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Facial nerve palsy

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course of facial nerve, causes of palsy, management and description of few causes, facial nerve decompression and animation techniques

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Facial nerve palsy

  1. 1. DR PRIYANKA SHASTRI FACIAL NERVE PALSY
  2. 2. ORIGIN AND COURSE OF FACIAL NERVE
  3. 3. Histology of facial nerve  Each nerve fibre : nerve cell body, axon : surrounded by myelin secreted by schwann cells  Endoneurium : to form tubule  Multiple tubules : perineurium  Epineurium : nerve sheath
  4. 4.  The facial nerve gets it’s blood supply from 4 vessels:  Anterior inferior cerebellar artery – at the cerebellopontine angle  Labyrinthine artery (branch of anterior inferior cerebellar artery) – within internal acoustic meatus  Superficial petrosal artery (branch of middle meningeal artery) – geniculate ganglion and nearby parts
  5. 5.  Stylomastoid artery (branch of posterior auricular artery) – mastoid segment  Posterior auricular artery supplies the facial nerve at & distal to stylomastoid foramen  Venous drainage parallels the arterial blood supply
  6. 6. Degrees of nerve injury  Neuropraxia : no wallerian degenration  Axonotmesis : distal wallerian degenration occurs, intact perineurium, total paralysis  Neurotmesis : wallerian degenration occurs
  7. 7. Sunderland classification  1°: Partial block: Neuropraxia  2°: Loss of axons, endoneurial tubes remain intact: axonotmesis  3°: Injury to the endoneurium: neurotemesis  4°: Injury to the perineurium in addition to above: partial transection  5°: Injury to the epineurium in addition to above: complete transection  The first three degrees are seen in viral and inflammatory disorders while 4th and 5th are seen in surgical or accidental trauma
  8. 8. CAUSES OF FACIAL PARALYSIS CENTRAL Brain abcess Pontine Gliomas Poliomyeliti s Multiple sclerosis GB syndrome INTRACRA NIAL Acoustic neuroma meningioma congenital cholesteato ma metastatic carcinoma meningitis. INTRATEMPORAL A. Idiopathic Bell’s palsy Melkersson’s syndrome B. Infections ASOM,CSOM, Herpes zoster oticus, malignant otitis externa C. Trauma – Mastoidectomy, Stapedectomy, # temporal bone D. NEOPLASMS Malignancies of external and middle ear glomus jugulare tumour facial nerve neuroma metastasis to temporal bone, cholesteatoma, VII nerve tumour, meningioma, schwannoma EXTRACRAN IAL Malignancy of parotid, sx of parotid, accidental injury in parotid region. Neonatal facial injury SYSTEMIC DISEASES DM, Hypothyroidism , uraemia,PAN, wegener’s granulomatosis , sarcoidosis,lepr osy, leukemia, demyelinating disease.
  9. 9. Altered function of facial nerve following injury  SYNKINESIS- Abnormal synchronization movement occuring with voluntary and reflex activity of muscle which normally do not contract together.  CROCODILE TEARS- Increased unilateral lacrimation on involved side associated with eating.  STAPEDIUS TENDON CONTRACTION – Hyperkinetic syndrome with faulty facial regeneration causes fullness and roaring in ear.  FACIAL MYOKYNIA – Continuous fine fibrillary movement of facial muscles giving “bag of worms” facial appearance.
