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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

5 Temporal Bone Radiology
75
fracture on CT is still signicant for the fracture. In addition, CT angiography, magnetic resonance (MR) angiography, and MR venography allow visualization of
injured vascular structures.
Ossicular injuries present as dislocations and fractures, often associated with
longitudinal fractures. Dislocations are most common at the incudostapedial and
incudomalleolar junctions. Ossicular fractures occur at the long process of the incus
and the stapes crura.
Facial canal fractures are associated with transverse fractures [12]. Complete
facial paralysis is seen in cases of nerve injury and may require surgical decompression [15].
A fracture line passing through the otic capsule may cause a pneumolabyrinth;
even if no obvious fracture line is seen on CT, it is suggestive of a fracture [13, 16].
Intralabyrinthine hemorrhage is also common but is unlikely to be seen on
CT.Therefore, MRI should be ordered in patients with sudden onset of sensorineural hearing loss associated with otic capsule trauma. Hemorrhage is hyperintense on
T1-weighted MR images and CSF is hypointense, especially on uid-attenuated
inversion recovery MR images [15].
Perilymphatic stulas may occur after oval or round window direct trauma, barotrauma, or iatrogenic stapes surgery. The pneumolabyrinth on CT is again a precautionary nding. Segmental enhancement of the membranous labyrinth in
contrast-enhanced T1-weighted images may be seen at the site of the stula [13, 15].
A fracture line including the tegmen tympani should usually be seen for CSF
leakage. However, it may be iatrogenic secondary to surgery or due to congenital
bone defects.
Carotid canal fractures may be associated with internal carotid artery (ICA)
injury, and air in the canal may sometimes be the only radiologic nding. In this
case, CT angiography and/or MR angiography are indicated. ICA dissection may
result in stenosis and ischemic infarction.
Sigmoid sinus and jugular bulb injuries are often associated with transverse fractures. CT may show air in the sinus or bulb. The most helpful diagnostic tools are
contrast-enhanced CT and CT venography [13].
The external ear cavity and temporomandibular joint may also be injured, usually by the mechanism of longitudinal trauma. Air may be seen in the joint capsule.
In high-energy trauma, the fracture lines may extend to the central skull base. The
carotid canal, cavernous sinus, and foramen ovale and associated neurovascular
structures may be injured.
Intracranial injuries are also present in almost all temporal bone trauma. These
injuries may be limited epidural hemorrhage or life-threatening pathologies such as
subarachnoid hemorrhage, subdural hematoma, cerebral contusion, cerebral edema,
herniation, and/or pneumocephalus [13, 15].

76
M. B. Eser et al.
5.2.4 Conclusion
The complex radiologic anatomy of the temporal bone presents both challenges and
opportunities for accurate imaging and diagnosis. The temporal bone is one of the
sites where knowledge of the anatomy and variations is most important in detecting
pathology. The anatomy of the temporal bone is complex enough to be the subject
of a book. This section has attempted to highlight the most important points of
radiologic anatomy for the clinician.
5.3 Radiologic Findings ofInfectious andInflammatory
Pathologies oftheTemporal Bone
5.3.1 Introduction
Infectious and inammatory conditions of the temporal bone present unique diagnostic challenges due to their diverse presentations and potential complications.
Radiologic imaging, primarily CT and MRI, plays a pivotal role in identifying,
characterizing, and guiding the management of these conditions. This section
reviews the radiologic ndings associated with infectious and inammatory temporal bone pathologies.
5.3.2 Necrotizing Otitis Externa
Necrotizing otitis externa is a rare and fatal complication of otitis externa, usually
seen in elderly, diabetic, and immunocompromised patients. The most common
pathogen is Pseudomonas aeruginosa, but Aspergillus fumigatus is also associated
in immunocompromised patients. Pathogens can spread to the temporomandibular
joint and skull base, causing osteomyelitis. Clinical symptoms are usually sufcient
for diagnosis. Imaging is necessary for complications [17].
Imaging ndings may range from fatty tissue inltration, soft tissue thickening,
and contrast enhancement to bone destruction. If osteomyelitis develops, CT may
show demineralization, erosion, and periosteal reaction. Hyperintensity may be
seen in these affected bones in the chronic phase. MRI is the best imaging modality
in the early stages of suspected fat marrow osteomyelitis (Fig.5.8). Widespread
hypointensity on T1 and hyperintensity and contrast enhancement on T2-weighted
images are highly suggestive of osteomyelitis. Retrocondylar, subtemporal, masticatory space, parapharyngeal fat planes, and the petroclival fat are the areas where
fatty inltration and soft tissue thickening may be seen. Cortical destruction of the
mastoid bone supports osteomyelitis, and jugular fossa involvement is extremely
important for intracranial spread of infection [18, 19]. Cranial nerve involvement
can also be demonstrated radiologically and is clearly associated with increased
mortality [20].

