing devices [33, 34]. Behaviors
observed involve increasing or decreasing movements,
starting or stopping sucking, opening eyes, searching, and
laughing at sounds. While some develop reexively, babies
as young as 5months may show searching, crying, and
laughing behaviors. The baby’s minimum level of response
to a sound is assessed. The responses fall into three
categories: 1. No observable response 2. There is a response
only at high-intensity levels (70–80dB) 3. There is a
response to relatively soft sounds (30–50dB) [35]
6–24Months Visual
Reinforcement
Audiometry
(VRA)
A supra-threshold auditory stimulus is presented with a visual
reinforcer. Once a reliable head turn is established (which can
take just a few trials), when the child turns to look for the visual
reinforcer on hearing the sound (a conditioned automatic
(involuntary) motor behavior), the hearing evaluation begins.
Ideally, earphones are used to establish separate ear minimum
response levels at 500–4000Hz [33–35]
25–60Months Conditioned
Play
Audiometry
(CPA)
The child is trained to respond to a sound by completing a
puzzle, throwing a ball into a bucket, building a tower, or
other play activities. Hearing thresholds can be established
for separate ears [33–35]
E. Kösemihal et al.
Table 8.5 Test battery with audiological test protocols for infants and children
Test name
Behavioral
audiometry
OAE TEOAE, DPOAE TEOAE, DPOAE TEOAE, DPOAE
Acoustic
immittancemetry
ABR Air and bone conduction
ASSR It should be used with
0–6Months 6–36Months
This test alone is not
enough. It only allows one
to observe the behavior of
the sound. It should be
used in conjunction with
objective assessments
1000-Hz probe tone 226-Hz probe tone 226-Hz probe tone
ABRs can be used
Click, chirp, and tone burst
stimuli may be used. Click
stimuli are used to test for
auditory neuropathy rather
than threshold seeking
ABR.Provides fast,
frequency-specic
evaluation
Evaluation can be made
using visual reinforcement
audiometry using tonal and
speech stimuli. In addition,
at least one objective
measure should be used
Preferred when behavioral
audiometry is unreliable
Preferred when behavioral
audiometry is unreliable.
Provides rapid, frequencyspecic evaluation
3–5Years
Play audiometry can be
performed. Tonal and
speech stimuli can be
used
Preferred when
behavioral audiometry
is unreliable and neural
pathology is suspected
Preferred when
behavioral audiometry
is unreliable and neural
pathology is suspected.
Provides rapid,
frequency-specic
evaluation

8 Behavioral andElectrophysiological Tests inAudiology
139
8.5 Objective Evaluation ofHearing
Subjective tests (pure-tone and speech audiometry) are not sufcient for the assessment of young children. Objective measures can provide more sensitive and specic
information to either complement or replace behavioral hearing evaluations. They
are particularly useful in the hearing evaluation of infants and young children, in
medico-legal cases, or in patients who cannot cooperate due to intellectual disability
or other challenges and whose behavioral audiometry is insufcient to determine
reliable hearing thresholds.
Beginning with middle ear measurements, this section explains which objective
measurements are used to make region-specic evaluations in anatomical order (the
cochlea, auditory nerve, central auditory nervous system). It also discusses the
results of behavioral tests and objective ndings and the relationship between them.
8.5.1 Acoustic Immittance Audiometry
Acoustic immittance combines acoustic impedance and admittance, opposing
forces used to evaluate middle ear function. It is a method consisting of tympanometry and acoustic reex measurements. Tympanometry evaluates middle ear function, while acoustic reex measurements additionally evaluate auditory function
from the cranial nerves (CNs) VII and VIII to the lower brainstem.
Acoustic impedance is the resistance of the middle ear system to transmission of
acoustic stimuli. This resistance consists of frictional force, mass effects, and system tension or stiffness. The unit of impedance is the ohm [4]. Acoustic admittance
refers to the exibility, compliance, mobility, and conductivity of the system, the
opposite of impedance. The unit of admittance is mmho. Impedance and admittance
properties change depending on pathologies in the middle and outer ear.
8.5.1.1 Tympanometry
Tympanometry measures the ability of the middle ear to transmit acoustic stimuli
based on the pressure created in the external ear canal. A tympanometry probe contains tubes connected to a pressure pump, a loudspeaker, and a microphone. The
acoustic stimulus is usually a 226-Hz probe tone, although a higher frequency tone
is used to test young infants. A disposable soft rubber tip is placed over the probe
with several small tubes, which need to be kept clear of wax and obstruction. The
principle of operation is as follows: The outer ear canal is tightly sealed with the
probe containing tubes connecting the pump, speaker, and microphone. The pump
varies the pressure between the eardrum and the probe between +200 and− 400
daPa. The acoustic stimulus is delivered through the loudspeaker. The microphone
records the variation in sound intensity of the transmitted stimulus due to reection
from the eardrum when the ear is pressurized [4, 37].
