Imaging Spectrum of Facial Nerve Lesions Achint K. Singh, MD,a Girish Bathla, DMRD, FRCR, MMeD (DR),b Wilson Altmeyer, MD,a Ruchi Tiwari, DNB,a Maria P. Valencia, MD,a Carlos Bazan III, MD,a and Bundhit Tantiwongkosi, MDa
The facial nerve is affected by a wide variety of pathologies, including congenital, traumatic, inflammatory, and neoplastic conditions. Imaging plays a vital role in the diagnosis of these pathologies. The facial nerve has a complex anatomy and course. A strong grasp of normal facial nerve anatomy is essential for the radiologist to maintain a high level of diagnostic sensitivity. This article details the normal imaging anatomy of the facial nerve and the imaging features of common facial nerve pathologies.
Introduction The facial nerve innervates the muscles of facial expression and supplies parasympathetic fibers to the lacrimal, submandibular, and sublingual glands. The facial nerve may be involved in a variety of lesions, including trauma, inflammation, or neoplasms. Imaging has an important role in the evaluation of facial nerve lesions. A detailed knowledge of the complex anatomical course of the facial nerve is paramount in the accurate characterization and diagnosis of facial nerve lesions.
Anatomy The facial nerve or cranial nerve VII (CN VII) has motor, sensory, and parasympathetic fibers that arise from 3 pontine nuclei. The motor nucleus, located in the anterolateral pontine tegmentum, is the largest CN VII nucleus. The motor nucleus innervates the muscles of facial expression, stapedius, and stylohyoid and the posterior belly of digastric muscles. The From the aUniversity of Texas Health Science Center, San Antonio, TX; and bUniversity of Iowa Hospitals and Clinics, Iowa city, IA. Reprint requests: Achint K. Singh, MD, 7703 Floyd Curl Dr, MC 7800, San Antonio, TX 78229. E-mail: [email protected]. Curr Probl Diagn Radiol 2014;XX:XX–XX. & 2014 Mosby, Inc. All rights reserved. 0363-0188/$36.00 + 0 http://dx.doi.org/10.1067/j.cpradiol.2014.05.011
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superior salivary nucleus, located dorsal to the motor nucleus, contributes parasympathetic secretomotor fibers to the lacrimal gland (via the greater superficial petrosal nerve [GSPN]) and the submandibular or sublingual gland (via the chorda tympani nerve). The nucleus solitarius, located posterolateral to the motor nucleus, is a sensory nucleus that receives information from the anterior two-thirds of the tongue and from the external auditory canal.1 The facial nerve can be divided into the following multiple segments: 1. Intra-axial segment (pons): The motor root of the facial nerve loops around the nucleus of the abducens nerve and creates the facial colliculus (bulge at the dorsal aspect of the pons in the floor of the fourth ventricle) (Fig 1A). The parasympathetic and sensory fibers join to form the nervus intermedius.2 The motor root and the nervus intermedius leave the brainstem at the pontomedullary junction. The nervus intermedius joins the motor root as it exits from the brainstem or near the meatus of the internal auditory canal (IAC).2 2. Cisternal segment: This segment starts as the nerve leaves the brainstem and crosses the cerebellopontine angle to its entry into the porus acusticus of the IAC. This segment is best seen on the heavily T2-weighted magnetic resonance (MR) sequences (Fig 1B). 3. Intratemporal segment: This segment can be further subdivided into 4 segments. (a) Intracanalicular segment (in the IAC): This segment extends from the porus acusticus medially to the fundus of the IAC laterally (Fig 1B). At the lateral end of the IAC, the facial nerve is separated from the cochlear and the inferior vestibular nerves by the crista
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FIG 2. An oblique sagittal reformatted heavily T2-weighted MR image at the level of the fundus of the IAC demonstrates 4 nerves in different quadrants: the facial nerve (long white arrow) in the anterior superior quadrant, the cochlear nerve (open arrow) in the anterior inferior quadrant, the superior vestibular nerve (short white arrow) in the posterior superior quadrant, and the inferior vestibular nerve (dotted arrow) in the posterior inferior quadrant.
FIG 1. Normal MR anatomy of the facial nerve on axial constructive interference in steady state (CISS) MR sequences. (A) The expected location of motor nucleus of the facial nerve (solid white circle) and the course of the facial nerve (white line) at the level of the facial colliculi (arrows). The looping of the facial nerve around the nucleus of the abducens nerve (dotted circle) can be noted. The expected course of the abducens nerve is marked by the dotted line. (B) The cisternal segment (black arrow) and the intracanalicular segment of the facial nerve (dotted arrow) are seen as linear hypointense structures. The superior vestibular nerve is also visualized (white arrow).
falciformis. The superior compartment is divided by the vertically oriented Bill bar, which separates the facial nerve anteriorly from the superior vestibular nerve posteriorly. Oblique sagittal reformatted heavily T2-weighted MR images can resolve these 4 nerves (Fig 2).
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(b) Labyrinthine segment: This is the narrowest and shortest segment and travels anterolaterally from the fundus of the IAC to the geniculate fossa, which contains the geniculate ganglion (Fig 3A). At this point (also known as the first or anterior genu), the facial nerve turns posteriorly to form the tympanic segment. The GSPN arises at the geniculate ganglion and carries the parasympathetic fibers to the lacrimal gland. (c) Tympanic segment: This segment runs in an anteroposterior direction and ends at the second or posterior genu, where the facial nerve turns inferiorly to form the mastoid segment (Fig 3B). The tympanic segment passes inferior to the lateral semicircular canal, which is a helpful landmark in its identification. (d) Mastoid segment: This segment extends from the second genu to the stylomastoid foramen (Fig 3C). The nerve to the stapedius muscle and the chorda tympani nerve arise from the mastoid segment. However, they are usually not seen on the routine imaging. 4. Extracranial segment: The facial nerve exits the skull at the stylomastoid foramen and then enters the parotid gland, where it
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FIG 3. Normal CT anatomy of the facial nerve. (A) An axial CT image demonstrates the labyrinthine (black arrow), first genu (white arrow), and proximal tympanic segments (dotted arrow) of the facial nerve. (B) An axial CT image demonstrates the entire tympanic segment of the facial nerve (black arrow). The cochlea (dotted black arrow), vestibule (V), and ossicles (white arrow) can also be noted. (C) A coronal CT image demonstrates a vertically oriented mastoid segment of the facial nerve (black arrow). The lateral (white arrow) and superior (dotted black arrow) semicircular canals can also be noted.
divides into multiple terminal branches, supplying the muscles of facial expression. This segment is difficult to resolve on the routine imaging; however, it usually courses lateral to the retromandibular vein, which serves as an important imaging landmark.3
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Imaging Techniques Computed tomography (CT) and magnetic resonance imaging (MRI) are complimentary imaging modalities in the evaluation of facial nerve pathology. In general, CT is preferred for the evaluation of lesions involving the labyrinthine, temporal, and mastoid segments of
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the facial nerve, and MRI is preferred if the lesion can be localized to the intracanalicular, cisternal, or intraaxial segments. CT is the preferred imaging modality for the evaluation of the facial nerve in the setting of congenital malformation; temporal bone fracture; middle ear pathology; and various osseous conditions, such as fibrous dysplasia, Paget disease, or osteopetrosis. MRI is preferred in the evaluation of perineural tumor spread (PTS), hemifacial spasm, and Bell palsy. Both CT and MRI are helpful for the evaluation of facial nerve tumors.
CT Technique Helical CT examination is preferred, as this technique allows the generation of isotropic voxels and subsequent reconstruction in any plane (without loss of resolution). Raw images are acquired from the top of petrous bone to 1 cm inferior to the mastoid tip. Axial images are reconstructed parallel to the plane of the lateral semicircular canal using a slice thickness of 0.6 mm with a gap of 0.3 mm using bone algorithm for each side with a FOV of 90-100 mm. Coronal images are then acquired perpendicular to the axial images. Stenvers and Pöschl reformats can be obtained from raw data in a plane perpendicular and parallel to the superior semicircular canal, respectively. Axial images are also reconstructed to include both ears using soft tissue algorithm.
MR Technique Small field of view and axial T1- and T2-weighted spin echo sequences are acquired for the IAC with a 3-mm slice thickness without interslice gap. Axial high-resolution 3-dimensional (3D) heavily T2-weighted images are acquired with a 1-mm thickness without gap. Postcontrast axial and coronal T1-weighted fat-saturated images are also acquired with a 3-mm thickness without gap.
