The facial nerve (VIIth cranial nerve) innervates the muscles of facial expression, lacrimal and salivary glands, as well as the palates, and provides sensation to the anterior 2/3rds of the tongue, to name a few.


Damage to the facial nerve can therefore lead to significant functional and psychological problems e.g. facial paralysis, dysarthria and dry conjunctivae [Image 1].


The aim of plastic surgery is to restore function - in the case of facial palsy this would be reanimation. If this is not possible, surgery can offer static support, e.g. resting symmetry or corneal protection, and improvement in the person's cosmetic appearence.




Facial nerve carries four different types of fibres:


  •  General Somatic Afferent (GSA) - sensory input from external acoustic meatus and the skin of small area posterior to the ear
  •  Special Afferent (SA) - taste from the anterior 2/3rds of the tongue
  •  General Visceral Efferent (GVE) - parasympathetic activity to the lacrimal gland, submandibular and sublingual salivary glands, mucous membranes of the nasal cavity and both the soft and hard palates
  •  Brachial Efferent (BE) - muscles of facial expression and the scalp, stapedius, posterior belly of digastric and stylohyoid 


Facial nerve originates from the lateral side of the border between the pons and the medulla oblongata. It consists of a large motor root (carrying BE fibres), and the intermediate nerve (a sensory root carrying GSA, SA and GVE fibres). These two roots exit the cranial cavity via the internal acoustic meatus, and enter the facial canal. Soon after entering the facial canal the two roots fuse to form the facial nerve and enlarge to form the geniculate ganglion. The geniculate ganglion gives off the greater petrosal nerve which supplies GVE fibres.


Facial nerve continues its course along the canal and whilst doing so gives off the nerve to stapedius and chorda tympani (carrying SA and GVE fibres). It finally exits the skull via the stylomastoid foramen. Before entering the parotid gland, facial nerve gives off the posterior auricular nerve and a muscular branch, which innervates the scalp. Once entering the parotid gland, facial nerve divides into five terminal branches: Temporal, Zygomatic, Buccal, Mandibular and Cervical [Image 2].


Mneumonic, frequently used for the five terminal branches, is: Ten Zebras Burgled My Car.



The five terminal branches innervate the muscles of facial expression [Image 3]. By identifying which actions are reduced/absent one can identify the lesion of the facial nerve [Table 1] and what treatment options are available.




Facial palsies can occur due to a number of causes [Table 2]. However, the most common cause of acquired facial palsy in the UK is Bell's palsy, with 1 in 70 people having Bell's palsy at sometime in their life. Bell's palsy is a sudden onset of facial paralysis, usually affecting only one side. It appears much like a stroke, however, as it is a lower motor neurone lesion, the forehead is NOT spared. (N.B. An upper motor neurone lesion such as a stroke does not paralyse the forehead due to bilateral innervation).


It is believed to be caused by inflammation around the facial nerve compressing it. The cause for the inflammation is still uncertain, however there is some evidence that it may be due to re-activation of the herpes simplex virus or the varicella zoster virus. The prognosis of Bell's palsy is very good (approximately 85% will make a full recovery and most will do so within a couple of months), however there are still some people who do not fully recover and need some further support and treatment.


Classification of facial paralysis


There are a variety of different grading systems to assess the extend of facial paralysis, but the most widely accepted is the House-Brackman classification:




  1. Normal
  2. Mild Dysfunction
  3. Moderate Dysfunction
  4. Moderately Severe Dysfunction
  5. Severe Dysfunction
  6. Total Paralysis


Grade I. Normal


Normal facial movement


Grade II. Mild Dysfunction



- slight weakness noticeable on close inspection

- may have slight synkinesis

- at rest: normal symmetry and tone



- FOREHEAD moderate to good function

- EYE complete closure with minimal effort

- MOUTH slight asymmetry


Grade III. Moderate Dysfunction



- obvious but not disfiguring difference between both sides

- noticable but not severe synkinesis, contracture or hemifacial spasm

- at rest: normal symmetry and tone



- FOREHEAD slight to moderate movement

- EYE complete closure with effort

- MOUTH slightly weak with maximum effort


Grade IV. Moderately Severe Dysfunction



- obvious weakness +/- disfiguring asymmetry

- at rest: normal symmetry and tone




- EYE incomplete closure

- MOUTH asymmetric with maximum effort


Grade V. Severe Dysfunction



- only barely perceptible motion

- at rest: asymmetry




- EYE incomplete closure

- MOUTH slight movement


Grade VI. Total Paralysis


No movement


1. Bell's Palsy


The most common cause of facial nerve palsy is Bell's Palsy. It classically presents as facial distortion, loss of taste, hyperacusis and a watery eye, however it is usually diagnosed by exclusion. Approximately 85% of patients will recover within a few months, but there will be some patients who will not and these patients may need surgical interventions.