  10. 10. APPROACH HISTORY onset duration Progression h/o head injury Recurrence PHYSICAL FINDINGS U/l or b/l pain over mastoid / preauricular area vesicles on the pinna / EAC s/s/o ASOM / CSOM Head & neck examn Showing mass or involvement of CN INVESTIGATIONS Topodiagnostic tests Electrodiagnostic Imaging
  11. 11. FACIAL NERVE PALSY
  12. 12. TOPOGNOSTIC TESTING
  13. 13.  SCHIRMER TEST- decrease in lacrimation of 75% or more as compared to normal side. Or < 10mm for both sides at 5 min.  STAPEDIAL REFLEX TESTING - if absent , site of lesion between geniculate ganglion and stapedius muscle. If present then site of lesion is distal to stapedius muscle.  TASTE TESTING – conc. Sweet, salt, sour and bitter solution tested along lateral margin of anterior 2/3 of tongue towards tip / electrogustometry ( EGM )  SUBMANDIBULAR GLAND FLOW- compared by sialometry using 6% citric acid.  TESTING FACIAL MOVEMENT
  14. 14. ELECTRICAL TESTING  Nerve Excitability Test - minimal current necessary to stimulate muscle movement when applied to a branch of facial nerve. A difference of 3.5mA or greater between two sides is thought to be significant.  Maximum Stimulation Test – strength and duration of stimulation is gradually increased from 1mA to 5mA. Useless <72 hrs.  ELECTRONEURONOGRAPHY - action potentials developed in the muscles by stimulation of the nerve is measured and expressed as % of degeneration compared to normal side. Surgical intervention in case of immediate paralysis with> 90% degeneration.No use < 72 hrs.
  15. 15. NERVE EXCITABILITY TEST (NET)  Compares transcutaneous current threshold required to elicit minimal muscle contraction between two sides  A difference of 3.5 milliamperes (mA) or more in thresholds between the two sides a reliable indicator of progressive degeneration :indicator for surgical decompression  If the paralysis becomes total, the test can determine whether a pure conduction block exists or whether degeneration is occurring, as indicated by progressive loss of excitability.
  16. 16. MAXIMAL STIMULATION TEST (MST)  Instead of measuring threshold, however, maximal stimuli (current levels at which the greatest amplitude of facial movement is seen) is employed.  degree of facial contraction is subjectively assessed as either equal, mildly decreased, markedly decreased, or without response compared with that on the normal side.  Movements on the paralyzed side are subjectively expressed as a percentage (0%, 25%, 50%, 75%, 100%) of the movement on the normal side.  Symmetric response within first ten days – complete recovery in > 90%  No response within first ten days – incomplete recovery with significant sequelae
  17. 17. ELECTROMYOGRAPHY  The recording of spontaneous and voluntary muscle potentials by needles introduced into the muscle is called electromyography (EMG).  Records motor unit potentials of the orbicularis oculi & orbicularis oris muscle during rest & voluntary contraction  In a normal resting muscle biphasic / triphasic potentials are seen every 30-50msec.
  18. 18.  EMG can be used to determine:- 1.If a nerve in question is in fact in continuity(volitional activity recorded) 2.Evidence of degenration ( fibrillation after 10-14 days) 3.If there are early sign of reinnervation (polyphasic innervation potentials after 4-6 weeks)
  19. 19.  Fibrillation potentials typically arises 2-3 weeks following injury  With regeneration of nerve after injury, polyphasic reinnervation potential replaces fibrillation potential  Reinnervation potentials may precede clinical signs of recovery by 6-12 weeks
  20. 20.  Polyphasic potential indicate regenrative process & surgical intervention is therefore not indicated  Fibrillation indicate lower motor neuron denervation but viable motor end plates, so surgical intervention needed(to achieve nerve continuity)  Electrical silence indicates atrophy of motor end plates & need for muscle transfer procedure
  21. 21. EVOKED ELECTROMYOGRAPHY (EEMG) OR EVOKED ELECTRONEURONOGRAPHY (EnoG)  Records compound muscle action potential (CMAP) with surface electrodes placed transcutaneously in the nasolabial fold (response) and stylomastoid foramen (stimulus)
  22. 22. EVOKED ELECTROMYOGRAPHY (EEMG) OR EVOKED ELECTRONEURONOGRAPHY (EnoG)  Waveform responses are analyzed to compare peak-to- peak amplitudes between normal and uninvolved sides where the peak amplitude is proportional to the number of intact axons.  Most valuable prognostic indicator---Its main indicaion acute onset complete facial paralysis  This method offers the potential advantage of an objective registration of electrically evoked responses, and the amplitude of response of the paralyzed side (in mV) can be expressed as a precise percentage of the normal side's response.
