Imaging plays a critical role in the evaluation of a number of facial nerve disorders. The facial nerve has a complex anatomical course; thus, a thorough understanding of the course of the facial nerve is essential to localize the sites of pathology. Facial nerve dysfunction can occur from a variety of causes, which can often be identified on imaging. Computed tomography and magnetic resonance imaging are helpful for identifying bony facial canal and soft tissue abnormalities, respectively. Ultrasound of the facial nerve has been used to predict functional outcomes in patients with Bell’s palsy. More recently, diffusion tensor tractography has appeared as a new modality which allows three-dimensional display of facial nerve fibers.
Imaging plays an important role in the evaluation of facial nerve disorders. The facial nerve has a complex anatomical course, and dysfunction can be due to congenital, inflammatory, infectious, traumatic, and neoplastic etiologies. Computed tomography is useful for identifying bony abnormalities of the intratemporal facial nerve, which can occur with congenital malformations, trauma, and cholesteatoma. Magnetic resonance imaging (MRI) is useful for identifying soft tissue abnormalities around the facial nerve, as seen in inflammatory disorders, neoplasms, and hemifacial spasm. Facial nerve ultrasound has been used in a recent study to predict functional outcomes in Bell’s palsy [
The facial nerve is composed of motor, sensory, and parasympathetic fibers. Complete separation of the facial and acoustic nerves and development of the nervus intermedius (or nerve of Wrisberg) occurs by 6 weeks of gestation. By the 16th week, the neural connections are completely developed. The bony facial canal develops until birth, enclosing the facial nerve in bone throughout its course except at the facial hiatus (the site of the geniculate ganglion) in the floor of the middle cranial fossa [
Facial motor fibers originate from cell bodies located in the precentral and postcentral gyri of the frontal motor cortex. These fibers travel in the posterior limb of the internal capsule inferiorly to the caudal pons. There, the motor fibers supplying the facial musculature beneath the brows cross the midline to reach the contralateral motor nucleus in the reticular formation of the lower pons (anterior to the fourth ventricle). The majority of motor fibers that supply the musculature of the forehead also cross the midline; however, a few fibers do not, instead traveling in the ipsilateral motor nucleus. Thus, muscles of the forehead receive innervation from both sides of the motor cortex, and so forehead-sparing facial paralyses can be indicative of a central etiology. The motor fibers the pass dorsally, loop medial-to-lateral around the abducens nucleus, and create the facial colliculus, which bulges into the floor of the fourth ventricle (Figure
Normal facial nerve on MRI. (a) Axial CISS image at the level of the pons demonstrates the facial colliculus (arrow) seen as a small bump along the anterior wall of the fourth ventricle. This is formed by the motor tracts of the facial nerve (purple curved line) coursing around the abducens nucleus (yellow dot). (b) Axial CISS sequence of the left CPA and IAC demonstrates the normal cisternal and intracanalicular segments of the left CN VII (solid arrow), anterior to CN VIII (double lined arrow).
The nervus intermedius contains sensory, special sensory and parasympathetic fibers. It provides sensation to the posterior concha and external auditory canal. The nervus intermedius’ special sensory fibers supply taste sensation to the anterior two-thirds of the tongue. The afferent fibers synapse with cell bodies in the geniculate ganglion at the first genu of the facial nerve. These sensory afferents then join the parasympathetic fibers, passing via the nervus intermedius to the nucleus tractus solitarius in the medulla. The parasympathetic portion of the nervus intermedius originates in the superior salivatory nucleus in the dorsal pons and provides the secretomotor function of the ipsilateral lacrimal gland, submandibular glands, sublingual glands, and minor salivary glands.
Both the motor root of the facial nerve and the nervus intermedius leave the brainstem near the dorsal pons at the pontomedullary junction (the cisternal segment of the facial nerve). Within the cerebellopontine angle (CPA), the nerve travels anterolaterally into the porus acousticus of the internal auditory canal (IAC), anterior to the vestibulocochlear nerve (Figure
The anterior inferior cerebellar artery (AICA) arises from the basilar artery near the junction of the pons and medulla. The AICA can have a variable course and territory. The AICA runs within the IAC and is frequently in proximity with the nerve within the IAC. In some cases, the AICA may run in the IAC between the facial and vestibulocochlear nerve [
The bony facial nerve canal (or fallopian canal) begins as the facial nerve exits the IAC at the fundus. The major blood supply for the facial nerve proximally within the canal is the superficial petrosal artery, a branch of the middle meningeal artery. The stylomastoid artery supplies the fallopian canal distally [
Normal facial nerve canal on CT. Axial temporal bone CT images demonstrate the intracanalicular (solid arrow in (a)), labyrinthine (double lined arrow in (a)), geniculate ganglion (double lined arrow in (b)), tympanic (solid arrow in (b)), and mastoid (arrow in (c)) segments of the facial nerve.
