FACIAL NV.pptx facial nerve cranial nerve number 7

facial nerve

1. Facial nerve By Dr Mallikarjun N Patil

2. INTRODUCTION The facial nerve (CN VII) is the nerve of second branchial arch. Facioacoustic primordium appears at 3 weeks of gestation and at 5–6 weeks geniculate ganglion can be appreciated. Complete separation of facial and acoustic nerve occurs and nervous intermedius develops. Its sensory root is also called nerve of Wrisberg and carries both secretomotor as well as gustatory fibers.

3. FUNCTIONAL DIVISIONS It is a mixed nerve and consists of following types of fibers: Branchial motor fibers (Special visceral efferents ): They supply muscles of facial expression (develop from the 2nd branchial arch) Parasympathetic preganglionic secretomotor fibers (General visceral efferents ): They supply to the lacrimal gland, submandibular and sublingual salivary glands and the glands in the nose and palate. Gustatory fibers (Special visceral afferent): They carry taste sensation from the anterior two-thirds of tongue and hard palate General sensations (General somatic afferent): They are carried from the concha, posterior part of external ear and retroauricular skin.

4. MOTOR NUCLEUS OF FACIAL NERVE Motor nucleus of facial nerve is situated in the pons near the nucleus of abducens. Upper part of the nucleus which innervates forehead muscles receives corticonuclear fibers from both the cerebral hemispheres, while the lower part of nucleus that supplies lower face gets only crossed fibers from opposite side of cerebral hemisphere. Facial motor nucleus also receives fibers from the thalamus by alternate routes and provides involuntary emotional expressions such as happy, sad, depressed and angry faces.

5. COURSE OF FACIAL NERVE The course of facial nerve is divided into three parts: Intracranial (23–24 mm) Intratemporal (20–30 mm) Extracranial (extratemporal 15–20 mm).

6. Intracranial course 15–17 mm Motor fibers first hook a round the nucleus of 6th nerve, and then are joined by the sensory root (nerve of Wrisberg ). Facial nerve along with the vestibulocochlear and abducens nerves leaves the brainstem at pontomedullary junction. It travels through the cerebellopontine angle (CPA) and along with vestibulocochlear nerve enters the internal auditory canal (IAC). At the fundus of IAC, facial nerve enters the bony fallopian canal.

7. Intratemporal course The part of the facial nerve, from internal acoustic meatus to stylomastoid foramen, is further divided into four segments: Meatal segment (8–10 mm): It lies within IAC. The meatal foramen is the most narrow aperture of facial canal. Labyrinthine segment (3–5 mm): It extends from IAC fundus (meatal foramen) to the geniculate ganglion where facial nerve takes a posterior turn forming the first “genu”. Labyrinthine segment lies posterosuperior to cochlea: The bony fallopian canal in the labyrinthine segment is most narrow and more prone to compression in Bell’s palsy.

8. c) Tympanic or horizontal segment (8–11 mm): It extends from geniculate ganglion to just above the pyramidal eminence, where it turns inferiorly and makes the second genu. d) Mastoid or vertical segment (10–14 mm): It extends from the pyramid to the stylomastoid foramen.

9. Extracranial course The facial nerve comes out of the temporal bone through the stylomastoid foramen. It crosses the styloid process and enters into the parotid gland. This extracranial part from stylomastoid foramen to the termination of its peripheral branches is situated in the substance of parotid gland.

10. BRANCHES OF FACIAL NERVE Greater superficial petrosal nerve : This first branch of the facial nerve arises from geniculate ganglion and carries preganglionic secretomotor fibers to lacrimal gland and the glands of nasal mucosa. Nerve to stapedius: This branch carries motor fibers to the stapedius muscle. Chorda tympani: It carries preganglionic parasympathetic secretomotor fibers to submandibular and sublingual salivary glands and gustatory fibers (taste sensation from anterior two-thirds of tongue).

11. 4. Communicating branch: It joins auricular branch (Arnold’s nerve) of vagus and supplies the concha, retroauricular groove, posterior part of meatus and the outer surface of tympanic membrane. 5. Posterior auricular nerve: It supplies muscles of pinna and occipital belly of occipitofrontalis muscle. 6. Muscular branches: They supply to stylohyoid and posterior belly of digastric, which are developed from the 2nd branchial arch. 7. Terminal branches [Pes anserinus (Goose's foot)]: The facial nerve, after crossing the styloid process, divides into two terminal divisions upper temporofacial and a lower cervicofacial.

