Tahani Al-Bohairy Rawan ALJaeed Joumana Mensef Facial nerve Tahani Al-Bohairy Rawan ALJaeed Joumana Mensef

Objective: Anatomy of facial nerve. Branches Of Facial Nerve Causes Of Facial Paralysis Clinical Features Diagnosis Prognosis Treatment

Anatomy of facial nerve Facial nerve runs from pons to parotid. It is a mixed nerve having motor and a sensory root (nerve of Wrisberg) which carries secretomotor fibres to the lacrimal gland and salivary glands, and brings fibres of taste and general sensation.

Components of the facial nerve include Components of the facial nerve include: 1. Special visceral efferent (motor): supplies all the muscles of facial expression, vestigial muscles, stylohyoid, posterior belly of digastric and the stapedius. 2. Special visceral afferent brings taste from the anterior two-thirds of tongue and soft and hard palate. 3. General visceral efferent supplies secretomotor fibres to the glands generally. 4. General somatic afferent (sensation) from the concha, posterosuperior part of external canal and the tympanic membrane.

The Course Of The Nerve The course of the nerve can be divided into three parts: 1- Intracranial 2-Intratemporal 3-Extracranual

BRANCHES OF FACIAL NERVE 1- Greater superficial petrosal nerve: It arises from geniculate ganglion. 2- Nerve to stapedius: It arises at the level of second genu and supplies the stapedius muscle. 3- Chorda tympani: It arises from the middle of vertical segment, passes between the incus and neck of malleus, and brings taste from anterior two-thirds of tongue. 4- Communicating Branches.

BRANCHES OF FACIAL NERVE 5-Posterior auricular Branches: it supplies muscles of pinna, occipital belly of occipitofrontalis. 6-Muscular branches: to stylohyoid and posterior belly of digastric. 7-Peripheral branches: two divisions; temporofacial and cervicofacial, the latter divides into smaller branches together forming pes anserinus (goosefoot) that supply all the muscles of facial expression.

Branches of the cervicofacial division of the peripheral branches.

They Supply All The Muscle Of Facial Expression

BLOOD SUPPLY OF FACIAL NERVE Arteries form an external plexus that lies in the epineurium 1- Anterior-inferior cerebellar artery 2- labyrinthine artery, supplies the nerve in internal auditory canal. 3- Superficial petrosal artery, which supplies geniculate ganglion and the adjacent region. 4- Stylomastoid artery, which supplies the mastoid and tympanic segment.

VARIATION AND ANOMALIES OF FACIAL NERVE (A) Normal. (B) Bony dehiscence. (C) Hump posteriorly, near the second genu. (D) Bifurcation. (E) Trifurcation. (F) Bifurcating and reuniting round the oval window. (G) Tympanic segment crossing between oval and round window

Causes Of Facial Nerve Paralysis The cause may be central or peripheral.The peripheral lesion may involve the nerve in its intracranial, intratemporal or extratemporal parts.Peripheral lesions are more common and about two-thirds of them are of the idiopathic variety IDIOPATIC INFECTIONS TRAUMA NEOPLASMS SYSTEMIC DISEASES AND FACIAL PARALYSIS

IDIOPATIC ”Bell’s Palsy” It is defined as idiopathic, peripheral facial paralysis or paresis of acute onset. 60 -75% of facial paralysis is due to Bell palsy Both sexes are affected with equal frequency. Any age group may be affected with increasing age. Risk of Bell palsy is more in diabetics (angiopathy) and pregnant women (retention of fluid).

Etiology 1- Viral infection: due to herpes simplex, herpes zoster or the Epstein–Barr virus 2- Vascular ischemia: It may be primary or secondary. Primary ischemia is: induced by: cold or emotional stress. Secondary ischemia is: the result of primary ischemia which causes increased capillary permeability leading to exudation of fluid, edema and compression of microcirculation of the nerve. 3. Hereditary: 10% of the cases of Bell palsy have a positive family history. 4. Autoimmune disorder: T-lymphocyte changes have been observed.

Clinical Features Onset is sudden. Patient is unable to close his eye, On attempting to close the eye, eyeball turns up and out (Bell phenomenon). Saliva dribbles from the angle of mouth. Face becomes asymmetrical. Tears flow down from the eye (epiphora ). Pain in the ear may precede or accompany the nerve paralysis. Some complain of noise intolerance (stapedial paralysis) or loss of taste (involvement of chorda tympani).

Examination of Facial nerve Ask the patient show his/her teeth open their mouth (cmpare the nasolabial folds). Ask the patient to close his/her eyes. Frown. wrinkle their forehead. raise eyebrows. Bare his/her teeth & open the mouth. Blow out their cheek. Pursuing the lips (for strength and weekness).

Diagnosis Diagnosis is always by exclusion. 1- careful history: complete otological and head and neck examination, X-ray studies, blood tests such as total count, peripheral smear, blood sugar and serology. 2- Nerve excitability tests: are done daily or on alternate days and compared with the normal side to monitor nerve degeneration. 3- Localizing the site of lesion (topo diagnosis): helps in establishing the etiology and also the site of surgical decompression of nerve, if that becomes necessary.