Diagram of the course of the intratemporal facial nerve from the fundus of the IAC to the stylomastoid foramen [
While the geniculate ganglion is typically covered by bone, in up to 18% of cases the ganglion is in direct contact with the dura of the middle cranial fossa [
The tympanic segment runs from the geniculate ganglion to the second (or posterior) genu [
The mastoid segment of the facial nerve runs posteromedially along the external auditory canal to its exit from the temporal bone at the stylomastoid foramen (13 mm in adults) [
Extratemporally, the facial nerve separates into two main branches at the pes anserinus: the temporofacial branch and the cervicofacial branch. Within the parotid gland, these branches further divide into five main branches that supply the facial musculature: temporal (or frontal), zygomatic, buccal, marginal mandibular, and cervical.
Imaging of the facial nerve should be tailored to both the suspected pathology and clinical localization of the lesion along the nerve’s course. Typically, if a facial palsy is localized to the cisternal or intracanalicular segments of the facial nerve or the pontine nuclei, contrast-enhanced MRI is indicated. If the lesion can be localized to the mastoid, tympanic, or labyrinthine segments of the facial nerve, high-resolution temporal bone CT is recommended to evaluate the fallopian canal. Contrast-enhanced MRI should be performed first in cases when the palsy cannot be definitively localized. Both MRI and temporal bone CT are typically performed for the evaluation of tumors involving the facial nerve.
CT is preferable for imaging the lateral course of the facial nerve from the porus acusticus to the stylomastoid foramen. CT evaluation of the facial nerve lateral to the porus acusticus should include high-resolution temporal bone CT. Temporal bone CT is particularly useful in the evaluation of the caliber and the course of the IAC and bony facial nerve canal in the temporal bone. Erosion and destruction of the facial nerve canal are best depicted with high-resolution temporal bone CT. In addition, CT has the advantage of demonstrating the relationship of the facial nerve canal to normal anatomic landmarks such as the ossicles which are not seen on MR. These relationships are critical during surgical planning. At our institution, we acquire noncontrast 0.3 mm axial slices through the bilateral temporal bones for our raw data, with 0.6 mm thick axial, coronal, and Pöschl reformats through the individual temporal bones. Dose settings are typically 120 kVp, CTDI volume 55.5—62.6, and 140–220 mAs. Administration of intravenous contrast is not part of the standard protocol but may be included if there is a clinical suspicion of a neoplasm or vascular abnormality.
Temporal bone CT can detect deviations in the course and caliber of the intratemporal facial nerve, which can provide key information regarding facial nerve pathology and prove critical in surgical planning for otologic surgery. Bony dehiscences of the fallopian canal can be identified preoperatively, leading to a decreased rate of iatrogenic facial nerve trauma. In cases of aural atresia, the facial nerve can vary in its course, making it more susceptible to injury during atresiaplasty and limiting the diameter of the reconstructed external auditory canal [
When using CT to evaluate the facial nerve, pathology often can only be inferred by visualization of erosion or destruction of the adjacent bony facial nerve canal. In contrast, MRI visualizes soft tissues well and so is better suited for evaluating soft tissue facial nerve abnormalities. MRI can be used to image the facial nerve from the brainstem to the fundus of the internal auditory canal and to determine the presence of perineural spread from parotid malignancies (Figure
In high-resolution T2-weighted images or CISS images, the normal facial nerve appears as a hypointense linear structure extending from the brainstem to the IAC, anterior to the vestibulocochlear nerve, surrounded by T2 hyperintense cerebrospinal fluid (Figure
When gadolinium contrast is used, the normal facial nerve faintly enhances in the geniculate ganglion, tympanic, and mastoid segments (Figure
Bell's palsy. T1- weighted contrast-enhanced MR images demonstrate abnormal enhancement of the distal left cisternal (arrow, (a)), labyrinthine (arrow, (b)), first genu (arrowhead, (b)), and mastoid (arrow, (d)) segment of the facial nerve. Enhancement of the first genu, tympanic and mastoid segments was asymmetrically greater than the normal contralateral side (not shown).
