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5 Temporal Bone Radiology
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fracture on CT is still signicant 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].
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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 ofInfectious andInflammatory
Pathologies oftheTemporal Bone
5.3.1 Introduction
Infectious and inammatory 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 inammatory 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 sufcient for diagnosis. Imaging is necessary for complications [17].
Imaging ndings may range from fatty tissue inltration, 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 inltration 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].
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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, signicant 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 andMastoiditis
Acute otitis media is the most common local infection in children under 5years 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 inamma­tion 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 opaci­cation, 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, decalcication, 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
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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 calcic 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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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 opacications 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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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 signi­cant destruction of the mastoid bone. (b) On diffusion-weighted axial MRI, the lesion is bright. (c) On an apparent diffusion coefcient map, the lesion is hypointense. (d) The apparent diffusion coefcient 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 inam­mation, 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 signicant contrast enhancement in the contrast-enhanced image
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Fig. 5.13 Labyrinthitis on magnetic resonance imaging. (a) Signicant 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 signicant contrast enhancement in the cochlea, vestibule, and semicircular canals (arrows)
ossication phase, referred to as labyrinthitis ossicans. In the late phase, patho­logic ossication 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 inammation 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 opacication 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 andVestibular 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 inammatory 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 inammatory 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 specic 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
andDiagnosis
5.4.1 Introduction
Temporal bone tumors, although rare, encompass a diverse spectrum of benign and malignant neoplasms that can pose signicant 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 ofTemporal Bone Tumors
Temporal bone tumors are classied 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 inltrate 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 neurobromatosis 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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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 Neurobromatosis 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. (df) Sporadic vestibular schwannomas are indicated by arrows in different patients