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Otology & Neurotology > Facial Nerve > Flashcards

Facial Nerve Flashcards

1
Q

√Describe the embryology of the facial nerve

A

3rd week: Facial nerve develops from neural crest cells (acousticofacial primordium) of the 2nd branchial arch
- Innervates structures derived from Reichert’s cartilage

  • 5th week: Distal facial primordium forms 2 branches: chorda tympani and the main facial nerve
  • 6th week: first and second genus develop
  • 7th week: nervus intermedius develops, extratemporal FN branches innervate muscles of facial expression.
  • 8th week: temporal segment pathway well developed
  • 16th week: FN becomes encased in bone (not always as some fallopian canals can be incompletely ossified)
  • 2nd year of life: mastoid develops causing the vertical segment to elongate
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2
Q

√What are the 6 segments of the facial nerve?

A

“I Must Learn To Make (Facial) Expressions”:

  1. Intracranial
  2. Meatal
  3. Labyrinthine
  4. Tympanic
  5. Mastoid
  6. Extratemporal
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3
Q

√What is the blood supply to the facial nerve?

A
  1. Labyrinthine artery (Anterior inferior cerebellar artery origin) - IAC portion
  2. Superficial petrosal artery (middle meningeal origin) - Perigeniculate region
  3. Stylomastoid artery (posterior auricular origin) - mastoid and tympanic regions

*Rich anastomoses between superficial petrosal and stylomastoid; poor in labyrinthine segments

Vancouver 267

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4
Q

√What are the functions of the facial nerve?

A

A. Afferent Functions
1. Somatosensory: EAC, auricle
2. Special Sensory: Taste to the anterior 2/3 of the tongue (glossopharyngeal nerve CNIX provides taste to posterior third)

B. Efferent Functions
1. Motor:
- Muscles of Facial Expression (Innervated by terminal branches; Orbicularis oculi, oris, posterior auricular, occipitalis)
- Posterior belly of the digastric
- Stapedius
- Stylohyoid muscle

  1. Parasympathetic:
    - Salivation to the Submandibular, Sublingual, and Minor Salivary glands (glossopharyngeal to Parotid)
    - Lacrimation
    - Parasympathetic innervation to the nasal mucosa

Kevan Facial nerve lecture

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5
Q

√Describe the nuclei of the facial nerve

A

Nuclei of the Facial Nerve
1. Afferent Functions
- Somatosensory: Spinal Trigeminal Nucleus
- Special Sensory: Nucleus Tractus Solitarius, aka Solitary Nucleus

  1. Efferent Functions
    - Motor Function: Facial Motor Nucleus
    - Parasympathetic: Superior Salivatory Nucleus (Inferior Salivatory nucleus goes to Parotid)

Kevan FN lecture

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6
Q

√Draw the pathway of the facial nerve

A

See Kevan lecture facial nerve

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7
Q

√What are the approximate lengths of the facial nerve segments?

A

Approximate Lengths of the Segments of the Facial Nerve
“I Must Learn To Make (Facial) Expressions”

  • I: Intracranial (23-24) = ~20mm
  • M: Meatal (8-10) = ~10mm
  • L: Labyrinthine (3-5) = ~5mm
  • T: Tympanic (8-10) = ~10mm
  • M: Mastoid (10-14) = ~15mm
  • E: Extracranial (15-20mm to pes) ~20mm

Start with 20, divide by 2 until 5, then keep adding 5 back to 20

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8
Q

√Where is the narrowest portion of the facial nerve? What is the diameter?

A

Fundus of IAC = 0.68mm (labyrinthine segment)

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9
Q

√Answer the following questions:
1. Facial nerve exits the brainstem where?
2. Facial nerve exits the skull base through what?
3. Facial nerve exits the temporal bone where?

A
  1. Facial nerve exits the brainstem at the: CPA (Cerebellopontine Angle), Pontomedullary Junction
  2. Facial nerve exits the skull base through the: Internal Auditory Meatus (ie. internal auditory canal, IAC)
  3. Facial nerve exits the Temporal Bone at the: Stylomastoid Foramen
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10
Q

√Regarding the intracranial segment of the facial nerve, discuss:
1. Discuss the components of this segment
2. Where does it start and where does it end?
2. What is the length?

A

START: Brainstem
END: Porous acousticus
LENGTH: ~20mm (23-24mm)

  • Exists the brainstem with CNVIII at the cerebellopontine angle (at the pontomedullary junction)
  • Exists the brainstem in 2 different bundles:
    1. Nervus Intermedius (Nerve of Wrisberg): contains non-motor fibers
    2. Facial nerve proper: contains motor fibers
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11
Q

√Regarding the meatal segment of the facial nerve, discuss:
1. Discuss the components of this segment
2. Where does it start and where does it end?
2. What is the length?

A

START: Porous acousticus
END: Fundus (end of IAC)
Length: ~10mm (8-10mm)

  • This section of the facial nerve travels through the internal auditory meatus (aka internal auditory canal)
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12
Q

√Describe the orientation of nerves that travels through the internal auditory meatus.

