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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

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E. Kösemihal et al.
conduction thresholds in conductive hearing loss and the degree of hearing loss in
cases where masking is required as well as for obtaining information about hearing
levels in individuals with atretic ears. However, because the maximum intensity
level at which the bone vibrator can be stimulated is usually 55–60dB nHL, this
limits the estimation of bone conduction hearing thresholds beyond mild- tomoderate degrees [72, 73].
8.5.3.3 Auditory Steady-State Responses
Auditory steady-state responses (ASSRs) reect electrical potentials produced by
stimulating the ear with a continuous and repetitive series of frequency (FM) and
amplitude modulations (AM). ASSR software are typically integrated into a device
with an ABR module. The electrode placement and earphones are the same as those
of the ABR.The ASSR test has recently been added to audiological test batteries.
This technique provides an objective testing option for threshold estimation with
automated and statistically based response analysis. No waveform analysis or interpretation is required [74, 75]; however, recording quality should be monitored and
results cross-checked with other tests to avoid artifactual results.
The ASSR is often evoked by pure-tone stimuli, which has the advantage of
frequency-specic threshold estimation. A carrier frequency between 500 and
8000Hz is used with different modulation frequencies and depths. In clinical
practice, 500–4000Hz is usually preferred due to time constraints. Frequency
modulation (FM), amplitude modulation (AM), or mixed modulation (MM),
which combines both, can be used to modulate the carrier frequency and enable
response detection [75]. It is possible to assess multiple frequencies simultaneously in both ears by modulating multiple stimuli at different frequencies at
different rates. Using pure tones as stimuli in ASSR, it is possible to assess
intensity levels of approximately 120dB HL.ABRs can measure responses up
to levels of about 100dB nHL [74]. High intensity levels are needed for threshold determination for cochlear implant candidates, especially young children.
As is the case for ABRs, ASSR measurements can be made with air and bone
conduction transducers. Standard test and stimulus parameters are provided in
Table8.8 [72].
Effect oftheStimulus Rate
Based on evidence for the response generators, ASSRs are typically divided into
40-Hz and 90-Hz ASSRs. The unit Hz used here refers to the approximate stimulus
modulation/presentation rate. The 90-Hz ASSR is used for sleeping subjects of all
ages (natural sleep, sedation, or general anesthesia), while the 40-Hz ASSR is used
for assessing awake adults and older children. The 40-Hz ASSR can be considered
similar to the middle latency response (MLR). The MLR is immature in neonates,
so its use in neonates is not recommended. The 40-Hz ASSR is appropriate for older
awake children (> 5years) and adults.
The 90-Hz ASSR is thought to originate from brainstem-level generators, similar
to the ABR.It is identical to the ABR, in that it can be recorded from birth, is mainly
unaffected by sleep, sedation, or general anesthesia, and is suitable for use at all

8 Behavioral andElectrophysiological Tests inAudiology
Table 8.8 Standard test and stimulus parameters for ASSR
Parameters Selections or options
Transducers Insert earphones, supra-aural earphones, bone oscillators, and
loudspeakers for stimulation in the sound eld
Carrier frequencies 250, 500, 1000, 2000, 4000, 8000Hz
Modulation
frequencies
Amplitude modulation
(AM)
Frequency modulation 10%
Advanced modulation
options
Stimulus intensity
range
Calibration reference dB HL
Different modulation rates from 70 to 110Hz
100%
Exposure modulation (AM2); phase-adjusted
0–125dB HL, depending on the frequency and the transducer
159
ages, including neonates. Since the ASSR stimulation rate is affected by the sleep
state, it is essential to correctly select the child or adult as asleep or awake from the
test protocols included in the software. Correction factors for the estimated HL to be
obtained vary according to test protocol—these correction factors are included in
the ASSR equipment [75, 76].
The ASSR also has potential disadvantages. Unlike the ABR, it is not a diagnostic test, and this test does not provide any information about the site of auditory
dysfunction and cannot identify ANSDs. Therefore, the combined use of the ABR
and ASSR is preferred for diagnostic evaluation and threshold estimation rather
than the ASSR alone. A graph is generated from the result of the ASSR test, indicating whether responses were obtained and at what intensity levels [75, 76].
8.5.3.4 Electrocochleography
This test records the electrical activity of the auditory nerve and cochlear hair
cells in response to auditory stimuli. Electrocochleography (ECochG) provides
information about the evaluation of peripheral auditory function, the diagnosis of
ANSDs, the diagnosis of Meniere’s disease, and the localization of peripheral
auditory dysfunction. Intraoperative neurophysiological monitoring of cochlear
and CN VIII status during surgery that puts these structures at risk is another use
of ECochG.
Electrocochleography response amplitudes vary with the type of electrode used.
The best response amplitudes are obtained with a small needle electrode placed on
the promontory through the ear canal via the transtympanic membrane approach.
Other options include placement of electrodes on the tympanic membrane and in
the ear canal [77, 78].
Cochlear microphonics (CMs), summation potential (SP), and action potential
(AP) are the three components of ECochG.Cochlear microphonics originate from
OHCs, whereas the summation potential mainly depends on inner hair cell activity
[77, 78]. The action potential is generated by the simultaneous ring of the distal
afferent eighth nerve bers and corresponds to ABR wave I [79].

