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BELLS PALSY

1. DEFINITION
Bells palsy is a form of facial paralysis of acute onset with an unknown etiology.
It is presume to be due to a non-suppurative inflammation of the facial nerve
inside its canal above the stylomastoid foramen. It was named after Sir Charles
Bell who stated that the facial nerve is the mother of the face.
Bells palsy occurs when a nerve transmits faulty signals to muscles in the face. It
happens with little or no warning symptoms may even suggest of stroke.
The functional components of the facial and intermediate nerve include: 1.)
Special visceral efferent (SVE, branchiomotor) fibers, 2.) General visceral
efferent (GVE, parasympathetic) fibers, 3.)
Special visceral efferent (SVE,
taste) and 4.) A few general somatic efferent (GSA, sensory) fibers. Special
visceral efferent fibers of the motor component innervate the muscles of facial
expression, the platysma, the buccinator and the stapedius muscles. Synapses
with the postganglionic neurons occur in the pterygopalatine and submandibular
ganglia. Postganglionic fibers from the pterygopalatine ganglion give rise to
secretory and vasomotor fibers that innervate the lacrimal gland and the mucous
membrane of the nose and mouth.
2. EPIDEMIOLOGY
Lifetime Prevalence: 6.4 per 100
Incidence: Increases with age
Overall: 0.5 per year per 1000
Age 20: 0.1 per year per 1000
Age 80: 0.6 per year per 1000
Season: Occurs at all times of the year
Equal prevalence between males and females
Recurrence: 7%
Side affected: Right side in 63%
3. ETIOLOGY
The exact cause of Bells Palsy is unknown. It commonly happens after:
Trauma to the facial nerve or
Pressure upon the facial nerve due to a tumor.
It also has been associated with:
A viral infection, like viral meningitis
Flue-like illness
Headaches and colds
Chronic middle ear infection
High blood pressure and diabetes
Temporal bone fractures
Hemorrhages
Infectious diseases
Three categories regarding the cause
Hereditary due to the diameter of the axons
Vascular ischemic theory exposure to cold
Viral theory
4. PATHOGENESIS
From the course of the illness, it is presumed that the acute non-suppurative
inflammation of unknown etiology causes swelling and/or edema and hyperemia
of the nerve sheath with the compression of the axons of the narrow facial canal,
thus impinging them.
Within a day or two from exposure, there might be a slight fever and pain and
stiffness in the neck region. The onset is sudden and acute. The patient often
finds the face paralyzed upon waking in the morning. He may notice that the
mouth is drawn to one side. The onset is accompanied by a dull ache behind the

