DEPARTMENT OF ORAL MEDICINE AND RADIOLOGY

BELL’S
PALSY
SUBMITTED TO SUBMITTED BY
DR NILOFER MOHAMMED AMEERSHA
HALIM M
DR FARZHANA 200022210
DR RUMAISHA FINAL YEAR PART I
 CONTENTS
 INTRODUCTION
 ANATOMY OF FACIAL NERVE
 FACIAL NERVE PALSY
 BELL’S PALSY
• ETIOLOGY
• EPIDEMIOLOGY
• CLINICAL FEATURES
• PATHOPHYSIOLOGY
• HISTORY AND PHYSICAL EXAMINATION
• INVESTIGATIONS
• TREATMENT
• DIFFRENTIAL DIAGNOSIS
• PROGNOSIS
 ASSOCIATED SYNDROMES
• MELKERSON ROSENTHAL SYNDROME
• RAMSAY HUNT SYNDROME
• CROCODILE TEARS SYNDROME
 CONCLUSION
 REFERENCE
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INTRODUCTION
 The facial nerve which is the 7 th Cranial nerve
supplies all the muscles of face concerned with
expression.
 A complete interruption of facial nerve at or
around the stylomastoid foramen produce
paralysis of all muscle of face .
 Bells palsy is the most common type of facial
nerve palsy . It can be of central or peripheral in
origin.
ANATOMY OF FACIAL NERVE
Facial nerve is the nerve of the second branchial arch.

Functional Component
 Special visceral or branchial efferent (SVE),
responsible for muscles of facial expression and for
elevation of the hyoid bone.
 General visceral efferent (GVE) or
parasympathetic fibres. These fibres are secretomotor
to the submandibular and sublingual salivary glands,
the lacrimal gland, glands of the nose, palate and
pharynx .
 General visceral afferent (GVA) component carries
afferent impulses from the above mentioned glands.
 Special visceral afferent (SVA) fibres carry tastes sensations

from the palate and from anterior two thirds of the tongue except

from vallate papillae.

 General somatic afferent (GSA) fibres probably innervate a

part of the skin of the ear. The nerve does not give any direct

branches to the ear.

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ORIGIN OF NERVE
 The facial nerve is attached to the brainstem
between the lower border of pons and upper end
of medulla the nerve lies lateral to abducent
nerve and medial to the 8th nerve.
The facial nerve arises by two roots - medial
larger motor root and lateral smaller sensory
root.
The roots enter the internal auditory meatus
along with vestibulocochlear nerve and
labyrinthine vessels.
At the lateral end of meatus, two roots unite to
form the trunk of the facial nerve:
BRANCHES AND DISTRIBUTION

1. Within the bony facial canal:

Greater petrosal nerve

Nerve to the stapedius

Chorda tympani.

2. At its exit from the stylomastoid foramen:

Posterior auricular

Digastric
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Stylohyoid.
3. Terminal branches within the parotid gland:

Temporal

Zygomatic

Buccal

Marginal mandibular

Cervical

4.Communicating braches with adjacent cranial and spinal nerves

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FACIAL PALSY
 Facial palsy refers to weakness or paralysis of the muscles on one
side of the face ,often caused by damage or dysfunction in the facial
nerve
 Facial nerve dysfunction can severely affect a patient’s quality of life .
The human face is a focal point for communication and expression
Facial Nerve carries motor, sensory and parasympathetic Fibres, so
facial palsy results in both a functional and cosmetic impairment.
 Facial nerve palsy is diagnosed upon clinical presentation with
weakness of the facial muscles. There may be immobility of the brow,
incomplete eye lid closure, dropping of the corner of the mouth,
impaired closure of the lips dry eye, hyperacusis, impaired taste or pain
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around the Ear.
CAUSES OF FACIAL NERVE PALSY
• NEUROLOGICAL 1. STROKE
2. GUILLIAN-BARRE SYNDROME
3. MULTIPLE SCLEROSIS

