FACIAL NERVE PALSY

ANATOMY OF FACIAL NERVE Facial nerve is a mixed nerve. Consists of 2 parts:

Facial nerve proper (motor) Nervus intermedius (sensory)

NUCLEUS OF FACIAL NERVE Facial nerve has 3 nuclei:-

Main motor nuclei (SVE) Upper part of nuleus

Innervates forehead muscle Receives fibre from both hemispheres

Lower part of nucleus Innervates lower face muscle Receives fibre from only one hemisphere

The motor nucleus of the facial nerve is found in the ventrolateral aspect of the tegmentum of the lower pons. Its axons take an aberrant course to exit the brainstem. They initially ascend in a dorsomedial direction to the region of the floor of the fourth ventricle. They then pass laterally over the abducens nucleus (CN VI) and descend in a ventrolateral trajectory, exiting the brainstem at the level of the caudal border of the pons (Fig. 14-8). Upon exiting the brain, fibers of the facial nerve enter the internal acoustic meatus and petrous portion of the temporal bone. The fibers then continue along and through the facial canal and, ultimately, exit the skull through the sty-lomastoid foramen.

The diagram show the petrous portion of temporal bone as mentioned in the previous slide.

Temporal bone consist of squamo, petrous, mastoid, tympanic parts and styloid process

NUCLEUS OF FACIAL NERVE - CONT Parasympathetic Nuclei

Superior Salivatory Nuclei Lacrimal Nuclei

Emotional response Reflex lacrimation secondary to irritation of cornea & conjunctiva

Sensory Nuclei

COURSE OF FACIAL NERVE Can be divided in to 3 parts:-

Stylomastoid foramen

Internal Acoustic Meatus

Intratemporal part is the longest part

COURSE OF FACIAL NERVE

BRANCHES OF FACIAL NERVE1. Greater superficial petrosal nerve

taste to soft palate preganglionic parasympathetic for lacrimal gland and glands of nasal & oral cavities

2. Nerve to stapedius3. Chorda tympani

preganglionic parasympathetic for submandibular & sublingual glands taste from anterior 2/3 tongue

4. Communicating branch Concha Retroauricular groove Posterior meatus Outer surface of tympanic membrane

BRANCHES OF FACIAL NERVE - CONT1. Posterior auricular nerve

Muscle of pinna Occipital belly of occipitofrontalis

2. Muscular branches Stylohyoid Posterior belly of diagastric

3. Peripheral branches

BLOOD SUPPLY OF FACIAL NERVE

SEVERITY OF NERVE INJURY

FACIAL NERVE PALSY Paralysis or loss of function of any structure innervated by facial nerve. Causes:-

Central Brain abscess Pontine gliomas Poliomyelitis Multiple sclerosis

Intracranial part (cerebellopontine angle) Acoustic neuroma Meningioma Congenital Cholesteatoma Metastatic carcinoma Meningitis

CAUSES OF FACIAL NERVE PALSY - CONT Intratemporal part

a) Idiopathic– Bell palsy (60-75% of total facial paralysis)– Melkersson syndrome

b) Infections– ASOM/ CSOM– Herpes zoster oticus– Malignant otitis externa

c) Trauma– Surgical (mastoidectomy/ Stapedectomy)– Accidental (fracture of temporal bone)

d) Neoplasms– Malignancies of external and middle ear– Glomus jugulare tumour– Facial nerve neuroma– Metastasis to temporal bone (from cancer of breast, bronchus, prostate)

CAUSES OF FACIAL NERVE PALSY - CONT Extracranial part

Malignancy of parotid Surgery of parotid Accidental injury in parotid

region Neonatal facial injury

(obstetrical forceps)

Systemic disease DM Hypothyroidism Uraemia Polyarteritis nodosa Wegener’s granulomatosis Sarcoidosis Leprosy Leukaemia Demyelinating disease

1. IDIOPATHIC Bell palsy Melkersson syndrome

BELL’S PALSY 60% to 75% of facial paralysis Idiopathic, peripheral facial paralysis or paresis of acute onset Affect both sexes equally Affect all age group but incidence higher with increasing age 6-8% of patient has positive family history Higher risk in diabetics (angiopathy) and pregnant lady (retention of fluids)

AETIOLOGY1. Viral infection

herpes simplex, herpes zoster, EBV

2. Vascular ischemia primary (induced by cold, emotional stress) secondary (result of primary ischemia which causes increased capillary permeability

leading to exudation of fluid, oedema and compression of microcirculation of the nerve.