MRI can also reveal enlargement of the facial nerve, as may be seen in a neoplastic process. Particularly in the areas outside of the bony fallopian canal, this enlargement can be missed in high-resolution temporal bone CT. Facial nerve schwannomas may appear as fusiform masses in the labyrinthine and mastoid segments. In the cisternal, intracanalicular, and tympanic segments, schwannomas can appear lobulated (Figure
MRI characteristics can be used to distinguish masses around the facial nerve that require surgical excision from those that should not be surgically removed until facial function has been affected. For instance, lipomas of the internal auditory canal and first genu will appear hyperintense on T1-weighted imaging without additional gadolinium and can be reliably identified with T1-weighted imaging with fat saturation (Figure
Reconstructed sagittal oblique CISS images through the internal auditory canals obtained perpendicular to the course of the IAC enable the evaluation of the caliber of the facial nerve. In patients with Moebius syndrome, CISS imaging is particularly useful in confirming the absence or small caliber of the facial nerve within the CPA and IAC (Figure
For patients with hemifacial spasm, a loop of the anterior inferior cerebellar artery, posterior inferior cerebellar artery, or vertebral artery compresses the ipsilateral facial nerve at the root exit zone, leading to involuntary contractions of the facial musculature. High-resolution T2-weighted or CISS images can directly visualize the vascular loop and compressed facial nerve (Figure
In a recent study, ultrasound has been utilized to predict facial nerve outcomes in Bell’s palsy. In this prospective, controlled study, patients with Bell’s palsy, ultrasound was performed 2–7 days after the onset of paralysis using a General Electric Logiq 7 Pro with a 5 to 10 MHz linear array transducer [
In cases of large vestibular schwannomas, it can be difficult to distinguish between the facial nerve and the tumor on MRI. Both the facial nerve and the schwannoma have similar signal intensities, and larger tumors cause thinning of the facial nerve, making the nerve even more difficult to identify. Additionally, there is typically no intervening cerebrospinal fluid between the schwannoma and the facial nerve [
Chen et al. [
Overall, DT tractography shows potential in evaluation of the course of the facial nerve, particularly in cases involving large vestibular schwannomas. Currently, this technique is computationally intensive and not automated, typically requiring intensive involvement of Ph.D. level personnel in the construction of these images. Further technological advancements in sensitivity and automation of the technique will likely lead to its greater clinical use.
The facial nerve can be affected by a number of different disorders resulting in weakness or paralysis of the facial musculature (Table
Disorders of the facial nerve.
Infectious | Acute OM |
Chronic OM | |
Cholesteatoma | |
Herpes zoster oticus | |
Lyme disease | |
| |
Traumatic | Temporal bone fracture |
Iatrogenic injury | |
Avulsion at brainstem | |
Penetrating trauma | |
| |
Neoplastic | Facial schwannoma |
Vestibular schwannoma | |
Hemangioma | |
Lipoma | |
Glomus tumors | |
Malignancy of skin/parotid | |
| |
Congenital | Moebius syndrome |
Displacement (atresia) | |
Aural atresia | |
CHARGE syndrome | |
Dehiscence of FC | |
| |
Vascular | MCA infarct |
Pontine artery infarct | |
Lacunar infarct | |
| |
Idiopathic | Bell’s palsy |
Multiple sclerosis | |
Sarcoidosis | |
| |
Inflammatory | Guillain-Barre |
OM: otitis media; FC: fallopian canal; and MCA: middle cerebral artery.
Facial dystonias and hyperkinetic states (hemifacial spasm, essential blepharospasm, and Meige’s syndrome) can also occur. All of these pathologies are discussed in detail below.
The most common cause of facial paralysis, Bell’s palsy, is characterized by the sudden onset of facial weakness. It has been associated with the reactivation of herpes simplex type 1 in the geniculate ganglion, leading to inflammatory edema of the facial nerve [
Several other idiopathic and inflammatory processes can cause facial paralysis. These include sarcoidosis, Guillain-Barre syndrome, and multiple sclerosis. These paralyses may have a more indolent onset than Bell’s Palsy, which is characterized by full onset of weakness within 72 hours. Typically these processes will involve other cranial nerves or parts of the brain in addition to the facial nerve. These pathologies are best evaluated utilizing MRI with gadolinium enhancement [
A variety of infectious disorders can affect the facial nerve. For instance, dehiscences of the fallopian canal can lead to facial paralyses in the setting of chronic or acute otitis media. These are best evaluated with high-resolution CT of the temporal bones. In cases where extension of the infection into the central nervous system is suspected, both high-resolution temporal bone CT and MRI of the brain with gadolinium will be indicated. Lyme disease is increasingly common in the United States and is the most common cause of acquired bilateral facial paralysis. MRI of the brain with gadolinium may be normal or may show bilateral enhancement of the facial nerves and, potentially, other nerves as well [
Traumatic injury to the facial nerve can occur at a variety of levels, from the brainstem to the distal periphery. Blunt force trauma from high-speed motor vehicle accidents can fracture the temporal bone, leading to either direct involvement of the fallopian canal and nerve injury or indirect injury via postconcussive injury and edema. Delayed facial palsy results from reactivation of herpes simplex type I virus within the geniculate ganglion and occurs 3–14 days after a traumatic injury [
Facial nerve injuries more commonly occur in transverse fractures (38–50% of cases), rather than longitudinal fractures (20% of cases) of the temporal bone [
Transverse temporal bone fracture. Coronal (a) and axial (b) CT images demonstrate a transverse fracture through the labyrinthine segment of facial nerve canal (arrows). Axial CT image (c) shows the fracture involving the otic capsule and basal turn of the cochlea (arrowhead). Note blood products in the middle ear cavity (asterisks).
