Computed Tomography Imaging of the Facial Nerve

Though imaging protocols vary, in most cases, intravenous contrast is not necessary for CT evaluation of the facial nerve. In general, 0.625 mm or thinner helically acquired axial images with reconstructions in the coronal plane form the basis of most CT protocols. Despite its inability to directly image the facial nerve itself, CT can play an important role in the appropriate clinical settings. Given its high resolution of bony structures (including of the facial nerve canal in all segments), CT is particularly well suited for evaluation of facial nerve injury related to temporal bone fracture, destructive osseous facial nerve lesions, or calcification that can be seen with hemangioma of the facial nerve.1 In addition, CT can play a critical role in assessing the intratympanic facial nerve and its relation to bony structures such as the footplate of the stapes or the lateral semicircular canal. More distally in its course, the relationship of the canal of the mastoid segment of the facial nerve and the jugular foramen is also well evaluated on CT. Besides the inability to directly visualize the facial nerve, another disadvantage of CT is its use of ionizing radiation, a particularly important consideration in pediatric populations. Nonetheless, when correctly utilized, CT demonstrates bony detail not possible with MRI and can serve as an important component of the imaging of facial nerve pathology.

Magnetic Resonance Imaging of the Facial Nerve

Generally, high-resolution multiplanar T1- and T2-weighted images along with gadolinium-enhanced, fat-suppressed T1-weighted images should be included in most standard imaging protocols of the facial nerve. Unlike CT, MRI allows direct visualization of the facial nerve, especially in the cisternal, intracanalicular, mastoid, and extracranial segments. In addition, if clinical findings suggest a lesion from the origin of the pontine nuclei of the facial nerve (or even from the cortex in a supranuclear facial palsy), MRI can offer far greater anatomic detail and contrast resolution of the brain. Heavily T2-weighted three-dimensional images are particularly useful in evaluating neural and vascular structures adjacent to the bright cerebrospinal fluid (allowing, for example, separation of the facial nerve from the components of the vestibulocochlear nerve in the internal auditory canal). In addition, MRI is valuable in demonstrating abnormal enhancement of the facial nerve in its cisternal, intracanalicular, and intratemporal segments, which can be seen in infectious, inflammatory, and neoplastic pathologies. In this regard, it is important to keep in mind that mild, symmetric perineural venous enhancement can normally be seen within the geniculate ganglion and the tympanic and mastoid segments.2 Finally, in the evaluation of suspected vascular lesions causing facial nerve symptoms (such as hemifacial spasm), magnetic resonance angiography can play a valuable role in assessing the relationship between anomalous/tortuous central vascular structures and the adjacent facial nerve.1

The authors’ simplified approach to choice of modality for imaging of facial nerve lesions is seen in Fig. 6.1 . Should physical exam and clinical findings localize a facial nerve deficit anywhere from cortical motor inputs to the cisternal segment of the internal auditory canal (IAC), precontrast and contrast-enhanced MRI should be the initial examination of choice. From the level of the IAC distally to the exit of the facial nerve through the stylomastoid foramen, both CT and MRI play complementary roles, and the first exam of choice depends on multiple factors as discussed and detailed as follows. Finally, distal to the stylomastoid foramen (e.g., for the evaluation of a suspected intraparotid lesion causing a facial nerve deficit) with its ability to resolve and characterize soft tissue lesions, MRI is the imaging exam of choice.

Bell Palsy

Patients with the typical symptoms of acute onset peripheral facial nerve palsy are frequently referred for imaging evaluation. Contrast-enhanced MRI is the mainstay for imaging of this clinical presentation, and the typical imaging is abnormal uniform enhancement of the facial nerve, which is usually normal in size or only slightly enlarged ( Fig. 6.2a, b ).3 Focal linear enhancement in the fundus of the IAC is a classic finding, with enhancement also frequently noted along the intratemporal portion of the nerve.4,5 Enhancement of more distal portions of the facial nerve, such as the mastoid segment, can occur, but is less frequently observed. Persistent enhancement of the nerve can lag clinical symptomatic improvement and can be seen for up to about 1 year in some cases. The mechanism of facial nerve enhancement in Bell palsy is not entirely clear but may be a function of the hyperemia of the perineural structures from inflammation or may be secondary to frank breakdown of the blood–nerve barrier. Nonetheless, depending on the timing of imaging, not all cases of Bell palsy demonstrate pathologic facial nerve enhancement with reported rates varying from 57–100%.1

Given its generally benign and self-limited clinical course, when a classic clinical presentation for Bell palsy is noted, imaging findings add little to patient management. However, in atypical presentations (slow insidious onset, progressive worsening of symptoms, failure of normal resolution within 4 months, etc.), MRI can provide valuable insight into other possible causes for facial nerve dysfunction along the entire course of the visualized nerve.6 In such cases, focal facial nerve enlargement or nodular, nonlinear enhancement should suggest an alternate diagnosis, and the possibility of a neoplastic entity should be entertained in the correct context. Slow insidious onset of facial paralysis or weakness requires imaging of the complete facial nerve including the entire parotid, temporal bone, and the central (brainstem) course.

Ramsay Hunt Syndrome

Thought to result from a similar reactivation of varicella zoster infection from the geniculate ganglion, the acute onset of symptoms including clinically apparent, sometimes hemorrhagic vesicles on the pinna and external auditory canal often result in the request for an imaging examination. Contrast-enhanced MRI is the imaging exam of choice, with variable findings, often indistinguishable from Bell palsy, including enhancement of the tympanic, geniculate, and mastoid segments of the facial nerve; it should be noted, however, that up to 50% of patients may not demonstrate abnormal enhancement of any component of the facial nerve.1 Though the physical exam findings should make the presence of lesions along the pinna and external auditory canal clear, MRI can confirm findings in cases with florid subcutaneous vesicular disease by demonstrating abnormal soft tissue enhancement ( Fig. 6.3a, b ).

Hemifacial Spasm

The anatomic basis for the clinical syndrome of hemifacial spasm is, in > 90% of cases, a redundant or tortuous vascular loop that causes compression of proximal cisternal segment of the facial nerve.1 The anterior inferior cerebellar, posterior inferior cerebellar, and vertebral arteries are most commonly responsible for this syndrome.7 MRI (typically combined with magnetic resonance angiography) can display, often in exquisite anatomic detail, the cisternal segment of the facial nerve and the culprit compressing vascular structure ( Fig. 6.4a, b ). The vessel causing compression usually exerts mass effect near the root exit zone of the facial nerve near the brainstem. Here, normally the medially positioned motor fibers are compressed by the anterolaterally positioned offending vessel.

Though a vascular loop can often be identified, absence of this finding on high-resolution MRI may occur because focal nerve compression may be secondary to a vessel that is below the spatial resolution threshold of MRI; therefore, a negative MRI study should not discourage surgical decompression in clinically appropriate cases.8 Conversely, an enlarged or prominent vessel in the cerebellopontine angle (CPA) cistern can be seen in up to a third of asymptomatic patients, many of whom display vertebrobasilar dolichoectasia secondary to long-standing hypertension. As such, imaging work-up for this syndrome should be considered an adjunct to clinical history and physical exam findings.8