REVIEW

Bell’s palsy: aetiology, clinical featuresand multidisciplinary careTimothy J Eviston,1 Glen R Croxson,2 Peter G E Kennedy,3 Tessa Hadlock,4

Arun V Krishnan1

1Prince of Wales ClinicalSchool, University of NSW,Sydney, New South Wales,Australia2Department ofOtolaryngology, Royal PrinceAlfred Hospital, Sydney,New South Wales, Australia3Department of Neurology,Glasgow University, SouthernGeneral Hospital, Glasgow, UK4Massachusetts Eye and EarInfirmary and Harvard MedicalSchool, Boston, Massachusetts,USA

Correspondence toDr Arun Krishnan, Prince ofWales Clinical School,University of New South Wales,Randwick, NSW 2031,Australia;Arun.Krishnan@unsw.edu.au

Received 23 December 2014Revised 19 February 2015Accepted 18 March 2015Published Online First9 April 2015

To cite: Eviston TJ,Croxson GR, Kennedy PGE,et al. J Neurol NeurosurgPsychiatry 2015;86:1356–1361.

ABSTRACTBell’s palsy is a common cranial neuropathy causingacute unilateral lower motor neuron facial paralysis.Immune, infective and ischaemic mechanisms are allpotential contributors to the development of Bell’s palsy,but the precise cause remains unclear. Advancements inthe understanding of intra-axonal signal molecules andthe molecular mechanisms underpinning Walleriandegeneration may further delineate its pathogenesisalong with in vitro studies of virus–axon interactions.Recently published guidelines for the acute treatment ofBell’s palsy advocate for steroid monotherapy, althoughcontroversy exists over whether combined corticosteroidsand antivirals may possibly have a beneficial role inselect cases of severe Bell’s palsy. For those withlongstanding sequaelae from incomplete recovery,aesthetic, functional (nasal patency, eye closure, speechand swallowing) and psychological considerations needto be addressed by the treating team. Increasingly,multidisciplinary collaboration between interestedclinicians from a wide variety of subspecialties hasproven effective. A patient centred approach utilisingphysiotherapy, targeted botulinum toxin injection andselective surgical intervention has reduced the burden oflong-term disability in facial palsy.

INTRODUCTIONBell’s palsy is an acute-onset peripheral facial neur-opathy and is the most common cause of lowermotor neuron facial palsy.1 The clinical presentationof the disorder is a rapid onset, unilateral, lowermotor 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 bythe anatomical construct of the human facial nerve,specifically its mixed nerve profile containingmotor, sensory and parasympathetic fibres. The pro-pensity for the facial nerve to form numerous con-nections with adjacent cranial nerves2 may alsoexplain the occasionally observed features of alteredfacial sensation (cranial nerve V), vestibular dysfunc-tion (cranial nerve VIII) or pharyngeal symptoms(cranial nerves IX and X).3 Reduced lacrimation andsalivation secondary to parasympathetic effects mayalso occur.3 Maximal disability occurs within thefirst 48–72 h and the severity of the palsy correlateswith the duration of facial dysfunction, the extent offacial 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

compression6 and autoimmunity7 may all play a role,yet the exact sequence and magnitude of these influ-ences remains unclear.

AnatomyThe human facial nerve is the seventh cranial nerve(CNVII) and comprises motor, sensory and para-sympathetic components. Its function is responsiblefor voluntary and mimetic facial movement, taste tothe anterior two-thirds of the tongue, and controlof salivary gland and lacrimal gland secretions.The facial nerve receives axons from the superior

