• Special visceral efferent (SVE). Branchial motor innervation to muscles of facial expression (including orbicularis oculi, orbicularis oris, zygomaticus major, levator anguli oris, risorius, depressor anguli oris, mentalis, buccinator, frontalis, occipitalis, corrugator supercilii, and platysma), stapedius, stylohyoid, and posterior belly of digastric.
• General visceral efferent (GVE). Visceral motor (parasympathetic) innervation to lacrimal gland (via greater superficial petrosal nerve; GSPN), oral and nasal mucosa (via GSPN), and submandibular and sublingual glands (via chorda tympani).
• General sensory afferent (GSA). Somatic sensory from external auditory meatus, auricle and retroauricular area
• Special afferent special sensory (SA) for taste from anterior two thirds of tongue and hard and soft palate (via chorda tympani) .
• Facial motor nucleus lies in caudal pontine tegmentum, anterolateral to cranial nerve (CN) VI nucleus (Figs. 7.1, 7.2). It sends axons dorsally toward the fourth ventricle; these axons loop around the CN VI nucleus (forming the genu of the facial nerve) and then travel ventrolaterally to emerge from the pontomedullary junction just above CN VIII. The facial colliculus is formed by this genu of the facial nerve and refers to a smooth hump that protrudes into the fourth ventricle.
• Supranuclear control is via corticobulbar fibers from the lower one third of the precentral gyrus via corona radiata, genu of internal capsule, and medial cerebral peduncle to the facial motor nucleus in the pons. Corticobulbar fibers project bilaterally to upper face motor neurons and contralaterally to lower face motor neurons. The peripheral course of CN VII is discussed below.
Nervus Intermedius (of Wrisberg)
• GVE, GSA, and SA (parasympathetic, somatic sensory, and special sensory).
• Exits the pons between the motor branch of CN VII (medially) and CN VIII (laterally), traverses the cerebellopontine angle cistern, and enters the internal auditory canal (IAC).
• GVE. The superior salivatory nucleus and associated lacrimal nucleus in the dorsal pons send preganglionic parasympathetic axons to the nervus intermedius and from there to (1) the greater superficial petrosal nerve (GSPN) to the pterygopalatine ganglion to the lacrimal gland and the mucosa of the nose and mouth (palatal and nasal glands); and (2) the chorda tympani nerve that joins with the lingual nerve (CN V3) and goes to the submandibular ganglion and on to the submandibular and sublingual glands for salivation (see below regarding taste function). The olfactory areas and the limbic system send input to the hypothalamus, which influences the superior salivatory nucleus by way of the dorsal longitudinal fasciculus.
• The geniculate ganglion is located in the petrous temporal bone lateral and posterior to the petrous internal carotid artery (ICA), posterior and medial to the foramen spinosum, and anterior to the superior semicircular canal. It consists of sensory nerve cell bodies for taste (from chorda tympani) and external ear sensation (from sensory auricular branch). Motor and parasympathetic fibers of CN VII pass through the geniculate ganglion without synapsing.
• GSA. Sensory information from the external auditory meatus, and the auricle and retroauricular area is carried via the sensory auricular branch to the geniculate ganglion (where cell bodies lie, at the facial genu in the petrous bone) to the nervus intermedius and back to the spinal trigeminal tract and spinal trigeminal nucleus in the medulla.
• SA. See below under Chorda Tympani Nerve.
• After emerging from the ventrolateral pons, the motor division and nervus intermedius traverse the cerebellopontine angle cistern with CN VIII and then enter the IAC in the petrous temporal bone, along with the labyrinthine artery and vein (Fig. 7.3). Four intratemporal segments of the nerve are described (Fig. 7.4):
Meatal (intracanalicular) segment. Within the IAC, the motor division of CN VII is located anterosuperior, the cochlear nerve anteroinferior, the superior vestibular nerve posterosuperior, and the inferior vestibular nerve posteroinferior. The nervus intermedius travels between CN VII and CN VIII at the porus acusticus and then joins CN VII to travel in the anterosuperior quadrant (superior to the crista falciformis and anterior to the Bill bar) (Fig. 7.3).
Labyrinthine segment. The bony fallopian canal courses anterolaterally from the fundus of the IAC and carries the labyrinthine segment of CN VII to the geniculate ganglion. The GSPN arises from the apex of the geniculate ganglion.
