1. Jiranut Chaibhuddanugul,MD.
Facial Nerve Test
Jiranut Chaibhuddanugul,MD.

2. Facial Nerve Test Topognostic test Electrophysiologic testing
Unconventional test

3. HOUSE-BRACKMANN FACIAL NERVE GRADING SYSTEM

4. HOUSE-BRACKMANN FACIAL NERVE GRADING SYSTEM

5. HOUSE-BRACKMANN FACIAL NERVE GRADING SYSTEM
Common mistake !!!
Upper eye lid movement
Remember
: Levator palpebrae m is innervated by
oculomotor N. (CN III)
 remain intact despite
total facial N paralysis.
K.J. Lee essential otolaryngology

7. Topognostic test
Simple principle: lesions below the point at which a particular branch leaves the facial nerve trunk will spare the function subserved by that branch.
Complete focal lesion such trauma, topognostic tests are reliable but usually are unnecessary.

8. Topognostic test
Bell's palsy usually is a mixed and partial lesion with varying degrees of conduction block and degeneration changes within different fibers and fascicles of the nerve trunk.
Topognostic tests are not expected to provide precise information about the level of the lesion.
In recent years, otologists use these tests only rarely.

9. Lacrimal Function Schirmer's test
Places a folded strip of sterile filter paper into the conjunctival fornix of each eye and compares the rate of tear production of the two sides.
The length of the wetted portion of the strip after a fixed interval (usually 5 minutes) is measured.
Positive if the affected side shows less than one-half the amount of lacrimation seen on the healthy side.

10. Lacrimal Function
A total response (sum of the lengths of wetted filter paper for both eyes) of less than 25 mm is considered abnormal.
Decrease to 25% of normal in any of these was associated with a 90% chance of a poor recovery.
Advantages
Simplicity, speed, and economy.
Evaluation protective mechanism of eye.
Disadvantages
Accuracy 60%
Not useful as prognostic test
Reflex is consensual ; Decrease tearing ,Excessive tearing

11. Stapedius Reflex
In patients with hearing loss, acoustic reflex testing is used to assess the afferent (auditory) limb of the reflex, but in cases of facial paralysis, the same test is used to assess the efferent (facial motor) limb.
An absent reflex or a reflex that is less than one-half the amplitude of the contralateral side is considered abnormal.
It is absent in 69% of cases of Bell's palsy (in 84% when the paralysis is complete).
No prognostic value.

12. Taste
Chorda tympani - taste from the anterior two thirds of the tongue.
Filter paper disks impregnated with aqueous solutions of salt, sugar, citrate, or quinine.
Electrical stimulation (electrogustometry ; EGM) - threshold responses are denoted by the current level's imparting a subjective sensation of one of the four cardinal tastes or of buzzing or tingling.

13. Taste
In healthy persons, the two sides of the tongue have similar thresholds for electrical stimulation, rarely differing by greater than 25%.
Little usefulness of taste testing, because results were abnormal in almost all patients who were in the acute phase of Bell's palsy and could not identify patients with a poor prognosis.

14. Taste

15. Salivary Flow Test
Cannulation of the submandibular ducts and comparison of stimulated flow rates on the two sides.
Lesion at or proximal to the point at which the chorda tympani nerve leaves the main facial trunk ; variable and may be anywhere in the vertical (mastoid) portion of the nerve.
Reduced salivary flow (less than 45% of flow on the healthy side after stimulation with 6% citric acid) correlates well with worse outcome in Bell's palsy ; accuracy 85%.

16. Salivary pH
Submandibular salivary pH of 6.1 or less predicts incomplete recovery in cases of Bell's palsy.
Only the duct on the affected side needs to be cannulated.
Overall accuracy of prediction was 91%.
Reported experience with salivary pH is very limited; it is unknown whether this test gives an earlier prognosis than other tests.