  23. 23. ELECTRONEURONOGRAPHY (EnoG) • )  Response <10% of normal in first 3 weeks-poor prognosis  Response >90% of normal within 3 weeks of onset- 80-100% probability of recovery  Testing every other day  Not useful until 4th day of paralysis as it takes about 3 days for degeneration to reach completion  Also of less value after three weeks bcoz of nerve fibre desynchronization  Advantages: Reliable  Disadvantages:  Uncomfortable  Cost  Test-retest variability due to position of electrodes
  24. 24. Limitation of electophysiological testing  Electric impulse can stimulate only normal/ neuropraxic fibres and can’t distinguish b/w axonotemesis or neurotemesis  Provides no useful information in cases of incomplete facial paralysis  It fails to provide information on the immediate post paralysis period( first 72 hours)
  25. 25. 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 (e.g., in a case of slowly progressive or longstanding weakness)  However, enhancement also occurs in most cases of Bell’s palsy and herpes zoster opticus, usually in the perigeniculate portions of the nerve. This enhancement may persist for more than 1 year after clinical recovery; can be distinguished from neoplasm by its linear, unenlarged appearance; and has no apparent prognostic significance.
  26. 26.  Computed tomography (CT) is valuable for surgical planning in cholesteatomas and temporal bone trauma involving facial nerve paralysis but probably is less useful than MRI in the investigation of atypical idiopathic paralysis.  Unfortunately, even MRI fails to detect a substantial number of malignant parotid tumors.  MRI shows the greatest utility in predicting location and depth of parotid gland tumors, but even in this capacity it is no better than simple manual palpation alone.
  27. 27. SIGN DIFFERENTIATING SUPRANUCLEAR FROM INFRANUCLEAR LESIONS SUPRANUCLEAR INFRANUCLEAR  Forehead intact bilaterally  FND, Hemiplegia on side of facial palsy  Ataxia  Reflexes intact  Tone maintained  Drooping corner of mouth  Slight flattening of nasolabial fold.  No muscle atrophy/ fasciculation  Total facial palsy  No FND  No hemiplegia  No ataxia  No reflexes  Flaccid  Not an isolated finding  Not an isolated finding  Muscle atrophy / fasciculations present.
  28. 28. BELL’S PALSY First described more than a century ago by Sir Charles Bell Bell palsy is certainly the most common cause of facial paralysis worldwide
  29. 29.  U/l spontaneous idiopathic lower motor neuron facial palsy  Incidence of Bell’s palsy is 20 to 30 patients per 100,000 population  The incidence is greater in patients  older than 65 years and lower in children younger than age 13.  The male-to-female ratio for Bell’s palsy is approximately equal,  except for a predominance in women younger than 20 years of age and a slight predominance in men older than 40  The left and right sides of the face are equally involved
  30. 30.  Diagnosis 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
  31. 31.  30% of patients will have incomplete paralysis on presentation  70% will have a complete paralysis.  Bilateral paralysis occurs in 0.3%  Have a history of previous paralysis.  A family history of Bell’s palsy can be elicited in 8% of patients
  32. 32. 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  Edema of nerve within inelastic fallopian canal  Recovery begins by 3 weeks, full recovery by 6months  70 % : 15 % : 15%
  33. 33.  most important prognostic factor is whether the paralysis is incomplete or complete.  The prognosis for affected persons in whom complete facial paralysis never develops is excellent: 95% to 100%  factors associated with poor outcome include hyperacusis; decreased hearing; age older than 60 years; diabetes mellitus; hypertension;and severe aural, anterior facial, or radicular pain
  34. 34. Ramsay Hunt Syndrome  Caused by reactivation varicella zoster virus (herpes virus type 3)  Facial paralysis + hearing loss +/- vertigo  Herpes zoster oticus  Two-thirds of patients have rash around ear  Other cranial nerves, particularly trigeminal nerves (5th CN) often involved  Worse prognosis than Bell’s (complete recovery: 50%)  Important cause of facial paralysis in children 6-15 years old
  35. 35.  The timing of the appearance of the vestibular eruption may have prognostic significance. In most cases, eruption and paralysis occur simultaneously.  In approximately 25% of cases, the eruption precedes the paralysis; these patients have a higher likelihood of recovery.  Patients with Ramsay Hunt syndrome also are more likely than patients with Bell’s palsy to have associated cranial nerve symptoms, including hyperacusis, hearing loss, and pain.  In approximately 10% of patients, the vesicular rash appears well after the initial facial paralysis, many patients demonstrate a rise in antibody to VZV without ever exhibiting cutaneous or mucous membrane vesicles—so-called Ramsay Hunt sine herpete.
