FACIAL NERVE AND ITS DISORDERS

Submitted byManjari ReshikeshIV BDS IIDEPARTMENT OF ORAL AND MAXILLOFACIAL SURGERY

FACIAL NERVE• Facial nerve is the seventh cranial nerve • Known as “QUEEN OF FACE”• Also known as “ Nervus facialis ”• Mixed nerve- both motor & sensory• Nerve of second branchial arch• It controls muscles of facial expressions• controls Taste sensations

EMBRYOLOGY• Develops from 2nd pharyngeal arch (hyoid)• Formation of facial nerve begins at 3rd week of

emryonic life • Course,branching,anatomic relations

completed at the end of 3rd month of prenatal life

• Not fully developed till 4yrs

ANATOMY

NUCLEI OF FACIAL NERVE1. Motor nucleus or branchiomotor2. Superior salivatory nuclus or parasympathetic3. Lacrimatory4. Nucleus tractus solitarius (NTS)

FUNCTIONAL COMPONENTS1. Special visceral or branchial efferent (SVE) to muscles of facial expression and elevation of hyoid bone2. General visceral efferent or parasympathetic scretomotor(GVE) to• submandibular &sublingual gland• Lacrimal gland• Glands of Nose, palate & pharynx3. General visceral afferent(GVA)- carries

impulses from above glands4. Special visceral afferent – carry taste

sensations from palate and anterior 2/3rd tongue5. General somatic afferent- a part of skin of ear

GSA

COURSE OF FACIAL NERVE

BRANCHES AND DISTRIBUTION1.Within the facial canal:• Greater petrosal nerve• Nerve to stapedius• Chorda tympani2. As it exits from stylohyoid foramen• Posterior auricular• Digastric• Stylohyoid

3.Terminal branches•Temporal•Zygomatic•Buccal•Marginal mandibular•Cervical4. Communicating branches with adj spinal &cranial nerves

FACIAL NERVE DISTURBANCE•Weakness of facial muscles to

perform motor functions – paresis(partial)

•Total flaccidity - paralysis•Dreaded functional & esthetic

complication•Loss of control of

lips&cheeks- affect drinking& mastication

• cornea- pain, visual acuity

•Facial assymetry

•Unilateral facial weakness•Loss of taste•Hyper acusis•Vesicles in the ear(shingles)•Facial pain]•decreased salivation•Decreased tear secretion

FACIAL NERVE PARALYSISFacial nerve paralysis is a common problem that

involves paralysis of any structures innervated by facial nerve.

Pathway of facial nerve is long and convoluted, so there are a number of causes that result in facial paralysis.

facial nerve paralysis classified as 1. Supranuclear lesions(UMN lesion)2. Infranuclear lesions(LMN lesion)

UMN LESION VS LMN LESION

Central Vs peripheral palsy

CLASSIFICATION OF FACIAL PALSY

House- Brackmann (1985)classificationGrade I: normal function without weakness

Grade II: Mild dysfunction with slight facial assymetry with minor degree of synkinesis

Grade III: Moderate dysfunctions-obvious assymetricwith contracture &/hemifacial spasm,but residual forehead movement

Grade IV: moderately sever dysfunction-obvious disfiguring assymetry with lack of forhead motion and incomplete eye closureGrade V: severe dysfunction-assymetry at rest and only slight movementGrade VI: Totalparalysis: complete absence of tone/motion

Rainer schmelzein et al (1999)based on causes1.Congenital Rare- congenital aplasia- moebius syndrome Myotonic dystrophy Melkersson-rosenthal syndrome Congenital cholesteatoma/facial palsy2.Neurologic: Myasthenia gravis Multiple sclerosis Gullain barre syndrome3. Neoplastic Tumors-schwannoma,neuro fibroma,neurogenic

sarcoma Glomus tumor,,parotid tumors,temporal tumors

4. Infection Otitis media,mastoditis Bacterial cause(diphtheria,TB) Viral causes(herpes zoster,lyme

disease, mumps, IMN)5. Other causes- Toxic, metabolic(DM), idiopathic(bells)6. Iatrogenic- parotidectomy, rhytidectomy,lat. skull base surgery7. Traumatic temporal bone #,penetrating trauma(gunshot)Facial lacerations,high altitude palsy

As a complication of IANB – into parotid gland

Systemic causes▫Diabetes Mellitus▫Hypothyroidism▫Uremia▫Polyarteritis Nodosa▫Wegener’s granulomatosis▫Sarcoidosis▫Leprosy- ALL▫Leukemia

NERVE INJURIES1. Seddons classification•Neuropraxia•Axonotmesis•neurotmesis2.Sunderland classification•1st degree( type I ,II,III)•2nd degree•3rd degree•4th degree•5th degree

NERVE INJURIESNeuropraxia: (Rev. conduction block)▀ Epineurium& endoneurium intact but nerve is just

compressed▀ No axonal degeneration distal to site▀ Temporary conduction block▀ No surgical intervention

