Facial Nerve Palsy
Dr. Saud ALROMAIH
Anatomy
Facial nerve is a mixed nerve, having
a motor root and a sensory root.
Motor root supplies all the mimetic
muscles of the face which develop
from the 2nd brachial arch.
Anatomy
Sensory root “nerve of Wrisberg”
carries taste fibers from the anterior
2/3 of the tongue and general
sensation from the concha and
retroauricular skin.
Anatomy
Also it carries secretomotor fibers to
the lacrimal, submandibular and
sublingual glands as well as those in
the nose and palate.
Anatomy: Nucleus
Pons.
precentral gyrus.
Upper part of the nucleus:
– Upper face
– Involuntary emotional movements
Anatomy: Course
Motor fibers originate…
Hooks around…
Joined by…
Facial n. leaves the brainstem…
Travels through…
Enters the IAC.
Then traverse the temporal bone through
facial n. canal
Leaves the temporal bone through
Finally divides into terminal branches.
Anatomy: Parts
Intracranial part
Intratemporal part
Extracranial part
Anatomy: Intratemporal segments
Meatal
Labyrinthine
Tympanic, horizontal
Mastoid, vertical
Anatomy: Branches
Greater superficial petrosal nerve:
Nerve to stapedius:
Chorda tympani:
Comunicating branch:
Posterior auricular nerve:
Muscular branches:
Peripheral branches: “Pes anserinus”
Anatomy: Surgical landmarks
Middle Ear and Mastoid Surgery:
– Processus chocleariformis
– Oval window and horizontal canal
– Short process of the incus
– Pyramid
Anatomy: Surgical landmarks
Parotid Surgery:
– Cartilaginous pointer:
– Styloid process
– Posterior belly pf digastric muscle
Anatomy: Structure of the nerve
From inside outward:
– Axon
– Myelin sheath
– Neurolimma
– Endoneurium
– Perineurium
– Epineurium
Anatomy: Severity of injury
Saunderland classification:
– 1°: Partial block: Neuropraxia
– 2°: Loss of axons: axonotemesis
– 3°: Injury to the endoneurium:
neurotemesis
– 4°: Injury to the perineurium: partial
transection
– 5°: Injury to the epineurium: complete
transection
History:
Onset: Sudden vs. Gradual
Duration:
Rate of progression:
Recuurent or familial
Associated symptoms
Medical history
Previous surgeries
Physical exam:
Complete vs. incomplete
Segmental vs. uniform involvement
Unilateral vs. bilateral
Cranial nerves assessment
Neurologic evaluation
Cerebellar signs
Physical exam:
Microscopic otoscopy
Complete head and neck exam
Physical exam:
Localization of facial nerve lesion:
Central vs. Peripheral.
Physical exam:
Localization of facial nerve lesion:
Peripheral:
– Level of nucleus
– CPA level:
– Bony canal level: Topodiagnostics
– Outside the Temporal bone
Physical exam:
Topodiagnostics:
– Schirmer’s test:
– Stapedial reflex:
– Taste test:
– Submandibular salivery flow test:
Warton’s ducts
Causes:
Central:
Intacranial part:
Intratemporal part:
Extracranial part:
Systemic:
Causes:
Central:
– Brain abscess
– Pontine glioma
– Poliomyelitis
– Multiple sclerosis
Causes:
Intacranial part:
– Acoustic neuroma
– Meningioma
– Metastatic CA
– Meningitis
Causes:
Intratemporal part:
– Idiopathic:
Bell’s palsy
Melkersson’s syndrome
Causes:
Intratemporal part:
– Infections:
ASOM
CSOM
Herpes Zoster Oticus
Causes:
Intratemporal part:
– Trauma:
Surgical: Mastoidectomy, Stapedectomy
Accidental:# temporal bone
Causes:
Intratemporal part:
– Neoplasms:
Glomus jugulare tumour
Facial nerve neuroma
Metastatic CA
Causes:
Extracranial part:
– Parotid gland CA
– Parotid gland surgery
– Parotid gland injury
– Neonatal facial nerve injury
Causes:
Systemic:
– DM
– Hypothyroidism
– Uremia
– PAN
– Wegener’s granulomatosis
– Sarcoidosis
– Leprosy
– Leukemia
Labs:
Pure-tune audiometry
Electrophysiologic tests
Imaging tests
Others
Labs:
Electrophysiologic tests:
– Nerve Excitability Test: NET
– Maximum stimulation Test: MST
– Electroneurography: ENoG
– Electromyography: EMG
Complications:
Incomplete recovery
Exposure keratitis
Synkinesis
Tics and spasms
Contractures
Crocodile tears
Frey’s syndrome “gustatory sweating”
Psychological and social problems
Bell’s Palsy
Dr. Saud ALROMAIH
Background:
one of the most common neurologic
disorders affecting the cranial
nerves.