• OTOLOGICAL 1. OTITIS MEDIA

2. FACIAL NERVE SCHWANOMMA

• ONCOLOGICAL 1. CREBRAL TUMOR

2. PAROTID TUMOR
3. LYMPHOMA

• INFLAMMATORY 1. SARCOIDOSIS
• INFECTIOUS 1. ENCEPHALITIS OR MENINGITIS
2. HERPES SIMPLEX VIRUS
3. HERPES ZOSTER VIRUS
4. LYME DISEASE

• TRAUMA 1. TEMPORAL BONE FRACTURE

2. IATROGENIC INJURY

• IDIOPATHIC 1. BELL’S PALSY

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 House - Brackmann scale of facial nerve weakness.
i. Grade 1-Normal
ii. Grade 2-Mild dysfunction
iii. Grade 3 –Mild- Moderate dysfunction
iv. Grade 4-Moderate dysfunction
v. Grade 5-Severe dysfunction
vi. Grade 6-Complete paralysis

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 BELL’SPALSY
 Bell’s palsy is one of the most common neurologic disorder
affecting the facial nerve . It is an ipsilateral, idiopathic and
acute lower motor neuron paralysis of seventh cranial nerve
that causes weakening of the facial muscles .
 Sir Charles Bell, the Scottish neurologist and
anatomist who described first .
 When Bell’s palsy occurs patients typically present
complaining of weakness and often numbness of
one side of the face , usually preceded 1 to 2 days
prior by a dull ache pain behind or within the ear .
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 Patients may report dry eye and potentially numbness of the tongue or a metallic taste
in mouth.

 upon awakening the patient or partner will frequently notice facial asymmetry and
may be concerned about the possibility of stroke
EPIDEMIOLOGY
 The annual incidence of bells palsy is 15 to 40 per 100000 individuals and the lifetime
risk in 1 in 60 with a recurrent rate of 8%to 12 % Sales

 According to 2022 paper published by Escalante et al , 16.30%

5.40%
16.30%

20.10%

41.90%

Grade III Grade IV Grade II Grade V Grade IV 14

CLINICAL FEATURES
 It occurs at any age
 No ethnic predilection
 No sex predilection
 The Bell’s phenomenon, also
called the palpebral-oculogyric
reflex, refers to the movement
of the eyeballs in an upward
direction when the eyelids are
forcefully closed.

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PATHOPHYSIOLOGY
Bell palsy, which is a unilateral hemifacial palsy of rapid onset, results from inflammation
of the facial nerve.

 The labyrinthine segment is the second intratemporal segment of the facial nerve and the
narrowest, with an average diameter of 0.7 mm and a length of 3 to 5 mm

 The narrowness of this portion of the facial nerve's canal predisposes it to dysfunction,
due to edema and impairment of perfusion when inflammation occurs, Bell’s palsy
more likely to occur in patients who have narrow labyrinthine segments of the facial
canal.

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HISTORY AND PHYSICAL EXAMINATION
Patients with Bell palsy present with progressive hemifacial paralysis that typically
reaches a peak in severity within 1 to 3 days of onset.
Patient will report :
I. Prodromal dull pain within or behind the ear .
II. Hyperacusis due to stapedius muscle weakness .
III. Metallic taste
IV. Numbness due to chorda tympani
V. Dry eyes
VI. Nasal obstruction
VII.Aesthetic self –consciousness because of facial asymmetry .

If the patient notes skin or mucosal rashes .Ramsay Hunt syndrome or lyme disease
should be considered . 17
INVESTIGATION
It is usually required to exclude facial palsy.

a) Blood pressure measurement (to exclude hypertension)

b) Blood tests that may include

Fasting blood sugar levels (to exclude diabetes).

Tests for HSV or other virus infections, such as HIV may need to be
considered.
Serum angiotensin converting enzyme levels as a screen for sarcoidosis.

