This document provides an overview of the anatomy and clinical management of Bell's palsy. It describes the course of the facial nerve from its central pathways through the various segments in the skull and temporal bone. Key points include use of steroids and possibly antivirals within 72 hours, eye protection for impaired closure, and selective use of electrodiagnostic testing or decompression surgery for patients with complete paralysis. Management aims to reduce inflammation and promote recovery of facial nerve function.

1. Facial nerve

2. Anatomy of Facial Nerve
1. Intracranial Part
2. Intra temporal part
3. Extra temporal part

3. Intra- cranial course of Facial nerve-
1. Central segment (tegmentum pontis).
2. Cisternal segment (CPA).
3. Canalicular segment (IAC).
4. Labyrinthine segment (Fallopian canal).
5. Geniculate ganglion.
6. Tympanic segment.
7. Stylomastoid segment.

4. Anatomy-
• Segment Location Length (mm)
1-Supranuclear Cerebral cortex
2-Brain stem Brain stem to IAC 24
3-Meatal IAM to Fundus 5-12
4-Labyrinthine Fundus of IAC to first genu 3-4
5-Tympanic Geniculate ganglion to pyramidal
eminence
8-11
6-Mastoid Pyramidal process to stylomastoid f 10-
14
7-Extra temporal Sf to pes anserinus 15-20
Distance between exit & entrance in IAC- 23-24 mm.

5. Facial Nuclei-
• Motor Nucleus- Lie in Reticular formation of
the brainstem, ventral to floor (tegmentum) of
the 4th ventricle.
• Non Motor Nuclei-
– Salivatory
– Solitary
– Spinal Trigeminal

6. Facial Nucleus-

7. 1-Central segment (Tegmentum Pontis)-
Facial colliculus

8. 2- Cisternal Segment-
Facial Nerve
AICA

9. Anatomy of Facial Nerve-

10. 3- Intra canalicular segment-
Facial nerve lies in Antero superior quadrant of the IAC.

11. Intra- canalicular segment-
1- Canalicular
segment
2- Geniculate
ganglion
3-Labrynthine
segment

12. Intra Temporal course-
4 segments-
1-Meatal
2- Labyrinthine
3-Tympanic/horizontal
4- Mastoid/vertical

13. Intra-Temporal course-
•Facial exits IAC via
fallopian canal.
•Fallopian Canal is
narrowest place
through its entire
course.
•Fallopian canal is
culprit for facial nerve
compression in bell’s
Palsy.
Fallopian Canal

14. 1-Meatal Segment-5-12 mm
Above the facial canal is the ceiling of the IAM, below is the falciform crest(transverse
crest) and externally a vertical crest(Bills bar).

16. Labyrinthine Segment- 3-5 mm, 0.68 mm
• Lies in Middle cranial fossa
• meningeal cover
• Narrow constriction (0.68mm)
• - 132 deg bend
• Slight constriction from vertical crest ,
thick periosteum
• Only segment of the facial nerve that
lacks anastomosing arterial cascades
• embolic phenomena, low-flow states,
or vascular compression

17. Tympanic Segment-
• The tympanic segment course posteriorly below
the lateral SCC.

18. Geniculate ganglion and its relationship-
- formed by the
junction of the
nervus intermedius
and the facial nerve
into a common
trunk

19. Greater Superficial Petrosal nerve-
• The GSPN is branch of the facial nerve that innervates the lacrimal
gland.
• It contains preganglionic parasympathetic fibers.
• It exits the superior surface of the temporal bone via the facial
hiatus.
• It passes under the Meckel’s cave to the foramen lacerum, at which
it joins the deep petrosal nerve to form the vidian nerve.
• The vidian nerve passes through the vidian canal to the
pterygopalatine fossa.

20. Mastoid Segment-15-20 mm

21. Chorda Tympani-
Leaves the parent nerve 5mm proximal to stylomastoid

22. Extra-Temporal facial nerve- Branches-
• 1. Ansa of Haller (inconstant)
• 2. Posterior auricular branch
• 3. Stylohyoid branch
• 4. Posterior belly of digastric branch
• 5. Pes anserinus

23. Extra-Temporal Facial nerve-
Runs anteriorly in the substance
of parotid gland, crosses the ECA
& divides at the posterior border
of ramus of mandible
into 2 primary branches:
1- Temporo- zygomatic
2- Cervico-facial