5 Temporal Bone Radiology
77
ab c
Fig. 5.8 Necrotizing otitis externa. (a) An axial CT image showing obliteration of the right exter-
nal auditory canal (arrow) in a 56-year-old male with diabetes. (b) A non-contrast MR image of
soft tissue thickening in the external auditory canal (arrow). (c) After contrast injection, signicant
contrast enhancement in the soft tissue (white arrow), also at the level of the temporomandibular
joint (black arrow) is remarkable
5.3.3 Middle Ear
5.3.3.1 Acute Otitis Media andMastoiditis
Acute otitis media is the most common local infection in children under 5years of
age. This is because the adenoid tissue of the nasopharynx is hypertrophied in children and the Eustachian tube is obstructed by the accumulation of secretions due to
its horizontal course [21]. Otitis media, usually of a bacterial origin, is an inammation of the ME.CT scans show uid accumulation, thickening of the ME mucosa,
and disruption of the ossicular chain. Acute otitis media presents with uid opacication, while chronic otitis media (COM) shows ossicular erosion, bony destruction, and cholesteatoma formation. Mastoiditis, an extension of otitis media, is
characterized by bony erosion within the mastoid air cells, which can be seen on CT
scans. In severe cases, imaging is helpful in determining the extent of bone destruction and possible intracranial involvement [21, 22]. While the diagnosis of acute
mastoiditis is based on clinical examination, imaging is required in chronic otomastoiditis, especially in the setting of complications.If the infection is not controlled
and secretions accumulate, the pressure in the ME cavity increases and the TM may
perforate. This initiates a complex process leading to acidosis, decalcication, bone
erosion, and ischemia. Subsequently, the walls of the mastoid air cells are destroyed
and coalescent mastoiditis develops. In acute coalescent mastoiditis, the thin bone
septa between the mastoid air cells are lysed by the infection, and this destruction is
seen on CT as a loss of density in the trabeculae. If the purulent material passes
through the periosteum to the emissary veins, a subperiosteal abscess may be seen
(Fig. 5.9) [21]. This was described as Bezold’s abscess in 1908. If the infection
causes destruction of the sigmoid sinus plate, an epidural abscess may occur, and, if
it causes a defect in the tegmen, the infection may spread to the middle cranial fossa
[21, 22].
5.3.3.2 Chronic Otitis Media
Chronic infection of the ME cavity is called COM, and, when the mastoid air cells
are also affected, it is called chronic otomastoiditis. COM can lead to damage or
xation of the ossicles and hearing loss. HRCT plays a role in assessing the exact