The tympanogram measurement begins with positive pressure being pumped
into the ear canal, which then decreases. When the pressure in the ear canal drops to
the point where it equals the ambient air pressure, assuming the middle ear is healthy
and aerated, the measurement of middle ear admittance reaches its peak value. As

140
E. Kösemihal et al.
air pressure then decreases in the negative direction, middle ear admittance
decreases. This change in pressure causes the immittance values shown on the tympanogram graph. The three measurements provided by tympanometry are external
ear canal volume (ECV), middle ear air pressure, and middle ear admittance, all of
which are critical for the diagnosis of middle ear dysfunction.
ECV is the value measured between the probe tip and the eardrum. During tympanometry, the tympanic membrane is at its most stiff at high air pressure levels.
The admittance measured at this point represents the equivalent ear canal volume of
the ear canal, excluding the middle ear, if the eardrum is intact and not perforated.
ECV within the normal range indicates an intact eardrum and the absence of excessive ear wax. Mean ear canal volumes range from 0.40 to 1.0cc (ml) in children and
from 0.6 to 1.5cc (ml) in adults [38]. The upper limit for adults is 2.5 cc [39].
Marked asymmetry in the volume of the two ear canals suggests the possibility of a
perforated eardrum or a patent (functional) ventilation tube.
Peak-balanced static acoustic admittance (SAA) of the middle ear includes
compliance (stiffness), mass, and resistance effects. Therefore, a simple reference to static compliance is not sufcient [40]. Instead, static (peak) acoustic
admittance (SAA) is used [6, 38–41]. The normal range of peak admittance for a
226-Hz probe tone is 0.3–1.30 mmho; however, the upper limit varies between
1.1 and 1.6 mmho [6, 39–42]. If the SAA value is below the normal range, this
indicates increased stiffness of the middle ear system, such as might occur in
ossicular xation. If it is above normal, this indicates excessive exibility of the
middle ear system, which could occur, for example, if there is ossicular discontinuity or the eardrum has an atrophic area due to scarring/previous middle ear
disease.
As sound travels from the external auditory canal to the cochlea, various factors
in the middle ear affect the transmission of sound energy, including stiffness, mass
and friction effects of the tympanic membrane, and middle ear structures such as the
ossicular mass, tendons, and ligaments. The effects of ossicular mass and stiffness
of the eardrum may either increase or decrease depending on the transmitted frequency. However, at a certain middle ear resonance frequency, the effects of stiffness and mass can cancel each other out. This resonance frequency can be determined
using multifrequency tympanometry and may provide additional information about
middle ear function in individuals, thus supplementing the standard tympanometric
ndings. The resonance frequency of the human middle ear is frequently reported to
be between 800 and 1200Hz [43, 44].
Tympanogram Interpretation
The slope of the tympanogram is related to the tympanogram width and gradient. In
the presence of otitis media with effusion, the gradient decreases and the tympanogram width increases [45]. To nd the tympanometric width, a horizontal line is
drawn at the half-way point between the peak and the baseline. The intersection of
this line with both sides of the tympanogram is measured, and the tympanogram
width is obtained. It is expressed in decapascal (daPa). Tympanometric width has
been found to be more sensitive to middle ear effusion than static admittance [42].

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As the peak widens, the static admittance decreases. The average peak width in the
normal adult ear is 77 daPa and varies from 51 to 114 daPa [43, 44].
Gradient is an alternative measure of tympanogram “peakiness” that is less
widely used. It is calculated by drawing a horizontal line at the point at which the
tympanogram width spans 100 daPa and by dividing the peak height above the line
by the total height between the tympanogram peak and base. Higher gradient values
indicate a more peaked tympanogram. A gradient value of <0.2 ml is associated
with uid in the middle ear.
Tympanometry is not a hearing test, but it is preferred as a diagnostic technique
owing to the rich information it provides when used together with other auditory
tests. The most commonly used tympanogram classication in the interpretation of
the obtained graph belongs to Jerger [46]. In this system, evaluation is made using
middle ear pressure and peak compliance values. Tympanograms obtained with a
226-Hz probe tone are classied as “A,” “B,” and “C” [9, 39]. A type A tympanogram indicates that middle ear pressure and mobility are within the normal range.