24. Landmarks for Extra Temporal facial nerve

25. Summary of Facial nerve and its supply-

26. Supra nuclear control-
Facial n & n of intermedius lie above & slightly ant to CN VIII

28. Facial Nerve- Sensory Roots-

29. Special Sensory Afferent- Taste
Origin : Unipolar
neurons in geniculate
Ganglia
•Central : Nucleus of
Tractus Solitarius
•Peripheral : Chorda
tympani nv
& lingual nv to
ant 2/3rd
tongue

30. General Visceral Efferent-
Origin : Sup
salivatory nucleus
Para sympathetic
secretomotor
Fibres

31. General Visceral Efferent-
• Superior salivatory nucleas-GSPN-
Pterygopalatine Ganglia-Lacrimal & Palatine
Gland
• Inferior salivatory nucleas- LSPN- Otic Ganglia
– Parotid Gland
• Chorda Tympani – Submandibular &
Sublingual Gland

32. Anatomical Localization of Facial nerve-

33. Vascular Supply of facial nerve-
The cortical motor area :
Rolandic branch
Pons : anterior inferior
cerebellar artery (AICA)
-Superficial petrosal
artery
-Posterior auricular
artery

34. House- Brackmann Facial n recovery
grading-
• Grade 1 : Normal
• Grade 2 : Mild dysfunction. Grossly there is a slight weakness
noticeable on close inspection, at rest, there is normal symmetry and
tone., Motion as observed in the forehead, is moderate to good. Eye
closure is complete with slight asymmetry of the mouth.
• Grade 3 : Moderate dysfunction. Grossly there is obvious but no
disfiguring difference between two sides and at rest there is normal
symmetry and tone. Motion as seen in the forehead is slight to
moderate, there is weakness of the angle of the mouth on maximal
effort and eye closure is complete with effort.
• Grade 4 : Moderately severe dysfunction. Grossly, there is obvious
asymmetry or disfigurement or both. At rest, there may be normal
symmetry and tone. There is no motion in the forehead, the eye
closure is incomplete even with maximal effort and there is mouth
movement with asymmetry on maximal effort.

35. House- Brackmann Facial n recovery
grading-
• Grade 5 : Severe dysfunction. Grossly there is
only barely perceptible motion at rest.
Forehead motion is none and eye closure is
incomplete with maximal effort and there is
very slight mouth movement.
• Grade 6 : Total paralysis, i.e. no movement.

36. Electro diagnostic test-
• Merits of Electro diagnostic Testing-
– Helps to detect subclinical evidence of early regeneration,
– Helps to differentiate birth trauma from embryogenic etiology
(Harris et al. 1983)
– Helps in determining the completeness of neural blockade by
testing for subclinical voluntary potentials.
• Demerits of Electro diagnostic Testing-
– EMG is not of much use in evaluation of acute paralysis because
14–21 days are required for the development of fibrillation
potentials from the time of onset of the facial nerve injury; hence
EMG is use only after 14–21 days of nerve injury.
– Slight electro dental positioning may produce variations in
amplitude of response making accurate assessment impossible.
– Temperature affects all electro diagnostic studies.
– Suboptimal stimulation can mimic demyelinations.

37. Facial Nerve Testing-
• Topographic test-
1. Lacrimation test (Schirmer’s test)
2. Stapedial Reflex
3. Salivatory Flow test
4. Test for sensation of taste on 1/3 of the tongue
• Prognostic test-
1. Electromyography
2. Nerve Excitability Test
3. Nerve conduction time
4. Maximal stimulation time
5. Electroneuronography

38. Facial Nerve Testing-
• Intra-operative monitoring-
– Electrically Evoked Potential
– Mechanically Evoked Potential

39. Bell’s palsy
• named after the Scottish anatomist, Sir
Charles Bell,
• most common acute mono-neuropathy,
affecting a single nerve,
• Bell’s palsy is defined as acute unilateral facial
nerve paresis or paralysis with onset in less
than 72 hours and without an identifiable
cause.

40. Risk factors -:
• Pregnancy
• Severe preeclampsia
• Obesity
• Hypertension and chronic hypertension
• Diabetes
• Upper respiratory ailments

42. Symptoms
• pain in the ear and postauricular region;
• weakness of facial musculature,
• inability to chew food;
• poor/ineffectual eye closure;
• alteration of taste,
• numbness or tingling of the cheek/mouth;
• ocular pain and tearing;
• family history of Bell’s palsy.
• Bell’s palsy presents disproportionately among
pregnant women ,diabetes, influenza, or other upper
respiratory illness.

