Imaging of the Cerebellopontine Angle

21

Outline Technical Considerations Classifications and Incidence of Cerebellopontine Angle Tumors Vestibular Schwannoma Meningioma and Simulants Epidermoid and Other Cysts

Chapter

Imaging of the Cerebellopontine Angle

Nonvestibular Posterior Fossa Schwannomas Vascular Lesions Extradural Lesions Intra-axial Tumors Intracanalicular Lesions Conclusion

TECHNICAL CONSIDERATIONS Modern imaging techniques for the cerebellopontine angle (CPA) and internal auditory canal (IAC) consist principally of magnetic resonance imaging (MRI) and computed tomography (CT). Angiography is occasionally employed when evaluating vascular lesions.1 Because of its superior soft tissue contrast, multiplanar capability, and lack of ionizing radiation, MRI holds a substantial advantage over CT in imaging the CPA.2 Furthermore, with paramagnetic contrast enhancement, MRI has become the unquestioned method of choice for visualization of small acoustic tumors.3 The frequent untoward reactions to intravenous (IV) iodinated contrast material for CT are obviated. Furthermore, recently developed heavily T2-weighted, submillimeter thinsection, spin-echo or gradient-echo images exquisitely outline cisternal nerves and vessels better than gas CTcisternography, and the otic labyrinth as well as or better than high-resolution CT.4–7 This chapter therefore focuses primarily on MRI. CT remains useful in special situations, for example, when MRI is not available, when patients are too claustrophobic or too large to be accommodated in the scanner, when visualization of calcium or bone changes is important,8 or when acute hemorrhage is in question.9,10 Although a detailed discussion of the technical aspects of MRI is beyond the scope of this chapter, a general understanding of the capabilities and limitation of the technique will greatly assist the clinician in effectively using MRI for investigation of the CPA or the IAC. Although not all CPA symptoms are caused by tumors, the principal concern raised is usually the presence or absence of a tumor. Because most of the tumors in the CPA are intradural extra-axial (outside the brain) and partly outlined by cerebrospinal fluid (CSF) and because T2-weighted images (T2WI) superbly outline nerves and

William W. M. Lo, MD Michael M. Hovsepian, MD

brain tissue against CSF, noncontrast, heavily T2-weighted, submillimeter thin-section images have been recommended for low-cost screening for acoustic tumors.11 Such images may be obtained by fast spin-echo (FSE) or by gradient-echo technique (constructive interference steady state, or CISS). Normal structures as demonstrated by CISS images are illustrated in Figure 21-1.4–7 However, gadolinium chelates as paramagnetic contrast agents administered intravenously, markedly enhance the signal intensity of most tumors, as well as inflammatory lesions on T1WI, and aid in characterization and differential diagnosis of lesions. Thus, contrast-enhanced T1WI is nearly always used for detection or evaluation of CPA and IAC tumors, in a comprehensive study.3,12–15 Normal T1WI are illustrated in Figure 21-2.16,17 Although T2WI add little to the detection of extra-axial tumors, they are useful in assisting characterization of tumors (e.g., in meningioma, lipoma, peritumoral cysts, peritumoral edema, hemorrhage, etc.). They are also more sensitive than T1WI for detection of intra-axial lesions (inside the brain) that can produce acoustic symptoms, such as occur in multiple sclerosis, infarct, and edema, as well as in hemosiderin deposition in superficial siderosis.18 Thus, a comprehensive study of the CPA would typically include T1WI in thin sections through the posterior fossa and IAC before and after the administration of gadolinium chelates, and T2WI in thicker sections to survey the brain. Under some circumstances, modified or additional techniques may be employed. For example, in neurofibromatosis 2 (NF2),19,20 in which multiple intracranial schwannomas and meningiomas, and spinal schwannomas, meningiomas, and ependymomas are often present, postcontrast T1-weighted surveys that include the entire head and spine may be desirable.19,21–22 When vascular lesions such as aneurysm, arteriovenous malformation (AVM), or vertebrobasilar dolichoectasia (VBD) are encountered or 349

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C

4

V

P

1 5

C sc

a

v

L

P IV

3 sc

F 2

B IV

A

B P

C sc

mp C v

IV

a IAC ce

P

C

ce

D

Figure 21-1. Normal structures in IAC on CISS images (A-C). A, CISS axial 0.8 mm through the superior aspect of the IAC demonstrating the parallel course of the facial nerve (1) anterior to the superior vestibular nerve (3). B, inferior aspect of the IAC where the divergent relationship or Y-shaped configuration of the cochlear nerve (4) anterior to the inferior vestibular nerve (5) is depicted. C, a prominent AICA loop is seen within the proximal IAC. D, T2W axial FSE 5.5 mm of posterior fossa. 1, facial nerve; 2, vestibulocochlear nerve; 3, superior vestibular nerve; 4, cochlear nerve; 5, inferior vestibular nerve; IV, fourth ventricle; a, AICA; B, basilar artery; C, cochlea; ce, cerebellar hemisphere; F, flocculus; L, lateral recess of the fourth ventricle; mp, middle cerebellar peduncle; P, pons; sc, semicircular canals; v, vestibule.

suspected, MR angiography may be added (Fig. 21-3).23 When confirmation of lipoma or fat, including operatively placed fat, is desired, a fat suppression technique may be invoked.24 Obviously, the desire for completeness and quality must be balanced against the constraints of time, cost, throughput, and patient tolerance. For practical purposes, a comprehensive study probably should not exceed half an hour per patient. A noncontrast, heavily T2-weighted, thin-section survey specifically used for screening for acoustic tumors may be accomplished in less than 15 minutes at considerably lower cost. Such a study, however, carries the disadvantage of not being able to differentiate lipomas or melanotic melanoma,25 which are hyperintense on preconstrast T1WI, from schwannomas, which are

isointense or mildly hypointense on precontrast images. Furthermore, multiple sclerosis (Fig. 21-4) or superficial siderosis (Fig. 21-5) may be completely missed, should either be present. A fat-suppressed postcontrast sequence is generally necessary for evaluation of postoperative recurrence.3 A precontrast T1-weighted sequence is necessary for evaluation of paragangliomas, which may become nearly isointense with bone marrow on postcontrast images (Fig. 21-6). Thus, each institution or facility must devise protocols best suited to its own needs or practice and adapt to new technical developments that emerge. Our current protocol is offered as an example in Table 21-1. Although one study showed that 5-mm sections compared favorably with 3-mm sections in detection of

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A

C

351

B

D

Figure 21-2. Normal structures in CPA. (A–H), Postcontrast T1WI (Gd-T1WI) overlapping 3-mm sections centered every 1.8 mm. A, Midpons. Dominant structure is pons itself (P) surrounded by prepontine cistern anteriorly, CPA cisterns bilaterally, and fourth ventricle (IV ) posteriorly, and connected to cerebellar hemispheres (CH) posterolaterally by middle cerebellar peduncles (mp). Trigeminal nerves traverse CPA cistern to enter Meckel cave (mc in B–E) inferior to attachment of tentorium cerebelli (TC). Basilar artery (B) ascends anterior to pons. B, Mid-lower pons. Contrast-enhanced choroid plexus (ch) is seen on roof of fourth ventricle (IV). Lateral recess (I) of the fourth ventricle leads toward foramen Luschka (black arrow in D). Meckel cave (mc) filled with CSF lies adjacent to contrast-enhanced cavernous sinus (CS). C, Lower pons. Facial (7) and acoustic (8) nerves traverse cistern toward IAC in close relationship to loop of anterior inferior cerebellar artery (a). Cochlear nuclei are located immediately anterior to lateral recess (I). Rostral ends of cerebellar tonsils (t) are seen flanking caudal end of inferior vermis (vr). Inferior petrosal sinus (IP) communicates with cavernous sinus (CS). Petrous apex (pa) is filled with hyperintense fatty marrow. D and E, Pontomedullary junction. Belly of pons (P) extends far anteriorly beyond medulla (M). Posterior to medulla is foramen of Majendie (white arrow) opening to vallecula (long white arrow) between the tonsils (t). Lateral recess is flanked by inferior cerebellar peduncle (ip) anteriorly and contrast-enhanced choroid plexus (ch) posteriorly. The latter protrudes into CPA cistern through foramen of Luschka (short black arrow) posterior to acoustic nerve (8) and inferior to flocculus (f in C). Continued

acoustic tumors,26 most facilities use the thinnest sections practicable for imaging of the IAC whenever permitted by the capability of their equipment, most commonly 2- to 3-mm sections,3,27 because intracanalicular tumors are often only a few millimeters in diameter and may be suboptimally visualized or even obscured by partial volume effect in thicker sections. The interslice gap also differs, from varying degrees of overlap up to perhaps 20% gaps. A minimum qualitative standard, which perhaps should be insisted on, is that the facioacoustic nerves through their cisternal and canalicular portions be recognizable bilaterally, either on T1WI or T2WI (see Figs. 21-1 and 21-2). An unfocused study of the brain with 5-mm or thicker sections is inadequate for imaging the IAC.

