Bell's palsy: Pathogenesis, clinical features,

and diagnosis in adults

Author:
Michael Ronthal, MD
Section Editor:
Jeremy M Shefner, MD, PhD
Deputy Editor:
April F Eichler, MD, MPH
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Jan 2019. | This topic last updated: Feb 09, 2018.

INTRODUCTION Sir Charles Bell first described the anatomy and

function of the facial nerve in the early 1800s [1,2]. Bell's initial description of facial
palsy related to facial paralysis caused by trauma to the peripheral branches of the
facial nerve.

Bell's palsy is the appellation commonly used to describe an acute peripheral facial
palsy of unknown cause. However, the terms "Bell's palsy" and "idiopathic facial
paralysis" may no longer be considered synonymous. A peripheral facial palsy is a
clinical syndrome of many causes, as discussed below, and evaluation requires
more than a superficial examination.

This review will discuss the pathogenesis, clinical features, and diagnosis of Bell's
palsy. The prognosis and treatment of Bell's palsy is discussed elsewhere.
(See "Bell's palsy: Treatment and prognosis in adults".)

ANATOMY OF THE FACIAL NERVE The facial nerve is a mixed

nerve, containing the following (figure 1):

●Motor fibers that innervate the facial muscles
●Parasympathetic fibers innervating lacrimal, submandibular, and sublingual
salivary glands
●Afferent fibers from taste receptors from the anterior two thirds of the tongue
●Somatic afferents from the external auditory canal and pinna

The facial nerve arises from two roots (one motor root and one visceral mixed root
known as the nervus intermedius) at the pontomedullary junction. It then courses
laterally through the cerebellopontine angle together with the vestibulocochlear
nerve to the internal auditory meatus, which is about 1 cm in length, and becomes
encased in periosteum and perineurium. The two roots then enter the facial
(fallopian) canal. The facial canal is about 33 mm in length, and consists of three
consecutive segments: labyrinthine, tympanic, and mastoid. Because the canal is
narrowest in the labyrinthine segment (average 0.68 mm in diameter), any swelling
of the nerve is more likely to result in compression here. The nerve runs laterally
toward the medial wall of the epitympanic recess where it bends sharply backward;
at the bend or genu is a swelling, the geniculate ganglion, lying in the labyrinthine
segment of the canal. The nerve then passes backward and downward to reach
the stylomastoid foramen. The precise anatomy and relationship to the vestibular
and auditory apparatus is of particular importance to surgeons operating in the
area.

The greater petrosal nerve branches off the facial nerve at the geniculate ganglion,
enters the middle cranial fossa extradurally, and exits through the foramen lacerum
toward the pterygopalatine ganglion (figure 1). It supplies the lacrimal and palatine
glands.

The next branch as the nerve passes downward is the nerve to the stapedius.
More distally, the chorda tympani arises from the main trunk of the facial nerve
about 6 mm above the stylomastoid foramen (figure 1). The chorda, the largest
branch of the facial nerve, passes across the tympanic membrane, separated from
the middle ear cavity only by a mucous membrane. It continues anteriorly to join
the lingual nerve and is distributed to the anterior two-thirds of the tongue. The
chorda tympani contains secretomotor fibers to sublingual and submandibular
glands, and visceral afferent fibers for taste. The cell bodies of the unipolar
gustatory neurons lie in the geniculate ganglion and travel via the nervus
intermedius to the tractus solitarius.

The remaining fibers of the facial nerve emerge at the stylomastoid foramen, turn
anterolaterally, and pass through the parotid gland. These fibers divide into five
groups of nerves between the deep and superficial lobes of the gland at the pes
anserinus (Latin "goose foot") and are distributed to the facial muscles in a variable
pattern (figure 1) [3].

EPIDEMIOLOGY Bell's palsy, defined as an acute peripheral facial

nerve palsy of unknown cause, represents about half of all cases of facial nerve
palsy [4]. The annual incidence rate is between 13 and 34 cases per 100,000
population [5]. There is no race, geographic, or gender predilection, but the risk is
three times greater during pregnancy, especially in the third trimester or in the first
postpartum week [6]. Diabetes is present in about 5 to 10 percent of patients [7,8].