A
  1. Anterosuperior: Facial nerve + nervus intermedius
  2. Anteroposterior: Cochlear nerve
  3. Posterosuperior: Superior vestibular nerve
  4. Posteroinferior: Inferior vestibular nerve

“7 up, coke down”

  • Bill’s Bar: Vertical bony crest that divides the facial nerve and superior vestibular nerve (divides anterior and posterior superior)
  • Falciform crest: Horizontal crest that divides superior and inferior IAC

Kevan’s FN lecture

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13
Q

√Regarding the labyrinthine segment of the facial nerve, discuss:
1. Discuss the components of this segment
2. Where does it start and where does it end?
2. What is the length?

A

START: Fundus (exit of IAC)
END: Geniculate Ganglion
Length: ~5mm (3-5mm)

Clinical Significance:
- Narrowest section of the facial nerve (< 0.76mm)
- Most common area with facial nerve compression (decompressing the facial nerve is generally this segment via a Middle Cranial Fossa (MCF) approach)

Geniculate Ganglion:
- Ganglion is at the point where the facial nerve has its first bend (“first genu”)
- Greater Superficial Petrosal Nerve (GSPN) exists the geniculate ganglion and enters the middle cranial fossa (carries parasympathetic fibers to the lacrimal gland and nasal mucosa)
- GSPN + Deep Petrosal Nerve = Vidian nerve
- Remainder of the facial nerve continues to the tympanic segment through the fallopian canal

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14
Q

√Regarding the tympanic segment of the facial nerve, discuss:
1. Discuss the components of this segment
2. Where does it start and where does it end?
2. What is the length?

A

START: Geniculate Ganglion
END: Second Genu (close to the horizontal/lateral SCC - landmark for FN depth; or posterior to the cochleariform process)
Length: ~10mm (8-11mm)

Details:
- Section of FN that travels across the middle ear within the fallopian canal

Clinical Significance:
- Segment of the facial nerve that is most commonly dehiscent (ie. no overlying bone)
- Dehiscent facial nerve may flop over the stapedius and prevent you from doing a stapedotomy

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15
Q

√What are 7 different anomalies that can occur to the tympanic segment during embryology?

A

Normal = Tympanic segment courses superior to the stapes

Abnormal:
1. FN inferior to stapes (if displaced anteriorly prior to stapes development)
2. FN courses through stapes (if FN courses through stapes, may form a mall during ossicular chain formation, and higher likelihood of malformed stapes)
3. Bifurcation anterior to the oval window
4. FN Overlying oval window
5. Through the stapedial arch
6. Inferior to the oval window
7. 2nd genu over the superior aspect of the horizontal SCC

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16
Q

√Regarding the mastoid (vertical) segment of the facial nerve, discuss:
1. Discuss the components of this segment
2. Where does it start and where does it end?
2. What is the length?

A

START: Second Genu (located near the horizontal SCC near the incus buttress)
END: Stylomastoid foramen
Length: ~15mm (10-14mm)

Components:
- Gives off nerve to stapedius (part of the stapedial reflex pathway)
- Gives off chorda tympani (taste to anterior 2/3 of the tongue)

Landmarks for the mastoid segment of the facial nerve:
1. Lateral SCC
2. Incus buttress
3. Digastric ridge

Kevan FN lecture

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17
Q

√What are 5 different anomalies that can occur to the mastoid segment during embryology?

A
  1. Bifurcation or trifurcation
  2. Hypoplastic facial nerve
  3. Posterior/anteriorly/laterally displaced
  4. Thickened chorda tympani (carrying motor fibers)
  5. With congenital aural atresia, mastoid segment can be absent or shortened, and exit near the TMJ
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18
Q

√Regarding the extracranial segment of the facial nerve, discuss:
1. Discuss the components of this segment
2. Where does it start and where does it end?
2. What is the length?

A

START: Stylomastoid foramen
END: Pes Anserinus

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19
Q

What are the extratemporal branches of the facial nerve? What other branches are given off the extracranial segment of the facial nerve?

A
  1. Temporal
  2. Zygomatic
  3. Buccal
  4. Marginal Mandibular
  5. Cervical

Other branches off the extracranial segment of the facial nerve:
- Nerve to the posterior belly of digastric
- Nerve to stylohyoid
- Posterior auricular nerve

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20
Q

√What are 4 intratemporal and 7 extratemporal landmarks for the facial nerve?

