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Bell's palsy: Aetiology, clinical features and multidisciplinary care

Article  in  Journal of Neurology, Neurosurgery, and Psychiatry · April 2015

DOI: 10.1136/jnnp-2014-309563 · Source: PubMed

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General neurology
1
Prince of Wales Clinical
School, University of NSW,
Sydney, New South Wales,
Australia
2
Department of
Otolaryngology, Royal Prince
Alfred Hospital, Sydney,
New South Wales, Australia
3
Department of Neurology,
Glasgow University, Southern
General Hospital, Glasgow, UK
4
Massachusetts Eye and Ear
Infirmary and Harvard Medical
School, Boston, Massachusetts,
USA
Correspondence to
Dr Arun Krishnan, Prince of
Wales Clinical School,
University of New South Wales,
Randwick, NSW 2031,
Australia;
Arun.Krishnan@unsw.edu.au
Received 23 December 2014
Revised 19 February 2015
Accepted 18 March 2015
Published Online First
9 April 2015
To cite: Eviston TJ,
Croxson GR, Kennedy PGE,
et al. J Neurol Neurosurg
Psychiatry 2015;86:
1356–1361.
1356
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REVIEW
Bell’s palsy: aetiology, clinical features
and multidisciplinary care
Timothy J Eviston,1 Glen R Croxson,2 Peter G E Kennedy,3 Tessa Hadlock,4
Arun V Krishnan1
ABSTRACT
Bell’s palsy is a common cranial neuropathy causing
acute unilateral lower motor neuron facial paralysis.
Immune, infective and ischaemic mechanisms are all
potential contributors to the development of Bell’s palsy,
but the precise cause remains unclear. Advancements in
the understanding of intra-axonal signal molecules and
the molecular mechanisms underpinning Wallerian
degeneration may further delineate its pathogenesis
along with in vitro studies of virus–axon interactions.
Recently published guidelines for the acute treatment of
Bell’s palsy advocate for steroid monotherapy, although
controversy exists over whether combined corticosteroids
and antivirals may possibly have a beneficial role in
select cases of severe Bell’s palsy. For those with
longstanding sequaelae from incomplete recovery,
aesthetic, functional (nasal patency, eye closure, speech
and swallowing) and psychological considerations need
to be addressed by the treating team. Increasingly,
multidisciplinary collaboration between interested
clinicians from a wide variety of subspecialties has
proven effective. A patient centred approach utilising
physiotherapy, targeted botulinum toxin injection and
selective surgical intervention has reduced the burden of
long-term disability in facial palsy.
INTRODUCTION
Bell’s palsy is an acute-onset peripheral facial neur-
opathy and is the most common cause of lower
motor neuron facial palsy.1 The clinical presentation
of the disorder is a rapid onset, unilateral, lower
motor neuron-type facial weakness with accom-
panying symptoms of postauricular pain, dysgeusia,
subjective change in facial sensation and hyperacu-
sis. This clinical presentation can be explained by
the anatomical construct of the human facial nerve,
specifically its mixed nerve profile containing
motor, sensory and parasympathetic fibres. The pro-
pensity for the facial nerve to form numerous con-
nections with adjacent cranial nerves2 may also
explain the occasionally observed features of altered
facial sensation (cranial nerve V), vestibular dysfunc-
tion (cranial nerve VIII) or pharyngeal symptoms
(cranial nerves IX and X).3 Reduced lacrimation and
salivation secondary to parasympathetic effects may
also occur.3 Maximal disability occurs within the
first 48–72 h and the severity of the palsy correlates
with the duration of facial dysfunction, the extent of
facial recovery and impairment of quality of life.
Despite extensive study of the condition, the exact
pathogenesis of Bell’s palsy is still controversial.4
Infection (herpes simplex type-1),5 nerve
Eviston TJ, et al. J Neurol Neurosurg Psychiatry 2015;86:1356–1361. doi:10.1136/jnnp-2014-309563
compression6 and autoimmunity7 may all play a role,
yet the exact sequence and magnitude of these influ-
ences remains unclear.
Anatomy
The human facial nerve is the seventh cranial nerve
(CNVII) and comprises motor, sensory and para-
sympathetic components. Its function is responsible
for voluntary and mimetic facial movement, taste to
the anterior two-thirds of the tongue, and control
of salivary gland and lacrimal gland secretions.
