Bell's Palsy

DR.RAHMAN
Bell's Palsy
 Introduction
 Bell's palsy is a form of temporary facial paralysis resulting from damage
or trauma to one of the two facial nerves.  It is the most common cause of
facial paralysis.
 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.  Symptoms
of Bell's palsy usually begin suddenly and reach their peak within 48
hours. 
Bell's Palsy
 Controversy surrounds the etiology and treatment of Bell palsy. The cause
of Bell palsy remains unknown, though the disorder appears to be a
polyneuritis with possible viral, inflammatory, autoimmune, and ischemic
etiologies.
 Increasing evidence implicates herpes simplex type I and herpes zoster
virus reactivation from cranial-nerve ganglia.
Bell's Palsy
 Bell palsy is one of the most common neurologic disorders affecting the
cranial nerves, and it is the most common cause of facial paralysis
worldwide.
 It is thought to account for approximately 60-75% of cases of acute
unilateral facial paralysis. Bell palsy is more common in adults, in people
with diabetes, and in pregnant women.
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 Neuroanatomy
o The facial nerve contains parasympathetic fibers to the nose, palate, and
lacrimal glands. Its course is tortuous, both centrally and peripherally. The
facial nerve travels a 30-mm intraosseous course through the internal
auditory canal (with the eighth cranial nerve) and through the internal
fallopian canal in the petrous temporal bone. This bony confinement limits
the amount that the nerve can swell before it becomes compressed.
Bell's Palsy
o The nucleus of the facial nerve lies within the reticular formation of the
pons, adjacent to the fourth ventricle. The facial nerve roots include fibers
from the motor, solitary, and salivatory nuclei. The preganglionic
parasympathetic fibers that originate in the salivatory nucleus join the
fibers from nucleus solitarius to form the nervus intermedius.
Bell's Palsy
o The nervus intermedius is composed of sensory fibers from the tongue,
mucosa, and postauricular skin, as well as parasympathetic fibers to the
salivary and lacrimal glands. These fibers then synapse with the
submandibular ganglion, which has fibers that supply the sublingual and
submandibular glands. The fibers from the nervus intermedius also supply
the pterygopalatine ganglion, which has parasympathetic fibers that supply
the nose, palate, and lacrimal glands.
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o The fibers of the facial nerve then course around the sixth cranial nerve
nucleus and exit the pons at the cerebellopontine angle. The fibers go
through the internal auditory canal along with the vestibular portion of the
eighth cranial nerve.The facial nerve passes through the stylomastoid
foramen in the skull and terminates into the zygomatic, buccal,
mandibular, and cervical branches. These nerves serve the muscles of
facial expression, which include the frontalis, orbicularis oculi, orbicularis
oris, buccinator, and platysma muscles. Other muscles innervated by the
facial nerve include the stapedius, stylohyoid, posterior belly of the
digastric, occipitalis, and anterior and posterior auricular muscles. All
muscles innervated by the facial nerve are derived from the second
branchial arch.
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 Causes
 Idiopathic
 Viral infection
 Vascular damage
 Trauma
 Cold exposure
Bell's Palsy
 Pathophysiology
 The precise pathophysiology of Bell palsy remains an area of debate. The
facial nerve courses through a portion of the temporal bone commonly
referred to as the facial canal. A popular theory proposes that edema and
ischemia result in compression of the facial nerve within this bony canal.
The cause of the edema and ischemia has not yet been established. This
compression has been seen in MRI scans with facial nerve enhancement.
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 The first portion of the facial canal, the labyrinthine segment, is the
narrowest; the meatal foramen in this segment has a diameter of only about
0.66 mm. This is the location that is thought to be the most common site of
compression of the facial nerve in Bell palsy. Given the tight confines of
the facial canal, it seems logical that inflammatory, demyelinating,
ischemic, or compressive processes may impair neural conduction at this
site.
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 Injury to the facial nerve in Bell palsy is peripheral to the nerve’s 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
 Clinical Presentation
o The diagnosis of Bell palsy must be made on the basis of a thorough
history and physical examination, as well as the use of diagnostic testing
when necessary. Bell palsy is a diagnosis of exclusion. Clinical features of
the disorder that may help to distinguish it from other causes of facial
paralysis include the sudden onset of unilateral facial paralysis and the
absence of signs and symptoms of CNS, ear, and cerebellopontine angle
disease.
