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 
1Prince of Wales Clinical School, University of NSW, Sydney, New South Wales, Australia 2Department of Otolaryngology, 
Royal Prince Alfred Hospital, Sydney, New South Wales, Australia 3Department of Neurology, Glasgow University, Southern 
General Hospital, Glasgow, UK 4Massachusetts 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; [email protected] 
Received 23 December 2014 Revised 19 February 2015 Accepted 18 March 2015 Published Online First 9 April 2015 
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 
1356 Eviston TJ, et al. J Neurol Neurosurg Psychiatry 2015;86:1356–1361. doi:10.1136/jnnp-2014-309563 

General neurology 
To cite: Eviston TJ, Croxson GR, Kennedy PGE, et al. J Neurol Neurosurg Psychiatry 2015;86: 1356–1361. 
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 
 
it correlation, provided a significant contribution to medical 
is not justifiable to assume a cause and effect 
relationship knowledge of his time. In particular, he was fascinated with the 
between the presence of HSV-1 in the patients’ 
endoneural fluid separation of sensory (trigeminal nerve) and motor supply 
and the development of Bell’s palsy. (facial nerve) to 
the face. It was his eloquent and logical descrip- 
HSV-1 is one of several human herpes viruses known 
to have tions that elevated his status among his contemporaries and 
a neurotrophic capacity for peripheral nerves, and other 
viruses ushered the ‘post-Bell’s’ era, which saw a rapid increase in the 
in this category include herpes simplex virus type 2 
(HSV-2) number of publications relating to acute idiopathic facial palsy 
and varicella zoster virus (VZV). They enter the body 
through —‘Bell’s palsy’. 
mucocutaneous exposure and establish their presence in 
latent Although Bell’s descriptions were admirable in their ability to 
form with highly restricted gene transcription in 
multiple inspire his contemporaries to document and study the disorder, 
ganglia throughout the neuroaxis for the entire life of 
the host, myriad other detailed descriptions exist in Greek, Persian and 
including in the cranial, dorsal root and autonomic 
ganglia.16 17 European medical texts as far back as the fifth century BCE,8 
This latent presence in ganglia in the absence of active 
viral rep- and there is prehistoric ceramic art depicting facial palsy identi- 
lication and assembly is characteristic, well described, 
and fied in ancient Peruvian culture.9 Other clinicians who recog- 
widely distributed through normal and diseased 
populations. nised the entity of acute idiopathic facial paralysis before Bell 
HSV has a global distribution and is a fundamentally 
resilient (and perhaps may have inspired some of his observations) 
virus. HSV and VZV can both reactivate in an 
immunocompe- include Sydenham, Stalpart van der Wiel, Douglas, Friedreich 
tent host, and in the presence of circulating antibodies, 
although and Thomassen á Thuessink.8 
reactivation is more likely in the setting of 
immunodeficiency, Approximately 1000 years before Bell, the Persian physician 
especially in the case of VZV. and scholar, Razi 
(865–925 CE), described facial palsy at length 
A possible cause of neural dysfunction due to HSV-1 
is the acti- in his seminal ninth century text ‘al-Hawi’.8 This remarkable 
vation of intra-axonal degradation and apoptotic 
pathways description referenced the contributions of Galen and Celsus, 
 driven by local direct and indirect responses of the axon 
to the among others, and included a diagnostic algorithm delineating 
virus itself in a susceptible phenotype. Although not 
previously peripheral facial palsy from more sinister central causes, which 
associated specifically with the pathogenesis of Bell’s 
palsy, the were accompanied by delirium, coma, hemiplegia, blindness, or 
emergence of literature pertaining to the role of 
intra-axonal deafness, and tended to have a poor prognosis. 
signal molecules (eg, SARM1),18 mitochondrial permeabilisa- tion19 and the molecular mechanisms underpinning Wallerian 
EPIDEMIOLOGY 
degeneration,18 suggests that acute axonal degeneration 
in the Bell’s palsy is a common cranial mononeuropathy. It affects 
context of viral infection may be an evolutionarily 
conserved males and females equally, and has a slightly higher incidence in 
innate immune response to prevent virus transport to the 
central mid and later life, but certainly occurs across all age ranges. The 
