various tests for facial nerve function

1. Dr. Rajendra Singh Lakhawat

2. Introduction
In facial paralysis, history and physical
examination usually provide more
useful information than laboratory
tests.

3. Sometimes, however, a more objective
evaluation of facial nerve function is
indicated to detect a facial nerve lesion;
to measure its severity; to localize it to
a particular intracranial, intratemporal,
or extratemporal site; to assess the
prognosis for recovery; to assist in
treatment decisions; or to detect and
avoid surgical injury.
Quantitative tests of facial nerve
function are then used.

4. Physical Examination
Facial weakness can be extremely
subtle, apparent only to a trained
examiner (and perhaps to the patient).
Paradoxically, mild unilateral facial
weakness sometimes can be more
easily detected by comparison with a
normal contralateral side by having the
patient perform nominal movements.

5. Rapid repetitive blinking also can
unmask a mild facial weakness, which
will manifest as slowed or reduced
blink frequency compared with that on
the normal side.
By contrast, when facial paralysis is
total or near-total, the diagnosis is
obvious; such impairment can be
devastating to the patient on
functional, social, and psychologic
levels.

6. Several systems of clinical
measurement of facial nerve function
have been devised, but since the mid-
1980s, the House-Brackmann system
has been most widely used.
This system is least ambiguous at its
extremes and most prone to intertest
variability at its intermediate grades II
to V.

7. House-Brackmann Facial Nerve
Grading System

10. Schematic diagram of
functional progression
in assigning
House-Brackmann
grade to degree of
facial paralysis.

11. Limitation of this System
Is in the evaluation ofACUTE facial
paralysis. The differentiation among
House-Brackmann grades II, III, IV,
and V rests partly on the presence and
severity of synkinesis, contracture,
hemifacial spasm, and asymmetry at
rest—all sequelae of long-term facial
nerve dysfunction and hence all absent
in the setting of acute facial paralysis.

12. The House-Brackmann system applied
in its strictest sense is well suited for
evaluation of long-standing facial
nerve dysfunction but not acute facial
paralysis.

13. Topognostic Tests
Topognostic tests were intended to
reveal the site of lesion by use of a
simple principle: Lesions below the
point at which a particular branch
leaves the facial nerve trunk will spare
the function subserved by that branch.

14. Accordingly, injury to the nerve in the
face cannot affect lacrimation,
salivation, taste, or the stapedius reflex.
Conversely, the combination of facial
paralysis and decreased lacrimation
can theoretically be caused only by a
lesion in the segment of the nerve in
which voluntary motor fibers and
parasympathetic fibers to the lacrimal
gland run together (i.e., from the
cerebellopontine angle to the
geniculate ganglion).

15. In complete focal lesions, topognostic tests
are reliable but usually are unnecessary,
because clinical examination and imaging
suffice to describe the site of lesion.
Bell’s palsy is a mixed and partial lesion
with varying degrees of conduction block
and degeneration changes within different
fibers and fascicles of the nerve trunk;
therefore, topognostic tests are not
expected to provide precise information
about the level of the lesion.
In recent years,these tests are used rarely.

16. Lacrimal function
physician 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.
Normally, the portion of the filter
paper in contact with the conjunctiva
acts as an irritant, stimulating an
increased flow of tears, which are then
wicked along the filter paper strip by
capillary action.

17. The length of the wetted portion of the
strip after a fixed interval (usually 5
minutes) is measured and is
proportional to the volume of tears
produced. A defect in the afferent (the
trigeminal nerve along the opthalmic
division, or V1) or efferent (the facial
nerve by way of the greater superficial
petrosal nerve) limb of this reflex may
cause reduced flow.

18. The reflex is consensual (i.e., a
unilateral irritating stimulus in either
eye causes tearing in both eyes, and a
unilateral sensory deficit in either eye
will reduce tearing bilaterally).
Schirmer’s test usually is considered
positive if the affected side shows less
than one-half the amount of
lacrimation seen on the healthy side.

19. Both the symmetry of the response and
its absolute magnitude are important; a
total response (sum of the lengths of
wetted filter paper for both eyes) of less
than 25 mm is considered abnormal.

20. Stapedius Reflex
The nerve to the stapedius muscle
branches off the facial trunk just past
the second genu in the vertical
(mastoid) part of the nerve. 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.