part of the solitary nucleus and superior salivarynucleus that form the nervus intermedius compo-nent (sensory and parasympathetic axons) andmotor efferent fibres from the facial nucleus, whichreceives synaptic input from the contralateralmotor cortex for all facial movements except theforehead, 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 angleto the internal acoustic meatus where it is accom-panied by the vestibulocochlear nerve (CNVIII).The intratemporal course of the facial nerve is longand tortuous. During its intratemporal course, thenerve encounters the geniculate ganglion and givesrise to the superior petrosal nerve, the nerve to sta-pedius and chorda tympani nerve branches, beforeexiting the skull base through the styloid foramen.The extratemporal facial nerve courses through thesubstance of parotid gland dividing it into deep andsuperficial lobes. It gives off the posterior auricularnerve and nerve to the posterior belly of digastricbefore dividing into its terminal facial branches.There is significant variation in the branchingpattern of the terminal facial branches, which aretraditionally conceptualised into temporal, zygo-matic, buccal, marginal mandibular and cervicalbranches. These terminal motor branches areresponsible for all facial expression and functionaltasks such as eye and mouth closure and nasalpatency during inspiration. Throughout its course,the facial nerve forms multiple communicationsbetween its own branches and with adjacent cranialnerves.2

HISTORYSir Charles Bell (1774–1842) was fascinated by thenervous system. As an accomplished anatomist,artist, surgeon and teacher, his work on the charac-terisation of the peripheral nervous system throughanatomical study, vivisection and clinical

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correlation, provided a significant contribution to medicalknowledge of his time. In particular, he was fascinated with theseparation 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 andushered the ‘post-Bell’s’ era, which saw a rapid increase in thenumber of publications relating to acute idiopathic facial palsy—‘Bell’s palsy’.

Although Bell’s descriptions were admirable in their ability toinspire his contemporaries to document and study the disorder,myriad other detailed descriptions exist in Greek, Persian andEuropean 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, Friedreichand Thomassen á Thuessink.8

Approximately 1000 years before Bell, the Persian physicianand scholar, Razi (865–925 CE), described facial palsy at lengthin his seminal ninth century text ‘al-Hawi’.8 This remarkabledescription referenced the contributions of Galen and Celsus,among others, and included a diagnostic algorithm delineatingperipheral facial palsy from more sinister central causes, whichwere accompanied by delirium, coma, hemiplegia, blindness, ordeafness, and tended to have a poor prognosis.

EPIDEMIOLOGYBell’s palsy is a common cranial mononeuropathy. It affectsmales and females equally, and has a slightly higher incidence inmid and later life, but certainly occurs across all age ranges. Thedescribed population incidence rates range from 11.5 to 40.2/100 00010 with specific studies demonstrating similar annualincidences 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. Anexception 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 detoxifiedEscherichia coli heat labile toxin adjuvant used in this form ofvaccine 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 isthere a racial or ethnic predilection. Some epidemiological datademonstrate seasonal variation, with a slightly higher incidencein cold months versus warm months,10 and a slight preponder-ance to arid over non-arid climates.12

AETIOLOGYThere is a diverse body of evidence implicating immune, infect-ive and ischaemic mechanisms as potential contributors to thedevelopment of Bell’s palsy, but the cause of classical Bell’s palsyremains unclear. One possible cause that has been suggested isthat of a reactivated herpes simplex virus (HSV-1) infectioncentred around the geniculate ganglion, a theory first outlinedby McCormick.5 The association with HSV-1 is supported bythe presence of HSV-1 in intratemporal facial nerve endoneuralfluid13 harvested during nerve decompression, and the ability toincite 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 unusualcompared with other diseases more commonly caused by HSV,such as herpes labialis (cold sores) and genital herpes.4 Further,

it is not justifiable to assume a cause and effect relationshipbetween the presence of HSV-1 in the patients’ endoneural fluidand the development of Bell’s palsy.

HSV-1 is one of several human herpes viruses known to havea neurotrophic capacity for peripheral nerves, and other virusesin this category include herpes simplex virus type 2 (HSV-2)and varicella zoster virus (VZV). They enter the body throughmucocutaneous exposure and establish their presence in latentform with highly restricted gene transcription in multipleganglia 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, andwidely distributed through normal and diseased populations.HSV has a global distribution and is a fundamentally resilientvirus. HSV and VZV can both reactivate in an immunocompe-tent host, and in the presence of circulating antibodies, althoughreactivation 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 pathwaysdriven by local direct and indirect responses of the axon to thevirus itself in a susceptible phenotype. Although not previouslyassociated specifically with the pathogenesis of Bell’s palsy, theemergence of literature pertaining to the role of intra-axonalsignal molecules (eg, SARM1),18 mitochondrial permeabilisa-tion19 and the molecular mechanisms underpinning Walleriandegeneration,18 suggests that acute axonal degeneration in thecontext of viral infection may be an evolutionarily conservedinnate immune response to prevent virus transport to the centralnervous system.19