78
M. B. Eser et al.
ab
c
de
Fig. 5.9 (a) Congestions in the mastoid bone and tympanic cavity in a 4-year-old girl with acute
otalgia and fever. (b) Destruction of mastoid air cell walls consistent with coalescent mastoiditis.
(c) A CT image of a subperiosteal abscess within the soft tissue density. (d) Mastoid congestion
(arrow) on MRI in a 9-year-old boy with headache and hearing loss. (e) A contrast-enhanced image
showing lling defects (arrows) in the transverse sinus; dural sinus thrombosis is a rare complication of mastoiditis
location of opacities and complications (Fig.5.10). There are fundamental questions that underlie the clinician’s motivation to request imaging. These are:
– Will my treatment be medical or surgical?
– If surgery is required, how will I plan?
– Does my patient have any anatomical variations (i.e., a high/dehiscent jugular
bulb, dilated emissary veins, a persistent stapedial artery, an aberrant carotid
artery) that may affect the success of surgery?
– Are there any complications such as tegmen defects, ossicular chain disruption,
inner ear stula, and facial nerve dehiscence?
A radiologic report of acceptable quality should clearly answer these questions
[23]. In a dry ear, where otoscopic evaluation of the ME is not possible because of
exocytosis, chronic calcic myringitis, etc., CT imaging provides data with a high
negative predictive value regarding the ME.However, CT cannot differentiate the
type of opacity. Cholesteatomas, cholesterol granulomas, granulation tissue, secretions, and pus all have the same opaque appearance on CT [24, 25].
5.3.3.3 Cholesteatomas
A cholesteatoma is an epidermoid cyst of the ME that presents a diagnostic challenge due to its variable appearance. CT scans show bony erosions and dense soft
tissue masses within the ME and mastoid. A cholesteatoma may be suspected

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a
d
Fig. 5.10 Chronic otitis media, labyrinthitis, and meningitis. (a) A CT image of a 38-year-old
male patient showing opacities in the tympanic cavity consistent with chronic otitis media and a
defect in the tegmen tympani (arrow). (b) On MRI, the normal signal of the cochlea and labyrinth
disappeared and became completely hypointense in the patient with severe tinnitus, vertigo, and
nuchal rigidity. (c) Contrast-enhanced MR series showing peripheral enhancement consistent with
an abscess (arrows) and contrast enhancement in the cochlea and semicircular canals (tail-ball
arrow). (d) Thickening and pathologic contrast enhancement consistent with meningitis are
observed in the temporal lobe dura (arrow)
because opacications have a nodular appearance on CT and cause destruction.
However, MRI is essential to differentiate an active cholesteatoma from granulation
tissue, with diffusion-weighted sequences showing restricted diffusion in the active
cholesteatoma. Today, non-echo planar diffusion-weighted imaging is known to be
superior to echo planar diffusion-weighted imaging in detecting cholesteatomas and
has become the standard of care. This is because non-EPI DWI avoids the artifact
and distortion caused by the air–bone transition in the temporal bone (Fig.5.11)
[26]. Radiologic assessment guides surgical planning and follow-up. Evaluation of
cholesteatomas using both CT and MRI guides treatment strategies and postoperative surveillance [27]. Fusion imaging, which combines CT and MR, is increasingly
being used for surgical planning [28].
Temporal bone infections can lead to intracranial complications, including meningitis, brain abscesses, and extradural abscesses. CT and MRI help identify these
complications by showing meningeal enhancement, intra- or extra-axial abscesses,
and bone destruction. Imaging is useful in planning surgery and monitoring response
to therapy.
5.3.3.4 Cholesterol Granulomas
The mechanism of formation of these lesions, also called cholesterol cysts, is not
fully understood, but it is believed that Eustachian tube dysfunction, negative

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a
d
Fig. 5.11 A cholesteatoma. (a) A cholesteatoma in the right ear of an 11-year-old girl. (a) An
axial computed tomographic image presents a large soft tissue density in the right ear with signicant destruction of the mastoid bone. (b) On diffusion-weighted axial MRI, the lesion is bright. (c)
On an apparent diffusion coefcient map, the lesion is hypointense. (d) The apparent diffusion
coefcient image of the lesion is bright and compatible with that of the cholesteatoma
pressure in the ME cavity, and the resulting vacuum phenomenon cause mucosal
edema and rupture of blood vessels. It has been suggested that erythrocytes in the
resulting hemorrhage increase cholesterol, leading to a foreign body reaction and
granulation tissue formation [29, 30].
Cholesterol granulomas have typical MRI features; T1 time is shortened due to
the blood elements they contain and they appear hyperintense. They are heterogeneously hyperintense on T2W images, a hypointense rim may be present, there is no
enhancement, and diffusion is limited (Fig.5.12). Trapped uid is important for
differentiating these lesions; uid is not expansile, whereas cholesterol granulomas
are [31, 32].
5.3.4 Inner Ear
5.3.4.1 Labyrinthitis
The most common cause of labyrinthitis is infection, but rare causes such as inammation, trauma, hemorrhage, and tumor can also cause labyrinthitis. Labyrinthitis
affects the inner ear structures and presents with vertigo, hearing loss, and tinnitus.
MRI is the modality of choice, showing enhancement and swelling within the
cochlea and vestibule. Diffusion-weighted imaging is particularly useful in detecting acute labyrinthitis, showing restricted diffusion within the affected labyrinthine
structures (Fig.5.13). The acute phase is followed by the brous phase and the nal

