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Autoimmunity Reviews 12 (2012) 323–328

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Autoimmunity Reviews
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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

article info abstract

Article history: Objectives: To review our current knowledge of the etiopathogenesis of Bell's palsy, including viral infection or
Received 19 May 2012 autoimmunity, and to discuss disease pathogenesis with respect to pharmacotherapy.
Accepted 30 May 2012 Systematic review methodology: Relevant publications on the etiopathogenesis, clinical presentation, diagno-sis and
Available online 8 June 2012 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 ac-counts 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
Bell's palsy
people. The peak incidence occurs between the second and fourth decades (15 to 45 years). The aetiology of
Aetiology Bell's palsy is unknown but viral infection or autoimmune disease has been postulated as possible
Pathogenesis pathomechanisms. Bell's palsy may be caused when latent herpes viruses (herpes simplex, herpes zoster) are
Therapy 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 de-myelinating cranial
neuritis, and in most cases, it is a mononeuritic variant of Guillain–Barré 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 reac-tion against peripheral nerve myelin
components, leading to the demyelination of cranial nerves, especially the facial nerve.

Given the safety profile 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 beneficial 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 specific
treatment guidelines in the management of Bell's palsy.
© 2012 Elsevier B.V. Open access under CC BY-NC-ND license.


1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 323
2. Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 325
2.1. Viral hypothesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 325
2.2. Immunological hypothesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 326
3. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 326
4. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 327
Take-home messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 327
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 327

1. Introduction nerve palsy may have a detectable cause (i.e. secondary facial nerve
palsy) or may be idiopathic (primary) without an obvious cause (i.e.
The most common causes of the abrupt onset of unilateral facial Bell's palsy) [2]. Secondary facial nerve palsy has a variety of causes
weakness are stroke and Bell's palsy [1]. Unilateral peripheral facial (Table a) and is generally less prevalent than Bell's palsy (25 vs. 75%)
[3]. Bell's palsy was first described by NA Friedreich in 1797 [4]. It is
Corresponding author at: Largo Valerio Bacigalupo 32 C, 00142 Rome, Italy. Tel.:
named after Sir Charles Bell (1774–1842), who described the
+39 03478404236. syndrome along with the anatomy and function of the facial nerve.
E-mail address: (GF. Macri).

1568-9972 © 2012 Elsevier B.V. Open access under CC BY-NC-ND

license. doi:10.1016/j.autrev.2012.05.008
324 A. Greco et al. / Autoimmunity Reviews 12 (2012) 323–328

