Facial Nerve Palsy

Overview of Presentation

• Introduction

• Review of facial nerve anatomy

• Clinical and Imaging features of Bell’s

palsy

– Typical

– Atypical

• Other causes of acute facial paralysis

Introduction

• Bell’s palsy accounts for 75% of cases of acute

facial nerve (7th cranial nerve) paralysis

• Imaging is not needed in majority of patients

unless they have atypical features

• W/atypical features, MR & CT may demonstrate

potentially treatable lesions affecting facial

nerves

• Facial nerves can be affected anywhere along

their course

Anatomy Review

• Facial nerve nuclei lie in

reticular formation of

brainstem, ventral to floor

(tegmentum) of 4th ventricle(4)

• Motor Nuclei:

– Efferent fibers surround nuclei

of CN VI & form small mounds

on floor of 4th ventricle

(facial colliculi)

• Non-Motor Nuclei:

– Salivatory

– Solitary

Facial colliculus

• Efferent fibers surround 6th CN nucleus & exit at

cerebellopontine angle (CPA)

• 7th nerve courses into internal auditory canal (IAC)

– Within superior anterior quadrant(6)

Ant Post

• Exits IAC via Fallopian

canal

– Narrowest point

throughout entire course

– Felt to be culprit in facial

nerve compression in

Bell’s palsy & other

causes of nerve swelling

Fallopian Canal

• Progress to geniculate

ganglion

– Gives rise to greater

superficial petrosal

nerve

• Contains taste axons

from tongue & somatic

fibers

Geniculate ganglion

• Fibers then course posteriorly under lateral semicircular canal in middle ear (tympanic portion)

• Fibers angle back & inferiorly at “second genu” diving the descending canal– Here last somatic & parasympathetic fibers separate from facial

nerve via the chorda tympani nerve

Tympanic Portion

Mastoid segment

• Facial nerve exits skull base at stylomastoid foramen

• Facial nerve angles superiorly & anteriorly behind posterior margin of vertical mandibular ramus– Just before entering parotid gland, inferior branches originate

• Posterior auricular, digastric & stylohyoid

– Within substance of parotid gland, superior branches arise

• Temporal, zygomatic, buccal, orbicularis oris, mandibular & cervical

Clinical Signs Suggesting Site of

Facial Nerve Lesion

• Upper facial territory is supplied by bilateral motor cortices

• Lower facial territory is supplied only by contralateral motor

cortex

• Therefore, unilateral central lesions spare upper face

• Lesions distal to geniculate ganglion

– Mostly motor abnormalities

• Lesions proximal to geniculate ganglion

– Motor, gustatory & autonomic abnormalities

Typical Bell’s Palsy

• Incidence – 15–30 per 100,000

– Usually during winter

• Etiology not entirely understood– Possibly viral (Herpes Simplex Virus) or idiopathic

• Viral infection of facial nerve results in demyelination, inflammation & swelling– Traps nerve in narrow confines of fallopian canal

• Diagnosis of exclusion– Made only when clinical & imaging (if necessary)

findings are supportive

• Usually a clinical diagnosis

– Acute onset unilateral (lower or upper) facial paralysis, posterior

auricular pain, decreased tearing, hyperacusis (30%) &

disturbances of taste

– By physical examination, Bell’s palsy divided according to

classification by House and Brackman

• Grades 1 & 2 have better outcomes with worse outcome as grade

increases.

• 80-90% recover completely

– Over age 60, only 40% recover completely

Imaging in Typical Bell’s Palsy

• Imaging in typical Bell’s palsy is not usually necessary– When necessary, MRI is best

• Normal facial nerve distal to geniculate ganglion may enhance– Facial nerve proximal to geniculate ganglion does not normally

enhance

• In patients with Bell’s palsy, enhancement of facial nerve in fallopian & ICA is typical

Atypical Bell’s Palsy

• Clinical features

– Slower onset of symptoms

– Bilateral

– Recurrence

• Numbness is not unusual

• Progression beyond seven days

suggests another cause

Imaging in Atypical Bell’s Palsy

Alternative Causes of Acute

Facial Nerve Paralysis

• Atypical signs & symptoms which suggest

etiology other than Bell’s palsy require

imaging

• Clinical history is crucial in distinguishing

etiologies

• Choice of imaging technique depends on

clinical suspicion

Lyme Disease

• Lyme disease (borreliosis)– Endemic areas (Northeast USA, central Europe,

Scandinavia, Canada)