A

INTRATEMPORAL:
1. Lateral SCC
2. Incus buttress
3. Cochleariform process
4. Digastric ridge

EXTRATEMPORAL:
1. Tragal pointer (1cm inferior and deep)
2. Tympanomastoid suture (A few mm deep and inferior)
3. Posterior belly of digastric (same plane, superiorly)
4. Retrograde Dissection (of distal nerve branches)
5. Stylomastoid foramen (follow anterior)
6. Retromandibular vein (deep)
7. Mastoidectomy

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21
Q

√List all the facial muscles that are supplied. bythe facial nerve (and which branches they are)

A

TEMPORAL BRANCH (4):
1. Occipitofrontalis
2. Orbicularis oculi
3. Corrugator Supercilli
4. Anterior and superior Auriculares

ZYGOMATIC BRANCH: (6)
1. Zygomaticus Major and Minor
2. Procerus
3. Levator labii superioris and alaeque nasi
4. Nasalis
5. Depressor septi nasi
6. Orbicularis oculi

BUCCAL BRANCH (3):
1. Buccinator
2. Orbicularis oris
3. Risorius

MARGINAL MANDIBULAR BRANCH (4):
1. Depressor anguli oris
2. Inferior Orbicularis oris
3. Depressor Labii inferioris
4. Mentalis

CERVICAL BRANCH (1):
1. Platysma

Vancouver Pg 267

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22
Q

√Define the Iter Chordae Posterior and Iter Chordae Anterior

A
  1. Iter Chordae Posterior = Posterior canal that the chorda tympani enters the mesotympanum through
  2. Iter Chordae Anterior = Anterior canal that the Chorda Tympani enters the petrotympanic fissure through (Canal of Huguier) to the infratemporal fossa
23
Q

√What are the most common areas of facial nerve dehiscence?

A
  1. Tympanic segment over oval win dow
  2. Geniculate Ganglion
  3. Adjacent to retrofacial air cells in mastoid region
24
Q

√What area of the facial nerve is most commonly injured in temporal bone injuries and why?

A

Labyrinthine segment
- Fallopian canal is the narrowest segment
- GSPN tethers the nerve
- “Watershed area” (area of vulnerability to ischemia because its located at the distal end of the blood supply, like a watershed that drains rain down) - Labyrinthine artery is the only blood supply

25
Q

√Describe the Sunderland-Seddon Classification of nerve injuries

A

Seddon (Neuropraxia, Axonotmesis, Neurotmesis), Sunderland I-V

  1. Class I: Neuropraxia
    - Causes: Local ischemia, traction, mild crush, compression
    - Recovery: Complete - hours up to a few weeks
    - Pathophysiology: No disruption of axon continuity, typically nerve conduction block
    - Tests: Abnormal EMG, all other tests normal
    - Surgical intervention: Typically not
  2. Class II: Axonotmesis
    - Causes: Nerve crush injury
    - Recovery: Complete - Weeks to months
    - Pahophysiology: Division of axons but all layers of the connective tissues remain in tact, wallerian degeneration back to a node of ranvier (These are the gaps formed between the myelin sheath where the axons are left uncovered. These ‘exposed’ areas without myelin sheath allow the generation of fast electrical impulse along the axon)
    - Surgical intervention: Typically not
  3. Class III: Axonotmesis
    - Causes: Nerve crush injury
    - Recovery: Incomplete and variable -months
    - Pathophysiology: Wallerian degeneration with disruption of myelin sheath and endoneurial layer. Synkinesis may occur
    - Surgical intervention: Typically not
  4. Class IV: Axonotmesis
    - Causes: Nerve crush injury
    - Recovery: Incomplete and variable - depending on injury and treatment can be months. toyears
    - Pathophysiology: Axon with myelin sheath, endoneurium, and perineurium disconnected
    - Surgical Intervention: Typically required; procedure depends upon findings
  5. Class V: Neurotmesis
    - Causes: Nerve laceration or transection
    - Recovery: Incomplete - months to years
    - Pathophysiology: Axon injury with myelin sheath, endoneurium, and epineurium disconnected
    - Surgical intervention: Required; early nerve healing or reconstruction

Layers of a nerve: https://images.squarespace-cdn.com/content/v1/5b427294372b967549fa8396/1533699102325-Z1B103JIWQUD2WY9PNR1/Unknown-1.jpeg

26
Q

√Describe the House-Brackman Grading scale of Facial Paralysis

A

GRADE 1: Normal
- Normal in all areas

GRADE 2: Mild dysfunction
- Slight weakness (± synkinesis) on close inspection
- Forehead: Slight weakness on close inspection, still good function
- Mouth: Slight asymmetry or weakness of mouth movement on close inspection
- Eye: Complete closure with minimum effort

GRADE 3: Moderate Dysfunction
- Normal at rest, obvious but not disfiguring with movement, synkinesis, contracture, or hemifacial spasm
- Forehead: Noticeable slight to moderate movement
- Mouth: Obvious but no disfiguring weakness/asymmetry
- Eye: Obvious weakness, eye closure with effort

GRADE 4: Moderately Severe Dysfunction
- Forehead: Obvious weakness or disfiguring asymmetry
- Mouth: Asymmetry at rest
- Eye: Incomplete eye closure

GRADE 5: Severe Dysfunction
- Forehead: Barely perceptible motion
- Mouth: Barely perceptible mouth movement
- Eye: Barely perceptible eyelid movement

GRADE 6: Total Paralysis
- Forehead: No movement
- Mouth: No movement
- Eye: No movement

27
Q

What are other facial paralysis grading scales?