Table a that carries taste sensation from the anterior two thirds of the tongue
Aetiologies of facial nerve palsy. through the chorda tympani nerve [10]. Parasympathetic fibres reach
From: Lorch M, Teach SJ. Facial nerve palsy: aetiology and approach to diagnosis and
the lacrimal glands via the greater superficial petrosal nerve, and they
treatment. Pediatric Emergency Care 2010; 26: 763–769.
reach the sublingual and submaxillary glands via the chorda tympani
Congential causes (Picture 1).
Birth trauma Genetic
Bell's palsy is diagnosed upon the abrupt onset of unilateral facial
Melkerson–Rosenthal syndrome Albers– weakness or complete paralysis of all the muscles on one side of the
Schönberg disease (osteopetrosis) face, dry eye, pain around the ear, an altered sense of taste,
Möbiuossyndrome hyperacusis (hypersensitivity to sounds), or decreased tearing [11]. In
Godenhar syndrome (oculoauriculovertebral dysplasia) patients with Bell's palsy, on attempted closure, the eye rolls upward
Acquired causes
Infections Lyme
(Bell's phenom-enon). The disease usually progresses from the onset
disease of symptoms to maximal weakness within three days.
Herpes simplex virus Various scoring systems are available to clinically assess the
Otitis media sever-ity of peripheral facial nerve palsy. The most widely applied is
Other (human herpesvirus type 6, mumps, coxsackie virus, adenovirus)
the House–Brackmann facial nerve grading system (HBS) (Table b).
Malignancy associated Approximately 10% of patients with Bell's palsy experience one or
Hypertension associated more recurrences after a mean latency of 10 years [12].
Idiopathic (Bell's palsy) The first step in diagnosis is to determine whether facial weakness
is due to a problem in the central nervous system or one in the pe-
Bell's palsy is an idiopathic peripheral nerve palsy involving the ripheral nervous system. Central nervous system lesions (e.g. multi-
facial nerve. It accounts for 60 to 75% of all cases of unilateral facial ple sclerosis, stroke, and tumour) can also cause facial nerve palsy.
paralysis [5]. The annual incidence is 15 to 30 cases per 100,000 However, some motor neurons to the forehead cross sides at the level
people [6]. of the brainstem, so the facial nerve fibres going to the forehead come
The peak incidence occurs between the second and fourth from both cerebral hemispheres. Supranuclear (central) lesions
decades (15 to 45 years) [7]. The median age at onset is 40 years, but affecting the facial nerve will not paralyse the forehead on the affect-ed
the dis-ease may occur at any age [8]. Different studies have reported side, resulting in a unilateral facial paralysis with forehead sparing.
either a slight female preponderance [7] or that women and men are Brain magnetic resonance imaging (MRI) is not routinely indicat-ed,
equally affected [9]. The prevalence is increased among pregnant but when it is performed, the most common abnormality ob-served is
women (43 cases per 100,000) [9]. contrast enhancement of the distal intracanalicular and labyrinthine
The facial nerve consists of a major motor component, which sup- segments of the facial nerve. The geniculate ganglion may also be
plies all the muscle of facial expression, and a small sensory branch involved [13].

Picture 1. Anatomy of facial nerve.

From: Gilden DH. Clinical practice. Bell's palsy. N Engl J Med 2004; 351: 1323–31.
A. Greco et al. / Autoimmunity Reviews 12 (2012) 323–328 325