Although it varies from source to source, healthy middle ear pressure is generally
accepted to be between +50 and−50 (−100) daPa [39]. A type As (A-shallow) tympanogram has a peak with an extremely low amplitude (<0.2ml). Middle ear pressure is normal. This is seen in ossicular chain xation (e.g., otosclerosis) or a scarred
tympanic membrane (tympanosclerosis) [39]. A type Ad tympanogram is a tympanogram of a markedly high peak amplitude with a normal peak pressure. The compliance of the middle ear system is higher than normal due to anomalies in the
middle ear and eardrum structures (e.g., ossicular chain dislocation or a accid tympanic membrane) [39].
In a type B tympanogram, the tympanogram has no prominent peak and a at
tympanogram shape, with high tympanometric width. This is most commonly associated with uid in the middle ear, if the ECV is in the normal range. If the ECV is
extremely low, a at tympanogram may indicate the presence of cerumen or a
blocked probe tip. A perforated tympanic membrane or an open tympanostomy tube
(grommet) causes the inability to create pressure in the external ear canal. A type B
(at) tympanogram with a high ECV is obtained [38]. The ECV should always be
recorded so that a type B tympanogram can be classied as either low- or highvolume (indicating middle ear effusion or a perforated eardrum, respectively).
A type C tympanogram shows negative middle ear pressure (peak pressure
more negative than −100 daPa) with normal peak static acoustic admittance. This
reects Eustachian tube dysfunction and may occur near the start or near the end
of middle ear effusion. The air pressure is lower in the middle ear than the ambient
air pressure, which causes a negative peak pressure to be recorded during tympanometry [39].
8.5.1.2 Multifrequency Tympanometry
Multifrequency tympanometry provides information on how conductance (G), mass
reactance, and stiffness reactance components change with the immittance probe
frequency. Differences between normal and pathological ndings are observed by
evaluating the changes resulting from this measurement. Changes in the

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transmission properties of the system cause changes that affect the resonant frequency (RF) of the middle ear system. Multifrequency or multicomponent tympanometry is based on the analysis of tympanograms obtained with multiple probe
tone frequencies ranging from 226Hz to 2000Hz [42].
8.5.1.3 Wideband Tympanometry
In wideband tympanometry (WBT), as in classical tympanometry, the probe,
which occludes the ear canal, contains a microphone, a speaker, and a pump. In
this test, a click stimulus is used that covers the frequency range between 226Hz
and 8000Hz. The test is interpreted by calculating the amount of reection or
absorption of the stimulus presented at a xed intensity level. Classical tympanometry measurements are also included [4, 47]. WBT has the potential to detect
more subtle effects of current and previous middle ear disease than is possible
using classical tympanometry. The following advantages of WBT have been
identied:
• Absorption measurement under pressurized and unpressurized conditions.
• Recording of middle ear response in a wide-frequency band.
• In addition to static compliance, it can also measure acoustic susceptance (mass
susceptance and compliant susceptance), which is the virtual component of
acoustic admittance, and acoustic conductivity, which is the real component of
acoustic admittance.
• Ability to calculate middle ear resonance.
• It is possible to collapse a number of frequencies and obtain absorbance data
over an averaged frequency range (a wideband-averaged tympanogram), which
might offer better clinical estimates for babies that are well and neonatal inten-
sive care unit (NICU) residents [4, 47].
8.5.1.4 Acoustic Reflex Test
The tensor tympani and stapes muscles are in the middle ear. These muscles contract involuntarily in response to a high-intensity sound. This contraction is called
an acoustic reex. An acoustic reex is generally considered a protective response,
but, more recently, it has been accepted that the stapedius muscle contracts to suppress one’s own internal noise and speaking voice. The stapedius muscle reex
response is recorded in response to high-intensity acoustic stimuli. These stimuli are
presented to the ipsilateral or contralateral ear. While the stapedius, a branch of CN
VII, innervates the stapes muscle, CN V innervates the tensor tympani muscle. At
high intensities, the movement of the stapes base causes the ossicular chain and
tympanic membrane to stiffen, making it more difcult for sound to travel from the
ossicular chain to the inner ear. The occurrence of the reex is used as evidence of
middle ear integrity and the functioning of the auditory structures that form the
acoustic reex arc. The stimulus presented to one ear causes the stapes muscles of
both ears to contract. Comparison of the ipsilateral (“non-crossed”) and contralateral (“crossed”) acoustic reex patterns is essential for audiological differential
diagnosis [48, 49].

