Autoimmunity Reviews 12 (2012) 323328

Contents lists available at SciVerse ScienceDirect

Autoimmunity Reviews
journal homepage: www.elsevier.com/locate/autrev

Review

Bell's palsy and autoimmunity

A. Greco, A. Gallo, M. Fusconi, C. Marinelli, G.F. Macri , M. de Vincentiis
Head and Neck Department ENT Department, Policlinico Umberto I University of Rome Sapienza, Italy

a r t i c l e

i n f o

a b s t r a c t
Objectives: To review our current knowledge of the etiopathogenesis of Bell's palsy, including viral infection
or autoimmunity, and to discuss disease pathogenesis with respect to pharmacotherapy.
Systematic review methodology: Relevant publications on the etiopathogenesis, clinical presentation, diagnosis and histopathology of Bell's palsy from 1975 to 2012 were analysed.
Results and conclusions: Bell's palsy is an idiopathic peripheral nerve palsy involving the facial nerve. It accounts for 60 to 75% of all cases of unilateral facial paralysis. The annual incidence of Bell's palsy is 15 to
30 per 100,000 people. The peak incidence occurs between the second and fourth decades (15 to 45 years).
The aetiology of Bell's palsy is unknown but viral infection or autoimmune disease has been postulated as
possible pathomechanisms. Bell's palsy may be caused when latent herpes viruses (herpes simplex, herpes
zoster) are reactivated from cranial nerve ganglia. A cell-mediated autoimmune mechanism against a myelin
basic protein has been suggested for the pathogenesis of Bell's palsy. Bell's palsy may be an autoimmune demyelinating cranial neuritis, and in most cases, it is a mononeuritic variant of GuillainBarr syndrome, a
neurologic disorder with recognised cell-mediated immunity against peripheral nerve myelin antigens. In
Bell's palsy and GBS, a viral infection or the reactivation of a latent virus may provoke an autoimmune reaction against peripheral nerve myelin components, leading to the demyelination of cranial nerves, especially
the facial nerve.
Given the safety prole of acyclovir, valacyclovir, and short-course oral corticosteroids, patients who present
within three days of the onset of symptoms should be offered combination therapy. However it seems logical
that in fact, steroids exert their benecial effect via immunosuppressive action, as is the case in some other
autoimmune disorders. It is to be hoped that (monoclonal) antibodies and/or T-cell immunotherapy might
provide more specic treatment guidelines in the management of Bell's palsy.
2012 Elsevier B.V. All rights reserved.

Article history:
Received 19 May 2012
Accepted 30 May 2012
Available online 8 June 2012
Keywords:
Bell's palsy
Autoimmunity
Aetiology
Pathogenesis
Therapy

Contents
1.
2.

Introduction . . . . . . . . . .
Aetiology . . . . . . . . . . .
2.1.
Viral hypothesis . . . . .
2.2.
Immunological hypothesis
3.
Treatment . . . . . . . . . . .
4.
Conclusions . . . . . . . . . .
Take-home messages . . . . . . . .
References . . . . . . . . . . . . .

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1. Introduction
The most common causes of the abrupt onset of unilateral facial
weakness are stroke and Bell's palsy [1]. Unilateral peripheral facial
Corresponding author at: Largo Valerio Bacigalupo 32 C, 00142 Rome, Italy. Tel.:
+ 39 03478404236.
E-mail address: giano1979@hotmail.com (GF. Macri).

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nerve palsy may have a detectable cause (i.e. secondary facial nerve
palsy) or may be idiopathic (primary) without an obvious cause (i.e.
Bell's palsy) [2]. Secondary facial nerve palsy has a variety of causes
(Table a) and is generally less prevalent than Bell's palsy (25 vs.
75%) [3]. Bell's palsy was rst described by NA Friedreich in 1797
[4]. It is named after Sir Charles Bell (17741842), who described
the syndrome along with the anatomy and function of the facial
nerve.