A
  1. Sunnybrook
  2. Yanighara scale
  3. Facial paralysis recovery index
28
Q

√Describe the History that should be taken for patients with facial nerve paralysis

A
  1. Otovestibular symptoms: hearing loss, hyperacusis, vertigo, imbalance, otorrhea, otalgia
  2. Focal neurologic deficits: e.g., diplopia, facial anesthesia
  3. Constitutional symptoms: fever, chills, fatigue, malaise, sweats, weight loss
  4. Meningitic symptoms: headache, nuchal rigidity
  5. Lyme: specific symptoms: recent tick bite or exposure, erythema migrans rash, arthralgias, myalgias, low back pain
  6. Inflammatory symptoms: orofacial swelling or parotitis, uveitis, or history of other autoimmune conditions.
29
Q

What are red flag signs of facial nerve paralysis on history of physical exam?

A
  1. Bilateral paralysis
  2. Slow onset of facial weakness (weakness in Bell palsy fully evolves over (24-72 hours)
  3. Asymmetric weakness across facial zones at onset
  4. Constitutional symptoms (fever, lethargy, malaise, myalgias)
  5. Headache (other than postauricular pain and otalgia, occurs frequently in Bell’s palsy)
  6. Other focal neurologic deficits (diplopia, hearing loss, vertigo)
  7. Absence of recovery of facial tone within 4 months of palsy onset
30
Q

√What are the components of the physical examination that should be done for patients with facial nerve palsy?

A

Oto/Neurotologic examination:
- Look for vesicles
- EAC evaluation
- Middle ear pathology: cholesteatoma, AOM, glomus tumour

Face:
- Characterize the deficit (House-Brackmann)
- Complete vs. incomplete paralysis
- Forehead involvement (LMN pattern) vs. forehead sparing (UMN pattern)
- Synkinesis and muscle bulk

Head & neck:
- Lymphadenopathy, parotid pathology
- Rule out malignant lesions

Neuro:
- CN examination, general neuro screen

31
Q

√List four types of electrophysiologic tests of facial nerve function

A
  1. Nerve Excitability Test (NET)
  2. Maximal stimulation test (MST)
  3. Electroneurography (ENoG)
  4. Electromyography (EMG)
32
Q

√How does the Nerve Excitability Test work for facial nerve testing? What is abnormal?

Criteria to consider facial nerve decompression?
What is the % to complete spotaneous recovery?

A
  • Definition: Minimum amount of stimulation necessary to elicit facial nerve activity (start with low amps and turn it up)
  • Stimulate at the stylomastoid foramen with a Hilger monitor

Results: Compare both sides, if >3.5mA difference = reilable sign of progressive degeneration, indication for decompression

Decompression indication:
1. 3.5mA threshold difference between control and affected

Percent chance to complete spontaneous recovery
1. > 3.5mA difference, 38% had complete spontaneous recovery

33
Q

√How does the Maximal stimulation test (MST) work for facial nerve testing?

Criteria to consider facial nerve decompression?
What is the % to complete spotaneous recovery?

A
  • Definition: Threshold/Degree of stimulation at which you get the Maximum degree of facial nerve activity (further stimulation above that maximum will not achieve greater facial nerve activity)
  • Stimulate at the stylomastoid foramen

How it works:
- Test to the maximum threshold on the normal side that you can get without pain, and compare it to the paretic side (this is a subjective test)
- Rank the difference as minimal, moderate, severe, or no response
- If no response on one side on MST –> indication for depression
- If MST remains normal for 10 days, 88% of patients have complete return of function

Criteria to consider facial nerve decompression:
1. No response to injured side at maximal stimulation

Percent chance to complete spontaneous recovery:
1. Equal responses bilateral = 92%
2. Markedly reduced/absent = 14%

34
Q

√How does Electroneurography work for facial nerve testing?

Criteria to consider facial nerve decompression?
What is the % to complete spontaneous recovery?

A
  • Definition: Objective measure of nerve function compared to the contralateral side (assuming normal function
  • Evoked EMG
  • Most commonly test used in real life

How it works:
- Stimulate at the stylomastoid foramen, and measure the distal response with EMG
- Records facial muscle componds amps at nasolabial fold with supramax stimulation
- Response is compared to the contralateral side (NEED to have a normal contralateral side)

Results:
- % Degeneration: Amount of decrease compared to normal side (ie. 10% activity compared to the contralateral side is a 90% degeneration)
- Generally used in sudden/complete facial nerve paralysis (HB 5/6) - cannot use well in mild FN paralysis

Interpretation:
- > 90% degeneration as compared to normal side within 14 days = poor prognosis
- Useful in following progression in acute period q1-2 days
- NOT useful BEFORE 3 days (Wallerian degeneration occurs) or AFTER 14 days

Indication for facial nerve decompression:
1. Percent degeneration = (CMAP (compound muscle action potential) of injured / CMAP normal); if result is >90% degeneration within 14 days of injury then decompress

Percent chance to complete spontaneous recovery:
1. ENoG < 90% indicates 83-94% chance for spontaneous recovery
2. ENoG > 90% indicates ~30% chance for spontaneous recovery

Vancouver 269; Chapter 171 Cummings

35
Q

√How does Electromyography (EMG) work for facial nerve testing? What are the types of potentials that can be seen, and what do they mean?