Images in a second orthogonal plane should be obtained when a tumor is encountered20 to demonstrate the relationship of tumor to the tentorium and the jugular fossa, and when volumetric measurements are desired. Gadolinium contrast agent should be routinely used in comprehensive studies because it markedly improves visualization of small tumors, permits identification of residual or recurrent tumor, and adds precision to the delineation of tumor in the IAC (Fig. 21-7).3 There are only a few contraindications to its use, and side effects rarely occur. Furthermore, gadolinium chelate enhancement confirms labyrinthitis28 and reveals nondestructive intralabyrinthine schwannomas.29,30 Numerous studies have been performed to identify the potential biologic effects of MRI, but none of them have

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E

F

G

H

Figure 21-2, cont’d. Facial nerve (7 ) and superior vestibular division of acoustic nerve (8) extend into labyrinthine facial nerve canal (7l ) and vestibule (v), respectively, in D; and cochlear and inferior vestibular divisions of acoustic nerve (8), respectively, into cochlea (c) and vestibule (v) in E. Geniculate ganglion (7g) and tympanic segment (7t) of facial nerve show normal contrast enhancement. Abducens nerve (6) crosses cistern to enter cavernous sinus (CS). Mastoid segment (7m) of facial nerve is at times paralleled by a fatty collection posteriorly (also in F, G, and H) F and G, Upper medulla. Glossopharyngeal and vagus nerves (9–10) extending from lateral medulla toward jugular foramen are difficult to separate from each other. Greater superficial petrosal nerve (gsp) extends from geniculate ganglion (7g in E) anteromedially on floor of middle fossa. Cranial opening of cochlear aqueduct (ca) closely overlies pars nervosa of jugular foramen (not well shown). H, Lower medulla. Spinal accessary nerve (11) ascending toward jugular foramen is also difficult to distinguish from glossopharyngeal and vagus (9–10 in F and G). Rootlets of hypoglossal nerve extend from preolivary sulcus anteriorly toward hypoglossal canal inferior to jugular tubercle (jt), which is separated from petrous apex (pa) by petro-occipital fissure (pof). Posterior inferior cerebellar artery (p) arises from vertebral artery (V). Artifact from flow is seen streaking between sigmoid sinuses (S ). Carotid artery (C), jugular vein (J ), tympanic cavity (T ), and external auditory canal (E ) are all signal-free.

A

B

Figure 21-3. Vertebrobasilar dolichoectasia. A, Axial Gd-T1WI. Tortuous left vertebrobasilar artery (long arrow) crosses left to right anterior to pons. Small arterial branch (open arrow) coursing toward left CPA probably represents left AICA. Note normal enhancement of geniculate ganglion and proximal tympanic facial nerve and posterior fossa veins (small arrows). Serration across cerebellum between sigmoid sinuses is caused by pulsating flow of blood in sigmoid sinuses. B, Coronal MR angiography. 3-D time-of-flight technique, maximum intensity projection. Same vertebrobasilar artery (long arrow) and probable left AICA (open arrow) as in A. Superior cerebellar and posterior cerebral arteries and right posterior inferior cerebellar artery (small arrows) are also seen. No contrast injection is necessary for MRA.

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B

Figure 21-4. Multiple sclerosis. A, T1WI. Subtle pontine lesion (arrowhead) shows easily overlooked minimal hypointensity. B, T2WI. Hyperintensity of lesion is obvious.

A

B

Figure 21-5. Superficial siderosis. Patient has bilateral progressive sensorineural hearing loss several years after surgical resection of left inferior frontal arteriovenous malformation. A, T1WI. No abnormality is apparent. B, T2WI. Thin layer of hypointensity from pial and subpial deposition of hemosiderin is visible on pons, cerebellum, and acoustic nerves (arrows). (Compare with Fig. 21-1). Thin layer of hypointensity is also present on inferior surfaces of cerebral hemisphere (not illustrated). Hypointensity of dentate nuclei may be physiologic.

A

B

Figure 21-6. Jugular paraganglioma (glomus jugulare tumor) with PF extension. A, T1WI. B, Gd-T1WI. Note loss of natural contrast between tumor and clivus marrow after Gd-DTPA and importance of precontrast images to serve as baseline. Tumor circumferentially narrows intrapetrous carotid (open arrow) and extends to protympanum (short arrow) to surround cochlea (arrow). Note dural tails (long thin arrows) and arterial branch (arrowhead) supplying tumor. (Compare with Fig. 21-28).

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TABLE 21-1. Sample Magnetic Resonance Protocol for Comprehensive Study of Cerebellopontine Angle/Internal Auditory Canal Axial survey of brain: T2WI, 5.5-mm thickness Axial posterior fossa detail: T1WI precontrast, 2.0-mm thickness Axial submillimeter posterior fossa detail: CISS, 0.8-mm thickness Axial survey of brain: DWI, 5.0-mm thickness Axial posterior fossa detail: T1WI post-Gd FS 2.0-mm thickness Coronal posterior fossa detail: T1WI post-Gd FS, 2.0-mm thickness If postoperative patient: Pre-Gd T1WI, FS, 2.0-mm thickness For NF2: include post-Gd T1WI axial and coronal whole brain, 5.5-mm thickness CISS, constructive interference steady state; DWI, diffusion-weighted images; FS, fatsuppressed; Gd, gadolinium chelate; NF2, neurofibromatosis 2; T1WI, T1-weighted images; T2WI, T2-weighted images.

determined any significant hazards.31,32 More directly related to otologic interest is acoustic noise produced by the activation and deactivation of the gradient magnetic filed.33,34 Reversible hearing loss may be induced by such noises.35 Disposable ear plugs or other noise reduction devices should be routinely used.31 Certain prosthetic implants and metallic materials are associated with potential hazards. Examples are cardiac pacemakers, ferromagnetic cerebrovascular aneurysm clips, and intraocular ferromagnetic foreign bodies.31 High-field MRI is strictly contraindicated for patients with cochlear implants,31,36 although low-field scanners may be safe. Stapes prostheses are safe for MRI with the exception of the Richards-McGee platinum-stainless steel piston manufactured in a relatively small quantity and only for a brief period after mid-1987, using C17NI4 stainless steel instead of the more common 316L stainless steel.37 Eyelid springs used for patients with facial nerve palsy have shown deflection in vitro but no significant ill effects in vivo.

A

CLASSIFICATIONS AND INCIDENCE OF CEREBELLOPONTINE ANGLE TUMORS Approximately 10% of intracranial tumors originate in the CPA.38 Most of them arise from the cranial nerve sheath, the meninges, the blood vessels, and the congenital rests located in the extra-axial compartment. Some arise from the petrous bone or the jugular foramen and are extradural in origin but intrude into the CPA. A few are exophytic growths of intra-axial lesions arising from the brain. Lesions in the CPA are extremely diverse. Provided in Table 21-2 for reference are the lesion types and numbers from three major series.39–41 The Brackmann series represents material from a neurotologic practice, excluding paragangliomas. Although the percentages differ, all three series show acoustic or vestibular schwannoma (VS), as by far the most common, comprising some 60% to 90% of all CPA lesions. The three series also agree that the distant second, third, and fourth most common tumors by narrow margins are meningioma, congenital intradural epidermoid tumor or cyst, and nonacoustic posterior fossa schwannomas, respectively. These four common tumor types account for about 75% to 98% of all CPA mass lesions. Beyond the four most common tumors, the types of mass lesions in the CPA are extremely diverse and numerous (see Table 21-2). The Revilla series of 205 CPA lesions includes 1 primary melanoma, 1 paraganglioma, and 13 cerebellar and petrous bone tumors infiltrating the CPA.40 The Brackmann series of 1354 CPA tumors includes 7 arachnoid cysts, 4 hemangiomas, 1 hemangioblastoma, 2 astrocytomas, 2 medulloblastomas, 3 metastatic tumors, 2 dermoids, 2 lipomas, 1 malignant teratoma, and 1 chondrosarcoma.39 The series of 455 CPA lesions of Valavanis41 includes among primary tumors, 1 melanoma and 3 hemangiomas; among secondary tumors, 47 paragangliomas, 1 ceruminoma, 2 chondrosarcoma, 8 chordoma, and 6 extensions of cerebellar and petrous bone

B

Figure 21-7. Intracanalicular vestibular schwannoma. A, T1WI. Typical small tumor isointense with brain without enlargement of IAC (arrow). Such a tumor may be isointense with CSF and not apparent on T2WI. B, Gd-T1WI. Extent of tumor (filling fundus of IAC) is more fully and precisely demonstrated postcontrast. (Compare with Figs. 21-30, 21-42, 21-43, 21-44, 21-46, and 21-47.)

