Bell's Palsy is an acute unilateral facial nerve paralysis that presents with weakness or paralysis of the muscles of facial expression. The most common cause is believed to be Herpes simplex virus infection of the facial nerve. Treatment involves oral corticosteroids combined with antiviral therapy if HSV or VZV infection is suspected. Prognosis is generally good, with most patients recovering, but complications can include synkinesis, hemifacial spasm, and gustatory lacrimation.
3. MOTOR COURSE OF THE FACIAL
NERVE: INTRACRANIAL
Nerve to stapedius
The first motor branch that arises
within the facial canal
Involvement of the stapedius
results in sound being hyperacute
(hyperacusis) and distorted in pitch
Bad prognostic sign as stapedius
involvement suggest that the facial
nerve is involved close to the
brainstem
4. CLUES FOR
INTRACRANIAL
INVOLVEMENT
OF THE FACIAL
NERVE
THE MUSCLES OF FACIAL EXPRESSION WILL BE
PARALYZED OR SEVERELY WEAKENED. THE OTHER
SYMPTOMS PRODUCED DEPEND ON THE LOCATION OF
THE LESION, AND THE BRANCHES THAT ARE AFFECTED:
• CHORDA TYMPANI – REDUCED SALIVATION AND LOSS
OF TASTE ON THE IPSILATERAL 2/3 OF THE TONGUE.
• NERVE TO STAPEDIUS – IPSILATERAL HYPERACUSIS
(HYPERSENSITIVE TO SOUND).
• GREATER PETROSAL NERVE – IPSILATERAL REDUCED
LACRIMAL FLUID AND NASAL MUCUS PRODUCTION.
• PREGANGLIONIC INPUT TO THE SPHENOPALATINE
CANAL
THE MOST COMMON CAUSE OF AN INTRACRANIAL LESION
OF THE FACIAL NERVE IS MIDDLE EAR PATHOLOGY –
SUCH AS A TUMOUR OR INFECTION. IF NO DEFINITIVE
CAUSE CAN BE FOUND THEN THE DISEASE IS TERMED
BELL’S PALSY.
5. Motor Course of the Facial Nerve
Between the stylomastoid foramen,
and the parotid gland, three motor
branches are given off:
Posterior auricular nerve – Ascends
in front of the mastoid process,
and innervates the intrinsic and
extrinsic muscles of the outer ear.
It also supplies the occipital part of
the occipitofrontalis muscle.
Nerve to the posterior belly of the
digastric muscle (suprahyoid
muscle of the neck). It is
responsible for raising the hyoid
bone.
Nerve to the stylohyoid muscle –
Innervates the stylohyoid muscle (a
suprahyoid muscle of the neck). It
is responsible for raising the hyoid
bone.
8. FACIAL NERVE INNERVATION OF THE MUSCLES OF FACIAL EXPRESSION
Within the parotid gland, the facial
nerve terminates by bifurcating into
five motor branches. These innervate
the muscles of facial expression:
Temporal branch – Innervates the frontalis,
orbicularis oculi and corrugator supercilia
Zygomatic branch – Innervates the
orbicularis oculi.
Buccal branch – Innervates the orbicularis
oris, buccinator and zygomaticus muscles.
Marginal Mandibular branch – Innervates the
mentalis muscle.
Cervical branch – Innervates the platysma.
9. PRESENTATION OF A BELL’S PALSY
Symptoms of Bell palsy include the following:
Acute onset of unilateral upper and lower facial paralysis (over a
48-hr period)
Posterior auricular pain
The pain frequently occurs simultaneously with the paresis, but pain
precedes the paresis by 2-3 days in about 25% of patients.
Decreased tearing
Hyperacusis
Taste disturbances
Otalgia
11. ETIOLOGIES OF A BELL’S PALSY
Herpes simplex virus (HSV) is
suspected as a common
cause of Bell palsy
•Autopsy studies have since shown HSV
in the geniculate ganglion of patients
with Bell palsy.
•Murakami et al performed polymerase
chain reaction (PCR) assay testing on
the endoneural fluid of the facial nerve
in patients who underwent surgery for
Bell palsy and found HSV in 11 of 14
cases.
1
Besides HSV infection,
possible etiologies for Bell
palsy include other infections
(eg, herpes zoster, Lyme
disease, syphilis, Epstein-
Barr viral infection,
cytomegalovirus, human
immunodeficiency virus
[HIV], mycoplasma)
2
Microvascular disease
(diabetes mellitus and
hypertension
3
Bell palsy may be secondary
to viral and/or autoimmune
reactions that cause the
facial nerve to demyelinate,
resulting in unilateral facial
paralysis.