  36. 36.  Severe ocular complications can occur with herpes zoster ophthalmicus.  These complications include uveitis, keratoconjunctivitis, optic neuritis, and glaucoma and are almost always associated with involvement of the ophthalmic division of the trigeminal nerve
  37. 37.  Management of patients with herpes zoster, including cephalic zoster, consists of systemic corticosteroids.  A specific benefit of corticosteroid therapy is a reduction in postherpetic neuralgia. The usefulness of corticosteroids in fostering recovery from the facial paralysis is controversial; however, early institution of corticosteroids seems to  relieve acute pain, reduce vertigo, and decrease the incidence of postherpetic neuralgia  The antiviral agent acyclovir also is recommended to treat herpes zoster facial
  38. 38. Congenital Facial Paralysis  The incidence of facial paralysis in newborns has been estimated at 0.23% of live births.  Birth trauma usually causes isolated facial paralysis and other signs of injury, including facial swelling, ecchymosis, and hemotympanum. Abnormalities of other cranial nerves or abnormalities on brainstem audiometry (prolongation of the I to III or I to V interval) suggest that the facial paralysis is congenital and not traumatic.  Of facial paralysis cases in infants, 78% are related to birth trauma.  These cases are equally divided between forceps deliveries and vaginal deliveries plus cesarean sections, suggesting that intrauterine facial nerve injury can occur from pressure on the infant’s face by the sacral prominence during birth
  39. 39.  Möbius’ syndrome represents a broad spectrum of clinical and pathologic findings ranging from isolated unilateral facial paralysis (usually associated with sixth cranial nerve paralysis) to bilateral absence of facial and abducens nerve function.  Multiple other cranial nerves,including the glossopharyngeal, vagus, hypoglossal, and other extraocular motor nerves, also may be affected
  40. 40. Infectious causes  Acute facial paralysis may result from bacterial or tuberculous infection of middle ear, mastoid & necrotizing otitis externa  Incidence of facial paralysis with otitis media: 0.16% ◦ Infection extends via bone dehiscences to nerve in fallopian canal leading to swelling, compression & eventually vascular compromise & ischemia  Immune compromised patients are at risk for pseudomona infection  Poor prognosis (complete recovery is < 50%)
  41. 41. Neoplasms  27% of patients with tumors involving the facial nerve develop acute facial paralysis  Most common causes: schwannomas, hemangiomas (usually near geniculate ganglion) & perineural spread such as with head and neck carcinoma, lymphoma & leukemia, congenital cholesteatoma  Other neoplasms can also involve the facial nerve ◦ Adults: metatstatic disease, glomus tumors, vestibular schwannomas & meningiomas ◦ Children: eosinophilic granuloma & sarcomas
  42. 42.  Slowly progressive facial paralysis  Early diagnosis : high degree of suspicion  h/o recurrent palsy, involvement of other cranial nerves.  CT and MRI  Tumout resection with grafting
  43. 43.  Recurrent facial palsy: seen in  Bell’s palsy,  Melkersson’s syndrome,  diabetes,  sarcoidosis  tumuors
  44. 44. Melkersson-Rosenthal Syndrome  Acute episodes of facial paralysis  Facial swelling  Fissured tongue  Very rare  Familial but sporadic  Usually begins in adolescence  Leads to facial disfigurement  No definite therapy
  45. 45. Bilateral simultaneous facial palsy  Moebius syndrome  GB Syndrome  Sarcoidosis  Myotonic dystrophy  Skull trauma  Infectious mononucleosis  CMV  Acute porphyria  Botulism  Lyme disease  Bell’s herpes simplex