21. 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) at the time of presentation;
the reflex recovers at about the same
time as for clinically observed
movements.

22. Taste
Psychophysical assessment can be
performed with natural stimuli, such as
filter paper disks impregnated with
aqueous solutions of salt, sugar, citrate,
or quinine, or with electrical
stimulation of the tongue.

23. Electrical stimulation of the tongue termed
electrogustometry (EGM), has the
advantages of speed and ease of
quantification.
EGM involves bipolar or monopolar
electrical stimulation of the tongue, with
current delivery on the order of 4 μA (−6
dB) to 4 mA (34 dB).
Taste function appears to recover before
visible facial movement in some cases, so if
the results are normal in the second week or
later, clinical recovery may be imminent.

24. Salivary Flow Test
The salivary flow test requires cannulation
of the submandibular ducts and comparison
of stimulated flow rates on the two sides. It
is time consuming and unpleasant for the
patient.
Reduced submandibular flow implies a
lesion at or proximal to the point at which
the chorda tympani nerve leaves the main
facial trunk; this is variable and may be
anywhere in the vertical (mastoid) portion
of the nerve.

25. Ekstrand stated that 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. Complete or
incomplete recovery could be predicted
with 89% accuracy.

26. Salivary pH
A submandibular salivary pH of 6.1 or
less predicts incomplete recovery in
cases of Bell’s palsy. Presumably only
the duct on the affected side needs to
be cannulated, because ass a study, all
of the control sides had pH levels of 6.4
or more. The overall accuracy of
prediction was 91%.

27. IMAGING
Gd enhanced MRI has revolutionized tumor
detection in the cerebellopontine angle and
temporal bone and is currently the study of
choice when a facial nerve tumor is
suspected (e.g., in a case of slowly
progressive or longstanding weakness).
 Enhancement also occurs in most cases of
Bell’s palsy and herpes zoster opticus,
usually in the perigeniculate portions of the
nerve.

28. This enhancement may persist for more
than 1 year after clinical recovery; can be
distinguished from neoplasm by its linear,
unenlarged appearance; and has no
apparent prognostic significance.
Computed tomography (CT) is valuable for
surgical planning in cholesteatomas and
temporal bone trauma involving facial
nerve paralysis but probably is less useful
than MRI in the investigation of atypical
idiopathic paralysis.

29. MRI shows the greatest utility in
predicting location and depth of
parotid gland tumors.
Fine needle aspiration biopsy
continues to be the “gold standard”
modality for preoperative evaluation of
parotid masses

30. Pathophysiology
Sunderland provided a simple, five-
category histopathologic classification
of peripheral nerve injury based on a
schematic framework proposed by
Seddon.

31. Class I
Pressure on a nerve trunk, provided that it
is not too severe, causes conduction block,
termed neurapraxia by Seddon. No
physical disruption of axonal continuity
occurs, and supportive connective tissue
elements remain intact.
When the pressure or other insult (e.g.,
local anesthetic infiltration) is removed, the
nerve can recover quickly.
e.g. an arm or leg that has “gone to sleep.”

32. Class II
A more severe lesion, whether caused
by pressure or some other insult (e.g.,
viral inflammation), may cause 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.

33. the connective tissue elements remain
viable, so regenerating axons may
return precisely to their original
destinations.
Removal of the original mechanism of
insult permits complete recovery, but
this is considerably delayed, because
the axon must regrow from the site of
the lesion to the motor end plate at a
rate of approximately 1 mm/day before
function returns. A class II injury is an
axonotmesis.

34. Class III
If the lesion disrupts the endoneurium,
wallerian degeneration occurs, but the
regenerating axons are free to enter the
wrong endoneurial tubes or may fail to
enter; this aberrant regeneration may be
associated with incomplete recovery,
manifested as an inability to make discrete
movements of individual facial regions
without involuntary movement of other
parts of the face—an abnormality termed
synkinesis.

35. Class IV
Perineurial disruption implies an even
more severe injury, in which the
potential for incomplete and aberrant
regeneration is greater.
Intraneural scarring may prevent most
axons from reaching the muscle,
resulting in not only greater synkinesis
but incomplete motor function
recovery.