Recent in vitro work has demonstrated local messenger RNAtranscription in peripheral nerve axons20 incited by the presenceof α-herpes virus particles. In this compartmentalised model,protein and signal transduction changes were not reliant onnuclear machinery, that is, when a virus enters an axon, theaxon responds locally. Earlier work examining cellular physi-ology in the setting of herpes infection demonstrated an acutedecrease 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 ofintracellular calcium. This aberration in calcium homoeostasisleads to protease activation and intra-axonal degeneration.These processes of axonal degeneration would drive the abruptonset of Bell’s palsy and explain the lack of a pronouncedimmune response. This would not necessarily discount the roleof compression to the pathogenesis but, rather, may answer thequestion as to why the nerve swells, leading to impingement, inthe first place.

Another possible contributor to the pathogenesis of Bell’s palsyimplicates the role of a cell-mediated immune response againstmyelin, 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 bloodpercentages of T and B lymphocytes, elevated chemokine concen-trations and in vitro reactivity to myelin protein (P1L) in bloodsamples taken from patients with Bell’s palsy.7

DIAGNOSISBell’s palsy is a clinical diagnosis. The characteristic findings areacute onset of unilateral lower motor neuron facial paralysis thataffects muscles of the upper as well as lower face and reaches itspeak by 72 h. These findings are frequently accompanied bysymptoms of neck, mastoid or ear pain, dysgeusia, hyperacusis

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or altered facial sensation. These associated symptoms arepresent in 50–60%23 and are reassuring for the diagnosis ofBell’s palsy.

The involvement of posterior auricular, petrosal, chordatympani and stapedius nerves implicates the site of dysfunctionbeing 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 ofthe facial nerve on contrast-enhanced MRI studies. This imagingfinding is hypothesised to represent disruption of the blood–brain barrier and vascular congestion of the facial nerve.Attempts to determine surrogate diagnosis through PCRtechniques 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 clinicalfeatures.24 These tests are therefore of limited value as diagnos-tic tools.

Differential diagnosisThe differential diagnosis for facial palsy is broad,25 and misdiag-nosis is not uncommon. Causes of facial palsy may be dividedinto congenital and acquired aetiologies. Congenital causesinclude genetic syndromes, birth-related trauma and isolated dis-orders of development (eg, developmental hypoplasia of facialmuscles). Acquired causes include infective (VZV, Lyme disease,mycobacterium tuberculosis, HIV), traumatic (iatrogenic or headtrauma), inflammatory (vasculitis, sarcoidosis, autoimmunedisease), neoplastic (benign or malignant) and cerebrovascularcauses, among others. In the experience of one of the authors(GC) in an expert referral setting, the rate of misdiagnosis ofBell’s palsy by the initial consulting clinician is 10.8%.26 Misseddiagnoses include tumours (eg, facial nerve schwannoma, parotidmalignancy and, rarely, acoustic neuroma), herpes zoster oticusand granulomatous diseases such as sarcoidosis and granulomato-sis with polyangiitis (Wegener’s granulomatosis).

A structured clinical approach that considers the pattern offacial palsy (figure 1) along with patient characteristics and a

thorough physical examination will generally provide evidencefor an alternative diagnosis, and prompt appropriate investiga-tion.25 Particular patterns of facial palsy that require thoughtfulconsideration 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 nerveneuroma); (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 parotidregion, a history of cutaneous malignancy or segmental facialnerve weakness should raise suspicion for a tumour. A history oftrauma, ear symptoms such as ipsilateral deafness, tinnitus, full-ness or discharge, or systemic symptoms such as fever, are alsored flags warranting further investigation and specialist oto-logical consultation.

