PD Warrick BScPhm, Meds '98 McMaster University

The complex anatomy of the seventh cranial nerve and its subsections must be understood in order to discriminate among the peripheral causes of facial nerve palsy, and to differentiate these from central etiologies.

• Supranuclear - from the precentral (motor) and postcentral (sensory) gyri through the genu of the internal capsule to the facial nucleus in the pons (ipsilateral and contralateral nucleus for upper face, contralateral only for lower face)
• Nuclear - facial nerve travels dorsomedially toward 4^th ventricle, loops laterally around abducent nucleus, then exits anterolaterally and inferiorly at the medullopontine junction
• Cerebellopontine angle (CPA) - travels with nervus intermedius (NI), alongside CN V, VIII to internal auditory canal
• Intratemporal
• Internal auditory canal (ICA) - travels anterosuperiorly with NI within canal for 5-12 mm alongside cochlear, vestibular nerves; lateral-most portion is surrounded by thicker periosteum
• Labyrinthine - beginning of " fallopian canal" travels almost totally inferiorly for 3-5 mm, then makes first (posterior) turn; gives off geniculate branch (NI) to form geniculate ganglion from which emerges the greater petrosal nerve (which controls lacrimation via the sympathetic plexus of internal carotid artery and pterygopalatine ganglion) and the lesser petrosal nerve (which controls salivation of parotid gland via the otic ganglion)

• Temporal - travels mostly posteriorly for 10-12 mm before reaching the second (inferior) turn just superior to middle ear
• Mastoid - gives off branch to stapedius, chorda tympani (which unites with lingual nerve of CN V₃ to cause salivation in submandibular and sublingual glands); travels 13 mm inferiorly and becomes more superficial before emerging from the stylomastoid foramen
• Extracranial - travels anteroinferiorly immediately entering parotid space, gives off branches to occipitalis, intrinsic muscles of ear (posterior auricular), posterior belly of digastric and stylohyoid, then separates into temporofacial and cervicofacial divisions - highly variable anatomy from this point, but essentially 5 main divisions:
• Temporal - function differentiates upper motor from lower motor neuron lesion
• Zygomatic - most important, as function prevents exposure keratitis of cornea
• Buccal
• Marginal Mandibular
• Cervical

Some of the most helpful findings to differentiate upper motor neuron (UMN) (otherwise known as central or supranuclear/nuclear) lesions of the facial nerve from lower motor neuron (LMN) (also referred to as peripheral or infranuclear) lesions are:

1) CN VII Temporal branch testing - intact forehead movement indicates UMN lesion

2) CN V₁, V₂, V₃ testing - alteration in facial sensation suggests CN V involvement, and therefore a CPA lesion

3) Corneal Reflex - corneal hypesthesia suggests afferent corneal lesion, CN V involvement, and therefore a CPA lesion

1. Onset - when, sudden vs. progressive

2. Duration

3. Is it recurrent

• 1. UMN vs. LMN - other focal neurological signs

• 2. CN V findings

• 3. Bell’s phenomenon (When the patient closes his/her eyes, the eyeballs rotate upward)

• 4. Loss of taste

• 5. Loss of lacrimation

• Otalgia/Aural fullness

• Vesicles around the auditory meatus (See picture)

• CN VIII symptoms

  - Hearing loss

  - Tinnitus

  - Vertigo

• CN V symptoms: Facial hemianesthesia/hypesthesia or slow/ absent afferent corneal reflex

• 1. Complete CN exam

• 2. Gross peripheral motor and sensory function - look for asymmetry

• 3. Otoscopy

• 4. Weber’s and Rinné’s tests

1. Audiometry (pure tone and speech)

2. Acoustic stapedial reflex testing

3. Viral ELISA isolation studies to differentiate herpes zoster from herpes simplex

4. Electroneurongraphy (ENoG)

5. Topognostic testing (Schirmer’s test, Hitselberger's test etc...probably more academic than useful)

6. CT head (if skull fracture suspected)

7. MRI with gadolinium enhancement to delineate labyrinthine or geniculate ganglion portions of nerve

8. High-resolution CT (HRCT) to delineate fallopian canal

-primarily due to cerebrovascular accident of the lacunar type within the genu of the internal capsule

-may occur as part of a human immunodeficiency virus (HIV)-related neurologic disorder

-facial palsy is rare (represents about 3% of all cases of peripheral nerve palsy), but may be found in either acute or chronic otitis media

-usually due to a dehiscence of the bony (fallopian) canal of facial nerve

-Otitis media with facial palsy as a complication requires urgent treatment, and most otolaryngologists would, at the least, perform a myringotomy to drain the middle ear effusion.

Pregnancy - 3.3 x increased risk; most common in third trimester

-preeclampsia may pose even greater (6 x) risk

Diabetes mellitus - 4.5 x increased risk of Bell's palsy; facial palsies often associated with ophthalmoplegia without pupil involvement

-recurrent triad of symptoms beginning in second decade (only 25% have all three symptoms):

1) nonpitting orofacial edema (defining symptom)

2) facial palsy (50% of patients)

3) lingua plicata (fissured tongue) (50% of patients)

-may be more prone to facial paralysis secondary to Bell's palsy, HZO, or in late disease, systemic lymphoma

-commonly have mucous membrane, skin, lymph node involvement, coronary artery aneurysms

-about 30% have neurologic involvement including aseptic meningitis, irritability and facial nerve palsy

-idiopathic, progressive, involuntary spasm of one side of the face or orbicularis oculus and upper face

-blepharospasm can lead to functional blindness; may respond to botulinum toxin therapy

Mattox DE. Clinical disorders of the facial nerve. In: Cummings CW, ed. Ololaryngology-Head and Neck Surgery, 2^nd ed. Toronto: Mosby, 1992, pp. 3217-32.

Otolaryngology Clinics of North America Vol. 24 No. 3, June 1991

Selesnick SH, Patwardhan A. Acute facial paralysis: evaluation and early management. Am J Otolaryngol 1994;15(6):387-408.