Axonotmesis: (prolonged conduction block) Loss of continuity of some axons(axonal

degeneration) Distal to site, WALLERIAN DEGENERATION

occurs After 3 months, initial signs of recovery

Neurotmesis; (total permanent conduction block) Complete severence of all layers of nerve Distal to injury wallerian degeneration occurs Space between proximal & distal filled by

scar tissue Surgical intervention must

Wallerian degeneration

SUNDERLAND CLASSIFICATION

1st degree (neuropraxia(seddon) no axon degeneration, only compression rapid and complete return of sensation3 types based on mechanism of injury:Type 1: mild compression anoxia. No axon degenerationReturn to normal within 24 hrsType 2: moderate compression injure capilaries conduction block intrafascicular edemaRecovery- 1 week

Type 3 : severe compression segmental demyelinationRecovery- 1-2 monthsSurgery not indicated2nd degree: Axonal injury with degeneration & regeneration.Compression ischemia edema/ demyelinationEpineurium, perineurium and endoneurium intact2-4 months- signs of sensation Complete recovery by 1 yearUnless an extraneurial irritant inhibits recovery, no surgery

3rd degree: severe compression not only axon, endoneurium damagedSensation within 2- 5 months. Recovery never completeEndoneurial fibrosis prevent axon regenration leading to neuroma 4th degree: 1. traction2. Compression3. Injection injury4. Chemical injuryAxon, endoneurium and perineurium damagedEpineurium intactPoor prognosis

5th degree: Severe disruptionTissue loss alsoLaceration & avulsionAll layers of nerve disruptedAmputation neuroma may occurPoor prognosisMicroconstructive surgery

indicated

BELL’S PALSYHISTORY

• from Sir Charles Bell (1774-1842)

• Studied facial anatomy extensively• Concluded that facial nerve

controlled facial expression

• “Respiratory nerve of Face”

• Demonstrated separation of the motor and sensory innervation of face

•DEFINITION : an idiopathic paresis or paralysis of facial nerve of sudden onset.

•Most common cause of facial paralysis•15-40 cases per 1 lakh•Both sexes equally affected•Seen more in middle aged•Diabetics r more prone•Family history •Mostly unilateral. Only 1% bilateral

Etiology•Idiopathic• autoimmune response•Viral hypothesis•Ischemic hypothesis: factors producing

vasospasm 1. cold2. anoxia3.Injury4.Toxicity5.Allergic

Signs and symptoms• Sudden onset• Unable to close eyes• Bells phenomenon( eyeball rolls

up and out on attempting to close the eye & white sclera visible)

• Dribbling of saliva• Epiphora• Assymetrical face• Noise intolerance• Loss of taste• Unable to smile on affected side• Drooping corners of mouth

* RAMSAY HUNT SYNDROME(Herpes zoster oticus)

*James Ramsay hunt (1907)*Caused by varicella zoster *Infection along facial nerve near inner ear*Syndrome occurs when geniculate ganglion is involved

due to reactivation*Classical triad:1. Ipsilateral facial paralysis2. Ear pain/hearingloss3. Vesicles in pinna,* Sensation of spinning* tinnitus

* MELKERSSON- ROSENTHAL SYNDROME*Also known as orofacial granulomatosis

*Idiopathic Neurological disorder*Non tender persistent swelling of one or both lip*Facial paralysis*Lingua plicata(fissured tongue)

MOEBIUS SYNDROME•Described by

Moebius(1888)•Rare neurological disorder•Congenital oculofacial

paralysis•Congenital defect -Paralysis

of VII and VI neves•Mask like face –

expressionless•Unable to close eyes-

corneal ulcerations•strabismus

GUILLAIN BARRE SYNDROME• first Described by Jean

landry (1800s)•Discovered by jean barre

and georges guillain(1916)

•Inflammatory demyelinating poly neuropathy affecting peripheral nerves including VII nerve causng facial palsy

•Treated by IVIG&•Plasma exchange

TRANSIENT FACIAL PALSY•Encountered during IANB•Due to injection of LA into parotid gland

ifneedle injected too backwards•Temporary paralysis of facial nerve•Effect wears off over a period of time(<3Hrs)

during which eye needs to be protected(eye patch)

Hyperkinetic disorders •Involuntary twitching of facial

muscles on one or both sides1. Hemifacial spasm- on one

side due to irritation of nerve @ cerebellopontine angle ( microvascular decompression, botulinum toxin)

2. Blepharospasm- limited to orbicularis oculi on both sides (bot toxin into periorbital muscles

1.Facial nerve evaluation careful case history for onset,duration and

degree of recovery Acute onset in morning- bell’s palsy Sudden onset –infectious/inflamatory Neoplasm-paresis over long period of time Trauma-definite history Delayed onset- better prognosis Full otologic investigation needed

2. Examination of face at rest & motion to differentiate paresis & paralysis

DIAGNOSIS

Raise eyebrowsClose eyes against resistanceForced smile- buccal & marginal mandibularDepth of nasolabial foldPuff out cheeks

Schirmer’s test• Measurement of wetting of filer paper (41 whatman)

(35x5mm)• Folded and placed @ juntion of middle and outer third of

lower lid• Asked to keep eyes closed• After 5 mins,measured• If +ve,lesion @ geniculateganglion