43. • a comprehensive physical examination may confirm a
suspected etiology or unidentified cause of the
paresis/paralysis.
• Careful inspection of : ear canal,
• tympanic membrane,
• parotid gland,
• skin of the head face and cheek is essential.
• vesicular rashes (indicative of zoster infection) must be
ruled out.
• The presence of ulcerative lesions on the skin suggestive of
skin cancer or masses of the cheek should be noted.
• characterization of the overall movement of the face,
• all cranial nerves should be assessed, paying specific
attention to the extent of facial weakness and whether all
nerve branches are involved.

45. Management of bell palsy

47. STATEMENT 1.
• PATIENT HISTORY AND PHYSICAL
EXAMINATION:
• Clinicians should assess the patient using
history and physical examination to exclude
identifiable causes of facial paresis or paralysis
in patients presenting with acute-onset
unilateral facial paresis or paralysis.

48. STATEMENT 2.
• LABORATORY TESTING:
• Clinicians should not obtain routine
laboratory testing in patients with new-onset
Bell’s palsy.

49. STATEMENT 3
• DIAGNOSTIC IMAGING:
• Clinicians should not routinely perform diagnostic
imaging for patients with new-onset Bell’s palsy.
• However any presentation of facial paresis/paralysis
inconsistent with Bell’s palsy should be further
evaluated by imaging.
• Features atypical of Bell’s palsy include:
• a second paralysis on the same side,
• paralysis of isolated branches of the facial nerve,
• paralysis associated with other cranial nerve
involvement,or
• no sign of recovery after 3 months.

50. • Magnetic resonance imaging of the entire
course of the facial nerve, with and without
contrast, is the imaging test of choice for
patients In above circumstances.
• Imaging should include both the internal
auditory canal (IAC) and face, to image the
whole course of the facial nerve.
• If an MRI is contraindicated, a contrast-
enhanced CT can be used.

51. STATEMENT 4
• ORAL STEROIDS:
• Clinicians should prescribe oral steroids within
72 hours of symptom onset for Bell’s palsy
patients 16 years and older.

52. • Inflammation and edema causing compression
of the
• facial nerve as it travels through the fallopian
(facial) canal is the leading posited mechanism
of Bell’s palsy. Potent anti-inflammatory
agents, such as oral corticosteroids, target the
inflammatory process, presumably decreasing
nerve edema and thereby facilitating the
return of facial nerve function.

53. • 10-day course of oral steroids with at least 5
days at a high dose
• Either prednisolone 50 mg for 10 days or
• Prednisone 60 mg for 5 days with a 5-day
taper initiated within 72 hours of symptom
onset

54. • side effects of oral corticosteroid use include
• gastrointestinal disturbances, reactivation of
peptic ulcer disease,
• loss of control of glucose levels,
• Elevated blood pressure,
• peripheral edema,
• mood swings or episodes of acute psychosis.
• rarely, avascular necrosis of the femoral head has
been reported.

55. Use of Steroids in Children with Bell’s
Palsy
• oral steroids may be considered in pediatric
patients with a large role for caregiver
involvement in the decision-making process.

56. STATEMENT 5A.
• ANTIVIRAL MONOTHERAPY:
Clinicians should not prescribe oral antiviral
therapy alone for patients with new-onset
Bell’s palsy.

57. STATEMENT 5B.
• COMBINATION ANTIVIRAL THERAPY:
• Clinicians may offer oral antiviral therapy in
addition to oral steroids within 72 hours of
symptom onset for patients with Bell’s palsy.

58. • antiviral therapy in addition to steroid therapy
has not been proven to be of benefit in the
treatment of Bell’s palsy in large, high-quality
clinical trials.
• although a small benefit cannot be completely
excluded.
• Due to the potential of a small benefit in facial
nerve functional recovery and the relatively low
risk of antiviral therapy, patients may be offered
combination therapy if treated within 72 hours of
onset of Bell’s palsy.

59. STATEMENT 6
• EYE CARE:
• Clinicians should implement eye protection for
Bell’s palsy patients with impaired eye closure.

