INDEX

INDEX......................................................................................................................................1
CHAPTER I..............................................................................................................................2
INTRODUCTION....................................................................................................................2
CHAPTER II.............................................................................................................................3
1.1 ANATOMY..................................................................................................................4
2.1. DEFINITION...............................................................................................................4
2.2. EPIDEMIOLOGY........................................................................................................5
2.3. ETIOLOGY..................................................................................................................5
2.4. PATOPHYSIOLOGY...................................................................................................5
2.5. CLINICAL
MANIFESTATION.......................................................................................................6
2.6. DIAGNOSIS.................................................................................................................6
2.7. DIFFERENTIAL DIAGNOSIS ...................................................................................8
2.8. TREATMENT...............................................................................................................9
2.9. COMPLICATION.......................................................................................................12
2.10
PROGNOSIS........................................................................................................
.......13
REFERENCES.........................................................................................................................15

CHAPTER I
INTRODUCTION
Bell's palsy is the most common cause of acute unilateral facial paralysis, accounting
for approximately 60-75% of such cases Bells palsy, named after the Scottish anatomist, Sir
Charles Bell, is the most common acute mono-neuropathy, or disorder affecting a single
nerve, and is the most common diagnosis associated with facial nerve weakness/paralysis.
Bells palsy is an idiopathic, acute peripheral-nerve paresis (weakness) or paralysis (complete
loss of movement) involving the facial nerve, which supplies all the muscles of facial
expression
Bell's palsy is characterized by a one sided facial droop that comes on within 72 hours.
The forehead loses the ability to furrow, and the corner of the mouth droops on the affected
side. The eyelids will not close and when the patient attempts to close them, the eyeball can
roll upward (this is known as Bell's phenomenon). Altough Bells palsy has a high rate of
spontaneous recovery however, patients who have incomplete recovery will have obvious
cosmetic sequelae and will often be dissatisfied with their outcome.

CHAPTER II

1.1 Anatomy

The seventh cranial nerve supplies all the muscles concerned with facial expression.
The sensory component is small (the nervus intermedius); it conveys taste sensation from the
anterior two-thirds of the tongue and probably cutaneous impulses from the anterior wall of
the external auditory canal. The motor nucleus of the seventh nerve lies anterior and lateral to
the abducens nucleus. After leaving the pons, the seventh nerve enters the internal auditory
meatus with the acoustic nerve. The nerve continues its course in its own bony channel, the
facial canal, and exits from the skull via the stylomastoid foramen. It then passes through the
parotid gland and subdivides to supply the facial muscles.1
A complete interruption of the facial nerve at the stylomastoid foramen paralyzes all
muscles of facial expression. The corner of the mouth droops, the creases and skinfolds are
effaced, the forehead is unfurrowed, and the eyelids will not close. Upon attempted closure of
the lids, the eye on the paralyzed side rolls upward (Bells phenomenon). The lower lid sags
and falls away from the conjunctiva, permitting tears to spill over the cheek. Food collects
between the teeth and lips, and saliva may dribble from the corner of the mouth. The patient
complains of a heaviness or numbness in the face, but sensory loss is rarely demonstrable and
taste is intact.1,3