Electrodiagnostic Tests These tests are useful to differentiate between neurapraxia and degeneration of the nerve. They also help to predictprognosis and indicate time for surgical decompression of the nerve. 1- Nerve excitability test (NET) 2-Maximal stimulation test (MST) 3-Electromyography (EMG) 4-Electroneuronography (evoked electromyography) (ENoG)

Electromyography The recording of spontaneous and voluntary muscle potentials by needles introduced into the muscles is called Electromyography (EMG). in a normal, resting muscle, biphasic/triphasic potentials are seen every 30-50 msec.

Treatment General: Reassurance. Relief of ear pain by analgesics. Care of the eye Eye must be protected against exposure to avoid keratitis. Physiotherapy

Medical: Steroids Prednisolone is the drug of choice, If patient reports within 1 week, the adult dose is 1 mg/kg/day divided into morning and evening doses for 5 days and the Patient is seen on the fifth day. If paralysis is incomplete or is recovering, dose is tapered during the next 5 days. If it remains complete, the same dose is continued for another 10 days and thereafter tapered in next 5 days (total of 20 days). Contraindications: pregnancy, diabetes, hypertension, peptic ulcer, pulmonary tuberculosis and glaucoma. 2. Other drugs: Vasodilators, vitamins, mast cell inhibitors and antihistaminics have not been found useful.

Surgical: Nerve decompression : Vertical and tympanic segments of nerve are decompressed. Some workers have suggested total decompression including labyrinthine segment by postaural and middle fossa approach.

Prognosis 85-90% of the patients recover fully. 10-15% recover incompletely and may be left with some stigmata of degeneration. Recurrent facial palsy may not recover fully. 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).

C. Recurrent facial palsy. B. MELKERSSON SYNDROME It is also an idiopathic disorder consisting of a triad of facial paralysis, swelling of lips and fissured tongue. Paralysis may be recurrent. Treatment is the same as for Bell palsy. C. Recurrent facial palsy. Recurrent facial palsy is seen in Bell palsy (3–10% cases), Melkersson syndrome, diabetes, sarcoidosis and tumours. Recurrent palsy on the same side may be caused by a tumour in 30% of cases. D. Bilateral facial paralysis. Simultaneous bilateral facial paralysis may be seen in Guillain- Barré syndrome, sarcoid- osis, sickle cell disease, acute leukaemia, bulbar palsy, lep- rosy and some other systemic disorders.

INFECTIONS HERPES ZOSTER OTICUS (RAMSAY–HUNT SYNDROME) There is facial paralysis along with vesicular rash in the external auditory canal and pinna .There may also be anaesthesia of face, giddiness and hearing impairment due to involvement of Vth and VIIIth nerves. Treatment is the same as for Bell palsy.

TRAUMA FRACTURES OF TEMPORAL BONE Fractures of temporal bone may be longitudinal, transverse or mixed. Facial palsy is seen more often in transverse fractures (50%). Paralysis is due to intraneural haematoma, compression by a bony spicule or transection of nerve. In these cases, it is important to know whether paralysis was of immediate or delayed onset. Delayed onset paralysis is treated conservatively like Bell palsy while immediate onset paralysis may require surgery in the form of decompression, reanastomosis of cut ends or cable nerve graft. B. EAR OR MASTOID SURGERY Facial nerve is injured during stapedectomy, tympanoplasty or mastoid surgery. Paralysis may be immediate or delayed and treatment is the same as in temporal bone trauma. C. 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.

NEOPLASMS INTRATEMPORAL NEOPLASMS TUMOURS OF PAROTID Carcinoma of external or middle ear, glomus tumour, rhabdomyosarcoma and metastatic tumours of temporal bone, all result in facial paralysis. Facial nerve neuroma occurs anywhere along the course of nerve and produces paralysis of gradual or sudden onset. It is treated by excision and nerve grafting. High-resolution CT scan and gadolinium- enhanced MRI is very useful for facial nerve tumour. TUMOURS OF PAROTID Facial paralysis with tumour of the parotid almost always implies malignancy

SYSTEMIC DISEASES AND FACIAL PARALYSIS Peripheral facial paralysis is mostly of idiopathic variety but always needs exclusion of diabetes, hypothyroidism, leukemia, leprosy, syphilis and demyelinating disease

COMPLICATIONS FOLLOWING FACIAL PARALYSIS Peripheral facial paralysis due to any cause may result in any of the following complications: Incomplete recovery. Facial asymmetry persists. Eye can not be closed resulting in epiphora. A weak oral sphincter causes drooling and difculty in taking food. Exposure keratitis. Eye cannot be closed, tear film from the cornea evaporates causing dryness, exposure keratitis and corneal ulcer. This is worse when tear production is also affected. It can be prevented by use of (methylcellulose drops) every 1–2 h, eye ointment and proper cover for the eye at night. Synkinesis (mass movement). When the patient wishes to close the eye, corner of mouth also twitches or vice versa. It is due to cross innervation of fibres; there is no treatment. Tics and spasms. They are the result of faulty regeneration of fibres . Involuntary movements are seen on the affected side of the face.

6. Frey’s syndrome (gustatory sweating). 5. Contractures. They result from brosis of atrophied muscles or fixed contraction of a group of muscles. They affect movements of face but facial symmetry at rest is good. 6. Frey’s syndrome (gustatory sweating). There is sweating and flushing of skin over the parotid area during mastication. It results from parotid surgery. Psychological and social problems. Drooling during eating and drinking and impairment of speech cause social problems.

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