The recurrence rate of Bell's palsy is discussed separately. (See "Bell's palsy:

Treatment and prognosis in adults", section on 'Recurrence'.)
 PATHOGENESIS Bell's palsy is the appellation commonly used to

describe an acute peripheral facial palsy of unknown cause. However, the terms
"Bell's palsy" and "idiopathic facial paralysis" may no longer be considered
synonymous [9-11]. A peripheral facial palsy is a clinical syndrome of many
causes, and herpes simplex virus activation is the likely cause of Bell's palsy in
most cases. Nevertheless, most patients with peripheral facial palsy are labelled as
having Bell's palsy because there is no established or widely available method of
confirming herpes simplex virus as the mechanism in clinical practice.

A herpes simplex-mediated viral inflammatory/immune mechanism was the subject

of controversy for years but was suspected based upon serological evidence [12].
Polymerase chain reaction DNA testing supports the notion of axonal spread and
multiplication of a reactivated neurotropic virus leading to inflammation,
demyelination, and palsy. Herpes simplex virus activation has become widely
accepted as the likely cause of Bell's palsy in most cases [13-15], though the
evidence is not entirely conclusive [16,17]. In one study, HSV-1 genomes were
identified in facial nerve endoneurial fluid and auricular muscle in 11 of 14 patients
undergoing decompression surgery for Bell's palsy but in no controls [18].

Herpes zoster is probably the second most common viral infection associated with
facial palsy. In a large series of 1701 cases of Bell's palsy, 116 had herpes zoster
[15]. Other infectious causes of acute peripheral facial palsy include
cytomegalovirus, Epstein-Barr virus, adenovirus, rubella virus, mumps, influenza B,
and coxsackievirus [19]. Two cases due to Rickettsial infection have also been
reported [20], and ehrlichiosis can present as facial diplegia [21].

An inactivated intranasal influenza vaccine that was introduced and since

withdrawn from the market in Switzerland was significantly associated with Bell's
palsy in a case-control study [22]. The peak occurrence of Bell's palsy was
between 31 and 60 days after intranasal vaccination, suggesting that the palsy was
not due to a direct toxic response but rather an induced immune response, such as
reactivation of latent herpes simplex or varicella-zoster virus [23].

Histopathology of the facial nerve in patients with Bell's palsy is consistent with an
inflammatory and possibly infectious cause, and the appearance is similar to that
found with herpes zoster infection, further supporting an infectious hypothesis.
Specifically, the facial nerve has a thickened, edematous perineurium with a diffuse
infiltrate of small, round, inflammatory cells between nerve bundles and around
intraneural blood vessels. Myelin sheaths undergo degeneration [24]. These
changes are seen throughout the bony course of the facial nerve, although nerve
damage is maximal in the labyrinthine part of the facial canal where edema causes
compression and the tenuous blood supply adds to the damage.

Alternate postulated mechanisms of Bell's palsy include a genetic predisposition in

some cases [25-27] and ischemia of the facial nerve [28,29]. Diabetes is a risk
factor for microangiopathy, which may lead Bell's palsy via to microcirculatory
failure of the vasa nervosum [30]. A retrospective study found that 190 (74 percent)
of 257 patients with Bell's palsy first noticed facial weakness in the morning,
suggesting that actual development of facial palsy occurred during sleep [29]; the
authors speculated that nocturnal onset suggested an ischemic mechanism.

The increased risk of Bell's palsy associated with pregnancy, which is most marked
in the third trimester and the first postpartum week, may be caused by pregnancy-
related fluid retention leading to compression of the nerve or perineural edema.
Other potential etiologic factors include hypercoagulability causing thrombosis of
the vasa nervosum and relative immunosuppression in pregnancy [31]. Several
studies have found an association of Bell's palsy with preeclampsia, again
suggesting extracellular edema as the mechanism [32-34].

CLINICAL FEATURES Patients with Bell's palsy typically present with

the sudden onset (usually over hours) of unilateral facial paralysis. Common
findings include the eyebrow sagging, inability to close the eye, disappearance of
the nasolabial fold, and drooping at the affected corner of the mouth, which is
drawn to the unaffected side (picture 1). Decreased tearing,
hyperacusis, and/or loss of taste sensation on the anterior two-thirds of the tongue
may help to site the lesion in the fallopian canal, but these findings are of little
practical use other than as indicators of severity.

An acute facial palsy is often devastating for patients. Of 22,594 patients surveyed
at the Edinburgh facial palsy clinic, one-half exhibited a considerable degree of
psychological distress and restriction in social activities as a consequence of their
facial palsy [35].