On the whole, treatment of Bell's Palsy is usually with steroids, antivirals and eye care to prevent exposure keratitis:


  •  Eye care education (natural tears, taping eyes when asleep, use of a moisture chamber)
  •  Oral prednisolone to prevent/lessen the degeneration, reduce synkinesis and relieve pain


Regieme 1: 1mg/kg/day (max 80mg/day) for 1 week then taper in 2nd week.

Regieme 2: 10-day tapering course starting with 60mg/day


  •  Acyclovir 400mg five times a day for 7 days... or
  •  Valacyclovir 1g three times a day for 7 days


If the patient has a complete paralysis, electoneurography (ENoG) is performed by an audiologist 4-6 days post-onset. ENoG examines and records the integrity and conductivity of a nerve by comparing the the affected side to the none affected side - so the paralysis must be unilateral!


For the facial nerve the stimulation electrode is placed on the stylomastoid foramen and the recording electrode is placed near the nasolabial fold. ENoG helps clinicians to decide on the patient's management:


  •  <90% degeneration: the usual course of action is steroids and antivirals, with a repeated ENoG within 2 weeks
  •  >90% degeneration: facial nerve decompression should be performed within 2 weeks to allow for axonal regeneration. (N.B. the commonest site of compression is within the meatal foramen as this is the narrowest part of the facial canal)


Permanent lesions are labelled as such if there is no recovery about 10 months post-onset. These patients are referred to plastics for individualised static or dynamic treatment.


2. Trauma


Trauma is the 2nd commonest cause of facial palsy. 10-20% of patients with temporal bone fractures will have facial nerve injury, with the majority occuring in the perigeniculate region.


Patients with a facial nerve injury and temporal bone fracture are split into two groups: those with a complete facial paralysis, and those with an incomplete facial paralysis.




A patient with an obvious fracture of the temporal bone on CT should be send to theatre for surgical exploration of the facial nerve (if of course the patient is in a stable condition). In theatre the surgeon will remove any compression caused by the fracture fragments and and haematomas within the nerve sheath.


If the surgeon discovers a complete transection of the nerve, a direct end-to-end anastomosis should be performed unless this would create tension or if the nerve is severly damaged or has missing segments. In this case the surgeon can perform an interpositional graft using the greater auricular, medial antebrachial cutaneous or sural nerve.




On day 4 facial nerve testing should be performed to see the extent of the damage. If the test shows that there is advanced nerve degeneration surgical exploration of the facial nerve and decompression is the most ideal management plan.


3. Ramsay-Hunt Syndrome


Ramsay-Hunt Syndrome (RHS) is caused by a reactivation of a dormant varicella zoster virus in the extramedullary cranial nerve ganglion. This condition is the 3rd most common reason for facial palsy, but can be confused with Bell's Palsy. However, unlike Bell's Palsy, RHS patients have only a 50% chance of regaining normal function.


Treatment for RHS is somewhat idential to that of Bell's Palsy due to the role of the varicella zoster virus.


4. Tumours


Tumours account for 5% of all facial palsy cases. Although this is only a small number of cases compared to Bell's Palsy for example, it is very important to exclude this possibility for obvious reasons.


Clinical findings which should raise suspicion include:


  •  slow developing paresis of more than 3 weeks
  •  facial twitching
  •  additional cranial nerve deficits
  •  recurrent ipsilateral involvement
  •  associated lymphadenopathy
  •  palpable neck or parotid mass


Once a tumour has been diagnosed with the help of a MRI/CT scan, the management plan depends upon the site of the lesion, size and its malignant potential.


The most common BENIGN tumour to cause facial palsy is a facial nerve schwanomma.


The most common MALIGNANT neoplasms are mucoepidermoid carcinoma and adenoid cystic carcinoma of the parotid gland.


Surgical options for facial palsy include transposition of the nerve, division, reanastomosis, interposition grafting and cranial nerve crossover (see section: Cranial Nerve Crossover).