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TABLE 21-2. Classification and Frequency of CPA Lesions Revilla (1947) No. Primary Tumors of the CPA Acoustic schwannoma Meningioma Epidermoid Arachnoid cyst Schwannoma of the fifth, seventh, ninth, tenth, and eleventh nerves Primary melanoma Hemangioma Lipoma, dermoid, teratoma Secondary Tumors of the CPA Paraganglioma Ceruminoma Chondroma-chondrosarcoma Chordoma Extension of cerebellar and petrous bone tumors Metastases Vascular Lesions Aneurysm Arteriovenous malformation Vertebrobasilar dolichoectasia

%

Brackmann (1980) No.

%

Valavanis (1987) No.

%

154 13 13 — 10 1 — —

75.1 6.3 6.3 — 4.9 0.5 — —

1236 42 32 7 19 — 4 5

91.3 3.1 2.4 0.5 1.4 — 0.3 0.4

275 31 17 9 18 1 3 —

60.5 6.8 3.7 2.0 4.0 0.2 0.7 —

1 — — — 13 —

0.5 — — — 6.4 —

— — 1 — 5 3

— — 0.1 — 0.4 0.2

47 1 2 8 6 12

0.3 0.2 0.4 1.8 1.3 2.6

— — —

— — —

— — —

— — —

4 4 17

0.9 0.9 3.7

From Lo WWM: Tumors of the temporal bone and the cerebellopontine angle. In Som PM, Bergeron RT (eds.): Head and Neck Imaging, 2nd ed, St. Louis, Mosby-Year Book, 1991.

tumors; among vascular lesions, 4 aneurysms, 4 AVMs, and 17 VBDs; and 12 metastases. Other rare lesions not listed may also appear as mass lesions in the CPA, for example, lymphoma,42 hypertrophic pachymeningitis,43 syphilis, sarcoidosis,44,45 rhabdoid tumor,46 and so forth. (See also Chapter 49, Rare Tumors of the Cerebellopontine Angle.) Such a long list of possibilities makes differential diagnosis difficult. To simplify discussion in this chapter, the CPA lesions are grouped into eight categories (Table 21-3). Five extra-axial groups: (1) vestibular schwannoma, (2) meningioma and simulants, (3) epidermoid and other cysts (arachnoid, cysticercal, dermoid, etc.), (4) nonvestibular posterior fossa (PF) schwannomas (V, VII, IX, X, XI, XII), and (5) vascular lesions (VBD, aneurysm, AVM, superficial siderosis, etc.); two extradural groups: (6) bone lesions (benign or malignant, primary or metastatic) and (7) paraganglioma; and finally an intra-axial group including astrocytoma, ependymoma, papilloma, hemangioblastoma, metastasis, lymphoma, and so on. Such a categorization does not follow traditional classifications based on cell origin but is more conducive to differential diagnosis based on location and appearance of the lesions as revealed by imaging. (See also Chapter 49, Rare Tumors of the Cerebellopontine Angle.) Intracanalicular lesions with a slightly different differential diagnosis are also discussed.

VESTIBULAR SCHWANNOMA Commonly but incorrectly termed acoustic neuromas,19,20,38 VSs are by far the most common tumor in the CPA and the IAC.39–41 Most characteristically they arise in the IAC and enlarge into the CPA, with a rounded mass in the CPA and a cone-shaped stem in the IAC enlarging the porus acusticus (Fig. 21-8). Some tumors arise in the CPA and

appear as a rounded mass centered at the porus (Fig. 21-9). As VSs enlarge they often assume an ovoid configuration with their long axis parallel to the posterior petrous wall (Fig. 21-10). Intracanalicular VSs initially appear as small TABLE 21-3. Imaging Differential Diagnosis of CPA Lesions I. Extra-axial Lesions A. Vestibular schwannoma B. Meningioma and simulants Leptomeningeal metastases Primary meningeal lymphoma Primary meningeal melanoma Meningeal sarcoidosis Hypertrophic pachymeningitis C. Epidermoid and other cysts Arachnoid cyst Cysticercal cyst Epithelial cyst Neuroenteric cyst Craniopharyngioma Lipoma D. Nonvestibular PF schwannomas V, VII, IX, X, XI, XII E. Vascular lesions VBD Berry aneurysm Giant aneurysm Arteriovenous malformation Superficial siderosis

II. Extradural Lesions A. Bone lesions 1. Cysts, e.g., cholesterol cyst epidermoid cyst mucocele 2. Tumors, e.g., chordoma chondroma chondrosarcoma giant cell tumor myeloma metastases xanthoma B. Paraganglioma (glomus jugulare tumor) III. Intra-axial Lesions A. Brainstem tumor Astrocytoma Lymphoma Hemangioma B. Cerebellar tumor Astrocytoma Hemangioblastoma Metastases Lymphoma Hemangioma Medulloblastoma C. Fourth ventricular tumor Ependymoma Choroid plexus papilloma D. Nontumorous Infarct Multiple sclerosis

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B

Figure 21-8. Typical large IAC-CPA VS. Smoothly marginated tumor mushrooms out of IAC into CPA, causing funnel-shaped widening of the IAC and forming an extra-axial mass deforming the pons. A, T1WI. Tumor is nearly homogeneous, mildly hypointense to brain, and hyperintense to CSF. A vessel is seen trapped between the tumor and pons (arrow). B, Gd-T1WI. Marked contrast enhancement is typical of VSs. Intratumoral cystic components (arrow) are much more obvious than precontrast.

A

B

Figure 21-9. Medium-sized cisternal VS. Tumor is extra-axial, smoothly marginated, rounded, and centered to porus acusticus. A, T1WI. Tumor is mildly hypointense to brain, hyperintense to CSF, and slightly granular in texture. B, Gd-T1WI. Tumor shows marked nearly homogeneous enhancement postcontrast. (Compare with Fig. 21-27.)

A

B

Figure 21-10. Giant cisternal VS. Tumor is extra-axial, smoothly marginated, ovoid, centered over porus acusticus, and deforming pons, cerebellum, and fourth ventricle. A, T1WI. Tumor is mildly hypointense to brain and hyperintense of CSF and nearly homogeneous except for cystic component (arrowhead). Vessels are seen between tumor and brain (arrows). B, Gd-T1WI. Tumor shows marked contrast enhancement except for cystic component. Giant tumors are often entirely extracanalicular as in this case.

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B

Figure 21-11. Vestibular schwannoma with dural tail. A, T1WI. B, Gd-T1WI. Otherwise typical appearing IAC-CPA vestibular schwannoma shows enhancing dural tail (arrow) extending to posterior petrous surface. This finding was present in only 1 of 100 VSs in an unpublished series.

rounded masses and then become sausage-shaped as they grow to fill the canal (see Fig. 21-7). At times, intracanalicular VSs may be lobulated or globular and focally erode the canal. Schwannomas are typically isointense or mildly hypointense to brain on T1WI, enhance markedly on gadolinium, and are between brain and CSF in intensity

A

on T2WI (see Figs. 21-7 through 21-12). As a group, they enhance far more than any other benign extra-axial tumor, but sufficient overlap occurs among tumors of different types so that the degree of enhancement alone cannot always be relied on to differentiate the type of tumor.47 The enhancement may or may not be homogeneous because microcyctic and macrocystic components within

B

Figure 21-12. NF2. A, T1WI. B, Gd-T1WI. C, Sagittal Gd-T1WI. Patient has bilateral VSs (vertical arrows), bilateral trigeminal schwannomas (horizontal arrows), left facial schwannoma (open arrow), and left posterior fossa, falx, and parasagittal meningiomas (oblique arrows). Note also occlusion of left lateral sinus (blank arrow) and dural “tails” (long thin arrows).

C

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the tumor are common in schwannomas, reflecting the presence of Antoni type B tissue (see Figs. 21-8 and 21-10).1,38,48,49 Initially, nonenhancing microcystic components on a short sequence may attain enhancement in time as equilibration of contrast material in extracellular space takes place.1 Schwannomas may also be accompanied by one or more overlying arachnoid cysts (Fig. 21-13), and at times be dominated by one.50 Calcification is rarely present in schwannomas.41,49,51–54 Rarely, intratumoral hemorrhage may cause focal hyperintensity or hypointensity depending on the age of the hemorrhage.55–58 Even more rarely, subarachnoid hemorrhage may be the presenting symptom of a large VS.59,60 However, acute subarachnoid hemorrhage may not be apparent on MRI even when obvious on CT.10 CT is therefore indicated when the signs and symptoms suggest subarachnoid hemorrhage.14 A dural “tail” often observed in meningiomas (Figs. 21-12, 21-14, and 21-15), on rare occasions may be seen associated with a VS (see Fig. 21-11).61