The facial nerve receives axons from the superior
part of the solitary nucleus and superior salivary
nucleus that form the nervus intermedius compo-
nent (sensory and parasympathetic axons) and
motor efferent fibres from the facial nucleus, which
receives synaptic input from the contralateral
motor cortex for all facial movements except the
forehead, which has bicortical input.
The path of the facial nerve has intracranial, intra-
temporal and extratemporal components. Its intra-
cranial course runs from the pontomedullary angle
to the internal acoustic meatus where it is accom-
panied by the vestibulocochlear nerve (CNVIII).
The intratemporal course of the facial nerve is long
and tortuous. During its intratemporal course, the
nerve encounters the geniculate ganglion and gives
rise to the superior petrosal nerve, the nerve to sta-
pedius and chorda tympani nerve branches, before
exiting the skull base through the styloid foramen.
The extratemporal facial nerve courses through the
substance of parotid gland dividing it into deep and
superficial lobes. It gives off the posterior auricular
nerve and nerve to the posterior belly of digastric
before dividing into its terminal facial branches.
There is significant variation in the branching
pattern of the terminal facial branches, which are
traditionally conceptualised into temporal, zygo-
matic, buccal, marginal mandibular and cervical
branches. These terminal motor branches are
responsible for all facial expression and functional
tasks such as eye and mouth closure and nasal
patency during inspiration. Throughout its course,
the facial nerve forms multiple communications
between its own branches and with adjacent cranial
nerves.2
HISTORY
Sir Charles Bell (1774–1842) was fascinated by the
nervous system. As an accomplished anatomist,
artist, surgeon and teacher, his work on the charac-
terisation of the peripheral nervous system through
anatomical study, vivisection and clinical
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correlation, provided a significant contribution to medical
knowledge of his time. In particular, he was fascinated with the
separation of sensory (trigeminal nerve) and motor supply
(facial nerve) to the face. It was his eloquent and logical descrip-
tions that elevated his status among his contemporaries and
ushered the ‘post-Bell’s’ era, which saw a rapid increase in the
number of publications relating to acute idiopathic facial palsy
—‘Bell’s palsy’.
Although Bell’s descriptions were admirable in their ability to
inspire his contemporaries to document and study the disorder,
myriad other detailed descriptions exist in Greek, Persian and
European medical texts as far back as the fifth century BCE,8
and there is prehistoric ceramic art depicting facial palsy identi-
fied in ancient Peruvian culture.9 Other clinicians who recog-
nised the entity of acute idiopathic facial paralysis before Bell
(and perhaps may have inspired some of his observations)
include Sydenham, Stalpart van der Wiel, Douglas, Friedreich
and Thomassen á Thuessink.8
Approximately 1000 years before Bell, the Persian physician
and scholar, Razi (865–925 CE), described facial palsy at length
in his seminal ninth century text ‘al-Hawi’.8 This remarkable
description referenced the contributions of Galen and Celsus,
among others, and included a diagnostic algorithm delineating
peripheral facial palsy from more sinister central causes, which
were accompanied by delirium, coma, hemiplegia, blindness, or
deafness, and tended to have a poor prognosis.
EPIDEMIOLOGY
Bell’s palsy is a common cranial mononeuropathy. It affects
males and females equally, and has a slightly higher incidence in
mid and later life, but certainly occurs across all age ranges. The
described population incidence rates range from 11.5 to 40.2/
100 00010 with specific studies demonstrating similar annual
incidences between the UK (20.2/100 000), Japan (30/100 000)
and the USA 25–30/100 000.10 Clustering and epidemic phe-
nomena are not demonstrated in the majority of studies. An
exception to this is the recent occurrence of an increase in inci-
dence of Bell’s palsy during a trial of intranasal vaccine delivery.
