Presentation is loading. Please wait.

Presentation is loading. Please wait.

Facial Nerve Palsy Dr. SUDEEP K.C..

Similar presentations

Presentation on theme: "Facial Nerve Palsy Dr. SUDEEP K.C.."— Presentation transcript:

1 Facial Nerve Palsy Dr. SUDEEP K.C.

2 Anatomy Facial nerve is a mixed nerve, having a motor root and a sensory root. Motor root supplies all the mimetic muscles of the face which develop from the 2nd brachial arch.

3 Anatomy Sensory root “nerve of Wrisberg” carries taste fibers from the anterior 2/3 of the tongue and general sensation from the concha and retroauricular skin. Also it carries secretomotor fibers to the lacrimal, submandibular and sublingual glands as well as those in the nose and palate.

4 Anatomy: Nucleus Pons. Precentral gyrus. Upper part of the nucleus:
Upper face Involuntary emotional movements

5 Anatomy: Course Motor fibers originate… Hooks around…
Joined by sensory nerve i.e wrissberg. Facial n. leaves the brainstem… Travels through… Enters the IAC. Then traverse the temporal bone through facial n. canal ( foramen)? Leaves the temporal bone through Finally divides into terminal branches.



8 Anatomy: Parts Intracranial part Intratemporal part Extracranial part

9 Anatomy: Intratemporal segments
From internal acoustic meatus to stylomastoid foramen. It divides into- Meatal Labyrinthine Tympanic, horizontal Mastoid, vertical



12 Anatomy: Branches Greater superficial petrosal nerve:
Nerve to stapedius: Chorda tympani: Comunicating branch: Posterior auricular nerve: Muscular branches: Peripheral branches: “Pes anserinus”

13 Anatomy: Surgical landmarks
Middle Ear and Mastoid Surgery: Processus chocleariformis Oval window and horizontal canal Short process of the incus Pyramid

14 Anatomy: Surgical landmarks
Parotid Surgery: Cartilaginous pointer: Styloid process Posterior belly pf digastric muscle

15 Anatomy: Structure of the nerve
From inside outward: Axon Myelin sheath Neurolimma Endoneurium Perineurium Epineurium

16 Anatomy: Severity of injury
Saunderland classification: 1°: Partial block: Neuropraxia 2°: Loss of axons: axonotemesis 3°: Injury to the endoneurium: neurotemesis 4°: Injury to the perineurium: partial transection 5°: Injury to the epineurium: complete transection


18 History: Onset: Sudden vs. Gradual Duration: Rate of progression:
Recurrent or familial Associated symptoms Medical history Previous surgeries

19 Physical exam: Complete vs. incomplete
Segmental vs. uniform involvement Unilateral vs. bilateral Cranial nerves assessment Neurologic evaluation Cerebellar signs

20 Physical exam: Microscopic otoscopy Complete head and neck exam

21 Physical exam: Localization of facial nerve lesion:
Central vs. Peripheral.

22 Physical exam: Localization of facial nerve lesion: Peripheral:
Level of nucleus CPA level: Bony canal level: Topodiagnostics Outside the Temporal bone

23 Physical exam: Topodiagnostics: Schirmer’s test: Stapedial reflex:
Taste test: Submandibular salivery flow test: Warton’s ducts

24 Causes: Central: Intacranial part: Intratemporal part:
Extracranial part: Systemic:

25 Causes: Central: Brain abscess Pontine glioma Poliomyelitis
Multiple sclerosis

26 Causes: Intacranial part: Acoustic neuroma Meningioma Metastatic CA

27 Causes: Intratemporal part:
Idiopathic: Trauma: Bell’s palsy Surgical: Mastoidectomy, Stapedectomy Melkersson’s syndrome Accidental:# temporal bone Infections: Neoplasms: ASOM Glomus jugulare tumour CSOM Herpes Zoster Oticus Facial nerve neuroma Metastatic CA