17. Imaging
MRI with intravenous gadolinium contrast : study of choice when a facial nerve tumor is suspected in the cerebellopontine angle and temporal bone.
However, enhancement also occurs in most cases of Bell's palsy and herpes zoster oticus, usually in the perigeniculate portions of the nerve.
May persist for more than 1 year after clinical recovery and no apparent prognostic significance.

18. Imaging
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.
CT is valuable for surgical planning in cholesteatomas and temporal bone trauma.
Less useful than MRI in the investigation of atypical idiopathic paralysis.

19. Electrophysiologic testing

20. Sunderland classification
Neurapraxia
Axonotmesis
Neurotmesis

21. Sunderland Class I No physical disruption of axonal continuity occurs.
Supportive connective tissue elements remain intact.
Conduction block, no impulses can cross the area of the lesion, but electrical stimulation distal to the lesion still produces a propagated action potential and a visible muscle twitch at all times after injury.

22. Sunderland Class II
Axonal disruption without injury to supporting structures.
Wallerian degeneration occurs and propagates distally from the site of injury to the motor end plate and proximally to the first adjacent node of Ranvier.
Connective tissue elements remain viable, so regenerating axons may return precisely to their original destinations.

23. Sunderland Class III Disrupts the endoneurium.
Wallerian degeneration - regenerating axons are free to enter the wrong endoneurial tubes or may fail to enter an endoneurial tube at all.
Synkinesis.

24. Sunderland Class IV Perineurial disruption
Incomplete and aberrant regeneration is greater.
Intraneural scarring prevent most axons from reaching the muscle - greater synkinesis but incomplete motor function recovery.

25. Sunderland Class V Complete transection of a nerve.
Almost no hope for useful regeneration.

26. Sunderland Class VI MacKinnon and associates
Mixed injury involving both neurapraxia and a variable degree of neurodegeneration.
Compressive, inflammatory, or traumatic in origin, can be heterogeneous in nature, with differing degrees of injury from fascicle to fascicle.

27. Electrophysiologic testing
A patient with a conduction block (class I injury) cannot move the facial muscles voluntarily, but a facial twitch can be elicited by transcutaneous electrical stimulation of the nerve distal to the lesion.
In classes II to VI, delay wallerian degeneration results in continued electrical stimulability of the distal segment for up to 3 to 5 days after injury.
During these first days after an insult, electrodiagnostic testing of any form cannot distinguish between neurapraxic and neurodegenerative injuries.

28. Electrophysiologic testing
After wallerian degeneration : Class I / classes II – V.
Cannot distinguish among the different classes of neurodegenerative lesions II, III, IV, and V.
Most facial nerve lesions are not pure but probably mixed.
Variable threshold of electrical stimulability commensurate with the proportion of neural degeneration across the nerve trunk.

29. Electrophysiologic testing
Mark May, the facial nerve 2nd edition 2000

30. Electrophysiologic testing
Nerve excitability test (NST)
Maximal stimulation test (MST)
Electroneurography (ENoG)
Electromyography (EMG)

31. Electrophysiologic testing
Determining prognosis.
Sometimes in stratifying patients for nonsurgical versus surgical management.
Rarely useful in differential diagnosis.
Intraoperative monitoring of facial nerve function (usually with electromyography).

32. Nerve Excitability Test
Hilger stimulator, model N

33. Nerve Excitability Test
The stimulating electrode is placed on the skin over the stylomastoid foramen or over one of the peripheral branches of the nerve.
Beginning with the healthy side, electrical pulses steadily increasing current levels until a facial twitch is noted.
The lowest current eliciting a visible twitch is the threshold of excitation.
Next, the process is repeated on the paralyzed side.

34. Nerve Excitability Test
A difference of 3.5 milliamperes (mA) or more
reliable sign of severe degeneration.
an indicator for surgical decompression.
Complete versus incomplete recovery can be predicted with 80% accuracy.
In a simple conduction block - no difference exists between the two sides.
Positive in Sunderland class II – VI.
Daily examinations, severe degeneration can be detected as early as possible.