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ear, mastoid region, around the angle of the jaw and spreading into the face. A
few hours after, the patient may describe the weakness as being woody, stiff or
numb on one side of the face, but sensory testing is always normal. The mouth is
dry and excessive tearing (crocodile tears) is usually present during the first few
days of the palsy. Impairment is always present to some degree in almost all
patients, but rarely beyond the second week of paralysis. About one-half of the
cases attain maximum paralysis in 2 days and practically all cases, within 5 days.
5. CLINICAL MANIFESTATIONS
Signs and symptoms depend upon the location of the lesions:
A. Lesion 1: outside the stylomastoid foramen. Since it is a LMN, the muscles of
both the upper and lower parts of the ipsilateral face are flaccid.
The forehead cannot be wrinkled
The upper eyelids closes slowly because of the pull of gravity
When an attempt to shut the eye is made, closure is incomplete and the
eyeball rolls up and outward (Bells Phenomenon)
Blinking or corneal reflex is lost on the affected side
Rolling of tears down the cheek
Saliva may dribble from the mouth
Due to paralysis of the Orbicularis Palpebrum, the palpebral fissure is
widened
The nasolabial fold is obliterated, the brow is wrinkled, the angle of the
mouth sags and the affected side is expressionless
The mouth is drawn to the actively contracting muscles on the opposite
side of the face
B. Lesion 2: Facial canal (involving chorda tympani). All the signs of Lesion 1 are
present with the addition of the following:
Loss of tastes in the anterior two thirds of the tongue. This is because the
Chorda Tympani, a peripheral sensory fiber of the facial nerve, carries
taste impressions form the anterior two thirds of the tongue.
Reduced salivation on the activated side. This is because of the
preganglionic parasympathetic secreto-motor innervation of the
submaxillary and the sublingual glands enter the Chorda Tympani before
finally ending in the submaxillary ganglion.
C. Lesion 3: Higher than the facial canal and involving the stapedius muscle. All
the signs of Lesion 1 are present in addition with the following:
Hyperacusis painful sensitivity to loud sound
D. Lesion 4: Involving the Geniculate Ganglion
Acute with pain behind and within the ear
Ramsey-hunt Syndrome associated with Herpes Zoster of the geniculate
ganglion
E. Lesion 5: In internal auditory meatus
Since the internal auditory meatus transmits the acoustic nerve and the motor and
sensory roots of the facial nerve, therefore, lesions at the site would naturally
present with:
Signs of Bells Palsy
Deafness from CN 8 involvement
Tinnitus or ringing in one or both ear
Defective vestibular responses
F. Lesion 6: At the emergence of the facial nerve from the pons (meningitis) this
presents with Bells palsy with involvement of the CN V, VI and VIII probably
because the nuclei of these nerves are located in the pons.
MARCUS-GUNN or JAW WINKING PHENOMENON seen in congenital ptosis,
is the elevation of the optic eyelid on movement of the jaw to the contralateral
side.
MARIN-AMAT SYNDROME observed after peripheral facial paralysis, is
referred to as an inverted Marcus-Gunn phenomenon. Closing of the eyes occurs
when the patient opens the mouth forcefully or maximally.

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6. COMPLICATIONS
The most serious complication that may happen with Bells palsy is the inability to
close the eyelids, exposing the eye to irritation and drying.
Complications that may appear after apparent recovery.
A. Crocodile tears there is lacrimation while chewing
The eye tears on the side of paralysis while taking strongly flavored food
into the mouth because of the saliva secretory fibers to the lacrimal nerve
to innervate the lacrimal gland
When marked contractures develops, the nasolabial furrow becomes
deeper on the paralyzed side
B. Facial spasms develops and persists indefinitely and initiated by facial
movements
Usually begins in the orbicularis oculi muscles and gradually spread to
other muscles on that side of the face
C. Associated movement synkinesis attempts to move one group of facial
muscles results in contraction of all of them
D. Nasal obstruction which could cause difficulty breathing through
7. DIAGNOSIS
Criteria for diagnosis:
A. Sudden onset of complete or partial paralysis of the muscles supplied by the
seventh cranial nerve
B. Absence of other signs CNS diseases
C. Absence of diseases of the middle ear or posterior fossa
D. Absence of Herpes Zoster
The 4 electrodiagnostic test in the assessment of Bells Palsy are:
A. Measurement of nerve excitability, this is done in the first 10 days following
onset of the lesion.
B. Measurement of the NCV, this is done in the first 10 days following onset of
lesion also.
C. The SDC, this is the graph of the excitability of the nerve, muscle or both; this
is done 10-14 days after onset when the motor endplate excitability is lost if
the lesion is marked.
D. EMG, this will detect action potentials elicited by nerve stimulation when the
muscle contraction is too weak to be observed by the unaided eye, with
denervation, fibrillation potentials will appear.
Though it is not essential, some literature recommends formal audiometry to rule
out associated nerve involvement and to evaluate the stapes reflex. Studies
have demonstrated that if the paralysis is incomplete and the stapedial reflex is
intact that full recovery is commonly seen in 3-6 weeks.
8. DIFFERENTIAL DIAGNOSIS
COMPARISON BELLS PALSY AND FACIAL PARALYSIS