  46. 46. Traumatic facial nerve palsy  Second most common cause of FN paralysis  - Represents 15% of all cases of FN paralysis  - Most common cause of traumatic facial nerve injury is temporal bone fracture
  47. 47. Temporal bone fractures Longitudinal Transverse  70-90%  Parietal , temporal trauma  Hemotymoanum, ossicular chain disruption  Facial nerve paralysis : 10-20 %: horizontal segment  10-30%  Occipital  Snhl, vestibular dysfn  Facial nerve palsy : 50%: labyrinthine segment  Can be from iac to horizontal segment
  48. 48. Iatrogenic – Surgical • Most common overall surgery with FN injury is parotidectomy • Most common otologic procedures with FN paralysis – Mastoidectomy – 55% of surgical related FN paralysis – Tympanoplasty – 14% – Mechanism - direct mechanical injury or heat generated from drilling – Most common area of injury – distal tympanic segment including the 2nd genu, followed by mastoid segment • Unrecognized injury during surgery in nearly 80% of cases
  49. 49. SURGICAL LANDMARKS OF FACIAL NERVE FOR MIDDLE EAR AND MASTOID SURGERY  Processus cochleariformis  Oval window and horizontal canal  Short process of incus  Pyramid  Tympanomastoid suture  Digastric ridge
  50. 50. For parotid surgery  Cartilaginous pointer of conley  Tympanomastoid suture  Posterior belly of digastric  Styloid process
  51. 51. Surgical management A. Facial nerve decompression B. Neurorrhaphy(nerve repair) 1.direct end to end anastomosis 2. interposition cable grafting C. Nerve transposition: hypoglossal-facial D. Muscle transposition: temporalis, masseter E. Micro-neuro-vascular muscle flap F. Static procedure: eyelid implant, facial sling
  52. 52. Intratemporal Approaches to Decompression • Nerve may be injured along multiple segments – localize injured site pre-operatively – Full exposure of the nerve from IAC to the stylomastoid foramen if can’t localize • Approach to full exposure is based on patient’s auditory and vestibular status – Intact - Transmastoid/Middle cranial fossa approach – Absent – Transmastoid/Translabyrinthine approach
  53. 53.  General principles  Monitoring of facial nerve  Instrumentation  Sharp dissection
  54. 54. Retrolabyrinthine and retrosigmoid approach Advantages Complications  Access to FN in CP angle without sacrificing the inner ear function  No cerebellar compression  AICA and other vessels easily manipulated  Visualization of nerve hampered by location of 8th nerve  Increased risk of hearing loss during separation from 8th nerve  Csf leak  Vascular complications
  55. 55. Middle cranial fossa approach
  56. 56. Advantages Complications  the only method that exposes the entire internal auditory canal and labyrinthine segment with preservation of hearing  most commonly used for decompression of the facial nerve in Bell’s palsy and with longitudinal temporal bone fractures.  Dural elevation can be difficult  Persistent CSF leakage  Conductive and sensorineural hearing losses can result
  57. 57. Transmastoid approach Advantages Complications  excellent exposure of the mastoid and tympanic segments of the facial nerve  used in conjunction with middle fossa and retrolabyrinthine approaches if total facial nerve exposure is required and inner ear function is to be preserved  limited access to the geniculate ganglion and the inability to reach the labyrinthine segment.  Conductive or sensorineural hearing loss also can be a complication if the incus is removed or touched by a rotating burr during the procedure.