Serum antinuclear antibodies to exclude connective tissue disease.

Lyme disease should be excluded by ELISA test.

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c) Electromyography and Nerve conduction
responses

 Facial nerve stimulation or needle

electromyography may be useful, along with
electrogustometry, nerve excitability tests,
electromyography and electroneuronography.

d) Schirmer's test for lacrimation

 It is performed by gently placing a strip of filter -

Physio paper on the lower conjunctival sac and
comparing the wetting of the paper with that on the
other side. 19
e) Test for loss of hearing/ Audiometry

 Pure-tone audiometry is a behavioural test used

to measure hearing sensitivity or loss of hearing.

f) Test for taste loss:

Test for taste loss by applying sugar ,salt ,lime

juice ,vinegar on the tongue and asking the

patient to identify each of them.

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g) Imaging studies

 Imaging with MRI or CT of the internal auditory

meatus, cerebellopontine angle and mastoid may be
needed to exclude a lesion, such as a tumour

For patients who are travelled to an endemic area ,Lyme titers

are checked and other conditions such as:
HIV

Syphilis

Tuberculosis

Leprosy

COVID
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Polio
TREATMENT

Most patients of Bell’s palsy recover within first few weeks or

months .Presence of incomplete paralysis in the first week is a good

prognostic sign.

Once Bell’s palsy is diagnosed ,management is very straight forward .

Steroids and antivirals prescribed with antihyperglycemic medication added

for parients with diabetes .

Corneal protection is provided .patients with high risk of keratopathy are

given a scleral contact lense . 22

PREDNISOLONE • Adults 60 mg daily for 5 days .Then 40 mg for 5 days .
• Children 2mg/kg daily for 7-10 days.

VALACYCLOVIR • Adults 100mg twice daily

• Children 1g/day in 3 divided dose for 7 days .

ACYCLOVIR • Adults 400mg 5 times daily for 7 days.

• Children older than 2 years :80 mg /kg daily divided every 6 hours
for 5 days .

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Periocular procedures
Periocular procedures are more often
employed for patients with long-term
facial paralysis due to nerve trauma.
Scleral contact lenses can be very useful
in cases of acute Bell palsy to prevent or
treat exposure keratopathy.

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 Surgical options for improving eye closure
include placement of a weight or a spring into
the upper eyelid, tightening of the lower
eyelid with medial or lateral canthopexy and
tarsal strip, and tarsorrhaphy or
tarsoconjunctival flap transfer.
 Common adverse effect is astigmatism . Most
tends to correct itself once the weight is
removed .

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Facial Neve Decompression
Decompression of the facial nerve may be offered to patients who are both willing and able
to undergo the operation.

Decompression of the tympanic through the mastoid segments of the facial nerve may be
accomplished via a postauricular mastoidectomy approach.

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Physiotherapy
• Facial rehabilitation therapy comprises a wide
range of techniques, including:
• mime therapy
• Neuromuscular reeducation.
• video self-modeling
• Massage
• stretching,
• relaxation.

• Neuromuscular reeducation (NMR) consists

of exercises to produce small but controlled
movements on the affected side of the face
while concentrating on symmetry. 27
 Chemodenervation

The use of botulinum toxin injection to reduce spasms or

asymmetric movement due to facial palsy has been found
to be effective in both pediatric and adult populations.

 There are currently several commercially available

botulinum toxin preparations, but the most
commonly used one is onabotulinumtoxinA

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• A good starting dose is 2 aliquots of 5 units of onabotulinumtoxinA. A fine
short needle on a small syringe is best for ensuring precise doses of toxin
administered to the target .

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Myomectomy
• Patients who have undergone botulinum toxin injections
but who desire a longer-term solution or who are losing
the effectiveness of the injections due to antibody
development may do myomectomy.