POINTS OF COMPARISON
1. Etiology
2. UMNL/LMNL
3. Type of lesion
4. Distribution
5. Muscle tone
6. Nerve affected
7. Skin condition

BELLSPALSY
Unknown
LMNL
Peripheral or nuclear
of the face, ipsilateral
Flaccid
Facial nerve
Dry

FACIAL PARALYSIS
CVA, tumors, vascular lesion
UMNL
Central or supranuclear
Lower of the face, contra.
Spastic
No specific nerve (affect all)
Dry

It is important to test the facial nerve by having the patient first lift his/her
eyebrows and then lower them. Mild weakness can be seen when the eyebrows
do not lift symmetrically. Ask the patient to close his/her eyelids tightly. When the
weakness is severe the eyelids do not close completely. Bells phenomena is
seen when this occurs. Ask the patient to then smile or show his/her teeth.
When paralysis results from an upper rather than a lower motor lesion,
involuntary contraction of the muscles of facial expression can occur in response

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to an emotional stimulus (but not for voluntary facial movement.) It is unclear
what the anatomic pathways are for involuntary facial movement.
Physical findings may also include hyperesthesia or dysesthesia of cranial nerve
5 & 9 along with the 2nd cervical nerve. Abnormalities in hearing are not seen
with Bells Palsy and should prompt the consideration of other diagnoses.
Acute facial muscle weakness:
Polyneuritis
Bells Palsy 75% of cases
Herpes Zoster Ramsey Hunt syndrome
Guillain-Barre syndrome
Myasthenia gravis
Idiopathic autoimmune disease
Trauma
Skull fracture or concussion basilar or facial
Surgery
Penetrating facial injury
Birth trauma
Infectious
Otitis media bacterial
Cholerteatoma
Lyme disease
Mumps
Tuberculosis
HIV related
Sarcoidosis
Cerebrovascular accidents
Neurologic disorders
Toxic
Thalidomide
INH
Melkersson-Rosenthal syndrome (recurrent alternating facial palsy,
furrowed tongue, faciolabial edema).
Progressive or Chronic facial muscle weakness
Tumors
Paratoid (any cell type)
Metastatic
Benign tumors
9. PROGNOSIS
The amount of paralysis varies in each case, depending on the severity of the
lesion. The total actual deficit may be determined for about 7 to 10 days because
damage nerve fibers may conduct in the process of degeneration, swollen but
undestroyed fibers temporarily may not function.
Spontaneous recovery may take places in mild cases within a few days at 85% of
untreated patients who improve, the initial change appears within 3 weeks. The
other 15% show signs of improvement within 3-6 months.
Some authors claim that more than a5 months, while some claim that most
patients recover within a few weeks or in a month or two.
Overall, 90% of patients are expected to recover from Bells palsy. However, for
some patients, the symptoms may last longer. In a few cases, the symptoms may
never completely disappear.
Good prognostic signs:
Incomplete paralysis in the first 5 to 7 days
Return of the voluntary power of the face at the end of 3 weeks from
onset
Slow progression
Younger age