Imaging Anatomy of the Facial Nerve
FIG 4. The normal enhancement of the facial nerve on MR image. (A) An axial fat-saturated postcontrast T1-weighted image demonstrates thin enhancement of the first genu and the proximal tympanic segments of the right facial nerve (solid arrow). It can be noted that there is no enhancement in the IAC (dotted arrow). (B) An axial fatsaturated postcontrast T1-weighted image demonstrates thin enhancement of the mastoid segment of the right facial nerve.
Pontine nuclei of the facial nerve are not delineated on CT or MRI scans. The facial colliculus, a prominent bulge along the floor of the fourth ventricle, is an important landmark in identifying the approximate location of the motor nucleus of the facial nerve (Fig 1A). The cisternal and the intracanalicular segments of the facial nerve are well visualized on highresolution 3D heavily T2-weighted images (Fig 1B).
An oblique sagittal reformatted image can be obtained from this sequence and is helpful in resolving the 4 individual nerves at the fundus of the IAC (Fig 2). The labyrinthine, temporal, and mastoid segments of the facial nerve may not be well visualized on the noncontrast MR images but are well seen on CT images (Fig 3). On postcontrast images, normal enhancement
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TABLE. Classification of facial nerve lesions Categories Lesions Preferred imaging modality Neoplasms
Distinguishing imaging features
Schwannoma
MRI
Perineural tumor spread
MRI
Ramsay Hunt syndrome
MRI
Lyme disease
MRI
Otitis media Cholesteatoma
CT CT
Bell palsy Sarcoidosis
MRI (only in atypical cases) MRI
Abnormal facial nerve enhancement with suggestive clinical symptoms (acuteonset, unilateral, peripheral facial nerve paralysis) Abnormal facial nerve enhancement with basilar leptomeningeal and dural enhancement
Traumatic
Temporal bone fracture
CT
Fracture extending into the facial nerve canal (typically with transverse-type fracture)
Vascular
Hemifacial spasm Venous malformation or hemangioma
MRI CT or MRI
Prominent vascular loop at the root exit zone of the facial nerve Enhancing lesion at the geniculate ganglion with bony spicules
Congenital
Moebius syndrome Aberrant course
MRI CT
Absent facial colliculi Comparison with the normal side is helpful
Pontine lesions
Infarct Multiple sclerosis
MRI MRI
Cavernoma
MRI
T2-FLAIR hyperintense lesions with diffusion restriction Pontine lesion with multiple other white matter lesions with or without enhancement “Popcorn”-like appearance on T2 with susceptibility artifacts
Infectious
Idiopathic
Enhancing lesion extending into the geniculate ganglion (along the course of the facial nerve) Extension of tumor along the course of the facial nerve with known primary malignancy Abnormal enhancement of the facial nerve with classic clinical features (otalgia, vesicles, and facial paralysis) Abnormal facial nerve enhancement with white matter lesions, meningeal enhancement, and classic clinical symptoms (erythema migrans, radiculoneuritis, and arthritis) Middle ear opacification abutting the facial nerve canal Middle ear opacification abutting the facial nerve canal with osseous erosion
FLAIR ¼ fluid attenuated inversion recovery.
FIG 5. Facial nerve schwannoma. An axial T1-W contrast-enhanced MR image demonstrates a large enhancing lesion involving the cisternal (black arrow), intracanalicular (dotted arrow), first genu (long white arrow), and tympanic (short white arrow) segments of the left facial nerve. Enhancement along the expected course of the facial nerve is the most helpful feature in the differentiation of this lesion from a vestibular schwannoma. T1-W, T1-weighted.
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FIG 6. Perineural tumor spread from adenoid cystic carcinoma of the parotid gland. A contrast-enhanced axial CT image demonstrates an infiltrative left parotid gland tumor (asterisk) with abnormal enhancement and widening in the region of the left stylomastoid foramen (black arrow). Compare with normal fat-filled right stylomastoid foramen (white arrow).
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of the facial nerve is seen at the geniculate ganglion and the tympanic and the mastoid segments (Fig 4).1 However, a comparison with the contralateral facial
FIG 8. Ramsay Hunt syndrome. An axial T1-W contrast-enhanced MR image demonstrates asymmetric enhancement of the right facial nerve involving the labyrinthine (dotted arrow) and the first genu (white arrow) segments. T1-W, T1-weighted.
nerve in these segments is essential, as asymmetric enhancement is considered abnormal. The cisternal, intracanalicular, labyrinthine, and parotid segments do not enhance normally, and enhancement of these segments is always suspicious for pathologic processes (Fig 4A).4
Classification of Facial Nerve Lesions For further details, see the Table.
Neoplasms Facial Nerve Schwannoma Schwannomas arise from Schwann cells in the outer layer of the nerve sheath. They account for less than 1% of all tumors of petrous temporal bone.5 They can arise from any segment of the facial nerve with the FIG 7. Perineural tumor spread from squamous cell carcinoma of the skin. (A) An axial T1-W fat-saturated contrast-enhanced MR image demonstrates an infiltrative mass involving the right parotid gland and overlying skin (asterisk) with asymmetric prominent enhancement of the mastoid segment of the right facial nerve (white arrow). (B) An axial T1-W fat-saturated contrast-enhanced MR image demonstrates enhancement along the intracanalicular (long arrow) and the tympanic (dotted arrow) segments of the right facial nerve. Enhancement in the right pterygopalatine fossa (short arrow) indicating involvement of the maxillary division of the trigeminal nerve (CN V2) can be noted. (C) An axial T1-W fat-saturated contrast-enhanced MR image demonstrates enhancement along the first genu and the labyrinthine segments of the right facial nerve (solid arrow). Enhancement of the right trigeminal ganglion and the cisternal segment of the right trigeminal nerve extending to the pons (dotted arrows) can be noted. T1-W, T1-weighted. 6
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FIG 10. Otitis media. A coronal CT image demonstrates opacification (asterisk) of the right tympanic cavity abutting the tympanic segment of the facial nerve (arrow).
FIG 9. Lyme disease. (A) An axial T1-W contrast-enhanced MR image demonstrates prominent enhancement of both the facial nerves. (B) An axial T1-W contrast-enhanced MR image demonstrates abnormal enhancement of both the trigeminal nerves. T1-W, T1-weighted.
geniculate ganglion being the most common site followed by the labyrinthine and the tympanic segments.6,7 Facial nerve schwannomas (FNSs) also tend to involve multiple segments of the nerve.7 The clinical symptoms depend on the location. However, patients typically present with unilateral facial weakness or hearing loss. On CT scans, FNSs usually show smooth osseous expansion without obvious erosion or destruction.7 The osseous expansion in the expected course of the facial nerve is a specific finding.2 On MR images, FNSs demonstrate isointense to hypointense signal on T1-weighted images and hyperintense signal on T2-weighted images. They usually
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demonstrate avid postcontrast enhancement. Large tumors may demonstrate cystic changes. An FNS in the intracanalicular segment can be confused with a vestibular schwannoma; however, a “dumbbell-shaped” lesion with extension of the enhancing component from the fundus of the IAC to the geniculate ganglion is characteristic of an FNS (Fig 5).8 High-resolution 3D heavily T2-weighted images are very helpful in the anatomical localization of temporal bone tumors. Parasagittal reformatted images from these sequences may be helpful in small IAC schwannomas to determine whether the origin of the lesion is the facial nerve (anterior superior quadrant), cochlear nerve (anterior inferior quadrant), or vestibular nerve (posterior superior and inferior quadrants).9
PTS Along the Facial Nerve PTS is the development of a tumor in a noncontiguous fashion along the endoneurium or the perineurium of a nerve. PTS is most commonly seen in adenoid cystic and squamous cell carcinoma of the head and neck.10 Other uncommon malignancies that may demonstrate PTS include lymphoma, melanoma, basal cell carcinoma, and rhabdomyosarcoma.11 The trigeminal and facial nerves are the most common CNs involved in PTS.11 Diagnosis of PTS often changes the management, necessitating the use of adjuvant chemotherapy, adjuvant radiotherapy, or wide surgical margins. Knowledge of CN anatomy is required for the appropriate
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trigeminal nerve branches, as there are multiple connections between the branches of the facial and the trigeminal nerves. The vidian nerve and branches of the maxillary nerve communicate in the sphenopalatine ganglion, allowing tumor spread from the vidian nerve to the GSPN in a retrograde fashion (the vidian nerve is formed by the GSPN and the deep petrosal nerve).12 The auriculotemporal branch of the mandibular nerve also communicates with the facial nerve branches within the parotid gland.13
Infections Ramsay Hunt Syndrome Ramsay Hunt syndrome is a complication of reactivation of the varicella-zoster virus in the geniculate ganglion. The classic clinical triad consists of otalgia, vesicles in the external auditory canal, and ipsilateral facial paralysis.14 This condition is typically diagnosed clinically and imaging studies (most commonly MRI) are reserved for atypical cases. Abnormal enhancement in any segment of the facial nerve can be seen on postcontrast T1-weighted sequences on MRI (Fig 8). Pontine nucleus enhancement has also been described with this syndrome.15 Facial nerve inflammation is often accompanied by neuritis of the vestibulocochlear nerve, which can cause sensorineural hearing loss, vertigo, and tinnitus. Associated pathologic enhancement of CN VIII may be observed on MR images.2 FIG 11. Bell palsy. (A) An axial T1-W contrast-enhanced MR image demonstrates prominent enhancement of both the facial nerves involving the intracanalicular (long arrow) and the first genu and the tympanic (dotted arrow) of the right facial nerve and the first genu (short arrow) of the left facial nerve. (B) A coronal T1-W contrastenhanced MR image demonstrates enhancement of the tympanic segments of both the facial nerves. T1-W, T1-weighted.
