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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

148
E. Kösemihal et al.
b
Fig. 8.3 (a) An example of a TEOAE result screen. The red column shows the signal, and the gray column shows the noise. The SNR, shown by the green line,
provides information about the test under appropriate conditions. (b) An example of a DPOAE result screen. SNR is indicated by the red line

8 Behavioral andElectrophysiological Tests inAudiology
Table 8.6 TEOAE test results and interpretation
TEOAE results
Present No answer “Inconclusive” or “not clear (NC)”
Amplitudes between
−10 and+30dB SPL
TE-NFa (SNR) ≥6dB
SPL
a
NF Noise oor
Table 8.7 DPOAE results and interpretation
DPOAE amplitude (dB SPL) Within normal
Signal-to-noise ratio
(SNR)=Distortion
product−Noise oor (dB)
Low noise level (LNL) Ideally
At low noise
levels (≤−5dB
SPL)
SNR ≤5dB SPL
DPOAE results
Present and
normal
limits (>0dB
SPL)
≥6dB ≥6dB
<−10dB SPL
Recording conditions are not sufcient (e.g.,
noisy environment or probe placement problem)
Possibly present but
abnormal Absent
Below normal limits
(e.g., <5% of normal
and<0dB SPL)
Ideally <−10dB SPL
149
Below noise
oor
<6dB
Ideally
<−10dB
SPL
8.5.3 Auditory Evoked Potentials
Auditory evoked potentials (AEPs) are waveforms that are generated by synchronized neural activity in the central auditory nervous system in response to acoustic stimuli. They can reect electrophysiological function at different levels in
the auditory system. Because AEPs objectively assess the integrity and function
of the peripheral and central auditory systems, they have become a powerful tool
for determining hearing thresholds in children who are too young to undergo
audiometric testing and others who are unable to comply with behavioral testing [54].
AEPs are widely used for purposes such as estimating hearing thresholds, evaluating central auditory nervous system function, newborn hearing screening, and
monitoring auditory nervous system function during surgery [55].
It is possible to categorize AEPs based on the region in the central auditory nervous system from which they are obtained and the latency interval during which the
response occurs (Fig.8.4).
Although there are several methods for grouping AEPs in audiological evaluations, the most commonly used method is to classify them according to the latency
intervals in which they are obtained:
• Electrocochleography (ECochG): This occurs within the rst 5ms after the sig-
nal presentation. It reects activity of the cochlea and CN VIII.

150
Fig. 8.4 Family of
auditory evoked potentials
E. Kösemihal et al.
• Auditory brainstem response (ABR): This occurs within 1–10 milliseconds (ms).
This is the most commonly used AEP.The ABR reects neural activity in CN
VIII and the brainstem.
• Middle latency response (MLR): This occurs within 10–50ms. The MLR wave-
form mainly reects activity in the midbrain, thalamocortical projections, and
primary auditory cortex.
• Late latency response (LLR): This occurs within 50–250ms (or later in infants).
It reects activity in the primary auditory regions of the cerebral cortex and
related structures.
• Auditory steady-state response (ASSR): The ASSR is evoked by a periodic stim-
ulus and reects phase-locked steady-state neural activity in response to an
ongoing stimulus. The ASSR is recorded in the frequency domain so that peri-
odic activity can be extracted. This differs from the transient evoked responses
(ECochG, ABR, MLR, LLR), which are usually analyzed by examining the
waveform in the time domain. The generators of the ASSR depend on the modu-
lation rate of the stimulus; responses to slow rates originate from more central
brain structures. In contrast, responses to high rates originate from the more
peripheral auditory nerve and brainstem structures [56].
8.5.3.1 Auditory Evoked Response Measurement Principles
andTechniques
Most clinically used auditory evoked responses (AERs) reect electrical brain
responses that are at lower voltages than responses obtained from other activities in
the brain and body (e.g., electroencephalography (EEG) and cardiac and muscle
activity). Therefore, unique techniques and equipment are used to measure and isolate the actual AERs from other sources of electrical “noise.” Although the measurement principles for AERs are the same, the recording parameters for each differ. All
AERs are typically recorded with electrodes placed on the scalp that collect electrical
voltages generated in the brain. The names of these electrode sites are standardized
according to the international 10–20 electrode system. In clinical practice, a three- or
four-electrode array is commonly used for single- and two-channel recordings.
However, a 32- or 64-electrode array with a unique cap is also used in neurological
examinations and experimental studies. In the most common electrode placement,
the non-inverting electrode (an active or positive electrode) is placed at the center of

