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FACIAL PALSY
INTRODUCTION Facial nerve is the VII CN. Facial muscles develop from the mesoderm of second branchial arch. Facial muscles are remnants of panniculuscarnosus ,the subcutaneous muscle of animals.
Motor nucleus of VII CN is antero lateral to VI CN nucleus  Red line motor fibers Parasympathetic fibres Visceral afferent fibres
Muscle action Frontalis –wrinkling Corrugatorsupercili — frowning,vertical wrinkles of forehead Orbicularisoculi—closure of eyes Orbicularisoris—whistling Buccinator –puffing the mouth Dilator of the mouth –showing the teeth Platysma-forcibly pulling the angle of mouth downwards and backwards.
Examination of facial nerve Show the teeth Open his mouth—compare nasolabial folds Close his eyes Frown Wrinkle forehead Raise eyebrows Bare his teeth and open his mouth Blowing out cheeks Pursuing the lips –strength and weakness
U M N FACIAL PALSY
L M N FACIAL PALSY
CASE A 28 yr old female had fever for 12 days followed by weakness of left  half  of the face 2 days after subsidence of fever.patient had numbness over the left half of face..mouth was noticed to be deviated to the right side.patient had difficulty in chewing  food.dribbling of saliva and running of tears from eyes. h/o pain in the ear and tinnitus prior to onset.patient has no ear disharge.not a diabetic. On examination patient was having no wrinkles on forehead..unable to close her eyes,whistle,blowout,motuh deviated to right side,could not put out platysma on left side.  A diagnosis of ACUTE COMPLETE LMN FACIAL PALSY was made.
Bell’s palsy
DEFINITION Acute onset of non suppurative  inflammation of the facial nerve above the stylomastoidforamen,producing a unilateral LMN FACIAL PALSY.
BELL’S PALSY IDIOPATHIC  L. M.N FACIAL PALSY HERPES SIMPLEX FACIAL PARALYSIS(ADAM AND VICTOR’S) HERPETIC FACIAL PARALYSIS—(ADAM AND VICTOR’S) Most common form of lower motor neuron facial palsy.  Sudden onset of LMN facial palsy. No other neurologic abnormalities.
BELL’S PALSYcont… Incidence is 23/1,00,000 Affects men and women equally , all ages ,all times of the year. Increased occurrence in the elderly diabetics, hypertensives than in the common people. Increased incidence in women during the third trimester of pregnancy 2 weeks preceding delivery ,first two weeks postpartum. 1 in 6o life time occurrence of single episode Facial palsy reccurs with each pregnancy .
Etiology: Idiopathic  Reactivation of the herpes simplex virus in the geniculate ganglion. Viral agent has long been suspected –(BARINGER)
Patho physiology HSV I DNA in the endoneural fluid .,post auricular muscle---due to reactivation of the virus in the geniuclate ganglion. Inactivated intra nasal influenza vaccine can cause bells palsy. No adequate  data to support the above relation.
Onset of bell’s palsy is acute. ½ of the cases attain maximum paralysis in 48 hours. All cases are clinically prominent by 5 days.
Pain behind the ear may precede the paralysis by a day or two . Impairement of taste is present to some degree in all cases –rarely beyond second week of paralysis. Hyperacusis or distortion of sound in ipsilateral ear ---paralysis of stapedius muscle.
Patient feels stiffness of face pulled to one side. Ipsilateral restriction of eye closure, difficulty with eating ,fine facial movements. Disturbance of taste –chorda tympani fibres Hyperacusis—fibers to stapedius
Paralysis is partial in 30%,complete in 70%cases. Emotional fibres are affected Jaw jerk is normal Corneal reflex is absent These differentiate it from UMN  palsy
BELL’S PHENOMENON Normally on closing the eye ,the eyeball moves upwards and inwards. This is obvious on the affected side due to ineffective closure of the eyelids.
Clinically Corner of mouth droops Crease and skin folds effaces Forehead is unfurrowed Eyelids will not close Eye on the paralysed side rolls upward –BELL’S PHENOMENON Lower lid sags and falls away from conjunctiva Tears spill over cheek Food collects between the teeth and lips Saliva may dribble from the corner of the mouth Heaviness or numbeness of the face Sensory loss rarely demonstratble
Enhancement of the facial nerve on gadolinium enhanced MRI Increased lymphocytes ,mononuclear cells in CSF. Other tests Tensilon test Shirmer test ESR Blood glucose levels
Prognosis 80% patients recover within a few weeks.2-12 weeks. 10%--permanent disfigurement.long term sequelae. 8%--recurrence Best clinical guide to progress is the severity of the palsy during the first few days after presentation. Recovery of taste precedes motor function.
Clinically complete palsy when first seen are less likely to make a full recovery—than incomplete one Advanced age Hyperacusis—persistent Severe initial pain.
If recovery of taste occurs in first week –good prognostic sign. Early recovery of motor function in the first 5-7 days— most favourable prognosis. Recurrence is due to reactivation of virus,pregnancy. Interval between periods is not predictable.
