Учебники / Otolaryngology - Basic Science and Clinical Review

with chronic otitis media, the mastoid never pneumatizes. The long-standing eustachian tube obstruction that leads to the development of cholesteatoma is invariably associated with a sclerotic or nonpneumatized mastoid; it is possible but rare to find a patient with cholesteatoma and a well-pneumatized mastoid bone. True mastoiditis is due to a bacterial infection, and the diagnosis should not be made on CT in the absence of the characteristic clinical features. Initially, mastoiditis is seen as varying degrees of mastoid air cell opacification, often with air/fluid levels, and at this point is radiographically indistinguishable from eustachian tube dysfunction. Mastoiditis can be complicated by loss of septations due to necrosis (osteomyelitis), with coalescence of air cells (coalescent mastoiditis), and eventual cortical destruction.

TEMPORAL BONE TRAUMA

Temporal bone fracture usually occurs in the setting of severe head trauma, and neurological injury must be assessed first, preferably with MRI. Radiographic evaluation of temporal bone fracture and ossicular disruption requires the use of CT. If a fracture is found to extend into the petrous carotid canal, MRA or catheter angiography must be performed to exclude dissection and pseudoaneurysm. If a sensorineural hearing loss is diagnosed and the CT is normal, then an MRI could be performed to detect hemorrhage into the membranous labyrinth, identified as high signal on the noncontrast T1W scan.

Most fractures of the temporal bone (70–90%) are oriented along the long axis of the petrous bone and are referred to as longitudinal fractures (Fig. 36-7). Approximately 10 to 20% of longitudinal fractures will involve the facial nerve; many will involve the ossicular chain. Less common is the transverse fracture, oriented perpendicular to the long axis of the petrous bone, half of which will have facial nerve involvement (Fig. 36-8). Many temporal bone fractures will be “mixed.” Regardless of fracture orientation, the images must be fully assessed for location and extent of injury.True fractures must be distinguished from normal structures that can simulate bone disruption, such as the petromastoid suture, subarcuate canal, cochlear and vestibular aqueducts, posterior ampullary canal, mastoid canaliculus, and inferior tympanic canaliculus.

When conductive hearing loss is diagnosed in the setting of head trauma, disruption of the ossicular chain or oval window has occurred.The least stable ossicle is the incus, which lacks significant attachments. Incudostapedial dislocation is most commonly encountered.

Figure 36-7 Longitudinal temporal bone fracture, axial computed tomography. A fracture line traverses the temporal bone, running parallel to the long axis of the bone (black arrows).The facial nerve was uninvolved, but the malleoincudal articulation was dislocated (not shown).However,note the abnormal configuration of the ossicular chain in the mesotympanum (white arrows).

Pneumolabyrinth (air in the membranous labyrinth) generally indicates fracture of the oval window. Fluid in the middle ear may, in the appropriate clinical setting, indicate the presence of a perilymphatic fistula. Penetrating EAC injuries (such as Q-Tip injuries) can result in

Figure 36-8 Transverse temporal bone fracture, axial computed tomography. A fracture line traverses the temporal bone,running perpendicular to the long axis of the bone (black arrows).The fracture traverses the vestibule (v) and extends into the geniculate ganglion (arrowhead).

protrusion of the stapes footplate and crura into the vestibule.

VASCULAR LESIONS

Evaluation of vascular masses behind an intact TM invokes a specific differential diagnosis that can often be resolved with appropriate imaging studies. When a middle ear lesion is found on otoscopy, the evaluation should begin with CT. Most of the time, the noncontrast examination will differentiate between an aberrant carotid canal or carotid artery aneurysm, large dehiscent jugular bulb with or without a diverticulum, and a glomus tympanicum tumor. If the noncontrast study is unclear, intravenous contrast injection may be useful to confirm or exclude carotid or jugular origin of the lesion by demonstrating enhancement equivalent to that of blood pool.A glomus tumor will enhance less than blood pool on immediate postcontrast images, and more than inflammatory disease. MRI/MRA may be useful, but they are subject to the limitations mentioned earlier. Location of a discrete mass along the medial wall of the middle ear cavity suggests a glomus tympanicum. A large glomus tympanicum bulges laterally against the TM and is associated with a surprising lack of ossicular erosion for its size (Fig. 36-9). Integrity of the osseous skull base is critical in determining extratympanic spread of a glomus tympanicum and in making the diagnosis of glomus jugulare. An irregular

Figure 36-9 Glomus tympanicum, axial computed tomography.A bilobed, smooth, well-circumscribed mass is seen along the medial wall of the middle ear, in the hypotympanum (asterisk).The adjacent bone is intact.

lytic, permeative, and often subtle destructive pattern of bone involvement will be seen. If bone involvement is found in a patient with glomus tympanicum and early jugular bulb invasion has occurred, the MRI will be negative. In this situation, a postcontrast CT scan will demonstrate a filling defect in the jugular bulb representing the tumor nodule.