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The acoustic reex pathway includes the conducting mechanism, inner ear, auditory nerve, cochlear nucleus, medial superior olivary complex (MSOC) (ipsilateral
and contralateral), motor nucleus of the facial nerve, and the stapedial nerve. The
schematic of the acoustic reex arc is shown in Fig.8.2.
The probe placed in the ear canal for the acoustic reex test should completely
occlude the ear, as it does for the tympanometric measurement. First, the pump is
set at the peak tympanometric pressure. The acoustic stimulus level is typically
increased in 5-dB increments, starting at 80dB.In most clinics, the maximum level
is 110 dB to avoid acoustic trauma. The reex is recorded 25–100ms after the
acoustic stimulus. As the threshold is approached, the reex is delayed in onset. As
the intensity level of the stimulus increases, the amplitude of the reex increases
and the onset latency is faster. The amplitude of the reex is proportional to the
increase in stiffness of the ossicular chain when the stapedius muscle contracts.
Traditionally, acoustic reexes are dened as ipsilateral and contralateral reexes,
depending on the ear to which the stimulus is presented [4, 47]. If a stimulus is
presented and recorded from the ear where the tympanometry probe is placed, it is
an ipsilateral reex. If a stimulus is presented to the ear opposite where a speaker
(earphone) is placed and the reex recording is made from the ear where the probe
is placed, it is a contralateral acoustic reex. For example, a right contralateral
acoustic reex means that the probe is placed in the left ear while the stimulus is
presented in the right ear.
Fig. 8.2 Ipsilateral and contralateral acoustic reex arcs for the right ear

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The acoustic reex threshold (ART) is the lowest stimulus level that produces
minimal reproducible change in middle ear admittance (shown as a downward
deection on the immittance instrument). For people with normal hearing, the ART
is typically >60dB (well above the hearing threshold) and is usually recorded with
stimuli at 80–90dB HL [48, 49]. Pure-tone signals at 500, 1000, 2000, and 4000Hz
and a broadband noise signal can be used for acoustic reex measurements.
The arc of the acoustic reex is a neural pathway; however, the occurrence of the
reex depends on the functioning of the external auditory canal and middle ear,
which transmit the stimulus to the cochlea. Therefore, even small conductive hearing loss or a middle ear pathology may prevent acoustic reex detection. Acoustic
reex thresholds of approximately 80–85dB HL for pure tones rule out most middle ear abnormalities. In infants and young children, a broadband noise signal may
be used rather than tones to quickly obtain test results, in which case the ART should
occur at a lower intensity level.
The eighth cranial nerve carries neural impulses generated by cochlear activation
to the ventral cochlear nucleus (VCN) [49]. Most axons in the ipsilateral facial
motor nucleus region project from the VCN to the ipsilateral acoustic reex pathways. The stapedius muscle is innervated by the afferent neurons originating from
the motor nucleus of the facial nerve. A portion of the bers of the VCN travel to the
contralateral MSOC after passing through the trapezoid body. The stapedius muscle
is innervated by efferent facial nerve bers that are contralateral to the stimulus ear
and are transmitted by the next set of neurons to the motor nucleus of the facial
nerve. Thus, intact ipsilateral and absent or elevated contralateral ARTs may indicate a brainstem auditory pathology affecting the MSOC or trapezoid body.
8.5.1.5 The Reflex Decay Test
At intensities above the ART, the decrease in reex amplitude depending on the
stimulus duration is called a reex decay. In clinical practice, an acoustic stimulus
is presented for 10sec at 10dB above the reex threshold. If a 50% decrease in
reex amplitude occurs in the rst 5sec, the reex decay is considered “positive”
and suggests the possibility of a retrocochlear pathology. Low-to-mid-frequency
stimuli (500 and 1000Hz) are the preferred test frequencies. Because there is a high
probability of a positive reex decay for stimuli at 2000 and 4000Hz, even in normal hearing subjects, testing at these frequencies is unreliable [4]. Reex decay as
a test for neural or retrocochlear pathology can complement otoneurologic ABR
testing to diagnose retrocochlear pathology; however, MRI of the auditory nerve, if
this is available, is a more sensitive and specic test.
