Dr. Zaimal ShahanPost Graduate TraineeENT DEPARTMENTCAPITAL HOSPITAL

Anatomy

Anatomy

Anatomy

Anatomy

Type of Fibers

Facial nerve is a mixed nerve, having a motor root and a sensory root.

Motor root supplies all the mimetic muscles of the face which develop from the 2nd brachial arch.

Sensory root “nerve of Wrisberg” carries taste fibers from the anterior 2/3 of the tongue and general sensation from the concha and retroauricular skin.

Also it carries secretomotor fibers to the lacrimal, submandibular and sublingual glands as well as those in the nose and palate.

Nuclei

Motor nucleus of facial nerve (SVE):

It lies in the lower part of the pons

Superior salivatory nucleus (GVE):

It lies in the pons lateral to the main motor nucleus of VII and gives rise to secretomotor

parasympathetic fibers that pass in greater superficial petrosal nerve and chorda tympani.

Nucleus solitarus (SVA):

It lies in the medulla, receives the taste sensation from the anterior 2/3 of the tongue via the central processes of the cells of the geniculate ganglion of the facial nerve

GSA fibers :

Through these fibers to acoustic meatus & back of auricle through communication from auricular branch of vagus. These fibers terminate in main sensory nucleus & spinal nucleus of 5 th nerve

Nucleus xxxx

Pons. precentral gyrus. Upper part of the nucleus:

Upper face Involuntary emotional movements

Course

Motor fibers originate… Hooks around the abducent nucleus in the floor of the

4th ventricle forming facial colliculus Joined by… Facial n. leaves the brainstem… Travels through… Enters the IAC. Then traverse the temporal bone through facial n.

canal Leaves the temporal bone through Finally divides into terminal branches.

Internal course: the motor fibres passes dorsally and medially forming a loop around the abducent nucleus in the floor of the 4th ventricle forming facial colliculus

COURSE OF FACIAL NERVE xxxx

Superficial origin: at the pontomedullary angle above the inferior cerebellar peduncle.

1- Facial nerve proper (motor): arising from facial motor nucleus in pons.

2- Nervus intermedius: it is the sensory root of facial lies position between the facial proper and vestibulcochlear nerve in the pontocerebellar angle.

Carrying para-sympathetic fibers (from superior salivary nucleus) and taste fibers ( to the solitary nucleus).

The facial nerve is formed mainly of two parts:

Course and relations: I- Intracranial (intrapetrosal) course

II- Extracranial course

I- The intrapetrous course:

A.Meatal segment

B.Labyrinthine segment

C.Tympanic segment

D.Mastoid segment

A.MEATAL SEGMENT

8-10 mm

B.LABYRINTHINE SEGMENT3.5-4.0mmObliquely forwardPerpendicular to temporal boneNARROWEST PARTChanges direction----- 1st GENU

GENICULATE GANGLION:Junction of FACIAL NERVE+NERVUS INTERMEDIUS

II- Extracranial course:

As it emerges from the stylomastoid foramen, it runs forwards in the substance of the parotid gland crosses the styloid process, the retromandibular vein and the external carotid artery.

It divides behind the neck of the mandible into its terminal branches which come out of the anteromedial surface of the gland.

BRANCHES1.PETROSAL NERVES

2.GREATER SUPERFICIAL PETROSAL NERVE

3.LESSER PETROSAL NERVE

4.EXTERBNAL PETROSAL NERVE

Parts

Intracranial part Intratemporal part Extracranial part

Intratemporal segments Meatal Labyrinthine Tympanic, horizontal Mastoid, vertical

Branches

Greater superficial petrosal nerve: Nerve to stapedius: Chorda tympani: Comunicating branch: Posterior auricular nerve: Muscular branches: Peripheral branches: “Pes anserinus”

Temporal Zygomatic Buccal Marginal Mandibular Cervical

Surgical landmarks

Middle Ear and Mastoid Surgery: Processus chocleariformis Oval window and horizontal canal Short process of the incus Pyramid

Parotid Surgery: Cartilaginous pointer: Styloid process Posterior belly of digastric muscle Tympanomastoid suture

Anatomy: Structure of the nerve

From inside outward: Axon Myelin sheath Neurolimma Endoneurium Perineurium Epineurium

Branches

Branches of communication Branches of distribution

Internal acoustic meatus

Vestibulocochlear nerve

Geniculate ganglion A. Greater petrosal nerve

B. Lesser petrosal nerve

C. External petrosal nerve

Facial canal Vagus nerve

Stylomastoid foramen IX & X cranial nerveGreater auricular nerveAuriculotemporal nerve