This was possibly due to the immune effects of the detoxified
Escherichia coli heat labile toxin adjuvant used in this form of
vaccine delivery.11 The incidence is higher in pregnancy, follow-
ing viral upper respiratory tract infection, in the immunocom-
promised setting, and with diabetes mellitus and hypertension.1
There is no distinct latitudinal variation for incidence, nor is
there a racial or ethnic predilection. Some epidemiological data
demonstrate seasonal variation, with a slightly higher incidence
in cold months versus warm months,10 and a slight preponder-
ance to arid over non-arid climates.12
AETIOLOGY
There is a diverse body of evidence implicating immune, infect-
ive and ischaemic mechanisms as potential contributors to the
development of Bell’s palsy, but the cause of classical Bell’s palsy
remains unclear. One possible cause that has been suggested is
that of a reactivated herpes simplex virus (HSV-1) infection
centred around the geniculate ganglion, a theory first outlined
by McCormick.5 The association with HSV-1 is supported by
the presence of HSV-1 in intratemporal facial nerve endoneural
fluid13 harvested during nerve decompression, and the ability to
incite facial palsy in an animal model through primary infec-
tion14 and reactivation induced by immune modulation.15
Despite this evidence, the behaviour of Bell’s palsy is unusual
compared with other diseases more commonly caused by HSV,
such as herpes labialis (cold sores) and genital herpes.4 Further,
Eviston TJ, et al. J Neurol Neurosurg Psychiatry 2015;86:1356–1361. doi:10.1136/jnnp-2014-309563
General neurology
it is not justifiable to assume a cause and effect relationship
between the presence of HSV-1 in the patients’ endoneural fluid
and the development of Bell’s palsy.
HSV-1 is one of several human herpes viruses known to have
a neurotrophic capacity for peripheral nerves, and other viruses
in this category include herpes simplex virus type 2 (HSV-2)
and varicella zoster virus (VZV). They enter the body through
mucocutaneous exposure and establish their presence in latent
form with highly restricted gene transcription in multiple
ganglia throughout the neuroaxis for the entire life of the host,
including in the cranial, dorsal root and autonomic ganglia.16 17
This latent presence in ganglia in the absence of active viral rep-
lication and assembly is characteristic, well described, and
widely distributed through normal and diseased populations.
HSV has a global distribution and is a fundamentally resilient
virus. HSV and VZV can both reactivate in an immunocompe-
tent host, and in the presence of circulating antibodies, although
reactivation is more likely in the setting of immunodeficiency,
especially in the case of VZV.
A possible cause of neural dysfunction due to HSV-1 is the acti-
vation of intra-axonal degradation and apoptotic pathways
driven by local direct and indirect responses of the axon to the
virus itself in a susceptible phenotype. Although not previously
associated specifically with the pathogenesis of Bell’s palsy, the
emergence of literature pertaining to the role of intra-axonal
signal molecules (eg, SARM1),18 mitochondrial permeabilisa-
tion19 and the molecular mechanisms underpinning Wallerian
degeneration,18 suggests that acute axonal degeneration in the
context of viral infection may be an evolutionarily conserved
innate immune response to prevent virus transport to the central
nervous system.19
Recent in vitro work has demonstrated local messenger RNA
transcription in peripheral nerve axons20 incited by the presence
of α-herpes virus particles. In this compartmentalised model,
protein and signal transduction changes were not reliant on
nuclear machinery, that is, when a virus enters an axon, the
axon responds locally. Earlier work examining cellular physi-
ology in the setting of herpes infection demonstrated an acute
decrease in sodium conductivity in the setting of HSV-1.21
Changes in sodium conductance can result in a reversed sodium-
calcium exchange (NCX)22 current and the accumulation of
intracellular calcium. This aberration in calcium homoeostasis
leads to protease activation and intra-axonal degeneration.
These processes of axonal degeneration would drive the abrupt
onset of Bell’s palsy and explain the lack of a pronounced
immune response. This would not necessarily discount the role
of compression to the pathogenesis but, rather, may answer the
question as to why the nerve swells, leading to impingement, in
the first place.
Another possible contributor to the pathogenesis of Bell’s palsy
implicates the role of a cell-mediated immune response against
myelin, akin to a mononeuropathic form of Guillain-Barré syn-
drome (GBS). The evidence for this stems from the indirect labora-
tory finding of GBS, such as changes in peripheral blood
percentages of T and B lymphocytes, elevated chemokine concen-
trations and in vitro reactivity to myelin protein (P1L) in blood
samples taken from patients with Bell’s palsy.7
DIAGNOSIS
Bell’s palsy is a clinical diagnosis. The characteristic findings are
acute onset of unilateral lower motor neuron facial paralysis that
affects muscles of the upper as well as lower face and reaches its
peak by 72 h. These findings are frequently accompanied by
symptoms of neck, mastoid or ear pain, dysgeusia, hyperacusis
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General neurology
or altered facial sensation. These associated symptoms are
present in 50–60%23 and are reassuring for the diagnosis of
Bell’s palsy.