Congenital malformations of the facial nerve can clinically be asymptomatic or present with facial weakness. Bony dehiscences of the facial nerve canal are the most common of these and typically occur in the tympanic segment superior to the oval window (Figure
Facial nerve dehiscence. Coronal CT image of right temporal bone demonstrates dehiscence of right CN VII tympanic segment at the level of oval window (arrow).
Aural atresia. Axial CT images (a)–(c) demonstrate abnormal facial nerve canal tympanic segment coursing posterolaterally to the middle ear cavity (arrows), instead of the normal posteromedial course. Coronal CT image (d) demonstrates the abnormal proximal tympanic segment of the facial nerve canal coursing superior to the middle ear cavity and ossicles (arrow), instead of its normal medial course. Coronal CT images (e)-(f) showing the abnormal distal tympanic segment and second genu of the facial nerve canal (arrows).
Congenital facial paralysis can occur as a result of facial nerve nucleus abnormalities in a variety of syndromes that include Moebius, DiGeorge, Goldenhar, CHARGE, trisomy 13, and trisomy 18. In Moebius syndrome, a constructive interference in steady-state (CISS) sequence can assist in early diagnosis by demonstrating the absence of the facial nerve [
A variety of central pathologies can affect the intracranial portion of the facial nerve, including cerebrovascular accident (CVA), brain tumors (primary and metastatic), and multiple sclerosis. Presentation of the paresis or paralysis is determined by the site of the intracranial lesion. Central paralyses occur when the lesion disrupts the facial nerve fibers prior to their decussation in the reticular formation of the caudal pons. Lesions affecting the facial nerve distal to the decussation can be mistaken for peripheral facial palsies; however, these are rare. Millard-Gubler syndrome is a mixed syndrome that is caused by lesions of the pons which lead to ipsilateral facial paresis, ipsilateral abducens paralysis, and contralateral hemiplegia. Millard-Gubler syndrome results from pathology disrupting the corticospinal tract prior to decussation plus the sixth and seventh nerve nuclei [
Pontine infarcts comprise approximately 7% of all ischemic strokes. These infarcts are most frequently lacunar infarcts involving paramedian, short, and long circumferential perforators arising from the basilar artery [
Central facial paralysis can also follow a CVA in the territory of the middle cerebral artery (MCA) or anterior cerebral artery (ACA) [
MRI with multiple sequences can accurately detect ischemic changes in patients with acute neurologic deficits. The following sequences are typically included: diffusion weighted imaging (DWI), T2-weighted (T2W) and fluid-attenuated inversion recovery (FLAIR), MR angiography (MRA), perfusion-weighted imaging (PWI), and gradient-recalled echo (GRE). DWI sequence can detect acute ischemia within minutes of onset as a focal area of hyperintensity [
Patients with hemifacial spasm suffer unilateral twitching or spasms of facial muscles. Tortuosity of the anterior inferior cerebellar artery, posterior inferior cerebellar artery, basilar artery, or vertebral artery can compress the facial nerve at the root exit zone, resulting in unilateral spasms. MRI can identify the artery compressing the facial nerve and, thus, serve as a guide for microvascular decompression. In essential blepharospasm, involuntary blinking occurs with increased frequency, particularly in response to stimuli such as wind, sunlight, noise, or stress [
A variety of neoplastic processes can affect facial nerve function. Schwannomas can occur anywhere along the course of the facial nerve. Most commonly, they arise in the perigeniculate, tympanic, or mastoid segments. Lipomas can occur in the CPA or IAC, entrapping unmyelinated facial nerve fibers. Hemangiomas arise from the vascular plexus surrounding the facial nerve, most commonly in the perigeniculate region. Less commonly, these lesions are found in the IAC or mastoid segment [
Facial nerve hemangioma. Axial CT (a) demonstrates a mass with trabecular bony matrix centered in the first genu of the facial nerve (arrow). Axial T1 postcontrast fat-saturated MRI (b) demonstrates the enhancing hemangioma (arrow).