Behind ear Lesser occipital

Face V nerve

Neck Transverse cutaneous nerve

Branches of Communication

Branches of Distribution

Facial canal A.Nerve to stapedius

B.Chorda tympani

In face A.Temporal

B.Zygomatic

C.Buccal

D.Marginal mandibular

E.Cervical

Stylomastoid foramen

A.Posterior auricular

B.Nerve to stylohyoid

C.Nerve to digastric (posterior belly)

Facial Nerve: Functional Components

Special Visceral Efferent/Branchial Motor

General Visceral Efferent/Parasympathetic

General Sensory Afferent/Sensory

Special Visceral Afferent/Taste

Special Visceral Efferent/Branchial Motor

Premotor cortex motor cortex corticobulbar tract bilateral facial motor nuclei (pons) facial muscles

Stapedius, stylohyoid, posterior digastric, buccinator

GANGLIA ASSOCIATED WITH THE FACIAL NERVE Geniculate ganglion

Submandibular ganglion

Pterygopalatine ganglion

Geniculate Ganglion

The geniculate ganglion (from Latin genu, for "knee") is an L-shaped collection of fibers and sensory neurons of the facial nerve located in the facial canal of the head.

It receives fibers from the motor, sensory, and parasympathetic components of the facial nerve and sends fibers that will innervate the lacrimal glands, submandibular glands, sublingual glands, tongue, palate, pharynx, external auditory meatus, stapedius, posterior belly of the digastric muscle, stylohyoid muscle, and muscles of facial expression.

Submandibular Ganglion

The submandibular ganglion is small and fusiform in shape. It is situated above the deep portion of the submandibular gland, on the hyoglossus muscle, near the posterior border of the mylohyoid muscle.

The ganglion 'hangs' by two nerve filaments from the lower border of the lingual nerve (itself a branch of the mandibular nerve, CN V3). It is suspended from the lingual nerve by two filaments, one anterior and one posterior. Through the posterior of these it receives a branch from the chorda tympani nerve which runs in the sheath of the lingual nerve.

Pterygopalatine Ganglion

The pterygopalatine ganglion (meckel's ganglion, nasal ganglion or sphenopalatine ganglion) is a parasympathetic ganglion found in the pterygopalatine fossa.

It's largely innervated by the greater petrosal nerve (a branch of the facial nerve); and its axons project to the lacrimal glands and nasal mucosa

Testing of Facial Nerve Branches

Testing the temporal branches of the facial nerve To test the function of the temporal branches

of the facial nerve, a patient is asked to frown and wrinkle his or her forehead.

Testing the Zygomatic branches of the facial nerve

The patient is asked to close their eyes tightly.

Testing the buccal branches of the facial nerve Puff up cheeks (buccinator) Smile and show teeth (orbicularis oris) Tap with finger over each cheek to

detect ease of air expulsion on the affected side

The marginal mandibular nerve may be

injured during surgery in the neck region,

especially during excision of the

submandibular salivary gland or during

neck dissections.

Evaluation of Facial paralysis

Clinical feature Central VS Peripheral facial paralysis Complete head and neck examination Cranial nerve evaluation Electrodiagnostic testing Topographic diagnosis

Central facial paralysis

Upper motor neuron lesion

Movements of the frontal and upper orbicularis oculi tend to be spared

Because of uncrossed contributions from ipsilateral supranuclear areas

Involvement of tongue

Involvement of lacrimation and salivation

Peripheral paralysis

Lower motor neuron lesion

At rest : less prominent wrinkles on forehead of affected

side, eyebrow drop, flattened nasolabial fold, corner of mouth turned down

Unable to : wrinkle forehead, raise eyebrow, wrinkle

nasolabial fold, purse lips, show teeth, or completely close eye

House-Brackmann grading system

Grade I - Normal Grade II - Mild dysfunction, slight weakness on close inspection, normal symmetry at rest Grade III - Moderate dysfunction, obvious but not disfiguring difference between sides, eye can be completely closed with effort Grade IV - Moderately severe, normal tone at rest, obvious weakness or asymmetry with movement, incomplete closure of eye Grade V - Severe dysfunction, only barely perceptible motion, asymmetry at rest Grade VI - No movement