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A. Greco et al. / Autoimmunity Reviews 12 (2012) 323328

Table a
Aetiologies of facial nerve palsy.
From: Lorch M, Teach SJ. Facial nerve palsy: aetiology and approach to diagnosis and
treatment. Pediatric Emergency Care 2010; 26: 763769.
Congential causes
Birth trauma
Genetic syndromes
MelkersonRosenthal syndrome
AlbersSchnberg disease (osteopetrosis)
Mbiuossyndrome
Godenhar syndrome (oculoauriculovertebral dysplasia)
Acquired causes
Infections
Lyme disease
Herpes simplex virus
Otitis media
Other (human herpesvirus type 6, mumps, coxsackie virus, adenovirus)
Traumic
Malignancy associated
Hypertension associated
Idiopathic (Bell's palsy)

Bell's palsy is an idiopathic peripheral nerve palsy involving the

facial nerve. It accounts for 60 to 75% of all cases of unilateral facial
paralysis [5]. The annual incidence is 15 to 30 cases per 100,000 people
[6].
The peak incidence occurs between the second and fourth decades
(15 to 45 years) [7]. The median age at onset is 40 years, but the disease may occur at any age [8]. Different studies have reported either a
slight female preponderance [7] or that women and men are equally
affected [9]. The prevalence is increased among pregnant women (43
cases per 100,000) [9].
The facial nerve consists of a major motor component, which supplies all the muscle of facial expression, and a small sensory branch

that carries taste sensation from the anterior two thirds of the tongue
through the chorda tympani nerve [10]. Parasympathetic bres reach
the lacrimal glands via the greater supercial petrosal nerve, and they
reach the sublingual and submaxillary glands via the chorda tympani
(Picture 1).
Bell's palsy is diagnosed upon the abrupt onset of unilateral facial
weakness or complete paralysis of all the muscles on one side of the
face, dry eye, pain around the ear, an altered sense of taste, hyperacusis
(hypersensitivity to sounds), or decreased tearing [11]. In patients with
Bell's palsy, on attempted closure, the eye rolls upward (Bell's phenomenon). The disease usually progresses from the onset of symptoms to
maximal weakness within three days.
Various scoring systems are available to clinically assess the severity of peripheral facial nerve palsy. The most widely applied is the
HouseBrackmann facial nerve grading system (HBS) (Table b).
Approximately 10% of patients with Bell's palsy experience one or
more recurrences after a mean latency of 10 years [12].
The rst step in diagnosis is to determine whether facial weakness
is due to a problem in the central nervous system or one in the peripheral nervous system. Central nervous system lesions (e.g. multiple sclerosis, stroke, and tumour) can also cause facial nerve palsy.
However, some motor neurons to the forehead cross sides at the
level of the brainstem, so the facial nerve bres going to the forehead
come from both cerebral hemispheres. Supranuclear (central) lesions
affecting the facial nerve will not paralyse the forehead on the affected side, resulting in a unilateral facial paralysis with forehead sparing.
Brain magnetic resonance imaging (MRI) is not routinely indicated, but when it is performed, the most common abnormality observed is contrast enhancement of the distal intracanalicular and
labyrinthine segments of the facial nerve. The geniculate ganglion
may also be involved [13].

Picture 1. Anatomy of facial nerve.

From: Gilden DH. Clinical practice. Bell's palsy. N Engl J Med 2004; 351: 132331.

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A. Greco et al. / Autoimmunity Reviews 12 (2012) 323328

Table b
HouseBrackman scale grading.
From: Rath B, Linder T, Cornblath D, et al. All that palsies is not Bell's the need to dene Bell's palsy as an adverse event following immunization. Vaccine 2007; 26: 114.
Grade 1 normal (100% function; measurementa: 8/8)
Normal facial function in all areas.
Grade 2 mild dysfunction (7699% function; measurementa 7/8)
Slight weakness noticeable only on close inspection. At rest: normal symmetry of
forehead, ability to close eye with minimal effort and slight asymmetry. No
synkinesis, contracture, or hemifacial spasm.
Grade 3 moderate dysfunction (5175% function; measurementa: 5/86/8)
Obvious but not disguring difference between two sides, no functional impairment;
noticeable but not severe synkinesis, contracture and/or hemifacial spasm. At rest:
normal symmetry and tone. Motion: slight to no movement of forehead, ability to
close eye with maximal effort and obvious asymmetry, ability to move corners of
mouth with maximal effort and obvious asymmetry. Patients who have obvious
but not disguring synkinesis, contracture, and/or hemifacial spasm are grade 3
regardless of degree of motor activity.
Grade 4 moderately severe dysfunction (2650% function; measurementa: 3/84/8)
Obvious weakness and/or disguring asymmetry. At rest: normal symmetry and
tone. Motion: no movement of forehead; inability to close eye completely with
maximal effort. Patients with synkinesis, mass action; and/or hamifacial spasm
severe enough to interfere with function are grade 4 regardless of motor activity.
Grade 5 severe dysfunction (125% function; measurementa: 1/82/8)
Only barely perceptible motion. At rest: possible asymmetry with droop of corner
of mouth and decreased or absence of nasal labial fold. Motion: no movement of
forehead, incomplete closure of eye and only slight movement of lid with
maximal effort, slight movement of corner of mouth. Synkinesis, contracture,
and hemifacial spasm usually absent.
Grade 6 total paralysis (0% function, measurementa: 0/8)
Loss of tone, asymmetry; no motion; no synkinesis, contracture, or hemifacial spasm.
a
Measurement is determined by measuring the superior movement of the midportion of the superior eyebrow and the lateral movement of the oral commissure. A
scale point of 1 is assigned for each 0.25 cm of motion up to 1 cm for both eyebrow
and commissure movement. The points are then added together. Thus, a total of
8 points can be obtained, if each structure moves 1 cm.