35. Nerve Excitability Test
The NET is useful only during the first 2 to 3 weeks of complete paralysis, before complete degeneration has occurred.
This test is unnecessary in cases of incomplete paralysis, in which the prognosis is always excellent.
If the paralysis becomes total, the test can determine whether a pure conduction block exists or whether degeneration is occurring.

36. Nerve Excitability Test
Once excitability is lost and this result is confirmed by repeat testing, further excitability tests are pointless, because clinically evident recovery always begins before any apparent electrical excitability returns (early deblocking).
Complete paralysis, if clinical recovery begins before degeneration is noted, continuing testing is unnecessary, because recovery will be rapid and complete.

37. Nerve Excitability Test
Because of relatively large intersubject variations in threshold compared with the small differences between the two sides of the face.
Mechelse and associates used as their criterion for decompression a 150% increase in threshold compared with the healthy side.

38. Maximum Stimulation Test
Nerve-stimulating equipment are the same as in the NET.
Maximal stimuli or supramaximal stimuli are used (Initial 5 mA  to level of patient’s tolerance).
On the unaffected side, the stimulus current intensity is increased until the maximum stimulation level.
Then used to stimulate the affected side, and the degree of facial contraction is subjectively assessed as either equal, mildly decreased, markedly decreased, or without response compared with that on the normal side.
(0%, 25%, 50%, 75%, 100%)

39. Maximum Stimulation Test
The theoretic basis of the MST is that by stimulating all intact axons.
Information should more reliably guide prognosis and treatment than that obtained with the NET.
Unfortunately, no good data comparing these, so this claim has not been proved.
Sx - no response on injured side at maximal stimulation.
May and coworkers, in Bell's palsy
MST normal - 88% of patients recovered completely.
Reduced movement - 27% chance of complete recovery.
Absence of electrically stimulated movement –incomplete recovery.

40. Electroneuronography (ENoG)
Facial nerve is stimulated transcutaneously, as in the NET, although a bipolar stimulating electrode is used.
Responses to maximal electrical stimulation of the two sides are compared, as in the MST, but they are recorded in a more objective fashion by measuring the evoked compound muscle action potential (CMAP) with a second bipolar electrode.
The average difference in amplitude between the two sides in healthy patients be only 3%.

41. Electroneuronography (ENoG)
Estimate the amout of severe nerve fiber degeneration.
Example, amplitude of the response on the paralyzed side is 10% of that on the normal side, an estimated 90% of fibers are degenerated.
May and colleagues ; severe ENoG amplitude reductions (<10% of the unaffected side) were highly correlated with incomplete recovery and indicated for Sx if degeneration within 14 days.

42. Electroneuronography (ENoG)

43. Electroneuronography (ENoG)
Most useful between 4 – 21 days after the onset of complete paralysis.
Not performed until 4th day , takes 3 days for wallerian degeneration to occur after severe injury.
Not useful after 3 weeks, false positive from deblocking.
Used in Bell’s palsy, trauma, otitis media.
Not useful in Ramsay Hunt syndrome due to multiple site of injury.
Glasscock –Shambaugh
Surgery of the Ear, 6th .

44. Electroneuronography (ENoG)
Tumor: Increase latency + decrease amplitude
Decrease amplitude = increasing tumor size
Bell’s palsy: decrease CMAP amplitude
Mark May, the facial nerve 2nd edition 2000

45. Electroneuronography (ENoG)
Patients reaching 95% degeneration within 2 weeks had a 50% chance of a poor recovery.
Gradual decrease in ENoG amplitude had a much better prognosis.
Cumming’s 5th .
If 90% degeneration dose not occur by 3 weeks after onset of Bell’s palsy  good prognosis.
Degeneration > 90% in 14 days of complete paralysis – poor recovery > 50% of patients.
Rate of degeneration is important – severe degeneration in 5th day have poorer prognosis than in several weeks.
Glasscock –Shambaugh ,6th .