Stapedius reflex test• Stapedius reflex – involuntary muscle contracion that occurs

in middle ear in response to high intensity sound stimuli• Absent reflex or reflex less than1 /2 of amplitude of

contralateral abnormal• Acoustic reflex equipment• 69% facial palsy- absent

Electro gustometry• Simplest regional evaluation of taste• EGM delivers taste sstimuli in controlled manner• To dtermine gustatorythresholds by electric stimulus on L/R or

A/P tongue• Stimulated chordatympani• electrode atached to tongue

• Current passed till patient feels metallic/sour taste

Submandbular Salivary flow test• Cannulate wharton duct on each side with no. 50

polyethylene tube• Stimulate saliva with lemon juice• Output measured• 25%reduction significant

Electromyography• Recording of spontaneous or voluntary muscle potenitials by

needle electrodes introduced to muscles is EMG• Records potential of muscles at function and rest• In early stage, use is limited (10-14 days post onset)Useful in assesing reinnervation after 2 weeks

ElectroNeurography(ENoG)• Most accurate prognostic test• Objective,qualitative measurement of neural degeneration• Nerve stimulated with impulse TC at using bipolar electrodes• Place electrodes one each on either sides of nose &forehead• Electrical stimulator used & placed in front of ear• Recordings obtained in computer• Peak to peak amplitude- intact axons• Two sides compared.• Reduction in amplitude <10 %- poor prognosis

Nerve excitability test/ hilgers test

• Commonly used • Minimum threshold current to elicit twitching/ visible muscle

movement on both affected and unaffected side and compare• Placement of stimulating electrode at stylomatoid foramen.• Difference .3.5 mA – poor prognosis

•Maximum stimulation test• Modified version of NET• Same equipment• Maximum stimulus applied on unaffected side until no Further increase in response obtained. Same stimuli applied on AS.• If no response, decompression is only option

IMAGING MRI with IV gadolinium contrast revolutionised tumor detetction In case of tumors, MRI is choice

CT – valuable in surgical planning of cholesteatoma and skull base fractures

Exclusion of other pathologies

Complications of facial paralysis• Synkinesis/ Mass movement• Tics & spasms• Crocodile tears/bogorad’s

syndrome• uncommon consequence of

regeneration causing communication between salivatory nucleus and lacrimal glands

• unilateral lacrimation with mastication(faulty regeneration )

• Exposure keratitis

TREATMENT• Based on etiology of nerve damage/

dysfunction treatment is planned.

1. Medical Management2. Surgical Management

Medical Management

• Physiotherapy- in case of bell’s palsy or paralysis, muscle atrphy may occur. So massage, excercises indicated

• Within 2- 3weeks of onset, prednisolone 1mg/kg for 10 -14 days with tapering

• Vitamins B1,B6,B12 administered• Antivirals like acyclovir 400 mg 5 times a day

SURGICAL MANAGEMENT

• Open injuries of facial nerve repaired surgically as soon as possible

• 12 months - limit for successful repair

• NERVE DECOMPRESSION• NEURORRHAPHY• NERVE TRANSFER• MUSCLE TRANSPOSITION• TARSORRAPHY• Static procedure: GOLD

IMPLANTS,

Facial Nerve Decompression

• Compression on facial nerve is relieved

• 2 approachesMiddle cranial approach is common• Used to relieve compression

of facial nerve in bell’s palsy and temporal bone fracture

• The bone fragments are removed and compression releived

NeurorraphyEND TO END ANASTOMOSIS

• Surgical repair of transected facial nerve is done with direct end to end approximation and suturing(Lacerations, iatrogenic injuries,benign conditions)

• May be epineural only or along with perineural suture• 9-0 8-0 nylon monfilament

2. NERVE GRAFTINGIf there is gap between proximal & distal- autogenous grafting done. And if gap>1cm – cable graft• The hypoglossal nerve • Sural nerve - 1cm posterior to

lateral malleolus • Great auricular nerve• Branches from cervical plexus

*Cross- facial nerve

grafting/Reanimation

*Employs a nerve graft typically sural nerve that acts a connection for motor axons from normal to affected facial nerve

*FISCH Technique- on nonparalysed side intact buccal branch connected to paralysed stem of facial nerve by sural graft

Facial hypoglossal transfer

When direct and grafting procedures not possible

An intact distal segment and muscles suitable for reinnervation

Nearly normal appearence at rest

With stump of 12th nerve hooked to end of 7th nerve,fac will move when tongue is moved

Nerve transfers

TEMPORALIS MUSCLE TRANSPOSITION

• Exposure of temporalis muscle through extended preauricular incision

• Elevation of temporalis muscle slings

• Slings brought forward through tunnel to commisure

• Tunneling near outer canthus of eye

• Slings transposed to upper and lower eyelids

Tarsorrhaphy0 Eyelids are partially sewn together to narrow eyelid

opening0 Done to protect cornea as in facial palsy

Mc Laughlins tarsorrhaphy incisons

Gold / platinum lid weights

Before and after placement

Facial Reanimation Results

BEFORE AFTER

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