Additional cranial neuropathies — Patients with Bell's palsy typically have only

isolated peripheral seventh cranial nerve neuropathy. However, clinical findings
suggestive of additional cranial neuropathies may infrequently occur. A prospective
case series of 51 patients diagnosed with Bell's palsy found four with additional
cranial neuropathies; these included contralateral trigeminal (one),
glossopharyngeal (two), and hypoglossal (one) [36].

In the same study, an additional 13 patients had ipsilateral facial sensory

impairment suggestive of ipsilateral trigeminal neuropathy [36]. Such ipsilateral
sensory loss in the setting of Bell's palsy has usually been attributed not to
neuropathy, but to abnormal perception based on droopy facial muscles, skin, and
associated tissue. Three additional patients had bilateral facial palsy, possibly from
the same pathogenesis as typical unilateral Bell's palsy.
 DIAGNOSIS The diagnosis of Bell's palsy is based upon the following

criteria:
●There is a diffuse facial nerve involvement manifested by paralysis of the
facial muscles, with or without loss of taste on the anterior two-thirds of the
tongue or altered secretion of the lacrimal and salivary glands.
(See 'Peripheral versus central lesions' below.)
●Onset is acute, over a day or two; the course is progressive, reaching
maximal clinical weakness/paralysis within three weeks or less from the first
day of visible weakness; and recovery or some degree of function is present
within six months.

An associated prodrome, ear pain, or dysacusis is variable.

A diagnosis of Bell's palsy is doubtful if some facial function, however small, has
not returned within four months [5,37,38]. Additional evaluation to determine the
etiology is warranted in this instance.

Examination — Facial movement is assessed by observing the response to

command for closing the eyes, elevating the brow, frowning, showing the teeth,
puckering the lips, and tensing the soft tissues of the neck to observe for platysma
activation. The evaluation also includes a general physical examination and
neurologic examination. Particular attention is directed at the external ear to look
for vesicles or scabbing (which indicates zoster) and for mass lesions within the
parotid gland. (See 'Differential diagnosis' below.)

Peripheral versus central lesions — Sparing of the forehead muscles on the

affected side of the face is suggestive of a central (upper motor neuron) lesion
because of bilateral innervation to this area. However, this finding does not exclude
a peripheral site of pathology in all cases. As an example, a partial lesion of the
facial nerve at the pes anserinus (between the deep and superficial lobes of the
parotid gland) that spares the temporal branch to the frontalis muscle results in
facial paralysis, but the patient is still able to wrinkle the forehead. Nonetheless,
forehead sparing should stimulate further evaluation of a possible central etiology.

A "peripheral" (lower motor neuron) pattern of facial weakness that involves the
forehead is usually due to a lesion of the ipsilateral facial nerve, but also can be
caused by a central (brainstem) lesion that involves the ipsilateral facial nerve
nucleus or facial nerve tract in the pons.

Central activation of the facial nerve is both volitional and automatic or emotional in
origin, and the facial nerve is the final common pathway. Thus, dissociation of
movement of the face to command from spontaneous movement, as in smiling,
indicates an upper motor neuron lesion. Lack of dissociation (absence of both
voluntary and spontaneous movement) indicates a lower motor neuron (peripheral)
lesion.
Diagnostic tests — Electrodiagnostic studies help determine the prognosis, and
imaging studies can define potential surgical causes of facial palsy. However,
these tests are not necessary in all patients. Patients with a typical lesion that is
incomplete and recovers do not need further study.

In contrast, electrodiagnostic studies may be warranted in patients with clinically

complete lesions for prognostic purposes. Imaging is warranted if the physical
signs are atypical, there is slow progression beyond three weeks, or if there is no
improvement at four months. Screening blood studies for underlying systemic
disease or infection should also be considered in these cases. However, no test
provides prognostic information sufficiently early as to be used for determining who
should or should not be treated.

Attempting to localize the site of the lesion with tests such as the Schirmer test for
lacrimation, stapedial reflex, and evaluation of taste and salivation have only
moderate accuracy and are of little practical benefit [39]. Furthermore, in patients
studied at surgery, only 6 percent had lesions distal to the geniculate ganglion [40],
the site that these tests target.