TOPOGNOSTIC TESTING

1. Schirmer test for lacrimation (GSPN)2. Stapedial reflex test (Stapedial branch)3. Taste testing (Chorda tympani nerve)4. Salivary flow rates & pH (Chorda tympani) ELECTROPHYSIOLOGIC TESTS

Nerve excitability test (NET)Electromyography(EMG) Maximal stimulation test (MST) Electroneuronography (ENoG)

DYES

Testing of Facial Nerve

Topographic Diagnosis

To determine the anatomical level of a peripheral lesion

Lacrimation Geniculate ganglion

Stapedius reflex motor nerve of stapedius muscle

Taste chorda tympani

Schirmer's Test

Geniculate ganglion & petrosal nerve function test

Schirmer’s test +ve when

Affected side shows less than half the amount of lacrimation seen on the normal side

Sum of the lengths of wetted filter paper for both eyes less than 25 mm

Lesion at or proximal to the geniculate ganglion

Schirmer's Test

Stapedius reflex

Nerve to stapedius muscle test

Impedence audiometry can record the presence or absence of stapedius muscle contraction to sound stimuli 70 to 100 db above hearing threshold

An absence reflex or a reflex less than half the amplitude is due to a lesion proximal to stapedius nerve

Taste (Electrogustometry)

Chorda tympani nerve test

Solution of salt, sugar, citrate, quinine or Electrical stimulation

Compares amount of current require for a response each side of tongue

Normal : difference < 20 uAmp (thresholds differening by more than 25%= abnormal)

Total lack of Chorda tympani : No response at 300 uAmp

Disadvantage : False +ve in acute phase of Bell’s palsy

Maximum stimulation Test: MST:

Indication: complete paralysis<3wks

Interpretation:

Marked weakness or no muscle contraction:

advanced degeneration with guarded prognosis

Electroneurography: ENoG

Indication: complete paralysis<3wks

Interpretation: < 90% degeneration: prognosis is good; > or = 90%: prognosis is a question

Limitation: False-positive results in deblocking phase.

Electromyography: EMG

Indication: Acute paralysis less than 1 week or chronic paralysis longer than 2 weeks

Interpretation:

Active mu: intact motor axons

Mu + fibrillation potentials: partial degeneration

Polyphasic mu: regenerating nerve

Limitation: cannot assess degree of degeneration or prognosis for recovery

Anatomy: Severity of injury

Saunderland classification: 1°: Partial block: Neuropraxia 2°: Loss of axons: axonotemesis 3°: Injury to the endoneurium: neurotemesis 4°: Injury to the perineurium: partial

transection 5°: Injury to the epineurium: complete

transection

History:

Onset: Sudden vs. Gradual Duration: Rate of progression: Recuurent or familial Associated symptoms Medical history Previous surgeries

Physical exam:

Complete vs. incomplete Segmental vs. uniform involvement Unilateral vs. bilateral Cranial nerves assessment Neurologic evaluation Cerebellar signs

Physical exam:

Microscopic otoscopy Complete head and neck exam

Physical exam:

Localization of facial nerve lesion: Central vs. Peripheral.

Physical exam:

Localization of facial nerve lesion:

Peripheral: Level of nucleus CPA level: Bony canal level: Topodiagnostics Outside the Temporal bone

Physical exam:

Topodiagnostics: Schirmer’s test: Stapedial reflex: Taste test: Submandibular salivery flow test: Warton’s

ducts

Causes:

Central: Intacranial part: Intratemporal part: Extracranial part: Systemic:

Disorders of Facial Nerve

1. Supra nuclear type:

Features:

a) Paralysis of lower part of face (opposite side)b) Partial paralysis of upper part of facec) Normal taste and saliva secretiond) Stapedius not paralysed

Facial Nerve Lesions

2. Nuclear type:

Features:

a) Paralysis of facial muscle (same side)

b) Paralysis of lateral rectus

c) Internal strabismus

3. Peripheral lesion

A.INTRACRANIAL(CPA)

Acoustic neuroma

Meningioma

Congenital cholesteatoma

Metastatic carcinoma

Meningitis

B.INTRATEMPORAL

1.IDIPOPATHIC

BELL PALSYMELKERSON SYNDROME

2.INFECTIONS:

ASOMCSOMHERPES ZOSTER OTICUSMALIGNANT OTITIS EXTERNA

3.TRAUMA:

A.SURGICAL:

Mastoidectomy + Stapedectomy

B.ACCIDENTAL:

Fracture TB

D.NEOPLASTIC:MalignanciesGlomus jugulareFacial nerve neuromaMetastasis to temporal bone

B.EXTRACRANIALParotid malignancyParotid surgeryAccidental traumaNeonatal trauma

Lesion at int acoustic meatus

SYSTEMIC DISEASESDMHypothyroidismUraemiaSarcoidosisLeprosyLeukemiaDemyelinating diseases

Lesion distal to geniculate ganglion

A.IDIOPATHIC

1.BELL PALSY

First described more than a century ago by Sir Charles Bell

Demographics of Bells palsy

Race: slightly higher in persons of Japanese descent. Sex: No difference exists Age: highest in persons aged 15-45 years.