– Consider in children w/atypical facial palsy

• Imaging: small white matter lesions similar to multiple sclerosis, enhancement of facial & other cranial nerves

• Bilateral facial paralysis: 25%

• Important to make diagnosis early because it is curable early w/antibiotics

Ramsay Hunt Syndrome

• Caused by reactivation varicella zoster virus (herpes

virus type 3)

• Facial paralysis + hearing loss +/- vertigo

– Herpes zoster oticus

• Two-thirds of patients have rash around ear

• Other cranial nerves, particularly trigeminal nerves (5th

CN) often involved

• Worse prognosis than Bell’s (complete recovery: 50%)

• Important cause of facial paralysis in children

6-15 years old

Infectious causes

• Acute facial paralysis may result from bacterial or tuberculous infection of middle ear, mastoid & necrotizing otitis externa

• Incidence of facial paralysis with otitis media: 0.16%– Infection extends via bone dehiscences to nerve in

fallopian canal leading to swelling, compression & eventually vascular compromise & ischemia

• Immune compromised patients are at risk for pseudomona infection

• Poor prognosis (complete recovery is < 50%)

Tuberculosis

Parotid & peri-parotid disease

HIV Infection

Bezold’s abscess & coalescent

mastoiditis

Trauma

• Most acute post traumatic facial palsies are due

to t-bone fractures

• Historically fractures classified as longitudinal or

transverse with transverse carrying risk of

permanent paralysis

– Longitudinal fracture usually leads to temporary

paralysis from concussion & swelling of nerve

– Transverse fracture can lead to transection of nerve

• In all types of paralysis due to fracture, usually

the region of geniculate ganglion is involved

Neoplasms

• 27% of patients with tumors involving the facial nerve develop acute facial paralysis

• Most common causes: schwannomas, hemangiomas (usually near geniculate ganglion) & perineural spread such as with head and neck carcinoma, lymphoma & leukemia

• Other neoplasms can also involve the facial nerve– Adults: metatstatic disease, glomus tumors,

vestibular schwannomas & meningiomas

– Children: eosinophilic granuloma & sarcomas

Hemangioma

Facial Nerve Schwannoma

Perineural Tumor Spread

Glomus Tumor

• Glomus tumors arising

from jugular bulb

(jugulare) and/or

middle ear

(tympanicum) may

involve the facial nerve

Other tumors

Rhabdomyosarcoma & squamous cell carcinoma of the EAC

Vestibular Schwannoma

• Common tumor

• However, facial nerve is resistant to compression

– Therefore, tends to produce facial paralysis mostly when

they attain a large size

Vestibular Schwannoma

-Common tumor

-However, facial nerve is resistant to compression, thus,

tends to produce facial paralysis mostly when they attain a

large size

Meningioma

• Second most common

primary tumor of

cerebellopontine angle

• Rarely results in facial

paralysis

Rhabdomyosarcoma

Miscellaneous Causes :

Hypertrophic Polyneuropathy

• Hypertrophic

polyneuropathies

occasionally lead to

facial paralysis

Wegener’s Granulomatosis

• Guillain-Barre Syndrome

– Ascending paralysis

• Iatrogenic

– Temporal bone surgery

• Excision of vestibular schwannoma has <10%

chance of paralysis

• Middle ear surgeries

– Babies who required forceps delivery

• >90% recovery

Melkersson-Rosenthal Syndrome

• Acute episodes of facial paralysis

– Facial swelling

– Fissured tongue

• “Scrotal” tongue

• Very rare

• Familial but sporadic

– Usually begins in adolescence

• Leads to facial disfigurement

• No definite therapy

Conclusion

• While Bell’s palsy does not typically require

imaging for diagnosis, imaging evaluation is

important in the work-up of patients with atypical

or unusual presentations of acute facial nerve

paralysis, identification of discreet lesions may

lead to a change in management of these

patients.