Electrodiagnostic studies — The simplest electrodiagnostic test is

electromyography (EMG). In patients who have a clinically complete lesion, EMG
may show some action potentials on active volition, which allows one to conclude
that the nerve is still in continuity with a potential for regrowth.

In the first days after symptoms onset, the blink reflex (stimulation of the
supraorbital nerve) can confirm the peripheral origin of weakness and assess the
degree of axonal conduction block [41,42].

Motor nerve conduction studies (NCS) of the facial nerve is a technique whereby
the facial nerve is supramaximally stimulated near the parotid, and the evoked
potential is measured by surface recording electrodes over the orbicularis oculi,
nasalis, or lower facial muscles, yielding a compound muscle action potential
(CMAP) reflecting activity in the muscles beneath the electrodes. At approximately
10 days after the onset of symptoms, the amplitude of the CMAP on the paralyzed
side compared with that on the normal side yields an estimate of the degree of
axonal loss [42].

The CMAP value obtained by facial nerve stimulation correlates histologically with
the number of degenerating motor neurons; a CMAP value of 10 percent of normal
corresponds with a degeneration or loss of 90 percent of the motor axons on that
side [43]. In one study, 90 percent degeneration was considered to be a critical
value below which recovery was poor; degeneration of greater than 98 percent
predicted a very poor result [44]. Recovery was variable with degeneration
between 90 and 98 percent, and often weakness and synkinesis resulted. In
another study, 75 percent was regarded as the critical cutoff [45].

Facial nerve stimulation to assess function in the peripheral nerve is most useful
when performed within two weeks after progression to complete facial paresis in
cases in which surgical decompression might be considered [46]. Severe
degeneration of the facial nerve is probably irreversible after two to three weeks
[47]. (See "Bell's palsy: Treatment and prognosis in adults", section on 'Surgical
decompression'.)

At approximately 20 to 30 days after onset, needle EMG may provide confirmation

of muscle denervation and the degree of axonal damage [42]. In patients with
axonal loss, needle EMG at about three months after onset may be used to assess
for evidence of subclinical reinnervation from the facial nerve. The patient is
interested mainly in prognosis – the EMG in this instance serves to define an
incomplete lesion with potential for recovery.

Additional electrodiagnostic studies include the following:

●The maximal stimulation test (MST) uses supramaximal stimulation to

achieve maximal stimulation, and the response is subjectively observed by the
tester. It is of doubtful value.
●Nerve excitability threshold testing is similar, but the tester attempts to
quantify the current required to produce a threshold response. A critical value
of 3.5 mA is said to correlate with 90 percent degeneration on motor NCS [48],
and implies a poor prognosis [49].

Imaging studies — As mentioned above, imaging is warranted if the physical

signs are atypical, there is slow progression beyond three weeks, or if there is no
improvement at four months. History of a facial twitch or spasm that precedes
facial weakness suggests nerve irritation from tumor and should also prompt
imaging [46]. For patients with acute onset of facial paralysis and negative imaging
studies at four months who have continued complete flaccid paralysis at seven
months, repeat imaging is warranted, and biopsy is suggested if repeat imaging is
negative [50].

Imaging in these cases should be performed with high resolution contrast-

enhanced CT or gadolinium-enhanced MRI and should include the brain, temporal
bone, and parotid gland [50]. High resolution CT scanning is excellent for bony
detail and will demonstrate erosion. MRI delineates the soft tissue structures, and
is the best study to evaluate the intraparotid facial nerve for inflammation, edema,
or neoplasm. In normal people there is mild to moderate enhancement of the
geniculate ganglion and the tympanic-mastoid segment within the facial canal
[51,52]. Pathological enhancement in Bell's palsy is reported in between 57 and
100 percent of patients [53], and absence of enhancement may be a good
prognostic sign [54,55]. Enhancement of the inner ear structures occurs only in
herpes zoster facial palsy and can be taken to suggest this diagnosis even without
a vesicular eruption [53].

Other investigations — Serologic testing for Lyme disease is recommended for

adults with acute-onset facial palsy when there is the possibility of exposure in
Lyme-endemic areas during the spring through autumn seasons, particularly for
those with bilateral facial palsy or other clinical manifestations of Lyme disease.
Serologic testing should follow the two-tier strategy, which uses a sensitive
enzyme-linked immunosorbent assay (ELISA) or an immunofluorescent assay
(IFA) in place of ELISA, followed by a Western blot if the ELISA or IFA is positive
or equivocal. (See "Nervous system Lyme disease", section on 'Serologic testing'.)

