Mais conteúdo relacionado


facial nerve

  2. CONTENTS • introduction • Embryology • Nuclei of origin • Functional components • Course of facial nerve • Branches and distribution • Surface marking of facial nerve • Ganglion associated with facial nerve • Blood supply • Age changes • Variations of facial nerve • Applied anatomy • Face nerve considerations in endodontics • Conclusion • References
  3. INTRODUCTION : • Seventh cranial nerve. • Mixed nerve Motor root Sensory root • 10,000 Neurons 7000 Motor 3000 Sensory and Secretomotor
  4. EMBRYOLOGY • Developmentally derived from • Motor division of facial nerve is derived from • Sensory division originates from the cranial neural crest.
  5. 3 rd week Facioacoustic primordium or crest develops 1st distinguishable feature of facial nerve 4th week Facial and acoustic portions are more distinct 5th week Apperance of Geniculate ganglion which separates into 2 branches-main trunk of facial nerve and chorda tymphani 6th week Facial motor nucleus is recognizable 7th week Nervus intermedius arises from the ganglion,formation of peripheral branches
  6. 8th week Formation of fallopian canal 10-15 weeks Peripheral branches are completely developed • course ,branching,anatomic relations are established during the first three months of prenatal life. • Important steps in facial nerve development occurs throughout gestation and the nerve is not fully developed until 4yrs after birth.
  7. NUCLEI OF FACIAL NERVE The fibres of the nerve arise from four nuclei situated in the lower pons. 1. Motor nucleus of brachiomotor 2.superior salivatory nucleus –parasympathetic 3.lacrimatory nucleus-parasympathetic 4.Nucleus tractus solitarus which is gustatory and also receives afferent fibres from the gland.
  8. FUNCTIONAL COMPONENTS • Special Visceral Efferent — Motor to striated muscles derived from the 2nd branchial arch i.e, muscles responsinble for facial expression and elevation of hyoid bone. • General Visceral efferent — these are secretomotor to submandibular, sublingual, lacrimal and glands of nose, palate and pharynx. • General visceral afferent — carries afferent impulses from the above mentioned glands. • special Visceral Afferent — carries taste sensation from the palate and from anterior two-thirds of the tongue except from vallate papillae. • General Somatic Afferent — innervate a part of skin of ear and carries the impulses of touch and temperature, carries proprioceptive impulses from muscles of face.
  9. COURSE OF FACIAL NERVE • The course of facial nerve is divided by stylomastoid foramen into Intracranial (intrapterous)part Extracranial part
  10. INTRACRANIAL PART : 2 roots attached to the lateral part of the lower border of pons,medial to CNVIII Both reach the internal acoustic meatus In the Meatus motor root lies in a groove on CNVIII(accompained by labrythine vessels) Two roots fuse in the bottom of the meatus to form a single trunk Single trunk lies in the pterous part of the temporal bone and enters the facial canal
  11. • Within the canal,the course of the nerve can be divided into three parts by 2 bends. • First part :directed laterally above the vestibule. • Second part :runs backwards into relation to the medial wall of the middle ear above promontory. • Third part:directed downwards behind the promontory. • First bend :also called genu,lies anteriosuperior to promontory. • Second bend: is between promontory and mastoid antrum.
  12. The facial nerve exits the posterior cranial fossa at the internal acoustic meatus
  13. Within the internal acoustic meatus ,facial nerve enters the facial canal
  14. The first branch –the greater superficial petrosal nerve branches from the geniculate ganglion within the genu of the facial canal and enters the middle cranial fossa by way of hiatus of the canal for the GSPN
  15. EXTRACRANIAL PART: • As it exits from the stylomandibular foramen,it gives rise to .posterior auricular .digastric .stylohyoid
  16. Lateral side of base of styloid process Then enters the parotid gland through posterolateral surface Behind the neck of the mandible ,it divides into 5 terminal branches Emerges out through anteriomedial surface
  17. Branches Branches of communication Branches of distrubution
  18. BRANCHES OF COMMUNICATION Internal acoustic meatus VIII cranial nerve Geniculate ganglion a. greater petrosal nerve b.lesser petrosal nerve C.External petrosal nerve Facial canal Vagus nerve Stylomastoid foramen IX & X cranial nerves Greater auricular nerve Auriculotemporal nerve Behind ear Lesser occipital nerve Face V cranial nerve Neck Transverse cutaneous nerve
  19. BRANCHES OF DISTRUBUTION FACIAL CANAL Greater petrosal nerve Nerve to stapedius Chorda tympani STYLOMASTOID FORAMEN a.posterior auricular b.nerve to stylohyoid c.nerve to digastric(posterior belly) IN FACE a.temporal b.zygomatic c.buccal d.marginal mandibular e.cervical
  20. SURFACE MARKING • Marked by a short horizontal line which joins the following two points: 1) A point at the middle of the anterior border of the mastoid process. 2)Behind the neck of the mandible.