8 Behavioral andElectrophysiological Tests inAudiology
151
the forehead toward the hairline (Fz) or at the vertex at the top of the head (Cz). The
inverting electrode (a reference or negative electrode) is placed on the right and/or
left earlobes (A1, A2) or on the mastoid bone (M1, M2). The ground electrode (a
neutral or common electrode) is placed on the forehead or root of the nose (Fpz).
Recording electrodes detect the minimal electrical voltages reecting activation
of the central auditory nervous system in response to repeated auditory stimuli and
transmit this information to a preamplier where the responses are amplied.
Filtering and signal averaging are performed to separate unwanted electrical activity
from the time-locked auditory neural responses to the stimuli. The aim is to increase
the quality and reliability of the measurement using methods such as digital ltering
of the resulting waveform, artifact rejection (AR) to eliminate muscle or other electrical noise, noise-weighted averaging, and checking the reproducibility rate/recording quality using metrics provided by the AER software. In short, the AER test
recording process requires well-connected, low-impedance electrodes, low-noise
ampliers, ltering, response averaging, and digital signal processing. Selection of
appropriate recording parameters is critical in AER measurement [56].
8.5.3.2 Auditory Evoked Brainstem Response
The auditory brainstem response (ABR), the most commonly used evoked potential,
is obtained at the brainstem level. It occurs within the rst 10ms of presentation of
an auditory stimulus. A typical ABR waveform consists of ve peaks separated by
approximately 1ms. The ve peaks that make up the ABR waveform are labeled
with Roman numerals. Waves I, III, and V are the peaks evaluated most often in
clinical applications [54]. Figure8.5 shows an example of the ABR waveform for
an adult with normal hearing.
The ABR test is sensitive to disorders at the level of CN VIII and the auditory
brainstem [54]. It is useful in the diagnosis of vestibular schwannoma and brainstem-level disorders. It can also be monitored during surgery to remove CN VIII
tumors to preserve hearing. In addition, it is widely used as an objective test to
estimate hearing thresholds in young children and for newborn hearing screening.
Normal outer, middle, and inner ear function is required for a normal ABR.The
latency and amplitude values of the obtained waveform are compared to normative
values and provide information on the integrity and status of the auditory nervous
system up to the upper brainstem [54, 55].
The ABR is used in newborn hearing screening and hearing loss diagnosis.
Information obtained from ABR testing should be combined with the results of
other objective measures, such as tympanometry, acoustic reexes, and OAEs, and
behavioral assessment to achieve accurate and precise hearing assessment [56].
The ABR can be recorded in newborns and premature infants after birth. The
latencies, amplitudes, and morphology of the waves reect developmental changes
in brainstem maturation and nerve myelination during the rst 18months of life. By
24months, brainstem maturation is complete and the ABR waveform becomes similar to that of adults. In clinics, normative data appropriate for the baby’s age and
months are necessary to analyze and interpret ABRs in infants younger than
18months [56].

152
a
b
E. Kösemihal et al.
Fig. 8.5 (a) An example of an adult ABR waveform obtained at 80dB nHL.Waves I, III, and V
are labeled. (b) The latency–intensity function. As the intensity increases, the latency is expected
to decrease
Stimulus Types
Click, chirp, or tonal stimuli are used for ABRs. Recently, speech stimuli have also
been used, although this is uncommon for audiometric assessment. Speech ABR has
been used as a diagnostic test for central auditory processing disorder.
The click stimulus can provide general information about hearing and hence may
be used for screening ABRs. The click stimulus is a broadband (100–10,000Hz)
and short-duration (0.1ms or 100μs) stimulus. Because of these characteristics, a
strong ABR can be elicited by synchronizing the ring of multiple auditory nerve
bers [57]. The click ABR does not reect frequency-specic hearing and hence
cannot be used to reliably measure hearing thresholds at different frequencies.
The chirp stimulus is created by taking into account the time delays that occur in
the cochlea because different stimulus frequencies activate different cochlear regions
due to the tonotopic structure (frequency mapping) of the cochlea, with low and high
frequencies activating apical and basal cochlear regions, respectively. A widely used
chirp stimulus is referred to in the literature as CE-Chirp, an abbreviation of the name
of Claus Elberling, who developed the chirp stimulus. The time-dependent frequency