Table b Associations with several infectious pathogens, such as cytomega-

House–Brackman scale grading. lovirus [21], Epstein–Barr virus [22], mumps [23], rubella [24] and
From: Rath B, Linder T, Cornblath D, et al. All that palsies is not Bell's — the need to de-fine
human immunodeficiency virus [25] have been documented. The an-
Bell's palsy as an adverse event following immunization. Vaccine 2007; 26: 1–14.
ecdotal reports do not unequivocally link these agents with the disor-
Grade 1 — normal (100% function; measurementa: 8/8) der [26]. However, for at least two infectious pathogens, the evidence
Normal facial function in all areas.
that they can and do indeed cause Bell's palsy is quite sound. These
Grade 2 — mild dysfunction (76–99% function; measurementa 7/8)
include Borrelia burgdorferi in Lyme disease [27] and zoster virus in
Slight weakness noticeable only on close inspection. At rest: normal symmetry of Ramsay-Hunt syndrome [28,29]. There are many reports on the asso-
forehead, ability to close eye with minimal effort and slight asymmetry. No ciation between facial paralysis and viral infections, for example,
synkinesis, contracture, or hemifacial spasm. Varicella zoster [30–32] and herpes simplex [17].
The herpes viruses are DNA viruses with the unique ability to es-
Grade 3 — moderate dysfunction (51–75% function; measurementa: 5/8–6/8)
Obvious but not disfiguring difference between two sides, no functional impairment; tablish latent infections in their hosts and cause recurrent disease by
noticeable but not severe synkinesis, contracture and/or hemifacial spasm. At reactivation. Of the human herpes viruses, herpes simplex viruses 1
rest: normal symmetry and tone. Motion: slight to no movement of forehead, (HSV-1) and 2 (HSV-2) and Varicella zoster virus are neurotropic;
ability to close eye with maximal effort and obvious asymmetry, ability to move
namely, they establish latent infections in the peripheral nervous sys-
corners of mouth with maximal effort and obvious asymmetry. Patients who have
obvious but not disfiguring synkinesis, contracture, and/or hemifacial spasm are tem, and the viral genome is maintained in the peripheral sensory
grade 3 regardless of degree of motor activity. ganglia for the entire life of the host [33]. These peripheral sensory
ganglia are the reservoir from which the neurotropic herpes viruses
Grade 4 — moderately severe dysfunction (26–50% function; measurementa: 3/8– can reactivate and cause neurological and mucocutaneous disorders.
4/8) Obvious weakness and/or disfiguring asymmetry. At rest: normal symmetry
The three neurotropic herpes viruses vary in their clinical presen-
and tone. Motion: no movement of forehead; inability to close eye completely with
maximal effort. Patients with synkinesis, mass action; and/or hamifacial spasm tation and differ in their molecular structure. However, they share
severe enough to interfere with function are grade 4 regardless of motor activity. several features that govern the biology of their infection of the human
nervous system: 1) The primary infection involves the muco-cutaneous
Grade 5 — severe dysfunction (1–25% function; measurementa: 1/8–2/8) surfaces, which serve as the portal of entry into the periph-eral nervous
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
system for the viral particles; 2) the primary and infectious recurrent
forehead, incomplete closure of eye and only slight movement of lid with maximal diseases caused by the same virus usually have the same cutaneous
effort, slight movement of corner of mouth. Synkinesis, contracture, and distribution; 3) under normal (i.e., immune com-petent) conditions, the
hemifacial spasm usually absent. reactivation infection usually does not spread beyond the anatomic
distribution and the vicinity of a single periph-eral sensory ganglion.
Grade 6 — total paralysis (0% function, measurementa: 0/8)
Loss of tone, asymmetry; no motion; no synkinesis, contracture, or hemifacial spasm.
a These features can be grouped under a unifying hypothesis that is
“Measurement” is determined by measuring the superior movement of the mid-