Plastic Surgery Techniques


Not all cases of facial palsy require surgery, particularly surgery in Bell's Palsy is rather contraversial, but many patients with chronic (>2 years) facial palsy will be offered plastic surgery whether it be a dynamic or static procedure.


Treatment options include:


  •  Selective ipsilateral and contralateral Botox chemodenervation
  •  Brow lift
  •  Fascia lata slings
  •  Alloderm
  •  Suture suspension
  •  Upper lid loading
  •  Lower lid cathoplasty
  •  Temporalis muscle transposition
  •  Free tissue transfer
  •  Nerve grafting
  •  Selective myectomy


Three of the most successful dynamic procedures are cranial-nerve crossover, temporalis muscle transfer and eyelid weighting.


Cranial Nerve Crossover

Patients who lose their facial nerve during excision of a tumour in the temporal bone, parotid gland or skull base, often undergo nerve crossover. The most popular is the hypoglossal (CN XII) to facial (CN VII) crossover.


The hypoglossal nerve is usually located inferior to the digastric muscle and is identified using nerve stimulation. The nerve is skeletonised distally towards the tongue and transected as distally as possible. The transected end of the hypoglossal nerve is anastomosed to the main trunk or a secondary division of the facial nerve [Image 4].



  •  Relatively simple
  •  Can be performed up to 2 years after lesion
  •  Over 90% of patients have improved tone and symmetry



  •  Not suitable for patients with degenerative conditions where the facial nerve distal to the lesion is not intact
  •  Can cause subtle articulaion problems
  •  Some patients (up to 15%) can have excessive facial tone, hyperactivity and/or spasms, but this is rarely severe enough to warrant a reversal


Temporalis Muscle Transfer


The temporalis muscle is a large fan-shaped muscle and, as such, can be used as a transfer to reanimate the mouth: when the patient clenches their teeth the transferred muscle causes the corner of the mouth to be elevated, producing a smile.


An incison is made in the preauricular crease and extended into the superior temporal line. The middle third of the temporalis muscle is harvested: the periosteum is separated from the skull base and the harvested muscle is elevated and folded in on itself, to allow to be passed through a made tunnel over the zygomatic arch.


A second incison is then made in the nasolabial fold to produce a symmetrical crease. the harvested muscle is then passed through the tunnel and attached to the orbicularis oris muscle [Image 5]. The procedure must be completed in an overcorrected state, because the operated side of the face relaxes after surgery.



The middle third of the temporalis muscle is used because the anterior third of the muscle tends to be short, bulky and poorly oriented whilst the posterior third is poorly oriented and lacks appropriate contacilility.


Before suturing is closed, the space created by the transferred temporalis muscle can be filled by use of local tissue or implants.



  •  Can be used when an intact facial neuromuscular system is absent
  •  Almost immediate response
  •  Produces a voluntary and more natural looking smile



  •  Invasive
  •  Removing a muscle from one area leaving a space which needs to be filled for and acceptable cosmetic outcome
  •  Patient has to eat a soft diet for 4 weeks post-op


Eyelid weighting


The facial nerve enables you to close your eyelid which protects the eye. A common problem in facial palsy is the loss of ability to close the eyelid increasing the risk of conjunctivitis, exposure keratitis and blindness.


One technique used by plastic surgeons involves inserting a gold or platinum weight into the upper eyelid, allowing the force of gravity to close the eyelid:


Firstly an external test is performed by taping several different sizes and weights to the outer eyelid to find the correct weight to enable rapid eye closure but without excessive drooping [Image 6]. This can also be used as a 'tester' if a patient is not sure about whether to have the procedure.


Once the correct weight is identified the surgeon makes a transverse incision in the skin of the lateral upper eyelid. The weight is then inserted into a pocket made behind the remnant of the orbicularis oculi muscle, so that it lies at the midpoint of the eyelid, and secured.



  •  Simple, quick operation
  •  Immediate results
  •  Reduces the need of use of eye lubricants



  •  Invasive
  •  Inserting a relatively inert metal may ulcerate the overlying skin
  •  Many patients can fear surgery near/to the eye




  •  The most common cause of facial palsy is Bell's Palsy, of which the majority of cases will resolve within a few months with minimal treatment
  •  REASSURE the patient - many Bell's Palsy patient's may think they've had a stroke and are therefore scared
  •  A slow onset of facial palsy with other cranial nerve deficits should raise suspision of a possible tumour
  •  Treatment for facial palsy is individualised
  •  If reanimation can not be achieved static support should be offered




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