A
  • Definition: Similar to ENoG, however instead of Evoked EMG (put a stimulation and measure a response), measures activity from spontaneous/voluntary action
  • aka. Spontaneous or voluntary EMG

Measure of regeneration:
- Early testing (< 3 days) if motor potential present in 4 or 5 muscle units = 90% chance of recovery, but can be misleading
- Polyphasic potentials (spontaneous or voluntary) suggests return of function (re-innervation) and precedes recovery 6-12 weeks (cannot tell if synkinesis or not); usually starts 4-6 weeks post-injury
- Fibrillation potential indicates denervation and does not occur until 10-14 days post-injury is when it starts
- Electrical silence: denervation with significant muscle fibrosis/atrophy (occurs after 1-2 years); can also mean congenital absence of muscle
- Normal voluntary action potentials: Functioning axons are connected and stimulating motor units

Indications:
- Only if complete paralysis, not paresis (because integrity not in doubt)
- MST, NET, ENoG not useful for prognosis until Wallerian degeneration has occurred (3 days)

36
Q

√Why can’t EMG be used at the outset of facial nerve injury, and what is the lag between EMG recovery and clinical return?

A
  • For the first 10-14 days, do not see muscular fibrillation potentials that indicate muscular degeneration (therefore not very useful to test at the onset of injury with EMG)
  • Polyphasic potentials (good prognosis, indicates regeneration) are seen 6-12 weeks prior to clinical recovery
37
Q

√Discuss the management of facial nerve testing in acute onset facial nerve paralysis

A

ENoG timing = > 3 days, < 14 days (to allow for Wallerian degeneration to occur if it’s going to occur - e.g. if you only test after 1 day it hasn’t had time to potentially START degenerating yet so you are getting inaccurate premature results cuz it hasn’t degenerated; don’t want to wait until after 21 days because after that nerve excitability is definitively lost, and nerve degeneration is complete (so not useful))

Threshold hold to consider decompression = 90% degeneration (some say 95%)

Other adjunctive testing:
- Consider facial nerve EMG (for < 90%)
- Reassuring = polyphasic action potentials
- Non-reassuring = fibrillations

See the flow diagram, but essentially 3 parts. In acute FN onset of paralysis:

  1. PARTIAL
    - Progressive?
    - If yes, do a CT/GdMRI
    - If no, start observation ± steroids ± acyclovir; if not resolved then do a CT/GdMRI
  2. COMPLETE
    A. First, depends if there are vesicles or no vesicles.
    - If vesicles, start Steroids, Acyclovir, then do an ENoG 3-14d
    - If no vesicles, start Steroids, ± Acyclovir, then do an ENoG 3-14d
    B. ENoG results depends on ≥ 90% degeneration, < 90%
    - ≥ 90%: Consider decompression
    - < 90%: Taper steroids; if not resolved then image with CT/GdMRI
  3. POST-TRAUMATIC
    - Depends on timing of injury; if < 21 days then do ENoG and proceed as #2 above
    - If ≥ 21 days, then do CT; if there is CT evidence of severe disruption of the fallopian canal, then consider surgical exploration/decompression (but if no, then observe)

Kevan FN lecture diagram

38
Q

√What are some localization/topognostic studies that can be used for facial nerve paralysis?

A
  1. Schirmer Test (test of lacrimation; used for Sjogren’s disease; strip of iodine inside the lower eyelid of each eye)
    - Injury past the geniculate ganglion on the lacrimal pathway / GSPN
    - Unilateral difference of >50% or a bialteral total of < 5mm after 5 minutes is significant
  2. Stapedial Reflex Testing
    - Injury proximal to the mastoid segment of the FN (where the stapedial muscle is and where the nerve is given off)
  3. Electrogustometry: Electrical way to assess taste (very uncomfortable)
    - Injury along the course of the chorda tympani (parasympathetic) - mastoid segment at least
  4. Salivary Flow Testing
    - Injury along the course of the chorda tympani/mastoid segment (parasympathetic branches are divided off there)
    - Unilateral reduction > 25% is abnormal;
  5. Salivary pH Testing
    - Injury along the course of the chorda tympani (parasympathetic)
    - pH > 6.4 generally normal
  6. Trigeminal (Corneal) Reflex:
    - Abnormal if lesion is proximal to orbicularis oculi muscle
  7. High Resolution CT and MRI have largely replaced these tests for localization
39
Q

√List a complete differential diagnosis of unilateral facial nerve paralysis. What is the most common?