If the lesion is in the middle-ear portion, taste is lost over the anterior two-thirds of the
tongue on the same side. If the nerve to the stapedius is interrupted, there is hyperacusis
(sensitivity to loud sounds). Lesions in the internal auditory meatus may affect the adjacent
auditory and vestibular nerves, causing deafness, tinnitus, or dizziness. Intrapontine lesions
that paralyze the face usually affect the abducens nucleus as well, and often the corticospinal
and sensory tracts.2
If the peripheral facial paralysis has existed for some time and recovery of motor
function is incomplete, a continuous diffuse contraction of facial muscles may appear. The
palpebral fissure becomes narrowed, and the nasolabial fold deepens. Attempts to move one
group of facial muscles may result in contraction of all (associated movements, or
synkinesis). Facial spasms, initiated by movements of the face, may develop (hemifacial
spasm). Anomalous regeneration of seventh nerve fibers may result in other troublesome
phenomena. 1
If fibers originally connected with the orbicularis oculi come to innervate the
orbicularis oris, closure of the lids may cause a retraction of the mouth, or if fibers originally
connected with muscles of the face later innervate the lacrimal gland, anomalous tearing
(crocodile tears) may occur with any activity of the facial muscles, such as eating. Another
facial synkinesia is triggered by jaw opening, causing closure of the eyelids on the side of the
facial palsy (jaw-winking).1,3
2.1 Definition
. Bells palsy, named after the Scottish anatomist, Sir Charles Bell, is the most common
acute mono-neuropathy, or disorder affecting a single nerve, and is the most common
diagnosis associated with facial nerve weakness/paralysis. Bells palsy is an idiopathic, acute
peripheral-nerve paresis (weakness) or paralysis (complete loss of movement) involving the
facial nerve, which supplies all the muscles of facial expression. The condition leads to the
partial or complete inability to voluntarily move facial muscles on the affected side of the
face. Although typically self-limited, the facial paresis/paralysis that occurs in Bells palsy
may cause significant temporary oral incompetence and an inability to close the eyelid,
leading to potential eye injury.2,3
2.2 Epidemiology
Bell's palsy is the most common cause of acute unilateral facial paralysis, accounting
for approximately 60-75% of such cases. The right side is generally affected more often, i.e.
63% of the time. Although bilateral facial paralysis can also occur, the occurrence rate is less
than 1% when compared to unilateral Bell's palsy. The condition can also be recurrent in 414% of affected individuals.
The annual incidence of Bell's palsy in the United States is approximately 23 cases per
100.000 persons, and in the United Kingdom 20 cases per 100.000 persons. Bell's palsy
affects both sexes equally, although the condition is more frequent in younger women (aged

10-19) compared to the same age group of men. Pregnancy can increase the risk threefold,
and in pregnant women Bell's palsy most commonly appears in the third trimester.
The condition is generally more common in adults. Peak ages are between 20 and 40
years of age. Diabetes and prediabetes are conditions frequently associated with Bell's palsy.
The risk of being affected by this condition is 29% higher in diabetic patients than in healthy
individuals. Patients with hypothyroidism and other autoimmune processes of the thyroid
gland also represent a susceptible group.
2.3 Etiology
Bells palsy is believed to be caused by inflammation of the facial nerve at the
geniculate ganglion, which leads to compression and possible ischemia and demyelination.
Classically, Bells palsy has been defined as idiopathic, and the cause of the inflammatory
process in the facial nerve remains uncertain. Recently, attention has focused on infection
with herpes simplex virus type 1 (HSV-1) as a possible cause because research has found
elevated HSV-1 titers in affected patients. However, studies have failed to isolate viral DNA
in biopsy specimens, leaving the causative role of HSV-1 in question.3
2.4 Patophysiology
A popular theory proposes that edema and ischemia result in compression of the facial
nerve within this bony canal. Seventh cranial nerve (facial nerve) passes through a portion of
temporal bone known as the facial canal. Inflammation of at the part of the nerve termed
geniculate ganglion (a group of fibers and sensory neurons) leads to compression within this
bony canal.4,5
This can in turn block the transmission of neural signals, result in ischemia and
demyelination, and cause facial paralysis or Bell's palsy. Injury is peripheral to the facial
nerve's nucleus, and such compression has been proven on MRI scans (magnetic resonance
imaging).4
Injury to the facial nerve in Bell palsy is peripheral to the nerves nucleus. The injury is
thought to occur near, or at, the geniculate ganglion. If the lesion is proximal to the geniculate
ganglion, the motor paralysis is accompanied by gustatory and autonomic abnormalities.
Lesions between the geniculate ganglion and the origin of the chorda tympani produce the
same effect, except that they spare lacrimation. If the lesion is at the stylomastoid foramen, it
may result in facial paralysis only.
Bell's palsy is considered an idiopathic condition, which means the cause of the
inflammation is not known and the exact pathophysiology remains uncertain. Several viruses
are associated with this disease, and herpes simplex virus type 1 (HSV-1) is thought to be the
most probable causative factor, as affected individuals have elevated antibody titers for this
virus. Other infectious agents may play a role in certain cases, such as Epstein-Barr virus and
cytomegalovirus (which both cause infectious mononucleosis), adenovirus, mumps and
rubella. Bilateral facial palsy has also been linked to acute HIV-infection.4
5