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Fig. 5.12 A cholesterol granuloma on magnetic resonance imaging. (a) A large-sized lesion
extending from the petrous apex level to the cerebellopontine angle and involving the clivus on the
right. A hypointense hemosiderin rim is observed at the periphery of the lesion. The signal of the
lesion on the T2-weighted image, heterogeneous and bright in posterior part of the lesion. (b) The
signal of the lesion is hyperintense on the non-contrast T1-weighted image. (c) The lesion does not
show signicant contrast enhancement in the contrast-enhanced image
c
Fig. 5.13 Labyrinthitis on magnetic resonance imaging. (a) Signicant signal loss in the left
cochlea and vestibule (arrows) on a T2W sequence in a 73-year-old man. Comparison of noncontrast (b) and non-contrast-enhanced (c) images showing signicant contrast enhancement in
the cochlea, vestibule, and semicircular canals (arrows)
ossication phase, referred to as labyrinthitis ossicans. In the late phase, pathologic ossication occurs in the cochlea and vestibular system [33].
5.3.4.2 Petrous Apicitis
The petrous bone apex is pneumatized in approximately one-third of the population.
Petrous apicitis is an infection of the apex of the petrous bone that may extend to the
skull base. MRI is valuable in assessing the extent of soft tissue inammation and

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possible cranial nerve involvement. Early detection aids in prompt medical management to prevent complications such as cranial nerve palsies.
CT scans show opacication of the air cells of the petrous apex and adjacent
bone erosion. Contrast-enhanced MRI is more useful in the diagnosis of petrous
apicitis and osteomyelitis [34, 35].
5.3.4.3 Facial andVestibular Nerves
In pathologies of the cranial nerves, an increase in nerve thickness and enhancement
can be seen radiologically. Therefore, contrast-enhanced MRI should be chosen
when imaging is to be performed. Contrast enhancement of cranial nerves can be
seen in many conditions, such as perineural extension, in addition to infectious and
inammatory causes. In particular, facial nerve enhancement should be evaluated
segmentally, as physiologic enhancement may be seen, especially in the tympanic
segment and geniculate ganglion. Pathologic and physiologic enhancement can be
differentiated by an experienced radiologist using special thin-slice MRI sequences.
Bell’s palsy is an acute idiopathic facial paralysis and is the most common cause of
facial paralysis [36, 37]. Ramsay Hunt syndrome is caused by reactivation of the
varicella zoster virus latent in the geniculate ganglion. Symptoms include otalgia,
vertigo, nausea, vomiting, facial paralysis, and, in a minority of patients, hearing
loss. It is important to look for vesicles on clinical examination. Thickening and
enhancement of the facial nerve are typical radiologic ndings.
Latent viruses such as herpes simplex and varicella zoster can also affect the
eighth nerve and cause vestibular neuritis. Vestibular neuritis is the most common
cause of benign paroxysmal positional vertigo and the second most common
cause of peripheral vestibular vertigo [38]. Imaging can be used to exclude causes
such as tumors, ischemia, and vascular stenosis. Contrast enhancement of the
vestibular nerves, especially the superior vestibular nerve, may be seen on MRI
(Fig.5.14) [39].
Fig. 5.14 When the non-contrast (a) and contrast-enhanced (b) images are evaluated together,
contrast enhancement is observed in the vestibular nerve tract (arrow) in the distal part of the internal auditory canal in a 72-year-old female patient who presented with facial paralysis and hearing
loss. On clinical examination, the patient has vesicles around the ear; the diagnosis was compatible
with Ramsay Hunt syndrome

