St.

Paul University Iloilo

General Luna St., Iloilo City

BELLS PALSY

In Partial Fulfillment
Of the Requirements in

Seminar 2

Presented to:
Mr. Raymund O. Guanco, PTRP, RPT

Prepared By:
Bianca Nicole Flores
Mary Catherine Rebitoy
Ma. Chyril Dagol
Fitz Patrick Coo
Frances Marie Pagdato
Krystal Joy Apostolero
Michelle Sotero
Chris Mikaela Villegas
Renzo Pacheco
BSPT-4A

April 3, 2017

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 DEFINITION OF TERMS
1. Axonotmesis a nerve injury characterized by disruption of the axon and myelin sheath
but with preservation of the connective tissue fragments, resulting in degeneration of the
axon distal to the injury site
2. Corona radiata- a bundle of white fibers which spreads out like a fan and connects the
cortex of the brain with the basal ganglia and spinal cord
3. Corticonuclear fibers- are nerve fibers traveling in the pyramidal tract to the nuclei of
cranial nerves
4. Electromyogram (EMG) - measures the electrical activity of muscles when they're at rest
and when they're being used
5. Geniculate ganglion - contains fibers for taste and somatic sensation and is located in the
petrous temporal bone
6. Hyperaemic - an excessive amount of blood in an organ or part
7. Hyperacusis - is a health condition characterized by an increased sensitivity to certain
frequency and volume ranges of sound
8. House Brackmann Scale most widely used tool for grading facial paralysis and for
predicting recovery.
9. Nervus intermedius a form of the central processes of the unipolar cells of the
geniculate ganglion. It contains the efferent preganglionic parasympathetic fibers from
parasympathetic nuclei.
10. Neuropraxia - is the least severe type of nerve injury. It results in complete block of nerve
transmission despite intact nerve fibers
11. Neurotmesis partial or complete severance of a nerve, with disruption of the axon and
its myelin sheath and the connective tissue elements
12. Paresis - a condition of muscular weakness caused by nerve damage or disease; partial
paralysis
13. Pterygopalatine ganglion - one of the four parasympathetic ganglia of the head and neck
and largest of the peripheral parasympathetic ganglia. It receives parasympathetic fibers
from the facial nerve
14. Reticular formation- throughout the midbrain, pons and medulla oblongata, groups of
scattered nerve cells and fibers are collectively known as the reticular formation.
15. Synkinesis - refers to "simultaneous movement" that occurs after Bell's palsy or instances
where the facial nerve has been cut and sewn back together.

INTRODUCTION
BELLS PALSY

It is the most common cause of facial paralysis.

Bell's palsy is named for Sir Charles Bell, a 19th century Scottish surgeon who described
the facial nerve and its connection to the condition.
Bells palsy is a form of temporary facial paralysis resulting from damage or trauma to
the facial nerves.
The facial nerve, also called the 7th cranial nerve travels through a narrow, bony canal in
the skull, beneath the ear, innervating the muscles on each side of the face.
In Bells palsy, the function of the facial nerve is disrupted, causing an interruption in the
messages the brain sends to the facial muscles. This interruption results in facial
weakness or paralysis.

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 Generally, Bell's palsy affects only one of the paired facial nerves and one side of the
face, however, in rare cases, it can affect both sides.

ANATOMY
The Facial nerve has three nuclei:
The Main motor nucleus
The Parasympathetic nuclei
The Sensory nucleus

Main Motor Nucleus

lies deep in the reticular formation of the lower part of the pons.
The part of the nucleus that supplies the muscles of the upper part of the face receives
corticonuclear fibers from both cerebral hemispheres.
The part of the nucleus that supplies the muscles of the lower part of the face receives
only corticonuclear fibers from the opposite cerebral hemisphere.

Parasympathetic Nuclei
lie Posterolateral to the main motor nucleus.
They are the Superior Salivatory and Lacrimal nuclei.
The Superior Salivatory Nucleus receives afferent fibers from the hypothalamus
through the descending autonomic pathways. Information concerning taste also
is received from the nucleus of the solitary tract from the mouth cavity.
The Lacrimal Nucleus receives afferent fibers from the hypothalamus for
emotional responses and from the sensory nuclei of the trigeminal nerve for
reflex lacrimation secondary to irritation of the cornea or conjunctiva.