now the dogma in herpes virology [34,35]. Following the primary in-
portion 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 fection, the virus gains access to axon endings within the mucocuta-
and commissure movement. The points are then added together. Thus, a total of 8 neous surfaces and is transported to the peripheral sensory ganglia.
points can be obtained, if each structure moves 1 cm. The viral genome is maintained within the peripheral sensory ganglia,
which serve as reservoirs for viral nucleic acids. Latent herpetic infec-
Liston and Kleid [14] found histologic changes in the facial nerve tion is a lifelong state. Under certain circumstances, the virus can
that can be summarised as follows: 1) The nerve was infiltrated by reactivate and travel to regions innervated by the respective periph-
small, round inflammatory cells from the internal acoustic meatus to eral sensory ganglia, causing recurrent disease there.
the stylomastoid foramen. 2) There was a breakdown of the neuron In Ramsey-Hunt syndrome, the acute facial paralysis is accompa-
myelin sheaths that involved the macrophages. 3) There was an in- nied with zostiform vesicles in the ear [36,37]. Varicella zoster virus is
crease in the spaces between the neurons, which was interpreted as most likely also the causative agent of Bell's palsy in a subgroup of
oedema. 4) The bony fallopian canal was normal, and there was no patients who have no cutaneous abnormality, but have serological
sign of facial nerve compression by the bone of the fallopian canal. evidence of a Varicella zoster virus reactivation.
The small round cells of lymphocytic nature and the breakdown of More convincing is recent molecular data demonstrating Varicella
myelin sheaths probably are the histologic expression of an autoim- zoster virus nucleic acids in the auricular skin exudates [38] and in the
mune response. peripheral mononuclear cells of patients with Bell's palsy [39]. The
The disparity of the histologic descriptions in previously reported latter is in accordance with the identification of the Varicella zos-ter
cases of Bell's palsy is not surprising. Bell's palsy is a clinical syn- virus genome in the peripheral mononuclear cells of patients with
drome, and it is entirely possible that more than one disease entity can zoster sine herpete [40]. Thus, Bell's palsy in a subgroup of patients
produce an idiopathic facial palsy. In fact, some causes of facial could eventually also be designated as ‘zoster sine herpete’.
paralysis have only been recognised recently [14]. For example, Lyme In 1972, Mc Cormick hypothesised that the herpes simplex virus
disease [15] was first recognised as a cause of facial paralysis within (HSV) might be the causative agent of Bell's palsy [17]. The first sup-
the past few years. port for this hypothesis arrived twenty years later, with studies that
identified herpes simplex virus nucleic acids in the geniculate gangli-on
2. Aetiology [41,42].
Bell's palsy has been associated with serological evidence of an ac-
The aetiology of Bell's palsy is unknown, but viral infection and auto- tive HSV-1 infection. HSV-1 DNA was detected during decompression
immune disease have been postulated as possible pathomechanisms [16]. surgery in the endoneural fluids of the facial nerve in patients with id-
iopathic facial palsy [43].
2.1. Viral hypothesis When considering the possibility that HSV-1 is responsible for Bell's
palsy, several facts that do not favour this hypothesis should be
Several features of Bell's palsy may be characteristic of a viral in- mentioned: 1) In humans, HSV-1 resides latent in the peripheral
fection [17]. These include 1) epidemicity [18], 2) a flu-like prodrome sensory ganglia (PSG), although latency in the motor neurons has
[19], and 3) gadolinium enhancement of the facial nerve during the been documented experimentally [44], and its mucocutaneous rea-
acute phase of the disease on imaging of the geniculate ganglion [20]. ctivations are not associated with motor impairment. 2) While
326 A. Greco et al. / Autoimmunity Reviews 12 (2012) 323–328