  21. GANGLIA ASSOCIATED WITH FACIAL NERVE GANGLION NATURE FUNCTION Geniculate sensory Taste fibers from anterior 2/3rds of the tongue submandibular parasympathetic Secretomotor fibres to submandibular and sublingual salivary glands pterygopalatine parasympathetic Secretomotor fibres to lacrimal gland
  22. VARIATIONS OF FACIAL NERVE 1. Buccal branch usually single, two branches in 15% cases 2. Marginal mandibular branch – pass bellow the lower border of mandible, incidence varying between 20-50% 3. Cervical branch – 20% cases, two branches 4.Baker and Conley reported trifurcation, quadrifurcation, or even a plexiform branching pattern of the trunk of the facial nerve
  23. DISORDERS OF FACIAL NERVE • Facial nerve lesions: 1)supranuclear type 2)nuclear type 3)peripherial lesions Injury at the internal acoustic meatus Injury distal to geniculate ganglion Injury at stylomastoid foramen
  24. SUPRANUCLEAR TYPE: • Features: • Paralysis of lower part of the face(opposite side) • Partial parlysis of upper part of the face • Normal taste and saliva secretion • Stapedius not paralysed
  25. NUCLEAR TYPE • Features: • Paralyses of the facial muscle of the same side • PERIPHERAL: A)Injury at the level of internal acoustic meatus: Features: • Paralysis of secretomotor fibres. • Hyper acusis • Loss of corneal reflex • Taste fibres unaffected • Facial expression and movements paralysed
  26. B)injury distal to geniculate ganglion • Features: • Complete motor paralysis(same side) • Loss of corneal reflex • No hyper acusis • Taste fibers affected • Facial expression and movements paralysed • C)injury at stylomastoid foramen: • Condition known as Bell's palsy
  27. CAUSES FOR FACIAL PALSY • Birth • Trauma • Infections • Toxic • Metabolic causes • Neoplastic • Iatrogenic • Idiopathic
  28. BIRTH: • Forceps delivery. • Dystrophia myotonica. • Moebius syndrome.
  29. TRAUMA • Basal skull fracture. • Facial injuries. • Penerating injury to middle ear. • Altitude paralysis(barotrauma).
  30. INFECTIONS • Malignant otitis Externa(skull base osteomyelitis) • Acute or chronic otitis media • Varicella zoster infection • Herpes zoster infection(Ramsey hunt syndrome) • Hiv infection • Parotitis • Mumps • Meningitis
  31. TOXIC • Thalidomide • Tetanus • Diphtheria • Carbon monoxide
  32. METOBOLIC CAUSES • Diabetes mellitus • Hyperthyroidism • Pregnancy • Hypertension • Acute porphyria
  33. NEOPLASTIC • Facial nerve tumor • Leukaemia • Meningioma • Haemangioblastoma • Sarcoma • Carcinoma(invading or metastatic)
  34. IATROGENIC • Mandibular block anesthesia • Head and neck surgery
  35. IDIOPATHIC • Myasthenia gravis • Guillian-barre syndrome • Sarcodiosis • Familial bell's palsy
  36. EVALUATION OF FACIAL PARALYSIS • Clinical features Central VS peripheral lesion Complete head and neck examination Cranial nerve evaluation • Electrodiagnostic testing • Tophographic diagnosis
  37. TOPHODIANOSTIC TESTS • Schirmer test for lacrimation (GSPN) • Stapedial reflex test (Stapedial branch) • Taste testing (Chorda tympani nerve) • Salivary flow rates & pH (Chorda tympani)
  38. ELECTROPHYSIOLOGIC TESTS • Nerve excitability test(NET) • Electromyography(EMG) • Maximal stimulation test(MST) • Electroneuronography(ENoG)
  39. IMAGING • Magnetic resonance imaging (MRI) with intravenous gadolinium contrast has revolutionized tumor detection in the cerebellopontine angle and temporal bone and is currently the study of choice when a facial nerve tumor is suspected. • Computed tomography (CT) is valuable for surgical planning in cholesteatomas and temporal bone trauma involving facial nerve paralysis.