Bell palsy is less common in those younger than 15 years and in those older than 60 years.

Pathophysiology of Bells palsy

IDIOPATHIC

1.ISCHEMIC THEORY

2.VIRAL THEORY

3.AUTOIMMUNE THEORY

Bell's phenomenon is the upward diversion of the eye ball on attempted closure of the lid is seen when eye closure is incomplete.

Features of Bell’s Palsy

Fore head

Diagnosis of Bells palsy

By exclusion

Criteria

Paralysis or paresis of all muscle groups of one side of the face

Sudden onset

Absence of signs of CNS disease

Absence of signs of Ear disease

Medical treatment

Corticosteroids :

Prednisolone 1 mg/kg/day 7-10 days Corticosteroids combine with antiviral drug is better

Acyclovir 400 mg 5 times/day Famciclovir and valacyclovir 500 mg bid

Surgical treatment

Facial nerve decompression

Indication:

Completely paralysis

ENoG less than 10% in 2 weeks

Appropriate time for surgery is 2-3 weeks after paralysis

2.MELKERSSON SYNDROMEA.FACIAL PARALYSIS

B.SWELLING OF LIPS

C.FISSURED TONGUE

B.INFECTIONS

RAMSAY HUNT SYNDROMEHERPES ZOSTER OTICUS

Symptoms:

Facial paralysis

Ear pain

Vesicles

Sensorineural

hearing loss

Vertigo

Herpes zoster oticus Ramsay Hunt syndrome type II

Moebius syndrome (congenital facial diplegia)Abnormal VI ,VII,XII Nerve nucleiFacial Nerve absent / smallerCongenital Extra ocular muscle & facial palsy

Congenital Facial nerve palsy

Cardiofacial Syndrome

Unilateral facial paralysis involving only the lower lip and congenital heart disease

The facial paralysis in these patients involves only those muscles concerned with pulling the lower lip downwards and outwards

These are the mentalis, depressor labii inferioris and depressor anguli oris muscles

All are supplied by the mandibular marginal branch of the facial nerve.

Lesions of this nerve have been recognized in adultsand children for many years The paralysis is only recognizable when the patienttalks, smiles or cries

Treacher collins syndrome (mandibulo facial dysostosis)

There is a set of typical symptoms within Treacher Collins Syndrome

The OMENS classification was developed as a comprehensive and stage-based approach to differentiate the diseases. O; orbital asymmetry M; mandibular hypoplasia E; auricular deformity N; nerve development and S; soft-tissue disease

Facial Nerve involvement in Treacher collins syndrome

N0: No facial nerve involvement

N1: Upper facial nerve involvement (temporal or zygomatic branches)

N2: Lower facial nerve involvement (buccal, mandibular or cervical)

N3: All branches affected

Goldenhars syndrome (oculoauriculo vertebral dysplasia)

It is a wide spectrum of congenital anomalies that involves structures arising from the first and second branchial arches.

Features of hemi facial microsomia, anotia, vertebral anomalies, congenital facial nerve palsy.

C.TRAUMA

1.FRACTURES TEMPORAL BONE

LONGITUDNAL

TRANSVERSE

MIXED

IMMEDIATE ONSET:

SURGICALDECOMPRESSIONRE-ANASTOMOSISCABLE NERVE GRAFT

DELAYED ONSET:TREAT LIKE BELL PALSY

2.EAR/MASTOID SURGERY

3.PAROTID SURGERY

D.NEOPLASMS

1.INTRATEMPORAL

2.TUMORS OF PAROTID

E.CONGENITAL

Facial Nerve Injury from Birth Trauma

Trauma (forceps delivery)

Congenital Facial Palsy

Mobius syndrome

Cardiofacial syndrome

Toxic Causes:

Thalidomide

Tetanus

Diphtheria

Carbon Monoxide

Lead Intoxication

Causes:

Central: Brain abscess Pontine glioma Poliomyelitis Multiple sclerosis

Causes:

Intacranial part: Acoustic neuroma Meningioma Metastatic CA Meningitis

Causes:

Intratemporal part: Idiopathic:

Bell’s palsy Melkersson’s syndrome

Causes:

Intratemporal part: Infections:

ASOM CSOM Herpes Zoster Oticus

Causes:

Intratemporal part: Trauma:

Surgical: Mastoidectomy, Stapedectomy Accidental:# temporal bone

Causes:

Intratemporal part: Neoplasms:

Glomus jugulare tumour Facial nerve neuroma Metastatic CA

Causes:

Extracranial part: Parotid gland CA Parotid gland surgery Parotid gland injury Neonatal facial nerve injury

Causes:

Systemic: DM Hypothyroidism Uremia PAN Wegener’s granulomatosis Sarcoidosis Leprosy Leukemia

Labs:

Pure-tune audiometry Electrophysiologic tests Imaging tests Others

Labs:

Electrophysiologic tests: Nerve Excitability Test: NET Maximum stimulation Test: MST Electroneurography: ENoG Electromyography: EMG

Complications:

Incomplete recovery Exposure keratitis Synkinesis Tics and spasms Contractures Crocodile tears Frey’s syndrome “gustatory sweating” Psychological and social problems

Bell’s Palsy

Dr. Saud ALROMAIH

Background:

one of the most common neurologic disorders affecting the cranial nerves.

abrupt, unilateral, peripheral facial paresis or paralysis without a detectable cause.

Background:

first described more than a century ago by Sir Charles Bell,

yet much controversy still surrounds its etiology and management.

Bell palsy is certainly the most common cause of facial paralysis worldwide.

Incidence:

United States Internationally

Incidence:

The incidence of Bell palsy in the United States is approximately 23 cases per 100,000 persons.

Internationally: The incidence is the same as in the United States.

Demographics:

Race: Sex: Age:

Demographics:

Race: slightly higher in persons of Japanese descent.

Sex: No difference exists Age: highest in persons aged 15-45 years.

Bell palsy is less common in those younger than 15 years and in those older than 60 years.

Pathophysiology:

Main cause of Bell's palsy is latent herpes viruses (herpes simplex virus type 1 and herpes zoster virus), which are reactivated from cranial nerve ganglia.

Polymerase chain reaction techniques have isolated herpes virus DNA from the facial nerve during acute palsy.

Pathophysiology:

Inflammation of the nerve initially results in a reversible neurapraxia,

Herpes zoster virus shows more aggressive biological behaviour than herpes simplex virus type 1

History:

The most alarming symptom of Bell's palsy is paresis

Up to three quarters of affected patients think they have had a stroke or have an intracranial tumour.

History:

The palsy is often sudden in onset and evolves rapidly, with maximal facial weakness developing within two days.

Associated symptoms may be hyperacusis, decreased production of tears, and altered taste.

History:

Patients may also mention otalgia or aural fullness and facial or retroauricular pain, which is typically mild and may precede the palsy.

A slow onset progressive palsy with other cranial nerve deficits or headache raises the possibility of a neoplasm

Physical exam:

Bell's palsy causes a peripheral lower motor neurone palsy,

which manifests as the unilateral impairment of movement in the facial and platysma muscles, drooping of the brow and corner of the mouth, and impaired closure of the eye and mouth.

Physical exam:

Bell's phenomenon—upward diversion of the eye on attempted closure of the lid—is seen when eye closure is incomplete.

Physical exam:

Polyposis or granulations in the ear canal may suggest cholesteatoma or malignant otitis externa.

Vesicles in the conchal bowl, soft palate, or tongue suggest Ramsay Hunt syndrome

Physical exam:

The examination should exclude masses in the head and neck.

A deep lobe parotid tumour may only be identified clinically by careful examination of the oropharynx and ipsilateral tonsil to rule out asymmetry.

Investigations:

Serum testing for rising antibody titres to herpes virus is not a reliable diagnostic tool for Bell's palsy.

Salivary PCR for herpes simplex virus type 1 or herpes zoster virus is more likely to confirm virus during the replicating phase, but these tests remain research tools.

Investigations:

MRI has revolutionised the detection of tumours.

Investigations:

Topognostic tests and electroneurography may give useful prognostic information but remain research tools.

