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FACIAL NERVE PATHOLOGIES AND IMAGING
CHARACTERISTICS
A Mohandas, M Haider, M Le, T Khairalseed, K Shah
Detroit Medical Center/Wayne State University
eEdE-154
DISCLOSURES
•
Aravind Narayan Mohandas – nothing to disclose.
•
Maera Haider – nothing to disclose.
•
Mark Le – nothing to disclose.
•
Tagwa Khairalseed – nothing to disclose.
•
Kamran Shah – nothing to disclose.
INTRODUCTION
•
The facial nerve (FN) has a complex
course which makes it’s assessment
during imaging challenging.
•
Adequate understanding of it’s
anatomy will facilitate assessment.
•
The aim of the presentation is to
review the normal anatomy with the
help of CT and MRI and to review
imaging characteristics of
pathological entities differentiated
along etiological origin.
ORIGIN
Nucleus
Function
Motor Nucleus
Motor supply to muscles of facial
expression
Superior salivary nucleus
Parasympathetic supply to the major
salivary glands and lacrimal gland
Nucleus of the tractus solitarius
Receives taste sensation from the
anterior two thirds of the tongue.
ORIGIN (CONT’D)
T2 images with illustrations depicting the origin of the FN in the pons.
SEGMENTS – CISTERNAL
•
Cisternal segment emerges from the
pons parallel and medial to the
vestibulocochlear nerve.
•
Nerve of Wrisberg (nervus
intermedius) carries parasympathetic
secretomotor fibres from the superior
salivary nucleus and relays taste
sensation from the anterior 2/3 rds of
the tongue to the nucleus of tractus
solitarius.
•
Nerve of Wrisberg joins the facial
nerve as it enters the internal auditory
canal.
SEGMENTS – CANNALICULAR
•
Cannalicular or meatal segment is the
portion of the FN within the internal
auditory canal.
•
Located in the anterosuperior quadrant
of the internal auditory canal.
•
Related medially to the
vestibulocochlear nerve.
SEGMENTS – LABRYNTHINE
•
Labrynthine segment courses between
the cochlea and vestibule.
•
Anterior genu – FN bends posteriorly
to continue as the tympanic segment.
•
Geniculate ganglion – located at the
junction of the labrynthine and
tympanic segments of the facial nerve
in front of the anterior genu.
•
Greater superficial petrosal nerve
arises from the geniculate ganglion
and supplies the lacrimal glands.
•
Geniculate ganglion also gives rise to
lesser and external petrosal nerves.
SEGMENTS – TYMPANIC
•
Continuation of the FN from the
anterior genu in the fallopian canal.
•
Courses posteriorly beneath the lateral
semicircular canal.
•
After travelling a short distance
posterior to the pyramidal eminence
the FN turns inferiorly forming the
posterior genu and continues as the
descending segment.
SEGMENTS – DESCENDING
•
The descending or mastoid segment
continues after the FN forms the
posterior genu within the fallopian or
facial canal.
•
Emerges from the temporal bone and
fallopian canal through the
stylomastoid foramen.
•
Nerve to stapedius and the chorda
tympani branch, which carries taste
sensation from the anterior 2/3 rd of
tongue, are branches from this
segment.
PATHOLOGICAL ENTITIES
•
Demyelinating disorders.
•
•
Infections and inflammations.
•
•
Multiple sclerosis.
Sarcoidosis, Bell’s palsy, fungal infections.
Neoplasms.
•
Benign.
• Schwannoma, hemangioma .
•
Malignant.
• Perineural spread of head and neck cancers .
•
Trauma.
•
•
Temporal bone fractures
Miscellaneous
•
Vascular loop syndrome, arachnoid cyst.
MULTIPLE SCLEROSIS
•
Demyelinating lesions in the
infratentorial, juxtacortical and
periventricular regions seen as
FLAIR hyperintensities.
•
Isolated cranial nerve involvement
may occur in 10% of cases [1].
•
Facial nerve affected in 4% of cases
[1].
•
Only half of these cases have MRI
findings in the pons [1].
FLAIR image shows demyelinating lesions in the
lower pons in the region of the right facial
colliculus (red arrow) including the facial nerve
tract and abducens nucleus and in the left
corticospinal tract (blue arrow).
SARCOIDOSIS
•
Granulomatous inflammation where
neurological involvement occurs in
5-15% of cases [2].