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 Symptoms of Bell palsy include the following:
o Acute onset of unilateral upper and lower facial paralysis (over a 48-h
period)
o Posterior auricular pain
o Decreased tearing
o Hyperacusis
o Taste disturbances
o Otalgia
Bell's Palsy
 Early symptoms include the following:
o Weakness of the facial muscles
o Poor eyelid closure
o Aching of the ear or mastoid (60%)
o Alteration of taste (57%)
o Hyperacusis (30%)
o Tingling or numbness of the cheek/mouth
o Epiphora
o Ocular pain
o Blurred vision
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 Onset
o The onset of Bell palsy is typically sudden, and symptoms tend to peak in
less than 48 hours. This sudden onset can be frightening for patients, who
often fear they have had a stroke or have a tumor and that the distortion of
their facial appearance will be permanent.
o Because the condition appears so rapidly, patients with Bell palsy
frequently present to the emergency department (ED) before seeing any
other health care professional. More people first notice paresis in the
morning. Because the symptoms require several hours to become evident,
most cases of paresis likely begin during sleep.
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 Facial paralysis
o The paralysis must include the forehead and lower aspect of the face. The
patient may report the inability to close the eye or smile on the affected
side. He or she also may report increased salivation on the side of the
paralysis. If the paralysis involves only the lower portion of the face, a
central cause should be suspected (ie, supranuclear). If the patient
complains of contralateral weakness or diplopia in conjunction with the
supranuclear facial palsy, a stroke or intracerebral lesion should be
strongly suspected.
Bell's Palsy
o If a patient has gradual onset of facial paralysis, weakness of the
contralateral side, or a history of trauma or infection, other causes of facial
paralysis must be strongly considered. Progression of the paresis is
possible, but it usually does not progress beyond 7-10 days. A progression
beyond this point suggests a different diagnosis. Patients who have
bilateral facial palsy must be evaluated for meningitis.
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o Many patients report numbness on the side of the paralysis. Some authors
believe that this is secondary to involvement of the trigeminal nerve,
whereas other authors argue that this symptom is probably from lack of
mobility of the facial muscles and not lack of sensation.
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 Ocular manifestations
 Early ocular complications include the following:
o Lagophthalmos (inability to close the eye completely)
o Paralytic ectropion of the lower lid
o Corneal exposure
o Upper eyelid retraction
o Decreased tear output/poor tear distribution
o Loss of the nasolabial fold
o Corneal erosion, infection, and ulceration (rare)
Bell's Palsy
 Late ocular manifestations include the following:
o Mild, generalized mass contracture of the facial muscles, rendering the
affected palpebral fissure narrower than the opposite one (after several
months)
o Aberrant regeneration of the facial nerve with motor synkinesis
o Reversed jaw winking (ie, contracture of the facial muscles with twitching
of the corner of the mouth or dimpling of the chin occurring
simultaneously with each blink)
o Autonomic synkinesis (ie, crocodile tears—tearing with chewing)
o Permanent, disfiguring facial paralysis (rare)
Bell's Palsy
 Posterior auricular pain
o Half of the patients affected with Bell palsy may complain of 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. Ask the
patient if he or she has experienced trauma, which may account for the
pain and facial paralysis.
o One third of patients may experience hyperacusis in the ear ipsilateral to
the paralysis, which is secondary to weakness of the stapedius muscle.
Bell's Palsy
 Taste disorders
o While only one third of patients report taste disorders, 80% of patients
show a reduced sense of taste. Patients may fail to note reduced taste,
because of normal sensation in the uninvolved side of the tongue. Early
recovery of the sense of taste suggests that the patient will experience a
complete recovery.
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 Facial spasm
o Facial spasm, a very rare complication of Bell palsy, occurs as tonic
contraction of 1 side of the face. Spasms are more likely to occur during
times of stress or fatigue and may be present during sleep. This condition
may occur secondary to compression of the root of the seventh nerve by an
aberrant blood vessel, tumor, or demyelination of the nerve root.
Bell's Palsy
o Facial spasm occurs most commonly in patients in the fifth and sixth
decades of life. Sometimes the etiology is not found. The presence of
progressive facial hemispasm with other cranial nerve findings indicates
the possibility of a brainstem lesion.
o Synkinesis is an abnormal contracture of the facial muscles while smiling
or closing the eyes. It may be mild and result in slight movement of the
mouth or chin when the patient blinks or in eye closure with smiling.