A

C

Funnel-shaped enlargement of the IAC is common in VSs and rarely seen in other lesions (see Figs. 21-8 and 21-11).41,54 The incidence of hydrocephalus roughly correlates with tumor size. One report noted hydrocephalus in 17 of 44 patients in whom a tumor of 3 cm or larger was present.62 Rarely, a large VS compressing the brain may cause peritumoral edema.41 CT and MRI have been extremely useful in studying the natural history of VS. Many such studies have been published.63–73 Their methodologies may vary, but the results appear to concur that most tumors are stable or slowly growing (of the order of 2 mm or less a year) but some grow as much as 1 cm or more a year. These results appear to correlate with those revealed by monoclonal antibody studies.74 To establish the growth rate of a tumor, an initial follow-up study in perhaps 6 months may be done. If the tumor is found to be stable or very slow growing, subsequent follow-up studies then may be repeated at 1- to 2-year intervals. In postoperative studies for residual or recurrent tumor, precontrast and postcontrast studies at matching levels are

B

D

Figure 21-13. VS with arachnoid cysts. Tumor is extra-axial, slightly lobulated, centered over porus acusticus, and lies predominantly in CPA cistern with an overlying arachnoid cyst as large as the tumor itself laterally and a smaller arachnoid cyst medially. A, T1WI. Tumor is mildly hypointense to brain; arachnoid cysts (arrows) are isointense to CSF. B, Gd-T1WI. Tumor shows marked contrast enhancement, and arachnoid cysts (arrows) show no enhancement. C, T2WI. Tumor is slightly hypointense to CSF and slightly granular in texture. Arachnoid cysts (arrows) are isointense to CSF and homogeneous. D, Coronal Gd-T1WI. Tumor extends superiorly to undersurface of tentorium (down arrow) and inferiorly over contrast-enhanced sigmoid sinus (up arrow) medial to enhanced high jugular bulb (open arrow).

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A

B

C

D

359

Figure 21-14. CPA meningioma with classic features. A, T1WI. B, Gd-T1WI. C, T2WI. D, Coronal Gd-T1WI. Tumor is an extra-axial, hemispherical mass with its broad base against the posterior petrous wall, obtuse bone tumor angle, underlying focal hyperostosis (open arrow), central vascular pedicle (long thin arrow), and transincisural (arrowheads) and transtentorial (paired white arrows) middle fossa extensions. Tentorium is indicated by black arrows. Central hypointensity is consistent with fibrosis and calcification. Note dural tails (tandem arrowheads) in B.

A

B

Figure 21-15. En-plaque meningioma with transpetrous tumor in posterior and middle fossas. A, T1WI. B, Gd-T1WI. Tumor (arrows) is isointense and inconspicuous precontrast, but markedly hyperintense postcontrast. Note dural tail over clivus (arrowhead), tumor filling right Meckel’s cave in contrast to unfilled left Meckel’s cave (open arrow), and underlying focal hyperostosis (small arrows). Note also tentorial attachment (curved arrows). (Courtesy of James J. Hodge, MD)

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important for differentiation of surgically placed fat from tumor.75 Fat suppression technique should be used.24 After hearing-conservation techniques have been performed to remove small VSs, enhancement of varying degrees at the operative site is usually present.76 Serial follow-up studies are necessary to establish the presence or absence of tumors.77 After stereotactic radiosurgery, one series shows VSs often shrank (22%) but more commonly remained stable in size (73%) and rarely continued to grow (4%).78 The corresponding numbers for untreated tumors were 3%, 59%, and 38%, respectively.78 The majority (79%) of tumors after radiosurgery showed loss of central enhancement, which sometimes returned (Fig. 21-16). Some 5 to 15 months after treatment, 9% developed hyperintensity on T2WI in the adjacent pons and the cerebellar peduncle with associated contrast enhancement on T1WI suggestive of breakdown in the blood-brain barrier. Some of these changes resolved after months and were not necessarily associated with neurologic symptoms. Similarly, contrast enhancement was observed in the trigeminal nerve in some of the patients. Up to 10% of the patients developed hydrocephalus months after radiosurgery and required ventriculoperiotoneal shunts.78–80 Some tumors continued to grow and required reradiation or eventually surgical resection.79 The distinction of neurofibromatosis 1 (NF1) (von Recklinghausen’s disease) from NF2 (bilateral acoustic

A

neurofibromatosis), established by the National Institute of Health (NIH) Consensus Development Conference as separate disorders, represents a significant advance in the understanding and management of these disorders.19 Although both disorders are autosomal-dominant and may be inherited or acquired by mutation, they are associated with defects in different chromosomes.81,82 Because both disorders may have central nervous system (CNS) involvement, the terms peripheral and central neurofibromatosis should be discarded.83 It is important to be aware of their differences so that the MRI examination may be appropriately tailored to the disorders.83,84 The diagnostic criteria for NF1 may be found in Chapter 46. The criteria for NF2 include (1) bilateral eighth nerve masses seen with appropriate imaging techniques, such as CT or MRI (see Fig. 21-12) or (2) a first-degree relative with NF2 and either a unilateral eighth nerve mass or two of the following: neurofibroma, meningioma, glioma, schwannoma, or juvenile posterior subcapsular lenticular opacity.19 Besides bilateral VSs, NF2 patients are at risk for schwannomas of other cranial and spinal nerves, and intracranial and spinal meningiomas, often multiple (see Fig. 21-12).21,83 Members of some kindreds also develop ependymomas.22 Choroid plexus calcification is common.85 NF2 patients, however, are not at risk for optic gliomas, focal cerebral hamartomas, and many other stigmata common in NF1.83

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Figure 21-16. VS after stereotactic radiosurgery. A, T1WI. Hypointensity in adjacent pons consistent with edema (arrow). B, Gd-T1WI. Central nonenhancement (curved arrow) consistent with cystic component or loss of enhancement seen in majority of VSs after stereotactic radiosurgery. Pontine enhancement (arrow) consistent with breakdown of blood-brain barrier seen in a small percentage of patients. C, T2WI. Hyperintensity in middle cerebellar peduncle and adjacent pons and cerebellum consistent with edema (arrows). (Courtesy of Barry D. Pressman, MD)

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Imaging of the Cerebellopontine Angle

MENINGIOMA AND SIMULANTS In the CPA, meningioma is a distant second to VS in incidence.39,40,86 It is most often the lesion difficult to differentiate from VS.41,52,86,87 (See Chapter 47.) Meningiomas in the CPA most commonly arise from the posterior petrous surface (Fig. 21-17). Like VSs they are extra-axial, but unlike VSs they are usually eccentric to the porus (see Fig. 21-14). Also unlike VSs, meningiomas frequently herniate into the middle cranial fossa, (see Figs. 21-14 and 21-17).41 They may grow into the middle fossa through the tentorium or the temporal bone (see Figs. 21-15 and 21-17).41,87 Most characteristically, meningiomas are sessile and hemispherical in configuration, with their broad base against the petrous bone (see Fig. 21-14). They show obtuse bone tumor angles (see Fig. 21-14) in contrast to VSs, which are typically spherical or ovoid and show acute bone tumor angles (see Figs. 21-8 through 21-13 and 21-16).41 Less commonly, meningiomas are flat or plaquelike (en plaque) (see Fig. 21-15), and rarely pedunculated and nearly rounded.38 The en plaque meningiomas are notably prone to cause deep infiltration of the petrous bone (see Fig. 21-15).38 The surface of meningiomas is usually smooth or slightly lobulated. On MRI, like VSs, meningiomas are isointense or slightly hypointense on T1WI but, unlike VSs, they vary from hyperintense to hypointense on T2WI (see Fig. 21-14).8 (Hypointensity on T2WI may be due to calcification, fibrous tissue, melanotic elements, hemosiderin, fat, etc.)58 Gentry and colleagues8 found that when the intensity of the CPA mass was equal to or less than that of gray matter on T2WI, meninigioma was the most likely diagnosis. The variability in signal intensity of meningiomas on T2WI appears to reflect the histopathologic diversity of meningiomas. Tumors significantly hypointense to brain cortex tend to be composed primarily of fibroblastic or transitional elements, whereas those significantly hyperintense tend to be composed primarily of syncytial (meningothelial) or highly vascular elements.38,88,89 Generally, however, accurate prediction of histology by imaging is not possible,90,91 and tumor aggressiveness and recurrence rate does not necessarily correlate with histology.92 Metabolic rate as revealed by positron emission tomography (PET) may be a better prognosticator of tumor aggressiveness and likelihood of recurrence.93

Figure 21-17. Diagrammatic representation of locations of 19 meningiomas producing CPA symptoms (left and right sides combined). (From House JW and O’Connor AF [eds.]: Handbook of Neurotological Diagnosis, New York, 1987, Marcel Dekker, Inc, p 290, by courtesy of Marcel Dekker, Inc.)