36. Class V
A complete transection of a nerve,
including its epineurial sheath, carries
almost no hope for useful regeneration,
unless the ends are approximated or
spanned and repaired.
Class III to V are NEUROTMESIS
injuries

37. Sunderland histopathologic
classification of peripheral
nerve injury.
Roman numerals I to V at
left denote the Sunderland
class corresponding to the
degree of injury depicted in
the diagram.

38. Class VI
Insults to the facial nerve trunk,
whether compressive, inflammatory, or
traumatic in origin, can be
heterogeneous in nature, with differing
degrees of injury from fascicle to
fascicle.
Such mixed injury involving both
neurapraxia and a variable degree of
neurodegeneration has been advocated
as an additional class of injury.

39. 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.
Because no wallerian degeneration
occurs, this electrical stimulability
distal to the site of lesion is preserved
indefinitely in isolated class I injury.

40. In classes II to VI, once wallerian
degeneration has occurred, electrical
stimulation of the nerve distal to the
lesion will fail to produce a propagated
action potential and muscle
contraction.
But, before axonal degeneration, the
distal segment is still electrically
stimulable.

41. Histopathologic degeneration of the distal
segment becomes apparent approximately 1
week after insult and continues for the
ensuing 1 to 2 months.
This delay in 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.

42. It cannot, distinguish among the different
classes of neurodegenerative lesions II, III,
IV, and V.
An important consideration in the use of
such testing is its limited ability to
distinguish between pure lesions associated
with an excellent prognosis for perfect
spontaneous recovery (class II) and those
associated with a poor prognosis for useful
recovery without surgical repair (class V).

43. Electrodiagnostic Testing
Tests based on these two principles,
electrical stimulation and recording of
the electromyographic response, are
useful in determining prognosis and in
stratifying patients for nonsurgical
versus surgical management.
They are rarely useful in differential
diagnosis.

44. In Bell’s palsy and traumatic facial nerve
paralysis, electrical tests most often are used
to identify patients whose nerves have
begun to degenerate, because these patients
may be candidates for decompression
surgery.
In this sense, outpatient evaluation of facial
paralysis with electrical testing only needs
to be performed if the physician is prepared
to recommend decompression in the event
that degeneration is discovered.

45. Intraoperative monitoring of facial
nerve function (usually with
electromyography) is in widespread use
in many types of intracranial and
intratemporal surgery.

46. Nerve Excitability Test
Introduced by Laumans and Jonkees.
Stimulating electrode is placed on the skin
over the stylomastoid foramen or over one
of the peripheral branches of the nerve,
with a return electrode taped to the
forearm.
Beginning with the healthy side, electrical
pulses, typically 0.3 msec in duration, are
delivered at steadily increasing current
levels until a facial twitch is noted.

47. The lowest current eliciting a visible
twitch is the threshold of excitation.
The process is repeated on the
paralyzed side, and the difference in
thresholds between the two sides is
calculated.

48. In a simple conduction block (e.g., after
infiltration of the perineural tissues with
lidocaine proximal to the point of stimulation),
no difference exists between the two sides.
After a more severe injury ( II to V) in which
distal axonal degeneration occurs, electrical
excitability is gradually lost, over a period of 3 to
4 days—even after a total section of the nerve.
Findings on the NET (electrical tests involving
distal stimulation), therefore, always lag several
days behind the biologic events themselves.

49. A difference of 3.5 milliamperes (mA)
or more in thresholds between the two
sides has been proposed as a reliable
sign of severe degeneration and has
been used as an indicator for surgical
decompression.
With use of this criterion, complete
versus incomplete recovery can be
predicted with 80% accuracy

50. 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; in these cases, the test result will be
normal when the segment of nerve distal to
the lesion is stimulated. If the paralysis
becomes total, the test can determine whether
a pure conduction block exists or whether
degeneration is occurring, as indicated by
progressive loss of excitability.

51. Total paralysis for longer than 1 month is
almost invariably associated with total loss
of excitability.
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.

52.  This disparity results because the regenerating
axons are smaller, more irregular in size, and
fewer in number than before the lesion occurred.
 Electrical stimulation generally is ineffective in
eliciting a synchronous and hence observable
twitch in the early stages of regeneration.
 As these early fibers regenerate, they may regain
electrical function individually, while group
function, measured as a clinically apparent twitch
on electrical stimulation, still is not evident. This
phenomenon is termed early deblocking, or
asynchronous firing of the facial nerve.