Bell's Palsy
 Cranial neuropathies
o Some believe that other cranial neuropathies may also be present in Bell
palsy; however, this is not uniformly accepted. The symptoms in question
include the following:
o Hyperesthesia or dysesthesia of the glossopharyngeal or trigeminal nerves
o Dysfunction of the vestibular nerve
o Hyperesthesia of the cervical sensory nerves
o Vagal or trigeminal motor weakness
Bell's Palsy
 Clinical features
 1.Onset is subacute, initially pain may present
 2.All parts of face affected, loss of taste, salivation, lacrimation,
hyperacusis if stapedius weak
 3.Weakness or paralysis of the facial muscles on one side, with failure of
eye closure
 4.Visible upward deviation of the eyes as this is tempted- Bell’s sign
 Dysarthria may present
Bell's Palsy
 Physical Examination
o Weakness and/or paralysis from involvement of the facial nerve affects the
entire face (upper and lower) on the affected side. A careful examination of
the head, ears, eyes, nose, and throat must be carried out in all patients
with facial paralysis. Time must also be taken to examine the patient’s skin
for signs of squamous cell carcinoma, which can invade the facial nerve,
and parotid gland disease.
Bell's Palsy
 Focus attention on the voluntary movement of the upper part of the face on
the affected side; in supranuclear lesions, such as occur in a cortical stroke
(upper motor neuron; above the facial nucleus in the pons), the upper third
of the face is spared in the majority of cases, while the lower two thirds are
paralyzed. The orbicularis, frontalis, and corrugator muscles are innervated
bilaterally at the level of the brainstem, which explains the pattern of facial
paralysis in these cases.
Bell's Palsy
• Initial inspection of the patient demonstrates flattening of the forehead and
nasolabial fold on the side affected by the palsy. When the patient is asked
to raise his or her eyebrows, the side of the forehead with the palsy will
remain flat. When the patient is asked to smile, the face will become
distorted and lateralize to the side opposite the palsy.
Bell's Palsy
 GradingThe grading system developed by House and Brackmann
categorizes Bell palsy on a scale of I to VI.
 Grade I is normal facial function.
 Grade II is mild dysfunction. Characteristics include the following:
o Slight weakness is noted on close inspectionSlight synkinesis may be
present
o Normal symmetry and tone are noted at rest
o Forehead motion is moderate to good
o Complete eye closure is achieved with minimal effort
o Slight mouth asymmetry is noted
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 Grade III is moderate dysfunction. The following characteristics are
found:
o An obvious, but not disfiguring, difference is noted between the 2 sides
o A noticeable, but not severe, synkinesis, contracture, or hemifacial spasm
is present
o Normal symmetry and tone are noted at rest
o Forehead movement is slight to moderate
o Complete eye closure is achieved with effort
o A slightly weak mouth movement is noted with maximal effort
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 Grade IV is moderately severe dysfunction. Signs include the
following:
o An obvious weakness and/or disfiguring asymmetry is noted
o Symmetry and tone are normal at rest
o No forehead motion is observed
o Eye closure is incomplete
o An asymmetrical mouth is noted with maximal effort
Bell's Palsy
 Grade V is severe dysfunction. Characteristics include the following:
o Only a barely perceptible motion is noted
o Asymmetry is noted at rest
o No forehead motion is observed
o Eye closure is incomplete
o Mouth movement is only slight.
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 Grade VI is total paralysis. The following are noted:
o Gross asymmetry
o No movement

 In this system, grades I and II are considered good outcomes, grades III
and IV represent moderate dysfunction, and grades V and VI describe poor
results. Grade VI is defined as complete facial paralysis; all of the other
grades are defined as incomplete. An incomplete facial paralysis denotes
an anatomically and, to some degree, functionally intact nerve.
Bell's Palsy
 Differential Diagnoses
 Anterior Circulation Stroke
 Benign Skull Tumors
 Brainstem Gliomas
 Cerebral Aneurysms
 Intracranial Hemorrhage
Bell's Palsy
• Investigations
 CBC
 VDRL/RPR
 RBS
 CSF study
 CT /MRI
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 Management
 1.About 70-80% pts recover spontaneously with in 2-12 wks
 2.Prednisolone 40-60 mg/day for 7 days
 3.Eye- artificial E/D with antibiotic E/D or E/O
 4.Surgical decompression of the facial nerve in the facial canal
 5.Aciclovir may be helpful.
Bell's Palsy
 Prognosis
o 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:
o Group 1 - Complete recovery of facial motor function without sequelae
o Group 2 - Incomplete recovery of facial motor function, but with no
cosmetic defects that are apparent to the untrained eye
o Group 3 - Permanent neurologic sequelae that are cosmetically and
clinically apparent