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sequence of the CE-Chirp stimulus is designed to match the frequency sensitivity of
the cochlea, progressing from apical to basal. Lower frequencies are delivered rst,
followed by higher frequencies. Because of the tonotopic organization, the entire
cochlea is stimulated simultaneously and synchronous neural activation is achieved,
optimizing ABR amplitudes. As a result, chirp responses are elicited at levels close
to the hearing threshold obtained with the click stimulus but with higher amplitudes.
The level-specic chirp stimulus (LS CE-Chirp) is a stimulus whose duration varies
as a function of stimulation intensity [57]. Frequency-specic threshold estimation in
infants is possible using chirps and tone burst stimuli. Both tone bursts and tonal
CE-Chirp stimuli can be used for frequency-specic assessment, to obtain frequencyspecic ABRs at 500, 1000, 2000, and 4000Hz. It is important to assess hearing
across the frequency range so that the auditory conguration can be determined to
support hearing aid tting for individuals who cannot complete pure-tone audiometry. Agreement between ABR and pure-tone audiometry thresholds is achieved using
appropriate equipment calibration and correction factors [58, 59].
Stimulus Polarity
Polarity refers to the direction in which the diaphragm in the headphone moves rst with
the stimulus presentation. “Rarefaction” is the term used for the direction in which the
pressure decreases in the ear canal, and “condensation” is used for the direction in which
it increases. Many AER instruments offer alternating polarity. That is, the earphone diaphragm moves in two directions, alternately. This is used to cancel electromagnetic
stimulus artifacts, but it is also clinically important to separately examine the waveform
evoked by single-polarity stimuli. For example, it is expected that the rarefaction polarity will be used for clicks because of the larger wave amplitudes and that the alternating
polarity will be used for tonal stimuli because of their longer duration and the need to
reduce stimulus-related artifacts to better observe responses to tonal stimuli. Separately
examining the waveform evoked by rarefaction and condensation polarities is essential
in diagnostic practice as this reveals the presence of cochlear microphonics (CMs),
which is a critical nding in the diagnosis of auditory neuropathy spectrum disorders
(ANSDs) [59, 60]. Because cochlear microphonics are preneural and reect cochlear
hair cell activity, the polarity of the response follows the stimulus polarity. The presence
of cochlear microphonics with an absent ABR is indicative of an ANSD.
Stimulus Presentation Rate
This refers to the number of stimuli delivered per second. A rate between 11/sec, 21/
sec, or 37/sec can be used. Stimulation rates of 60/sec or higher could degrade the
response and hence are not recommended for hearing threshold assessment. The
higher the rate, the shorter the time needed for assessment, however. A high-rate
stimuli of 70–90/sec may be useful for the diagnosis of neurodegenerative diseases
such as multiple sclerosis, where neural synchronization is affected [59].
Stimulus Intensity
Neural evaluation of the ABR is performed at high-stimulus intensity levels (>
70 dB nHL (decibels normalized hearing level)) where all wave components

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(waves I–V) are visible. For diagnostic evaluation, it is recommended that normative values (peak latency values of waves, interpeak latencies, and amplitudes)
be obtained at the same intensity level as that used in the test battery for diagnostic ABR.This is because, as the intensity level decreases, latencies increase and
amplitudes decrease. Waves I and III may not be seen as the intensity decreases.
Wave V is the most robust component that is monitored down to 20dB nHL for
clinical threshold assessment. People with normal hearing are expected to have
wave V at 20dB nHL, although at 500Hz, 30dB nHL is the typical “pass” level
for infant hearing assessment. Elevated ABR thresholds indicate hearing loss
[59, 60].
The unit of intensity level for all auditory potential tests is dB nHL.This unit is
a value that reects the average hearing thresholds for the ABR stimuli of a group
of individuals with normal hearing. As mentioned earlier, frequency-specic correction factors adjust the thresholds obtained with tonal stimuli to those obtained
with pure-tone audiometry in dB HL.Some instruments can use dB SPL for clinical
testing and research purposes; however, care needs to be taken when equating these
levels to audiometric thresholds [59, 60].
Analysis Time (Recording Epoch)
ABRs typically do not exceed 10 ms, even in pathological cases. Therefore, an
analysis time of 12–15 ms is appropriate. If a longer analysis time is used, the waves
may appear more elongated with smaller amplitudes, making it difcult to determine thresholds. In very young infants with conductive hearing loss, a longer time
window of 20ms may be required to identify ABR wave V and the following negative peak.
Filters
In diagnostic ABR testing, unwanted physiological noise is recorded in addition to
the responses generated by the auditory stimuli, but the energy of this noise is generally <100Hz. A high-pass lter set at 100Hz is preferred for click ABR; however,
a lower value of high-pass lter (30Hz) is optimal for frequency-specic ABR.The
choice of high-pass lter should effectively reduce artifacts and unwanted noise
without affecting the ABR amplitude. A low-pass lter should be selected to avoid
excessive “rounding” of the waveform. The optimal low-pass lter is 2500 or
3000Hz for accurate and precise recording of peak ABR latencies. A 30–1500-Hz
bandpass lter may be preferred for tonal air and bone ABR testing [59, 60].
Artifact Rejection Level
The artifact rejection (AR) level should be as low as possible to achieve a good
signal-to-noise ratio in AEP testing whilst still allowing for clinically acceptable
recording times. Efforts should be made to reduce muscle activity and electrical
noise picked up by the electrodes. Under good recording conditions, an artifact
rejection level of no more than ±10μV is suggested, but, depending on the conditions, a higher value (e.g., ±40μV) may be preferred. Noise-weighted averaging can
also help reduce noise and improve waveform quality.