12. Congenital Anomalies • Dehiscent canal: The nerve becomes more prone to infection in patients with suppurative otitis media. Facial canal may be dehiscent over: – 1.Oval window (most common) 2. Geniculate ganglion 3.Retrofacial mastoid air cells. • Prolapse from dehiscence: Prolapse may make stapes surgery challenging. • Abnormal courses: 1.Posterior hump near the lateral semicircular canal. 2. Running between oval and round window • Abnormal branches: 1.Bifurcation enclosing oval window 2.Multiple terminal branches of mastoid segment

13. BLOOD SUPPLY Following are the arteries and areas of facial nerve supplied by them: Labyrinthine artery, branch of anterior inferior cerebellar artery: Meatal segment within the IAC and labyrinthine segment. Petrosal artery, branch of middle meningeal artery: Perigeniculate area. Stylomastoid artery, branch of posterior auricular artery: Mastoid and tympanic segments.

14. CLINICAL EVALUATION OF FACIAL PALSY Onset: Sudden or gradual; events preceding the onset of facial nerve palsy such as trauma, surgery, ear pain, exposure to extreme of temperature. The most important prognostic clinical factor is whether the onset of facial palsy occurred immediately or over days after injury. Unilateral/bilateral Duration and progression Associated symptoms: Ear discharge, vertigo, dysphagia, dysphasia. Past history of facial palsy Major medical illness Central nervous system examination: Especially cranial nerves, cerebellum and motor system.

15. PATHOPHYSIOLOGY OF NERVE INJURY A nerve fiber consists of axon, myelin sheath and neurilemma and is covered by endoneurium A bundle of nerve fibers forms a fascicle, which is enclosed in a sheath called perineurium. The fascicles are bound together by epineurium. The degree of nerve injury determines the degeneration and regeneration of nerve and its functions

16. Seddon Classification of Neural Injury Seddon described three types of progressive nerve injuries: Neuropraxia: It is reversible blockage of nerve impulses due to pressure. There is no distal Wallerian degeneration. Axonotmesis: There occurs blockage of axoplasmic flow and distal Wallerian degeneration. Neurotmesis: It is total nerve transaction.

17. Sunderland classification Based on anatomical structure of the nerve, Sunderland classified the severity of nerve injuries into five degrees. First degree (obstruction to axoplasm)-neuropraxia: In this conduction block, flow of axoplasm through the axons is obstructed. No morphological changes are seen. In this type of injury, recovery of function is complete. Second degree (injury to axon)—axonotmesis: There is loss of axons, but endoneurial tubes remain intact. Wallerian degeneration occurs distal to the lesion.During regeneration, axons will grow into their respective tubes. Recovery is good.

18. 3. Third degree (injury to endoneurium)-neurotmesis: It is an injury to nerve fiber along with both Wallerian degeneration and loss of endoneurium. During regeneration, axon of one tube can grow into another. There are chances of synkinesis (such as mouth movement with eye closure). 4. Fourth degree (injury to perineurium): Partial transaction of nerve occurs. Scarring occurs and impairs regeneration of axons. 5 . Fifth degree (injury to epineurium): There occurs complete nerve transaction. The scar filling the gap does not allow regrowth of axons and neuromuscular reanastomosis . Recovery: Axons grow at a rate of 1 mm/day and accounts for faster recovery in first-degree palsy compared to second degree palsy .

19. DIFFERENCES BETWEEN UPPER AND LOWER MOTOR NEURON PALSY Upper Motor Neuron Facial Paralysis The paralysis is of only the lower half of face on the contralateral side. Frontalis muscle movements are retained due to bilateral innervation of upper part of motor facial nucleus. Involuntary emotional expressions and the tone of facial muscles remain intact Central facial paralysis is caused by cerebrovascular accidents (hemorrhage, thrombosis or embolism), tumor or an abscess.

20. Lower Motor Neuron Facial Paralysis In the peripheral facial paralysis, all the ipsilateral muscles of the face become paralyzed. Patient is unable to frown, close the eye, purse the lips and whistle.

21. INVESTIGATIONS Electrical Tests Nerve excitability test Maximum stimulation test Electroneurography Electromyography Nerve conduction velocity

22. Topodiagnostic Tests They are done to find the site of lesion in the intratemporal segment of facial nerve. Schirmer’s test Stapedial reflex Taste test or Electrogustometry Submandibular salivary flow

23. CAUSES OF FACIAL NERVE PARALYSIS

24. SEQUELAE/COMPLICATION OF FACIAL NERVE PALSY Incomplete recovery: It can result in facial asymmetry, epiphora (due to inability to close eye), drooling of saliva and difficulty in chewing food (due to weak oral sphincter). Drooling during chewing and drinking and impairment of speech may result in social problems. Exposure keratitis: Evaporation of tears from the open eye results in dryness that leads to keratitis and corneal ulcer. The findings of corneal irritation are redness, itching, foreign body sensation and visual blurring.