abrupt, unilateral, peripheral facial
paresis or paralysis without a
detectable cause.
Background:
first described more than a
century ago by Sir Charles
Bell,
yet much controversy still
surrounds its etiology and
management.
Bell palsy is certainly the
most common cause of
facial paralysis worldwide.
Incidence:
United States
Internationally
Incidence:
The incidence of Bell palsy in the
United States is approximately 23
cases per 100,000 persons.
Internationally: The incidence is the
same as in the United States.
Demographics:
Race:
Sex:
Age:
Demographics:
Race: slightly higher in persons of
Japanese descent.
Sex: No difference exists
Age: highest in persons aged 15-45
years. Bell palsy is less common in
those younger than 15 years and in
those older than 60 years.
Pathophysiology:
Main cause of Bell's palsy is latent
herpes viruses (herpes simplex virus
type 1 and herpes zoster virus),
which are reactivated from cranial
nerve ganglia.
Polymerase chain reaction techniques
have isolated herpes virus DNA from
the facial nerve during acute palsy.
Pathophysiology:
Inflammation of the nerve initially
results in a reversible neurapraxia,
Herpes zoster virus shows more
aggressive biological behaviour than
herpes simplex virus type 1
History:
The most alarming symptom of Bell's
palsy is paresis
Up to three quarters of affected
patients think they have had a stroke
or have an intracranial tumour.
History:
The palsy is often sudden in onset
and evolves rapidly, with maximal
facial weakness developing within
two days.
Associated symptoms may be
hyperacusis, decreased production of
tears, and altered taste.
History:
Patients may also mention otalgia or
aural fullness and facial or
retroauricular pain, which is typically
mild and may precede the palsy.
A slow onset progressive palsy with
other cranial nerve deficits or
headache raises the possibility of a
neoplasm
Physical exam:
Bell's palsy causes a peripheral lower
motor neurone palsy,
which manifests as the unilateral
impairment of movement in the
facial and platysma muscles,
drooping of the brow and corner of
the mouth, and impaired closure of
the eye and mouth.
Physical exam:
Bell's phenomenon—upward
diversion of the eye on attempted
closure of the lid—is seen when eye
closure is incomplete.
Physical exam:
Polyposis or granulations in the ear
canal may suggest cholesteatoma or
malignant otitis externa.
Vesicles in the conchal bowl, soft
palate, or tongue suggest Ramsay
Hunt syndrome
Physical exam:
The examination should exclude
masses in the head and neck.
A deep lobe parotid tumour may only
be identified clinically by careful
examination of the oropharynx and
ipsilateral tonsil to rule out
asymmetry.
Investigations:
Serum testing for rising antibody
titres to herpes virus is not a reliable
diagnostic tool for Bell's palsy.
Salivary PCR for herpes simplex virus
type 1 or herpes zoster virus is more
likely to confirm virus during the
replicating phase, but these tests
remain research tools.
Investigations:
MRI has revolutionised the detection
of tumours.
Investigations:
Topognostic tests and
electroneurography may give useful
prognostic information but remain
research tools.
Diagnosis:
Bell palsy is a diagnosis of exclusion.
Other disease states or conditions
that present with facial palsies are
often misdiagnosed as idiopathic.
Management:
The main aims of treatment in the acute
phase of Bell's palsy are to speed recovery
and to prevent corneal complications.