3. Hereditary Narrow fallopian canal (makes the nerve susceptible to early compression with the

slightest oedema)

4. Autoimmune disorder T-lymphocyte changes have been observed.

CLINICAL FEATURES Sudden onset Unable to close eyes, eyeball turns up and out (Bell’s Phenomenon) Drooping of mouth Epiphora ( tears flow down from the eye ) Noise intolerance ( stapedial paralysis ) Loss of taste ( chorda tympani involvement )

DIAGNOSIS Exclusional diagnosis Requires

complete history, ontological, head and neck examination. X-ray Blood test eg. Total count, peripheral smear, sedimentation rate, blood sugar and

serology Nerve excitability tests (done daily or on alternate days and compared with the

normal side to monitor nerve degeneration)

TREATMENT General

ReassuranceAnalgesics to relieve ear painEye protection to prevent exposure keratitis and corneal ulcer

- artificial tears (methylcellulose drops every 1-2hrs)- eye paddling-spectacles if outdoor

Physiotherapy or massage of the facial muscles Medical

Steroids (e.g. prednisolone) Surgical

Nerve decompression (relieves pressure on the nerve and thus improves the microcirculation of the nerve)

PROGNOSIS 85% to 90% fully recover 10% to 15% has incomplete recover and left with some stigmata of

degeneration Recurrent facial palsy may not fully recover Prognosis is good in incomplete bell palsy (95% complete recovery) and in

those where clinical recovery starts within 3 weeks of onset (75% complete recovery)

MELKERSSON’S SYNDROME Idiopathic disorderConsists of a triad of:-

Facial paralysisSwelling of the lipsFissured tongue

Paralysis may be recurrentTreatment is the same as Bell’s Palsy

2. INFECTIONHerpes Zoster OticusAcute Otitis MediaChronic Otitis MediaMalignant Otitis Externa

HERPES ZOSTER OTICUS (RAMSAY-HUNT SYNDROME)• Herpes zoster oticus (HZ oticus) is a viral infection of the inner, middle,

and external ear. HZ oticus manifests as severe otalgia (ear pain) and associated cutaneous vesicular eruption, usually of the external canal and pinna.

• When associated with facial paralysis, the infection is called Ramsay Hunt syndrome.

• Reactivation of latent varicella-zoster virus (VZV) that has remained dormant within sensory ganglia (commonly the geniculate ganglion) of the facial nerve

• Precipitating factor : • Immunocompromised (carcinoma, radiation therapy, chemotherapy, HIV infection )• Physical stress • Emotional stress

CLINICAL FEATURES Severe otalgia Painful, burning blisters in and around the ear, on the face, in the mouth or on the tongue

Vertigo, nausea, vomiting Hearing loss, hyperacusis, tinnitus Eye pain, lacrimation Associated symptoms :

Anaesthesia of face Hearing impairment Giddiness

due to involvement of CN V & CN VIII

HERPES ZOSTER OTICUS. IMAGE COURTESY OF MANOLETTE ROQUE, MD, OPHTHALMIC CONSULTANTS PHILIPPINES CO, EYE REPUBLIC OPHTHALMOLOGY CLINIC

* Other viral infection also can cause facial paralysis, such as herpes simplex / Epstein-Barr virus

TREATMENT Generally supportive including warm compresses, narcotic analgesics and antibiotic for secondary bacterial infection. Antiviral (acyclovir) = play a role in limiting the severity and duration of symptoms if given early in the course of the illness + increased rate of facial nerve function recovery and prevented further nerve degeneration. Corticosteroids (prednisone) = used to relieve acute pain, decrease vertigo, and limit the occurrence of postherpetic neuralgia

ACUTE OTITIS MEDIA Facial nerve is normally well protected in its bony canal. Sometimes, the bony canal is dehiscent, and the nerve

lies just under the middle ear mucosa. It is in these cases that inflammation of middle ear spreads to epi- and perineurium, causing facial paralysis.

Facial nerve function fully recovers if acute otitis media is controlled with systemic antibiotics.

Surgical Treatment : Myringotomy or cortical mastoidectomy

MYRINGOTOMYA surgical procedure of the tympanic membrane, performed by making a small incision with a myringotomy knife through the layers of tympanic membrane which permits direct access to the middle ear space and allows the release of middle-ear fluid.

CHRONIC OTITIS MEDIA Either result from cholesteatoma (abnormal skin growth in

the middle ear behind the eardrum, consists of squamous epithelium) or from penetrating granulation tissue.

Cholesteatoma destroys bony canal and then causes pressure on the nerve, further aided by edema of associated inflammatory process.