Horizontal (tympanic) segment. From the geniculate ganglion, CN VII travels posteriorly and horizontally just inferior to the lateral semicircular canal. No branches arise from this segment of the facial nerve.
Mastoid (vertical) segment. At the posterior aspect of the middle ear, CN VII turns inferiorly to form the mastoid segment. Three branches arise from this segment of CN VII: the nerve to the stapedius muscle, the chorda tympani nerve (see above), and the sensory auricular branch (innervates external auditory meatus and the auricle and retroauricular area). CN VII then exits the bony facial canal at the level of the stylomastoid foramen and immediately gives off the posterior auricular nerve (to occipitalis, posterior auricular, and oblique auricular muscles), the digastric branch (to the posterior belly of the digastric muscle), and the stylohyoid branch (to the stylohyoid muscle).
CN VII then enters the parotid gland and divides into temporofacial and cervicofacial branches. These then divide into temporal, zygomatic, buccal, marginal mandibular, and cervical branches (TEN ZEBRAS B IT MY CLOCK), which innervate the many muscles of facial expression (listed at beginning of chapter).
The distribution and functions of CN VII are summarized in Fig. 7.5.
Greater Superficial Petrosal Nerve
• GVE (parasympathetic).
• GSPN arises from the geniculate ganglion, courses anteromedially, and exits the petrous temporal bone via the greater petrosal foramen (facial hiatus) to the middle fossa.
• GSPN passes deep to the trigeminal (gasserian) ganglion in Meckel’s cave and down the foramen lacerum to the pterygoid canal (vidian canal), where it joins with the deep petrosal nerve (sympathetic fibers from ICA plexus; cell bodies in superior cervical ganglion) to form the nerve of the pterygoid canal (vidian nerve).
Nerve of the Pterygoid Canal (Vidian Nerve)
• GVE (parasympathetic) + sympathetic.
• Traverses pterygoid (vidian) canal to the pterygopalatine fossa, where the parasympathetics synapse in the pterygopalatine (sphenopalatine) ganglion.
• Postganglionic parasympathetics then travel with the zygomatic nerve (branch of CN V2) into the inferior orbital fissure to join the lacrimal nerve (branch of CN V1) to innervate the lacrimal gland.
• Other postganglionic parasympathetics travel with other CN V2 branches (nasal and palatine nerves) to the oral and nasal mucosa to innervate nasal and palatal glands.
Chorda Tympani Nerve
• GVE (parasympathetic) + SA (taste).
• Arises from the mastoid segment of CN VII (see below).
• Traverses the middle ear cavity medial to the tympanic membrane, then exits the cranium via a part of the petrotympanic fissure known as the canal of Huguier to join the lingual branch of CN V3 ~1 cm below the foramen ovale at the submandibular ganglion.
• Preganglionic parasympathetics synapse in the submandibular ganglion.
• Postganglionic parasympathetics then travel with the lingual nerve to the submandibular and sublingual glands (for salivation).
• Taste sensation (SA) from the anterior two thirds of the tongue and hard and soft palates is transmitted via the chorda tympani nerve to the geniculate ganglion, then via nervus intermedius to the rostral nucleus solitarius (also called “gustatory nucleus”) in the medulla.
• Taste information then ascends via the central tegmental tract to the ventropostereomedial nucleus (VPM) of the thalamus, synapses, and terminates in the gustatory cortex located in the postcentral parietal operculum and insula.
Facial Nerve: Normal Images
• Both computed tomography (CT) and magnetic resonance imaging (MRI) play an important role in the assessment of facial nerve disorders, and appropriate indications for each are discussed below and summarized in Table 7.1. CT is generally done with thin sections (1.25 mm or less) and a high-resolution bone algorithm. This allows for precise assessment of the bony facial canal, as well as adjacent temporal bone structures. For MR, in addition to the routine T1- and T2-weighted images that would generally be done as part of any MR scan of the brain, head and neck, or skull base, thin-section high-resolution heavily T2-weighted sequences such as fast imaging employing steady-state acquisition (FIESTA) or constructive interference in steady-state (CISS) should be performed. These sequences produce a “myelographic effect” with the nerve in sharp contrast to surrounding high signal intensity cerebrospinal fluid (CSF) and allow a high-resolution assessment of the cisternal and intracanalicular segments of the nerve. Post-gadolinium T1-weighted images with fat saturation are performed to assess for pathology of the brainstem and meninges, as well as abnormal enhancement of the nerve itself.
|CT Indications||MR Indications|
|Congenital anomalies (e.g., EAC atresia)||Suspected brainstem disease|
|Cisternal or intracanalicular disease|
|Inflammatory disease/cholesteatoma||Atypical Bell’s palsy|
|Temporal bone fracture||Parotid mass or history of parotid cancer|
|Hemangioma||Intracranial complications of inflammatory disease|
Note: in many cases, CT and MR are complementary.