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Meningiomas often calcify on CT (25%).41,94 On MRI, calcification appears hypointense on both T1 and T2WI (see Fig. 21-14), although hyperintense calcification has also been reported.95 MRI is less sensitive to calcification than CT and may not detect faint calcifications. Underlying hyperostosis is infrequently seen but strongly diagnostic when present (see Figs. 21-14 and 21-15).41 The IAC is rarely if ever enlarged. Cystic foci may be present in the tumor but appear much less commonly in meningiomas that in VSs.52 Peritumoral edema is more commonly associated with meningiomas than with VSs. Meningeal blood supply in the form of an arborizing signal void is highly characteristic if present. Marginal vessels and surrounding CSF cleft may be seen but are nonspecific.96 Dural thickening surrounding meningiomas, best seen with gadolinium enhancement (see Figs. 21-12, 21-14, and 21-15)97 has been variously termed meningeal sign, dural tail, and flare sign.98–100 Initially found to correspond to tumoral extension within or around the dura,97,99 the dural thickening in many subsequent cases has been found to contain only connective tissue, hypervascularity, and no tumor.101 Hence, to establish the histopathology in a peritumoral meningeal thickening, biopsy is necessary. In most cases, the thickening represents reactive rather than neoplastic changes.102 Dural thickening has been found in 52% to 72% of the meningiomas on postcontrast MRI.98–100 It has also been found, although much less frequently, in nonmeningiomas, including oligodendroglioma, schwannoma (see Fig. 21-11),61,100 glioblastoma, metastases, and other tumors (see Figs. 21-6, 21-18, 21-19, and, later in this chapter, Fig. 21-35).102 Thus, peritumoral dural thickening is strongly suggestive but not diagnostic of meningioma. Aoki and coworkers98 found dural thickening and enhancement extending into the IAC in two of four CPA meningiomas that simulated the stem of a VS. Several rare neoplastic and inflammatory diseases involving the meninges may simulate meningiomas on CT or MRI. Among the neoplasms are loculated leptomeningeal metastasis (meningeal carcinomatosis)

Figure 21-18. Loculated and diffuse meningeal metastases from carcinoma of the prostate. Gd-T1WI, Loculated metastases are present in both IACs (arrows) and diffuse metastasis (long thin arrows) similar to dural “tail.” Differential diagnosis: meningeal lymphoma, melanoma, sarcoidosis, tuberculosis, syphilis, idiopathic pachymeningitis.

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Figure 21-19. Idiopathic hypertrophic pachymeningitis. A, Sagittal T1WI. B, T2WI. C, Gd-T1WI. D, Coronal Gd-T1WI. Mass (black arrows) is extra-axial, dural-based on clivus and posterior petrous surface, slightly inhomogeneous and hypointense on T1WI, A, and inhomogeneous in intensity of T2WI, B, with mild inhomogeneous enhancement postcontrast, C and D, except for dural tails (white arrow) where enhancement is more intense. The patient is a 50-year-old woman who had rubbery hypovascular prepontine mass at transtemporal exploration and well-formed granulomas and chronic inflammation of histopathologic examination. No organisms were found on stains and cultures. (Courtesy of Robert K. Jackler, MD.)

(Figs. 21-18 and 21-20),103–105 primary meningeal lymphoma,42,106 and primary malignant melanoma.41,107,108 Among the inflammatory diseases are meningeal sarcoidosis,44,109 tuberculosis, syphilis, and idiopathic hypertrophic cranial pachymeningitis (see Fig. 21-19).43 All of the preceding conditions may appear as diffuse dural thickening simulating en plaque meningiomas or localized dural-based masses simulating sessile meningiomas. However, they are not expected to have underlying hyperostosis, intratumoral calcification, or discernible arborizing meningeal arterial feeders.

EPIDERMOID AND OTHER CYSTS Congenital intradural epidermoid tumors or cysts are the third most common mass lesion in the CPA (Figs. 21-21 and 21-22).39,41 They may be anterolateral or posterolatral to the brainstem. They tend to expand where the physical resistance is low, often extending into the prepontine and suprasellar cisterns and “dumbbell” into the contralateral cistern or

the middle cranial fossa. Their shapes are thus quite variable. They tend to burrow into the surface crevices of the brain and possess a fine surface irregularity reminiscent of that of cauliflower.110 The petrous apex may be eroded.41,111 On CT they are well known to be isodense with CSF.8 But, rarely they may be hyperdense (see Fig. 21-22).112–114 On MRI they are slightly hyperintense to CSF on T1WI and isointense on T2WI in the vast majority of cases.8,110,115,116 But, rarely, they show reversed signal intensities and are hyperintense on T1WI and hypointense on T2WI (“white epidermoids”) (see Fig. 21-22).117,118 They often show fine internal strands and at times a thin capsule of brain intensity.116 They may surround rather than displace the cisternal arteries.116 Small punctate calcifications are infrequently seen in the periphery.119 Epidermoid cysts are nonenhancing (see Fig. 21-12).119 Association of an enhancing component should arouse the suspicion of a squamous carcinoma arising from an epidermoid cyst.120,121 A number of other cysts may simulate epidermoid cysts in the CPA. They are all nonenhancing extra-axial masses of nearly CSF attenuation (on CT) and intensity (on

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Figure 21-20. Loculated leptomeningeal metastasis simulating meningioma. Patient had right hearing loss for only 2 weeks, an unusually short duration of symptoms for a meningioma, and had previously had a malignant melanoma removed from her trunk. Metastatic melanoma was surgically confirmed. A, GdT1WI. Hemispherical homogeneously enhancing extra-axial mass eccentric to porus acusticus with extension into IAC, entirely consistent with a meningioma. B, Coronal Gd-T1WI. Subtle symmetric additional metastases within foramen magnum are seen (arrows). (Courtesy of Peter W. Joyce, MD.)

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Figure 21-21. Intradural congenital epidermoid cyst (tumor). A, T1WI. B, Gd-T1WI. C, T2WI. D, Coronal Gd-T1WI. Irregular extra-axial mass displaces pons and insinuates toward fourth ventricle through widened lateral recess (arrowheads). Tumor is slightly hyperintense to CSF on T1WI, A, nonenhancing postcontrast, B, and nearly isointense to CSF on T2WI, C, and shows fine internal inhomogeneity and fine surface irregularity (A, B, and C). Note herniation (arrows in D) through tentorial incisura displacing midbrain.

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Figure 21-22. Intradural “white” congenital epidermoid. A, Noncontrast CT. B, T1WI. C, T2WI. This very rare “white” epidermoid in the right CPA deforming the medulla is hyperdense of CT, A, hyperintense of T1WI, B, and hypointense on T2WI, C, in complete reversal to the relatively common and more typical “black” epidermoid in the preceding figure. The MR intensities of a “white” epidermoid are similar to those of lipoma (see Figs. 21-25 and 21-44); the CT hyperdensity, however, is in contrast to the hypodensity characteristic of lipoma or fat. (Courtesy of Robert K. Jackler, MD.)

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MRI)—hypointense on T1WI and hyperintense on T2WI. Lipoma is also considered at this time because it is nonenhancing, although its x-ray attenuation and MR signal intensities of fat are distinctive from those of most cysts.122,123 Arachnoid cysts in the CPA are usually large masses and, like epidermoid cysts, hypointense on T1WI and hyperintense on T2WI (Fig. 21-23).124,125 (See Chapter 55, Neurotologic Aspects of Posterior Fossa Arachnoid Cysts.) But unlike epidermoid cysts, their surfaces are smooth and their contents homogeneous. They displace rather than surround the arteries in the cistern. An attempt to differentiate the two lesions on the basis of imaging is worthwhile, since the symptoms of arachnoid cysts may be controlled by diuretics alone.126 Diffusion-weighted and fluid-attenuated MR sequences may help in differentiating the two lesions when routine spine-echo studies are inconclusive.127 Cysticercosis should be considered in endemic areas. Cisternal cysticercal cysts are also of CSF attenuation and intensity, but are usually smaller than arachnoid cysts and often detected only by the presence of focal cisternal widening (Fig. 21-24).128 Unlike parenchymal and ventricular cysticercal cysts, which are separate from one another, cisternal cysts are racemose, a few centimeters in diameters, and lack a scolex.128 The majority are detectable only

on T1WI, but T2WI demonstrate the surrounding parenchymal reaction to greater advantage.129 Coexistent parenchymal, ventricular, or additional cisternal cysts, when present, strongly support the diagnosis. Very rare congenital cysts that may be encountered in the CPA include epithelial cysts,130–133 neurenteric cysts,134 and craniopharyngioma.17,135 Although their CT and MR images have been illustrated, generalization of their findings is difficult on the basis of the very few cases reported. Some of them show CT attenuation and MR intensities atypical of uncomplicated cysts.132,134,135 In contrast to most CPA tumors and cysts, lipomas are hyperintense on T1WI and hypointense on T2WI and parallel the signal intensity of orbital and subcutaneous fat (Fig. 21-25).122,136–140 They show no contrast enhancement, and their hyperintensities on T1WI are diminished by fat suppression sequences.24 Without pregadolinium images for comparison, their inherent hyperintensity on T1WI will not be recognized when only postgadolinium T1WI are obtained; nor will their characteristic short T2 values be appreciated without adequate T2WI. Because conservative management for lipomas may be advisable,122,136,137,139,141–143 diagnosis on the basis of imaging findings is of considerable importance. Besides the characteristic MRI intensities, the negative Hounsfield values of lipomas on CT are also diagnostic.42,123,141

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Figure 21-24. CPA cysticercal cysts. T1WI. Bilateral cisternal cysts (arrows) isointense with CSF indent pons and slightly bow left facioacoustic nerves (curved arrow).