2.5 Clinical Manifestation

Patient may report that exposure to cold preceed their symptoms, and they may
complain facial numbness or stiffness without any objective sensory deficit. 5 Bell's palsy is
characterized by a one sided facial droop that comes on within 72 hours. 6 The classic sign of
the disease is the involvement of only one side of the face. Both sides of the face are
simultaneously affected in less than 1% of cases. Symptoms usually peak in less than 48
hours and pain behind the ear sometimes occurs as a preceding symptom.
The paralysis includes the forehead and lower aspect of the face. The forehead loses the
ability to furrow, and the corner of the mouth droops on the affected side. The eyelids will not
close when the patient attempts to close them, the eyeball can roll upward (this is known as
Bell's phenomenon). Although tear production decreases, the loss of lid control allows tears
to spill freely from the eye, thus creating the appearance of excessive tearing. Loss of
sensation along the external auditory canal sometimes also occurs, which is known as a
positive Hitselberger sign.
Parts of the cranial nerve that supply the ear and the tongue can also be affected,
resulting in inappropriate reaction to loud noises (hyperacusis) and a loss of taste on the
frontal two-thirds of the tongue. Normal lip movement is usually heavily affected by Bell's
palsy, resulting in the inability to purse the lips and show the teeth on the affected side. Facial
spasm can rarely occur, more likely as a result of fatigue or stress, and usually in patients in
their fifth or sixth decades of life.
A large proportion of patients report numbness on the side of the face affected by
paralysis. Although this symptom could be attributed to the lack of mobility of the facial
muscles, it could also indicate a secondary involvement of the trigeminal nerve. General
(albeit mild) contracture of the facial muscles can result in a narrower fissure of the eyelids of
the affected side when compared to the opposite part. This manifestation usually occurs after
several months.
It is of utter most importance to differentiate Bells palsy from a stroke. Both of these
conditions can cause unilateral paralysis; however, presence of other symptoms can be used
to distinguish between them. Bell's palsy affects only the facial nerve; hence the symptoms
are limited to facial symptoms (muscle paralysis or weakness, taste problems and decreased
tearing). On the other hand, stroke can cause additional problems in active speaking or
understanding others, paralyze the arm or leg on the same side and severely impair vision
quality. In essence, Bell's palsy affects the peripheral nerve and causes weakness of the eyelid
and (most importantly) forehead, while stroke represents a problem with central nervous
system and typically affects only muscles of the lower face.4
2.6 Diagnosis
The diagnosis of Bells palsy can usually be made clinically in patients with :
6

1.
2.
3.
4.

a typical presentation
no risk factors or preexisting symptoms for other causes of facial paralysis,
absence of cutaneous lesions of herpes zoster in the external ear canal,
a normal neurologic examination with the exception of the facial nerve.