A

A. CONGENITAL
1. Congenital Unilateral Lower Lip Palsy (CULLP)
2. Moebius syndrome (congenital condition that causes underdevelopment of the facial nerves)
3. Myotonic dystrophy

B. INFECTIOUS & IDIOPATHIC
1. Bell’s palsy (idiopathic; most common 48%)
2. Meningitis
3. Herpes Zoster Oticus/Ramsay Hunt Syndrome (5-9%)
4. Lyme disease
5. EBV
6. HIV
7. TB
8. Syphillis
9. Acute bacterial otitis media (most common in pediatrics - suggest dehiscent facial nerve)
10. Chronic bacterial otitis media

C. NEUROLOGIC:
1. Clostridial (tetanus, botulism) - Neurologic
2. Cerebrovascular disorder - central or peripheral
3. Guillain-Barre syndrome
4. Myasthenia gravis
5. Benign intracranial hypertension
6. Multiple sclerosis
7. ALS

C. TRAUMA (Second most common, 20%)
1. Temporal bone trauma
2. Birth trauma
3. Iatrogenic (e.g. surgical)
4. Barotrauma otitis
5. Necrotizing otitis external neoplastic

D. MALIGNANT NEOPLASM
1. Primary or metastatic parotid tumor

E. BENIGN NEOPLASM
1. CN VII Hemangioma (90% between IAC and 2nd genu, superior surface)
2. Schwannoma (~20%/segment between labyrinthine and mastoid)
3. Glomus tumor
4. Leukemia/lymphoma
5. Cholesteatoma

F. SYSTEMIC (“PHD MASK KCP”)
1. Pregnancy
2. Hyperthyroidism
3. Diabetes mellitus
4. Melkerson-Rosenthal syndrome
5. Autoimmune disease
6. Sarcoidosis (Heerfordt’s disease)
7. Kawasaki disease
8. Collagen Vascular diseases
9. Polyarteritis Nodosa

40
Q

List the differential diagnosis of bilateral facial nerve palsy

A

A. CONGENITAL
1. Moebius syndrome
2. Congenital syphillis

B. INFECTIOUS & IDIOPATHIC
1. Bacterial meningitis
2. Brainstem encephalitis
3. Lyme disease
4. Bell’s palsy - bilateral in 0.3% of cases

C. TRAUMA
1. Bilateral temporal bone trauma
2. Birth trauma
3. Iatrogenic

D. NEOPLASM:
1. Leukemia/lymphoma

E. NEUROLOGIC:
1. Guillaume-Barre syndrome
2. Myasthenia Gravis
3. Multiple idiopathic cranial neuropathies
4. Benign intracranial hypertension
5. Multiple sclerosis
6. ALS

F. SYSTEMIC
1. Sarcoidosis
2. Diabetes Mellitus
3. Hyperthyroidism
4. Melkersson-Rosenthal syndrome
5. Osteoporosis (Albers-Schoenberg) - hereditary, bony obliteration of foramina/compression of CNs; decompression rarely indicated
6. Collagen Vascular diseases
7. Polyarteritis Nodosa (PAN)

41
Q

√List the possible causes of congenital facial paralyss

A
  1. Mononeural agenesis
  2. Congenital unilateral lower lip palsy (caused by absence of activity of depressor labii inferioris muscle; caused by brainstem lesion)
  3. Mobius SYndrome (can be unilateral, usually also involves CNVI;; Can also be bilateral, may involve other cranial nerves)
  4. Hemifacial microsomia
  5. Oculoauriculovertebral dysplasia (Goldenhar) - occasionally interchangeable with hemifacial microsomia, but this specifically also has internal orgn and vertebrae disruption
  6. Poland syndrome (associated with agenesis of the pectoralis major muscle; in some cases also facial palsy - sometimes referred to as poland-mobius syndrome)
  7. Secondary to teratogens, thalidomide
  8. Congenital rubella
  9. Congenital syphillis
42
Q

√Describe the complete diagnostic workup for patients presenting with facial palsy

A

Investigations are guided by Clinical Judgment

A. Bloodwork
1. CBC with differential
2. Monospot/heterophile antibody (EBV, Leukemia)
3. ESR, Ca/ACE, ANA, RF (Sarcoid, collagen vascular dx, PAN)
4. Lyme serologies
5. Glucose tolerance test (DM)
6. FTA-ABS (Syphillis)

B. Radiographic
1. CT or MRI of brainstem/CPA/TB/SB ± Parotid
2. CXR (Sarcoidosis, lymphoma, carcinoma)

C. Special tests
1. LP/CSF (Meningitis, encephalitis, GBS, MS, Meningeal carcinomatosis)
2. Bone marrow (leukemia, lymphoma)

D. Urinary
1. Porphyrins and uPorphobilinogen (acute porphyria)
2. uCalcium (Sarcoidosis)
3. uGlucose (DM)
4. Fecal - C. Botulinum toxin (Botulism)

43
Q

√Regarding Bell’s Palsy, discuss:
1. Definition
2. Etiologies
3. Clinical Presentation
4. Risk Factors
5. Pathology
6. Diagnosis
7. Prognosis and Risk factors of Poor prognosis
8. Medial treatment options
9. Surgical treatment options