 Common targets include the platysma and the

depressor anguli oris, in which diminished
function will improve smile, and the orbicularis
oculi - myomectomy will reduce involuntary
eye closure and squinting
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Selective Neurectomy Selective neurectomy is a technique that identifies
zygomatic branches of the facial nerve that innervate the
orbicularis oculi muscle,

It is done under general anesthesia.

Patients report early symptomatic improvement, but

nerve branches to the orbicularis oculi muscle tend to
regenerate after a few months, thereby negating the effects
of the surgery.

Selective neurectomy may be combined with

myomectomy and may also be combined with nerve or
muscle transfer.
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Nerve transfer.
 For restoring function in cases of facial paralysis,
typically either traumatic or iatrogenic, nerve
transfer may also be used to improve coordination of
a particular muscle or muscle group
by"disconnecting" it from the synkinetic control of
the facial nerve and reinnervating it with a different
motor nerve, such as the hypoglossal or masseteric
nerve.

It is ideally performed within the first 6 to 12

months after onset of paralysis.
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Muscle Transfer
 For patients where nerve transfer has failed ,muscle transfer techniques such as those used
for smile reanimation.

 Of these, the best studied is the Gracilis free muscle transfer, which takes a portion of the
gracilis muscle from the medial thigh and transfers it into the face. This permit the patient to
produce a close lipped smile .

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DIFFRENTIAL DIAGNOSIS

I. Infectious Disease
 Herpes zoster oticus

 Lyme disease

 Syphilis

II. Neurologic causes

 Stroke

 Multiple sclerosis

 Guillain –Barre syndrome

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III.Tumors
 Parotid tumors
 Schwannoma
IV.Traumatic causes
 Temporal bone fracture
 Iatrogenic injury
V.Autoimmune
 Sarcoidosis
 Systemic lupus erythematosus

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STAGING
House-Brackmann scale is simple and easy to use for surgeons, emergency medicine
providers, and primary care clinicians, but it provides very little detail, particularly
concerning the function of individual zones

 The first facial paralysis grading scheme published was that of

Naoaki Yanagihara in 1976, requiring patients to perform 9 facial
movements and a resting evaluation. The strength of each is
graded as :
 4 Points (normal or nearly normal )
 2 Points (weak)
 0 Points (no movements ) 36
 The 9 movements are :

 Eye brow elevation  Puffing of the cheeks

 Gentle eye closure  Whistling

 Forceful eye closure  Smiling

 Closure of affected eye only  Depression of the lip.

 Wrinkling of the nose

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PROGNOSIS

• Bell palsy resolves completely without treatment in approximately 80% of cases, with the
remaining patients developing synkinesis[60 years and above] and complete paralysis.

• Oral corticosteroids with or without antivirals increase the chance of recovery from 90% to
97%.

• Recurrence does occur in 8% to 12% of affected individuals, with a mean latency of 10

years between episodes.

• Some patients are typically young and healthy with incomplete palsy and may exhibit
complete recovery in as few as 2 weeks, most patients will take several months to a year to
recover.
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ASSOCIATED SYNDROMES

MELKERSSON –ROSENTHAL SYNDROME

• Melkersson-Rosenthal syndrome is a rare neurological disorder characterized by

recurring facial paralysis, swelling of the face and lips and the development of folds and
furrows in the tongue. Onset is in childhood or early adolescence.

• After recurrent episodes (ranging from days to years in between), swelling may persist
and increase, eventually becoming permanent.

• The lip may become hard, cracked, and fissured with a reddish-brown discoloration.

• The cause of Melkersson-Rosenthal syndrome is unknown, but there may be a genetic

predisposition.. 39
Treatment  Symptomatic treatment

 NSAIDs and corticosteroids to reduce

swelling

 Antibiotics

 Immunosuppressants

 Surgery may be recommended to

relieve pressure on facial nerve and to
reduce swollen tissues.