Facial Nerve Lesions
• Lead to contralateral paresis/palsy of lower portion of face (“central CN VII” lesion).
• Upper part of the face is spared due to bilateral supranuclear innervation.
Nuclear and Fascicular Lesions
• Lead to ipsilateral paresis/palsy of entire face (“peripheral CN VII” lesion).
• Lesion within pons may affect nearby structures, for example, CN V, CN VI, paramedian pontine reticular formation (PPRF), corticospinal tract (CST), spinothalamic tract (STT).
• Millard-Gubler syndrome. Lesion in ventral pons affecting CN VI, CN VII, CST. CN VII involvement is due to involvement of the fascicles of CN VII, not the more dorsally located CN VII motor nucleus. Characterized by ipsilateral peripheral CN VII paralysis, ipsilateral abducens palsy, contralateral hemiplegia.
• Foville syndrome. Lesion in pons affecting CN VII, CN VI, PPRF, CST. Characterized by ipsilateral peripheral CN VII paralysis, ipsilateral conjugate gaze paralysis, contralateral hemiplegia.
• See Appendix A (The Brainstem) for a review of anatomical details .
Cerebellopontine Angle Lesions
• In the cerebellopontine angle (CPA) cistern, CN VII travels with nervus intermedius and near CN VIII. Masses of the CPA cistern (e.g., acoustic neuroma, meningioma) result variably in ipsilateral peripheral CN VII paralysis, loss of taste over anterior two thirds of tongue, hyperacusis, ipsilateral tinnitus, hearing loss, and/or vertigo. CPA masses affect CN VIII function far more commonly than CN VII function.
• Lesions in CPA may displace or compress pons, cerebellum, or other CNs (e.g., CN V, CN VI).
• Hemifacial spasm. Usually due to neurovascular compression of the motor root of CN VII in the CPA (see Case 7.8).
• Geniculate neuralgia (also called nervus intermedius neuralgia or Hunt neuralgia). Neuralgia affecting the sensory root of CN VII (nervus intermedius), causing paroxysmal otalgia similar to the ear form of glossopharyngeal neuralgia (see Chapter 9). Attributed to vascular—usually anterior inferior cerebellar artery (AICA)—compression of nervus intermedius. Treatment is with carbamazepine, microvascular decompression, or sectioning of the nervus intermedius and/or geniculate ganglion.
More Peripheral Lesions
• Most common causes of unilateral complete facial paralysis are Bell’s palsy, trauma, and Ramsay Hunt syndrome (herpes zoster oticus).
• Bell’s palsy (idiopathic facial palsy). Unilateral CN VII dysfunction with sudden onset (see case discussion below).
• Ramsay Hunt syndrome (herpes zoster oticus) (see Case 7.6).
• Posttraumatic facial palsy. The facial nerve is the most commonly injured motor CN (see Case 7.13).
• Möbius syndrome. Congenital bilateral CN VI and CN VII palsies due to neural underdevelopment.
• Additional causes of peripheral facial palsy include
Malignancy (e.g., parotid, temporal bone).
Infectious/inflammatory (e.g., varicella-zoster virus [VZV], Lyme disease, syphilis, acquired immunodeficiency syndrome [AIDS], mononucleosis, Guillian-Barré syndrome [Miller-Fisher variant]).
Iatrogenic (e.g., parotid surgery, temporal bone surgery).
Granulomatous and connective tissue diseases (e.g., sarcoidosis, Wegener granulomatosis).
• Facial nerve dysfunction is most commonly described using the House-Brackmann classification scheme (Table 7.2).
|I||Normal facial function|
|II||Slight weakness noticeable on close inspection|
|Eye—complete closure with minimal effort|
|III||Obvious weakness, but not disfiguring|
|Eye—complete closure with effort|
|Mouth—slightly weak with maximum effort|
|IV||Obvious weakness and/or disfiguring asymmetry|
|Mouth—asymmetric with maximum effort|