A

DEFINITION:
- Acute unilateral facial nerve paresis or paralysis with onset < 72 hours

ETIOLOGY: (theories)
1. Idiopathic disease
2. Attributed to viral (most likely)
3. Vasa vasorum failure
4. Neuropathy
5. Autoimmune

SYMPTOMS:
1. Pain in the ear and postauricular region
2. Weakness of facial musculature, including the inability to chew food without difficulty
3. Poor/ineffective eye closure
4. Alteration of taste
5. Occasionally accompanied by numbness or tingling of the cheek/mouth; ocular pain and tearing; or a family history of bell’s palsy

RISK FACTORS:
1. Pregnancy
2. Pre-eclampsia
3. DM
4. HTN
5. Obesity
6. URTI

PATHOLOGY:
- Diffuse demyelination throughout intratemporal course of facial nerve, worst at meatal and labyrinthine portions (esp labyrinthine as its the narrowest part)

DIAGNOSIS: Diagnosis of EXCLUSION - rule out any trauma, infection, or neoplasm
1. AAO recommends against ROUTINE lab testing or diagnostic imaging (strong rec against)
2. Electrodiagnostic tests (ENoG and EMG) - should NOT be performed in incomplete palsy (rec against), but may offer (option) in patient’s with complete palsy Day 7-14

PROGNOSIS:
1. Incomplete paralysis (30%) - approx 95% full recovery without intervention
2. Complete paralysis (70%) - approx 61% full recovery without intervention
3. 7% recurrent
4. ENoG prognosis scores
- If more than 90% degeneration by 14 days, 42% chance of recovery to HB I-II without surgical intervention, and 91% with surgical intervention
- 90-94% beneficial; 90-100% very highly beneficial

RISK FACTORS OF POOR PROGNOSIS
1. Complete paralysis (most important factor)
2. Hyperacusis (decreased stapedial reflex)
3. Decreased lacrimation
4. Age > 60
5. Diabetes
6. Hypertension
7. Severe aural, anterior facial, radicular pain

MEDICAL:
1. Steroids (Strong Rec AAO): 10 Days course of oral steroids with at least 5 days at a high dose, initiated within 72 hours of symptom onset. Benefit of treatment after 72 hours is less clear (either Pred 50mg x 10 days, or 60mg x 5 days with 5d taper)
2. Antivirals (Strong Rec AGAINST AAO): Should NOT prescribe oral antiviral therapy ALONE for patients with new-onset Bell’s palsy. MAY (option) offer antivirals in addition to PO steroids within 72 hours of symptom onset. note: Canadian guidelines weak recommendation for steroids + antivirals together only if severe to complete paralysis. – Valacyclovir 1000mg or Famvir 750mg TID x 7 days
3. Eye protection if incomplete eye closure (Strong Rec AAO)

SURGICAL (No AAO recs; Canadians rec against..)
1. Indications for decompression: Over 90% degeneration of motor fibers on ENoG, and no voluntary activity on EMG (performed between 7-14d)
- Best result if surgery within 14d symptom onset
- Maximal nerve injury occurs at meatal foramen/labyrinthine segment - best approached through middle fossa, unroofing labyrinthine segment ± incising perineurium
- Given the complexities of offering ENoG + EMG + surgery within 14 days and uncertain benefits, there is no recommendation (AAO)

  1. Physical therapy, acupunture - no recommendation AAO

FOLLOW UP:
1. If incomplete recovery after 3 months, consider alternative diagnosis: get imaging
- MRI enhancement not correlated with prognosis
- Refer to facial reanimation specialist
2. If new or worsening neurologic findings then FU
3. Ocular symptom devleopment then FU

TREATMENT BASED ON SYMPTOMS:
1. Incomplete eye closure: Artificial tears q1h PRN, lacrilube, tapine at night, ophthalmology referral
2. Mild to Moderate HB up to IV - oral corticosteroids and calcium
3. Severe to Complete IV-VI - oral corticosteroids, antivirals can be considered (weak recommendation) - valacyclovir
4. Incomplete recovery or progression - imaging to r/o neoplasm, electroneuronography
5. If > 90% on ENOG at 14 days, do Facial nerve EMG, if poor prognosis then surgical decompression can be offered (fib potentials and shart waves)

44
Q

√What are eight poor prognostic indicators in Bell’s palsy?

A
  1. Complete loss of function
  2. Hyperacusis
  3. Decreased lacrimation
  4. Hypertension
  5. Severe aural, facial, radicular pain
  6. Facial spasm
  7. Other cranial nerve palsy
  8. Age > 60 years old
  9. Recovery time > 3 months
  10. Diabetes mellitus
45
Q

√What are the effects that steroids have in facial palsy?

A
  1. Reduced edema
  2. Prevent wallerian degeneration
  3. Speed recovery
  4. Lessen synkinesis
46
Q

√What are the indications for imaging in facial paralysis?