25. Synkinesis (mass movement): While closing the eye, corner of mouth twitches. It may happen vice versa. It occurs due to cross innervation of fibers during axon regeneration after Wallerian degeneration. Tics and spasms: Involuntary movements of the facial muscles occur, which are due to the faulty regeneration of fibers. Contractures: The fixed contraction or fibrosis of atrophied muscles affects movements of face. The facial symmetry is maintained at rest. Crocodile tears (gustatory lacrimation): The condition is characterized by the ipsilateral lacrimation during mastication. Frey’s syndrome (gustatory sweating): This condition is characterized by the ipsilateral sweating and flushing of skin over the parotid during mastication. It happens in some cases of parotid surgery.

26. Bell’s palsy Idiopathic demyelinating disease. characterized by an acute isolated unilateral lower motor neuron facial paralysis. Risk factors include diabetes (angiopathy) and pregnancy (retention of fluid).

27. Etiology Viral infection Vascular ischemia Hereditary Autoimmunity

28. Clinical Features Inability to close eye Bell’s phenomenon Dribbling of saliva Asymmetrical face Epiphora Earache Hyperacusis iminished taste sensation

29. Diagnosis Laboratory tests - Radiological studies -Complete blood count -Peripheral blood smear -Sedimentation rate -Blood sugar and serology Nerve excitability tests Topodiagnostic tests

30. Differential Diagnoses Preceding history of temporal bone trauma or surgery Presence of acute suppurative otitis media (ASOM), cholesteatoma, vesicles in and around ear, glomus tumors, malignant tumors of ear and CPA, CNS diseases (such as strokes). Multiple cranial nerve palsies Bilateral facial nerve paralysis Facial palsy at birth Gradual onset of facial paralysis Failure to recover within 6 months.

31. Teatment General Measures Reassurance Analgesics Eye care Physiotherapy

32. Medical Treatment Steroids Acyclovir Other drugs: : Vasodilators Vitamins Mast cell inhibitors Antihistaminics Surgical Facial Nerve Decompression

33. MELKERSSON’S SYNDROME Idiopathic disorder Triad of facial paralysis, swelling of lips and fissured tongue. Patients get recurrent attacks of facial palsy. Treatment is similar to Bell’s palsy

34. RAMSAY HUNT SYNDROME OR HERPES ZOSTER OTICUS (VARICELLA-ZOSTER VIRUS) VIRUS -Varicella-Zoster Virus

35. Clinical Features Prodrome of severe otalgia Stimuli for viral reactivation: Immunosuppression, physical and psychological stressors. Painful vesicles with erythematous base appear in the canal and concha, behind pinna and/or soft palate. Later vesicles rupture and form crusts. Unilateral facial palsy and deep ear pain manifest 1–2 days later. Facial paresis usually recovers over weeks. About 25% patients have vertigo, nystagmus, tinnitus and hearing loss. Sensorineural hearing loss occurs only in 6% of cases. Caloric responses are either decreased or absent

36. Diagnosis Gadolinium-enhanced MRI of temporal bone: Enhancement of geniculate ganglion of facial nerve. HPE: Multinucleated giant cells in vesicle scrapings. Varicella-Zoster virus from vesicle fluid Varicella-Zoster virus DNA by polymerase chain reaction (PCR) assay in vesicle fluid or cerebrospinal fluid (CSF).

37. Treatment Tablet acyclovir 800 mg five times a day or famcyclovir 500 mg tds or valacyclovir 1 g tds for 7 days. Tablet prednisone—tapering dose of 6 days course, beginning usually with 1 mg/kg Topical antibiotic/steroid ear drops Eye care

38. TEMPORAL BONE FRACTURE Pertinent anatomy - Five components Squamous Tympanic Mastoid Petrous Styloid process

39. Clinical presentation Vertigo with vegetative symptoms SNHL herald labyrinthine damage Nystagmus

40. Types Three categories 1)Transverse 2) Longitudinal 3) Oblique/mixed

41. Management of Temporal Bone Fracture Secure airway, control bleeding, examine neurological status, stabilize and evaluate cervical spine. Assess facial nerve function at the earliest . Examine EAC for fracture along the scutum and roof, CSF otorrhea, degree of hemorrhage, presence of brain herniation. Blood and cerumen may be aspirated but never irrigated. Look for any tympanic membrane perforations and hemotympanum. Ear packing is discouraged and done only in cases of significant bleeding. Profuse bleeding not controlled by packing is managed by carotid ligation or angiography for balloon occlusion. Early ear canal stenting is required in cases of severely traumatized ear canals. Benign paroxysmal positional vertigo needs repositioning maneuver. Positive fistula test, which is not done in acute setting (for the fear of introduction of air and infection in the ear) and in cases of CSF fistula, indicates perilymph fistula that presents with vertigo and nystagmus for more than a week and fluctuating or progressive SNHL Audiogram in cases of CSF fistula and facial palsy. CT head assesses intracranial hemorrhage. HRCT of temporal bone Delayed paralysis is treated conservatively. Immediate facial paralysis usually requires surgery (decompression, reanastomosis of cut ends or cable nerve graft), which is performed 3 weeks after injury

