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Bell’s Palsy:
Presentation,
Differential and
Management
Randy M Rosenberg
MD FAAN FACP
Associate Professor of
Neurology
Lewis Katz School of
Medicine at Temple
University
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
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.
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.
Posterior Auricular Motor Function
Stylohyoid and Posterior Belly of the
Digastric Muscle Function
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.
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
FACIAL WEAKNESS
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
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
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.
RAMSAY HUNT SYNDROME (ZOSTER OTICUS)
AAN EVIDENCE BASED GUIDELINES
FOR ACUTE BELL’S PALSY
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
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.
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
COMPLICATIONS OF BELL’S PALSY
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.
Hemifacial Spasm
Note rapid and stereotypic
movements but not
particularly rhythmic
Similar to synkinesia
Don’t confuse this with focal
seizure activity
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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Bell's Palsy

  • 1. Bell’s Palsy: Presentation, Differential and Management Randy M Rosenberg MD FAAN FACP Associate Professor of Neurology Lewis Katz School of Medicine at Temple University
  • 2.
  • 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.
  • 7. Stylohyoid and Posterior Belly of the Digastric Muscle Function
  • 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.
  • 14. RAMSAY HUNT SYNDROME (ZOSTER OTICUS)
  • 15. AAN EVIDENCE BASED GUIDELINES FOR ACUTE BELL’S PALSY
  • 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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