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Imaging in
Acute Facial Nerve Paralysis
M Castillo, MD, FACR
Department of Radiology
University of North Carolina, Chapel Hill
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
Fallopian Canal
• 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
Geniculate ganglion
• Progress to geniculate
ganglion
– Gives rise to greater
superficial petrosal
nerve
• Contains taste axons
from tongue & somatic
fibers
• 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
Mastoid segment
Tympanic Portion
• 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
Typical Bell’s Palsy
• 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
C/o Dr. M. Michel, Wisconsin
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
C/o Dr. M. Michel, Wisconsin
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
C/o Dr. M. Michel, Wisconsin
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
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
Other Causes
• 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.