diagnosis of perineural spread.12 PTS along the facial nerve typically takes place from malignant tumors of the parotid gland. Tumor typically spreads in a retrograde fashion from the stylomastoid foramen to the geniculate ganglion. Osseous expansion of the stylomastoid foramen and the facial nerve is appreciated on CT scans (Fig 6). A postcontrast fat-suppressed T1-weighted MRI sequence demonstrates abnormal enhancement and thickening of the facial nerve, indicating PTS (Fig 7). Tumor can also spread along the facial nerve from
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Lyme Disease Lyme disease is caused by spirochete Borrelia burgdorferi. The nervous system is involved in 10%15% of patients with infection.16 The characteristic clinical triad is lymphocytic meningitis, cranial neuritis, and radiculoneuritis.17 The facial nerve is the most common CN to be involved.16 Lyme disease occurs in stages with an incubation period of 3-32 days. Stage 1 is characterized by erythema migrans with flulike symptoms.18 Neurologic and cardiac symptoms are seen in stage 2. Stage 3 is characterized by monoarticular or oligoarticular arthritis. The most common abnormality seen on MR images is periventricular or subcortical nonspecific white matter T2 hyperintense signal with or without enhancement.19 Lyme disease should be included in the differential diagnosis if diffuse meningeal or CN enhancement is seen (Fig 9).19
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FIG 12. Sarcoidosis. (A) An axial T1-W contrast-enhanced MR image demonstrates abnormal enhancement of intracanalicular segment of both the facial nerves. (B) An axial T1-W contrast-enhanced MR image demonstrates pathologic enhancement of both the trigeminal nerves (doubleheaded arrows). A small enhancing lesion in the right superior cerebellum (black arrow) can be noted. (C) An axial T1-W contrast-enhanced MR image demonstrates pathologic enhancement of both the optic nerves (arrows). T1-W, T1-weighted.
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viruses, such as Cytomegalovirus23 and Epstein-Barr virus,24 have also been suggested as possible causes. A cell-mediated autoimmune response to peripheral nerve basic protein has also been proposed as the pathogenesis of Bell palsy.25 Bell palsy is characterized by acute onset of facial paralysis, which peaks at 48 hours with gradual spontaneous improvement. Imaging is not routinely performed when the diagnosis is clinically obvious. Imaging is reserved for atypical cases with persistent or recurrent symptoms and for patients with slowly progressive paralysis. MRI with contrast is the study of choice, and abnormal enhancement of the facial nerve in the region of geniculate ganglion, labyrinthine, and proximal tympanic segment is seen without enlargement (Fig 11).12
Sarcoidosis FIG 13. An axial CT image demonstrates transverse-type fracture (black arrow) of the right temporal bone with involvement of the inner ear and the tympanic segment of the facial nerve (dotted arrow). Opacification of the mastoid antrum can also be noted.
Other Infectious or Inflammatory Conditions Involving the Facial Nerve Other inflammatory causes of facial nerve palsy include otitis media, cholesteatoma, and malignant otitis externa. Facial nerve paralysis is seen in 5% of patients with acute otitis media and 1% of patients with cholesteatoma.12 The tympanic segment of the facial nerve is most vulnerable, especially in patients with congenital dehiscence of the facial nerve canal. Opacification of middle ear cavity abutting the facial nerve canal with or without associated osseous erosion or destruction may be observed on CT scans (Fig 10). Contrast-enhanced MRI may provide additional information and demonstrate asymmetric intense enhancement of the facial nerve.
Idiopathic Bell Palsy Bell palsy is the most common cause of acuteonset, idiopathic, unilateral, peripheral facial nerve palsy and accounts for 60%-75% of cases of unilateral facial paralysis.20,21 The etiology is unknown, but viral infections and autoimmune diseases have been recognized as possible causes. Herpes simplex virus has been implicated as a causative agent,22 but other
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Sarcoidosis is an idiopathic systemic disease characterized by formation of noncaseating granulomas. Approximately 5% of patients exhibit central nervous system involvement.26 Isolated central nervous system involvement is seen in less than 1% of patients without systemic involvement.27 Neurologic symptoms are nonspecific and depend on the site of involvement. CN palsy is a common finding with the facial nerve being the most commonly involved CN.28 Other common symptoms are seizures, signs of meningeal irritation, visual disturbances, polyuria, and polydipsia (diabetes insipidus). The diagnosis of neurosarcoidosis is usually based on clinical signs and classic imaging features with evidence of systemic sarcoidosis, which is typically done by biopsy.29 The most common radiologic finding is dural involvement.29 Dural enhancement can be focal or diffuse with hypointense signal on T2-weighted images (a helpful feature suggesting sarcoidosis).30 Leptomeningeal enhancement involving the basilar meninges is a typical finding.27 CN enhancement can be seen without leptomeningeal involvement. The facial and the optic nerves are commonly involved and demonstrate enhancement on postcontrast T1-weighted MR sequences (Fig 12).
Trauma Facial nerve injuries are reported in up to 50% of temporal bone fractures, particularly when the fracture is transverse in orientation. Longitudinal fractures result in injury to the geniculate ganglion, and transverse fractures
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FIG 14. Venous malformation of the facial nerve. (A) An axial CT image demonstrates enlargement of the facial nerve in the region of the first genu. (B) An axial CT image demonstrates bony spicules within the lesion, which is characteristic of venous malformation. (C) An axial T2-W MR image demonstrates hyperintensity at the same location. (D) An axial T1-W contrast-enhanced MR image demonstrates avid enhancement of the lesion. T1-W, T1-weighted.
are more likely to cause injury to the labyrinthine segment. Facial paralysis is usually delayed and incomplete. Immediate facial paralysis after trauma suggests severe nerve injury or transection. Temporal bone fractures with facial nerve involvement are best diagnosed by CT examination (Fig 13).
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Vascular Facial Nerve Venous Malformation or Hemangioma Facial nerve hemangiomas are benign, slow-growing vascular lesions and may be as common as FNSs.31-33
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FIG 15. Hemifacial spasm. An axial CISS MR image demonstrates prominent loop of left vertebral artery (dotted arrow) at the root exit zone of the left facial nerve (white arrow). CISS, constructive interference in steady state.
Benign vascular tumor is another term used interchangeably with hemangioma.34 Recently, it has been proposed that these lesions should be classified as “venous malformations of the facial nerve.”35 Mulliken and Glowacki36 introduced a new classification system in 1982, where they classified vascular lesions into 2 categories based on clinical and histopathologic features: vascular tumors (infantile hemangioma and congenital hemangioma) and vascular malformations (capillary, venous, lymphatic, or arteriovenous malformations). The most common site of facial nerve venous malformation is in the region of the geniculate ganglion followed by the IAC.11,37 Patients' symptoms depend on the tumor location: slowly progressive facial paralysis from lesions located in the geniculate ganglion and unilateral progressive sensorineural hearing loss from lesions located in the IAC.38,39 The term “ossifying hemangioma” is used for these lesions when they form bone.14 On CT images, these lesions have irregular margins with a tendency to produce bony spicules or amorphous “honeycomb” bony changes (Fig 14A and B).14,40 The honeycomb appearance is pathognomonic but seen in only approximately 50% of cases. These lesions demonstrate variable signal intensity on T1-weighted images and high signal intensity on T2-weighted images with strong contrast enhancement
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FIG 16. Moebius syndrome in a neonate with congenital facial palsy. (A) An axial T2-W MR image demonstrates absent facial colliculi. (B) An axial T2-W MR image demonstrates normal facial colliculi in a different patient (for comparison). T2-W, T2-weighted.