•
Variable appearance mimicking
other diseases with both supra and
infratentorial involvement.
•
T2 hyperintense lesions which
enhance along with leptomeningeal
enhancement.
(A) FLAIR image shows diffuse hyperintense
lesions in the pons, cerebellum and bilateral facial
nerves (red arrows).
SARCOIDOSIS
•
Facial nerve is the most commonly
affected cranial nerve [3].
•
Heerfordt syndrome – variant of
sarcoidosis with fever, parotid
enlargement, facial palsy and
anterior uveitis.
(B) Post contrast image shows intense nodular
enhancement in the pons, cerebellum and
bilateral facial nerves (red arrows).
BELL’S PALSY
•
Idiopathic facial neuropathy.
•
Reactivation of herpes simplex virus
from geniculate ganglion considered
as possible cause.
•
Tympanic and mastoid segments
normally enhance slightly due to rich
venous plexus in temporal bone.
•
Slight enhancement of the
intracannalicular and labrynthine
segments is normal due to rich
venous plexus within the temporal
bone.
Post contrast image shows abnormal enhancement of
the cannalicular, labrynthine segment and anterior
genu (red arrow) of the right facial nerve. Contiguous
enhancement of the tympanic segment also noted
which is normal.
FUNGAL INFECTIONS
•
Fungal infections of the brain occur
particularly in immuno-compromised
patients.
•
May result from hematogenous
spread or angiotropic and perineural
spread from adjacent sites.
(A) Post contrast image show abscess forming
blastomycosis impinging on the origin of the left
facial nerve at the cerebellopontine angle (red
arrow).
FUNGAL INFECTION
•
Fungal malignant external otitis has
a predilection for FN involvement
(50%) [4].
•
Organisms – Aspergillus,
Mucomycosis, Blastomycosis,
Candida, etc.
(B) T2 weighted images show abscess forming
blastomycosis impinging on the origin of the left
facial nerve at the cerebellopontine angle (red
arrow).
SCHWANNOMA
•
Most common primary neoplasm of
facial nerve.
•
Multisegmental involvement with
geniculate ganglion most commonly
affected [5].
•
Iso to hypointense on T1, iso to
hyperintense on T2 with
homogenous enhancement.
•
Cystic change in 20% of cases [5].
•
CT may show bone remodelling and
scalloping if intratemporal in
location.
(A) CT temporal bone - schwannoma of descending
segment expanding facial canal (red arrow). (B)
Post contrast MRI - enhancement of the mass
(green arrow). Blue arrow – Internal jugular vein.
SCHWANNOMA
(A) & (B) Axial CT images show schwannoma of the right FN within the deep lobe of the right parotid gland (red
arrow) with resultant facial palsy and right buccinator (blue arrow) and platysma (yellow arrow) atrophy.
SCHWANNOMA
Post contrast T1 images emphasizing multi-segmental involvement of the FN (red arrows).
HEMANGIOMA
•
Venous vascular malformation of the
facial nerve.
•
Predeliction for the geniculate
ganglion.
•
Facial palsy out of proportion to the
size of the lesion.
•
Heterogeneously hyperintense T2
mass with punctate foci of
hypointensity which enhances.
(A) Iso to slightly
hyperintense T1
lesion in the
geniculate
ganglion of left
facial nerve (red
arrow).
(B) T2
hyperintense mass
from left facial
nerve geniculate
ganglion (blue
arrow)
PERINEURAL SPREAD OF TUMOR
•
Metastatic tumor spread through
perineurium or endoneurium to non
contiguous areas.
•
Associated with squamous cell
carcinoma of head and neck and
parotid malignancy.
•
Incidence of approximately 10-30%
in parotid malignancy [6].
•
Most common in adenoid cystic
carcinoma of the parotid (50%) [7].
•
Neural thickening, enhancement and
canal and foraminal widening.
PERINEURAL SPREAD
(A) &(B) Pre and post contrast T1 images shows multiple masses in
the left parotid (blue arrow) extending along the FN into the digastric
groove (red arrow) with homogenous enhancement. (C) Coronal
post contrast image shows expansion of the facial canal and
enhancement of the descending segment (yellow arrow).
PERINEURAL SPREAD
(A) Axial CT shows expansion of the left facial canal
(red arrow). (B) and (C) Post contrast axial MRI
images show enhancing descending portion of the left
FN (red arrow) and geniculate ganglion (blue arrow).