The consideration of cerebrovascular disease as a cause offacial palsy is important with this being the main concern formany patients and clinicians, often prompting expert neurologyconsultation. The preservation of upper facial movement (fron-talis contraction) is a discriminator between cortical (central)and peripheral facial nerve weakness. Rarely, ipsilateral pontinepathology may result in lower motor neuron pattern facialweakness due to direct compromise of the facial nucleus. Thiswill be accompanied by other cranial nerve, and long tractsymptoms and signs. Ipsilateral abducens nerve (CNVI) dysfunc-tion (lateral gaze palsy) is a particularly useful sign.

GradingThe most widely used systems for recording the severity ofBell’s palsy are the House-Brackmann27 (HB) scale or the FacialNerve Grading Scale28 (also known as the Sunnybrook system).The subjective nature of these scales makes them prone to somemisinterpretation and interobserver variability; however, theirease of use has cemented their role in clinical practice for com-municating the overall degree of dysfunction, for monitoringoutcomes and for the presentation of group data in a research

Figure 1 Patterns of facial palsy.

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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 recordingof standardised facial movements (eyebrow raise, gentle eyeclosure, tight eye closure, snarl, open and closed lip smiles, lipdepression and lip puckering) is emphasised for the accurateoutcome assessment of interventions such as chemodenervation,physiotherapy or surgery, which may be considered in thosepatients who have an incomplete recovery.

NeurophysiologyThere have been a number of studies exploring the potentialutility of neurophysiological assessment for treatment selectionand prognosis. In the past, nerve conduction studies of thefacial nerve, also referred to as electroneuronography (ENoG)in the surgical literature, have been suggested in some studies tobe useful in the selection of patients who may require surgicaldecompression of the facial nerve. The demonstration of agreater than 90% reduction in compound muscle action poten-tial in the first 10 days of onset compared with the unaffectedside 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, riskand lack of efficacy.30 With this trend away from surgery, thetime and cost of neurophysiology assessment outweighs thebenefit for the vast majority of patients. An exception to this isthe clinical setting of complete paralysis. Here, neurophysiologyprovides useful information with the presence of a residualresponse 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 neurophysiologicalresponse is suggestive of complete degeneration and a prolongedparalysis with incomplete recovery that may be complicated bysynkinesis. The knowledge of a prolonged recovery may swaythe clinician and patient towards surgical eye protection proce-dures and the proactive involvement of a facial therapist early inthe course of recovery.

TREATMENTAcute treatmentThe American Academy of Neurology31 (AAN) and theAmerican Academy of Otolaryngology—Head and Neck SurgeryFoundation30 (AAO-HNSF) have recently published guidelinesfor the treatment of Bell’s palsy. Although the structure andscope of these guidelines are different, they are essentially com-plementary documents that reinforce the role of corticosteroidsin the treatment of Bell’s palsy and argue against the routine useof antiviral therapy. Furthermore, the AAO-HNSF guidelines dis-courage routine laboratory, imaging or neurophysiological testingat the first presentation of typical Bell’s palsy. The dose of oralsteroids should be started in the first 72 h of onset and a regimemirroring either of the Scottish32 or European33 randomisedcontrolled trials (RCTs) should be used. This is either 50 mgprednisone for 10 days or 60 mg for the first 5 days, thenreducing by 10 mg each day for the next 5 days. Both seemeffective.34 It has been argued that the lack of significancedemonstrated by combined corticosteroid and antiviral therapyover corticosteroids alone in double-blind RCTs represents a dilu-tion effect of mild and moderate palsies, which have a high rateof spontaneous recovery, masking any demonstrable benefit forthe severe palsy subgroup. Supporting this are the positive find-ings in favour of combined therapy in non-double-blindedstudies.35 36

The key rationale for giving patients with Bell’s palsy antiviraltreatment with the antiherpes drug acyclovir is the possible roleof HSV-1, based on the current circumstantial evidence.Another reason given for using antiviral therapy in the settingof clinical equipoise is that a portion of those given a provi-sional diagnosis of Bell’s palsy will have zoster sine herpete, thatis, symptomatic VZV reactivation without the typical vesiculareruption pathognomonic of a typical VZV infection (Ramsay-Hunt syndrome).