  40. HOUSE BRACKMANN FACIAL NERVE GRADING SYSTEM GRADING DEGREE OF INJURY FEATURES GRADE 1 NORMAL normal functions GRADE II SLIGHT DYSFUNCTION At rest: normal symmetry & tone At motion: slight weakness Complete closure of eye with mini mum effort Slight asymmetry of mouth GRADE III MODERATE DYSFUNCTION At rest- normal symmetry & tone At motion: obvious dysfunction but not disfiguring difference between two sides complete closure of eye with effort Hemi facial spasm
  41. GRADE IV MODERATE SEVERE DYSFUNC TION At rest: normal symmetry & t one At motion: obvious weakness Disfiguring asymmetry Incomplete closure of eye Mouth- asymmetric GRADE V SEVERE DYSFUNCTION At rest: asymmetry At motion: barely perceptible motion Eye- incomplete closure Mouth- slight movement
  42. BELLS PALSY • Bell's palsy is an idiopathic, acute, unilateral paresis or paralysis of the face in a pattern consistent with peripheral facial nerve dysfunction, and may be partial or complete, occurring with equal frequency on the right and left sides of the face. • Named after Sir Charles Bell (1774-1842), who first described the syndrome along with the anatomy and function of the facial nerve. • Bell palsy is certainly the most common cause of facial paralysis worldwide
  43. DEMOGRAPHICS OF BELL'S PALSY • Race:slightly higher in persons of japanese descent. • Sex:no diference exists. • Age: it is more common in persons aged 15-45 years. • Bell's palsy is less common in those younger than 15 years and in those older than 60 years.
  44. PATHOPHYSIOLOGY OF BELL'S PALSY • Two most common proposed theories are: 1.) infection with virus.(HSV1, Herpes zoster) 2.) Compression of the nerve.
  45. 1.)Reactivated herpes viruses from the geniculate ganglion of the facial nerve may play a key role in the development of this condition. Primary viral infection (herpes) sometime in the past. The virus lives in the nerve (geniculate ganglion) from months to years. The virus becomes reactivated at a later date The virus reproduces and travels along the nerve.
  46. The virus infects the cells surrounding the nerve resulting in inflammation. The immune system responds to the damaged Schwann cells, which causes inflammation of the nerve and subsequent weakness or paralysis of the face. The course of the paralysis and the recovery will depend upon the degree and amount of damage to the nerve.
  47. 2.)Compression of the nerve: • Edema and ischemia result in compression of the facial nerve within fallopian or facial canal. • The first portion of the facial canal, the labyrinthine segment, is the narrowest. • The meatal foramen in this segment has a diameter of only about 0.66 mm. This is the location that is thought to be the most common site of compression of the facial nerve in Bell palsy.
  48. FEATURES OF BELL'S PALSY • Unilateral involvement. • Loss of nasolabial fold. • Drooping of the corner of the mouth. • Slight widening palpebral fissure. • Inability to close eyelid (bell's sign). • Mask like appearance of face. • Inability to smile , close eye or raise eyebrow . • Whistling impossible. • Inability to puffing cheeks. • Inability to wrinkle forehead . • Slurred speech. • Loss/alteration of taste.
  49. DIAGNOSIS OF BELL'S PALSY • By exclusion • Criteria: • Paralysis or paresis of all the muscles groups on side of the face. • Sudden onset. • Absence of signs of CNS disease. • Absence of signs of ear disease.
  50. HISTORY • Patient also mentoin otalgia or aural fullness and facial or retroauricular pain,which is typically mild and may precede the palsy. • The palsy is often sudden in onset and evolves rapidly ,with maximal facial weakness developing within two or three days. • Associated symptoms may be hyperacusis,decresed production of tears and altered taste. • The most alamring symptom of bell's palsy is paresis.
  51. PHYSICAL EXAMINATION • Bell's phenomenon —upward diversion of the eye on attempted closure of the lid—is seen when eye closure is incomplete. • Careful inspection of the ear canal, tympanic membrane, and oropharynx. • Evaluation of peripheral nerves function in the extremities. • Palpation of the parotid gland.