asymptomatic reactivations of HSV-1 and 2, namely viral shedding role of viruses and immune responses in the etiopathogenesis of
without mucocutaneous disease, may take place [33], the opposite demy-elinating diseases of both the central and peripheral nervous
situation (‘herpes sine herpetica’ with neurological abnormality) has systems [61,62]. Viruses and immune mechanisms involvement have
never been documented. 3) HSV-1 causes recurrent reactivations, also been proposed in Bell's palsy, suggesting that it may be caused
which raises the question of why Bell's palsy is an isolated episode in by an autoim-mune postviral disease [47,63].
the overwhelming majority of cases. 4) The HSV-1 genome seems to A viral infection may be the etiologic cause of Bell's palsy and GBS.
be present in more trigeminal [45] than geniculate ganglia [41,42], but A viral infection may prompt an autoimmune reaction against a com-
by a factor less than the order of 1. This raises the ques-tion of why ponent of the peripheral nerve myelin, leading to the demyelination of
Bell's palsy is such a rare condition when compared to cold sores [46]. cranial nerves, especially the facial nerve, in a way that is not yet clear
An examination of the serum samples of patients with Bell's palsy
2.2. Immunological hypothesis shows elevated concentrations of the cytokines interleukin-1 (IL-1), IL-
6, and tumour necrosis factor-alpha (TNF-alpha) compared with
A cell-mediated autoimmune mechanism has been suggested as control populations [64], suggesting an activation of cell-mediated
the pathogenesis of Bell's palsy [47–49]. Aviel et al. conducted a clin- effectors.
ical study of adults and found some alterations in the lymphocyte Some authors [65] have proposed that a breakdown of peripheral
subsets of the peripheral blood during the acute stage of the disease tolerance occurred in patients with hepatitis C virus infection as a
[50]. consequence of interferon (IFN)-alpha therapy, which led to aug-
Following the description by Abramsky et al. of immune-mediated mented cell-mediated immune responses. Given that the majority of
mechanisms against the basic myelin protein in the disease's pathogen- cases of uncomplicated Bell's palsy recover fully, it may be that the
esis, cellular and humoural immunologic alterations have been reported in main lesion is not of the nerve itself, but of the myelin sheath and its
adult patients with Bell's palsy [51]. Decreased percentages of total T cells native cell, the Schwann cell. Further, the pharmacologic doses of IFN-
(CD3) and T helper/inducer cells (CD4) have been documented in the alpha used may cause a failure of peripheral tolerance by stimu-lating
acute phase of disease compared with control patients [52]. a pool of lymphocytes already sensitised to native Schwann cell
Some evidence implicates the involvement of immune mechanisms in membrane antigens, as described previously [47]. This failure of
Bell's palsy. Many reports have indicated the association between fa-cial tolerance occurs with induced autoimmune thyroid disease, which is
paralysis and Guillain–Barré syndrome (GBS) [53], a condition that was more common than Bell's palsy in IFN-alpha-treated patients [65].
recently shown to be a cell mediated, autoimmune neuritis [54]. The appearance of Bell's palsy in children after vaccination [66,67]
Abramsky et al. [47] demonstrated a defined in vitro response to a supports the immunological hypothesis. Intranasal administration of
human basic protein (P1L) of peripheral nerve myelin in patients with influenza vaccines may reduce the transmission of influenza more ef-
Bell's palsy. They suggested that cell-mediated autoimmune ficiently than parenteral administration because it stimulates both
mechanisms may be of importance in the pathogenesis of Bell's palsy. mucosal and systemic immune responses [68]. Over a seven-month
Approximately the same in vitro transformation in the presence of period, the Swiss Drugs Monitoring Centre received 46 case reports of
P1L protein was found in cases with GBS [55]. The specific in vitro Bell's palsy among flu vaccine recipients. The risk of Bell's palsy was
stimulation of lymphocytes from Bell's palsy and GBS patients using highest during the second month after intranasal vaccination
peripheral P1L basic protein suggests that an in vivo sensitisation to suggesting an immunological mechanism [69].
such self protein may occur in these two conditions, and that
cell-mediated autoimmune mechanisms may be an important factor in
the pathogenesis of the paralysis. 3. Treatment
The similarities between GBS and Bell's palsy with regard to the
lymphocyte sensitisation to the same P1L protein suggest that Bell's Any evaluation must consider that 71% of untreated patients re-
palsy may be a variant of GBS. cover completely, and 84% achieve near-normal function [70]. Thus,
The percentage of T lymphocytes was reduced in Bell's palsy patients the 20 to 30% who do not recover fully remain the focus of treatment.
[56], and a reduction in the percentage of total T lymphocytes has also In the past, the efficiency of prednisone in alleviating the disease
been found in patients with acute Guillain–Barré syndrome [57]. [71] has been attributed to its ability to reduce inflammation and oede-
In Bell's palsy patients, the percentage of T suppressor cells was ma. However, it seems logical that steroids in fact exert their beneficial
significantly reduced, whereas the percentage of T helper cells was effect by means of immunosuppressive action, as in the case of some
normal [56]. This is in line with the findings in patients with acute other autoimmune disorders [72]. Therefore, it seems warranted to
Guillain–Barré syndrome [58]. rec-ommend the prednisone for patients with Bell's palsy based on
Aviel et al. found that Bell's palsy patients had a significant in- findings concerning the autoimmune aspects of this disease's
crease in the percentage of B lymphocytes and a significant decrease pathogenesis. Meta-analyses have compared glucocorticoids with
in the percentage of T lymphocytes [50]. Most suggestive is the fact placebo. One such analysis showed significant improvement of facial
that similar changes in peripheral blood lymphocyte subpopulations weakness with glu-cocorticoid therapy [73].
were also described in the course of several demyelinating diseases, According to viral theory, one randomised trial with no placebo
such as in acute exacerbations of multiple sclerosis and during the group compared oral prednisone with acyclovir. This study indicated
acute stage of Guillain–Barré syndrome [49,57,59]. that facial-muscle strength was better after treatment with predni-sone
Bell's palsy, like Guillain–Barré syndrome, is an acute than it was after treatment with acyclovir [74].
demyelinating disease of the peripheral nervous system. In both Although a 2004 Cochrane review found insufficient evidence to
diseases, an inflam-matory demyelination neuritis has been found. The support the use of these antivirals alone [75], two recent placebo-
immunological sim-ilarities between Bell's palsy and Guillain–Barré controlled trials demonstrated full recovery in a higher percentage of
syndrome suggest that the diseases may share a similar aetiology and patients treated with an antiviral drug in combination with predniso-
pathogenesis [50]. In most cases, Bell's palsy is a mononeuritic variant lone than with prednisolone alone [76].
of Guillain–Barré syn-drome [60]. Prednisone is typically prescribed in a 10-day tapering course,
It has also been proposed that Bell's palsy is in fact a polyneuropathy, starting at 60 mg per day. Acyclovir 400 mg can be given five times
as the facial paralysis may be associated with involvement of other cra-nial per day for seven days, and valacyclovir 1 g can be given three times
nerves [5]. Recent decades were rich with studies concerning the per day for seven days.
A. Greco et al. / Autoimmunity Reviews 12 (2012) 323–328 327