 Physiotherapy and electrical

stimulation . 40
RAMSAY HUNT SYNDROME
• Ramsay Hunt syndrome is peripheral facial
nerve palsy accompanied by an erythematous
vesicular rash on the ear (zoster oticus) or in
the mouth.
It is now known that varicella zoster virus (VZV)
• J Ramsay Hunt, who described various
causes Ramsay Hunt syndrome.
clinical presentations of facial paralysis and
rash, other frequent symptoms and signs such
as:

• tinnitus, hearing loss, nausea, vomiting,

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vertigo, and nystagmus.
• It is now known that varicella zoster virus (VZV)
causes Ramsay Hunt syndrome.
• Change in taste ,dry eyes
hyperacusis, dysarthria and nasal
obstruction are few uncommon
symptoms .

• The rash is red and vesicular ,filled

with fluid and associated with pain
affecting the pinna.

• Rash can also seen in mouth and

soft palate . 42
TREATMENT
1.Acyclovir-500 mg 3 times a day

2.Valacyclovir-1000 mg 3 times a day

3.Famciclovir-500 mg 3 times a day

• Oral prednisolone 60 mg daily for 3 weeks and is stopped gradually

• The treatment is continued for up-to weeks or ten days

• Further treatment is aimed at providing symptomatic release from pain and rash.

• Carbamazepine is given to prevent seizure.

• Anticholinergics and antihistamine are given to suppress vertigo.

• Diazepam relieves pain and dizziness. 43

CROCODILE TEARS SYNDROME
“Crocodile tears syndrome,” also known as Bogorad syndrome, is the shedding of
tears while eating or drinking in patients recovering from Bell palsy.

It is also referred to as gustatory lacrimation..

ETIOLOGY

 There are different theories regarding the

cause of crocodile tears syndrome.
 The widely accepted theory is due to Bell
palsy or traumatic disruption of the nervus
intermedius.
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TREATMENT
1. Botulinum Toxin (Botox) Injections

2. Topical Anticholinergic Drops

3. Surgical Options

4. Physical Therapy or Facial Nerve Rehabilitation

45
CONCLUSION

Bell's palsy is an ipsilateral, idiopathic and acute lower motor neuron paralysis of
seventh cranial nerve that causes weakening of the facial muscles and significantly
impart the patients appearance and the standard of living and psychosocial well-
being.

Symptoms begins with mild weakness in facial muscles without any neurological
abnormalities in the first week and then steadily diminish over 3 weeks to 3 months
even without any medical treatment but may result in various complications and
leave the patient with varying degree of residual paralysis.

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 Diagnosis is one of exclusion and requires a vigilant history and through clinical
examination of stipulated by medical history or risk factors testing for Lyme disease
and diabetes are suggested .

Incomplete closure of lids with resultant dry eyes dysphagia and slurred speech are
common short term complications.An uncommon long term complication is
permanent weakening of facial muscles. Although most patients undergo spontaneous
recovery treatment with a short course of valacyclovir or acyclovir and a dose of
prednisolone.

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REFERENCE
1. B .D Chaurasia’s Human Anatomy Volume 4 .
2. Peeyush Shivhare ,Ajay Parihar .Textbook of Oral Medicine and Oral Radiology .
3. Shafer’s Textbook of Oral Pathology .
4. Hohman MH, Warner MJ, Varacallo M. Bell Palsy. [Updated 2024 Oct 6]. In:
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
Available from: https://www.ncbi.nlm.nih.gov/books/NBK482290/
5. https://www.ninds.nih.gov/health-information/disorders/melkersson-rosenthal-
syndrome
6. Sweeney CJ, Gilden DH. Ramsay Hunt syndrome. J Neurol Neurosurg Psychiatry.
2001 Aug;71(2):149-54. doi: 10.1136/jnnp.71.2.149. PMID: 11459884; PMCID:
PMC1737523.
7. Modi P, Arsiwalla T. Crocodile Tears Syndrome. 2023 Jan 18. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. PMID: 48
30247828..
THANK YOU

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