Treatment should begin immediately to
inhibit viral replication and the effect on
subsequent pathophysiological processes
that affect the facial nerve.
Psychological support is also essential,
and for this reason patients may require
regular follow up.
Management, Eye care
Management, Eye care
It focuses on protecting the cornea from
drying and abrasion due to problems with
lid closure and the tearing mechanism.
The patient is educated to report new
findings such as pain, discharge, or
change in vision.
Lubricating drops should be applied hourly
during the day and a simple eye ointment
should be used at night.
Management, Steroid
Management, Steroid
Two systematic reviews concluded
that Bell's palsy could be effectively
treated with corticosteroids in the
first seven days, providing up to a
further 17% of patients with a good
outcome in addition to the 80% that
spontaneously improve.
Management, Steroid
Usual regimen is 1mg/kg/day for 1
week.
To be tapered in the 2nd week.
Management, Steroid
Cochrane review*:
“There is insufficient evidence about the effects of
corticosteroids for people with Bell's palsy, although
their anti-inflammatory effect might prevent nerve
damage.”
*Salinas RA, Alvarez G, Ferreira J. Corticosteroids
for Bell's palsy (idiopathic
facial paralysis). Cochrane Database of Systematic Reviews 2004, Issue 4.
Art. No.: CD001942.
Management, Antivirals
It seems logical in Bell's palsy
because of the probable involvement
of herpes viruses.
Aciclovir, a nucleotide analogue,
interferes with herpes virus DNA
polymerase and inhibits DNA
replication.
Management, Antivirals
Usual regimen is 4000mg/24hrs
divided into 5 doses for 7 to 10 days
Bell’s palsy:
Antivirals:
Cochrane review*:
“More evidence is needed to show whether the antiviral
drugs acyclovir or valacyclovir are effective in aiding
recovery from Bell's palsy.”
* Allen D, Dunn L. Acyclovir
or valaciclovir for Bell's palsy (idiopathic facial
paralysis). Cochrane Database of Systematic Reviews 2004, Issue 3. Art.
No.: CD001869.
Outcomes:
It has a fair prognosis without
treatment, with almost three
quarters of patients recovering
normal mimetical function and just
over a tenth having minor sequelae.
A sixth of patients are left with either
moderate to severe weakness,
contracture, hemifacial spasm, or
synkinesis.
Outcomes:
Patients with a partial palsy fair
better, with 94% making a full
recovery.
The outcome is worse when herpes
zoster virus infection is involved in
partial palsy.
Outcomes:
In patients who recover without
treatment, major improvement
occurs within three weeks in most.
If recovery does not occur within this
time, then it is unlikely to be seen
until four to six months, when nerve
regrowth and reinnervation have
occurred.
Bad Prognostic Factor:
Complete facial palsy
No recovery by three weeks
Age over 60 years
Severe pain
Ramsay Hunt syndrome (herpes zoster
virus)
Associated conditions—hypertension,
diabetes, pregnancy
Severe degeneration of the facial nerve
shown by electrophysiological testing
Thanks
Labs:
Nerve Excitability Test: NET :
– Indication: complete paralysis<3wks
– Interpretation: < or = 3.5 mA
threshold: Prognosis Good
– Limitation: Not useful in the 1st 3 days
or during recovery.
Labs:
Maximum stimulation Test: MST:
– Indication: complete paralysis<3wks
– Interpretation: Marked weakness or no
muscle contraction: advanced
degeneration with guarded prognosis
– Limitation: Not Objective.
Labs:
Electroneurography: ENoG :
– Indication: complete paralysis<3wks
– Interpretation: < 90% degeneration:
prognosis is good; > or = 90%:
prognosis is question
– Limitation: False-positive results in
deblocking phase.
Labs:
Electromyography: EMG
– Indication: Acute paralysis less than 1 week or
chronic paralysis longer than 2 weeks
– Interpretation:
Active mu: intact motor axons
Mu + fibrillation potentials: partial degeneration
Polyphasic mu: regenerating nerve
– Limitation: cannot assess degree of
degeneration or prognosis for recovery.