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C Figure 21-23. CPA arachnoid cyst. A, T1WI. B, T2WI. C, Postcontrast CT. Cyst is isointense with CSF on MRI, A and B, and isodense with CSF on CT, C, and nonenhancing, similar to a typical epidermoid but is distinguishable from the latter by being smooth surfaced and homogeneous. Note notching on surface by basilar artery in A and B.

B Figure 21-25. CPA lipoma. A, T1WI. B, T2WI. Note characteristic hyperintensity on T1WI (arrow in A) and hypointensity on T2WI (arrow in B) in reverse of CSF. See also Fig. 21-44.

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NONVESTIBULAR POSTERIOR FOSSA SCHWANNOMAS Schwannomas arising from PF cranial nerves other than the vestibular are rare.38,44 They resemble VSs in appearance but differ from them in location.41,144 Not infrequently, facial and intracranial jugular foramen schwannomas are associated with symptoms relating primarily to the eighth nerve. Careful assessment of their relationship to the cranial foramina is important so that the correct diagnosis can be made and inappropriate use of the translabyrinthine approach avoided.145 Among the PF schwannomas, trigeminal schwannoma is a distant second to VS in frequency of occurrence.144 Trigeminal schwannomas may arise intradurally from the nerve root in the CPA and the Meckel cave or extradurally from the gasserian ganglion in the middle cranial fossa (Fig. 21-26).146–149 They often dumbbell into the posterior and middle fossae through the porus trigeminus.86,147–149 The foramen ovale or foramen rotundum (or both) may be enlarged. They tend to be larger than the average VS,149 and more often contain cystic components.41,150

Facial schwannomas are, in most cases, indistinguishable from VSs on CT or MRI when they arise in the CPA or the IAC (Fig. 21-27).1,138,151 When they arise in the CPA or the IAC, they tend to show vestibulocochlear symptoms and may be indistinguishable from VSs clinically as well,151–153 unless a cisternal facial schwannoma lies clearly anterior to the course of the acoustic nerve. Schwannomas of the glossopharyngeal, vagus, and spinal accessory nerves (jugular foramen schwannomas) may be predominantly intracranial (type A), predominantly in the skull base (type B), or predominantly extracranial (type C).154 Type A tumors tend to present with eighth nerve and cerebellar signs and symptoms, and type B and C tumors tend to present with palsies of the ninth, tenth, or eleventh cranial nerves.154–157 Thus type A tumors mainly need to be differentiated from VS and type B tumors from paraganglioma (glomus jugulare tumor), meningioma, and other tumors that may involve the jugular foramen (Fig. 21-28). (See also Chapter 61.) On CT the jugular foramen enlarged by a schwannoma shows a smooth rounded margin.1 On MRI, the prominent serpentine arborizing signal voids common in large paragangliomas are seldom present,158 and on angiography the

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Figure 21-26. Cystic trigeminal schwannoma. A, T1WI. B, Gd-T1WI. C, PDWI. D, T2WI. Bulk of tumor lies in posterior fossa with a small middle fossa component enlarging left Meckel’s cave (arrow). Note similarity of tumor to arachnoid cyst (Fig. 21-19) on noncontrast images (A, C, and D). Tumor is nearly of CSF intensity of T1WI, A, because of predominance of intratumoral cystic components, and more obvious in B postcontrast, but also subtly suggested in A and C.

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Figure 21-27. CPA facial schwannoma. A, T1WI. B, Gd-T1WI. Isointense rounded extraaxial tumor centered at porus acusticus, A, intensely enhancing postcontrast, B, indistinguishable from VS (see Fig. 21-9).

tumors are less vascular than paragangliomas but more so than meningiomas.154,155,159 (See also Chapters 22 and 61.) When the pars nervosa of the jugular canal is selectively expanded, a glossopharyngeal schwannoma can be recognized. When the entire jugular foramen is diffusely and enlarged, however, differentiation among the jugular foramen schwannomas is not possible by imaging.1 Rarely a hypoglossal schwannoma may also appear as a mass in the CPA. Its identity can be traced if the hypoglossal canal is smoothly and selectively enlarged.160–162 When the bone erosion incorporates the adjacent jugular foramen, identification of precise origin of the tumor is then no longer possible.160

VASCULAR LESIONS Vascular lesions in the CPA are rare, but a number of them may clinically mimic neoplasms and should be considered in the differential diagnosis on imaging.163

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VBD, or elongation and dilatation of the vertebrobasilar arteries, is probably the vascular lesion most commonly associated with compressive symptoms of the PF cranial nerves (Figs. 21-3 and 21-29).164 The basilar artery may be considered ectatic if its diameter is more than 4.5 mm (see Fig. 21-29) and elongated if it deviates beyond the lateral margin of the clivus (see Fig. 21-3) or the dorsum sellae or if it bifurcates above the plane of the suprasellar cistern.165 Patients with VBD may or may not be symptomatic.166 The incidence of cranial nerve compressive symptoms, however, appears to correlate with the degree of tortuosity.167 A symptomatic patient with a tortuous basilar artery of normal caliber is more likely to have involvement of a single cranial nerve (see Fig. 21-3); conversely, one with a dilated and tortuous artery is likely to have multiple compressive or ischemic neurologic deficits or hydrocephalus (see Fig. 21-29).164 In most cases the actual compression of a cranial nerve is exerted by the superior cerebellar artery on the trigeminal,

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Figure 21-28. Jugular foramen schwannoma. A, T1WI. B, Gd-T1WI. Patient has NF2. Tumor is slightly lobulated and located partly in posterior fossa, deforming medulla and cerebellum, and partly in jugular foramen. It is mildly hypointense to brain, A, and intensely enhancing postcontrast, B. Vascularity is more prominent in this tumor than in a typical schwannoma, raising the question of a paraganglioma (see Fig. 21-6). Note signal from slowly flowing blood in left sigmoid sinus enhancing postcontrast.

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Figure 21-29. Vertebrobasilar dolichoectasia. A, Sagittal T1WI. Dilated and tortuous basilar artery (curved arrow) shows peripheral laminar hyperintensity due to very slow flow or thrombi (or both) and central moderate intensities due to moderately slow flow within the patent lumen. Normal flow void is seen in the undilated proximal and distal arteries (straight arrows). B, Gradient echo image. Flowing blood appears hyperintense on such images. Basilar artery (curved arrows) shows marked fusiform dilatation and marked tortuosity. Signal intensities in such dilated arteries are often complex due to presence of thrombi of varying are and flow of varying velocity. Similar complex intensity patterns may be also found in giant aneurysms, although the latter lesions are rounded or ovoid rather than fusiform. (Courtesy of William P. Dillon, MD.)

the anterior inferior cerebellar artery (AICA) on the facial or vestibulocochlear, or the posterior inferior cerebellar artery (PICA) on the glossopharyngeal. Hence, vascular cross-compression by a branch of the vertebrobasilar artery may occur without the vertebrobasilar itself necessarily being substantially dilated or tortuous. In fact, the offending vessel may at times be a vein instead of an artery.168 Furthermore, vessel-nerve contact or even vascular grooving of the nerve does not necessarily mean disease.169 Positive identification of the offending vessel by imaging is difficult. Angiographic localization, which visualizes the vessel but not the nerve, is indirect and invasive.170,171 CT with IV contrast shows the vertebrobasilar arteries and the brainstem but not adequately the branches of the vertebrobasilar or the cranial nerves in question.172 MRI offers improved resolution of the structures, but experience with MRI in this application is as yet limited.173–175

With future improvements MR angiography may become a useful adjunct (see Fig. 21-3).23 For preoperative diagnosis of neurovascular crosscompression, some centers use CT or MRI only to exclude other causes of symptoms,168,176 whereas others use, in addition, gas-CT cisternography for positive identification of the offending vessel before surgical microvascular decompression (Fig. 21-30).9,177 The point of contact may be in the cistern, the porus, or the canal and not necessarily limited to the canal as described in some reports.169,177 Concerns about postprocedural morbidity,178 even with 25-gauge rather than the “standard” 22-gauge spinal needles,179 have discouraged continued use of the gas-CT cisternogram in favor of the MR cisternogram with fast spin echo or CISS (see Fig. 21-1).4,5,11 Aneurysms of the vertebrobasilar system comprise about 10% of intracranial aneuryms.180 The common locations

Figure 21-30. AICA loop in IAC (also see Fig 21-1). High-resolution gas-CT cisternogram. Loop on AICA is marked with curved arrow; facial nerve, short arrow; acoustic nerve, long arrow.