Liston and Kleid [14] found histologic changes in the facial nerve
that can be summarised as follows: 1) The nerve was inltrated by
small, round inammatory cells from the internal acoustic meatus
to the stylomastoid foramen. 2) There was a breakdown of the neuron
myelin sheaths that involved the macrophages. 3) There was an increase in the spaces between the neurons, which was interpreted as
oedema. 4) The bony fallopian canal was normal, and there was no
sign of facial nerve compression by the bone of the fallopian canal.
The small round cells of lymphocytic nature and the breakdown of
myelin sheaths probably are the histologic expression of an autoimmune response.
The disparity of the histologic descriptions in previously reported
cases of Bell's palsy is not surprising. Bell's palsy is a clinical syndrome, and it is entirely possible that more than one disease entity
can produce an idiopathic facial palsy. In fact, some causes of facial
paralysis have only been recognised recently [14]. For example,
Lyme disease [15] was rst recognised as a cause of facial paralysis
within the past few years.
2. Aetiology
The aetiology of Bell's palsy is unknown, but viral infection and autoimmune disease have been postulated as possible pathomechanisms [16].
2.1. Viral hypothesis
Several features of Bell's palsy may be characteristic of a viral infection [17]. These include 1) epidemicity [18], 2) a u-like prodrome
[19], and 3) gadolinium enhancement of the facial nerve during the
acute phase of the disease on imaging of the geniculate ganglion [20].