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Number ofSweeps
Under optimum conditions, 1500–2000 sweeps per waveform are usually sufcient.
In cases where the residual noise level is high, more sweeps may be required. The
relationship between AR level and sweeps follows a quadratic law; if the AR level is
doubled to ±20μV to achieve the same residual noise, the number of sweeps must be
quadrupled from 2000 to 8000 [59, 61]. However, rather than simply increasing the
number of sweeps, it may be more benecial to stop the test, ensure proper conditions, and restart. Using a xed number of sweeps is not appropriate in all situations.
Electrodes
Disposable electrodes are gradually replacing reusable electrodes. Disposable Ag/
AgCl electrodes are available. Although disposable adhesive electrodes may resemble electrocardiogram (ECG) electrodes, adhesive electrodes designed for neurological assessment are preferred. These electrodes are placed in regions numbered
and named according to the international 10–20 system. According to this system,
the ground (common) electrode is placed on the forehead, the positive (noninverting) electrode is placed on the upper forehead (Fz) or vertex (Cz), and the
negative (inverting) electrode is placed on the mastoid (M1–M2) or earlobe (A1–
A2). Placement in different regions affects wave amplitudes and morphologies. For
example, the non-inverting electrode on the forehead compared to the vertex can
reduce the signal-to-noise ratio, resulting in a smaller waveform, but this is not a
substantial effect. Placing the mastoid electrode farther from the ear (as is often
done in threshold ABR testing) can reduce the amplitude of wave I.Impedances
should generally be <5kΩ and inter-electrode impedances should ideally be <3kΩ
for optimal recording [62].
In addition to the technical parameters of the ABR, variables dependent on the
individual being tested also affect the results. As mentioned previously, the brainstem of infants continues to mature until 18months of age. Therefore, longer latencies may be obtained [62].
There are also gender differences. Waves III, IV, and V are shorter in some adult
females than in males. Differences in cochlear size have been suggested as a reason
for this. It should be noted that these sex differences are small enough not to affect
clinical normative values [63].
Another factor is the individual’s body temperature. A decrease in body temperature can cause a prolongation of wave latencies and a reduction in amplitudes.
Although not at levels that differ from normative values, it is helpful to record body
temperature during testing for research purposes and intraoperative monitoring. It is
recommended to use a correction factor of 0.2ms below 37°C and 0.15ms at each
level for 38–42°C [64, 65].
Although pharmacological agents affect ABR results, especially in cases of hearing loss due to ototoxicity, drugs that do not directly affect hearing do not signicantly affect the latency and amplitude of ABR waves in clinical ndings. It has
been noted that some anesthetics, which are sometimes utilized in order to perform
the test under anesthesia in complex or difcult-to-test cases, cause prolongation of
brainstem response latencies but have no signicant effect on amplitudes [66, 67].