nervous system.19 described population incidence rates 
range from 11.5 to 40.2/ 
Recent in vitro work has demonstrated local 
messenger RNA 100 00010 with specific studies demonstrating similar annual 
transcription in peripheral nerve axons20 incited by the 
presence incidences between the UK (20.2/100 000), Japan (30/100 000) 
of α-herpes virus particles. In this compartmentalised 
model, and the USA 25–30/100 000.10 Clustering and epidemic phe- 
protein and signal transduction changes were not reliant 
on nomena are not demonstrated in the majority of studies. An 
nuclear machinery, that is, when a virus enters an axon, 
the exception to this is the recent occurrence of an increase in inci- 
axon responds locally. Earlier work examining cellular 
physi- dence of Bell’s palsy during a trial of intranasal vaccine delivery. 
ology in the setting of herpes infection demonstrated an 
acute This was possibly due to the immune effects of the detoxified 
decrease in sodium conductivity in the setting of 
HSV-1.21 Escherichia coli heat labile toxin adjuvant used in this form of 
Changes in sodium conductance can result in a reversed 
sodium- vaccine delivery.11 The incidence is higher in pregnancy, follow- 
calcium exchange (NCX)22 current and the 
accumulation of ing viral upper respiratory tract infection, in the immunocom- 
intracellular calcium. This aberration in calcium 
homoeostasis promised setting, and with diabetes mellitus and hypertension.1 
leads to protease activation and intra-axonal 
degeneration. There is no distinct latitudinal variation for incidence, nor is 
These processes of axonal degeneration would drive the 
abrupt there a racial or ethnic predilection. Some epidemiological data 
onset of Bell’s palsy and explain the lack of a 
pronounced demonstrate seasonal variation, with a slightly higher incidence 
immune response. This would not necessarily discount 
the role in cold months versus warm months,10 and a slight preponder- 
of compression to the pathogenesis but, rather, may 
answer the ance to arid over non-arid climates.12 
question as to why the nerve swells, leading to impingement, in the first place. AETIOLOGY 
Another possible contributor to the pathogenesis of 
Bell’s palsy There is a diverse body of evidence implicating immune, infect- 
implicates the role of a cell-mediated immune response 
against ive and ischaemic mechanisms as potential contributors to the 
myelin, akin to a mononeuropathic form of 
Guillain-Barré syn- development of Bell’s palsy, but the cause of classical Bell’s palsy 
drome (GBS). The evidence for this stems from the 
indirect labora- remains unclear. One possible cause that has been suggested is 
tory finding of GBS, such as changes in peripheral 
blood that of a reactivated herpes simplex virus (HSV-1) infection 
percentages of T and B lymphocytes, elevated 
chemokine concen- centred around the geniculate ganglion, a theory first outlined 
trations and in vitro reactivity to myelin protein (P1L) 
in blood by McCormick.5 The association with HSV-1 is supported by 
samples taken from patients with Bell’s palsy.7 the 
presence of HSV-1 in intratemporal facial nerve endoneural fluid13 harvested during nerve decompression, and the ability to 
DIAGNOSIS incite facial palsy in an animal model 
through primary infec- 
Bell’s palsy is a clinical diagnosis. The characteristic 
findings are tion14 and reactivation induced by immune modulation.15 
acute onset of unilateral lower motor neuron facial 
paralysis that Despite this evidence, the behaviour of Bell’s palsy is unusual 
affects muscles of the upper as well as lower face and 
reaches its compared with other diseases more commonly caused by HSV, 
peak by 72h. These findings are frequently 
accompanied by such as herpes labialis (cold sores) and genital herpes.4 Further, 
symptoms of neck, mastoid or ear pain, dysgeusia, hyperacusis 
Eviston TJ, et al. J Neurol Neurosurg Psychiatry 2015;86:1356–1361. doi:10.1136/jnnp-2014-309563 1357 

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 

General neurology 
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 
 
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 
10days or 60mg for the first 5days, then reducing by 10mg each day for the next 5days. 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 
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 
Eviston TJ, et al. J Neurol Neurosurg Psychiatry 2015;86:1356–1361. doi:10.1136/jnnp-2014-309563 1359 