325

Associations with several infectious pathogens, such as cytomegalovirus [21], EpsteinBarr virus [22], mumps [23], rubella [24] and
human immunodeciency virus [25] have been documented. The anecdotal reports do not unequivocally link these agents with the disorder [26]. However, for at least two infectious pathogens, the evidence
that they can and do indeed cause Bell's palsy is quite sound. These
include Borrelia burgdorferi in Lyme disease [27] and zoster virus in
Ramsay-Hunt syndrome [28,29]. There are many reports on the association between facial paralysis and viral infections, for example,
Varicella zoster [3032] and herpes simplex [17].
The herpes viruses are DNA viruses with the unique ability to establish latent infections in their hosts and cause recurrent disease
by reactivation. Of the human herpes viruses, herpes simplex viruses
1 (HSV-1) and 2 (HSV-2) and Varicella zoster virus are neurotropic;
namely, they establish latent infections in the peripheral nervous system, and the viral genome is maintained in the peripheral sensory
ganglia for the entire life of the host [33]. These peripheral sensory
ganglia are the reservoir from which the neurotropic herpes viruses
can reactivate and cause neurological and mucocutaneous disorders.
The three neurotropic herpes viruses vary in their clinical presentation and differ in their molecular structure. However, they share
several features that govern the biology of their infection of the
human nervous system: 1) The primary infection involves the mucocutaneous surfaces, which serve as the portal of entry into the peripheral nervous system for the viral particles; 2) the primary and
infectious recurrent diseases caused by the same virus usually have
the same cutaneous distribution; 3) under normal (i.e., immune competent) conditions, the reactivation infection usually does not spread
beyond the anatomic distribution and the vicinity of a single peripheral sensory ganglion.
These features can be grouped under a unifying hypothesis that is
now the dogma in herpes virology [34,35]. Following the primary infection, the virus gains access to axon endings within the mucocutaneous surfaces and is transported to the peripheral sensory ganglia.
The viral genome is maintained within the peripheral sensory ganglia,
which serve as reservoirs for viral nucleic acids. Latent herpetic infection is a lifelong state. Under certain circumstances, the virus can
reactivate and travel to regions innervated by the respective peripheral sensory ganglia, causing recurrent disease there.
In Ramsey-Hunt syndrome, the acute facial paralysis is accompanied with zostiform vesicles in the ear [36,37]. Varicella zoster virus
is most likely also the causative agent of Bell's palsy in a subgroup
of patients who have no cutaneous abnormality, but have serological
evidence of a Varicella zoster virus reactivation.
More convincing is recent molecular data demonstrating Varicella
zoster virus nucleic acids in the auricular skin exudates [38] and in
the peripheral mononuclear cells of patients with Bell's palsy [39].
The latter is in accordance with the identication of the Varicella zoster virus genome in the peripheral mononuclear cells of patients with
zoster sine herpete [40]. Thus, Bell's palsy in a subgroup of patients
could eventually also be designated as zoster sine herpete.
In 1972, Mc Cormick hypothesised that the herpes simplex virus
(HSV) might be the causative agent of Bell's palsy [17]. The rst support for this hypothesis arrived twenty years later, with studies that
identied herpes simplex virus nucleic acids in the geniculate ganglion [41,42].
Bell's palsy has been associated with serological evidence of an active HSV-1 infection. HSV-1 DNA was detected during decompression
surgery in the endoneural uids of the facial nerve in patients with idiopathic facial palsy [43].
When considering the possibility that HSV-1 is responsible for
Bell's palsy, several facts that do not favour this hypothesis should
be mentioned: 1) In humans, HSV-1 resides latent in the peripheral
sensory ganglia (PSG), although latency in the motor neurons has
been documented experimentally [44], and its mucocutaneous reactivations are not associated with motor impairment. 2) While

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A. Greco et al. / Autoimmunity Reviews 12 (2012) 323328

asymptomatic reactivations of HSV-1 and 2, namely viral shedding

without mucocutaneous disease, may take place [33], the opposite
situation (herpes sine herpetica with neurological abnormality) has
never been documented. 3) HSV-1 causes recurrent reactivations,
which raises the question of why Bell's palsy is an isolated episode
in the overwhelming majority of cases. 4) The HSV-1 genome seems
to be present in more trigeminal [45] than geniculate ganglia
[41,42], but by a factor less than the order of 1. This raises the question of why Bell's palsy is such a rare condition when compared to
cold sores [46].
2.2. Immunological hypothesis
A cell-mediated autoimmune mechanism has been suggested as
the pathogenesis of Bell's palsy [4749]. Aviel et al. conducted a clinical study of adults and found some alterations in the lymphocyte
subsets of the peripheral blood during the acute stage of the disease
[50].
Following the description by Abramsky et al. of immune-mediated
mechanisms against the basic myelin protein in the disease's pathogenesis, cellular and humoural immunologic alterations have been reported
in adult patients with Bell's palsy [51]. Decreased percentages of total T
cells (CD3) and T helper/inducer cells (CD4) have been documented in
the acute phase of disease compared with control patients [52].
Some evidence implicates the involvement of immune mechanisms
in Bell's palsy. Many reports have indicated the association between facial paralysis and GuillainBarr syndrome (GBS) [53], a condition that
was recently shown to be a cell mediated, autoimmune neuritis [54].
Abramsky et al. [47] demonstrated a dened in vitro response to a
human basic protein (P1L) of peripheral nerve myelin in patients
with Bell's palsy. They suggested that cell-mediated autoimmune
mechanisms may be of importance in the pathogenesis of Bell's palsy.
Approximately the same in vitro transformation in the presence of
P1L protein was found in cases with GBS [55]. The specic in vitro
stimulation of lymphocytes from Bell's palsy and GBS patients using
peripheral P1L basic protein suggests that an in vivo sensitisation to
such self protein may occur in these two conditions, and that
cellmediated autoimmune mechanisms may be an important factor
in the pathogenesis of the paralysis.
The similarities between GBS and Bell's palsy with regard to the
lymphocyte sensitisation to the same P1L protein suggest that Bell's
palsy may be a variant of GBS.
The percentage of T lymphocytes was reduced in Bell's palsy patients
[56], and a reduction in the percentage of total T lymphocytes has also
been found in patients with acute GuillainBarr syndrome [57].
In Bell's palsy patients, the percentage of T suppressor cells was
signicantly reduced, whereas the percentage of T helper cells was
normal [56]. This is in line with the ndings in patients with acute
GuillainBarr syndrome [58].
Aviel et al. found that Bell's palsy patients had a signicant increase in the percentage of B lymphocytes and a signicant decrease
in the percentage of T lymphocytes [50]. Most suggestive is the fact
that similar changes in peripheral blood lymphocyte subpopulations
were also described in the course of several demyelinating diseases,
such as in acute exacerbations of multiple sclerosis and during the
acute stage of GuillainBarr syndrome [49,57,59].
Bell's palsy, like GuillainBarr syndrome, is an acute demyelinating
disease of the peripheral nervous system. In both diseases, an inammatory demyelination neuritis has been found. The immunological similarities between Bell's palsy and GuillainBarr syndrome suggest that
the diseases may share a similar aetiology and pathogenesis [50]. In
most cases, Bell's palsy is a mononeuritic variant of GuillainBarr syndrome [60].
It has also been proposed that Bell's palsy is in fact a polyneuropathy,
as the facial paralysis may be associated with involvement of other cranial nerves [5]. Recent decades were rich with studies concerning the