4
12. Bell’s Palsy in Pregnancy
• Increased risk of Bell's palsy associated
with pregnancy, which is most marked in
the third trimester and the first
postpartum week
• May be caused by pregnancy-related
fluid retention leading to compression of
the nerve or perineural edema.
• Other potential etiologic factors include
hypercoagulability causing thrombosis of
the vasa nervosum and relative
immunosuppression in pregnancy.
• Several studies have found an
association of Bell's palsy with
preeclampsia, again suggesting
extracellular edema as the mechanism
13. RAMSAY HUNT
SYNDROME
Reactivation of the varicella zoster virus (VZV)
along the distribution of the sensory nerves
innervating the ear, which usually includes the
geniculate ganglion, is responsible for herpes
zoster (HZ) oticus.
Associated symptoms, such as hearing loss and
vertigo, are thought to occur as a result of
transmission of the virus via direct proximity of
cranial nerve (CN) VIII to CN VII at the
cerebellopontine angle or via vasa vasorum that
travel from CN VII to other nearby cranial nerves.
Ramsay Hunt syndrome accounts for up to 12%
of all facial paralyses and generally causes more
severe symptoms and has a worse prognosis
than Bell’s Palsy
Return-to-baseline neurologic function is
predicted partially by severity of paralysis.
In several studies, only 10-22% of individuals
with significant facial paralysis had complete
recovery. In one study, however, 66% of patients
with incomplete paralysis had complete
recovery.
16. Antiviral
Management
If herpes simplex virus (HSV-1 or HSV-2) or
varicella zoster virus (VZV) is suspected as
the etiology, an antiviral agent may be
added to the oral corticosteroid, as follows:
HSV: Acyclovir 400 mg PO 5 times daily for
10d or valacyclovir (Valtrex) 500 mg PO BID
for 5d
VZV: Acyclovir 800 mg PO 5 times daily for
10d or valacyclovir 1000 mg PO TID for 5d
17. Caveat for
Acute
Treatment of
Bell’s Palsy
Limited evidence of the efficacy of steroids and
antivirals in important Bell palsy subgroups:
Those with a lower probability of recovery
because of severe palsy at presentation
Those with possible zoster sine herpete
Because studies included only patients presenting early
after palsy onset, it is difficult to determine the effect
of steroid or antiviral treatment in patients presenting
later in the course of their illness (e.g., one week after
the onset of facial weakness).
Likewise, although it seems reasonable to assume that
an equivalent dose of alternative steroids would also
be effective, decisions regarding alternative steroid
dosing regimens necessarily require clinician judgment.
18. SURGICAL OPTIONS FOR A BELL’S PALSY
• Facial nerve decompression
• Subocularis oculi fat (SOOF) lift
• Implantable devices (eg, gold weights) placed into the eyelid
• Tarsorrhaphy
• Transposition of the temporalis muscle
• Facial nerve grafting
• Direct brow lift
20. Facial Synkinesia
Synkinesis is an abnormal
involuntary associated facial
movement that occurs in nearly all
cases of facial nerve degeneration
Synkinesis begins 3–4 months
after regeneration of FNP and
continues for up to 2 years.
The etiology of synkinesis is not
fully understood; however,
aberrant regeneration of the facial
nerve has been the most
commonly reported cause
The best treatment protocol among
rehabilitation program is
biofeedback.
21. Hemifacial Spasm
Note rapid and stereotypic
movements but not
particularly rhythmic
Similar to synkinesia
Don’t confuse this with focal
seizure activity
22. GUSTATORY LACRIMATION OR “CROCODILE TEARS SYNDROME”
GUSTATORY LACRIMATION OR “CROCODILE
TEARS SYNDROME,” IS THE SHEDDING OF
TEARS WHILE EATING OR DRINKING IN PATIENTS
RECOVERING FROM BELL’S PALSY.
IN THE RECOVERY PERIOD FOLLOWING FACIAL
NERVE INJURY, THE REGENERATING SALIVARY
NERVE FIBERS UNDERGO SYNKINESIS OR ARE
MISDIRECTED TO ULTIMATELY INNERVATE THE
LACRIMAL GLAND INSTEAD OF THE
SUBMANDIBULAR GLAND.
ANY STIMULI SUCH AS THE SMELL OR TASTE OF
FOOD, INSTEAD OF CAUSING SALIVATION,
EXCITES THE LACRIMAL GLAND TO PRODUCE
IPSILATERAL TEARING.
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