The involvement of posterior auricular, petrosal, chorda
tympani and stapedius nerves implicates the site of dysfunction
being within the temporal bone. Localisation to the intratem-
poral facial nerve is further supported by unilateral enhance-
ment of the geniculate, labyrinthine and meatal segments of
the facial nerve on contrast-enhanced MRI studies. This imaging
finding is hypothesised to represent disruption of the blood–
brain barrier and vascular congestion of the facial nerve.
Attempts to determine surrogate diagnosis through PCR
techniques with VZV and HSV primers applied to posterior aur-
icular, tear or facial muscle specimens have failed to demon-
strate any consistent correlation between viral load and clinical
features.24 These tests are therefore of limited value as diagnos-
tic tools.
Differential diagnosis
The differential diagnosis for facial palsy is broad,25 and misdiag-
nosis is not uncommon. Causes of facial palsy may be divided
into congenital and acquired aetiologies. Congenital causes
include genetic syndromes, birth-related trauma and isolated dis-
orders of development (eg, developmental hypoplasia of facial
muscles). Acquired causes include infective (VZV, Lyme disease,
mycobacterium tuberculosis, HIV), traumatic (iatrogenic or head
trauma), inflammatory (vasculitis, sarcoidosis, autoimmune
disease), neoplastic (benign or malignant) and cerebrovascular
causes, among others. In the experience of one of the authors
(GC) in an expert referral setting, the rate of misdiagnosis of
Bell’s palsy by the initial consulting clinician is 10.8%.26 Missed
diagnoses include tumours (eg, facial nerve schwannoma, parotid
malignancy and, rarely, acoustic neuroma), herpes zoster oticus
and granulomatous diseases such as sarcoidosis and granulomato-
sis with polyangiitis (Wegener’s granulomatosis).
A structured clinical approach that considers the pattern of
facial palsy (figure 1) along with patient characteristics and a
Figure 1 Patterns of facial palsy.
1358 Eviston TJ, et al. J Neurol Neurosurg Psychiatry 2015;86:1356–1361. doi:10.1136/jnnp-2014-309563
thorough physical examination will generally provide evidence
for an alternative diagnosis, and prompt appropriate investiga-
tion.25 Particular patterns of facial palsy that require thoughtful
consideration include: (1) fluctuant, step-wise or slowly progres-
sive (beyond 72 h), facial palsy; (2) bilateral palsy (GBS, carcin-
omatosis, lymphoma); (3) recurrent facial palsy (facial nerve
neuroma); (4) prolonged complete palsy (>4 months) and (5)
sudden complete facial palsy (haemorrhage into a tumour).
These patterns should prompt a detailed search for an under-
lying cause. Likewise, the presence of a mass in the parotid
region, a history of cutaneous malignancy or segmental facial
nerve weakness should raise suspicion for a tumour. A history of
trauma, ear symptoms such as ipsilateral deafness, tinnitus, full-
ness or discharge, or systemic symptoms such as fever, are also
red flags warranting further investigation and specialist oto-
logical consultation.
The consideration of cerebrovascular disease as a cause of
facial palsy is important with this being the main concern for
many patients and clinicians, often prompting expert neurology
consultation. The preservation of upper facial movement (fron-
talis contraction) is a discriminator between cortical (central)
and peripheral facial nerve weakness. Rarely, ipsilateral pontine
pathology may result in lower motor neuron pattern facial
weakness due to direct compromise of the facial nucleus. This
will be accompanied by other cranial nerve, and long tract
symptoms and signs. Ipsilateral abducens nerve (CNVI) dysfunc-
tion (lateral gaze palsy) is a particularly useful sign.
Grading
The most widely used systems for recording the severity of
Bell’s palsy are the House-Brackmann27 (HB) scale or the Facial
Nerve Grading Scale28 (also known as the Sunnybrook system).
The subjective nature of these scales makes them prone to some
misinterpretation and interobserver variability; however, their
ease of use has cemented their role in clinical practice for com-
municating the overall degree of dysfunction, for monitoring
outcomes and for the presentation of group data in a research
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or audit setting. In a recent survey of facial nerve specialists,29
photography and videography were ubiquitous among respon-
dents and, indeed, the use and importance of video recording
of standardised facial movements (eyebrow raise, gentle eye
closure, tight eye closure, snarl, open and closed lip smiles, lip
depression and lip puckering) is emphasised for the accurate
outcome assessment of interventions such as chemodenervation,
physiotherapy or surgery, which may be considered in those
patients who have an incomplete recovery.