Subjective tinnitus with a normal middle ear exam poses a different clinical problem.An MRI is the imaging modality of choice to evaluate the posterior fossa and skull base to exclude neoplasm and vascular lesions such as aneurysm, arteriovenous malformation (AVM), and dural arteriovenous fistula (AVF). If the MRI is completely normal, the MRA will invariably be negative as well. Dural arteriovenous fistulas can go undetected on all cross-sectional imaging studies including MRA, and conventional angiography is necessary to confirm this diagnosis. However, without venous hypertension or parenchymal varices, both of which would be detected on MRI, a dural AVF is unlikely to bleed. Glomus jugulare tumors large enough to produce tinnitus will be well delineated on MRI (Fig. 36-10).These chemodectomas have a characteristic hyperintense, speckled appearance on T2W MRI and demonstrate marked contrast enhancement. MRA will delineate many but not all of the arterial feeders. If surgery is selected for treatment, catheter angiography will be necessary for vascular mapping and preoperative embolization.

PETROUS APEX

Lesions of the petrous apex raise yet another differential diagnosis. Both CT and MRI are usually indicated for complete evaluation: the CT defines the character of bony involvement, and the MRI defines the character of the lesion contents.

Petrous apicitis (including Gradenigo’s syndrome) is characterized by the presence of a pneumatized but opacified petrous apex, with identification of preserved septations on CT; as the infection progresses, cortical and septal destruction can occur, representing osteomyelitis. High signal intensity will be noted on the T2W MRI with enhancement on the postcontrast T1W images. Outlet obstruction of petrous air cells can result in a petrous apex mucocele. This is a smooth expansile lesion with a thin bony rim. A mucocele can demonstrate either low or high signal intensity onT1W MRI and is generally high in signal intensity on T2W images. The pattern of signal intensity reflects the degree of hydration and protein content of the mucocele. Cholesterol granulomas (Fig. 36-11) may occur in the petrous apex and can be identical to mucoceles on CT.

A

C

Figure 36-10 Glomus jugulare. (A) AxialT2-weighted magnetic resonance imaging (MRI). A lobulated hyperintense mass is seen in the right skull base,centered at the jugular bulb (white arrows). Numerous rounded and linear low-signal foci represent flowing blood in the feeding vessels (black arrows).Anterior and inferior extension has obstructed the eustachian tube, and high-signal fluid has accumulated in the mastoid air cells (white arrowhead). C, cerebellum; M, medulla; L, longus colli muscle; p, torus tubarius and palatine musculature. (B) Sagittal T1-weighted MRI with contrast. The lesion enhances densely with gadolinium. Posterior fossa extension is well seen in this projection (arrowheads). Notice that the vessels

Both lesions are sharply circumscribed and smoothly expansile. Cholesterol granulomas may be larger and more irregular in shape.The characteristic MRI feature of cholesterol granuloma is high signal intensity (homogeneous or heterogeneous) on the T1W sequence due to the presence of hemoglobin degradation products and cholesterol debris. These lesions are hyperintense

B

D

maintain flow voids (arrows) despite contrast administration. (C) Magnetic resonance angiography of the neck,time-of-flight technique, oblique projection. The ascending pharyngeal artery is enlarged (arrowhead). A tangle of tumoral vessels is identified (arrows). C,internal carotid artery;M,internal maxillary artery.(D) Magnetic resonance angiography of the neck and skull base, time-of-flight technique, axial compression image. There is no flow in the right transverse and sigmoid sinuses and jugular bulb due to the glomus tumor.Note the normal venous drainage on the left side (solid arrows). V, vertebral arteries; open arrows, overlap of the cervical carotid arterial system and tumor.

on T2W MRI and do not enhance after contrast injection. Congenital cholesteatomas (epidermoid cyst) can arise in the petrous apex and are lytic on CT, with sharply defined margins. On MRI, these lesions are low in signal on T1W and high in signal on T2W sequences. They may therefore appear purely cystic or have some degree of increased T1 signal intensity compared with

A

Figure 36-11 Cholesterol granuloma. (A) Axial computed tomography (CT). (B) Sagittal T1-weighted magnetic resonance imaging (MRI).There is a well-circumscribed rounded lesion in the right petrous apex (asterisk). The thin but intact cortical margin on CT (arrows) indicates the slow expansile character of the lesion that allows

CSF. Aneurysms of the petrous carotid artery are rare. Fusiform dilation of the carotid canal will be present. If patent, flow characteristics will be visible on MRA; if thrombosed, clot will be identified on MRI, with stenosis or occlusion on MRA. Primary and metastatic bone lesions may also involve the petrous apex.These will be seen as irregular destructive lesions with ill-defined margins on CT. MRI will confirm the cellular nature of the lesion: hypointense to isointense onT1W and isointense to hyperintense on T2W sequences, with varying degrees of contrast enhancement.