With the exception of the first four to six weeks after infection, serologic testing is
highly sensitive and specific for the diagnosis of Lyme disease. Occasionally the
cranial neuropathy occurs before the patient has become seropositive; in such
patients, follow-up serology in several weeks is typically diagnostic. Cerebrospinal
fluid analysis is of limited utility if Lyme disease is limited to the peripheral nervous
system. (See "Nervous system Lyme disease", section on
'Diagnosis' and "Diagnosis of Lyme disease".)

Parotid gland biopsy is suggested for patients with acute onset facial paralysis
when there is no recovery and imaging studies (see 'Imaging studies' above) are
negative at seven months [50]. (See 'Imaging studies' above and "Salivary gland
tumors: Epidemiology, diagnosis, evaluation, and staging".)

DIFFERENTIAL DIAGNOSIS Facial nerve palsy may be caused by a

variety of disorders that can be confused with Bell's palsy, including herpes zoster
infection, Guillain-Barré syndrome, otitis media, Lyme disease (neuroborreliosis),
HIV infection, and others discussed below. In addition, a "peripheral" pattern of
facial weakness involving the forehead and all muscles of facial expression can be
caused by a central lesion, such as a stroke, that involves the ipsilateral facial
nerve nucleus or facial nerve tract in the pons.

Herpes zoster — Herpes zoster is diagnosed if vesicles are found in the external

meatus. Ramsay Hunt syndrome refers to either herpes zoster oticus (geniculate
herpes) or any cephalic zoster complicated by facial paralysis or by auditory or
vestibular symptoms. (See "Epidemiology, clinical manifestations, and diagnosis of
herpes zoster", section on 'Ramsay Hunt syndrome (herpes zoster oticus)'.)

Seroconversion is occasionally seen in the absence of vesicles, known as zoster

sine herpete [56,57]. Dermatomal pain and dysesthesia that occurs before the
presence of vesicles is known as preherpetic neuralgia, and it may be the only sign
that herpes zoster is the etiology [58]. Up to one-third of Bell's palsy cases
previously considered idiopathic may be caused by zoster sine herpete [59].

Otitis media — Facial paralysis is a potential complication of otitis media (bacterial

infection of the middle ear), which is usually diagnosed easily by simple inspection
of the external meatus and tympanic membrane. (See "Acute otitis media in
adults" and "Chronic otitis media, cholesteatoma, and mastoiditis in adults".)

Lyme disease — Facial nerve palsy is the most common cranial neuropathy

associated with Lyme disease. It occurred in 63 percent of patients with Lyme
meningitis in a European series and in 50 percent of patients in an American series
[60,61]. Involvement of the facial nerve can be unilateral or bilateral, and usually
lasts less than two months [62]. (See "Nervous system Lyme disease", section on
'Cranial neuropathies'.)

The approach to facial nerve palsy in children who live in areas endemic for Lyme
disease is reviewed elsewhere. (See "Facial nerve palsy in children", section on
'Lyme disease'.)

Findings suggestive of possible Lyme disease (table 1) include the development of

facial palsy in a young patient (with or without a known history of tick bite or
antecedent skin rash), heart block, arthritis, vertigo, and hearing loss. Painless,
non-tender swelling and erythema of the face preceding the facial palsy are
distinctive features [63]. The likelihood that Lyme disease is the cause of a seventh
nerve palsy diminishes in either nonendemic areas or at a time of year when Lyme
disease is not prevalent. (See "Nervous system Lyme disease" and "Epidemiology
of Lyme disease".)

The diagnosis of Lyme disease is discussed in detail separately. (See "Diagnosis

of Lyme disease".)

Guillain-Barré syndrome — The cardinal features of Guillain-Barré syndrome

(GBS) are progressive, mostly symmetric muscle weakness and absent or
depressed deep tendon reflexes, making it rather uncomplicated to distinguish
from Bell's palsy in most cases. Facial weakness occurs in more than 50 percent of
patients with GBS, and is typically bilateral and symmetric. Uncommonly, GBS or
one of its variants can present with bilateral facial palsy and relatively little limb
weakness. Unilateral facial palsy as a manifestation of GBS is rare [64,65].