Sensory Nucleus
upper part of the nucleus of the Tractus Solitarius and lies close to the motor nucleus.
Sensations of taste travel through the peripheral axons of nerve cells situated in the
geniculate ganglion on the seventh cranial nerve.
The central processes of these cells synapse on nerve cells in the nucleus.
Efferent fibers cross the median plane and ascend to the ventral posterior medial nucleus
of the opposite thalamus and to a number of hypothalamic nuclei.
From the thalamus, the axons of the thalamic cells pass through the internal capsule and
corona radiata to end in the taste area of the cortex in the lower part of the postcentral
gyrus.

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Course of the Facial Nerve
The Facial nerve consists of a motor and a sensory root. The fibers of the motor root first travel
posteriorly around the medial side of the abducent nucleus. They then pass around the nucleus
beneath the colliculus facialis in the floor of the fourth ventricle and, finally, pass anteriorly to
emerge from the brainstem.

The sensory root (nervus intermedius) is formed of the central processes of the P.347 unipolar
cells of the geniculate ganglion. It also contains the efferent preganglionic parasympathetic fibers
from the parasympathetic nuclei.

The two roots of the facial nerve emerge from the anterior surface of the brain between the pons
and the medulla oblongata. They pass laterally in the posterior cranial fossa with the
vestibulocochlear nerve and enter the internal acoustic meatus in the petrous part of the temporal
bone.
At the bottom of the meatus, the nerve enters the facial canal and runs laterally through the inner
ear. On reaching the medial wall of the tympanic cavity, the nerve expands to form the sensory
geniculate ganglion and turns sharply backward above the promontory. At the posterior wall of
the tympanic cavity, the facial nerve turns downward on the medial side of the aditus of the
mastoid antrum, descends behind the pyramid, and emerges from the stylomastoid foramen.

Important Branches of the Facial Nerve

Greater petrosal nerve
arises from the nerve at the geniculate ganglion.
It contains preganglionic parasympathetic fibers that synapse in the pterygopalatine
ganglion.
The postganglionic fibers are secretomotor to the lacrimal gland and the glands of the
nose and the palate.
The greater petrosal nerve also contains taste fibers from the palate

Nerve to stapedius
supplies the stapedius muscle in the middle ear.

Chorda tympani
arises from the facial nerve in the facial canal in the posterior wall of the middle ear.
It runs forward over the medial surface of the upper part of the tympanic membrane and
leaves the middle ear through the petrotympanic fissure, thus entering the infratemporal
fossa and joining the lingual nerve.

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 The chorda tympani contains preganglionic parasympathetic secretomotor fibers to the
submandibular and the sublingual salivary glands. It also contains taste fibers from the
anterior two thirds of the tongue and floor of the mouth.

Posterior auricular, the posterior belly of the digastric, and the stylohyoid nerves
are muscular branches given off by the facial nerve as it emerges from the stylomastoid
foramen.
Five terminal branches to the muscles of facial expression.
Temporal
Zygomatic
Buccal
Mandibular
Cervical

The facial nerve thus controls facial expression, salivation, and lacrimation and is a pathway for
taste sensation from the anterior part of the tongue and floor of the mouth and from the palate.

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 INCIDENCE
Females > Males
Blacks and Hispanics had higher rates did than those in the White/Asian/Native
American group.
Incidence rate of 42.77 per 100,000 person-years among active-duty members of the US
Armed forces.
33% higher among those assigned to arid regions of the United States compared with
those who were assigned to nonarid regions of the country.
Two physical stressors: residence in arid climate and exposure to cold.
More common among young and middle aged adults.

CLASSIFICATION
THE MODIFIED HOUSE-BRACKMANN CLASSIFICATION OF FACIAL FUNCTION

GRADE DESCRIPTION CHARACTERISTICS

I Normal Normal facial function

II Mild dysfunction Slight weakness noticeable on

close inspection. May have
slight synkinesis

III Moderate dysfunction Obvious, but not disfiguring,

difference between two sides.
Complete eye closure with
effort. Noticeable but not
severe synkinesis, contracture

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 or hemifacial spasm.

IV Moderately severe Obvious weakness or

dysfunction disfiguring asymmetry.
Normal symmetry or tone at
rest. Incomplete eye closure.

V Severe dysfunction Only barely perceptible

motion. Asymmetry at rest

VI Total paralysis No movement

ETIOLOGY
Idiopathic, acute peripheral-nerve palsy involving the facial nerve, which supplies all the
muscles of facial expression (inflammation or compression)

Nerve that controls the facial muscles is swollen, inflamed, or compressed, resulting in facial
weakness or paralysis.