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Neural Generators ofABRs
The ABR originates from various parts of the auditory nervous system, from the
vestibulocochlear nerve (eighth nerve) to the upper brainstem. The generators of
ABR components are thought to be as follows:
Wave I: Obtained from the distal part of the auditory nerve.
Wave II: Obtained from the proximal part of the auditory nerve.
Wave III: Originates from many nerve sources in the cochlear nucleus and superior
olivary complex regions.
Wave IV-V: Wave IV-V is thought to be generated by neural activity as the lateral
lemniscus bers enter the contralateral inferior colliculus. However, it is reported
that there is more than one source for components responsible for wave III and
later peaks [68–70].
Auditory Brainstem Response Analysis andInterpretation
The purpose of neurotological ABR evaluation is quite different from threshold
determination. Neurotological ABRs can provide information about the location of
a pathology in the auditory pathway. Detailed analyses of many wave components
of the ABR waves, including their morphology, repeatability, absolute and interpeak
latency values, amplitude relationships, and differences between the two ears, are
particularly important for diagnostic ABRs [71].
Morphology refers to the general appearance of the resulting ABR wave.
Because it requires the experience of the clinician, morphological analysis is subjective. The intensity level of the stimulus affects the morphology. As the intensity
level decreases, the amplitude of the waveform decreases and the latency is longer.
At a high-intensity stimulus level such as 80dB nHL, waves I, III, and V are seen.
The most robust component is wave V; waves I and III can disappear at threshold
levels [71].
The repeatability of a waveform is another aspect of morphology. Latency and
amplitude values should be obtained under the same conditions [59, 71]. If the reliability of the waveform is low, this may indicate a retrocochlear pathology as a
result of asynchronous/disrupted neural transmission [71].
Waves I, III, and V peak latencies obtained from each ear after stimulus presentation are compared to normative data for latency assessment. The similarity of absolute latencies between the two ears is also examined. The latency of an ABR
component reects the time it takes for neural activity to reach the neural generator/s
[71]. ABR wave latencies increase steadily as stimulus intensity decreases. In normal hearing, at the 80-dB nHL stimulus intensity level, wave I is obtained about
1.5ms after the stimulus and waves III and V occur at 2-ms intervals later than this.
The obtained peak latencies, interpeak latencies, and interaural latency of wave V
are compared with existing normative data [59, 71].
The latency–intensity function curve is a clinical graph that presents the decrease
in latency as a function of increasing intensity (Fig.8.5). A clinician can easily
compare the wave absolute latencies and I–III, III–V, and I–V interpeak latencies in
the same ear or between the ears with normative data in this graph. The similarity of

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interpeak latencies between the two ears is evaluated. In general, the I–V interpeak
latency should not exceed 4.5ms in adults and children over 18months of age. The
I–V interpeak latency range in healthy newborns is 5ms. In symmetric or nearly
symmetric hearing, the interaural difference of wave V peak latency should not
exceed 0.3ms, otherwise a retrocochlear pathology should be suspected [71, 72].
An abnormality is dened as more than two standard deviations above the clinical
mean (normative) or an appropriate normative database for the measurement of
absolute wave latencies and interwave latency values.
For amplitude ratio assessment, wave V to wave I amplitude ratio is calculated.
The result is compared with normative data. The amplitude of wave V is typically
twice that of wave I, and the V/I amplitude ratio is 2.0. An amplitude ratio of <0.5
is considered abnormally reduced, suggesting a retrocochlear or auditory brainstem
pathology. In infants younger than 18months with normal hearing, wave I amplitude is larger than wave V amplitude [71, 72].
In neurological evaluation, the accuracy or sensitivity of the ABR for auditory
nerve lesions is high (>90%). The specicity is 85%–90% [72]. A functional problem involving CN VIII and lower brainstem is evidenced by ABR abnormalities on
the ipsilateral side, and rostral auditory brainstem pathology is mostly associated
with contralateral ABR abnormalities [72, 73].
Clinical Use ofABRs forChildren
The purpose of newborn hearing screening is to detect the possibility of hearing
loss, not to estimate the threshold. Therefore, the intensity level for screening has
been set at 35dB nHL.If an ABR wave V is present at this level, the likelihood of
signicant hearing loss is relatively low. The ABR has been endorsed by the Joint
Committee on Infant Hearing (JCIH) as the standard for newborn hearing screening [73].
In newborn hearing screening programs, ABR measurement can be performed
with conventional instruments, but portable devices are now widely available. These
devices include algorithms for automatic detection and analysis of wave V, providing a “pass” or “refer” result. If there is no risk factor for newborns, the “pass” result
means that the hearing system works well up to the upper auditory brainstem structures. The “refer” result indicates that follow-up screening is needed (depending on
the screening protocol), and the second “refer” result means a diagnostic hearing
evaluation is required [73].
The OAE and automated ABR measurements were suggested by the JCIH to be
used for newborn screening in 2007. However, OAE screening can miss cases of
auditory neuropathy spectrum disorder. In addition, OAEs are extremely sensitive
to minor middle ear disease, earwax, and measurement conditions. False positive
results for OAE hearing screening and high referral rates due to technical issues can
lead to increased costs and unnecessary anxiety for parents associated with the diagnostic follow-up of infants. Therefore, ABRs alone or a combination of ABRs and
OAEs is ideal for screening [73].
ABRs can also obtained with a bone vibrator used to determine bone conduction
thresholds in pure-tone audiometry. This is a valuable test for determining bone
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