8.5.1.6 Eustachian Tube Evaluation
A normally functioning Eustachian tube provides air pressure equalization on both
sides of the tympanic membrane. Ideally, the air pressure in the middle ear should
be at or near atmospheric pressure (0 daPa). It is generally considered normal in the
range of +50/−50 daPa. Eustachian tube dysfunction may be indicated by middle
ear pressure that is either positive or negative outside of this range. Eustachian tube
function (ETF) tests are used to determine whether or not the Eustachian tube is

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patent. The Valsalva maneuver and the Toynbee maneuver are the two main tests of
the Eustachian tube.
The Valsalva test begins with standard tympanometry. Next, the patient is
instructed to gently hold his or her nose and blow air into the back of the nasopharynx. Another tympanogram is recorded. If the Eustachian tube is functional, a positive shift of the tympanometric peak pressure is expected [41].
In the Toynbee test, the patient is asked to swallow while holding the nose. The
peak pressure in the tympanogram recorded after the maneuver is expected to shift
in a negative direction [41].
Although Eustachian tube function tests are simple to perform, they cannot
detect a specic pathology. In addition to these tests, evaluation should be performed if Eustachian tube dysfunction is suspected based on the patient’s complaints, history, or the presence of a negative peak pressure. If a change in peak
pressure is recorded during Eustachian tube testing, it is concluded that the
Eustachian tube can be opened with active pressure. However, this does not fully
explain how the Eustachian tube works during different real-life activities and conditions. If no change in peak pressure is observed during the Eustachian tube test,
this indicates a risk factor for recurrent otitis media or barotrauma due to activities
such as ying or diving [41].
Some diagnostic tympanometers provide a special ETF module, in which positive and negative pressure changes are created through the pressure pump in the
external ear canal. The patient is asked to take one sip of water to check whether the
Eustachian tube can change middle ear pressure to equalize the external canal pressure. A change of at least 20 daPa between trials indicates healthy ETF.
8.5.2 Otoacoustic Emissions
Otoacoustic emissions (OAEs) are generated by the motility of outer hair cells
(OHCs) in the organ of Corti. This generated energy can be measured in the external
ear canal [50]. It is propagated from the cochlea to the middle ear and to the outer
ear canal by vibration of the tympanic membrane. Active biological mechanisms in
the cochlea contribute to frequency selectivity, increased sensitivity, and the nonlinear properties of cochlear responses. Sensory pathologies that cause hearing loss
affect OHC function in the cochlea. Therefore, OAEs are an effective and sensitive
measure for diagnosing OHC dysfunction. Damage to OHCs results in decreased
hearing sensitivity, poorer frequency tuning (selectivity), and loudness recruitment
(abnormal growth of loudness as intensity increases).
The amount of amplication provided by the active processes in the cochlea
associated with OHC activity is thought to be in the order of 40–50dB.However,
the residual energy reaching the ear canal (OAEs) is in the range of 0–15 dB
SPL.OAEs are preneural responses—they do not depend on the integrity of the
afferent eighth (auditory) nerve bers. Hence, OAE measurement plays a crucial
role in the diagnosis of cochlear or retrocochlear dysfunction and auditory neuropathy spectrum disorders (ANSDs) [51].

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8.5.2.1 Classification ofOtoacoustic Emissions
OAEs are divided into two types according to their generation mechanism.
Spontaneous otoacoustic emissions are recorded without an acoustic stimulus, and
evoked otoacoustic emissions are recorded after an acoustic stimulus.
Spontaneous otoacoustic emissions (SOAEs) are recorded by a probe microphone placed in the ear canal without a stimulus. SOAE energy peaks between 800
and 4000Hz and is most commonly observed between 12 and 20dB SPL in the
1000–2000-Hz range. Because spontaneous OAEs are observed in only 50% of
normal hearing subjects, they are not preferred for clinical use [52].
Stimulated otoacoustic emissions are widely used in clinical practice. There are
two subtypes of evoked OAEs: transient evoked OAEs (TEOAEs) and distortion
product OAEs (DPOAEs). Both types of evoked OAEs reect active cochlear mechanisms. Therefore, failure to obtain OAEs may indicate a disorder of the outer hair
cells, the generating mechanism [52].
Transient evoked OAEs (TEOAEs) occur when brief (transient) sounds, such as
clicks or tone bursts, are presented. TEOAEs are typically recorded in the frequency
range of 500–4000Hz. For measurement, the stimulus intensity should be set at
80±4dB SPL and response reproducibility and stability of the presented stimulus
with probe placement should be ensured [52].