(Fig 14C and D). Low signal intensity foci may be seen on T1- or T2-weighted images, corresponding to the ossific changes seen on CT images.41
Hemifacial Spasm Hemifacial spasm is characterized by involuntary, unilateral, sudden contraction of the muscles supplied by the facial nerve. The disease starts with the
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FIG 17. An axial CT image demonstrates right labyrinthine aplasia with hypoplastic facial nerve (black arrow). Normal inner ear structures and normal course of the facial nerve on the left side, for comparison, can be noted.
contraction of the orbicularis oculi muscle with gradual extension to the other facial muscles. It is typically caused by a prominent vascular loop of the
FIG 18. Multiple sclerosis. An axial FLAIR MR image demonstrates a large hyperintense lesion (long white arrow) in the left pons at the expected location of the facial nerve motor nucleus. Other small lesions in the ventral pons and the left middle cerebellar peduncle (short arrows) can also be noted. FLAIR, fluid attenuated inversion recovery.
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anterior inferior cerebellar artery, posterior inferior cerebellar artery, or vertebral artery compressing the root exit zone (the region where the nerve exits the brainstem) of the facial nerve.42,9 The root exit zone of the facial nerve is the transition zone between central and peripheral myelination, which may explain the increased vulnerability of this segment of facial nerve to compression.43,44 Other rare causes of hemifacial spasm include Bell palsy, facial nerve injury, brainstem demyelination, and vascular insults.45 MRI is a useful modality in the identification of these causes. A high-resolution T2-weighted sequence is very helpful in identifying the relationship of vascular loop to the facial nerve (Fig 15). Multiplanar reformatted images can be obtained from this sequence for the evaluation of facial nerve compression in different planes.2
Congenital Congenital facial nerve palsy (CFNP) occurs in approximately 2.1 per 1000 live births in the United States and may be seen at birth or shortly thereafter.46 It most frequently occurs secondary to birth-related trauma, in which case it is often isolated and recovers in approximately 90% cases over several weeks.47 CFNP occurs in the absence of birth trauma and may be an isolated finding or part of underlying syndrome such as Moebius, Goldenhar, or Poland syndrome.
FIG 19. Pontine cavernoma. An axial T2-W MR image demonstrates heterogeneous “popcorn”-like lesion in the pons at the expected location of left facial nerve motor nucleus. T2-W, T2-weighted.
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Irrespective of the etiology, patients with developmental CFNP may show a spectrum of imaging findings, including focal brainstem lesions, brainstem hypoplasia, hypoplasia, or agenesis of the facial nerve.46 Moebius syndrome is characterized by facial weakness and impairment of ocular abduction and is frequently bilateral.48 These patients often have hypoplasia or agenesis of the CN VII nuclei and the accompanying facial nerve along with brainstem hypoplasia (Fig 16). Patients with Goldenhar syndrome demonstrate unilateral CFNP associated with vertebral defects, facial hypoplasia, and preauricular skin tags. Patients with Poland syndrome have absent pectoralis muscles and upper limb deformity in addition to unilateral CFNP.46 Not unexpectedly, patients with developmental CFNP often do not show any improvement with time. An anomalous facial nerve course often occurs in association with developmental anomalies of CN VIII, IAC, middle ear, or inner ear (Fig 17). In these cases, the facial nerve may follow an aberrant course through the temporal bone, exit prematurely from the IAC, and overlie the stapes footplate or cochlear promontory.49
Central Causes of Facial Nerve Palsy The facial nerve can also be affected by a variety of intracranial lesions, such as infarcts, multiple sclerosis plaques (Fig 18), cavernomas (Fig 19), neoplasms (Fig 20), and arteriovenous malformations. MRI is the modality of choice for the characterization of these lesions.
Conclusion
FIG 20. Brain metastases from lung cancer with involvement of the right facial nerve motor nucleus. (A) An axial T2-W MR image demonstrates hyperintense lesion in the right pons at the level of the facial colliculi. (B) An axial T1-W contrast-enhanced MR image demonstrates avid enhancement (white arrow) of the pontine lesion with another large lesion in the right occipital lobe (dotted arrow). T2-W, T2-weighted.
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The facial nerve is affected by a wide variety of pathologies, including congenital, traumatic, inflammatory, and neoplastic conditions. Any segment of the facial nerve, from the brainstem to the parotid gland, can be involved by these pathologies. Familiarity with the anatomy, normal pattern of enhancement, and pathologic imaging findings is important for appropriate patient management.
REFERENCES 1. Al-Noury K, Lotfy A. Normal and pathological findings for the facial nerve on magnetic resonance imaging. Clin Radiol 2011;66:701-7.
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2. Jager L, Reiser M. CT and MR imaging of the normal and pathologic conditions of the facial nerve. Eur J Radiol 2001;40:133-46. 3. Casselman J, Mermuys K, Delanote J, et al. MRI of the cranial nerves—More than meets the eye: Technical considerations and advanced anatomy. Neuroimaging Clin N Am 2008;18:197-231 [preceding x]. 4. Gupta S, Mends F, Hagiwara M, et al. Imaging the facial nerve: A contemporary review. Radiol Res Pract 2013;2013: 248039. 5. Rosenblum B, Davis R, Camins M. Middle fossa facial schwannoma removed via the intracranial extradural approach: Case report and review of the literature. Neurosurgery 1987;21:739-41. 6. Parnes LS, Lee DH, Peerless SJ. Magnetic resonance imaging of facial nerve neuromas. Laryngoscope 1991;101:31-5. 7. Wiggins RH 3rd, Harnsberger HR, Salzman KL, et al. The many faces of facial nerve schwannoma. Am J Neuroradiol 2006;27:694-9. 8. Salzman KL, Davidson HC, Harnsberger HR, et al. Dumbbell schwannomas of the internal auditory canal. Am J Neuroradiol 2001;22:1368-76. 9. Veillon F, Taboada LR, Eid MA, et al. Pathology of the facial nerve. Neuroimaging Clin N Am 2008;18:309-20 [x]. 10. Caldemeyer KS, Mathews VP, Righi PD, et al. Imaging features and clinical significance of perineural spread or extension of head and neck tumors. Radiographics 1998;18: 97-110 [quiz 47]. 11. Ojiri H. Perineural spread in head and neck malignancies. Radiat Med 2006;24:1-8. 12. Raghavan P, Mukherjee S, Phillips CD. Imaging of the facial nerve. Neuroimaging Clin N Am 2009;19:407-25. 13. Diamond M, Wartmann CT, Tubbs RS, et al. Peripheral facial nerve communications and their clinical implications. Clin Anat 2011;24:10-8. 14. Adour KK. Otological complications of herpes zoster. Ann Neurol 1994;35(suppl):S62-4. 15. Sartoretti-Schefer S, Kollias S, Valavanis A. Ramsay Hunt syndrome associated with brain stem enhancement. Am J Neuroradiol 1999;20:278-80. 16. Halperin JJ. Nervous system Lyme disease. Infect Dis Clin North Am 2008;22:261-74 [vi]. 17. Reik L, Steere AC, Bartenhagen NH, et al. Neurologic abnormalities of Lyme disease. Medicine 1979;58:281-94. 18. Hengge UR, Tannapfel A, Tyring SK, et al. Lyme borreliosis. Lancet Infect Dis 2003;3:489-500. 19. Agarwal R, Sze G. Neuro-lyme disease: MR imaging findings. Radiology 2009;253:167-73. 20. Adour KK, Byl FM, Hilsinger RL Jr., et al. The true nature of Bell's palsy: Analysis of 1000 consecutive patients. Laryngoscope 1978;88:787-801. 21. Greco A, Gallo A, Fusconi M, et al. Bell's palsy and autoimmunity. Autoimmun Rev 2012;12:323-8. 22. Takasu T, Furuta Y, Sato KC, et al. Detection of latent herpes simplex virus DNA and RNA in human geniculate ganglia by the polymerase chain reaction. Acta Otolaryngol 1992;112: 1004-11.