TEMPORAL BONE FRACTURES
•
Due to motor vehicle collision,
assault and falls.
•
Up to 20% of patients with
craniofacial trauma have temporal
bone fractures [8].
•
Complex course of FN within the
temporal bone makes it vulnerable
to injury at multiple points.
•
FN injury occurs in 5-10% of
patients with temporal bone
fractures [8].
•
Geniculate ganglion is the most
commonly injured part [8].
(A) Axial CT shows comminuted fracture of the temporal
bone affecting the tympanic (red arrow) and descending
(blue arrow) segments.
TEMPORAL BONE FRACTURES
(B) & (C) Coronal CT shows transverse fracture (yellow arrow) crossing the geniculate fossa and
lateral semi circular canal resulting in it’s lateral displacement (green arrow).
VASCULAR LOOP SYNDROME
•
Compression of FN by a vessel is an
accepted cause of hemifacial spasm.
•
Trigeminal nerve is the most
commonly affected cranial nerve
followed by FN involvement with an
incidence of about 0.8/100,000 [9].
•
Presents with spasm of the eyelids
initially and then spreads downwards.
•
MRI is excellent at demonstrating
vascular compression of the FN.
T2 image showing a dolichoectatic left vertebral artery (blue
arrow) compressing the left FN at its root of exit and
causing mass effect on the adjacent pons (red arrow).
VASCULAR LOOP SYNDROME
•
Root of exit of FN is its weakest point
and most susceptible to compression.
•
The most common offending vessel
causing hemifacial spasm is the
posteroinferior cerebellar artery (70%)
followed by the vertebral artery (41%)
and anteroinferior cerebellar artery
(28%) [10].
•
The frequency of multiple offending
vessels in the same patient is high
(38%) [10].
FLAIR image shows compression of the left FN at its root
of exit (red arrow) by the dolichoectatic left vertebral
artery (blue arrow).
ARACHNOID CYST
•
Arachnoid cyst at the CP angle is
usually asymptomatic and
developmental arising from splitting of
the arachnoid and contains
cerebrospinal fluid.
•
Rare cause of hemifacial spasm.
•
T2 and FLAIR sequences used to
demonstrate properties of
cerebrospinal fluid within the cyst.
T2 (A) and FLAIR (B) images showing mass at
the left cerebellopontine angle with properties of
cerebrospinal fluid (red arrows).
REFERENCES
1.
Zadro, I., et al., Isolated cranial nerve palsies in multiple sclerosis. Clin Neurol Neurosurg, 2008. 110(9): p. 886-8.
2.
Segal, B.M., Neurosarcoidosis: diagnostic approaches and therapeutic strategies. Curr Opin Neurol, 2013. 26(3): p. 307-13.
3.
Pickuth, D., R.P. Spielmann, and S.H. Heywang-Kobrunner, Role of radiology in the diagnosis of neurosarcoidosis. Eur
Radiol, 2000. 10(6): p. 941-4.
4.
Hamzany, Y., et al., Fungal malignant external otitis. J Infect, 2011. 62(3): p. 226-31.
5.
Thompson, A.L., et al., Magnetic resonance imaging of facial nerve schwannoma. Laryngoscope, 2009. 119(12): p. 2428-36.
6.
Terhaard, C.H., et al., Salivary gland carcinoma: independent prognostic factors for locoregional control, distant metastases,
and overall survival: results of the Dutch head and neck oncology cooperative group. Head Neck, 2004. 26(8): p. 681-92;
discussion 692-3.
7.
Carlson, M.L., et al., Occult Temporal Bone Facial Nerve Involvement by Parotid Malignancies with Perineural Spread.
Otolaryngol Head Neck Surg, 2015. 153(3): p. 385-91.
8.
Kennedy, T.A., G.D. Avey, and L.R. Gentry, Imaging of temporal bone trauma. Neuroimaging Clin N Am, 2014. 24(3): p. 46786, viii.
9.
Auger, R.G. and J.P. Whisnant, Hemifacial spasm in Rochester and Olmsted County, Minnesota, 1960 to 1984. Arch Neurol,
1990. 47(11): p. 1233-4.
10.
Sherif Elaini, J.M., Arnaud Deveze, Nadine Girard, Magnetic resonance imaging criteria in vascular compression syndrome.
The Egyptian Journal of Otolaryngology, 2013. 29(1): p. 10-15.