Neurophysiology
There have been a number of studies exploring the potential
utility of neurophysiological assessment for treatment selection
and prognosis. In the past, nerve conduction studies of the
facial nerve, also referred to as electroneuronography (ENoG)
in the surgical literature, have been suggested in some studies to
be useful in the selection of patients who may require surgical
decompression of the facial nerve. The demonstration of a
greater than 90% reduction in compound muscle action poten-
tial in the first 10 days of onset compared with the unaffected
side is associated with a 50% chance of incomplete recovery6
and was a trigger for operative intervention in some centres.
In contemporary practice, facial nerve decompression has
increasingly fallen out of the normal domain due to cost, risk
and lack of efficacy.30 With this trend away from surgery, the
time and cost of neurophysiology assessment outweighs the
benefit for the vast majority of patients. An exception to this is
the clinical setting of complete paralysis. Here, neurophysiology
provides useful information with the presence of a residual
response on neurophysiology suggesting a predominantly neuro-
praxic injury, in which case the prospect of a good recovery
(HB I or II) is high. The absence of a neurophysiological
response is suggestive of complete degeneration and a prolonged
paralysis with incomplete recovery that may be complicated by
synkinesis. The knowledge of a prolonged recovery may sway
the clinician and patient towards surgical eye protection proce-
dures and the proactive involvement of a facial therapist early in
the course of recovery.
TREATMENT
Acute treatment
The American Academy of Neurology31 (AAN) and the
American Academy of Otolaryngology—Head and Neck Surgery
Foundation30 (AAO-HNSF) have recently published guidelines
for the treatment of Bell’s palsy. Although the structure and
scope of these guidelines are different, they are essentially com-
plementary documents that reinforce the role of corticosteroids
in the treatment of Bell’s palsy and argue against the routine use
of antiviral therapy. Furthermore, the AAO-HNSF guidelines dis-
courage routine laboratory, imaging or neurophysiological testing
at the first presentation of typical Bell’s palsy. The dose of oral
steroids should be started in the first 72 h of onset and a regime
mirroring either of the Scottish32 or European33 randomised
controlled trials (RCTs) should be used. This is either 50 mg
prednisone for 10 days or 60 mg for the first 5 days, then
reducing by 10 mg each day for the next 5 days. Both seem
effective.34 It has been argued that the lack of significance
demonstrated by combined corticosteroid and antiviral therapy
over corticosteroids alone in double-blind RCTs represents a dilu-
tion effect of mild and moderate palsies, which have a high rate
of spontaneous recovery, masking any demonstrable benefit for
the severe palsy subgroup. Supporting this are the positive find-
ings in favour of combined therapy in non-double-blinded
studies.35 36
Eviston TJ, et al. J Neurol Neurosurg Psychiatry 2015;86:1356–1361. doi:10.1136/jnnp-2014-309563
General neurology
The key rationale for giving patients with Bell’s palsy antiviral
treatment with the antiherpes drug acyclovir is the possible role
of HSV-1, based on the current circumstantial evidence.
Another reason given for using antiviral therapy in the setting
of clinical equipoise is that a portion of those given a provi-
sional diagnosis of Bell’s palsy will have zoster sine herpete, that
is, symptomatic VZV reactivation without the typical vesicular
eruption pathognomonic of a typical VZV infection (Ramsay-
Hunt syndrome).
VZV is an important differential diagnosis in all acute lower
motor neuron facial palsies. Ramsay-Hunt syndrome has a
worse prognosis than Bell’s palsy and, on average, presents as a
more severe palsy. It is more responsive to combined antiviral
and steroid therapy, and the rate of complications from antiviral
therapy is low. Since VZV is known to cause facial palsy, the use
of antivirals in Ramsay-Hunt syndrome has a clear evidence
base, and is justified and rational.4 A typical regime to
adequately cover VZV would be 3000 mg/day (1000 mg valacy-
clovir three times a day) for 7 days. Valacyclovir has a higher
bioavailability than acyclovir.