42. LYME DISEASE (BANNWARTH’S SYNDROME) Multisystem spirochete disease involves skin, nervous system, heart and joints. Transmitted by Ixodes ticks primary reservoirs – white footed mice and white-tailed deer

43. Clinical Features Acute facial nerve palsy, which is usually unilateral, recovers completely and spontaneously after weeks to few months. There may be preceding history of ear pain, facial pain or paresthesias . Intensely red and violet nodules ( lymphocytoma ) are present on the ear lobe. Sudden SNHL, positional vertigo and Ménière like symptoms have been reported.

44. Diagnosis Clinical in endemic regions Enzyme-linked immunosorbent assay and Western blotting: Detection of specific antibody to B. burgdorferi.

45. Treatment Highly sensitive to doxycycline. Other antibiotics are amoxicillin, erythromycin, cefuroxime, ceftriaxone and imipenem.

46. SARCOIDOSIS Chronic multisystem disease of unknown etiology Frequently affects lungs and occurs in 3rd–4th decade of life

47. Clinical Features Cough and granulomatous skin rashes and bilateral hilar adenopathy Triad of uveoparotid fever ( Heerfordt’s syndrome ): Parotitis, uveitis, facial nerve palsy and mild fever. Otologic: Sensorineural hearing loss, vestibular dysfunction and occasionally granulomatous lesion in EAC, middle ear and mastoid. CN VII palsy: Often bilateral, sudden and resolve spontaneously. Eye: Iridocyclitis and keratoconjunctivitis. Nervous system: Peripheral mononeuritis or polyneuritis. Lymphadenopathy and hepatosplenomegaly Myalgia and arthralgia Cardiac failure.

48. Investigations X-ray chest: Hilar adenopathy Serum: Hypercalcemia, elevated serum angiotensinconverting enzyme Biopsy: Noncaseating epithelioid granulomas.

49. Treatment Spontaneous resolution occurs First-line agent: Corticosteroids in progressive disease with involvement of eye, heart and CNS. Second-line agents: Cytotoxic drugs such as methotrexate, azathioprine, and cyclophosphamide Infliximab: It inhibits the release or blocks the effect of a key cytokine, which appears to be tumor necrosis factor.

50. MOBIUS SYNDROME Congenital facial palsy Associated with bilateral abducens palsy Concomitant tongue weakness and clubfoot are common

51. IATROGENIC OR SURGICAL TRAUMA Damaged accidentally during stapedectomy, tympanoplasty or mastoid surgery. The paralysis may be immediate (needs earliest surgical decompression and repair) Delayed (treated conservatively). The exposed nerve may be pressed by the pressure of ear packing. This just needs removal of ear pack.

52. Prophylaxis Thorough anatomical knowledge and temporal bone dissection Always work along the course of facial nerve and never across the nerve. Constant irrigation during the drilling avoids thermal injury to the facial nerve. Diamond burr must be used, when working near the nerve. If nerve is exposed, do not get scared. Just handle the nerve gently. Avoid unnecessary handling and instrumentations. Do not remove those granulations which penetrate facial nerve

53. Management of postoperative facial palsy after mastoidectomy • Remove the pack and get CT scan done. • Re-exploration for correction is indicated, if there is no recovery within first few hours.

54. HYPERKINETIC DISORDERS OF FACIAL NERVE Hemifacial Spasm Involuntary unilateral repeated twitching of facial muscles. Two types of hemifacial spasms— 1) Idiopathic 2) Secondary:

55. Essential or idiopathic . Cause is not known. Treatment Selective section of the branches of facial nerve in the parotid Puncturing the facial nerve with a needle in its tympanic segment Injection of botulinum blocks the neuromuscular junction by preventing release of acetylcholine in the affected muscle

56. Secondary The irritation of facial nerve by Acoustic neuroma Congenital cholesteatoma Glomus tumor – Vascular loop at the cerebellopontine angle: Treated by microvascular decompression through posterior fossa craniotomy

57. Blepharospasm Twitching and spasms of the orbicularis oculi muscles on both sides results in closure of both the eyes causing functional blindness. Etiology: The cause, which is yet not certain, perhaps lies in the basal ganglia. Treatment Selective section of nerves supplying muscles around the eye on both sides. Injection botulinum A into the peripheral muscles gives relief for 3–6 months. It can be repeated, if required.

58. SURGICAL TREATMENT OF FACIAL NERVE PALSY Decompression End-to-end anastomosis Nerve graft (cable graft) Hypoglossal-facial anastomosis Plastic procedures