CEREBELLOPONTINE ANGLE

Acoustic neuroma (vestibular schwannoma) is the most common lesion of the CPA. These lesions may be entirely intracanalicular or both intracanalicular and cisternal (Fig. 36-12). MRI is the imaging modality of choice to evaluate these tumors, clearly delineating the location and extent of disease. The typical acoustic neuroma is isointense on both T1W and T2W MRI sequences, and enhances densely following contrast administration.When the cisternal component is larger than 2 to 3 cm, intratumoral cystic areas can be seen; arachnoid cysts may be found at the periphery of large acoustic neuromas. In patients who are unable to undergo MRI, CT of the posterior fossa with contrast injection can be performed. Small intracanalicular

B

the bone to remodel as it enlarges.This type of expansion can displace and distort the carotid canal without eroding into it.High-signal intensity on the noncontrast T1-weighted MRI represents hemorrhagic degradation products and cholesterol crystals, and is the most characteristic imaging feature of this lesion.C,petrous carotid canal;E,external auditory canal.

Figure 36-12 Acoustic neuroma. Axial T1-weighted magnetic resonance imaging following intravenous contrast injection.There is a bulky, enhancing mass lesion (asterisk) in the right cerebellopontine angle (CPA), internal auditory canal (IAC), and a widened porus acusticus (arrows). It extends 1 cm into the IAC; the 3 cm cisternal component has compressed the pons (P), brachium pontis or middle cerebellar peduncle (B), and cerebellar hemisphere (C) with partial effacement and distortion of the fourth ventricle (arrowhead). The lesion makes an acute angle with the petrous bone (curved arrow). Note the normal IAC and porus on the left side (double arrows).

Figure 36-13 Meningioma.Axial T1-weighted magnetic resonance imaging following intravenous contrast injection. There is a broad, flat, enhancing lesion in the posterior fossa centered at the clivus and posterior petrous bone (asterisk). The mass occupies the prepontine cistern, compressing the pons (P), and partially encasing the basilar artery (arrowhead). It extends into the left cerebellopontine angle and internal auditory canal (arrow) but does not widen the porus acusticus. The lesion makes an obtuse angle with the petrous bone (curved arrow).

tumors will be missed; bony erosion, however, will be readily detected.A cisternal component larger than 3 to 4 mm will be seen on a high-quality CT performed with contrast administration. Far less common than acoustic neuroma, but the second most common CPA mass, is the meningioma (Fig. 36-13).These tumors are benign, arise from the leptomeninges, and will therefore be broad based along the posterior wall of the petrous bone. A rim of dural enhancement frequently surrounds a meningioma and is called the “dural tail” sign. This finding is suggestive of meningioma, but it can be seen in association with other lesions as well. At the margin of a meningioma, an obtuse angle is characteristically formed between tumor and petrous bone, whereas an acoustic neuroma makes an acute angle as it balloons out of the IAC. Meningiomas can extend into the IAC and mimic schwannoma.

Arachnoid and epidermoid cysts are occasionally found in the CPA. Arachnoid cysts form within the leaves of the arachnoid membrane and are similar in density and signal intensity to CSF, and do not enhance with contrast. An epidermoid cyst can be similar in appearance to an arachnoid cyst. Epidermoid cysts exhibit high signal on the diffusion-weighted sequence, while arachnoid cysts are low in signal. The epidermoid cyst grows along paths of least

resistance, insinuating around and between various structures in the subarachnoid space. An arachnoid cyst will displace structures as it enlarges.

CONGENITAL MALFORMATIONS

A complete discussion of congenital anomalies is well beyond the scope of this chapter. Here we will consider two abnormalities most frequently encountered: microtia with aural atresia, and the Mondini’s malformation.

