History

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.
Symptoms of Bell palsy include the following:

Acute onset of unilateral upper and lower facial paralysis (over a 48-h period)
Posterior auricular pain
Decreased tearing
Hyperacusis
Taste disturbances
Otalgia
Early symptoms include the following:

Weakness of the facial muscles

Poor eyelid closure
Aching of the ear or mastoid (60%)
Alteration of taste (57%)
Hyperacusis (30%)
Tingling or numbness of the cheek/mouth
Epiphora
Ocular pain
Blurred vision

Onset
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.
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.

Facial paralysis
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.
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 Guillain-Barr syndrome, Lyme
disease, and meningitis.
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.

Ocular manifestations
Early ocular complications include the following:

Lagophthalmos (inability to close the eye completely)

Paralytic ectropion of the lower lid
Corneal exposure
Brow droop
Upper eyelid retraction
Decreased tear output/poor tear distribution
Loss of the nasolabial fold
Corneal erosion, infection, and ulceration (rare)
Late ocular manifestations include the following:

Mild, generalized mass contracture of the facial muscles, rendering the affected palpebral fissure
narrower than the opposite one (after several months)
Aberrant regeneration of the facial nerve with motor synkinesis
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)
Autonomic synkinesis (ie, crocodile tearstearing with chewing)
Permanent, disfiguring facial paralysis (rare)
Two thirds of patients complain about tear flow.[10] This results from the reduced function of the orbicularis oculi
in transporting the tears. Fewer tears arrive at the lacrimal sac, and overflow occurs. The production of tears is
not accelerated.

Posterior auricular pain

Half of the patients affected with Bell palsy may complain of posterior auricular pain. [10] 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.
One third of patients may experience hyperacusis in the ear ipsilateral to the paralysis, which is secondary to
weakness of the stapedius muscle.

Taste disorders
While only one third of patients report taste disorders,[10] 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.

Facial spasm
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.
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.
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.
Crocodile tears can be observed; patients shed tears while they eat.

Cranial neuropathies
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:

Hyperesthesia or dysesthesia of the glossopharyngeal or trigeminal nerves

Dysfunction of the vestibular nerve
Hyperesthesia of the cervical sensory nerves

Vagal or trigeminal motor weakness

Diagnosis
Examination for Bell palsy includes the following:

Otologic examination: Pneumatic otoscopy and tuning fork examination, particularly if evidence of
acute or chronic otitis media

Ocular examination: Patient often unable to completely close eye on affected side

Oral examination: Taste and salivation often affected

Neurologic examination: All cranial nerves, sensory and motor testing, cerebellar testing
Grading
The grading system developed by House and Brackmann categorizes Bell palsy on a scale of I to VI, [3, 4, 5] as
follows:
Grade I: normal facial function
Grade II: mild dysfunction
Grade III: moderate dysfunction
Grade IV: moderately severe dysfunction
Grade V: severe dysfunction
Grade VI: total paralysis
See Clinical Presentation for more specific information on patient history and physical examination for Bell
palsy.
Testing
Although there are no specific diagnostic tests for Bell palsy, the following may be useful for identifying or
excluding other disorders:

Rapid plasma reagin and/or venereal disease research laboratory test or fluorescent treponemal
antibody absorption test
HIV screening by enzyme-linked immunosorbent assay and/or Western blot
Complete blood count
Erythrocyte sedimentation rate
Thyroid function
Serum glucose
CSF analysis
Blood glucose
Hemoglobin A1c
Antineutrophil cytoplasmic antibody levels
Salivary flow
Schirmer blotting test
Nerve excitability test
Computed tomography
Magnetic resonance imaging
See Workup for more specific information on testing and imaging modalities for Bell palsy.
In many cases, the history and physical examination of the patient establish the diagnosis of Bell palsy. If the
clinical findings are doubtful or if paralysis lasts longer than 6-8 weeks, further investigations should be
considered.[11]

No specific diagnostic tests are available for Bell palsy, though the following may be useful for identifying or
excluding other disorders:

Rapid plasma reagin (RPR) and/or venereal disease research laboratory (VDRL) test or fluorescent
treponemal antibody absorption (FTA-ABS) test
HIV screening by means of enzyme-linked immunosorbent assay (ELISA) and/or Western blot
Complete blood cell (CBC) count
Erythrocyte sedimentation rate measurement
Thyroid function studies
Serum glucose level
Cerebrospinal fluid analysis
In addition to the above tests, blood glucose or hemoglobin A1c levels may be obtained to determine if the
patient has undiagnosed diabetes. Persons with diabetes have a 29% higher risk of being affected by Bell
palsy than do persons without diabetes.
Serum titers for herpes simplex virus (HSV) may be obtained. However, this test is usually not helpful, owing to
the ubiquitous nature of this virus.
Antineutrophil cytoplasmic antibody (cANCA) levels are indicated, if applicable, to exclude Wegener
granulomatosis. In areas where Lyme disease is endemic, serum titers (immunoglobulin M [IgM] and IgG)
for Borrelia burgdorferi should be obtained.
Serum titers (IgM and IgA) for Mycoplasma pneumoniae may be obtained. A study in Germany measured titers
in patients with Bell palsy and found that several patients had elevated titers for M pneumoniae, though only 2
of those who tested positive had respiratory symptoms. [37]

Salivary flow test

Salivary flow also may be tested. The physician places a small catheter into the paralyzed and normal
submandibular glands. The patient is then asked to suck on a lemon, and the salivary flow is compared
between the 2 sides. The normal side is the control.

Schirmer blotting test

The Schirmer blotting test may be used to assess tearing function. The use of benzene will stimulate the
nasolacrimal reflex, and the degree of tearing can be compared between the paralyzed and normal sides.

Nerve excitability test

The nerve excitability test determines the threshold of the electrical stimulus needed to produce visible muscle
twitching. This test is technically challenging and has very limited clinical availability.

Imaging considerations
If the history and physical examination lead to a diagnosis of Bell palsy, then immediate imaging is not
necessary, because most patients with Bell palsy improve within 8-10 weeks. If the paralysis does not improve
or worsens, imaging may be useful. If the patient has a palpable parotid mass, imaging may be necessary

9. CT Scanning and MRI

Imaging with CT scanning or other methods is indicated if there are other associated physical findings or if the
paresis is progressive and unremitting. CT scanning demonstrates the architecture of the temporal bone and
may be used if some other pathology is suspected.
MRI is useful as a means of excluding other pathologies as the cause of paralysis and is preferred for imaging
the cerebellopontine angle.

MRI in patients with Bell palsy may show enhancement of the seventh cranial nerve (facial nerve) at or near the
geniculate ganglion. Alternatively, MRI may demonstrate a neoplasm compressing the facial nerve. Tumors that
compress or involve the facial nerve include schwannoma (most common), hemangioma, meningioma, and
sclerosing hemangioma.
Perform gadolinium-enhanced MRI when findings are atypical or when the facial nerve paralysis appears
central, to rule out a tumor or vascular compression. [38]Increased signal intensity of the premeatal or
intratemporal segment of the facial nerve after administration of gadolinium has been noted in patients with Bell
palsy.[39, 40] Attempts to correlate outcome with quantification of signal intensity increases have yielded
contradictory results.

Conduction Testing and EMG

Useful tests for evaluation of the function of the facial nerve include nerve conduction testing and EMG. Nerve
conduction velocities and EMG produce a graphic readout of the electrical currents, displayed by stimulating
the facial nerve and recording the excitability of the facial muscles it supplies. These tests may aid in assessing
the outcome of a patient who has persistent and severe Bell palsy.
This testing is not part of the acute workup; the tests are most useful when performed 3-10 days after the onset
of paralysis. Note that most electromyographic/nerve conduction studies do not show an abnormality for 3
weeks following a peripheral nerve injury.
Comparison to the contralateral side helps to demonstrate the extent of nerve injury and has prognostic
implications. Nerve conduction responses are abnormal if a difference of 50% in amplitude between the
paralyzed and normal side is detected; a difference of 90% between the 2 sides suggests a poorer prognosis.
May et al demonstrated that prognosis may be favorable if the motor amplitude of the affected side is greater
than 25% of that of the normal side. An incomplete recovery was observed in patients whose results
demonstrated less than 25% amplitude on the paralyzed side. [41] Blink reflexes can be used to measure
conduction across the involved segment, but they are commonly absent in Bell palsy.