Facial nerve swells and becomes inflamed in reaction to the infection, causing pressure within
the Fallopian canal and leading to ischemia (the restriction of blood and oxygen to the nerve
cells).

Exact reason Bell's palsy occurs isn't clear, it's often linked to exposure to a viral infection.
Viruses that have been linked to Bell's palsy include the virus that causes:

Cold sores and genital herpes (herpes simplex)

Chickenpox and shingles (herpes zoster)
Mononucleosis (Epstein-Barr)
Cytomegalovirus infections
Respiratory illnesses (adenovirus)
German measles (rubella)
Mumps (mumps virus)
Flu (influenza B)
Hand-foot-and-mouth disease (coxsackievirus)

PATHOMECHANISM
Facial nerve becomes swollen or hyperaemic. Within the facial canal, in which there is
limited space, the nerve rapidly becomes compressed and conductivity is lost. Swelling of the
inflamed nerve causes compression against the bony walls, tending to the compression of blood
supply, ischemia and further swelling. In its more severe form, infarction of the nerve may occur
with prolonged and not infrequently, an incomplete process of regeneration.

Disorders of the facial nerve results in paresis of the muscles of facial expression and loss
of taste of the anterior 2/3 of the tongue. Facial weakness, however, also results from a lesion
involving the direct activation of pathways descending feom the cortex to innervate the facial

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nuclei. It is of clinical importance to distinguish between upper motor neuron (central) facial
weakness involving the lower part of the face and the lower motor neuron (peripheral) facial
weakness involving both the upper and the lower portions of the face.

SIGNS AND SYMPTOMS

Location of Lesion Description Signs and symptoms

1. Outside the stylomastoid Muscles of both the upper A. Forehead cannot be

foramen and lower parts of the
ipsilateral face are involved
in flaccid paralysis; A
Lower motor lesion
2. Facial canal and involving the Chord tympani carries taste
chord tympani impressions from anterior
2/3 of the tongue.
wrinkled
B. Palperbral fissure is
widened
C. The Upper eyelid closes
slowly
D. Demostrates Bells
phenomenon
E. Loss of blinking reflex on
the affected side
F. Saliva may dribble on the
mouth
G. No deviation of tongue or
jaw
All the signs of Lesion 1 are
present, as well as:

The Preganglionic

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3. Higher in the Facial canal
involving Stapedius muscle
4. Geniculate Ganglion
5.Internal Auditory Meatus
6. Emergrence of the facial nerve This presents with Bells
from Pons (Meningitis)
DIFFERENTIAL DIAGNOSIS
Condition
Ramsay Hunt Syndrome
CVA
parasymptathetic secreto-
motor innervations of the
sublingual and submaxillary
glands enter the Chorda
tympani
The action of the stapedius
is to reflexly calm the
vibrations of the
stapes;when it is affected,
the middle ear cannot fully
carry out its protective
function of reducing the
amplitude of vibrations
accompanying intense
sounds of low frequency.
The sensory geniculate
ganglion is just an
expansion of the facial
nerve reaching the medial
wall of the tympanic cavity.
AKA Internal Acoustic
Meatus; concerned with
hearing
A. Marcus-Gunn
palsy with involvement of
the facial nerves, 5,8 and at
times CN 6, 11 & 12, 7
Cause Similarities
Herpes Zoster Severe Facial
Virus
Palsy
Ischemia or
Hemmorhage
A. Loss of taste in ant. 2/3 of
the tongue
B. Reduced salivation on the
affected side
All the signs of Lesion 1 and 2
are present, as well as:
A. Hyperacusis (painful
sensitivity to loud sound)
A. Herpetic eruptions on the
ipsilateral eardrum, post. Part
of auricle, tympanic
membrane, external auditory
canal, pinna or soft palate
B. Facial Paralysis
C. Facial Numbness
D. Ipsilateral deafness
A. Tinnitus
B. Defective Vestibular
responses
C. Signs of Bells palsy
D. Deafness
B. Maran Amat Syn observed
after Peripheral Facial
Paralysis
Distinguishing factors
Pronounced prodrome
of pain; vesicular
eruption in ear canal
or pharynx
Cortical CVA: sparing
of upper third of face,
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 presence of other
neurological deficits.

Pontine CVA:
typically involves all
regions of the face,
presence of other
neurological deficits.