Facial paralysis is insidious but slowly progressive.

Treatment : Urgent exploration of the middle ear and mastoid. - - Facial canal is inspected from the geniculate ganglion to the stylomastoid foramen. - If granulation tissue or cholesteatoma has entered the bony canal, uncapped the area of involvement.- Granulation tissue surrounding the nerve is removed but if it invades the nerve sheath, it is left in place. - If a segment of the nerve has been destroyed by the granulation tissue, resection of the nerve and grafting are better left to a second stage when infection has been controlled and fibrosis has matured.

MALIGNANT (NECROTISING) OTITIS EXTERNA Caused by pseudomonas infection Usually in diabetic elderly/those on

immunosuppressant drugs Early manifestation resemble otitis

externa but there is excruciating pain and granulations in the meatus

Facial paralysis is common (cranial nerve involvement indicates a poor prognosis)

May spread to skull base and jugular foramen multiple nerve involvement

Anteriorly, infection can spreads to temporomandibular fossaPosteriorly to the mastoidMedially to middle ear and petrous boneTreatment :High dose of IV antibiotics for 6-8weeks or longerDiabetes must be controlledSurgical debridement of devitalised tissue/bone

3. TRAUMA Fracture of temporal bone Ear or mastoid surgery Parotid surgery and trauma to face

FRACTURE OF TEMPORAL BONE

May be longitudinal, transverse or mixed fractures. Transverse fracture more commonly cause facial nerve palsy

Facial palsy is more often seen in transverse fractures (50%)

Paralysis is due to intraneural hematoma, compression by a bony spicule or transection of nerve.

CLINICAL FEATURES Facial nerve paralysis Hearing loss Vertigo Dizziness Otorrhagia (hemorrhage from the ear) CSF otorrhea (Ear discharge) Tympanic membrane perforation Hemotympanum (The presence of blood in the middle ear)

TREATMENT Delayed onset:

Treat conservatively like Bell’s Palsy Caused edema of the surrounding structure

Immediate onset: Surgical intervention in the form or decompression, re-anastomosis

of cut ends or cable nerve graft.

EAR OR MASTOID SURGERY Injured during stapedectomy,

tympanoplasty, or mastoid surgery. Sometimes, nerve is paralysed due

to pressure of packing on the exposed nerve and this should be relieved first.

Paralysis may be immediate or delay

Treatment same as fractured temporal bone.

PAROTID SURGERY AND TRAUMA TO FACE

Facial nerve may be injured in surgery of parotid tumours or deliberately excised in malignant tumours.

Accidental injuries in the parotid region can also cause facial paralysis.

Application of obstetrical forceps may also result in facial paralysis in the neonate due to pressure on the extratemporal part of nerve.

4. NEOPLASMS -Intratemporal Neoplasms -Tumours OF Parotid

i) Intratemporal NeoplasmsCarcinoma of external or middle ear, glomus tumour, rhabdomyosarcoma and metastatic tumours of temporal bone. Facial nerve neuroma can occur anywhere along the course of the nerve and produce paralysis of gradual or sudden onsetInvestigation : High resolution CT scan and gadolinium-enhanced MRI is very useful for facial nerve tumourManagement : Excision and nerve grafting

ii) Tumours of Parotid Facial paralysis with tumour of the parotid almost alwaysimplies malignancy

COMPLICATIONS FOLLOWING FACIAL PARALYSIS

1. Incomplete recoveryfacial asymmetry, epiphora(excessive tearing), drooling and difficulty in taking food

2. Exposure keratitiseyes cannot be closed tear film evaporates dryness, exposure keratitis, corneal ulcerTreatment : artificial tears (methylcellulose drops) every 1-2 hours, eye ointment and proper cover for eye at night

3. Synkinesis (mass movement)Due to cross innervation of fibresWhen patient wishes to close the eye, corner of mouth also twitches or vice versa

4. Tics & spasms Faulty regeneration of fibres. Involuntary movements are seenon the affected side of the face .

5. ContracturesFibrosis of atrophied muscle or fixed contraction of a group of muscles

6. Crocodile tears (gustatory lacrimation)Unilateral lacrimation with masticationDue to faulty regeneration of parasympathetic fibres which now supply lacrimal gland instead of the salivary glandTreated by section of greater superficial petrosal nerve or tympanic neurectomy

7. Frey’s syndrome (gustatory sweating)Sweating and flushing of skin over parotid area during mastication It results from parotid surgery

8. Psychological and social problemsDrooling during eating/drinkingImpairment of speech