General neurology 
 
sequelae. in the setting of flaccid facial paralysis. Using a straw for liquids 
In the setting of acute steroid use the rate of 
full and tending towards soft foods are often helpful. The inability 
recovery is over 90%.32 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. 
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 Physiotherapy 
swallowing) and psychological considerations need to 
be From an evidence-based perspective, this diverse modality of 
addressed by the treating team. Over the last three 
decades, the treatment, which broadly encompasses heat therapy, electrosti- 
treatment of incomplete recovery of facial palsy has 
evolved mulation, massage, mime therapy and biofeedback,30 is hard to 
from static techniques aimed at suspension of the oral 
commis- analyse as a whole. There is a plethora of treatment regimes, and 
sure and eye closure, into a multimodal,38 zonal-based 
approach their timing and variability in implementation make their 
that utilises the complementary aspects of 
physiotherapy, che- broader assessment of utility complex. Although not recom- 
modenervation and selective surgical procedures to 
maximise mended for all suffers of Bell’s palsy,30 there are subgroups of 
the cosmetic and functional outcome needs of each 
patient. patients for whom there is evidence supporting the use of physio- 
Increasingly, multidisciplinary collaboration between 
interested therapy.37 These include patients who have incomplete recovery 
clinicians from a wide variety of subspecialties has 
proven and who have developed hypertonia, hyperkinesis or synkinesis, 
effective. and in these groups neuromuscular retraining 
is trialled before 
In outlining treatment modalities and their 
appropriateness, consideration of chemodenervation.38 Physiotherapy and chemo- 
one must consider incomplete recovery of facial 
function as a denervation are complementary in the treatment of synkinesis. 
heterogeneous entity that encompasses different degrees of flac- cidity, hypertonicity and synkinesis. Each of these issues can 
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 
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. have not experienced some 
recovery in the first 3–4 months after onset are more likely to have incomplete recovery of facial 
Synkinesis function, with or without spasm and 
synkinesis. Prolonged pain 
Synkinesis refers to abnormal facial muscular 
contraction during is also a predictor of worse outcome. 
voluntary facial movements and has been traditionally 
attributed The natural history of Bell’s palsy has been elucidated 
to aberrant re-innervation of facial musculature 
following nerve through a number of large studies.1 3 25 Based on conclusions 
injury. It can be seen as involuntary eye-closure during 
midface drawn from these large studies, clinicians can expect that 
movement such as eating or smiling (oro-ocular 
synkinesis); as without intervention, approximately 70% of patients will 
lip excursion during eye closure (oculo-oral synkinesis); 
or as experience full recovery. Of those who do not recover fully, half 
chin dimpling or muscular neck cords during midface 
move- will have mild sequelae, and the remainder moderate-to-severe 
ment due to involuntary mentalis or platysma activation. The 
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. 

General neurology 
1360 Eviston TJ, et al. J Neurol Neurosurg Psychiatry 2015;86:1356–1361. doi:10.1136/jnnp-2014-309563 
 