Melkersson-Rosenthal Unknown, rare Facial Edema (labial),

syndrome Syn Plication of the
tongue

Otitis Media Bacterial Gradual onset; ear

or Cholesteatoma pathogens pain, fever, and
conductive hearing
loss

Others:

1. Multpile Sclerosis
2. Lymes Disease
3. Facial hemiatrophy of Rhomberg
4. Blepharospasm

PROGNOSIS
The amount of paralysis varies in each case, depending on the severity of the lesion.
Spontaneous recovery may take in mild cases within a few days with 85% of untreated
patients. The initial change appears within 3 weeks.
The other 15% shows signs of improvement within 3 to 6 months.
Good prognosis signs:
1. If recovery of taste occurs in the 1st week.
2. Incomplete paralysis in the first 5 to 7 days is the most favorable prognostic sign.
3. If within a few days after the onset , EMG shows that there are motor units under
voluntary conduction remains normal or slightly slowed, then in all probability, the lesion
is mainly neuropraxial and recovery is likely to be rapid and complete.
4. If at the end of 3 weeks from the onset there is some return of voluntary power in the
face, the recovery is likely to be rapid and probably be complete in a few weeks.

Factors associated with a poorer prognosis than average or with which patients are at risk of
not recovering completely are:

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 1. Age > 60 y.o.
2. Hypertension
3. Hyperacusis
4. Diminished lacrimation
5. DM
6. If the lesion or paralysis is complete
7. If no motor units can be detected by needle electrode exploration of the facial
musculature.
8. If within a few days the facial nerve is totally unexcitable.

Recovery:
Recovery of taste precedes recovery of motor function.
Usual order of return of function:
1. Buccinators
2. Zygomatic
3. Inferior levator
4. Orbicularis oculi
5. Frontalis

ANCILLARY PROCEDURES
1. EMG
2. Nerve conduction velocity

PT EVALUATION
Clinical examination should include a complete neurologic and general examination, including
otoscopy and attention to the skin and parotid gland. Vesicles or scabbing around the ear should
prompt testing for herpes zoster. Careful observation during the interview while the patient is
talking may re- veal subtle signs of weakness and provide additional clues.
A systematic approach to the assessment of a patient with suspected Bell palsy is recommended

1. Does the patient have peripheral facial palsy?

In Bell palsy, wrinkling of the forehead on the affected side when raising the eyebrows is
either asymmetrical or absent.
If the forehead muscles are spared and the lower face is weak, this signifies a central
lesion such as a stroke or other structural abnormality and not a peripheral lesion of the
facial nerve (eg, Bell palsy).

2. Can the patient close the eyes tightly?

In Bell palsy, when the patient attempts to close the eyes, the affected side shows
incomplete closure and the eye may remain partly open.
Assess the strength of the orbicularis oculi by trying to open the eyes. The patient who is
attempting to close the eyelids tightly but cannot will demonstrate the Bell phenomenon,

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 ie, the examiner is able to force open the eyelids, and the eyes are deviated upward and
laterally.
Closely observe the blink pattern, as the involved side in Bell palsy may slightly lag be-
hind the normal eye, and the patient may be unable to close the eye completely.

3. Is the smile symmetric?

Note flattening of the nasolabial fold on one side, which indicates facial weakness.

4. Can the patient puff out the cheeks?

Ask the patient to hold air in the mouth against resistance. This assesses the strength of
the buccinator muscle.

5. Can the patient purse the lips?

Ask the patient to pucker or purse the lips and observe for asymmetry or weakness on the
affected side.
Test the orbicularis oris muscle by trying to spread the lips apart while the patient resists,
and observe for weakness on one side.

6. Is there a symmetric grimace?

This will test the muscles involved in depressing the angles of the mouth and platysma.

7. Are taste, sensation, and hearing intact?

Other testable functions of the facial nerve, including taste, sensation, and hearing, do not
always need to be assessed but can be in patients with specific sensory deficits.
Somatic sensory fibers supplied by the facial nerve innervate the inner ear and a small
area behind the ear, but these may be difficult to assess objectively. Formal audiologic
testing may be needed if hearing is impaired.