At the present the use of combined acyclovir and corticoster-
oids in treating classical Bell’s palsy remains controversial, with
conflicting data emerging from different trials and, indeed, from
different meta-analyses.4 Based on current evidence, particularly
the extensive Scottish Bell’s palsy study32 of 551 patients in a
double-blind, placebo-controlled, randomised study, it seems
reasonable to treat classic Bell’s palsy with oral corticosteroids
alone, without acyclovir. However, combined acyclovir and cor-
ticosteroids may possibly have a beneficial role in cases of severe
Bell’s palsy, and this issue needs to be resolved in a large pro-
spective clinical trial. In cases where the patient is severely
immunocompromised, consideration may be given to intraven-
ous regimes of acyclovir to prevent possible central nervous
system complications.
Eye care
The institution of an eye protection strategy for each patient
with incomplete closure is of paramount importance.
Lacrimation occurs at the lateral aspect of the conjunctival
membrane and is swept lateral to medial as a film by the action
of the orbicularis oculi during blink and effective eye closure.
Loss of this mechanism results in epiphora (tearing) due to an
ineffective pump mechanism to spread the tear film, and expos-
ure and irritation of the eye itself. Prolonged drying and irrita-
tion will progress to keratitis and ulceration, and eventually can
threaten sight. At the first consultation, the clinician must enact
a strategy to avoid ocular exposure, and refer any cases of
concern to an ophthalmologist. Effective eye protection uses
barrier protection (eg, wrapped sunglasses), lubrication (artificial
tears during the day, ointment at night) and taped closure at
night. Particular environments that may present a challenge for
the patient include showering and swimming, and dusty and
windy environments; these situations are best avoided.
The early use of an eyelid weight should be considered in the
elderly, those with diabetes, with pre-existing eye disease, com-
plete facial palsy with no response on neurophysiology and the
presence of ongoing irritation despite the use of the eye-
protective therapies described above.25
Oral care
Loss of the sphincter function of the orbicularis oris confers the
social inconvenience of oral incontinence and predisposes the
lip and inner cheek to abrasion during mastication and subse-
quent ulceration. Strategic eating may lessen the impact of these
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General neurology
in the setting of flaccid facial paralysis. Using a straw for liquids
and tending towards soft foods are often helpful. The inability
to lower and evert the lower lip precludes eating certain foods.
Temporary dental ‘spacers’ adhered to the lateral aspect of the
molar teeth may be used to prevent chewing of the buccal
mucosa.
Physiotherapy
From an evidence-based perspective, this diverse modality of
treatment, which broadly encompasses heat therapy, electrosti-
mulation, massage, mime therapy and biofeedback,30 is hard to
analyse as a whole. There is a plethora of treatment regimes, and
their timing and variability in implementation make their
broader assessment of utility complex. Although not recom-
mended for all suffers of Bell’s palsy,30 there are subgroups of
patients for whom there is evidence supporting the use of physio-
therapy.37 These include patients who have incomplete recovery
and who have developed hypertonia, hyperkinesis or synkinesis,
and in these groups neuromuscular retraining is trialled before
consideration of chemodenervation.38 Physiotherapy and chemo-
denervation are complementary in the treatment of synkinesis.
Prognosis
Natural history studies have demonstrated that ∼85% of patients
experience some recovery in the first 3 weeks.1 Predictors of
incomplete recovery include severe facial palsy, the length of
time prior to onset of recovery, and persistent pain. Patients
with complete facial palsy (House-Brackman grades 5–6) who
have not experienced some recovery in the first 3–4 months
after onset are more likely to have incomplete recovery of facial
function, with or without spasm and synkinesis. Prolonged pain
is also a predictor of worse outcome.
The natural history of Bell’s palsy has been elucidated
through a number of large studies.1 3 25 Based on conclusions
drawn from these large studies, clinicians can expect that
without intervention, approximately 70% of patients will
experience full recovery. Of those who do not recover fully, half
will have mild sequelae, and the remainder moderate-to-severe
Figure 2 Botulinum toxin injection
sites for the treatment of synkinesis.
Blue (affected side) and green
(unaffected side) dots represent
planned point of injection for 1.5–3 IU
of onabotulinum A. The preapplication
of topical local anaesthetic cream and
the use of a fine bore needle size
(25–30 gauge) are used to reduce the
pain of injection. Subcutaneous
injection is as effective as
intramuscular.