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23. Traavik T, Storvold G, Sundsfjord A, et al. Peripheral facial palsy and coincidental cytomegalovirus infection or reactivation. Scand J Infect Dis 1983;15:233-8. 24. Grose C, Feorino PM, Dye LA, et al. Bell's palsy and infectious mononucleosis. Lancet 1973;2:231-2. 25. Abramsky O, Webb C, Teitelbaum D, et al. Cellular immune response to peripheral nerve basic protein in idiopathic facial paralysis (Bell's palsy). J Neurol Sci 1975;26:13-20. 26. Gascon-Bayarri J, Mana J, Martinez-Yelamos S, et al. Neurosarcoidosis: Report of 30 cases and a literature survey. Eur J Intern Med 2011;22:e125-32. 27. Smith JK, Matheus MG, Castillo M. Imaging manifestations of neurosarcoidosis. Am J Roentgenol 2004;182:289-95. 28. Christoforidis GA, Spickler EM, Recio MV, et al. MR of CNS sarcoidosis: Correlation of imaging features to clinical symptoms and response to treatment. Am J Neuroradiol 1999;20: 655-69. 29. Zajicek JP, Scolding NJ, Foster O, et al. Central nervous system sarcoidosis—Diagnosis and management. Q J Med 1999;92:103-17. 30. Seltzer S, Mark AS, Atlas SW. CNS sarcoidosis: Evaluation with contrast-enhanced MR imaging. Am J Neuroradiol 1991;12:1227-33. 31. Fisch U, Rüttner J. Pathology of intratemporal tumors involving the facial nerve. In: Fisch U, editor. Facial Nerve Surgery. Birmingham, AL: Aesculapius; 1997. p. 448-56. 32. Lo WW, Horn KL, Carberry JN, et al. Intratemporal vascular tumors: Evaluation with CT. Radiology 1986;159: 181-5. 33. Juliano AF, Maya MM, Lo WW, et al. Temporal bone tumors and cerebellopontine angle lesions. In: Som PM, Curtin HD, editors. Head and Neck Imaging. 5th ed. St. Louis, MO: Mosby; 2011. p. 1364-5. 34. Lo WW, Shelton C, Waluch V, et al. Intratemporal vascular tumors: Detection with CT and MR imaging. Radiology 1989;171:445-8. 35. Benoit MM, North PE, McKenna MJ, et al. Facial nerve hemangiomas: Vascular tumors or malformations? Otolaryngol Head Neck Surg 2010;142:108-14. 36. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: A classification based on endothelial characteristics. Plast Reconstr Surg 1982;69: 412-22. 37. Curtin HD, Jensen JE, Barnes L Jr., et al. “Ossifying” hemangiomas of the temporal bone: Evaluation with CT. Radiology 1987;164:831-5. 38. Eby TL, Fisch U, Makek MS. Facial nerve management in temporal bone hemangiomas. Am J Otol 1992;13:223-32. 39. Salib RJ, Tziambazis E, McDermott AL, et al. The crucial role of imaging in detection of facial nerve haemangiomas. J Laryngol Otol 2001;115:510-3. 40. Phillips CD, Hashisaki G, Veillon F. Anatomy and development of the facial nerve. In: Swartz JD, Loevner LA, editors. Imaging of the Temporal Bone. 4th ed. New York, NY: Thieme; 2009. p. 469-70. 41. Mijangos SV, Meltzer DE. Case 171: Facial nerve hemangioma. Radiology 2011;260:296-301.
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42. Girard N, Poncet M, Caces F, et al. Three-dimensional MRI of hemifacial spasm with surgical correlation. Neuroradiology 1997;39:46-51. 43. Nielsen VK. Electrophysiology of the facial nerve in hemifacial spasm: Ectopic/ephaptic excitation. Muscle Nerve 1985;8:545-55. 44. Rosenstengel C, Matthes M, Baldauf J, et al. Hemifacial spasm: Conservative and surgical treatment options. Dtsch Arztebl Int 2012;109:667-73. 45. Yaltho TC, Jankovic J. The many faces of hemifacial spasm: Differential diagnosis of unilateral facial spasms. Mov Disord 2011;26:1582-92.
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46. Jemec B, Grobbelaar AO, Harrison DH. The abnormal nucleus as a cause of congenital facial palsy. Arch Dis Child 2000;83:256-8. 47. Sasaki M, Imamura Y, Sato N. Magnetic resonance imaging in congenital facial palsy. Brain Dev 2008;30:206-10. 48. Verzijl HT, Valk J, de Vries R, et al. Radiologic evidence for absence of the facial nerve in Mobius syndrome. Neurology 2005;64:849-55. 49. Al-Mazrou KA, Alorainy IA, Al-Dousary SH, et al. Facial nerve anomalies in association with congenital hearing loss. Int J Pediatr Otorhinolaryngol 2003;67:1347-53.
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The facial nerve is affected by a wide variety of pathologies, including congenital, traumatic, inflammatory, and neoplastic conditions. Imaging plays a vital role in the diagnosis of these pathologies. The facial nerve has a complex anatomy and course. A strong grasp of normal facial nerve anatomy is essential for the radiologist to maintain a high level of diagnostic sensitivity. This article details the normal imaging anatomy of the facial nerve and the imaging features of common facial nerve pathologies.
Introduction The facial nerve innervates the muscles of facial expression and supplies parasympathetic fibers to the lacrimal, submandibular, and sublingual glands. The facial nerve may be involved in a variety of lesions, including trauma, inflammation, or neoplasms. Imaging has an important role in the evaluation of facial nerve lesions. A detailed knowledge of the complex anatomical course of the facial nerve is paramount in the accurate characterization and diagnosis of facial nerve lesions.
Anatomy The facial nerve or cranial nerve VII (CN VII) has motor, sensory, and parasympathetic fibers that arise from 3 pontine nuclei. The motor nucleus, located in the anterolateral pontine tegmentum, is the largest CN VII nucleus. The motor nucleus innervates the muscles of facial expression, stapedius, and stylohyoid and the posterior belly of digastric muscles. The From the aUniversity of Texas Health Science Center, San Antonio, TX; and bUniversity of Iowa Hospitals and Clinics, Iowa city, IA. Reprint requests: Achint K. Singh, MD, 7703 Floyd Curl Dr, MC 7800, San Antonio, TX 78229. E-mail: [email protected]. Curr Probl Diagn Radiol 2014;XX:XX–XX. & 2014 Mosby, Inc. All rights reserved. 0363-0188/$36.00 + 0 http://dx.doi.org/10.1067/j.cpradiol.2014.05.011
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superior salivary nucleus, located dorsal to the motor nucleus, contributes parasympathetic secretomotor fibers to the lacrimal gland (via the greater superficial petrosal nerve [GSPN]) and the submandibular or sublingual gland (via the chorda tympani nerve). The nucleus solitarius, located posterolateral to the motor nucleus, is a sensory nucleus that receives information from the anterior two-thirds of the tongue and from the external auditory canal.1 The facial nerve can be divided into the following multiple segments: 1. Intra-axial segment (pons): The motor root of the facial nerve loops around the nucleus of the abducens nerve and creates the facial colliculus (bulge at the dorsal aspect of the pons in the floor of the fourth ventricle) (Fig 1A). The parasympathetic and sensory fibers join to form the nervus intermedius.2 The motor root and the nervus intermedius leave the brainstem at the pontomedullary junction. The nervus intermedius joins the motor root as it exits from the brainstem or near the meatus of the internal auditory canal (IAC).2 2. Cisternal segment: This segment starts as the nerve leaves the brainstem and crosses the cerebellopontine angle to its entry into the porus acusticus of the IAC. This segment is best seen on the heavily T2-weighted magnetic resonance (MR) sequences (Fig 1B). 3. Intratemporal segment: This segment can be further subdivided into 4 segments. (a) Intracanalicular segment (in the IAC): This segment extends from the porus acusticus medially to the fundus of the IAC laterally (Fig 1B). At the lateral end of the IAC, the facial nerve is separated from the cochlear and the inferior vestibular nerves by the crista
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FIG 2. An oblique sagittal reformatted heavily T2-weighted MR image at the level of the fundus of the IAC demonstrates 4 nerves in different quadrants: the facial nerve (long white arrow) in the anterior superior quadrant, the cochlear nerve (open arrow) in the anterior inferior quadrant, the superior vestibular nerve (short white arrow) in the posterior superior quadrant, and the inferior vestibular nerve (dotted arrow) in the posterior inferior quadrant.
FIG 1. Normal MR anatomy of the facial nerve on axial constructive interference in steady state (CISS) MR sequences. (A) The expected location of motor nucleus of the facial nerve (solid white circle) and the course of the facial nerve (white line) at the level of the facial colliculi (arrows). The looping of the facial nerve around the nucleus of the abducens nerve (dotted circle) can be noted. The expected course of the abducens nerve is marked by the dotted line. (B) The cisternal segment (black arrow) and the intracanalicular segment of the facial nerve (dotted arrow) are seen as linear hypointense structures. The superior vestibular nerve is also visualized (white arrow).
falciformis. The superior compartment is divided by the vertically oriented Bill bar, which separates the facial nerve anteriorly from the superior vestibular nerve posteriorly. Oblique sagittal reformatted heavily T2-weighted MR images can resolve these 4 nerves (Fig 2).