8. Facial nerve reflexes

A number of facial reflexes can be tested, including the orbicularis oculi, palpebral-
oculogyric, and corneal reflexes
The orbicularis oculi reflex is tested by gentle finger percussion of the glabella while
observing for involuntary blinking with each stimulus. This reflex is weakened or absent
on the affected side.
The palpebral-oculogyric reflex, or Bell phenomenon, produces upward and lateral
deviation of the eyes when attempting forceful eyelid closure. In Bell palsy, this reflex is
visible because of failure of adequate eyelid closure.
The corneal reflex is elicited by stimulating the cornea with a wisp of cotton, causing
reflexive closure of the both eyes. The affected side may show slowed or absent lid
closure when tested on either side. The sensory afferent fibers are carried by the
trigeminal nerve, and the motor efferent fibers are carried by the facial nerve.

9. Grading of facial paralysis (The House-Brackmann scale)

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 Special Tests:

1. Bells Phenomenon
(+)upon eye closure, eye rolls upward & outward

2. Chvostek Test
tapping the parotid gland or cheeks
(+) facial twitch

3. Marcus Gun Phenomenon

resisted lateral jaw deviation
(+)blinking or winking of the eye

4. Marin Amat
resisted mouth opening
(+) partial closing of the eye

5. Crocodile Tears
upon chewing
(+) tearing if the eye
aka Bogorad's syndrome

MEDICAL MANAGEMENT

1. Oral Steroids to reduce inflammation

2. Surgery
3. Eyelids may be stitched to protect the eye
4. Prodnisone

PT MANAGEMENT

A. Assessment
1. Converse with the patient
2. Observe the patient at rest
3. Close eyes and lips and forcefully open
4. Show teeth/ grimace voluntarily
5. Let the patient perform act of whistling and blowing
6. Taste test
7. Test for frontal muscle
8. Test for hyperacusis
9. Electrical test

B. Course of Treatment
Paralysis
1. US cover the nerve trunk just front of the tragus or the ear for inflammation reduction
2. Massage
- Stroking in upward and outward direction

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 - Slow finger kneading applied in paralyzed muscle to maintain suppleness and
muscle elasticity
- Should be done ( 3 ) three minutes daily to maintain lymphatic and blood flow,
prevent contracture
3. Advice
- Lie down in intervals throughout the day to reduce the effects of gravity on the
paralyzed muscle
- Blink regularly because the normal blinking reflex is lost and dust particles
collect and results to conjunctivitis

C. Acute and Subacute stage

1. Splinting - to relieve strain on relax muscle and to preserve tonus and cosmesis
2. Facial massage - five ( 5 ) mins., 2x/day
3. Googles or plain glasses - to protect cornea from damage
4. Infrared ray - increase blood supply and decrease skin resistance prior to ES
5. ES - galvanic or faradic current for regeneration and preparation for rein-nervation
6. HMP - to hasten recover and pain relief

D. Recovery stage
1. Mild IR - to warm the muscle and improve function
2. Eye must be protected with a wool
3. PNF - for muscle reeducation
1. Quick stretch
2. Hold relax
4. Icing, brushing, tapping or brisk stroking may be applied along the muscle length

E. Exercises
1. Look surprised then frown
2. Squeeze eyes, close, then wide open
3. Smile, grin and say "OH"
4. Say " A, E, I, O, U
5. Hold straw in the mouth then blow
6. Whistle

F. Prognosis
- the amount pf paralysis varies in each case, depending on the severity of the lesion. The
total actual deficit may not be determined or about 7 to 10 days, because damaged nerve
fibers may conduct during the process of degeneration and swollen undestroyed fibers
temporarily may not function.

Good prognosis sign:

1. Recovery of taste occurs first week
2. Incomplete paralysis of 5 to 7 days
3. EMG conduction remains normal and slightly slowed
4. End of 3 weeks from the onset there is some return of voluntary power

Factors associated with power prognosis or at risk of not recovering

1. Age greater than 60
2. Hypertension
3. Hyperacusis
4. Diminished Lacrimation
5. DM
6. No motor unit can be detected by needle electrode exploration
7. Lesion or paralysis is complete
8. Facial nerve is totally unexcitable
9. Evidence of denervation after 10 days

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 Order of function:
- Buccinator
- Zygomaticus
- Inferior Levator
- Orbicularis Oculi
- Frontalis

Complications after apparent recovery

1. State of overtoning or contracture
2. Associated movement of synkinesis
3. Crocodile tears
4. Hemifacial Spasm

References:
1. Snell, R.S. (2010). Clinical Neuroanatomy (7th ed.) Philadelphia: Lippincott
Williams & Wilkins.
2. Patel, D.K. & Levin, K.H. (2015). Bell Palsy: Clinical Examination and
Management. Cleveland Clinic Journal of Medicine. 82(7), 419-426.

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