53. Partial degeneration and a bad outcome are
not synonymous.
Laumans and Jonkees state that even
patients who show degeneration (threshold
difference greater than 3.5 mA) have a 38%
chance for complete spontaneous recovery;
in the remainder, development of
complications such as permanent weakness
(not total paralysis) and synkinesis is
typical.

54. Maximum Stimulation Test
The MST is similar to the NET in that it
involves visual (i.e., subjective) evaluation
of electrically elicited facial movements.
Instead of measuring threshold, maximal
stimuli (current levels at which the
greatest amplitude of facial movement is
seen) or supramaximal stimuli are used.

55. On the unaffected side, the stimulus
current intensity is increased above the
threshold level incrementally—with
corresponding increases in subjective facial
twitch magnitude—until the maximum
stimulation level is reached.
This maximum stimulation level is 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.

56. The theoretic basis of the MST is that
by stimulating all intact axons, the
proportion of fibers that have
degenerated can be estimated; this
information should more reliably guide
prognosis and treatment than that
obtained with the NET.
In a study, An absence of electrically
stimulated movement was always
associated with incomplete recovery

57. Electroneuronography (ENoG)
The facial nerve is stimulated
transcutaneously at the stylomastoid
foramen, as in the NET, although a bipolar
stimulating electrode used.
Responses to maximal electrical stimulation
of the two sides are compared, but they are
recorded by measuring the evoked
compound muscle action potential (CMAP)
with a second bipolar electrode pair placed
(usually) in the nasolabial groove.

58. A supramaximal stimulus often is used
Peak-to-peak amplitude is measured in
millivolts (mV). The average difference
in response amplitude between the two
sides in healthy patients is only 3%.
 The term “electroneuronography” is
actually a misnomer, because it is the
facial muscle CMAP that is measured
and recorded.
Synonym evoked electromyography.

59. This method offers the potential
advantage of an objective registration of
electrically evoked responses, and the
amplitude of response on the paralyzed
side can be expressed as a precise
percentage of that on the healthy side.
 e.g. if the amplitude of the response on
the paralyzed side is only 10% of that on
the normal side, an estimated 90% of
fibers are said to have degenerated on
the paralyzed side.

60. Most investigators require a 30% or greater
asymmetry (or change over time) for results
to be considered abnormal.
Electrical recording of the muscle response
also offers the possibility of measuring
latency, which is the time elapsed between
stimulus and response.
Joachims and et. al. stated that increased
latency in the first 72 hours (before any
observable change in threshold or response
amplitude) was a reliable predictor of a
poor outcome.

61. The limitation described for the NET, also
applies to the MST and to ENoG.
 e.g. its inapplicability in cases of partial
paralysis, after the beginning of clinical
recovery and after excitability has been lost.
In acute facial paralysis, all of these tests are
useful only in tracking the early course of a
completely paralyzed nerve until clinical
recovery begins or the nerve shows
complete loss of excitability.

62. In time course of Bell’s palsy, the acute
phase rarely exceeds 10 days.
Decreases in ENoG amplitude after the 10th
day were a/w substantial latency increases
and were attributed to desynchronization of
surviving fibers, rather than to increased
degeneration.
The time elapsed since the onset of paralysis
should be taken into account in the
interpretation of ENoG results.

63. Patients reaching 95% degeneration
(amplitude of response equals 5% of that
on the healthy side) within 2 weeks had a
50% chance of a poor recovery, whereas
patients exhibiting a more gradual decrease
in ENoG amplitude had a much better
prognosis.
ENoG is used mainly to obtain an early
prognosis in acute facial paralysis or to
select patients for decompression surgery

64. Kartush pointed out that ENoG also
can document subclinical facial nerve
involvement by tumors especially
acoustic neuromas. Patients with
acoustic tumors who had ENoG
evidence of nerve involvement (despite
clinically normal facial movement)
were more likely to have postoperative
weakness.

66. Electromyography
EMG is the recording of spontaneous
and voluntary muscle potentials using
needles introduced into the muscle. Its
role in the early phase of Bell’s palsy is
limited, because it does not permit a
quantitative estimate of the extent of
nerve degeneration (the percentage of
degenerated fibers).

67. Decompression for Bell’s palsy is based
primarily on NET or ENoG,but it also
require confirmatory EMG if it shows
voluntarily active facial motor units
despite loss of excitability of the nerve
trunk, the prognosis for a good
spontaneous recovery is excellent.This
application of EMG in Bell’s palsy
probably is underused.