VZV is an important differential diagnosis in all acute lowermotor neuron facial palsies. Ramsay-Hunt syndrome has aworse prognosis than Bell’s palsy and, on average, presents as amore severe palsy. It is more responsive to combined antiviraland steroid therapy, and the rate of complications from antiviraltherapy is low. Since VZV is known to cause facial palsy, the useof antivirals in Ramsay-Hunt syndrome has a clear evidencebase, and is justified and rational.4 A typical regime toadequately cover VZV would be 3000 mg/day (1000 mg valacy-clovir three times a day) for 7 days. Valacyclovir has a higherbioavailability than acyclovir.

At the present the use of combined acyclovir and corticoster-oids in treating classical Bell’s palsy remains controversial, withconflicting data emerging from different trials and, indeed, fromdifferent meta-analyses.4 Based on current evidence, particularlythe extensive Scottish Bell’s palsy study32 of 551 patients in adouble-blind, placebo-controlled, randomised study, it seemsreasonable to treat classic Bell’s palsy with oral corticosteroidsalone, without acyclovir. However, combined acyclovir and cor-ticosteroids may possibly have a beneficial role in cases of severeBell’s palsy, and this issue needs to be resolved in a large pro-spective clinical trial. In cases where the patient is severelyimmunocompromised, consideration may be given to intraven-ous regimes of acyclovir to prevent possible central nervoussystem complications.

Eye careThe institution of an eye protection strategy for each patientwith incomplete closure is of paramount importance.Lacrimation occurs at the lateral aspect of the conjunctivalmembrane and is swept lateral to medial as a film by the actionof the orbicularis oculi during blink and effective eye closure.Loss of this mechanism results in epiphora (tearing) due to anineffective 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 canthreaten sight. At the first consultation, the clinician must enacta strategy to avoid ocular exposure, and refer any cases ofconcern to an ophthalmologist. Effective eye protection usesbarrier protection (eg, wrapped sunglasses), lubrication (artificialtears during the day, ointment at night) and taped closure atnight. Particular environments that may present a challenge forthe patient include showering and swimming, and dusty andwindy environments; these situations are best avoided.

The early use of an eyelid weight should be considered in theelderly, those with diabetes, with pre-existing eye disease, com-plete facial palsy with no response on neurophysiology and thepresence of ongoing irritation despite the use of the eye-protective therapies described above.25

Oral careLoss of the sphincter function of the orbicularis oris confers thesocial inconvenience of oral incontinence and predisposes thelip and inner cheek to abrasion during mastication and subse-quent ulceration. Strategic eating may lessen the impact of these

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in the setting of flaccid facial paralysis. Using a straw for liquidsand tending towards soft foods are often helpful. The inabilityto lower and evert the lower lip precludes eating certain foods.Temporary dental ‘spacers’ adhered to the lateral aspect of themolar teeth may be used to prevent chewing of the buccalmucosa.

PhysiotherapyFrom an evidence-based perspective, this diverse modality oftreatment, which broadly encompasses heat therapy, electrosti-mulation, massage, mime therapy and biofeedback,30 is hard toanalyse as a whole. There is a plethora of treatment regimes, andtheir timing and variability in implementation make theirbroader assessment of utility complex. Although not recom-mended for all suffers of Bell’s palsy,30 there are subgroups ofpatients for whom there is evidence supporting the use of physio-therapy.37 These include patients who have incomplete recoveryand who have developed hypertonia, hyperkinesis or synkinesis,and in these groups neuromuscular retraining is trialled beforeconsideration of chemodenervation.38 Physiotherapy and chemo-denervation are complementary in the treatment of synkinesis.

PrognosisNatural history studies have demonstrated that ∼85% of patientsexperience some recovery in the first 3 weeks.1 Predictors ofincomplete recovery include severe facial palsy, the length oftime prior to onset of recovery, and persistent pain. Patientswith complete facial palsy (House-Brackman grades 5–6) whohave not experienced some recovery in the first 3–4 monthsafter onset are more likely to have incomplete recovery of facialfunction, with or without spasm and synkinesis. Prolonged painis also a predictor of worse outcome.