28 Causes: Extracranial part: Parotid gland CA Parotid gland surgery
Parotid gland injury Neonatal facial nerve injury

29 Causes: Systemic: DM Hypothyroidism Uremia PAN
Wegener’s granulomatosis Sarcoidosis Leprosy Leukemia

30 Labs: Pure-tune audiometry Electrophysiologic tests Imaging tests

31 Labs: Electrophysiologic tests: Nerve Excitability Test: NET
Maximum stimulation Test: MST Electroneurography: ENoG Electromyography: EMG

32 Complications: Incomplete recovery Exposure keratitis Synkinesis
Tics and spasms Contractures Crocodile tears Frey’s syndrome “gustatory sweating” Psychological and social problems

33 TIRED ???????

34 Bell’s Palsy

35 Background: one of the most common neurologic disorders affecting the cranial nerves. abrupt, unilateral, peripheral facial paresis or paralysis without a detectable cause.

36 Background: First described more than a century ago by Sir Charles
Bell, Yet much controversy still surrounds its etiology and management. Bell palsy is certainly the most common cause of facial paralysis worldwide.

37 Incidence: United States Internationally
The incidence of Bell palsy in the United States is approximately 23 cases per 100,000 persons. Internationally: The incidence is the same as in the United States.

38 Demographics: Race: slightly higher in persons of Japanese descent.
Sex: No difference exists Age: highest in persons aged years. Bell palsy is less common in those younger than 15 years and in those older than 60 years.

39 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. Polymerase chain reaction techniques have isolated herpes virus DNA from the facial nerve during acute palsy.

40 Pathophysiology: Inflammation of the nerve initially results in a reversible neurapraxia, Herpes zoster virus shows more aggressive biological behaviour than herpes simplex virus type 1

41 History: The most alarming symptom of Bell's palsy is paresis
Up to three quarters of affected patients think they have had a stroke or have an intracranial tumour.

42 History: The palsy is often sudden in onset and evolves rapidly, with maximal facial weakness developing within two days. Associated symptoms may be hyperacusis, decreased production of tears, and altered taste.

43 History: Patients may also mention otalgia or aural fullness and facial or retroauricular pain, which is typically mild and may precede the palsy. A slow onset progressive palsy with other cranial nerve deficits or headache raises the possibility of a neoplasm

44 Physical exam: Bell's palsy causes a peripheral lower motor neurone palsy, Which manifests as the unilateral impairment of movement in the facial and platysma muscles, drooping of the brow and corner of the mouth, and impaired closure of the eye and mouth.


46 Physical exam: Bell's phenomenon—upward diversion of the eye on attempted closure of the lid—is seen when eye closure is incomplete.


48 Physical exam: Polyposis or granulations in the ear canal may suggest cholesteatoma or malignant otitis externa. Vesicles in the conchal bowl, soft palate, or tongue suggest Ramsay Hunt syndrome


50 Physical exam: The examination should exclude masses in the head and neck. A deep lobe parotid tumour may only be identified clinically by careful examination of the oropharynx and ipsilateral tonsil to rule out asymmetry.

51 Investigations: Serum testing for rising antibody titres to herpes virus is not a reliable diagnostic tool for Bell's palsy. Salivary PCR for herpes simplex virus type 1 or herpes zoster virus is more likely to confirm virus during the replicating phase, but these tests remain research tools.

52 Investigations: MRI has revolutionised the detection of tumours.

53 Investigations: Topodiagnostic tests and electroneurography may give useful prognostic information but remain research tools.

54 Diagnosis: Bell palsy is a diagnosis of exclusion.
Other disease states or conditions that present with facial palsies are often misdiagnosed as idiopathic.

55 Management: The main aims of treatment in the acute phase of Bell's palsy are to speed recovery and to prevent corneal complications. Treatment should begin immediately to inhibit viral replication and the effect on subsequent pathophysiological processes that affect the facial nerve. Psychological support is also essential, and for this reason patients may require regular follow up.