1360 Eviston TJ, et al. J Neurol Neurosurg Psychiatry 2015;86:1356–1361. doi:10.1136/jnnp-2014-309563
sequelae. In the setting of acute steroid use the rate of full
recovery is over 90%.32
Managing incomplete recovery
Chronic facial palsy is a disabling condition that has a dramatic
impact on social function, emotional expression and quality of
life. Aesthetic, functional (nasal patency, eye closure, speech and
swallowing) and psychological considerations need to be
addressed by the treating team. Over the last three decades, the
treatment of incomplete recovery of facial palsy has evolved
from static techniques aimed at suspension of the oral commis-
sure and eye closure, into a multimodal,38 zonal-based approach
that utilises the complementary aspects of physiotherapy, che-
modenervation and selective surgical procedures to maximise
the cosmetic and functional outcome needs of each patient.
Increasingly, multidisciplinary collaboration between interested
clinicians from a wide variety of subspecialties has proven
effective.
In outlining treatment modalities and their appropriateness,
one must consider incomplete recovery of facial function as a
heterogeneous entity that encompasses different degrees of flac-
cidity, hypertonicity and synkinesis. Each of these issues can
range in severity from absent to severe. Generally, functional
issues such as brow ptosis, nasal valvular collapse and eye
closure, are addressed through directed structural interventions
including nasal valvular suspension, brow ptosis correction, plat-
inum weight insertion into the upper eyelid, lower lid suspen-
sion or tarsorrhaphy to improve eye closure.
Synkinesis
Synkinesis refers to abnormal facial muscular contraction during
voluntary facial movements and has been traditionally attributed
to aberrant re-innervation of facial musculature following nerve
injury. It can be seen as involuntary eye-closure during midface
movement such as eating or smiling (oro-ocular synkinesis); as
lip excursion during eye closure (oculo-oral synkinesis); or as
chin dimpling or muscular neck cords during midface move-
ment due to involuntary mentalis or platysma activation. The
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treatment of synkinesis centres around physiotherapy, with a 12
particular focus on biofeedback exercises to retrain facial sym-
metry, and selective chemodenervation using directed botulinum 13
toxin to problem areas (figure 2). Most patients express a high
degree of satisfaction with this approach, and objective improve-
ment is seen in the majority.38 14
Treatment of synkinesis with botulinum toxin is tailored
according to the individual patient. Injection points focused on 15
orbicularis occuli and platysma relieve spasm and synkinesis
while selective use of contralateral (unaffected side) brow and
depressor angularis oris injection points enhances facial sym- 16
metry and cosmesis. Injection of the weak/synkinetic zygomati- 17
cus muscles is best avoided due to the debilitating effect of
losing smile function from an already weakened face. Some 18
patients have a reduced benefit with repeated injections while
19
for others the requirement for recurrent injections three to four
times per year is unsatisfactory. In selected cases, a more per- 20
manent solution can be achieved through surgical interventions
such as selective myectomy. Recently, selective neurectomy has
also proven to be very effective.39 21
Facial reanimation 22
In the setting of incomplete recovery with ineffective smile,
nerve-to-nerve transfer, and regional and free tissue transfer
23
techniques offer the opportunity to restore midface movement.
A regional tendon transfer technique that relocates the tempor- 24
alis muscle tendon to the oral commissure has been popularised
by the French surgeon, Labbe.40 Alternatively, innervated free
muscle transfer techniques that utilise the gracilis muscle can be 25
inserted into the face with nerve coaptation from the contralat- 26
eral facial nerve and/or from the ipsilateral mandibular branch
of the trigeminal nerve. Nerve-to-nerve transfers are also
becoming increasingly popular for those with autopreservation 27
of facial musculature but a frozen oral commissure. Donor
28
nerves include the masseteric branch of the trigeminal nerve,
and cross face nerve grafting. These complex reconstructive pro- 29
cedures offer an opportunity for smile reanimation, and the sub-
sequent benefits in social function and quality of life.
30
Competing interests None.
31
Provenance and peer review Commissioned; externally peer reviewed.
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Bell's palsy: aetiology, clinical features and

multidisciplinary care
Timothy J Eviston, Glen R Croxson, Peter G E Kennedy, Tessa Hadlock
and Arun V Krishnan

J Neurol Neurosurg Psychiatry 2015 86: 1356-1361 originally published

online April 9, 2015
doi: 10.1136/jnnp-2014-309563

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