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5.3.5 Conclusion
Radiologic imaging is essential in the diagnosis and management of infectious and
inammatory conditions of the temporal bone. The ability to visualize soft tissue
and bony changes allows for timely and accurate diagnosis, facilitating appropriate
treatment strategies and minimizing potential complications. By understanding the
specic imaging patterns associated with various conditions, radiologists and clinicians can work together to improve patient outcomes and guide therapeutic
decisions.
5.4 Temporal Bone Tumors: Radiologic Evaluation
andDiagnosis
5.4.1 Introduction
Temporal bone tumors, although rare, encompass a diverse spectrum of benign and
malignant neoplasms that can pose signicant diagnostic and management challenges. Radiologic evaluation, primarily by CT and MRI, plays a critical role in
characterizing these tumors and allowing for accurate diagnosis, treatment planning, and monitoring. This section reviews the radiologic approach to temporal
bone tumors, highlighting their imaging characteristics and clinical implications.
5.4.2 Classification ofTemporal Bone Tumors
Temporal bone tumors are classied according to their origin, including primary
tumors arising from the temporal bone structures and secondary tumors arising
from adjacent regions. The rst question is in which part of the temporal bone the
tumor is located. Tumors may arise from the cerebellopontine angle (CPA), petrous
apex, external auditory canal, ME, or mastoid bone. Primary tumors include vestibular schwannomas, glomus tumors, and cholesteatomas. Secondary tumors often
arise from the parotid gland, skull base, or intracranial structures and inltrate the
temporal bone.
5.4.2.1 Cerebellopontine Angle Tumors
MRI can identify tumors of the cerebellopontine angle with high accuracy. IAC
extension, brainstem and cranial nerve compression, development of hydrocephalus
are all evaluated with imaging.
Vestibular Schwannomas
Vestibular schwannomas (acoustic neurinomas) are the most common CPA tumors
that arise from the Schwann cells of the cochlear or vestibular nerve. These tumors
occur sporadically in the fth to seventh decade of life. A bilateral vestibular
schwannoma is one of the diagnostic criteria for neurobromatosis type 2. MRI is

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the preferred modality and shows a well-circumscribed mass along the cochlear or
vestibular nerve. T1-weighted imaging shows heterogeneous signal intensity, while
T2-weighted imaging shows hyperintense signals. Schwannomas are hyperintense
tumors. As the tumor grows, cystic degeneration may develop and enhancement
may become heterogeneous (Fig. 5.15). Tumor extension changes the surgical
approach; suboccipital, translabyrinthine, or middle cranial fossa approaches are
used. Stereotactic radiosurgery is an alternative, especially for high-risk patients
and residual tumors [5].
Arachnoid Cysts
Arachnoid cysts are lesions that originate from arachnoid cap cells and show the
same signal characteristics as CSF in all sequences. They do not restrict diffusion [40].
Meningiomas
Meningiomas are classic non-diffusing lesions with a dural tail and homogeneous
enhancement. Although benign, these lesions may show extension into the middle
cranial fossa, ME, IAC, petrous bone, and cavernous sinus (Fig.5.16). When lesions
extend into the IAC, they usually do not expand [5, 40].
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def
Fig. 5.15 A vestibular schwannoma. (a) Bilateral lesions originating from the CPA and extending
into the internal auditory canal are shown on T2W MRI in an Neurobromatosis II patient. (b) The
lesions show contrast enhancement and extend into the internal auditory canals. (c) Other extraaxial lesions are seen in the same patient; these are meningiomas and are not surprising in an NF
II patient. (d–f) Sporadic vestibular schwannomas are indicated by arrows in different patients
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