  52. COURSE AND PROGNOSIS • Partial paralysis always resolves completely within a few weeks. • Recovery from complete paralysis takes longer (months)and is complete in only about 60-70% cases. • Approximately 15% of patients are left with troublesome residual palsy and or synkinesis.
  53. MANAGEMENT • The main aims of treatment in the acute phase of Bell's palsy are to speed recovery and to prevent corneal complications. • Psychological support is also essential, and for this reason patients may require regular follow up. • There is general agreement that 70-80% of these patients recover completely ,while the reminder develop various sequelae within one to three months
  54. • Eye care: • It focuses on protecting the cornea from drying and abrasion due to problems with lid closure and the tearing mechanism. • Lubricating drops (carboxy methyl cellulose)should be applied hourly during the day and a simple eye ointment should be used at night.
  55. MEDICAL TREATMENT • Corticosteroids : • Prednisolone 1mg/kg/day 7-10 days • Corticosteroids combine with antiviral drugs is better. • Acyclovir 400mg 5 times/day. • Famciclovir and valacyclovir 500mg bid
  56. SURGICAL TREATMENT • Facial nerve decompression. • INDICATION: • Completely paralysis. • Appropiate time for surgery is 2-3 weeks after paralysis.
  58. HERPES ZOSTER OTICUS SYNDROME • Symptoms: • Facial paralysis • Ear pain • Vesicles • Hearing loss • vertigo
  59. MELKERSSON ROSENTHAL SYNDROME • Recurrent attacks of facial paralysis. • Associated with mulitple episodes of non-pitting ,non-inflammatory painless edema of the face. • Chelitis granulomatosa. • Fissured tongue.
  60. TREACHER COLLINS SYNDROME • Features : • 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 disease. • O; orbital asymmetry • M; mandibular hypoplasia • E; auricular deformity • N; Abberent Nerve development and • S; soft-tissue disease
  61. Facial nerve involvement in treachers 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
  62. MOEBIUS SYNDROME(CONGENITAL FACIAL DIPLEGIA) • Abnormal VI ,VII,XII Nerve nuclei • Facial Nerve absent / smaller • Congenital Extra ocular muscle & facial palsy
  63. CROCODILE TEAR SYNDROME • Due to injury to facial nerve ,proximal to geniculate ganglion,there may be misdirection of nerve fibers to lacrimal gland instead of going to submandibular gland,through the greater pterosal nerve. • As a result ,patient lacrimates is termed as crocodile tear syndrome and can be treated by dividing the greater petrosal nerve.
  64. AURICULOTEMPORAL NERVE SYNDROME • Is a complication of paradicetomy . • Abberant nerve regeneration after injury(a complication develops between auriculo temporal and greater auricular nerves such thst the parasympathetic fibers migrate into cutaneoussympathetic nerves that supply the swaet glands .
  66. • Through dental or surgical procedures; dentist may cause the transient or permanent facial palsy. • An dentist may treat a patient with FP or • The first medical professional to observe FP in a patient or • Even induce iatrogenic errors themselves
  67. SUMMARY • In endodontics facial nerve palsy is caused by : • Direct anaesthesia to the facial nerve. • Reflex vasospams of the external carotid artery ischemia of the facial nerve. • Direct damage with the irrigants. • Dental infections may secondarily infect the facial nerve.
  68. CONCLUSION • The diagnosis,clarification of etiology and treatment of facial paralysis require a multidisciplinary team with neurosurgeon, otorhinolaryngologist, oral and maxillofacial surgeon. • The dentist must evaluate and remove the dental foci. • The dentist should avoid inducing iatrogenic facial paralysis in the dental office. • Dentist should have a thorough knowledge of facial nerve, its complications, clinical findings, diagnosis and should have an essential treatment plan of FNP in dental office • The dentist can make oral devices to implement multifunctional rehabilition and must also rehabilitate an asymmetric oral cavity with functional disorders ,in order to improve the quality of life of patients with facial paralysis.
  69. REFERENCES • B.D.chausaria 's human anatomy 4th edition. • Gray's anatomy 2 nd edition. • The facial nerve –May's 2nd edition. • Shafers textbook of oral pathology-5th edition. • Management of patients with facial paralysis in the dental office: A brief review of the literature and case report:Aranka Ilea,Alxendaru cristea ,Viorica Tarmure,Veronica E. Trombita,Radu S Campian,Silviu Albu.