Treatment Controversial Symptomatic Protection of eye during the sleep   patch Massage of the weakened muscles    Lubricating eye drops Prednisolone 60-80 mg/day in divided doses intial 4-5 days,then taper over next 7-10 days. Decreases the possibility of permanent paralysis From swelling of facial nerve in facial canal. Decreases the severe pain.
Acyclovir alone is not useful. No evidence that surgical decompression of facial nerve is effective ---may be harmful Acyclovir 400mg 5 times a day –10 days is not recommended Valacyclovir 1000mg /day 5-7 days-not recommended.
Complications Contracture develops in the paralysed muscles—normal appearance---evident when patient smiles.
Denervation after ten days---axonal degeneration. Electromyography  Nerve excitability  Nerve conduction studies are useful for prognosis.
Long delay in the onset of recovery—3months Regeneration of nerve –2 years Incomplete Crocodile tears Jaw winking Synkinesis Facial spasms Sequelae
Hemifacial spasms Painless  Irreuglar contractions on one side of the face. As a sequelae to bell’s palsy. Irritative lesion of facial nerve.---acoustic neuroma,aberrantartery.,basilar aneurysm Treatment – carbamazepine,gabapentin, Resistant cases – baclofen Local injection of botulinum toxin  Surgical decompression 2 marks
SEQUELAE
Facial diplegia b/l LMN facial palsy Seen in  Guillainbarre syndrome Miller fischer variant Sarcoidosis Lyme disease Mobius syndrome Melkersonrosenthal  syndrome
L M N FACIAL PALSY
L M N FACIAL PALSY B/L
MELKERSSEN ROSENTHAL SYNDROME RECURRENT FACIAL PARLAYSIS LABIAL EDEMA PLICATION OF TONGUE 2 MARKS
D.DIAGNOSIS Lyme disease Ramsay hunt syndrome Sarcoidosis Guillainbarre syndrome Leprosy Diabetes Sjogrens Amyloidosis Melkersonrosenthal syndrome Acoustic neuroma Mutiple sclerosis Middle ear infections Carotid body tumors Cholesteatoma
summary Idiopathic LMN  FACIAL palsy is bells’; palsy Recovery is the rule Prednisolone 60- 80 mg for five days .
Thank you

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Bell’s palsy

  • 2. INTRODUCTION Facial nerve is the VII CN. Facial muscles develop from the mesoderm of second branchial arch. Facial muscles are remnants of panniculuscarnosus ,the subcutaneous muscle of animals.
  • 3. Motor nucleus of VII CN is antero lateral to VI CN nucleus Red line motor fibers Parasympathetic fibres Visceral afferent fibres
  • 4.
  • 5. Muscle action Frontalis –wrinkling Corrugatorsupercili — frowning,vertical wrinkles of forehead Orbicularisoculi—closure of eyes Orbicularisoris—whistling Buccinator –puffing the mouth Dilator of the mouth –showing the teeth Platysma-forcibly pulling the angle of mouth downwards and backwards.
  • 6. Examination of facial nerve Show the teeth Open his mouth—compare nasolabial folds Close his eyes Frown Wrinkle forehead Raise eyebrows Bare his teeth and open his mouth Blowing out cheeks Pursuing the lips –strength and weakness
  • 7.
  • 8. U M N FACIAL PALSY
  • 9. L M N FACIAL PALSY
  • 10. CASE A 28 yr old female had fever for 12 days followed by weakness of left half of the face 2 days after subsidence of fever.patient had numbness over the left half of face..mouth was noticed to be deviated to the right side.patient had difficulty in chewing food.dribbling of saliva and running of tears from eyes. h/o pain in the ear and tinnitus prior to onset.patient has no ear disharge.not a diabetic. On examination patient was having no wrinkles on forehead..unable to close her eyes,whistle,blowout,motuh deviated to right side,could not put out platysma on left side. A diagnosis of ACUTE COMPLETE LMN FACIAL PALSY was made.
  • 12. DEFINITION Acute onset of non suppurative inflammation of the facial nerve above the stylomastoidforamen,producing a unilateral LMN FACIAL PALSY.
  • 13. BELL’S PALSY IDIOPATHIC L. M.N FACIAL PALSY HERPES SIMPLEX FACIAL PARALYSIS(ADAM AND VICTOR’S) HERPETIC FACIAL PARALYSIS—(ADAM AND VICTOR’S) Most common form of lower motor neuron facial palsy. Sudden onset of LMN facial palsy. No other neurologic abnormalities.
  • 14. BELL’S PALSYcont… Incidence is 23/1,00,000 Affects men and women equally , all ages ,all times of the year. Increased occurrence in the elderly diabetics, hypertensives than in the common people. Increased incidence in women during the third trimester of pregnancy 2 weeks preceding delivery ,first two weeks postpartum. 1 in 6o life time occurrence of single episode Facial palsy reccurs with each pregnancy .