A patient with an acute onset of unilateral facial weakness most likely has Bells palsy.
A careful history of the onset and progress of paralysis is important because gradual onset of
more than two weeks duration is strongly suggestive of a mass lesion. Medical history should
include recent rashes, arthralgias, or fevers; history of peripheral nerve palsy; exposure to
influenza vaccine or new medications; and exposure to ticks or areas where Lyme disease is
endemic.1,3
The physical examination should include careful inspection of the ear canal, tympanic
membrane, and oropharynx, as well as evaluation of peripheral nerve function in the
extremities and palpation of the parotid gland. In order to assess forehead involvement,
physical examination should also include evaluation of cranial nerve function, including all
facial muscles.1
Particular attention to the eighth cranial nerve, which courses near to the facial nerve in
the pontomedullary junction and in the temporal bone, and to other cranial nerves is essential.
In atypical or uncertain cases, an ESR, testing for diabetes mellitus, a Lyme titer, angiotensinconverting enzyme and chest imaging studies for possible sarcoidosis, a lumbar puncture for
possible Guillain-Barr syndrome, or MRI scanning may be indicated. MRI often shows
swelling and enhancement of the facial nerve in idiopathic Bells palsy.3
Laboratory testing is not usually indicated. However, because diabetes mellitus is
present in more than 10 percent of patients with Bells palsy, fasting glucose or A1C testing
may be performed in patients with additional risk factors (e.g., family history, obesity, older
than 30 years). Lyme antibody titers should be performed if the patients history suggests
possible exposure. Signs and symptoms atypical for Bells palsy should prompt further
evaluation. Patients with insidious onset or forehead sparing should undergo imaging of the
head.4
If the paralysis does not improve or becomes even worse, imaging studies like magnetic
resonance imaging (MRI) may also help rule out a tumor, especially if the patient has a
palpable parotid mass. Electroneurography, which uses electricity for stimulating facial
muscles on both sides of the face, may be used to provide prognostic information in cases of
complete facial paralysis. Degree of nerve degeneration can be successfully quantified by
mutual comparison of the responses on both sides of the face.4
The hearing threshold is usually not affected by Bell palsy, thus audiography and auditory
evoked potentials should be pursued if hearing loss is suspected. Computer-based analysis of
eyelid motion (also known as blepharokymographic analysis) may prove helpful in
establishing diagnosis, predicting prognosis and evaluating therapy response. Schirmers tear
testing to measure the eyes ability to produce tears.4

One of diagnostic scales are used to grade the severity of Bell's palsy. Those are HouseBrackmann Facial Nerve Grading System. House-Brackmann system categorizes the
condition into six different categories, with first category representing normal facial function
and sixth category a state of complete paralysis. It can also help clinicians monitor disease
progression and evaluate recovery of the patient.4

2.7 Differential Diagnosis

Many conditions can produce isolated facial nerve palsy identical to Bells palsy.
Structural lesions in the ear or parotid gland (e.g., cholesteatoma, salivary tumors) can
produce facial nerve compression and paralysis. Other causes of peripheral nerve palsies
include Guillain-Barr syndrome, Lyme disease, otitis media, Ramsay Hunt syndrome (an
outbreak of herpes zoster in the facial nerve distribution), sarcoidosis, and some influenza
vaccines. Although these conditions can present as isolated facial nerve palsies, they usually
have additional features that distinguish them from Bells palsy.
Patients with Lyme disease often have a history of tick exposure, rash, or arthralgias.
Facial nerve palsies from acute and chronic otitis media have a more gradual onset, with
accompanying ear pain and fever. Patients with Ramsay Hunt syndrome have a pronounced
prodrome of pain and often develop a vesicular eruption in the ear canal and pharynx,
although cases without the vesicular eruption (i.e., zoster sine herpete) have been reported.
Polyneuropathies (e.g.,Guillain-Barr syndrome, sarcoidosis) will more often affect both
facial nerves.
Tumors will present with a more insidious onset of symptoms over weeks or months.
Central nervous system lesions (e.g., multiple sclerosis, stroke, tumor) can also cause facial
nerve palsy. However, some motor neurons to the forehead cross sides at the level of the
brainstem, so the fibers in the facial nerve going to the forehead come from both cerebral
hemispheres. Supranuclear (central) lesions affecting the facial nerve will not paralyze the
forehead on the affected side, resulting in a unilateral facial paralysis with forehead sparing.
Often, there will be at least some weakness of extremities on the affected side as well.