treatment  of  synkinesis  centres  around  physiotherapy,  with  a  particular  focus  on  biofeedback  exercises  to  retrain  facial  sym- 
metry,  and  selective  chemodenervation  using  directed  botulinum  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 
Treatment  of  synkinesis  with  botulinum  toxin  is  tailored  according  to  the  individual  patient.  Injection  points  focused  on 
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- metry and cosmesis. Injection of the weak/synkinetic zygomati- cus 
muscles  is  best  avoided due to the debilitating effect of losing smile function from an already weakened face. Some patients have 
a  reduced  benefit  with  repeated  injections  while  for  others the requirement for recurrent injections three to four times per year is 
unsatisfactory.  In  selected  cases,  a  more  per-  manent  solution  can  be  achieved  through  surgical  interventions  such  as  selective 
myectomy. Recently, selective neurectomy has also proven to be very effective.39 
Facial reanimation In the setting of incomplete recovery with ineffective smile, nerve-to-nerve transfer, and regional and free 
tissue transfer techniques offer the opportunity to restore midface movement. A regional tendon transfer technique that relocates 
the tempor- 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 inserted into the face with nerve coaptation from 
the contralat- 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 of facial musculature but a frozen oral commissure. Donor 
nerves include the masseteric branch of the trigeminal nerve, and cross face nerve grafting. These complex reconstructive pro- 
cedures offer an opportunity for smile reanimation, and the sub- sequent benefits in social function and quality of life. 
Competing interests None. Provenance and peer review Commissioned; externally peer reviewed. 
REFERENCES 
1 Peitersen E. Bell’s palsy: the spontaneous course of 2,500 peripheral facial nerve 
palsies of different etiologies. Acta Otolaryngol Suppl 2002;122:4–30. 2 Diamond M, Wartmann CT, Tubbs RS, et al. Peripheral 
facial nerve communications 
and their clinical implications. Clin Anat 2011;24:10–18. 3 Adour KK, Byl FM, Hilsinger RL Jr, et al. The true nature of 
Bell’s palsy: analysis of 
1,000 consecutive patients. Laryngoscope 1978;88:787–801. 4 Kennedy PG. Herpes simplex virus type 1 and Bell’s palsy—a 
current assessment of 
the controversy. J Neurovirol 2010;16:1–5. 5 McCormick DP. Herpes-simplex virus as cause of Bell’s palsy. Lancet 
1972;299:937–9. 6 Gantz BJ, Rubinstein JT, Gidley P, et al. Surgical management of Bell’s palsy. 
Laryngoscope 1999;109:1177–88. 7 Greco A, Gallo A, Fusconi M, et al. Bell’s palsy and autoimmunity. Autoimmun Rev 
2012;12:323–8. 8 Sajadi MM, Sajadi M-RM, Tabatabaie SM. The history of facial palsy and spasm: 
hippocrates to Razi. Neurology 2011;77:174–8. 9 Canalis RF, Cino L. Ceramic representations of facial paralysis in ancient 
Peru. 
Otol Neurotol 2003;24:828–31. 10 De Diego JI, Prim MP, Madero R, et al. Seasonal patterns of idiopathic facial 
paralysis: a 16-year study. Otolaryngol Head Neck Surg 1999;120:269–71. 11 Lewis DJM, Huo Z, Barnett S, et al. Transient 
facial nerve paralysis (Bell’s palsy) 
following intranasal delivery of a genetically detoxified mutant of Escherichia coli heat labile toxin. PLoS ONE 2009;4:e6999. 
12 Campbell KE, Brundage JF. Effects of climate, latitude, and season on the incidence 
of Bell’s palsy in the US Armed Forces, October 1997 to September 1999. Am J Epidemiol 2002;156:32–9. 13 Murakami S, 
Mizobuchi M, Nakashiro Y. Bell palsy and herpes simplex virus: 
identification of viral DNA in endoneurial fluid and muscle. Ann Inter Med 1996;124:27–30. 14 Sugita T, Murakami S, 
Yanagihara N. Facial nerve paralysis induced by herpes simplex virus in mice: an animal model of acute and transient facial 
paralysis. Ann Otol Rhinol Laryngol 1995;104:574–81. 15 Esaki S, Yamano K, Katsumi S, et al. Facial nerve palsy after 
reactivation of herpes 
simplex virus type 1 in diabetic mice. Laryngoscope 2014;125:E143-8. doi: 10.1002/lary.24994. Epub 2014 Oct 31. 16 Steiner I, 