In patients presenting with facial weakness, the presence of associated limb

weakness, bulbar weakness, ophthalmoplegia, or absent or depressed deep
tendon reflexes should prompt an evaluation for GBS. In a retrospective study that
identified 356 cases potentially misdiagnosed as Bell's palsy in the emergency
department, GBS was one of the most frequent alternate diagnoses at follow-up
[66].

The clinical features and diagnosis of GBS are discussed in detail elsewhere.
(See "Guillain-Barré syndrome in adults: Clinical features and diagnosis".)

HIV infection — Mononeuropathies are an uncommon clinical manifestation of

neurologic disease in human immunodeficiency virus (HIV)-positive patients, and
can involve either cranial or peripheral nerves. Thus, HIV infection rarely causes
facial palsy. The etiology of facial nerve palsy in HIV-infected individuals is
unknown, although the usual occurrence of this finding at the time of HIV
seroconversion suggests a direct relationship to the virus itself. Other causes of
facial palsy in patients with HIV infection include herpes zoster, Treponema
pallidum, and lymphomatous meningitis.
Sarcoidosis — Cranial neuropathy, including peripheral facial nerve palsy, is a
frequent manifestation of neurosarcoidosis. The facial nerve palsy can be unilateral
or bilateral (simultaneous or sequential) and recurrent. Neurosarcoidosis is an
important diagnostic consideration in patients with known sarcoidosis who develop
neurologic findings. Patients who develop a neurologic illness consistent with
neurosarcoidosis but are not known to have sarcoidosis present a diagnostic
challenge, as reviewed elsewhere. (See "Neurologic sarcoidosis".)

Sjögren syndrome — Sjögren syndrome can cause multiple cranial neuropathies,

and the facial nerve is one of the most commonly affected cranial nerves.
However, isolated facial nerve palsy due to Sjögren syndrome is unusual [67].
(See "Clinical manifestations of Sjögren's syndrome: Extraglandular disease",
section on 'Peripheral nervous system'.)

Tumor — Mass lesions of the temporal bone, internal acoustic canal,

cerebellopontine angle, or parotid gland can compress or infiltrate the facial nerve
and cause an ipsilateral facial weakness [68]. A prolonged, slowly progressive, or
relapsing course of facial weakness suggests a tumor as the cause, especially if
paralysis persists with no recovery [69]. Less often, tumor is the cause of sudden-
onset or recurrent facial weakness [68,70]. Discrete involvement of only one or two
distal branches of the facial nerve also suggests tumor, and active middle ear
disease or a parotid mass suggests that the palsy is associated with that finding
[71]. Additional clues consistent with tumor as the cause include a facial twitch or
spasm (suggesting ongoing facial nerve irritation) and hearing loss [46,68].

Tumor types that may cause facial nerve palsy include schwannoma of the facial
nerve and parotid gland tumor. Another consideration is cholesteatoma, which is
an abnormal collection of squamous epithelium within the middle ear or mastoid
that can be congenital or acquired, usually as a result of chronic middle ear
disease [11,70]. (See "Salivary gland tumors: Epidemiology, diagnosis, evaluation,
and staging", section on 'Differential diagnosis' and "Chronic otitis media,
cholesteatoma, and mastoiditis in adults" and "Cholesteatoma in children".)

Stroke — Ischemic and hemorrhagic stroke can present with unilateral facial

weakness, which in most cases spares the forehead muscles because it the
impairment is that of an upper motor neuron type (see 'Peripheral versus central
lesions' above). However, a stroke that affects the ipsilateral facial nerve nucleus
or facial nerve tract in the pons can cause a lower motor neuron lesion that mimics
Bell’s palsy with a pattern of ipsilateral weakness involving all the muscles of facial
expression, including the forehead. Such cases are considered rare [72,73], but
limited evidence suggests that a substantial proportion of cases misdiagnosed as
Bell’s palsy are due to ischemic stroke [66].

Melkersson-Rosenthal syndrome — The Melkersson-Rosenthal syndrome is a

rare condition with a female predominance characterized by recurrent episodes of
facial paralysis, episodic facial swelling, and a fissured tongue [74,75]. Age at
onset varies from early childhood to late adulthood. Incomplete forms of this
syndrome outnumber those with the classic triad. Granulomatous inflammation is
seen in the edematous tissue [76,77], but the cause is unknown, and treatment
unproven.