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E. Kösemihal et al.
Electrocochleography Analysis
ECochG analysis involves conrming the presence of CMs, calculating amplitude
and latency values for summation and action potentials, and calculating the SP/AP
amplitude ratio. The SP/AP ratio is expressed as a percentage. SP/AP normative
values vary depending on the electrode type. The normative SP/AP percentages for
each electrode type are as follows: ear canal electrode type SP/AP >50%, tympanic
membrane electrode SP/AP >40%, and transtympanic needle electrode SP/AP
>30% [72, 80, 81].
In Meniere’s disease, an abnormally high SP/AP ratio is observed. The sensitivity of the transtympanic membrane electrode technique was reported to be between
50% and 60% and its specicity was more than 90% in the diagnosis of endolymphatic hydrops [81]. Another advantage of ECochG is that it is an important test in
the diagnosis of ANSDs [82, 83]. Detection and analysis of ECochG wave morphol-
ogy and wave components may allow for distinguishing whether dysfunction is in
the presynaptic or postsynaptic region. The ECochG result contributes to cochlear
implantation decisions in patients with ANSD.However, due to difculties in clinical practice, it is preferred to evaluate the presence or absence of CMs in ABRs for
the diagnosis of ANSDs [82, 83]. ECochG recordings can be more invasive and
time-consuming than ABR recordings, so it is more common for clinicians to check
for CMs by examining the early part of the ABR waveform in response to separate
polarity, high-level click stimuli.
8.5.3.5 Cortical Auditory Evoked Potentials
Cortical auditory evoked potentials (CAEPs) are brain responses generated in the
auditory cortex and nearby areas in response to (typical) longer-duration auditory
stimuli. They are the late latency members of the auditory evoked potentials family.
The purposes of measuring these potentials are to assess the neural transmission of
sound to the level of the auditory cortex and objectively evaluate auditory discrimination skills, to evaluate individuals with hearing disorders, and to monitor auditory
rehabilitation outcomes [84–86].
Time-locked evoked cortical activity provides information about the timing and
magnitude of sound processing as evidenced by CAEP latencies and amplitude.
Some components occur within 50 ms after stimulus presentation in adults, but
these are later in children. The late-latency responses have four components, referred
to as P1, N1, P2, and N2. The rst of these components, P1, is the same as Pb, the
last component of the MLR.The P1 wave occurs at approximately 50ms, the N1
wave at approximately 100ms, and the P2 wave at approximately 200ms. The nal
wave, N2, occurs at around 300–350ms but is often ignored in clinical evaluations
as it is less prominent that the P1–N1–P2 complex. More than one source is cited as
the generators of these components. Although CAEPs mainly originate from the
thalamus and primary auditory cortex in the supratemporal region, they are also
affected by the auditory association areas and the frontal cortex [84–86].
CAEP wave morphology shows signicant variability with age. The wave morphology we observe as the P1–N1–P2 complex in adults consists of a large and
broad P1 component in the early years of life. As this wave formally differentiates