56 Management, Eye care It focuses on protecting the cornea from drying and abrasion due to problems with lid closure and the tearing mechanism. The patient is educated to report new findings such as pain, discharge, or change in vision. Lubricating drops should be applied hourly during the day and a simple eye ointment should be used at night.

57 Management, Steroid Two systematic reviews concluded that Bell's palsy could be effectively treated with corticosteroids in the first seven days, providing up to a further 17% of patients with a good outcome in addition to the 80% that spontaneously improve.

58 Management, Steroid Usual regimen is 1mg/kg/day for 1 week.
To be tapered in the 2nd week.

59 Management, Steroid Cochrane review*:
“There is insufficient evidence about the effects of corticosteroids for people with Bell's palsy, although their anti-inflammatory effect might prevent nerve damage.” *Salinas RA, Alvarez G, Ferreira J. Corticosteroids for Bell's palsy (idiopathic facial paralysis). Cochrane Database of Systematic Reviews 2004, Issue 4. Art. No.: CD

60 Management, Antivirals
It seems logical in Bell's palsy because of the probable involvement of herpes viruses. Aciclovir, a nucleotide analogue, interferes with herpes virus DNA polymerase and inhibits DNA replication.

61 Management, Antivirals
Usual regimen is 800mg 5 times a day for 10 days.

62 Bell’s palsy: Antivirals: Cochrane review*:
“More evidence is needed to show whether the antiviral drugs acyclovir or valacyclovir are effective in aiding recovery from Bell's palsy.” * Allen D, Dunn L. Acyclovir or valaciclovir for Bell's palsy (idiopathic facial paralysis). Cochrane Database of Systematic Reviews 2004, Issue 3. Art. No.: CD

63 Outcomes: It has a fair prognosis without treatment, with almost three quarters of patients recovering normal mimetical function and just over a tenth having minor sequelae. A sixth of patients are left with either moderate to severe weakness, contracture, hemifacial spasm, or synkinesis.

64 Outcomes: Patients with a partial palsy fair better, with 94% making a full recovery. The outcome is worse when herpes zoster virus infection is involved in partial palsy.

65 Outcomes: In patients who recover without treatment, major improvement occurs within three weeks in most. If recovery does not occur within this time, then it is unlikely to be seen until four to six months, when nerve regrowth and reinnervation have occurred.

66 Bad Prognostic Factor:
Complete facial palsy No recovery by three weeks Age over 60 years Severe pain Ramsay Hunt syndrome (herpes zoster virus) Associated conditions—hypertension, diabetes, pregnancy Severe degeneration of the facial nerve shown by electrophysiological testing

67 ?

68 Labs: Nerve Excitability Test: NET :
Indication: complete paralysis<3wks Interpretation: < or = 3.5 mA threshold: Prognosis Good Limitation: Not useful in the 1st 3 days or during recovery.

69 Labs: Maximum stimulation Test: MST:
Indication: complete paralysis<3wks Interpretation: Marked weakness or no muscle contraction: advanced degeneration with guarded prognosis Limitation: Not Objective.

70 Labs: Electroneurography: ENoG :
Indication: complete paralysis<3wks Interpretation: < 90% degeneration: prognosis is good; > or = 90%: prognosis is question Limitation: False-positive results in deblocking phase.

71 Labs: Electromyography: EMG
Indication: Acute paralysis less than 1 week or chronic paralysis longer than 2 weeks Interpretation: Active mu: intact motor axons Mu + fibrillation potentials: partial degeneration Polyphasic mu: regenerating nerve Limitation: cannot assess degree of degeneration or prognosis for recovery.

72 Thank you for your attention BEST OF LUCK FOR UR CARD FINAL

Download ppt "Facial Nerve Palsy Dr. SUDEEP K.C.."

Similar presentations

Ads by Google