The natural history of Bell’s palsy has been elucidatedthrough a number of large studies.1 3 25 Based on conclusionsdrawn from these large studies, clinicians can expect thatwithout intervention, approximately 70% of patients willexperience full recovery. Of those who do not recover fully, halfwill have mild sequelae, and the remainder moderate-to-severe

sequelae. In the setting of acute steroid use the rate of fullrecovery is over 90%.32

Managing incomplete recoveryChronic facial palsy is a disabling condition that has a dramaticimpact on social function, emotional expression and quality oflife. Aesthetic, functional (nasal patency, eye closure, speech andswallowing) and psychological considerations need to beaddressed by the treating team. Over the last three decades, thetreatment of incomplete recovery of facial palsy has evolvedfrom static techniques aimed at suspension of the oral commis-sure and eye closure, into a multimodal,38 zonal-based approachthat utilises the complementary aspects of physiotherapy, che-modenervation and selective surgical procedures to maximisethe cosmetic and functional outcome needs of each patient.Increasingly, multidisciplinary collaboration between interestedclinicians from a wide variety of subspecialties has proveneffective.

In outlining treatment modalities and their appropriateness,one must consider incomplete recovery of facial function as aheterogeneous entity that encompasses different degrees of flac-cidity, hypertonicity and synkinesis. Each of these issues canrange in severity from absent to severe. Generally, functionalissues such as brow ptosis, nasal valvular collapse and eyeclosure, are addressed through directed structural interventionsincluding nasal valvular suspension, brow ptosis correction, plat-inum weight insertion into the upper eyelid, lower lid suspen-sion or tarsorrhaphy to improve eye closure.

SynkinesisSynkinesis refers to abnormal facial muscular contraction duringvoluntary facial movements and has been traditionally attributedto aberrant re-innervation of facial musculature following nerveinjury. It can be seen as involuntary eye-closure during midfacemovement such as eating or smiling (oro-ocular synkinesis); aslip excursion during eye closure (oculo-oral synkinesis); or aschin dimpling or muscular neck cords during midface move-ment due to involuntary mentalis or platysma activation. The

Figure 2 Botulinum toxin injectionsites for the treatment of synkinesis.Blue (affected side) and green(unaffected side) dots representplanned point of injection for 1.5–3 IUof onabotulinum A. The preapplicationof topical local anaesthetic cream andthe use of a fine bore needle size(25–30 gauge) are used to reduce thepain of injection. Subcutaneousinjection is as effective asintramuscular.

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treatment of synkinesis centres around physiotherapy, with aparticular focus on biofeedback exercises to retrain facial sym-metry, and selective chemodenervation using directed botulinumtoxin to problem areas (figure 2). Most patients express a highdegree of satisfaction with this approach, and objective improve-ment is seen in the majority.38

Treatment of synkinesis with botulinum toxin is tailoredaccording to the individual patient. Injection points focused onorbicularis occuli and platysma relieve spasm and synkinesiswhile selective use of contralateral (unaffected side) brow anddepressor 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 oflosing smile function from an already weakened face. Somepatients have a reduced benefit with repeated injections whilefor others the requirement for recurrent injections three to fourtimes per year is unsatisfactory. In selected cases, a more per-manent solution can be achieved through surgical interventionssuch as selective myectomy. Recently, selective neurectomy hasalso proven to be very effective.39

Facial reanimationIn the setting of incomplete recovery with ineffective smile,nerve-to-nerve transfer, and regional and free tissue transfertechniques 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 popularisedby the French surgeon, Labbe.40 Alternatively, innervated freemuscle transfer techniques that utilise the gracilis muscle can beinserted into the face with nerve coaptation from the contralat-eral facial nerve and/or from the ipsilateral mandibular branchof the trigeminal nerve. Nerve-to-nerve transfers are alsobecoming increasingly popular for those with autopreservationof facial musculature but a frozen oral commissure. Donornerves 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.

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