  • 15. Etiology: Idiopathic Reactivation of the herpes simplex virus in the geniculate ganglion. Viral agent has long been suspected –(BARINGER)
  • 16. Patho physiology HSV I DNA in the endoneural fluid .,post auricular muscle---due to reactivation of the virus in the geniuclate ganglion. Inactivated intra nasal influenza vaccine can cause bells palsy. No adequate data to support the above relation.
  • 17. Onset of bell’s palsy is acute. ½ of the cases attain maximum paralysis in 48 hours. All cases are clinically prominent by 5 days.
  • 18. Pain behind the ear may precede the paralysis by a day or two . Impairement of taste is present to some degree in all cases –rarely beyond second week of paralysis. Hyperacusis or distortion of sound in ipsilateral ear ---paralysis of stapedius muscle.
  • 19. Patient feels stiffness of face pulled to one side. Ipsilateral restriction of eye closure, difficulty with eating ,fine facial movements. Disturbance of taste –chorda tympani fibres Hyperacusis—fibers to stapedius
  • 20. Paralysis is partial in 30%,complete in 70%cases. Emotional fibres are affected Jaw jerk is normal Corneal reflex is absent These differentiate it from UMN palsy
  • 21. BELL’S PHENOMENON Normally on closing the eye ,the eyeball moves upwards and inwards. This is obvious on the affected side due to ineffective closure of the eyelids.
  • 22. Clinically Corner of mouth droops Crease and skin folds effaces Forehead is unfurrowed Eyelids will not close Eye on the paralysed side rolls upward –BELL’S PHENOMENON Lower lid sags and falls away from conjunctiva Tears spill over cheek Food collects between the teeth and lips Saliva may dribble from the corner of the mouth Heaviness or numbeness of the face Sensory loss rarely demonstratble
  • 23. Enhancement of the facial nerve on gadolinium enhanced MRI Increased lymphocytes ,mononuclear cells in CSF. Other tests Tensilon test Shirmer test ESR Blood glucose levels
  • 24. Prognosis 80% patients recover within a few weeks.2-12 weeks. 10%--permanent disfigurement.long term sequelae. 8%--recurrence Best clinical guide to progress is the severity of the palsy during the first few days after presentation. Recovery of taste precedes motor function.
  • 25. Clinically complete palsy when first seen are less likely to make a full recovery—than incomplete one Advanced age Hyperacusis—persistent Severe initial pain.
  • 26. If recovery of taste occurs in first week –good prognostic sign. Early recovery of motor function in the first 5-7 days— most favourable prognosis. Recurrence is due to reactivation of virus,pregnancy. Interval between periods is not predictable.
  • 27. Treatment Controversial Symptomatic Protection of eye during the sleep patch Massage of the weakened muscles Lubricating eye drops Prednisolone 60-80 mg/day in divided doses intial 4-5 days,then taper over next 7-10 days. Decreases the possibility of permanent paralysis From swelling of facial nerve in facial canal. Decreases the severe pain.
  • 28. Acyclovir alone is not useful. No evidence that surgical decompression of facial nerve is effective ---may be harmful Acyclovir 400mg 5 times a day –10 days is not recommended Valacyclovir 1000mg /day 5-7 days-not recommended.
  • 29. Complications Contracture develops in the paralysed muscles—normal appearance---evident when patient smiles.
  • 30. Denervation after ten days---axonal degeneration. Electromyography Nerve excitability Nerve conduction studies are useful for prognosis.
  • 31. Long delay in the onset of recovery—3months Regeneration of nerve –2 years Incomplete Crocodile tears Jaw winking Synkinesis Facial spasms Sequelae
  • 32. Hemifacial spasms Painless Irreuglar contractions on one side of the face. As a sequelae to bell’s palsy. Irritative lesion of facial nerve.---acoustic neuroma,aberrantartery.,basilar aneurysm Treatment – carbamazepine,gabapentin, Resistant cases – baclofen Local injection of botulinum toxin Surgical decompression 2 marks
  • 34.
  • 35.
  • 36. Facial diplegia b/l LMN facial palsy Seen in Guillainbarre syndrome Miller fischer variant Sarcoidosis Lyme disease Mobius syndrome Melkersonrosenthal syndrome
  • 37. L M N FACIAL PALSY
  • 38. L M N FACIAL PALSY B/L
  • 39. MELKERSSEN ROSENTHAL SYNDROME RECURRENT FACIAL PARLAYSIS LABIAL EDEMA PLICATION OF TONGUE 2 MARKS
  • 40. D.DIAGNOSIS Lyme disease Ramsay hunt syndrome Sarcoidosis Guillainbarre syndrome Leprosy Diabetes Sjogrens Amyloidosis Melkersonrosenthal syndrome Acoustic neuroma Mutiple sclerosis Middle ear infections Carotid body tumors Cholesteatoma
  • 41. summary Idiopathic LMN FACIAL palsy is bells’; palsy Recovery is the rule Prednisolone 60- 80 mg for five days .