8 Behavioral andElectrophysiological Tests inAudiology
161
by age 7 or later, N1 and P2 components appear. CAEP waves, which can be
obtained from birth, begin with a long latency (about 200–400ms). During adolescence, CAEPs reach adult latency and amplitude values between the ages of 14 and
16. This is considered an indicator of auditory cortical maturation [87].
Auditory pathways and centers in the brain become more efcient with increased
myelination, neural synchronization, and axon density. As the auditory system
matures, there is an increase in complex abilities such as increased sensitivity to and
discrimination of auditory stimuli, automaticity in information processing, adaptive
attention, learning, and memory [87].
Clinical applications of CAEP measures include:
– Evaluation of hearing aid and cochlear implant performance in infants and
children.
– Assessment of cortical maturation by examining P1 latency.
– Estimation of the hearing thresholds of patients who have difculty cooperating
for behavioral testing or sleeping for ABR or in medico-legal cases.
– Evaluation of auditory processing disorders, including those with comorbid lan-
guage or learning difculties.
– Monitoring the progression of neurodegenerative or psychological diseases [87].
CAEP measurements are obtained by changing parameters and using a different
protocol within the equipment used for ABR testing. It is a test that requires being
awake and still. When performed during sleep, the response amplitudes decrease.
The patient can watch videos during testing, or infants/children can be distracted
with quiet toys or books. Electrode placement is similar to the ABR, but different
placements can be used according to device guidelines. Typical parameters that may
be recommended for cortical auditory measurements for clinical purposes are listed
in Table8.9.
8.5.3.6 Event-Related Auditory Potentials
P300
The P300 response is a cortical response that occurs 250–350ms after stimulus
presentation. It reects whether two different presented stimuli can be discriminated
in the brain. Many anatomical regions in the brain may contribute to the formation
of the P300. It is thought to originate in the hippocampus, which is responsible for
conscious memory. The sensory cortex, centroparietal cortex, and frontal lobe are
also thought to contribute [84, 86].
The P300 response, rst described in the 1960s, is also known as the P3 or P3b.
It is presented with a stimulus train called the oddball paradigm. The P300 recording task involves actively detecting an infrequent “oddball” stimulus amongst presentations of a frequent standard stimulus. The ratio of frequent-to-infrequent
stimulus is typically 80–85% to 10–15%. P300 recording requires active participation of the patient. It is necessary to be alert, attentive, and cooperative during the
test and hence is not suitable for very young children. The patient may be asked to

162
Table 8.9 Typical parameters for cortical auditory evoked potential testing
Parameters Tone burst, speech (recorded or synthetic syllables or phonemes)
Stimulus
duration
Level of
intensity
Polarity Alternate/rarefaction
Stimulus
repetition
Number of
averages
Filter 1–30Hz
Artifact
rejection
Analysis time
Electrode
montage
20–200ms
70–80dB (for supra-threshold measurement) can be the lowest level in
threshold estimation
1.1/s
100–300
±100μV
−100ms/+600ms
Cz, Fpz, M1–M2, or A1–A2 (electrode placement can also be placed in the
supraorbital–lateral canthus to prevent artifacts caused by eye movements)
E. Kösemihal et al.
mentally count or press the button in their hand when they perceive the infrequent
stimulus. Infrequent stimuli may vary in frequency, duration, or intensity compared
to the standard (Fig.8.6a). The P300 potential elicited in response to the stimulus
presented within the oddball paradigm, which includes stimuli that differ in frequency, is shown. In this measurement, at 80 dB nHL, the frequent stimulus is
1000Hz and the infrequent/rare stimulus is 4000Hz [84, 86].
The P300 response has two subcomponents: P3a and P3b. The P3a response
indicates that new signals from the brain are being perceived. Its latency is shorter,
and its amplitude is lower. The P3b component occurs in response to rare stimuli
with activation of memory and attention. The highest amplitude responses are
obtained from the parietal region [84, 86, 88].
The P300 is an endogenous response. As the difference between infrequent and
frequent stimuli increases, it becomes easier to distinguish between them. Thus, the
latency may be shorter and the amplitude more robust. The equipment, electrode
placement, and parameters used to measure the P300 are similar to those used to
measure the late latency responses. However, a separate protocol must be opened
and preferences made for frequent and infrequent stimuli. The P300 response can be
used to electrophysiologically assess higher-order processing in patients with hearing aids and/or cochlear implants. It is also used in the diagnosis and follow-up of
central nervous system disorders such as dementia, brain injury, cerebrovascular
events, depression, alcoholism, auditory processing disorders, epilepsy, Parkinson’s
disease, or schizophrenia. In such cases, a decrease in P300 response amplitude and
a prolonged latency have been reported [89, 90].
Mismatch Negativity
Mismatch negativity (MMN) is a neurophysiological response that reects the
brain’s automatic ability to discriminate minor acoustic differences. It is a negative
response that occurs approximately 200ms after stimulus presentation. It was rst

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b
Fig. 8.6 (a) Examples of the P300 test result and the (b) MMN record