Kennedy PG. Molecular biology of herpes simplex virus type 1 latency in 
the nervous system. Mol Neurobiol 1993;7:137–59. 17 Mitchell BM, Bloom DC, Cohrs RJ, et al. Herpes simplex virus-1 and 
varicella-zoster 
virus latency in ganglia. J Neurovirol 2003;9:194–204. 18 Conforti L, Gilley J, Coleman MP. Wallerian degeneration: an 
emerging axon death 
pathway linking injury and disease. Nat Rev Neurosci 2014;15:394–409. 19 Galluzzi L, Blomgren K, Kroemer G. Mitochondrial 
membrane permeabilization in 
neuronal injury. Nat Rev Neurosci 2009;10:481–94. 20 Koyuncu OO, Perlman DH, Enquist LW. Efficient retrograde 
transport of 
pseudorabies virus within neurons requires local protein synthesis in axons. Cell Host Microbe 2013;13:54–66. 21 Storey N. 
Selective internalization of sodium channels in rat dorsal root ganglion neurons infected with herpes simplex virus-1. J Cell Biol 
2002;158:1251–62. 22 Persson AK, Kim I, Zhao P, et al. Sodium channels contribute to degeneration of dorsal root ganglion 
neurites induced by mitochondrial dysfunction in an in vitro model of axonal injury. J Neurosci 2013;33:19250–61. 23 Croxson 
GR. The assessment of facial nerve dysfunction. J Otolaryng Soc Austral 
1990;4:252–63. 24 Stjernquist-Desatnik A, Skoog E, Aurelius E. Detection of herpes simplex and 
varicella-zoster viruses in patients with Bell’s palsy by the polymerase chain reaction technique. Ann Otol Rhinol Laryngol 
2006;115:306–11. 25 Hohman MH, Hadlock TA. Etiology, diagnosis, and management of facial palsy: 2000 patients at a facial 
nerve center. Laryngoscope 2014;124:E283–93. 26 Croxson G, Coulson SE, Mukherjee P. Mistaken diagnoses in facial nerve 
disorders 
[conference presentation]. 12th International Facial Nerve Symposium. Boston: 7 June 2013. 27 House JW, Brackmann DE. 
Facial nerve grading system. Otolaryngol Head Neck Surg 
1985;2:146–7. 28 Ross B, Fradet G, Nedzelski J. Development of a sensitive clinical facial grading 
system. Otolaryngol Head Neck Surg 1996;114:380–6. 29 Fattah AY, Gavilan J, Hadlock TA, et al. Survey of methods of 
facial palsy 
documentation in use by members of the Sir Charles Bell Society. Laryngoscope 2014;124:2247–51. 30 Baugh RF, Basura GJ, 
Ishii LE, et al. Clinical practice guideline Bell’s palsy. 
Otolaryngol Head Neck Surg 2013;149(3 Suppl):S1–27. 31 Gronseth GS, Paduga R, American Academy of Neurology. 
Evidence-based guideline 
update: steroids and antivirals for Bell palsy: report of the Guideline Development Subcommittee of the American Academy of 
Neurology. Neurology 2012;79:2209–13. 32 Sullivan FM, Swan IRC, Donnan PT, et al. Early treatment with prednisolone or 
acyclovir in Bell’s palsy. N Engl J Med 2007;357:1598–607. 33 Engström M, Berg T, Stjernquist-Desatnik A, et al. 
Prednisolone and valacyclovir in Bell’s palsy: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet Neurol 
2008;7:993–1000. 34 Salinas RA, Alvarez G, Daly F, et al. Corticosteroids for Bell’s palsy (idiopathic facial 
paralysis). Cochrane Database Syst Rev 2010;3:CD001942. 35 Minnerop M, Herbst M, Fimmers R, et al. Bell’s palsy: 
combined treatment of 
famciclovir and prednisone is superior to prednisone alone. J Neurol 2008;255:1726–30. 36 Hato N, Yamada H, Kohno H, et al. 
Valacyclovir and prednisolone treatment for 
Bell’s palsy: a multicenter, randomized, placebo-controlled study. Otol Neurotol 2007;28:408–13. 37 Robinson M, Hadlock TA. 
Comprehensive facial rehabilitation improves function in people with facial paralysis: a 5-year experience at the Massachusetts 
Eye and Ear Infirmary. Phys Ther 2010;90:391–7. 38 Hadlock TA, Greenfield LJ, Wernick-Robinson M, et al. Multimodality 
approach to 
management of the paralyzed face. Laryngoscope 2006;116:1385–9. 39 Hohman MH, Lee LN, Hadlock TA. Two-step highly 
selective neurectomy for 
 refractory periocular synkinesis. Laryngoscope 2013;123:1385–8. 40 Labbé D, Bénateau H, Bardot J. Surgical procedures for 
labial reanimation in facial 
paralysis. Ann Chir Plast Esthet 2002;47:580–91. 
Eviston TJ, et al. J Neurol Neurosurg Psychiatry 2015;86:1356–1361. doi:10.1136/jnnp-2014-309563 1361 

General neurology