Nerve Excitability Test: NET : Indication: complete paralysis<3wks Interpretation: < or = 3.5 mA threshold:

Prognosis Good Limitation: Not useful in the 1st 3 days or during

recovery.

Maximum stimulation Test: MST: Indication: complete paralysis<3wks Interpretation: Marked weakness or no muscle

contraction: advanced degeneration with guarded prognosis

Limitation: Not Objective.

Electroneurography: ENoG : Indication: complete paralysis<3wks Interpretation: < 90% degeneration: prognosis

is good; > or = 90%: prognosis is question Limitation: False-positive results in deblocking

phase.

Electromyography: EMG Indication: Acute paralysis less than 1 week or chronic

paralysis longer than 2 weeks Interpretation:

Active mu: intact motor axons Mu + fibrillation potentials: partial degeneration Polyphasic mu: regenerating nerve

Limitation: cannot assess degree of degeneration or prognosis for recovery.

Diagnosis:

Bell palsy is a diagnosis of exclusion. Other disease states or conditions that

present with facial palsies are often misdiagnosed as idiopathic.

Management:

The main aims of treatment in the acute phase of Bell's palsy are to speed recovery and to prevent corneal complications.

Treatment should begin immediately to inhibit viral replication and the effect on subsequent pathophysiological processes that affect the facial nerve.

Psychological support is also essential, and for this reason patients may require regular follow up.

Management, Eye care

Management, Eye care

It focuses on protecting the cornea from drying and abrasion due to problems with lid closure and the tearing mechanism.

The patient is educated to report new findings such as pain, discharge, or change in vision.

Lubricating drops should be applied hourly during the day and a simple eye ointment should be used at night.

Management, Steroid

Management, Steroid

Two systematic reviews concluded that Bell's palsy could be effectively treated with corticosteroids in the first seven days, providing up to a further 17% of patients with a good outcome in addition to the 80% that spontaneously improve.

Management, Steroid

Usual regimen is 1mg/kg/day for 1 week. To be tapered in the 2nd week.

Management, Steroid

Cochrane review*:“There is insufficient evidence about the effects of

corticosteroids for people with Bell's palsy, although their anti-inflammatory effect might prevent nerve damage.”

*Salinas RA, Alvarez G, Ferreira J. Corticosteroids for Bell's palsy (idiopathic facial paralysis). Cochrane Database of Systematic Reviews

2004, Issue 4. Art. No.: CD001942.

Management, Antivirals

It seems logical in Bell's palsy because of the probable involvement of herpes viruses.

Aciclovir, a nucleotide analogue, interferes with herpes virus DNA polymerase and inhibits DNA replication.

Management, Antivirals

Usual regimen is 4000mg/24hrs divided into 5 doses for 7 to 10 days

Bell’s palsy:

Antivirals:Cochrane review*:“More evidence is needed to show whether the

antiviral drugs acyclovir or valacyclovir are effective in aiding recovery from Bell's palsy.”

* Allen D, Dunn L. Acyclovir or valaciclovir for Bell's palsy (idiopathic facial paralysis). Cochrane Database of Systematic Reviews 2004, Issue 3. Art. No.: CD001869.

Outcomes:

It has a fair prognosis without treatment, with almost three quarters of patients recovering normal mimetical function and just over a tenth having minor sequelae.

A sixth of patients are left with either moderate to severe weakness, contracture, hemifacial spasm, or synkinesis.

Outcomes:

Patients with a partial palsy fair better, with 94% making a full recovery.

The outcome is worse when herpes zoster virus infection is involved in partial palsy.

Outcomes:

In patients who recover without treatment, major improvement occurs within three weeks in most.

If recovery does not occur within this time, then it is unlikely to be seen until four to six months, when nerve regrowth and reinnervation have occurred.

Bad Prognostic Factor:

Complete facial palsy No recovery by three weeks Age over 60 years Severe pain Ramsay Hunt syndrome (herpes zoster virus) Associated conditions—hypertension,

diabetes, pregnancy Severe degeneration of the facial nerve

shown by electrophysiological testing

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Thanks

MUSCLE ACTION

Risorius Smile

Buccinator Aids chewing by holding cheeks flat

Levator Labii Superioris Elevates upper lip

Levator labii superioris alaeque nasi

Snarl

Levator Anguli Oris Soft smile

Nasalis Flare Nostrils

Orbicularis oris muscle Purse Lips

Depressor Septi Nasi Depresses Nasal Septum

Procerus Moves Skin of Forehead

The buccal branch supplies these muscles