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(b) Labyrinthine segment: This is the narrowest and shortest segment and travels anterolaterally from the fundus of the IAC to the geniculate fossa, which contains the geniculate ganglion (Fig 3A). At this point (also known as the first or anterior genu), the facial nerve turns posteriorly to form the tympanic segment. The GSPN arises at the geniculate ganglion and carries the parasympathetic fibers to the lacrimal gland. (c) Tympanic segment: This segment runs in an anteroposterior direction and ends at the second or posterior genu, where the facial nerve turns inferiorly to form the mastoid segment (Fig 3B). The tympanic segment passes inferior to the lateral semicircular canal, which is a helpful landmark in its identification. (d) Mastoid segment: This segment extends from the second genu to the stylomastoid foramen (Fig 3C). The nerve to the stapedius muscle and the chorda tympani nerve arise from the mastoid segment. However, they are usually not seen on the routine imaging. 4. Extracranial segment: The facial nerve exits the skull at the stylomastoid foramen and then enters the parotid gland, where it
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FIG 3. Normal CT anatomy of the facial nerve. (A) An axial CT image demonstrates the labyrinthine (black arrow), first genu (white arrow), and proximal tympanic segments (dotted arrow) of the facial nerve. (B) An axial CT image demonstrates the entire tympanic segment of the facial nerve (black arrow). The cochlea (dotted black arrow), vestibule (V), and ossicles (white arrow) can also be noted. (C) A coronal CT image demonstrates a vertically oriented mastoid segment of the facial nerve (black arrow). The lateral (white arrow) and superior (dotted black arrow) semicircular canals can also be noted.
divides into multiple terminal branches, supplying the muscles of facial expression. This segment is difficult to resolve on the routine imaging; however, it usually courses lateral to the retromandibular vein, which serves as an important imaging landmark.3
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Imaging Techniques Computed tomography (CT) and magnetic resonance imaging (MRI) are complimentary imaging modalities in the evaluation of facial nerve pathology. In general, CT is preferred for the evaluation of lesions involving the labyrinthine, temporal, and mastoid segments of
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the facial nerve, and MRI is preferred if the lesion can be localized to the intracanalicular, cisternal, or intraaxial segments. CT is the preferred imaging modality for the evaluation of the facial nerve in the setting of congenital malformation; temporal bone fracture; middle ear pathology; and various osseous conditions, such as fibrous dysplasia, Paget disease, or osteopetrosis. MRI is preferred in the evaluation of perineural tumor spread (PTS), hemifacial spasm, and Bell palsy. Both CT and MRI are helpful for the evaluation of facial nerve tumors.
CT Technique Helical CT examination is preferred, as this technique allows the generation of isotropic voxels and subsequent reconstruction in any plane (without loss of resolution). Raw images are acquired from the top of petrous bone to 1 cm inferior to the mastoid tip. Axial images are reconstructed parallel to the plane of the lateral semicircular canal using a slice thickness of 0.6 mm with a gap of 0.3 mm using bone algorithm for each side with a FOV of 90-100 mm. Coronal images are then acquired perpendicular to the axial images. Stenvers and Pöschl reformats can be obtained from raw data in a plane perpendicular and parallel to the superior semicircular canal, respectively. Axial images are also reconstructed to include both ears using soft tissue algorithm.
MR Technique Small field of view and axial T1- and T2-weighted spin echo sequences are acquired for the IAC with a 3-mm slice thickness without interslice gap. Axial high-resolution 3-dimensional (3D) heavily T2-weighted images are acquired with a 1-mm thickness without gap. Postcontrast axial and coronal T1-weighted fat-saturated images are also acquired with a 3-mm thickness without gap.
Imaging Anatomy of the Facial Nerve
FIG 4. The normal enhancement of the facial nerve on MR image. (A) An axial fat-saturated postcontrast T1-weighted image demonstrates thin enhancement of the first genu and the proximal tympanic segments of the right facial nerve (solid arrow). It can be noted that there is no enhancement in the IAC (dotted arrow). (B) An axial fatsaturated postcontrast T1-weighted image demonstrates thin enhancement of the mastoid segment of the right facial nerve.
Pontine nuclei of the facial nerve are not delineated on CT or MRI scans. The facial colliculus, a prominent bulge along the floor of the fourth ventricle, is an important landmark in identifying the approximate location of the motor nucleus of the facial nerve (Fig 1A). The cisternal and the intracanalicular segments of the facial nerve are well visualized on highresolution 3D heavily T2-weighted images (Fig 1B).
An oblique sagittal reformatted image can be obtained from this sequence and is helpful in resolving the 4 individual nerves at the fundus of the IAC (Fig 2). The labyrinthine, temporal, and mastoid segments of the facial nerve may not be well visualized on the noncontrast MR images but are well seen on CT images (Fig 3). On postcontrast images, normal enhancement
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TABLE. Classification of facial nerve lesions Categories Lesions Preferred imaging modality Neoplasms
Distinguishing imaging features
Schwannoma
MRI
Perineural tumor spread
MRI
Ramsay Hunt syndrome
MRI
Lyme disease
MRI
Otitis media Cholesteatoma
CT CT
Bell palsy Sarcoidosis
MRI (only in atypical cases) MRI
Abnormal facial nerve enhancement with suggestive clinical symptoms (acuteonset, unilateral, peripheral facial nerve paralysis) Abnormal facial nerve enhancement with basilar leptomeningeal and dural enhancement
Traumatic
Temporal bone fracture
CT
Fracture extending into the facial nerve canal (typically with transverse-type fracture)
Vascular
Hemifacial spasm Venous malformation or hemangioma
MRI CT or MRI
Prominent vascular loop at the root exit zone of the facial nerve Enhancing lesion at the geniculate ganglion with bony spicules
Congenital
Moebius syndrome Aberrant course
MRI CT
Absent facial colliculi Comparison with the normal side is helpful
Pontine lesions
Infarct Multiple sclerosis
MRI MRI
Cavernoma
MRI
T2-FLAIR hyperintense lesions with diffusion restriction Pontine lesion with multiple other white matter lesions with or without enhancement “Popcorn”-like appearance on T2 with susceptibility artifacts
Infectious
Idiopathic
Enhancing lesion extending into the geniculate ganglion (along the course of the facial nerve) Extension of tumor along the course of the facial nerve with known primary malignancy Abnormal enhancement of the facial nerve with classic clinical features (otalgia, vesicles, and facial paralysis) Abnormal facial nerve enhancement with white matter lesions, meningeal enhancement, and classic clinical symptoms (erythema migrans, radiculoneuritis, and arthritis) Middle ear opacification abutting the facial nerve canal Middle ear opacification abutting the facial nerve canal with osseous erosion
FLAIR ¼ fluid attenuated inversion recovery.
FIG 5. Facial nerve schwannoma. An axial T1-W contrast-enhanced MR image demonstrates a large enhancing lesion involving the cisternal (black arrow), intracanalicular (dotted arrow), first genu (long white arrow), and tympanic (short white arrow) segments of the left facial nerve. Enhancement along the expected course of the facial nerve is the most helpful feature in the differentiation of this lesion from a vestibular schwannoma. T1-W, T1-weighted.
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FIG 6. Perineural tumor spread from adenoid cystic carcinoma of the parotid gland. A contrast-enhanced axial CT image demonstrates an infiltrative left parotid gland tumor (asterisk) with abnormal enhancement and widening in the region of the left stylomastoid foramen (black arrow). Compare with normal fat-filled right stylomastoid foramen (white arrow).
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of the facial nerve is seen at the geniculate ganglion and the tympanic and the mastoid segments (Fig 4).1 However, a comparison with the contralateral facial
FIG 8. Ramsay Hunt syndrome. An axial T1-W contrast-enhanced MR image demonstrates asymmetric enhancement of the right facial nerve involving the labyrinthine (dotted arrow) and the first genu (white arrow) segments. T1-W, T1-weighted.
nerve in these segments is essential, as asymmetric enhancement is considered abnormal. The cisternal, intracanalicular, labyrinthine, and parotid segments do not enhance normally, and enhancement of these segments is always suspicious for pathologic processes (Fig 4A).4
Classification of Facial Nerve Lesions For further details, see the Table.