TREATMENT The treatment of Bell's palsy is discussed separately.

(See "Bell's palsy: Treatment and prognosis in adults".)

SOCIETY GUIDELINE LINKS Links to society and government-

sponsored guidelines from selected countries and regions around the world are
provided separately. (See "Society guideline links: Bell's palsy".)

INFORMATION FOR PATIENTS UpToDate offers two types of

patient education materials, "The Basics" and "Beyond the Basics." The Basics
patient education pieces are written in plain language, at the 5 th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a
given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education
pieces are longer, more sophisticated, and more detailed. These articles are
written at the 10th to 12th grade reading level and are best for patients who want in-
depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage
you to print or e-mail these topics to your patients. (You can also locate patient
education articles on a variety of subjects by searching on "patient info" and the
keyword(s) of interest.)

●Basics topics (see "Patient education: Bell's palsy (The Basics)")

●Beyond the Basics topics (see "Patient education: Bell's palsy (Beyond the
Basics)")

SUMMARY

●About one-half of all cases of facial palsy qualify for the label "Bell's palsy,"
defined as an acute peripheral facial nerve palsy of unknown cause. The
annual incidence rate is between 13 and 34 cases per 100,000 population.
There is no race, geographic, or gender predilection, but the risk is three times
greater during pregnancy, especially in the third trimester or in the first
postpartum week. (See 'Epidemiology' above.)
●Herpes simplex virus activation is the likely cause of Bell's palsy in most
cases. Nevertheless, most patients with peripheral facial palsy are labelled as
having Bell’s palsy because there is no established method of confirming
herpes simplex virus as the mechanism in clinical practice. Herpes zoster is
probably the second most common viral infection associated with facial palsy.
(See 'Pathogenesis' above.)
●Bell's palsy typically presents with the sudden onset (usually over hours) of
unilateral facial paralysis. Common findings include the eyebrow sagging,
inability to close the eye, disappearance of the nasolabial fold, and the mouth
drawn to the unaffected side (picture 1). Associated manifestations may
include decreased tearing, hyperacusis, and/or loss of taste sensation on the
anterior two-thirds of the tongue. (See 'Clinical features' above.)
●The diagnosis of Bell's palsy is based upon the following criteria:
•There is a diffuse facial nerve involvement (figure 1) manifested by
paralysis of the facial muscles, with or without loss of taste on the anterior
two-thirds of the tongue or altered secretion of the lacrimal and salivary
glands. (See 'Peripheral versus central lesions' above.)
•Onset is acute, over a day or two; the course is progressive, reaching
maximal clinical weakness/paralysis within three weeks or less from the
first day of visible weakness; and recovery or some degree of function is
present within six months. (See 'Diagnosis' above.)
●Patients with a typical Bell's palsy that is incomplete and recovers do not
need further study. However, imaging of the brain, temporal bone, and parotid
gland with high resolution contrast-enhanced CT or gadolinium-enhanced MRI
is warranted if the physical signs are atypical, there is slow progression
beyond three weeks, or if there is no improvement at four months. In patients
with clinically complete lesions, electrodiagnostic studies may be useful for
prognostic purposes. Serologic testing for Lyme disease is recommended for
adults with acute-onset facial palsy when there is the possibility of exposure in
Lyme-endemic areas during the spring through autumn seasons, particularly
for those with bilateral facial palsy or other clinical manifestations of Lyme
disease. (See 'Diagnostic tests' above.)
●Facial nerve palsy may be caused by a variety of disorders that can be
confused with Bell's palsy. The differential diagnosis includes (see 'Differential
diagnosis' above):
•Herpes zoster infection (see 'Herpes zoster' above)
•Otitis media (see 'Otitis media' above)
•Lyme disease (see 'Lyme disease' above)
•Guillain-Barré syndrome (see 'Guillain-Barré syndrome' above)
•Human immunodeficiency virus (HIV) infection (see 'HIV infection' above)
•Sarcoidosis (see 'Sarcoidosis' above)
•Sjögren syndrome (see 'Sjögren syndrome' above)
•Tumor (see 'Tumor' above)
•Stroke (see 'Stroke' above)
•Melkersson-Rosenthal syndrome (see 'Melkersson-Rosenthal
syndrome' above)
●The treatment of Bell's palsy is discussed separately. (See "Bell's palsy:
Treatment and prognosis in adults".)
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