  58. 58. Translabyrinthine approach Advantages Complications  The translabyrinthine exposure of the facial nerve is used primarily when the cochlear and vestibular functions have been lost preoperatively.  The greatest advantage with this technique of facial nerve exposure is the ability to access the entire nerve using one approach  Hearing and balance function must be sacrificed for total exposure of the nerve  CSF leakage and infection are the greatest risks
  59. 59. Facial Reanimation  Facial reanimation is a family of different surgical techniques to make one's paralyzed face move more normally. 74
  60. 60. Assessment and Planning  Cause of facial paralysis  Functional deficit/extent of paralysis  Time course/duration of paralysis  Likelihood of recovery  Other cranial nerve deficits  Patient’s life expectancy  Patient’s needs/expectations
  61. 61. Primary Nerve Repair  End-to-end anastomosis preferred  Can be performed with defect < 17 mm  Extratemporal repair performed < 72 hrs of injury  Most common methods  Group fascicular repair  Epineural repair Group fascicular repair
  62. 62. Primary Nerve Repair  Severed ends of nerve exposed  Devitalized tissue/debris removed with fine scalpel  Small bites of epineurium  Epineural sheath approximated with 9-0 nonabsorbable suture  Epineural repair recommended for injury proximal to pes anserinus and intratemporal  Horizontal segment rarely accessible to suture repair Epineural repair technique
  63. 63. Nerve Repair • Recovery of function begins around 4-6 months and can last up to 2 years following repair • Nerve regrowth occurs at 1mm/day • Goal is tension free, healthy anastomosis • Rule is to repair earlier than later - – After 12-18 months, muscle reinnervation becomes less efficient even with good neural anastomosis – Some authors have reported improvement with repairs as far out as 18-36 months • 2 weeks following injury -> collagen and scar tissue replace axons and myelin – Nerve endings must be excised prior to anastomosis for this reason if this far out
  64. 64.  The clinical uses of interposition grafts  (1) radical parotidectomy with nerve sacrifice;  (2) temporal bone resection;  (3) traumatic avulsions;  (4) cerebellopontine angle tumor resection;  (5) any other clinical situation in which viable proximal nerve can be sutured and distal elements of facial nerve can be identified
  65. 65. Interposition Grafting  Cable grafts  Used when defect > 17mm; nerve cannot be reapproximated w/o tension  Most common  Greater Auricular Nerve  Sensory nerves from superficial cervical plexus  Sural nerve  Medial antebrachial cutaneous nerve
  66. 66.  Useful features  Proximity to facial nerve  Cross-sectional area (~equal)  Limited morbidity  Limitations  Reconstruction of long defects and/or branching nerve gaps  maximum of 10 cm
  67. 67.  Pros:  Length (70cm)  Accessibility  Low morbidity associated with sacrifice  Two team approach  Reduced surgical time  Cons:  Variable caliber  Often too large  Difficult to make graft approximation  Unsightly scar
  68. 68. MBCN  Important landmarks:  Medial epicondyle of humerus  Biceps tendon  Basilic and medial cubital veins  Fascial plane separating bicep from tricep  Upper extremity can be prepped from axilla to wrist or continuous with the head/neck.  Nerve diameter and branching pattern are  similar to those of the facial nerve, and donor site morbidity is minimal  with nerve harvest
  69. 69. Surgical Technique  For the surgical technique of neurorrhaphy, interrupted sutures using  9-0 or 10-0 monofilament nylon are preferred.  Both ends of the nerve graft and the proximal and distal stumps should be transected cleanly with a fresh sterile blade.  Epineural sutures  Approximation of the nerve ends using an acrylic glue has been  described : Histacryl or cyano-butyl-acrylate  The nerve graft should lie in the healthiest possible bed of supporting tissue  Suction drainage systems should be placed away from any portions of the nerve graft.