60. • Bell’s palsy is a condition that predisposes the eye to
injury,
• due to incomplete closure of the eyelid
(lagophthalmos) from upper eyelid retraction or lower
lid ectropion,
• failure of the lacrimal pump mechanism,
• decreased blink and tear production, and
• loss of the corneal ‘‘squeegee effect’’ on the side
affected by facial palsy.
• Incomplete closure of the eyelid may lead to
deposition of foreign particles in the eye, corneal
abrasions, exposure keratitis and/or corneal
ulcerations.
• Clinicians should be aware of symptoms such as
burning, itching, eye irritation, changes in vision, and
pain.

61. • Use of sunglasses
• Frequent administration of lubricating ophthalmic
drops during the day
• Ophthalmic ointments At night
• Use of a moisture chamber using a polyethylene cover
• Eye patching or taping
• Combination of the above treatments
• Use of botulinum toxin injections,
• temporary or permanent tarsorrhaphy
• surgery to weight the upper eyelid

62. STATEMENT 7A.
• ELECTRODIAGNOSTIC TESTING WITH
INCOMPLETE PARALYSIS:
• Clinicians should not perform
electrodiagnostic testing in Bell’s palsy
patients with incomplete facial paralysis.

63. • Bell’s palsy, the chances of complete recovery
are very high.
• with rates ranging from approximately 70%
with no treatment to 94% with steroids
• The cost, inconvenience, and discomfort of
invasive EMG testing are outweighed by the
likelihood of full recovery in most patients

64. STATEMENT 7B
• ELECTRODIAGNOSTIC TESTING WITH
COMPLETE PARALYSIS:
• Clinicians may offer electrodiagnostic testing
to Bell’s palsy patients with complete facial
paralysis.
• Patients with complete facial paralysis need to
have electrodiagnostic testing (ENoG and
EMG) performed after day 7 but before 14
days after onset of paralysis.

65. • With complete paralysis, electrophysiologic testing
results become stable, and therefore informative,
approximately 7 days following symptom onset
• Electroneuronography: Surface electrodes are placed
over selected facial muscles and the main trunk of the
facial nerve is stimulated electrically.The amplitude of
the maximal response (mV) is recorded and compared
with the unaffected side.
• Electromyography: Needle electrodes are inserted into
the facial muscles and depolarizations are recorded at
rest and following voluntary attempts to contract the
facial muscles.

66. ENoG
• If the response amplitude on the damaged side
exceeds 10% of the amplitude on the
contralateral(intact) side, most patients recover
normal or nearnormal facial movement.
• If the amplitude is less than 10% of the normal
side, higher percentage of patients do not
achieve normal or near-normal
• EMG testing may offer additional information in
patients with complete paralysis and ENoG
showing less than 10% function on the affected
side

67. • can help to define a small subset of patients
with poorer prognosis who may be counseled
appropriately regarding potential
reconstructive options or who, at the
discretion of the clinician, may consider
surgical decompression of the facial nerve

68. STATEMENT 8.
• SURGICAL DECOMPRESSION:
• No recommendation can be made regarding
surgical decompression for Bell’s palsy
patients.

69. • Patients with complete paralysis, greater than
90% reduction in amplitude on ENoG testing,
and absent volitional nerve activity on EMG
are less likely to recover spontaneously or
with medical treatment alone.

70. • Bell’s palsy, the site of constriction is thought
to be at the most narrow portion of the facial
nerve canal- the labyrinthine segment starting
at the meatal foramen.
• The meatal foramen is at the lateral internal
auditory canal where the labyrinthine
segment of the facial nerve exits the IAC .

71. • conductive or sensorineural hearing loss;
• injury to the facial nerve;
• risk of cerebrospinal fluid leak;
• infection;
• risks of temporal lobe retraction such as
temporary or permanent
• aphasia, seizures, and stroke;
• nonspecific risks with general anesthesia

72. • transmastoid decompression of the facial
nerve alone is not appropriate,
• yet there are limited data supporting surgical
decompression of the meatal segment of the
facial nerve in patients with complete
paralysis, with electrodiagnostic testing
demonstrating severe denervation within 2
weeks of onset of paralysis.

73. STATEMENT 9.
• ACUPUNCTURE:
• No recommendation

74. STATEMENT 10.
• PHYSICAL THERAPY:
• No recommendation can be made regarding
the effect of physical therapy in Bell’s palsy
patients.

75. STATEMENT 11.
• PATIENT FOLLOW-UP:
• Clinicians should reassess or refer to a facial
nerve specialist those patients with
(1) new or worsening neurologic findings at any
point,
(2) ocular symptoms developing at any point,
(3) incomplete facial recovery 3 months after
initial symptom onset.