Electroneurography
Electroneurography is a physiologic test that uses EMG to objectively measure the difference between
potentials generated by the facial musculature on both sides of the face in response to a supramaximal
electrical stimulation of the facial nerve. Because all electrodiagnostic testing is performed on the nerve distal
to the proposed site of injury, sufficient time is needed for wallerian degeneration to occur, usually 48-72 hours.
Testing should begin 3 days from the onset of complete paralysis.
Electrodiagnostic testing measures the facial nerve degeneration indirectly. If a patient does not reach 90%
degeneration within the first 3 weeks of the onset of paralysis, some studies suggest that the prognosis is
excellent, with over 80-100% of the patients recovering with excellent function.
The patients who reach over 90% degeneration within the first 3 weeks of the onset of paralysis have a much
more guarded prognosis, with only 50% having good recovery of facial motion. The rate of degeneration also
predicts the prognosis. Patients who have 90% degeneration by 5 days have a worse prognosis than those
with 90% degeneration at 14 days

Brainstem Auditory Evoked Response and Audiometry

Brainstem auditory evoked response (BAER) may be obtained in patients with peripheral facial nerve lesions
and other neurologic involvement. This test measures the transmission of response through the brainstem and
is effective in detecting, notably, retrocochlear lesions.
Hendrix and Melnick evaluated the BAER of 17 patients with Bell palsy and found no evidence of retrocochlear
lesions of the auditory system in any of the patients. [42] In study by Shannon et al, BAER was recorded in 27
patients with Bell palsy; only 6 patients had prolonged brainstem transmission but normal auditory function. [43]
These studies were small and do not support routine use of BAER in patients with Bell palsy. However, when a
patient presents with multiple cranial neuropathies (eg, of the seventh and eighth cranial nerves), BAER may
be useful.

If hearing loss is suspected, audiography and auditory evoked potentials (AEPs) should be pursued once an
underlying structural lesion has been excluded. Typically, the hearing threshold is not affected by Bell palsy.
Impedance testing may reveal an absent or diminished stapedial reflex because of paresis of the stapedial
branch of the facial nerve.

Blepharokymographic Analysis
Blepharokymographic analysis, a high-speed eyelid motion-analysis system, has been used to evaluate
movement of the eyelids. Computer-based analysis may prove helpful in diagnosing Bell palsy, predicting
prognosis, and evaluating response to therapeutic measures such as placement of a gold weight in the affected
upper eyelid (used in cases in which spontaneous recovery has been limited)

Histologic Findings
In a review of 12 autopsy cases of patients with Bell palsy, most cases showed inflammatory changes around
the mastoid cells and walls of the arteries.[44] The most common site of involvement was the geniculate ganglion.
Surgical findings described constriction of the nerve at the stylomastoid foramen, with swelling of the nerve
itself. Microscopic findings showed an inflammatory reaction with infiltration of macrophages on the nerve.

History: The most obvious symptom of Bell's palsy is an unexplained episode of unilateral facial
weakness or paralysis. Individuals may report other symptoms, including a headache, tearing, changes in
the amount of saliva and tears, drooling, difficulty eating and drinking, change in facial appearance,
impairment of taste, and hearing loss. Some individuals report having a mild cold, influenza, or
other upper respiratory tract infection within a week prior to the onset of Bell's palsy. The individual may
report a history of diabetes or prior herpes infection with a recent outbreak. A complete history of current
and prior illnesses is usually obtained.
Physical exam: The exam reveals facial asymmetry, drooling, increased distance between the top and
bottom eyelids (palpebral fissure width), a smooth forehead, and a flattened crease between the nose and
the upper lip (nasolabial fold). No other evidence of central nervous system signs is usually noted. The
ear and neck will be examined fully for any conditions contributing to the symptoms. If the face is
paralyzed except for the forehead, a central nervous system cause is sometimes suspected. The extent
of facial dysfunction will be graded (grades I through VI) according to standard definitions.
Tests: No specific test confirms Bells palsy; the initial diagnosis is made through observation. Laboratory
testing may include complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive
protein, antinuclear antibodies, and blood chemistries to rule out underlying illness such as autoimmune
or other immunologic disease, diabetes, neoplastic disease, or infectious disease. Serological laboratory
tests may be done to rule out Lyme disease. An antineutrophil cytoplasmic antibody (cANCA) test may be
performed if Wegener granulomatosis is a possible underlying diagnosis.
A careful cranial nerve examination is typically performed, including a tuning fork examination to test
hearing and testing for corneal sensation. A simple test of taste should be performed. Audiometry may
also be used to evaluate hearing. Nerve excitability testing may also be performed through the use
of electromyography (EMG) for assessing facial paralysis by measuring voluntary motor activity, and
electroneuronography for determining the extent of nerve fiber degeneration. EMG usually is not thought
to be reliable sooner than 18 days after onset of the paralysis. Blepharokymographic analysis may be
used to evaluate eyelid motion, which can confirm the diagnosis and help predict the prognosis. Imaging
(x-ray, MRI, or CT) may be performed to evaluate other possible pressure sources such as infection,
tumor, or skull fracture (Bells Palsy)