Facial Nerve

Front 1

Functions

Back 1

• Special visceral efferent (SVE). Branchial motor innervation to muscles of facial expression (including orbicularis oculi, orbicularis oris, risorius, depressor anguli oris, zygomatic major, mentalis, buccinator, frontalis, occipitalis, corrugator supercilii, platysma), stapedius, stylohyoid and posterior belly of digastric.

• General visceral efferent (GVE). Visceral motor (parasympathetic) innervation to lacrimal gland (via greater superficial petrosal nerve), oral and nasal mucosa (via greater superficial petrosal nerve). and submandibular and sublingual glands (via chorda tympani).

• General sensory afferent (GSA). Somatic sensory from external auditory meatus, auricle and retroarticular area

• Special afferent special sensory (SA) for taste from anterior two-thirds of tongue and hard and soft palate (via chorda tympani)

Front 2

Anatomy: Motor division

Back 2

Motor Division

• SVE

• Facial motor nucleus lies in caudal pontine tegmentum, anterolateral to abducens nerve (CN) VI nucleus. 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

Front 3

Anatomy: Nervus intermedius of Wrisberg

Back 3

• 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), transverses the cerebellopontine cystern and enters the internal auditory canal.

• 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 the greater superficial petrosal nerve to the pterygopalatine ganglion to the lacrimal gland and the mucosa of the nose and mouth (palatal and nasal glands); and the chorda tympani nerve that joins with the lingual nerve (V3) and goes to the submandibular ganglion and on to the submandibular and sublingual glands for salivation.

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, posterior and medial to the foramen spinosum, and anterior to the superior semicircular canal. It consists of sensory nerve cell bodies for taste (chorda tympani) and external ear sensation (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.

Front 4

Anatomy: peripheral CN VII

Back 4

• After emerging from the ventrolateral pons, the motor division and nervus intermedius transverse the cerebellopontine angle cistern with CN VIII and then enter the internal auditory canal in the petrous temporal bone, along with the labyrinthine artery and vein.

Four intratemporal segments:

- Meatal: within the IAC, the CN VII is anterosuperior and CN VIII is inferior. Here, the nervus intermedius joins CN VII

- Labyrinthine: travels through the bony fallopian canal to the geniculate ganglion, where the greater superficial petrosal nerve arises.

- Horizontal segment: CN VII travels posteriorly and horizontally just inferior to the lateral semicircular canal. No branches arising from here

- Mastoid segment: Posterior to middle ear. The nerve turns inferiorly and gives off three branches: to stapedius, chorda tympani and sensory auricular branch (innervation of external auditory meatus and the auricle and retroauricular area).

Exit from the bony facial canal at the level of the stylomastoid foramen. The posterior auricular nerve, the digastric branch and the stylohyoid are given off here.

At this point, it enters the parotid gland and divides into temporofacial and cervicofacial branches, dividing into temporal, zygomatic, buccal, marginal mandibular, cervical branches (TEN ZEBRAS BIT MY CLOCK)

Front 5

Central facial palsy: VII + VI palsy

Back 5

- Möbius syndrome is an extremely rare congenital neurological disorder which is characterized by facial paralysis and the inability to move the eyes from side to side. Möbius syndrome results from the underdevelopment of the VI and VII cranial nerves.

- The facial (VII) nerve fascicle loops around the nucleus of the sixth (VI) nerve, creating the facial colliculus, and turns anterolaterally to join the eighth nerve in its exit from the lower pons. Of note, lesions of the cerebellopontine angle (especially acoustic neuroma or meningioma) may involve the sixth and other contiguous cranial nerves

Front 6

Sites of lesions and their manifestations

Back 6

1. Intrapontine lesions:

Peripheral motor facial paralysis associated with eye movement abnormalities (ipsilateral abducens or horizontal gaze palsies) and contralateral motor paralysis.

2. Intracranial and/or internal auditory meatus:

All symptoms of 3, 4, and 5, plus deafness due to involvement of eighth cranial nerve.

3. Geniculate ganglion:

All symptoms of 4 and 5 with diminished lacrimation plus pain behind ear. Herpes of tympanum and of external auditory meatus may occur.

4. Facial canal: All symptoms of 5, plus loss of taste in anterior tongue and decreased salivation on affected side due to chorda tympani involvement. Hyperacusis due to effect on nerve branch to stapedius muscle.

5.Below stylomastoid foramen (parotid gland tumor, trauma):

Facial paralysis (mouth draws to opposite side) on affected side with patient unable to close eye or wrinkle forehead; food collects between teeth and cheek due to paralysis of buccinator muscle).

Front 7

Diagnosis for peripheral CN VII palsy

Back 7

History:

I. OTOLOGICS SYMPTOMS (Hearing loss, Tinnitus, Vertigo, Ear Discharge)

II. NEUROLOGIC SYMPTOMS

III. TRAUMA

IV. RECURRENCE

V. TICK BITES (borreliosis)

Physical examination:

When a patient presents with facial weakness, differentiation should be made between peripheral facial nerve lesions and CNS processes.

- With the latter (central), when the patient is relaxed, subtle suggestions of a facial nerve lesion may be appreciated by nasolabial fold flattening on the affected side. Brain lesions such as cerebral infarction, tumor, inflammation, or demyelination are often associated with other findings that can help with localization. For example, a small lesion near the Broca area may result in motor aphasia and facial weakness.

- Peripheral facial weakness involves the upper and lower part of the face to the same degree, upper motor neuron lesions typically present with a gradient of weakness, with relative preservation of movement in the brow and forehead (orbicularis oculi and frontalis muscles). This is due to presumed dual hemispheric innervation of the forehead muscles.