Neoplasms Facial Nerve Schwannoma Schwannomas arise from Schwann cells in the outer layer of the nerve sheath. They account for less than 1% of all tumors of petrous temporal bone.5 They can arise from any segment of the facial nerve with the FIG 7. Perineural tumor spread from squamous cell carcinoma of the skin. (A) An axial T1-W fat-saturated contrast-enhanced MR image demonstrates an infiltrative mass involving the right parotid gland and overlying skin (asterisk) with asymmetric prominent enhancement of the mastoid segment of the right facial nerve (white arrow). (B) An axial T1-W fat-saturated contrast-enhanced MR image demonstrates enhancement along the intracanalicular (long arrow) and the tympanic (dotted arrow) segments of the right facial nerve. Enhancement in the right pterygopalatine fossa (short arrow) indicating involvement of the maxillary division of the trigeminal nerve (CN V2) can be noted. (C) An axial T1-W fat-saturated contrast-enhanced MR image demonstrates enhancement along the first genu and the labyrinthine segments of the right facial nerve (solid arrow). Enhancement of the right trigeminal ganglion and the cisternal segment of the right trigeminal nerve extending to the pons (dotted arrows) can be noted. T1-W, T1-weighted. 6
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FIG 10. Otitis media. A coronal CT image demonstrates opacification (asterisk) of the right tympanic cavity abutting the tympanic segment of the facial nerve (arrow).
FIG 9. Lyme disease. (A) An axial T1-W contrast-enhanced MR image demonstrates prominent enhancement of both the facial nerves. (B) An axial T1-W contrast-enhanced MR image demonstrates abnormal enhancement of both the trigeminal nerves. T1-W, T1-weighted.
geniculate ganglion being the most common site followed by the labyrinthine and the tympanic segments.6,7 Facial nerve schwannomas (FNSs) also tend to involve multiple segments of the nerve.7 The clinical symptoms depend on the location. However, patients typically present with unilateral facial weakness or hearing loss. On CT scans, FNSs usually show smooth osseous expansion without obvious erosion or destruction.7 The osseous expansion in the expected course of the facial nerve is a specific finding.2 On MR images, FNSs demonstrate isointense to hypointense signal on T1-weighted images and hyperintense signal on T2-weighted images. They usually
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demonstrate avid postcontrast enhancement. Large tumors may demonstrate cystic changes. An FNS in the intracanalicular segment can be confused with a vestibular schwannoma; however, a “dumbbell-shaped” lesion with extension of the enhancing component from the fundus of the IAC to the geniculate ganglion is characteristic of an FNS (Fig 5).8 High-resolution 3D heavily T2-weighted images are very helpful in the anatomical localization of temporal bone tumors. Parasagittal reformatted images from these sequences may be helpful in small IAC schwannomas to determine whether the origin of the lesion is the facial nerve (anterior superior quadrant), cochlear nerve (anterior inferior quadrant), or vestibular nerve (posterior superior and inferior quadrants).9
PTS Along the Facial Nerve PTS is the development of a tumor in a noncontiguous fashion along the endoneurium or the perineurium of a nerve. PTS is most commonly seen in adenoid cystic and squamous cell carcinoma of the head and neck.10 Other uncommon malignancies that may demonstrate PTS include lymphoma, melanoma, basal cell carcinoma, and rhabdomyosarcoma.11 The trigeminal and facial nerves are the most common CNs involved in PTS.11 Diagnosis of PTS often changes the management, necessitating the use of adjuvant chemotherapy, adjuvant radiotherapy, or wide surgical margins. Knowledge of CN anatomy is required for the appropriate
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trigeminal nerve branches, as there are multiple connections between the branches of the facial and the trigeminal nerves. The vidian nerve and branches of the maxillary nerve communicate in the sphenopalatine ganglion, allowing tumor spread from the vidian nerve to the GSPN in a retrograde fashion (the vidian nerve is formed by the GSPN and the deep petrosal nerve).12 The auriculotemporal branch of the mandibular nerve also communicates with the facial nerve branches within the parotid gland.13
Infections Ramsay Hunt Syndrome Ramsay Hunt syndrome is a complication of reactivation of the varicella-zoster virus in the geniculate ganglion. The classic clinical triad consists of otalgia, vesicles in the external auditory canal, and ipsilateral facial paralysis.14 This condition is typically diagnosed clinically and imaging studies (most commonly MRI) are reserved for atypical cases. Abnormal enhancement in any segment of the facial nerve can be seen on postcontrast T1-weighted sequences on MRI (Fig 8). Pontine nucleus enhancement has also been described with this syndrome.15 Facial nerve inflammation is often accompanied by neuritis of the vestibulocochlear nerve, which can cause sensorineural hearing loss, vertigo, and tinnitus. Associated pathologic enhancement of CN VIII may be observed on MR images.2 FIG 11. Bell palsy. (A) An axial T1-W contrast-enhanced MR image demonstrates prominent enhancement of both the facial nerves involving the intracanalicular (long arrow) and the first genu and the tympanic (dotted arrow) of the right facial nerve and the first genu (short arrow) of the left facial nerve. (B) A coronal T1-W contrastenhanced MR image demonstrates enhancement of the tympanic segments of both the facial nerves. T1-W, T1-weighted.
diagnosis of perineural spread.12 PTS along the facial nerve typically takes place from malignant tumors of the parotid gland. Tumor typically spreads in a retrograde fashion from the stylomastoid foramen to the geniculate ganglion. Osseous expansion of the stylomastoid foramen and the facial nerve is appreciated on CT scans (Fig 6). A postcontrast fat-suppressed T1-weighted MRI sequence demonstrates abnormal enhancement and thickening of the facial nerve, indicating PTS (Fig 7). Tumor can also spread along the facial nerve from
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Lyme Disease Lyme disease is caused by spirochete Borrelia burgdorferi. The nervous system is involved in 10%15% of patients with infection.16 The characteristic clinical triad is lymphocytic meningitis, cranial neuritis, and radiculoneuritis.17 The facial nerve is the most common CN to be involved.16 Lyme disease occurs in stages with an incubation period of 3-32 days. Stage 1 is characterized by erythema migrans with flulike symptoms.18 Neurologic and cardiac symptoms are seen in stage 2. Stage 3 is characterized by monoarticular or oligoarticular arthritis. The most common abnormality seen on MR images is periventricular or subcortical nonspecific white matter T2 hyperintense signal with or without enhancement.19 Lyme disease should be included in the differential diagnosis if diffuse meningeal or CN enhancement is seen (Fig 9).19
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FIG 12. Sarcoidosis. (A) An axial T1-W contrast-enhanced MR image demonstrates abnormal enhancement of intracanalicular segment of both the facial nerves. (B) An axial T1-W contrast-enhanced MR image demonstrates pathologic enhancement of both the trigeminal nerves (doubleheaded arrows). A small enhancing lesion in the right superior cerebellum (black arrow) can be noted. (C) An axial T1-W contrast-enhanced MR image demonstrates pathologic enhancement of both the optic nerves (arrows). T1-W, T1-weighted.
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viruses, such as Cytomegalovirus23 and Epstein-Barr virus,24 have also been suggested as possible causes. A cell-mediated autoimmune response to peripheral nerve basic protein has also been proposed as the pathogenesis of Bell palsy.25 Bell palsy is characterized by acute onset of facial paralysis, which peaks at 48 hours with gradual spontaneous improvement. Imaging is not routinely performed when the diagnosis is clinically obvious. Imaging is reserved for atypical cases with persistent or recurrent symptoms and for patients with slowly progressive paralysis. MRI with contrast is the study of choice, and abnormal enhancement of the facial nerve in the region of geniculate ganglion, labyrinthine, and proximal tympanic segment is seen without enlargement (Fig 11).12
Sarcoidosis FIG 13. An axial CT image demonstrates transverse-type fracture (black arrow) of the right temporal bone with involvement of the inner ear and the tympanic segment of the facial nerve (dotted arrow). Opacification of the mastoid antrum can also be noted.
Other Infectious or Inflammatory Conditions Involving the Facial Nerve Other inflammatory causes of facial nerve palsy include otitis media, cholesteatoma, and malignant otitis externa. Facial nerve paralysis is seen in 5% of patients with acute otitis media and 1% of patients with cholesteatoma.12 The tympanic segment of the facial nerve is most vulnerable, especially in patients with congenital dehiscence of the facial nerve canal. Opacification of middle ear cavity abutting the facial nerve canal with or without associated osseous erosion or destruction may be observed on CT scans (Fig 10). Contrast-enhanced MRI may provide additional information and demonstrate asymmetric intense enhancement of the facial nerve.