Figure 21-31. AICA berry aneurysm. Selective vertebral angiogram. Patient had subarachnoid hemorrhage and hearing loss. Aneurysm (arrow) shows nipple-like configuration suggestive of recent bleeding. (Reprinted from Lo WWM: Tumors of the cerebellopontine angle. In Som PM, Bergeron RT [eds.]: Head and Neck Imaging, 2nd ed. St. Louis, Mosby-Year Book, 1991.)

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Figure 21-32. Giant PICA aneurysm. A, Precontrast. B, Postcontrast CT. Aneurysm at PICA origin is partially thrombosed and slightly hyperdense to brain precontrast, A, and shows nonenhancing thrombus (open arrow) and enhancing lumen (long arrow) and outer rim (short arrow) postcontrast, B. (Courtesy of Duane E. Blickenstaff, MD.)

are the basilar bifurcation, the basilar trunk, the vertebral artery, and the PICA. Berry aneurysms usually present with subarachnoid hemorrhage (SAH) (Fig. 21-31), whereas giant aneurysms (those exceeding 2.5 cm) usually present instead as mass lesions (Fig. 21-32).181 AICA aneurysms, representing only 1% of intracranial aneurysms, are quite rare.182 In the past, AICA aneurysms have often been operated on with the erroneous diagnosis of acoustic tumor.182,183 A review of 22 reported cases revealed that 16 had acoustic and 14 had facial nerve symptoms and signs. Most had headaches, nausea, and vomiting, and 13 had documented SAH.182 Most were in the 5- to 7-mm range, although two exceeded 15 mm. Although VSs may on rare occasions present with SAH, they tend to be large, not small tumors.59,60 Berry aneurysms appear as signal voids on MRI and enhancing lesions on CT. Angiography is diagnostic (see Fig. 21-31). Giant aneurysms are usually partially thrombosed.41,181 A partially thrombosed aneurysm appears on MRI with a signal void in the patent lumen surrounded by layers of thrombi of varying signal intensities and sometimes a low-intensity outer rim (see Fig. 21-29).184–187 Signal loss from pulsating CSF around the basilar artery may mimic the signal void of an aneurysm.188 MR angiogram or contrast-enhanced CT would show the true size of the basilar artery. On CT a partially thrombosed aneurysm shows an enhancing outer rim with an isoattenuating nonenhancing mural thrombus surrounding an enhancing lumen (see Fig. 21-32), superficially resembling a partially enhancing cystic schwannoma.1,41,181,189 A thrombosed aneurysm is filled with a nonenhancing thrombus, and an unthrombosed one contains only the enhancing lumen.41 AVMs in the CPA are exceedingly rare (Fig. 21-33). Although they are generally intracerebral and cause primarily intracerebral hemorrhage, totally extracerebral AVMs, which are predisposed to primary subarachnoid bleeding, may be seen in the CPA.189 One or more cerebral aneurysms coexist with AVMs in about 20% of cases.190

Dilated enhancing vessels may be seen in the CPA on CT and serpentine hypointense loops on MRI.41,189 Superficial siderosis (SS), or pial siderosis of the acoustic nerves, is not a vascular lesion in itself but the result of chronic subarachnoid hemorrhage, often of venous or capillary origin such as from an occult ependymoma.191 It is rare, but has been recognized with increasing frequency with greater awareness and the increasing availability of high-field MRI. It should be considered in the differential diagnosis of CPA lesions since the affected patients commonly complain of bilateral progressive sensorineural hearing loss and ataxia (see Fig. 21-5).18,191,192 SS is characterized by intracellular and extracellular deposition of hemosiderin in the leptomeninges and subpial tissue of the brain, spinal cord, and cranial nerves. The acoustic nerve with its long glial-lined segment appears especially vulnerable. The characteristic hypointensity of pial and subpial tissue and the cranial nerves is seen only on T2WI on high-field MRI and gradient-echo imaging.18,192

Figure 21-33. CPA arteriovenous malformation. Selective vertebral angiogram. Principal feeder appears to be right AICA. (Courtesy of Livia G. Solti-Bohman, MD.)

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EXTRADURAL LESIONS

INTRA-AXIAL TUMORS

Bone lesions and paragangliomas are extradural lesions and are detailed in Chapter 22, Imaging of the Lateral Skull Base. Here they are briefly discussed only as a reminder that they may intrude into the CPA.1 Bone lesions in the petrous apex include cystic lesions such as cholesterol granuloma (cholesterol cyst) (Fig. 21-34), congenital intrapetrous epidermoid cyst, and petrous apex mucocele193; solid tumors such as chordoma, chondroma, chondrosarcoma (Fig. 21-35), giant cell tumor, myeloma, metastases, xanthoma,194 and so on; and intrapetrous carotid aneurysm. Papillary endolymphatic sac tumors, which may also protrude into the CPA, are discussed in Chapter 23, Imaging of the Facial Nerve. The more aggressive of the extradural tumors may at times transgress the dura and form an intradural mass (see Fig. 21-35). The same may be said for paragangliomas from the jugular foramen (see Fig. 21-6). The associated bone changes of an apparently intradural mass may reveal its true origin.

Intra-axial tumors arise from the brain and a detailed discussion is beyond the scope of this chapter. Some of them produce exophytic masses in the CPA and must be considered in the differential diagnosis. Intra-axial PF tumors arise from the brainstem, the cerebellum, or the fourth ventricle. Tumors of the brainstem are mainly astrocytomas that occur in children or young adults (Fig. 21-36).195–197 Exophytic growths are common. Tumors in the cerebellum may arise from the vermis or the hemispheres. The vermian tumors are principally medulloblastomas in childhood, now classified as primitive neuroectodermal tumors (PNETs).196,198,199 The hemispheric tumors include astrocytomas,196 usually of the pilocystic variety in young adults, hemangioblastomas in middle-aged individuals,200 and metastases.196 Any of the three may be cystic or solid.96 Lymphoma of the brain is seen with increasing frequency in recent years, particularly among immunosuppressed patients (Fig. 21-37).196,201

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Figure 21-34. Triloculated cholesterol granuloma (cholesterol cyst) of petrous apex. Huge extra-axial mass partly in posterior and partly in middle fossa. A, T1WI shows markedly hyperintense contents in two of the loculations but a mixture of hyperintensities and hypointensities in the third. B, T2WI shows markedly hyperintense contents in two of the loculations but markedly hypointense contents in the third. Note increased thickness of hypointensity in capsule as compared to A. C, Postcontrast CT shows isodense contents and thin opaque capsules, in part formed by remodelled bone. D, Coronal HRCT shows extradural intrapetrous origin of mass, which has expanded into posterior and middle fossas (arrowheads). Note partitions between loculations (short arrow) and erosion of cochlea and semicircular canal (open arrows).

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B

Figure 21-35. Petrous apex chondrosarcoma. A and B, Gd-T1WI. Highly conspicuous markedly enhancing intradural component (arrowhead) of tumor in CPA indenting pons represents merely “tip-of-iceberg” of the much larger but less conspicuous inhomogeneously enhancing extradural intrapetrous tumor extending into posterior fossa (twin arrows), middle ear (arrow), and Meckel’s cave (crossed arrow). Tumor also extends below skull base (black arrow). Note dural tail (long thin arrow).

Although any intra-axial tumor may grow into the CPA, tumors from the fourth ventricle are particularly prone to do so.202 They are ependymomas (Fig. 21-38)203,204 and choroids plexus papillomas (Fig. 21-39).205–208 Both of these tumors often contain granular calcifications. Although extra-axial tumors are more common in the CPA in adults and older teens,209 exophytic intra-axial tumors are more common in childhood.199 Nonneoplastic brain lesions such as multiple sclerosis (see Fig. 21-4)210–211 and infarct (Fig. 21-40)210,212 also enter into the differential diagnosis, as do AVMs,213 cavernous angiomas,214,215 developmental venous anomaly (venous angiomas), and capillary telangiectasia.214

In the IAC as in the CPA, tumors other than VSs are uncommon, but because therapeutic implications for some of the lesions are significantly different from those of VSs, each of the lesions should be carefully considered and if possible preoperatively identified. In general, few intracanalicular schwannomas, either vestibulocochlear or facial, are associated with signs of facial nerve involvement. Presence of such signs in a patient with an intracanalicular tumor should be a clinicoradiologic clue that arouses suspicion of a nonschwannomatous tumor.216 1. Vestibular schwannomas again constitute about 90% of the tumors.48,179,216 2. Facial schwannomas are rare and usually indistinguishable from VSs preoperatively.1,152,153 3. Meningiomas have been said to cause facial palsy more often than VSs but rarely have they been fully documented.217,218 They may be accompanied by hyperostosis or dural tail.

INTRACANICULAR LESIONS Intracanalicular lesions of the IAC carry a slightly different differential diagnosis from lesions of the CPA (Table 21-4).

A

B

Figure 21-36. Pontine astrocytoma. A, PDWI. B, T2WI. Intra-axial mass is mildly to moderately hyperintense and poorly marginated from pons and cerebellum (short arrows) and deforms fourth ventricle. Exophytic growth of tumor fills CPA cistern (open arrows). (Courtesy of Anton N. Hasso, MD.)