In addition, corticobulbar tract involvement, as in various suprabulbar palsies, leads to absence of voluntary facial movement but retained reflexive movements such as in response to emotional stimuli.

Front 8

Peripheral facial nerve: Bell's palsy

Back 8

It is a diagnosis of exclusion. Due to HSV reactivation.

Incidence of 30 per 100,000.

Pregnant females: 3.3 times greater; Diabetics 4-5 times greater

Equal gender distribution in middle age

Bilateral involvement in less than 1%

Recovery: 1-2 months

No other symptoms

The onset of Bell's palsy is acute: about one-half of cases attain maximum paralysis in 48 h and practically all within 3 or 4 days.

Pain behind the ear may precede the paralysis by a day or two and in a few patients is intense and persistent. Although a report by the patient of fullness or numbness in the face is common, in a small number there is hypesthesia in one or more branches of the trigeminal nerve.

The explanation of this finding is not clear.

Impairment of taste is present in most patients but it rarely persists beyond the second week of paralysis. This indicates that the lesion has extended proximal to the point at which the chorda tympani joins the facial nerve. Hyperacusis or distortion of sound is then experienced in the ipsilateral ear and, as mentioned, indicates paralysis of the stapedius muscle.

Front 9

Peripheral palsy: etiology

Back 9

• LYME DISEASE: Facial paralysis is the most common focal manifestation of neuroborreliosis; 40% of these patients have cranial neuropathies, and approximately 80% have CN-VII involvement

• INTRACRANIAL TUMOURS

• GUILLAIN-BARRE SYNDROME

Front 10

Peripheral palsy: Ramsay-Hunt syndrome

Back 10

The Ramsay–Hunt syndrome, caused by reactivation of the varicella-zoster virus (VZV) within the geniculate ganglion, is the second most common cause of atraumatic facial palsy.

Clinically, it is characterized by the triad of:

- acute facial palsy

- neuralgic pain

- eruption of herpetic vesicles within the external auditory canal, ipsilateral palate, and anterior two-thirds of the tongue.

The areas of pain and rash are appropriate to the general sensory innervation of the afferent facial nerve branches.

Front 11

Peripheral palsy: parotid neoplasm

Back 11

Several primary and metastatic malignancies may cause a facial palsy.

Carcinomatous meningitis usually affects multiple cranial nerves; the most common sources are the lung, the breast, gastrointestinal cancers, and lymphomas.

Typically, these tumors have an aggressive clinical course; those that present with an isolated CN-VII lesion soon demonstrate signs of multiple cranial or spinal nerve root involvement or both. Certain benign tumors may exert chronic extrinsic pressure on the facial nerve. Schwannomas from the vestibular portion of CN-VIII, typically occurring within the acoustic meatus at the CP angle, or less commonly meningiomas at similar sites, affect CN-VII very gradually over time. When they eventually do so, they tend to predominantly and subtly affect sensory fibers over the motor fibers that are more resilient to chronic deformation. Therefore, the only sign of early CN-VII involvement may be relatively minor numbness behind the ear, on the floor of the ear canal, in the posterior inferior quadrant of the eardrum (Hitzelberger sign), or a combination of these.

The change in hearing, however, usually leads to the diagnosis. Signs of a motor CN-VII lesion do not occur until these lesions become large. Malignant distal infiltration of CN-VII is seen with parotid tumors

Front 12

Peripheral palsy: Trauma

Back 12

LONGITUDINAL:

• The fracture runs along the external auditory canal and the anterior border of the petrous pyramid

• The most common fracture

• COMPLICATIONS:

- conductive hearing loss

- peripheral facial palsy ( -> TYMPANIC OR MASTOID SEGMENT): 10% cases

- Cerebrospinal fluid leak -> CSF otorrhea (± BLOOD OTORRHEA)

TRANSVERSAL:

• The fracture runs across the petrous pyramid along the internal auditory canal and/or through the labyrinth

• Not common fracture • COMPLICATIONS:

-Sensorineural hearing loss

- Vestibular dysfunction

- Peripheral facial palsy (-> labyrinthine tract): 50% of cases

- Cerebrospinal fluid leak (-> CSF rhinorrhea through the Eustachian Tube)

Front 13

Diagnosis

Back 13

OTOLOGIC EXAMINATION:

• Evaluate for pathology of eighth cranial nerve

• Retrocochlear pathology

– Asymmetrical thresholds

– Acoustic reflex decay: Acoustic Reflex Adaptation (or Decay). Reflex decay is defined as a decline in the contraction of the muscle during a sustained stimulating signal. This is also helpful in interpreting and differentiating auditory test results. In patients with normal middle ear and reflex thresholds, there is no decay during the presentation of the tone. Patients with lesions of the cochlea, eighth nerve or auditory brainstem may have evidence of decay.

• Bell’s palsy

– Symmetric audiological function

– Absent ipsilateral acoustic reflex

IMAGING

• Localize lesion

• Computed tomography

– Trauma

– Mastoiditis

– Cholesteatoma

• Magnetic resonance imaging (MRI)

– Nerve enhancement

– No correlation with site or degree of enhancement

– Exclude neoplasm

Front 14

Diagnosis in trauma

Back 14

• Schirmer test → greater petrosal nerve

The Schirmer test of lacrimal flow depends on an intact geniculate ganglion, the site of the most proximal anatomic branch point along the course of CN-VII, giving rise to the greater superficial petrosal nerve.

• Stapedial reflex → stapedial branch

• Electrogustometry → chorda tympani

• Salivary flow → chorda tympani

If the fracture is in the mastoid tract shimmer test is normal but you may have a deficit of the stapedial branch (so stapedial reflexes are absent) and the chorda tympani is also involved with a problem in the gustatory cells.