2.8 Treatment

Nonpharmacologic
It is universally accepted that eye care is imperative in Bell palsy. The patients eye is at
risk for drying, corneal abrasion, and corneal ulcers. In most cases, topical ocular lubrication
(with artificial tears during the day and lubricating ophthalmic ointment at night, or
occasionally ointment day and night) is sufficient to prevent the complications of corneal
exposure. Occluding the eyelids by using tape or by applying a patch for 1 or 2 days may
help to heal corneal erosions. Care must be taken to prevent worsening the abrasion with the
tape or patch by ensuring that the eyelid is securely closed.5
Other therapies such as physical therapy, facial massage or acupuncture may provide a
potential small improvement in facial nerve function and pain.5
Pharmacologic

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Corticosteroids
Oral corticosteroids have traditionally been prescribed to reduce facial nerve
inflammation in patients with Bells palsy. Prednisone is typically prescribed in a 10-day
tapering course starting at 60 mg per day. A 2004 Cochrane review and meta-analysis of three
randomized controlled trials comparing corticosteroids with placebo found small and
statistically nonsignificant reductions in the percentage of patients with incomplete recovery
after six months (relative risk [RR] = 0.86; 95% confidence interval [CI], 0.47 to 1.59) and
the percentage of patients with cosmetic complications (RR = 0.86; 95% CI, 0.38 to 1.98).
However, these trials included only 117 patients; larger prospective trials are needed to
establish the benefit of corticosteroids.5
Antivirals
Because of the possible role of HSV-1 in the etiology of Bells palsy, the antiviral drugs
acyclovir (Zovirax) and valacyclovir (Valtrex) have been studied to determine if they have
any benefit in treatment. Either acyclovir 400 mg can be given five times per day for seven
days or valacyclovir 1 g can be given three times per day for seven days.
Although a 2004 Cochrane review found insufficient evidence to support the use of
these antivirals alone, two recent placebo-controlled trials demonstrated full recovery in a
higher percentage of patients treated with an antiviral drug in combination with prednisolone
than with prednisolone alone (100 percent versus 91 percent and 95 percent versus 90
percent). However, no benefit was seen when treatment was delayed more than four days
after the onset of symptoms (86 percent versus 87 percent).5
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Spontaneous recovery
It is difficult to establish a statistically significant benefit of treatment in placebocontrolled trials because Bells palsy has a high rate of spontaneous recovery. The
Copenhagen Facial Nerve Study evaluated 2,570 persons with untreated facial nerve palsy,
including 1,701 with idiopathic (Bells) palsy and 869 with palsy from other causes; 70
percent had complete paralysis. Function returned within three weeks in 85 percent of
patients, with 71 percent of these patients recovering full function. Of the 29 percent of
patients with sequelae, 12 percent rated it slight, 13 percent rated it mild, and 4 percent rated
it severe.
Because of these findings, some persons have questioned whether treatment for Bells
palsy should be routinely indicated; however, patients who have incomplete recovery will
have obvious cosmetic sequelae and will often be dissatisfied with their outcome. Given the
safety profile of acyclovir, valacyclovir, and short-course oral corticosteroids, patients who
present within three days of the onset of symptoms and who do not have specific
contraindications to these medications should be offered combination therapy. Patients who
present with complete facial nerve paralysis have a lower rate of spontaneous recovery and
may be more likely to benefit from treatment.5
Other treatments
In the past, surgical decompression within three weeks of onset has been recommended
for patients who have persistent loss of function (greater than 90 percent loss of
electroneurography) at two weeks. However, the most widely cited study supporting this
approach only reported results for a total of 34 treated patients at three different sites,
included a nonrandomized control group, and lacked a blinded evaluation of outcome.
The most common complication of surgery is postoperative hearing loss, which affects
3 to 15 percent of patients. Based on the significant potential for harms and the paucity of
data supporting benefit, the American Academy of Neurology does not currently recommend
surgical decompression for Bells palsy. Some published studies have reported benefit with
acupuncture versus steroids and placebo, but all had serious flaws in study design and
reporting summarizes the available treatments.5
2.9 Complications
Both major and minor long-term complications can ensue from Bells palsy in 30% of
the patients, and 5% of them are left with a high degree of sequelae. In case of incomplete or
aberrant regeneration of damaged nerve fibers, a phenomenon known as synkinesis can occur.
During regrowth, some nerve fibers originating from facial nerve can sidetrack and
erroneously connect with the lacrimal ducts instead of the salivary glands. In such instances
patients will shed tears while eating, which is in medical literature also known as crocodile
tear syndrome, Bogorad's syndrome or gustatolacrimal reflex.
Other example of synkinesis is when the nerves controlling the eye muscles misdirect
and regrow connections with the muscles of the mouth. Abnormal movement or different
12