Idiopathic Bell Palsy Bell palsy is the most common cause of acuteonset, idiopathic, unilateral, peripheral facial nerve palsy and accounts for 60%-75% of cases of unilateral facial paralysis.20,21 The etiology is unknown, but viral infections and autoimmune diseases have been recognized as possible causes. Herpes simplex virus has been implicated as a causative agent,22 but other
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Sarcoidosis is an idiopathic systemic disease characterized by formation of noncaseating granulomas. Approximately 5% of patients exhibit central nervous system involvement.26 Isolated central nervous system involvement is seen in less than 1% of patients without systemic involvement.27 Neurologic symptoms are nonspecific and depend on the site of involvement. CN palsy is a common finding with the facial nerve being the most commonly involved CN.28 Other common symptoms are seizures, signs of meningeal irritation, visual disturbances, polyuria, and polydipsia (diabetes insipidus). The diagnosis of neurosarcoidosis is usually based on clinical signs and classic imaging features with evidence of systemic sarcoidosis, which is typically done by biopsy.29 The most common radiologic finding is dural involvement.29 Dural enhancement can be focal or diffuse with hypointense signal on T2-weighted images (a helpful feature suggesting sarcoidosis).30 Leptomeningeal enhancement involving the basilar meninges is a typical finding.27 CN enhancement can be seen without leptomeningeal involvement. The facial and the optic nerves are commonly involved and demonstrate enhancement on postcontrast T1-weighted MR sequences (Fig 12).
Trauma Facial nerve injuries are reported in up to 50% of temporal bone fractures, particularly when the fracture is transverse in orientation. Longitudinal fractures result in injury to the geniculate ganglion, and transverse fractures
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FIG 14. Venous malformation of the facial nerve. (A) An axial CT image demonstrates enlargement of the facial nerve in the region of the first genu. (B) An axial CT image demonstrates bony spicules within the lesion, which is characteristic of venous malformation. (C) An axial T2-W MR image demonstrates hyperintensity at the same location. (D) An axial T1-W contrast-enhanced MR image demonstrates avid enhancement of the lesion. T1-W, T1-weighted.
are more likely to cause injury to the labyrinthine segment. Facial paralysis is usually delayed and incomplete. Immediate facial paralysis after trauma suggests severe nerve injury or transection. Temporal bone fractures with facial nerve involvement are best diagnosed by CT examination (Fig 13).
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Vascular Facial Nerve Venous Malformation or Hemangioma Facial nerve hemangiomas are benign, slow-growing vascular lesions and may be as common as FNSs.31-33
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FIG 15. Hemifacial spasm. An axial CISS MR image demonstrates prominent loop of left vertebral artery (dotted arrow) at the root exit zone of the left facial nerve (white arrow). CISS, constructive interference in steady state.
Benign vascular tumor is another term used interchangeably with hemangioma.34 Recently, it has been proposed that these lesions should be classified as “venous malformations of the facial nerve.”35 Mulliken and Glowacki36 introduced a new classification system in 1982, where they classified vascular lesions into 2 categories based on clinical and histopathologic features: vascular tumors (infantile hemangioma and congenital hemangioma) and vascular malformations (capillary, venous, lymphatic, or arteriovenous malformations). The most common site of facial nerve venous malformation is in the region of the geniculate ganglion followed by the IAC.11,37 Patients' symptoms depend on the tumor location: slowly progressive facial paralysis from lesions located in the geniculate ganglion and unilateral progressive sensorineural hearing loss from lesions located in the IAC.38,39 The term “ossifying hemangioma” is used for these lesions when they form bone.14 On CT images, these lesions have irregular margins with a tendency to produce bony spicules or amorphous “honeycomb” bony changes (Fig 14A and B).14,40 The honeycomb appearance is pathognomonic but seen in only approximately 50% of cases. These lesions demonstrate variable signal intensity on T1-weighted images and high signal intensity on T2-weighted images with strong contrast enhancement
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FIG 16. Moebius syndrome in a neonate with congenital facial palsy. (A) An axial T2-W MR image demonstrates absent facial colliculi. (B) An axial T2-W MR image demonstrates normal facial colliculi in a different patient (for comparison). T2-W, T2-weighted.
(Fig 14C and D). Low signal intensity foci may be seen on T1- or T2-weighted images, corresponding to the ossific changes seen on CT images.41
Hemifacial Spasm Hemifacial spasm is characterized by involuntary, unilateral, sudden contraction of the muscles supplied by the facial nerve. The disease starts with the
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FIG 17. An axial CT image demonstrates right labyrinthine aplasia with hypoplastic facial nerve (black arrow). Normal inner ear structures and normal course of the facial nerve on the left side, for comparison, can be noted.
contraction of the orbicularis oculi muscle with gradual extension to the other facial muscles. It is typically caused by a prominent vascular loop of the
FIG 18. Multiple sclerosis. An axial FLAIR MR image demonstrates a large hyperintense lesion (long white arrow) in the left pons at the expected location of the facial nerve motor nucleus. Other small lesions in the ventral pons and the left middle cerebellar peduncle (short arrows) can also be noted. FLAIR, fluid attenuated inversion recovery.
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anterior inferior cerebellar artery, posterior inferior cerebellar artery, or vertebral artery compressing the root exit zone (the region where the nerve exits the brainstem) of the facial nerve.42,9 The root exit zone of the facial nerve is the transition zone between central and peripheral myelination, which may explain the increased vulnerability of this segment of facial nerve to compression.43,44 Other rare causes of hemifacial spasm include Bell palsy, facial nerve injury, brainstem demyelination, and vascular insults.45 MRI is a useful modality in the identification of these causes. A high-resolution T2-weighted sequence is very helpful in identifying the relationship of vascular loop to the facial nerve (Fig 15). Multiplanar reformatted images can be obtained from this sequence for the evaluation of facial nerve compression in different planes.2
Congenital Congenital facial nerve palsy (CFNP) occurs in approximately 2.1 per 1000 live births in the United States and may be seen at birth or shortly thereafter.46 It most frequently occurs secondary to birth-related trauma, in which case it is often isolated and recovers in approximately 90% cases over several weeks.47 CFNP occurs in the absence of birth trauma and may be an isolated finding or part of underlying syndrome such as Moebius, Goldenhar, or Poland syndrome.
FIG 19. Pontine cavernoma. An axial T2-W MR image demonstrates heterogeneous “popcorn”-like lesion in the pons at the expected location of left facial nerve motor nucleus. T2-W, T2-weighted.
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Irrespective of the etiology, patients with developmental CFNP may show a spectrum of imaging findings, including focal brainstem lesions, brainstem hypoplasia, hypoplasia, or agenesis of the facial nerve.46 Moebius syndrome is characterized by facial weakness and impairment of ocular abduction and is frequently bilateral.48 These patients often have hypoplasia or agenesis of the CN VII nuclei and the accompanying facial nerve along with brainstem hypoplasia (Fig 16). Patients with Goldenhar syndrome demonstrate unilateral CFNP associated with vertebral defects, facial hypoplasia, and preauricular skin tags. Patients with Poland syndrome have absent pectoralis muscles and upper limb deformity in addition to unilateral CFNP.46 Not unexpectedly, patients with developmental CFNP often do not show any improvement with time. An anomalous facial nerve course often occurs in association with developmental anomalies of CN VIII, IAC, middle ear, or inner ear (Fig 17). In these cases, the facial nerve may follow an aberrant course through the temporal bone, exit prematurely from the IAC, and overlie the stapes footplate or cochlear promontory.49
Central Causes of Facial Nerve Palsy The facial nerve can also be affected by a variety of intracranial lesions, such as infarcts, multiple sclerosis plaques (Fig 18), cavernomas (Fig 19), neoplasms (Fig 20), and arteriovenous malformations. MRI is the modality of choice for the characterization of these lesions.
Conclusion
FIG 20. Brain metastases from lung cancer with involvement of the right facial nerve motor nucleus. (A) An axial T2-W MR image demonstrates hyperintense lesion in the right pons at the level of the facial colliculi. (B) An axial T1-W contrast-enhanced MR image demonstrates avid enhancement (white arrow) of the pontine lesion with another large lesion in the right occipital lobe (dotted arrow). T2-W, T2-weighted.
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The facial nerve is affected by a wide variety of pathologies, including congenital, traumatic, inflammatory, and neoplastic conditions. Any segment of the facial nerve, from the brainstem to the parotid gland, can be involved by these pathologies. Familiarity with the anatomy, normal pattern of enhancement, and pathologic imaging findings is important for appropriate patient management.
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