Monoclonal antibodies represent the almost faster growing class of • Due to this disease's possible viral or autoimmune pathogenesis, a
therapeutics in autoimmunity. They offer the possibility to specifi-cally combination therapy of antivirals and oral corticosteroids should be
target immunologically relevant molecules which appear critical in the administered. It is to be hoped that (monoclonal) antibodies and/or T-
pathogenesis of peripheral nervous system autoimmune dis-eases, cell immunotherapy might provide more specific treatment guide-
like Bell's palsy. Based on theoretical grounds such approaches lines in the management of Bell's palsy. The role of surgical decom-
appear very promising, however, the side effect profile of these drugs, pression remains controversial, and it is not currently recommended
especially in long-term use, is not completely understood. As we because of its potential for harm and the paucity of data supporting
learned from the natalizumab trial in multiple sclerosis, severe com- its benefits.
plications or worsening of symptoms, can occur after therapy has been
initiated [77,78].
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Terjemahan :

Tujuan: Untuk meninjau pengetahuan kita saat ini
etiopatogenesis dari Bell palsy, termasuk infeksi
virus atau autoimunitas, dan mendiskusikan
patogenesis penyakit sehubungan dengan
Tinjauan sistematik metodologi: publikasi yang
relevan pada etiopatogenesis, presentasi klinis,
Diagno-sis dan histopatologi dari Bell palsy 1975-
2012 dianalisis.
Hasil dan kesimpulan : Bell palsy adalah
kelumpuhan saraf perifer idiopatik yang melibatkan
saraf wajah . Ini ac - jumlah untuk 60 sampai 75 %
dari semua kasus kelumpuhan wajah unilateral .
Kejadian tahunan Bell palsy adalah 15 sampai 30
per 100.000 orang . Insiden puncak terjadi antara
dekade kedua dan keempat ( 15 sampai 45 tahun ) .
Etiologi Bell palsy tidak diketahui tetapi infeksi
virus atau penyakit autoimun telah didalilkan
mungkin pathomechanisms . Bell palsy bisa
disebabkan ketika virus herpes laten ( herpes
simpleks , herpes zoster ) yang diaktifkan dari
kranial ganglia saraf . Mekanisme autoimun sel -
dimediasi terhadap protein dasar mielin telah
disarankan untuk patogenesis Bell palsy . Bell palsy
mungkin merupakan de - myelinating neuritis
tengkorak autoimun , dan dalam kebanyakan kasus ,
itu adalah varian mononeuritic sindrom Guillain -
Barré , gangguan neurologis dengan imunitas
seluler diakui terhadap antigen mielin saraf perifer .
Di Bell palsy dan GBS , infeksi virus atau reaktivasi
virus laten dapat menimbulkan autoimun reaksi
yang - tion terhadap perifer komponen mielin saraf ,
menyebabkan demielinasi saraf kranial , terutama
saraf wajah .
Mengingat profil keamanan acyclovir , valacyclovir
, dan jangka pendek kortikosteroid oral , pasien
yang datang dalam waktu tiga hari dari timbulnya
gejala harus ditawarkan terapi kombinasi . Namun
tampaknya logis bahwa sebenarnya , steroid
mengerahkan efek menguntungkan mereka melalui
tindakan imunosupresif , seperti yang terjadi di
beberapa gangguan autoimun lainnya . Itu harus
berharap bahwa ( monoklonal ) antibodi dan / atau
imunoterapi T - sel mungkin memberikan pedoman
pengobatan yang lebih spesifik dalam pengelolaan
Bell palsy