A
  1. Segmental paralysis
  2. Presence of other neuro deficits
  3. Suspicious of malignancy/tumors
  4. Palpation of any masses in the parotid
  5. Bell’s palsy not improving after 3 months
  6. Recurrent paralysis
47
Q

√Regarding Herpes Zoster Oticus/Ramsay Hunt Syndrome, discuss:
1. Definitions
2. Etiology and Pathophysiology
3. Clinical Presentation/Symptoms
4. Diagnosis
5. Complications
6. Prognosis
7. Treatments

A

Definitions:
1. Ramsay Hunt = Facial palsy + vesicles
2. Herpes Zoster Oticus = Vesicles alone

Etiology/pathophysiology:
1. Varicella Zoster Virus (HHV3) [reactivation] of the geniculate ganglion
Second most common cause of facial paralysis (5-9%)

Clinical Presentation/Symptoms:
1. Present with painful vesicles on the pinna, retroauricular area, face, mouth, often precedes palsy
2. Acute facial palsy
3. 25% will have hyperacusis (stapedial tendon down), tinnitus, hearing loss, pain, vertigo (CNVIII involved)
4. CN that might also be involved are: IX, X, V, VI (innervates lateral rectus)
5. Dysgeusia (chorda tympani involvement)

Complications:
1. Postherpetic neuralgia

DIAGNOSIS:
1. Clinical diagnosis
2. Complement fixation and serum titers of ZVZ confirm diagnosis

PROGNOSIS: (Depends on sevierity) - worse than Bell’s
1. Complete loss = full recovery in 10% (vs. 61% in Bell’s)
2. Incomplete loss = full recovery in 66% (vs. > 95% in Bell’s)

TREATMENTS:
1. Corticosteroids (reduces acute pain, postherpetic neuralgia, and vertigo)
2. Valcyclovir 1g PO TID x 7 days (reduces pain, post-herpetic neuralgia & shortens time to resolution of vesicles, and increases rate of facial nerve recovery
3. EYE PROTECTION
4. No role for surgical decompression

48
Q

√Regarding Melkersson-Rosenthal syndrome, discuss:
1. Symptoms
2. Diagnosis
3. Associations

A

TRIAD OF SYMPTOMS:
1. Recurrent orofacial edema (defining feature)
2. Recurrent facial paralysis (50-90%, may be bilateral)
3. Fissured tongue (lingua plicata) - 50%

Assocations:
1. Sarcoidosis
2. IBD

DIAGNOSIS:
1. Lip biopsy = Non-caseating epithelioid cell granulomas surrounded by histiocytes, lymphocytes, and plasma cells
2. High serum ACE in some cases (angiotensin converting enzyme)

49
Q

√What is Heerfordt-Waldenstrom syndrome? What are the clinical features, labs, and associations?

A

“Uveoparotid fever”

Clinical features: PUFF:
1. Parotitis
2. Uveitis
3. Facial nerve paralysis
4. Fevers

Associated with sarcoidosis

Labs:
1. Elevated ACE
2. Calcium (non-caseating granulomas, secrete vitamin D)

50
Q

√Regarding Lyme disease, discuss:
1. Cause
2. Stages
3. Chance of facial palsy
4. Treatment

A

CAUSE:
1. Borrelia Burgdorferi, transmitted by Ixodes (deer) ticks

STAGES:
1. Stage I: Acute erythema migrans (target), influenzae-like prodrome, lymphadenopathy, malaise
2. Stage II: Weeks-months later, meningitis, cranial and peripheral neuropathies
3. Stage III: Months-years later, chronic arthritis, neurologic deficits, recurrent meningitis, mental disorders

Facial nerve palsy seen in 5% of patients, can be unilateral or bilateral, usually complete resolves

TREATMENT:
1. Ceftriaxone x 2 weeks for neurologic symptoms; otherwise
2. Doxycycline, Amoxicillin, or Cefuroxime x 2 weeks
3. Steroids for disseminated involvement/FN paralysis

51
Q

√What is the most common cause of bilateral facial nerve paralysis in adults and in children?

A

Adults = Guillain-Barre Syndrome
Children = Lyme disease

52
Q

√What are the indications for facial nerve monitoring intraoperatively?

A

STANDARD OF CARE:
1. Vestibular Schwannoma
2. Skull base surgery
3. EAC atresia repair
4. Revision mastoid surgery

RECOMMENDED:
1. Mastoidectomy
2. Exostosis Surgery
3. Cochlear implant
4. Parotid surgery

Not routinely used:
1. Stapedectomy
2. Tympanoplasty

53
Q

√Discuss the management of unexpected facial weakness post ear surgery

A
  1. If incomplete palsy: observe ± remove packing
  2. If complete palsy:
    - Observe, allowing local to wear off
    - If no recovery –> consult and re-explore with 2nd surgeon present

Preparation for OR: No paralysis by Anesthesia, prep donor nerve graft site (e.g. GAN), NIM monitor
- If bone spur: decompress
- If transected: epineurial repair (vancouver notes says ?no stitching, just lay beside each other?)

54
Q

Neoplasms of the Facial Nerve*

A

Otology & Neurotology (17 decks)

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