372

A

NEURORADIOLOGY

B

Figure 21-37. Primary cerebellar lymphoma. A, Gd-T1WI. B, PDMI. C, T2WI. Moderately enhancing intraaxial tumor in region of flocculus (arrow) mildly hyperintense on PDWI, B, and T2WI, C, with peritumoral edema (small arrows) not apparent on Gd-T1WI, A. Differential diagnosis: solid astrocytoma, hemangioblastoma, and metastasis.

C

A

B

Figure 21-38. CPA ependymoma. A, T1WI. B, T2WI. Exophytic tumor from foramen of Luschka, widening lateral recess and displacing medulla (short arrow) and fourth ventricle (arrow) from left cerebellum (open arrow). As in other exophytic intra-axial tumors (Fig. 21-36), brain tumor margins are less distinct than in extra-axial tumors. (Compare with Fig. 21-39.)

Imaging of the Cerebellopontine Angle

A

373

B

Figure 21-39. CPA choroid plexus papilloma. A, T1WI. B, T2WI. Tumor from foramen Luschka widening lateral recess, and displacing medulla (short arrow) and fourth ventricle (arrow) from right cerebellum (open arrow). Tumor is mildly hypointense on T1WI, A, and mildly hyperintense on T2WI, B. Because the choroid plexus is extra-axial, brain tumor margins of papilloma are better defined than in ependymoma (see Fig. 21-38) (Courtesy of Val M. Runge, MD.)

4. Intracanalicular vascular tumors (hemangioma/vascular malformation) are probably a distant second to VSs in incidences in the IAC.219–222 They tend to cause a greater degree of nerve deficits and are more commonly accompanied by facial nerve symptoms than VSs of comparable size.216,221,223–225 Some of them contain intratumoral bone spicules discernible on high-resolution CT with bone algorithm (Fig. 21-41)226,227; some may be associated with honeycomb changes of the adjacent bone (see Fig. 21-41).221 On MRI, some are isointense or hyperintense to CSF on T2WI and a few are moderately hyperintense on T1WI, but often they are indistinguishable from schwannomas, especially when precontrast T1WI and adequate T2WI are lacking (Fig. 21-42).220,222 5. Intracanalicular metastases may be suspected from a short duration of symptoms, facial weakness, a known history of malignancy, and a rapid growth rate on serial studies.1,228,229 Not infrequently they are bilateral (Figs. 21-18 and 21-43).

6. Lipochoristomas (lipomas) contain adipose and other ectopic mature mesenchymal tissues, such as smooth muscle, in varying proportions, with fat usually predominating. Fat shows distinctive MR signal intensities, being markedly hyperintense on T1WI and moderately hypointense on T2WI (Fig. 21-44)142,230 and can be confirmed by precontrast fat-suppressed T1WI.24,139 7. Melanotic melanomas are also hyperintense on T1WI and hypointense on T2WI, but amelanotic melanomas do not follow such a pattern (see Figs. 21-20 and 21-43).58,108,231 8. Lymphoma in the IAC may involve the leptomeninges.232 9. Glioma of the acoustic nerve is an extreme rarity.233 10. Osteomas of the IAC are also rare and are better demonstrated on CT than on MRI (Fig. 21-45). Osteomas containing purely cortical bone are hypointense on all sequences; those containing fatty marrow simulate lipomas in intensities.

TABLE 21-4. Intracanalicular Lesions Neoplastic Vestibular schwannoma Facial schwannoma Meningioma Hemangioma Metastasis Melanoma Lymphoma Glioma Osteoma

Nonneoplastic

Figure 21-40. AICA infarct. T2WI. Nonexpansile hyperintense right pontocerebellar lesion (open arrow) in territory of anterior inferior cerebellar artery hardly discernible on T1WI (not illustrated). (Compare with Fig. 21-4.) Note also hyperintensity from slowly flowing blood in tortuous basilar artery (arrow).

Lipochoristomas (lipomas) AICA loop AICA aneurysm Meningitis Neuritis Hamartoma AICA, anterior inferior cerebellar artery.

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A

B

C

D

Figure 21-41. IAC hemangioma A, T1WI. B, Gd-T1WI. C, T2WI. D, and E, HRCT. Tumor (white arrow) extending slightly anterointeriorly beyond IAC is nearly isointense on T1WI, A, strongly enhancing postcontrast, B, and hyperintense on T2WI C, similar to schwannomas. HRCT reveals characteristic intratumoral bone spicule (black arrow) in D and “honeycomb” bone erosion (black arrow) of the floor of IAC in E. Some hemangiomas however do not show the characteristic bone changes (see Fig. 21-37). (Courtesy of Malcolm D. Graham, MD.)

E

Hamartoma of the acoustic nerve has also been reported.216,234 Other nonneoplastic IAC lesions include (1) AICA loop in the IAC (see Figs. 21-30 and 21-1),169,177,235 which may at times simulate a tumor,236 (2) AICA aneurysm as previously discussed (see Fig. 21-31),182,183 (3) meningeal inflammation and adhesion (Fig. 21-46),237,238 and (4) neuritis of the facial or acoustic nerves (Fig. 21-47).239–243 One report described four cases of vestibulocochlear neuritis with hearing loss, positive auditory brainstem response, and MRI finding of focal nerve enhancement indistinguishable from small intracanalicular VSs.244 A period of observation was

thus advised for very small lesions to verify persistence of symptoms or tumor growth.244,245

CONCLUSION The variety of tumors and other lesions that may arise in the CPA and the IAC are indeed enormous. However, the common extra-axial types, which are well over 90% of the lesions, are quite consistent in their appearance on imaging. These include VS, meningioma, epidermoid and

Imaging of the Cerebellopontine Angle

Figure 21-42. IAC hemangioma/vascular malformation. Gd-T1WI. Tumor is markedly hyperintense postcontrast and indistinguishable from IAC schwannomas. Compare with Figs. 21-7 and 21-41.

A

B

Figure 21-43. Bilateral IAC metastases from melanoma. A, T1WI. B, Gd-T1WI. C, T2WI. Tumors are isointense on T1WI, mildly enhancing of Gd-T1WI. One is isointense with gray matter and one with white matter on T2WI. Patient had bilateral rapidly progressive hearing loss and facial palsies.

C

375

376

NEURORADIOLOGY

A

B

Figure 21-44. IAC lipoma. A, Gd-T1WI. B, T2WI. On Gd-T1WI alone, hyperintense tumor is indistinguishable from a schwannoma or hemangioma (see Figs. 21-7 and 21-42). Hypointensity of tumor (arrow) on T2WI, however, suggests fat. See also Fig. 21-25. (Courtesy of Kenneth L. Kidd, MD.)

A

B

Figure 21-45. IAC osteoma. A, Coronal CT. Osteoma (arrow) consisting entirely of cortical bone arising from anterosuperior wall of porus acusticus caused sensorineural hearing loss relieved by resection. B, Gd-T1WI. Tumor (arrow) is hypointense in all sequences and nonenhancing postcontrast. A marrowcontaining osteoma would have shown central hyperintensity on T1WI similar to marrow in petrous apices. (Courtesy of Derald E. Brackmann, MD.)

A

B

Figure 21-46. Chronic inflammation. A, T1WI. B, Gd-T1WI. Small isointense soft tissue in fundus of IAC (arrowhead) enhancing postcontrast (arrow), indistinguishable from small VS except for perhaps presence of a small dural tail (small arrow). Compare with Figs. 21-7 and 21-47. Patient had progressive left sensorineural hearing loss of 3-year duration. Mass in fundus of left IAC adherent to dura and involving acoustic nerve was completely removed. Pathologic diagnosis: nongranulomatous active chronic nonspecific inflammation. (Courtesy of Robert D. Sostrin, MD.)

Imaging of the Cerebellopontine Angle

A

377

B

Figure 21-47. Focal cochlear neuritis. A, T1WI. B, Gd-T1WI. Globular thickening of acoustic nerve (arrow) with marked postcontrast enhancement (arrow) indistinguished from intracanalicular VS (see Fig. 21-7). Patient had progressive right sensorineural hearing loss of 1-year duration and abnormal acoustic brainstem reflex. C, Gd-T1WI, obtained 10 weeks after A and B. Considerable decrease in thickening and enhancement since initial study, B, with now only residual enhancement in cochlear nerve. Lack of clinical improvement lead to exploration by middle fossa approach, which found no tumor. (Courtesy of Michael J. O’Leary, MD.)

C other cysts, nonvestibular PF schwannomas, and vascular lesions. Most of the extradural and the intra-axial lesions are also recognizable under systematic analysis. With attention to technical detail, careful analysis of findings, a systematic approach to differential diagnosis, and close clinicoradiologic correlation, a correct radiologic diagnosis is possible, even for many of the rare lesions.

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