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Recovery of taste occurs in the first week
Electrodiagnostic tests normal
If within a few days after onset electromyography shows that there is
motor voluntary control in the facial muscles and facial nerve conduction
remains normal or slightly slowed, recovery is likely to be rapid and
complete.
Factors associated with poorer prognosis:
Age greater than 60 years old
Hypertension
Diabetes Mellitus
Hyperacusis
Diminished lacrimation
If the lesion of paralysis is complete
If no motor units can be detected by needle electrode exploration of the
facial musculature
If within a few days, the facial nerve is totally unexcitable. Spontaneous
fibrillation potentials recorded from the muscles within 2 to 3 weeks
indicate that at least has undergone Wallerian degeneration
Evidence of denervation after 10 days indicates a long delay in recovery
and sometimes is incomplete
Complete facial weakness
Pain other than ear pain
Changes in tearing
Usual Order of Recovery
1) Buccinator
2) Zygomatic muscles
3) Inferior levator
4) Orbicularis oculi
5) Frontalis
10. MEDICAL AND SURGICAL MANAGEMENT
Medical management
Eye patch or sunglasses are used to protect the eye and prevent
scratching of the cornea form dust and fingers.
Artificial tears are used in the daytime
Moisture chamber is used at nighttime
Bland ointment is applied during bedtime
A plastic wrap over the eye, fixated with a hairnet tape is used to keep the
eye moist
Consult an ophthalmologist if the patient complains of eye discomfort or if
the eye looks irritated even with usual care.
Pharmacological management
Oral steroids are used to reduce the inflammation and swelling of the
facial nerve
Analgesics are taken to relieve pain
Antiviral agents (acyclovir, famiclovir) may also be used to limit or reduce
damage to the nerve from possible viral causes.
Prednisone to the eye is used to prevent denervation, autonomic
synkinesia and progression of the palsy to paralysis and shortens the
course of the weakness. A standard prednisone dose of 1 mg/kg/day for
10-14 days is used for patients seen within 21 days after the onset. It is
followed by a tapering dose.
Surgical management
Surgery is rare in Bells palsy but may be used in long-standing cases for
aesthetic purposes. The eyelids may be stitched together for protection.
Surgery is indicated if:
o Paralysis is slowly progressing

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o No recovery after 6 months

o If there is a mass in the parotid or between the mandible and the
mastoid.
o There are progressions of other cranial deficits.
o Branches of the facial nerve is spared
o There is previous history of malignancy
o There is trauma with support for a traumatic resection
11. PHYSICAL THERAPY ASSESSMENT
Talk with the patient. Observe facial movements bilaterally. A total facial
weakness suggests a nuclear nerve lesion while partial paralysis suggests a
supracondylar lesion.
Observe patients face at rest. This test will help differentiate a supracondylar
from nuclear involvement with the same principle as No. 1
Let the patient close the eyes and lips and then forcefully open them. The
amount of mouth and eyeball movement or opening visible is tested with
resistance.
Let the patient show teeth or grimace voluntarily. A positive test would mean
impaired mouth movements.
Let the patient whistle or blow. Patient may exhibit difficulty in holding in air.
Tapping the cheek makes this test harder.
Taste test. Apply sugarcoated gauze to the anterior parts of the tongue and on
the sides id difficulty is present. This will assess the sweet taste sensations
bilaterally.
Test the frontalis muscle. Upon looking up, the eyebrows elevate and the
forehead frowns.
Test for hyperacusis. Patient will usually cover the involved ear in the
presence of a loud stimulus.
Electrical tests are conducted.
12. PHYSICAL THERAPY MANAGEMENT
During the acute and subacute stage.
Splinting for the paralyzed muscle to relieve the strain and preserve tone
for cosmesis.
Facial massage for 5 minutes twice a day in a chin-to-forehead direction to
maintain the tone.
Use eye patches, goggle or sunglasses to protect cornea from damage
and irritation.
IR to increase the blood supply and decrease skin resistance before ES
application.
ES application to the nerve and muscle.
HMP to hasten recovery and for relief of pain.
During paralysis
US over the nerve trunk, in front of the tragus of the ear to reduce
inflammation.
Massage is taught to the patient. The motion is upward and outward
applied to the paralyzed muscle to maintain skin suppleness, muscle
elasticity and maintenance of blood and lymphatic flow.
Patient education and advice. Patient should lie down at intervals to
reduce the effects of gravity upon the paralyzed muscle. The eye should
be blinked regularly because the blink reflex is lost.
Recovery stage
Mild IR to improve function and warmth to the muscle.
PNF for reeducation
Quick stretch technique to regain raising of eyebrows and corners of the
mouth.
Brushing, tapping or stroking along the length of the muscle.

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Exercises for the muscles of the face performed in supine first then
progresses to sitting. Practiced for twice a day.