46. Electromyography (EMG)
Recording of spontaneous and voluntary muscle potentials.
Role in the early phase of Bell's palsy is limited, because it does not quantitative estimate the percentage of degenerated fibers.
Uses to confirmed surgery when voluntarily active facial motor units (despite loss of excitability of the nerve trunk)

47. Electromyography (EMG)
EMG may give prognostically useful after muscle loss of excitability.
After 10 to 14 days, fibrillation potentials may be detected, confirming the presence of degenerating motor units ; 81% of patients - incomplete recovery.
Polyphasic reinnervation potentials, 4 to 6 weeks after the onset of paralysis, detectable recovery and predicts a fair to good recovery.

48. Electromyography (EMG)
Assessment of long-standing facial paralysis (> 3 weeks) to determine the possible success of anastomosis or cross-facial anastomosis for restoring facial motion.
In the setting of acute paralysis (< 3 weeks), the finding of active motor unit potential in the present of complete paralysis + > 90% degeneration in EnoG means deblocking is occur and prognosis is good.
EMG also can help assess whether a nerve repair is unsuccessful - no polyphasic reinnervation potentials at 15 months the anastomosis should be considered a failure.

49. Electromyography (EMG)
EMG-muscle at rest
A-needle insertion activity
(normal)
B-positive sharp waves
(~denervation)
C-fibrillations
(denervation- invisible contraction)
D-bizarre discharges
(~myopathies and neuropathies)
Mark May, the facial nerve 2nd edition 2000

50. Electromyography (EMG)
EMG-muscle contracting
A-Normal: mV
B-Partial interference pattern
Severe neuropathy
C-small but prolonged polyphasic motor
Early nerve regenertion
D- Short duration low-amplitude triphasic,polyphasic
Myopathiy
Mark May, the facial nerve 2nd edition 2000

51. Electromyography (EMG)
Degeneration : Defibrillation potential
Reinnervation
: Polyphasic potential

52. Facial Nerve Monitoring
Simple observation fails to detect many small muscular contractions and in any case demands constant vigilance.
Electrodes in or near the facial muscles record EMG potentials that can be amplified and made audible with a loudspeaker.
Active : electrical stimulation of the facial nerve is used along with measurement of facial CMAPs.
Passive : visually monitor the face for twitches during parotid surgery, applying needle electrodes to the facial muscles and recording CMAPs

53. Facial Nerve Monitoring
Monopolar electrode
Activates a wide area (depending on current intensity)
Sensitive for locating and mapping facial N.
 Best use for tumor mapping
Flexible with blunt tips  convenient for access to cramped areas.
Stimulation of adjacent N. (vestibular and auditory) often activate facial N.  false-positive.

54. Facial Nerve Monitoring
Bipolar electrode
Best for differentiating neural tissue or facial N form adjacent neural structure
Current is mostly confined to tissue bet. forceps tips  quite specific.
Small surface area of probe
 reduce possibility of false positive

55. Facial Nerve Monitoring – Sound Feed back
Thump / burst
stimulates the nerve electrically.
gentle mechanical stimulation (e.g., touching the nerve with an instrument).
near-instantaneous nerve stimulation.
popcorn popping / train
tension on the nerve or caloric or thermal stimulation.
signify ongoing stimulation of the nerve, which can be potentially more damaging.

56. Facial Nerve Monitoring - Errors
Detached or shorted electrodes.
incorrect wiring of electrodes.
malfunction of a nerve monitor or stimulator
Direct anesthesia of the facial nerve from local anesthetic infiltration to the stylomastoid foramen.
Pharmacologic muscular paralysis from induction agents used in anesthetic management
Muted speaker.
nonfunctional nerve.