Distortion product OAEs (DPOAEs) are another type of evoked OAE.Two pure
tones, referred to as f1 and f2, are presented simultaneously at specic intensity
levels, referred to as L1 and L2. The frequency ratio for the tonal stimuli is selected
to optimize the 2f1–f2 DPOAE amplitude (e.g., an f2/f1 ratio of 1.22), and the
intensity levels are preferably closely spaced, such as 65 and 55 dB SPL (f2>f1;
L1> L2). Although DPOAEs are recorded in the 0.5–6-kHz frequency range in
clinical practice, they can be recorded up to 10–12kHz in studies.
8.5.2.2 Performing Otoacoustic Emission Tests
The OAE test is noninvasive and technically simple to record. This test typically
takes 2–3min for each ear. OAE testing does not require sedation. A behavioral
response is not required to participate, so the patient’s motivation, attention, or cognitive state does not affect the procedure. The test can be performed while the patient
is quiet and awake. If this is not possible, the test may be administered during natural
sleep. Children can be distracted by watching a silent video during testing.
A disposable probe tip is preferred. This soft probe tip is gently inserted into the
ear canal. Signal leakage and measurement contamination from external noise are
prevented by sealing the probe tip rmly in the ear canal. At the start of the test, the
system automatically checks that the probe is correctly placed in the ear. The
loudspeaker/s in the probe (two loudspeakers for DPOAEs) produces acoustic stimuli to evoke cochlear response. The stimuli are transmitted through the middle ear to
the cochlea. A sensitive microphone in the probe detects and records OHC energy
that back-propagates mechanical vibration through the middle ear system and sound
into the ear canal that is recorded by a microphone in the OAE probe. The algorithms
in the OAE system distinguish OAE activity from other environmental and physiological noise, and the presence of otoacoustic emissions is statistically conrmed [53].

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8.5.2.3 Analysis andInterpretation ofOtoacoustic Emissions
Automated data analysis software is typically included with modern OAE equipment. However, visual inspection of OAE data with manual analysis is essential for
the reliable interpretation of OAE results. An example of screenshots of TEOAE
and DPOAE results is shown in Fig.8.3. Noise levels must be low enough to accurately measure OAE (Table8.6).
The TEOAE test criteria may change for clinical applications. For example, the
existence of TEOAE in two or more half-octave bands may be considered a “pass”
in newborn hearing screening. However, in some cases, such as when monitoring
for noise-induced hearing loss, changes in one or more half-octave bands may
indicate an abnormality in the OHCs indicative of noise damage. TEOAEs are
generally not detected in cochlear hearing loss >30dB HL.When the audiometric
thresholds are better than 20dB HL, TEOAEs are present in 99% of cases, but
TEOAEs may not be present in individuals with mild cochlear dysfunction, even
when hearing thresholds are within normal limits. TEOAEs are abnormally reduced
or absent in patients with OHC dysfunction and pure-tone thresholds between 25
and 35dB HL or when hearing is poorer than this. Normal OAEs may be recorded
in individuals with varying degrees of hearing loss associated with inner hair cell
dysfunction or neural or nonorganic hearing loss. It is always necessary to crosscheck OAE results with other audiometric test ndings to guide diagnosis. Table8.7
lists the required criteria for DPOAE results of “present, normal, abnormal,
absent” [53].
OAEs depend on normal cellular metabolism; they are extremely sensitive to
subtle effects on cochlear function. OAEs are an index of OHC activity. OHCs are
typically the rst affected by an insult to the cochlea such as an anoxic event.
Middle ear dysfunction impacts OAE measurement. An abnormality of the middle
ear or external ear canal can cause the absence of OAE even when OHC function
is normal. If there is normal middle ear function (normal tympanometry), OAE
abnormalities are an indicator of cochlear dysfunction related to the OHCs. Care
must be taken to ensure that the OAE probe is kept clean as even a small amount
of cerumen can block the small openings in the probe and interfere with the OAE
measurement. The areas listed below are where OAE measurements are currently used.
– Newborn and pediatric hearing screening.
– Diagnosis of auditory neuropathy spectrum disorders.
– Differentiation of cochlear/retrocochlear hearing loss.
– Patient populations that cannot cooperate readily with behavioral audiometry
(e.g., infants and young children, children with developmental delay, autism, or
intellectual disability).
– Early detection of noise-induced hearing loss.
– Ototoxicity monitoring in people receiving ototoxic agents for medical treatment.
– Assessment of medial superior olivary complex suppression (efferent auditory
function).
– As a cross-check tool for behavioral audiological thresholds.
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