  70. 70. Grafting and Nerve Transfer - Overview  Approach is based on availability of proximal nerve ending  Performed for defects > 17mm  Results in partial or complete loss of donor nerve function  Best functional results are obtained with cable grafting when a segment of the facial n. is disrupted  Also recommended if there is tension at the anastomotic site of a primary nerve repair  Graft should be aprox. 25% longer than needed to allow for a tension free anastomosis
  71. 71. Facial nerve transposition  Reinnervation by connecting an intact proximal facial nerve to the distal ipsilateral facial nerve
  72. 72. Hypoglossal-Facial  Technique modification aka partial XII-VII transfer  Donor nerve harvested  One end of donor nerve is sutured to severed main trunk of CN VII; other end hooked up to proximal segment of partially severed CN XII  The procedure has been modified by only partially sectioning the hypoglossal nerve and interposing, by end to-side anastomoses,by a greater auricular nerve graft between the hypoglossal and facial nerves.  Since the hypoglossal nerve is transected only halfway, tongue function can be preserved.  Limits tongue dysfunction and atrophy
  73. 73. Cross-facial Nerve Grafting  Contralateral CN VII used to reinnervate paralyzed side using a nerve graft ◦ Sural nerve often employed ◦ ~25-30cm of graft needed  Restitution of smile and eye blinking when successful  Disadvantage ◦ 2nd surgical site ◦ Violation of the normal facial nerve
  74. 74. Cross-facial Nerve Grafting  4 techniques 1. Sural nerve graft routed from buccal branch of normal CN VII to stump of paralyzed CN VII 2. Zygomaticus and buccal branch of normal CN VII used to reinnervate zygomatic and marginal mandibular portions respectively 3. 4 separate grafts from temporal, zygomatic, buccal and marginal mandibular divisions of normal CN VII to corresponding divisions on paralyzed side. 4. Entire lower division of normal side grafted to main trunk on paralyzed side.
  75. 75. Muscle Transposition (aka “Dynamic Sling”)  When to use:  Facial neuromuscular system absent  Neural techniques unsuitable  i.e. congenital facial paralysis  Facial nerve interruption of at least 3 years  Loss of motor endplates  Crossover techniques not possible due to donor nerve sacrifice
  76. 76.  Muscle transposition most commonly employs the temporalis muscle because of its good location, length,contractility, and vector of pull.  good for reanimation of the mouth in patients with long-standing (at least 1 year in length) paralysis.  Allows patients to have a voluntary smile. Temporalis
  77. 77. Temporalis  Overcorrection at oral commissure is critical  2nd or 3rd molar of upper dental arch should be exposed when procedure is finished  Harvest and placement of temporoparietal facial flap recommended to fill donor site  Oral support possible within 6 weeks  Movement achieved by clenching the jaws  Unnatural contraction requiring rehabilitation/Physiotherapy
  78. 78. Masseter  Used when temporalis muscle is not available  May be preferred due to avoidance of large facial incision  Disadvantage:  Less available muscle compared to temporalis  Vector of pull on oral commisure is more horizontal than superior/oblique like temporalis
  79. 79. Facial Paralysis (Acute < 3 wks) Intermediate (3 wks-2 years) Chronic (>2 years) CN VII decompression Nerve repair Primary Cable graft -G. auricular -Sural -MACN Nerve transfer -hypoglossal -masseteric -spinal acc. Cross-facial Graft Regional Muscle Transfer -Temporalis -Masseter -Digastric Free Muscle Transfer -Gracilis -serratus -L. dorsi -Pec minor +/-Static Techniques: Slings, Gold weight/Lid procedures, etc Reanimation Summary
  80. 80. THANK U

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