57. Facial Nerve Monitoring
False-positive identification
Stimulation of the trigeminal nerve – Masseter m.
Stimulation of the adjacent vestibular or cochlear nerves.
Use in
Acoustic neuroma surgery
Skull base surgery
Parotidectomy
Middle ear and mastoid surgery

58. Unconventional Tests of Facial Nerve Function
Acoustic Reflex Evoked Potentials
Antidromic Potentials
Blink Reflex
Magnetic Stimulation
Optical Stimulation
Transcranial Electrical Stimulation–Induced Facial Motor Evoked Potentials

59. Acoustic Reflex Evoked potentials
Hammerschlag and associates
Scalp-recorded potential response to acoustic stimulation contralateral to the recording site and attributed this to facial motor pathway activation.
The response persisted after paralysis during anesthesia - intraoperative monitoring of facial nerve function.
the response was extremely small and slow to record (12- to 15-msec latency).

60. Antidromic Potentials
If a motor nerve is electrically or mechanically stimulated, action potentials will be propagated in two directions
Orthodromic or antegrade impulse will travel distally toward the muscle.
M-wave (muscle action potential) is the same potential recorded in ENoG.
Antidromic or retrograde impulse will travel proximally toward the cell body.
F-wave antidromic impulse reflected back along that neuron's axon in an orthodromic direction
recorded by electrodes on the proximal nerve (near field) or at a distance (far field).

61. Antidromic Potentials
F-waves are easily disrupted by even the mildest degree of facial paresis, even when clinical examination of facial nerve function yields normal findings.
Delayed latency or decreased amplitude or absent in patients with acoustic tumors.
However, they do not predict postoperative function.
Intraoperative facial nerve monitoring - Wedekind and Klug believe that F-wave monitoring provides earlier and better prognostic information to the surgeon than that obtained with continuous EMG monitoring.

62. Blink Reflex
Electrical or mechanical stimulation of the supraorbital branch of the trigeminal nerve elicits a reflex contraction (blink) of the orbicularis oculi muscle, which is innervated by the facial nerve.
Two studies found blink reflex abnormalities (recorded by EMG) in many patients with acoustic tumors (far more than were found by ENoG).
Suggests that subclinical facial nerve involvement is more common than has been clinically appreciated.
No evidence of any prognostic information to that available from tumor size.

63. Optical Stimulation
Stimulating the facial nerve without direct tissue contact - neural stimulation without mechanical trauma.
Ultraviolet wavelength excimer laser.
Pulsed short- and medium-wavelength infrared laser light.
Advantage for use in locations in which mechanical dissection must be kept to a minimum, such as at the cerebellopontine angle (does not have a protective layer of epineurium for support.

64. Transcranial Electrical Stimulation–Induced Facial Motor Evoked Potentials (MEPs)
Active stimulation - intraoperative facial nerve monitoring.
Spiral electrodes are placed at Cz and C3/C4 overlying the facial motor cortex contralateral to the side of the lesion.
Electrical stimulation of these facial corticobulbar neurons is propagated across the pyramidal decussation to stimulate facial nucleus neurons on the side ipsilateral to the lesion.

65. Transcranial Electrical Stimulation – Induced Facial MEPs
Lower motor neuron stimulation propagates to the facial musculature, where a muscle action potential is recorded.
The integrity of the entire facial motor tract is tested by this technique.
MEP recordings before tumor microdissection (baseline), intraoperatively and immediately after completion of dissection (final).
The final-to-baseline MEP amplitude ratio is calculated to determine the likelihood of an intact or disrupted facial motor tract.

66. Transcranial Electrical Stimulation – Induced Facial MEPs
Constraints
Necessity for nonvolatile anesthesia (only propofol and narcotic infusions are used for maintenance of anesthesia, as volatile agents adversely affect corticobulbar stimulability).
Pause surgical dissection during MEP acquisition.
Possibility of epileptic discharge during cortical stimulation.

67. Transcranial Electrical Stimulation – Induced Facial MEPs
Final-to baseline MEP amplitude ratios greater than 50% appear to correlate well with good immediate postoperative facial function (reported as House-Brackmann grade I or II).
Ratios less than 50% correlate with varying degrees of worse function (reported as House-Brackmann grades III to VI).
This technique is in its infancy and is likely to undergo continued refinement.

68. Thank You.