facial muscle group occurs afterwards, since movement of one muscle can now affect the
other one. For example, the corner of the mouth can involuntarily lift when the affected
individual closes the eye. Such synkinesis is often treated with botulinum toxin injections
(Botox) and facial reanimation by means of cosmetic surgery. Botulinum injections are
sometimes administered to the non-affected side as well, in order to improve facial symmetry.
Incomplete motor regeneration is also an important long-term complication. As the
largest portion of the facial nerve contains efferent fibers for stimulation of facial muscles
and formation of facial expressions, subpar regeneration in this part of the nerve can result in
permanent paralysis of all or several muscles on that side of the face. That can in turn
manifest as an inadequate function of the mouth, excessive tearing (epiphora) and nasal
obstruction.
Incomplete sensory regeneration can also occur as a result of Bell's palsy. Deterioration
or loss of taste (also known as dysgeusia or ageusia, respectively) can occur after partial
regeneration of the chorda tympani (an important branch of the facial nerve that carries taste
information from the anterior part of the tongue). If other afferent branches are affected, a
change or sensation to normal stimuli can occur. This condition is known as dysesthesia,
although it is still a controversial topic as it seems other cranial (glossopharyngeal or
trigeminal) nerves are also involved.
Recent studies show that Bells palsy can increase the risk of non-hemorrhagic stroke.
That particular finding can be linked to previous research that has shown an increased risk of
stroke in patients with HSV-1. The pathogen in question has also been implicated in
inflammation, vasculopathy and atherosclerosis in the cerebral blood vessels. All things
considered, a multi-specialist approach is needed when dealing with a myriad of
complications arising as a result of Bell's palsy.4
2.10 Prognosis
The natural course of Bell palsy varies from early complete recovery to substantial nerve
injury with permanent sequelae (eg, persistent paralysis and synkinesis). Prognostically,
patients fall into 3 groups:

Group 1 - Complete recovery of facial motor function without sequelae

Group 2 - Incomplete recovery of facial motor function, but with no cosmetic defects
that are apparent to the untrained eye

Group 3 - Permanent neurologic sequelae that are cosmetically and clinically apparent

Approximately 80-90% of patients with Bell palsy recover without noticeable

disfigurement within 6 weeks to 3 months. Use of the Sunnybrook grading scale for facial
nerve function at 1 month has been suggested as a means of predicting probability of
recovery

13

Bell palsy recurs in 4-14% of patients, with one source suggesting a recurrence rate of
7%. It may recur on the same or opposite side of the initial palsy. Recurrence usually is
associated with a family history of recurrent Bell palsy

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REFERENCES
1. Beal MF, et al. Trigeminal Neuralgia, Bells Palsy, and Other Cranial Nerve
Disorders In Harrisons Neurology In Clinical Medicine 3rd Ed. New York :
McGraw-Hill. 2013. p. 394-397
2. Baugh RF, et al. Clinical Practice Guidelines : Bells Palsy. [online] 2013. Available
at : http://oto.sagepub.com/ . Diakses tanggal 15 oktober 2016
3. Tiemstra JD, et al. Bells Palsy Diagnosis and Management. [online] 2007. Available
at : http://aafp.org/ . Diakses tanggal 15 Oktober 2016
4. Metrovi, T. Bells palsy. [online] 2014. Available at : http://www.news-medical.net/.
Diakses tanggal 15 Oktober 2016
5. Taylor, DC. Bell Palsy. [online] 2016. Available at : http://emedicine.medscape.com/.
Diakses tanggal 16 Oktober 2016
6. Balakrishnan A. Bells Palsy: Causes, Symptoms, Diagnosis And Treatment. [online]
2015. Available at : http://jpsr.pharmainfo.in/ . Diakses tanggal 16 Oktober 2016

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