164
E. Kösemihal et al.
described by Naatanen, Gaillard, and Mantsalo (1978). In addition to the auditory
cortex, the frontal cortex and auditory subcortical areas have been reported to be
sources of MMN.The MMN response is also elicited by the oddball paradigm but
in a passive listening situation without the need for a patient response. Frequent and
infrequent stimuli are presented 15–20% and 80–85% of the time, respectively.
MMN latency and amplitude vary with the size of the difference between the stimuli. A longer latency and lower amplitude response can be obtained when similar
stimuli are presented [91].
MMN recording is performed using similar parameters and electrode placement to
the P300. Unlike the P300, it is a test that does not require patient participation. For this
reason, it can be assessed in infants and toddlers. Maturation differences are observed
into adulthood. While there may be no signicant age differences in the MMN response
obtained with simple stimuli, as the task becomes more difcult (with complex stimuli
such as speech), a reduction in latency is observed into adulthood (Fig.8.6b). The
recording in Fig.8b was obtained by changing both the stimulus and intensity of the
infrequent stimulus. The frequent stimulus was presented at 1000Hz and 80dB nHL,
and the infrequent stimulus was presented at 4000Hz and 70dB nHL [91–93].
Because MMN does not require attention and participation in the test, it can be
assessed in all age groups. It evaluates the effects of auditory experience, maturation, treatment, training, and learning on the central auditory system. It is an adjunctive test for evaluating hearing aid and cochlear implant performance and for
diagnosing and monitoring neurological and psychological conditions [91–93].
Acoustic Change Complex
The acoustic change complex (ACC) assesses neural processing ability in response
to acoustic changes, similar to MMN.It was rst described by Ostroff (1998) [94].
The ACC consists of two separate P1–N1–P2 complexes within the same waveform,
as a result of presenting two different tonal or speech stimuli sequentially. The ACC
represents discrimination ability at the level of the auditory cortex. It has been used
to assess speech perception and has the ability to detect auditory differences [95] and
to evaluate auditory skills, especially in hearing aid and cochlear implant users, as
well as in psychiatric cases [85, 95–97]. It has been reported that differences of up to
3dB in intensity between two stimuli can be detected using the ACC [85, 96, 97].
The electrode placement used in the ACC is similar to other cortical potential
measures, but the stimulus presentation is different. Two different stimuli are presented an equal number of times. Each stimulus can last up to 500ms. For this
reason, it is preferred that the analysis window be at least 1000ms. When long-term
sustained stimulation is used, the time for neural ring to recover increases and
waves with larger amplitudes are obtained. Stimulus characteristics vary depending
on the purpose of the assessment.
The ACC obtains two separate waves in a single trace. It does not require evaluating the difference between the separate waveforms of two stimuli as in MMN
or P300 evaluation. Because of this ease of use, it is preferred to MMN in some
clinics.

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165
If we summarize CAEPs overall, these responses are obtained from auditory
cortical areas and associated areas during the presentation of auditory stimuli. Sleep
or sedation is not required. The P1–N1–P2 complex indicates that the sound has
reached the cortex and that neural processing has begun. When more complex
recording techniques are used for the P300, MMN, and ACC, the variables affecting
response increase. Therefore, a single set of normative data has not been developed.
It is recommended that each clinic obtains normative data according to their methods [85, 96, 97].
Failure to obtain a CAEP response or an abnormal response may not directly
reect a cortical problem. Failure to obtain a response despite reliable testing may
reect a problem at any stage in the auditory pathway from the outer ear to the auditory cortex. Because the thresholds obtained correlate with behavioral thresholds in
adults, CAEP estimation of thresholds is preferred in medicolegal cases. ACC and
MMN tests do not require attention and provide information about sound discrimination. The P300 response requires attention to the stimuli and is hence inuenced
by cognition. For this reason, it is used in children over the age of 7 and in cooperative adults.
CAEPs are a tool that allows us to electrophysiologically image neural processing and evaluate the impact of auditory rehabilitation processes in the brain.
Technological innovations will make these tests even more powerful in the future
[85, 96, 97].
8.6 Conclusion
This section provides an overview of audiological assessments for neurotologists. It
is recommended that audiology textbooks be consulted for detailed information on
audiological testing. Best practices in diagnostic audiology require a test battery
with appropriate behavioral and electrophysiological tests. In audiology, each test is
of particular importance in evaluating the entire auditory function. The audiologist
is responsible for selecting these tests according to the patient’s needs. With an
appropriate test battery, diagnostic audiological tests can provide valuable information to guide decisions in the diagnosis and management of auditory and neurotological disorders.
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