role of viruses and immune responses in the etiopathogenesis of demyelinating diseases of both the central and peripheral nervous systems
[61,62]. Viruses and immune mechanisms involvement have also been
proposed in Bell's palsy, suggesting that it may be caused by an autoimmune postviral disease [47,63].
A viral infection may be the etiologic cause of Bell's palsy and GBS.
A viral infection may prompt an autoimmune reaction against a component of the peripheral nerve myelin, leading to the demyelination
of cranial nerves, especially the facial nerve, in a way that is not yet
clear [50].
An examination of the serum samples of patients with Bell's palsy
shows elevated concentrations of the cytokines interleukin-1 (IL-1),
IL-6, and tumour necrosis factor-alpha (TNF-alpha) compared with
control populations [64], suggesting an activation of cell-mediated
effectors.
Some authors [65] have proposed that a breakdown of peripheral
tolerance occurred in patients with hepatitis C virus infection as a
consequence of interferon (IFN)-alpha therapy, which led to augmented cell-mediated immune responses. Given that the majority of
cases of uncomplicated Bell's palsy recover fully, it may be that the
main lesion is not of the nerve itself, but of the myelin sheath and
its native cell, the Schwann cell. Further, the pharmacologic doses of
IFN-alpha used may cause a failure of peripheral tolerance by stimulating a pool of lymphocytes already sensitised to native Schwann
cell membrane antigens, as described previously [47]. This failure of
tolerance occurs with induced autoimmune thyroid disease, which
is more common than Bell's palsy in IFN-alpha-treated patients [65].
The appearance of Bell's palsy in children after vaccination [66,67]
supports the immunological hypothesis. Intranasal administration of
inuenza vaccines may reduce the transmission of inuenza more efciently than parenteral administration because it stimulates both
mucosal and systemic immune responses [68]. Over a seven-month
period, the Swiss Drugs Monitoring Centre received 46 case reports
of Bell's palsy among u vaccine recipients. The risk of Bell's palsy
was highest during the second month after intranasal vaccination
suggesting an immunological mechanism [69].

3. Treatment
Any evaluation must consider that 71% of untreated patients recover completely, and 84% achieve near-normal function [70]. Thus,
the 20 to 30% who do not recover fully remain the focus of treatment.
In the past, the efciency of prednisone in alleviating the disease
[71] has been attributed to its ability to reduce inammation and oedema. However, it seems logical that steroids in fact exert their benecial
effect by means of immunosuppressive action, as in the case of some
other autoimmune disorders [72]. Therefore, it seems warranted to recommend the prednisone for patients with Bell's palsy based on ndings
concerning the autoimmune aspects of this disease's pathogenesis.
Meta-analyses have compared glucocorticoids with placebo. One such
analysis showed signicant improvement of facial weakness with glucocorticoid therapy [73].
According to viral theory, one randomised trial with no placebo
group compared oral prednisone with acyclovir. This study indicated
that facial-muscle strength was better after treatment with prednisone than it was after treatment with acyclovir [74].
Although a 2004 Cochrane review found insufcient evidence to
support the use of these antivirals alone [75], two recent placebocontrolled trials demonstrated full recovery in a higher percentage of
patients treated with an antiviral drug in combination with prednisolone than with prednisolone alone [76].
Prednisone is typically prescribed in a 10-day tapering course,
starting at 60 mg per day. Acyclovir 400 mg can be given ve times
per day for seven days, and valacyclovir 1 g can be given three times
per day for seven days.