Perineural tumor spread along CN VII. Axial T1 (a) and coronal (b) postcontrast fat-saturated images demonstrate an enlarged, enhancing left facial nerve in the stylomastoid foramen and mastoid segment of the facial nerve canal (arrows), indicating perineural tumor spread from invasive squamous cell carcinoma (arrowhead) of the left external auditory canal.
Normal facial nerve on MRI. Postcontrast fat-saturated T1-weighted MRI images of normal enhancing tympanic (a) and mastoid (b) CN VII segments.
Right CN VII schwannoma in the cerebellopontine angle (CPA) in a patient with neurofibromatosis type II. Axial CISS sequence (a) demonstrates a small lesion along CNVII (black arrow), which courses anterior to CNVIII (white arrowhead) in the right CPA cistern. Axial T1 postcontrast fat-saturated images (b)-(c) demonstrate the enhancement of the right facial schwannoma (solid white arrow, (b)). Also note the vestibular schwannoma in the right IAC (dashed white arrow, (c)) and residual enhancement with postsurgical changes in the region of the left IAC.
CPA Lipoma. Noncontrast T1-weighted image (a) demonstrates a globular hyperintense lesion in the right CPA (white arrow). (b) Postcontrast fat-saturated T1-weighted MR image shows signal dropout indicating that this lesion is composed of fat. There is no associated enhancement of this lesion.
Recurrent cholesteatoma. Axial diffusion-weighted image (a) demonstrates abnormal hyperintense signal in the left temporal bone consistent with a focus on recurrent cholesteatoma (white arrow). Axial T2-weighted sequence (b) shows fat packing material in the left temporal bone (arrowhead) following mastoidectomy with blind sac closure.
Moebius syndrome. Sagittal oblique CISS sequence of the internal auditory canal in a patient with Moebius syndrome (a) demonstrates the small caliber of the hypoplastic facial nerve in the anterior superior aspect of the canal (arrow). The normal vestibulocochlear nerve is seen posteriorly (double lined arrow). Sagittal oblique CISS image in a normal patient (b) demonstrates the normal caliber of the facial (solid arrow) and vestibulocochlear (double lined arrow) nerves for comparison.
Neurovascular compression in a patient presenting with left hemifacial spasm. Axial CISS (a) and T1 postcontrast MRI (b) images demonstrate the left vertebral artery (arrow) abutting the left facial nerve at the root entry zone. Axial noncontrast CT scan (c) demonstrates the hyperdense postsurgical material from microvascular decompression surgery.
Paragangliomas are highly vascular tumors that originate in the paraganglionic tissue of the carotid bifurcation (carotid body tumors), jugular foramen (glomus jugulare), vagus nerve (glomus vagale), and tympanic plexus on the promontory (glomus tympanicum). They can occur sporadically or in association with tumor syndromes such as multiple endocrine neoplasia type II (MEN II), von Hippel-Lindau syndrome, or neurofibromatosis type I. Rare cases of facial nerve paragangliomas occurring along the mastoid segment have also been reported [
Neoplasms in the middle ear can infiltrate or compress the tympanic segment of the facial nerve. These lesions include adenomas, schwannomas, and paragangliomas. Adenomas arise from the glands of the middle ear mucosa and often present as a middle ear mass with conductive hearing loss. CT typically shows a middle ear mass without evidence of bony erosion.
Malignant tumors of the parotid can affect the extratemporal facial nerve. Primary malignant neoplasms include mucoepidermoid carcinoma, adenoid cystic carcinoma, adenocarcinoma, malignant mixed tumors, acinic cell carcinoma, lymphoma, and squamous cell carcinoma. In particular, adenoid cystic carcinoma frequently exhibits perineural invasion (70–75%) [
Imaging can provide critical information for diagnosis and treatment of facial nerve disorders. MRI of the brain and brainstem is most useful for central pathologies affecting the facial nerve as well as lesions of the facial nerve proximal to the porus acusticus. High-resolution CT of the temporal bone best visualizes the course of the nerve within the fallopian canal to the stylomastoid foramen. Soft tissue CT with contrast or MRI can be used to evaluate areas of the distal course of the facial nerve within the parotid and soft tissues of the face. Facial nerve ultrasound may be useful in predicting functional outcomes 3 months after the onset of paralysis in patients with Bell’s palsy. DT tractography is a new modality that shows promise for 3D visualization of facial nerve fibers, potentially lowering the risk of facial nerve injury during treatment of vestibular schwannomas.
The authors declare that they have no conflict of interests.