Microtia is frequently associated with external canal stenosis or atresia as well as a spectrum of anomalies involving the ossicular chain and facial nerve canal. A CT examination of the temporal bone is indicated if and when surgical correction of the conductive hearing loss is planned. The thickness of the atresia plate, degree of EAC stenosis, and fibrous content of a stenotic canal will be clearly delineated. The middle ear cavity will often be narrow, and there is usually some abnormality of the ossicular chain. Most commonly seen is clumping of the malleus and incus into an amorphous mass that is then fused to the atresia plate (Figs. 36-4 and 36-14). The course of the posterior tympanic facial nerve canal, the posterior genu, and

Figure 36-14 Microtia and aural atresia, coronal computed tomography posterior to Fig 36-9.The short incudal process is seen on this posterior slice.The facial nerve is aberrant with the descending segment (open arrow), located at the anterior rim of the lateral semicircular canal (L) rather than the tympanic segment.The crista falciformis is well delineated in A (black arrow). C, basal turn cochlea; S, superior semicircular canal.

Figure 36-15 Mondini malformation.Axial computed tomography. The cochlea (c) is dysplastic.There is no septation between the apical and middle turns,so that they appear as a single sac.The basal turn was completely normal on an inferior slice (not shown). The vestibule is slightly large (V), and the vestibular aqueduct is dilated (arrows).The internal auditory canal (asterisk), semicircular canals, and middle ear structures are normal.

the descending canal is frequently abnormal, with a foreshortened tympanic segment, anterior location of the genu, and a short, anteriorly angulated mastoid segment.

The Mondini’s malformation is a common anomaly of the cochlea, due to an interruption of the developmental sequence at 7 weeks of gestation. At this point, the cochlea has elongated to produce 11⁄2 turns: the basal turn is fully formed, but the separation between the middle and apical turns has not yet occurred. Therefore, the Mondini’s malformation is characterized by incomplete septation of the middle and apical cochlear turns. The CT scan confirms the presence of a normal basal turn and round window.The middle and apical turns are seen as a single sac without the intervening osseous spiral lamina (Fig. 36-15).The original description of this entity by Mondini included dilation of the vestibular aqueduct; in practice, this anomaly may or not be associated.

SUMMARY

Interpretation of temporal bone imaging studies is complex, requiring the integration and triangulation of many facts and findings. The key to understanding temporal bone imaging lies in realizing the strengths

TABLE 36-1 COMPARISON OF COMPUTED TOMOGRAPHY

AND MAGNETIC RESONANCE IMAGING FOR

TEMPORAL BONE IMAGING

*Bold lettering indicates the preferred modality.

CPA, cerebellopontine angle; CT, computed tomography; MRI, magnetic resonance imaging.

and limitations of each imaging modality; that is, understanding what structures may or may not be delineated, and what questions may or may not be answered. Beginning a radiographic evaluation with a definite or proposed clinical diagnosis is extremely useful and can be used to direct the initial examination (Table 36-1). Using this method, 80 to 90% of single modality studies will be diagnostic, necessitating a second study in the minority of cases.

SUGGESTED READINGS

Jackler RK, LuxfordWM, HouseWF. Congenital malformations of the inner ear: a classification based on embryogenesis. Laryngoscope 1987;97(suppl 40):2–24

Mayer TE, Brueckmann H, Siegert R, Witt A, Weerda H. Highresolution CT of the temporal bone in dysplasia of the auricle and external auditory canal. AJNR Am J Neuroradiol 1997;18:53–65

Osborn AG. Brain tumors and tumor like masses: cerebellopontine angle masses, internal auditory canal and temporal bone masses. In: Osborn AG, ed. Diagnostic Neuroradiology. St. Louis: MosbyYearbook; 1994:437–450

Swartz JD, Harnsberger HR. Imaging of theTemporal Bone.3rd ed. NewYork:Thieme Medical Publishers; 1998

Valvassori GE, Buckingham RA. Radiology of the temporal bone. In:Valvassori GE, Buckingham RA, Carter BL, Hanafee WN, Mafee MF, eds. Head and Neck Imaging. New York: Thieme Medical Publishers;1988:1–8

Weissman JL. Hearing loss. Radiology 1996;199:593–611

SELF-TEST QUESTIONS

For each question select the correct answer from the lettered alternatives that follow.To check your answers, see Answers to Self-Tests on page 716.

1.For evaluation of tinnitus, the optimal imaging modality is

A.Computed tomographic (CT) scan with intravenous (IV) contrast

B.Positron emission tomographic (PET) scanning

C.Angiography

D.T2-weighted magnetic resonance imaging (MRI)

E.MRI with IV contrast

2.Petrous apex lesions include cholesterol granulomas, cholesteatomas, and mucoceles. These lesions are optimally evaluated with

A.T2-weighted MRI

B.MRI with IV contrast

C.CT scan

D.Combination of plain CT and MRI with IV contrast

3.Temporal bone trauma causing facial nerve paralysis is best evaluated by

A.Surgical exploration

B.CT scan with IV contrast

C.MRI

D.CT scan without contrast high resolution