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A. Greco et al. / Autoimmunity Reviews 12 (2012) 323328

Monoclonal antibodies represent the almost faster growing class

of therapeutics in autoimmunity. They offer the possibility to specically target immunologically relevant molecules which appear critical
in the pathogenesis of peripheral nervous system autoimmune diseases, like Bell's palsy. Based on theoretical grounds such approaches
appear very promising, however, the side effect prole of these drugs,
especially in long-term use, is not completely understood. As we
learned from the natalizumab trial in multiple sclerosis, severe complications or worsening of symptoms, can occur after therapy has
been initiated [77,78].
Multiple sclerosis is an autoimmune disease characterized by
chronic demyelination affecting the central nervous system but usually not the peripheral nervous system, although subclinical peripheral nervous system involvement has occasionally been described [79].
In the past, surgical decompression within three weeks of onset
was recommended for patients with persistent loss of function. The
most common surgical complication is postoperative hearing loss.
Based on the signicant potential for harms and the paucity of data
supporting benet, the American Academy of Neurology does not
currently recommend surgical decompression for Bell's palsy [80].
Regarding indications for surgical decompression, it is unlikely that
the decompression will alter the course of viral infection or autoimmune reaction.
One of the greatest problems with Bell's palsy is the involvement
of the eye if the lid ssure remains open. In this case, eye care focuses
on protecting the cornea from dehydration, drying, or abrasions due
to insufcient lid closure or tearing [9]. Eye ointment is proposed during day and night, supported by a watch glass bandage day and night.
Permanent eyelid weakness may require tarsorrhaphy or the implantation of gold weights in the upper lid.
Facial asymmetry and muscular contractures may require cosmetic surgical procedures or botulinum toxin (Botox) injections. In these
cases, consultation with an ophthalmologist or cosmetic surgeon is
needed [9,81].
4. Conclusions
In conclusion Bell's palsy is probably an autoimmune disease. A
viral infection may prompt an autoimmune reaction against a component of the peripheral nerve myelin, leading to the demyelination of
the facial nerve.
Overall, the data suggest that glucocorticoids decrease the incidence of permanent facial paralysis, although more studies are needed to determine whether antiviral therapy confers additional benets.
This therapeutic consideration ex adiuvantibus enhances the autoimmune hypothesis. However, given the safety prole of acyclovir,
valacyclovir, and short-course oral corticosteroids, patients who present within three days of the onset of symptoms should be offered
combination therapy.
It is to be hoped that (monoclonal) antibodies and/or T-cell immunotherapy might provide more specic treatment guidelines in the
management of Bell's palsy. Some cases of acute Bell's palsy result
from cell-mediated immunity against peripheral nerve antigens, but
the majority of these precise antigens have not been identied.
These results encourage further research in steroids and other immunotherapies for patients with Bell's palsy and related disorders [82].
Take-home messages
Bell's palsy is an idiopathic peripheral nerve palsy involving the facial
nerve. Its etiopathogenesis includes viral infection caused by latent
herpes viruses (herpes simplex, herpes zoster) or an autoimmunity
cell-mediated reaction against a protein of the peripheral nerve myelin. Bell's palsy may be a mononeuritic variant of GuillainBarr
syndrome.

327

Due to this disease's possible viral or autoimmune pathogenesis, a

combination therapy of antivirals and oral corticosteroids should be
administered. It is to be hoped that (monoclonal) antibodies and/or
T-cell immunotherapy might provide more specic treatment guidelines in the management of Bell's palsy. The role of surgical decompression remains controversial, and it is not currently recommended
because of its potential for harm and the paucity of data supporting
its benets.

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