68. After loss of excitability, NET and ENoG
are no longer useful.
However, EMG may give prognostically
useful information during this phase of
the illness.
After 10 to 14 days, fibrillation potentials
may be detected, confirming the presence
of degenerating motor units; in 81% of
patients with such findings, incomplete
recovery is the rule

69. More useful are the polyphasic
reinnervation potentials that may be
seen as early as 4 to 6 weeks after the
onset of paralysis. Presence of these
potentials precedes clinically
detectable recovery and predicts a fair
to good recovery.

70. EMG also can help assess whether a nerve
repair (e.g., in the cerebellopontine
angle) is unsuccessful. If no clinical
recovery occurs and EMG shows no
polyphasic reinnervation potentials at 15
months (or at 18 months at the latest).
The anastomosis should be considered a
failure, and another operation should be
considered (e.g., hypoglossal-facial
anastomosis).

71. Facial Nerve Monitoring
It is possible to watch for facial movements
in response to mechanical or electrical
stimulation of the nerve, simple
observation fails to detect many small
muscular contractions and in any case
demands constant vigilance.
By contrast, electrodes in or near the facial
muscles record EMG potentials that can be
amplified and made audible with a
loudspeaker.

72. Active versus passive monitoring.
PASSIVE whereby facial muscle movement
is activated only with direct mechanical,
stretch, caloric, or other nonelectrical
stimulation of the facial nerve
e.g. 1. assistant visually monitor the face for
twitches during parotid surgery. 2. By
applying needle electrodes to the facial
muscles and recording CMAPs, the activity
of the facial nerve can be monitored in a
more standardized, precise, and sensitive
fashion.

73. When electrical stimulation of the
facial nerve is used along with
measurement of facial CMAPs, the
technique is termed active facial
nerve monitoring. Electrical
stimulation is delivered by a
monopolar or bipolar electrode.

74. Electrical stimulation activates a
surrounding volume of tissue with the
delivered current intensity, and
modulation of current intensity can
provide the surgeon with good
sensitivity for locating and mapping
the facial nerve.
As dissection is carried closer to the
nerve, lowering the current level allows
for more precise determination of
nerve location.

75. When the surgeon stimulates the nerve
electrically, a CMAP is recorded and can be
plotted on an oscilloscope, and the
loudspeaker emits a characteristic thump.
Gentle mechanical stimulation (e.g.,
touching the nerve with an instrument) will
produce a similar sound.

76. Tension on the nerve from mechanical
stretching or caloric or thermal
stimulation of the nerve from irrigation
often will produce a prolonged irregular
series of discharges that sounds like
popcorn popping.
Prass et.al. termed these two
characteristic sounds bursts and trains,
respectively.

77. Bursts imply near-instantaneous nerve
stimulation; trains signify ongoing stimulation
of the nerve, which can be potentially more
damaging.
Stimulation of the trigeminal nerve occasionally
can cause electrical confusion, or crosstalk; the
facial muscle electrodes may pick up EMG
signals from the nearby masseter muscle.
Similarly, stimulation of the adjacent vestibular
or cochlear nerves can sometimes activate the
facial nerve as well, leading to a false-positive
identification.

78. The idea that audible EMG monitoring
makes acoustic tumor surgery easier,
faster, and probably more successful in
terms of facial nerve preservation has
become widely accepted.
Postoperative facial nerve function is
better in patients who have been
monitored (at least during operations
for resection of large tumors).

79. Intraoperative facial nerve monitoring
has been shown to be cost-effective for
both primary and revision middle ear
and mastoid surgical procedures, with
a higher number of quality-adjusted
life-years and lower average cost than
for a no-monitoring strategy.

80. Unconventional Tests of Facial
Nerve Function
1. Acoustic Reflex Evoked Potentials
 A scalp-recorded potential at 12- to 15-msec latency in
response to acoustic stimulation contralateral to the
recording site, attributed to facial motor pathway
activation.
 The response persisted after paralysis during
anesthesia,it can be used for intraoperative monitoring
of facial nerve function.
 However, the response is extremely small (much lower in
amplitude than that of the auditory brainstem response)

81. 2. Antidromic Potentials
If a motor nerve is electrically or
mechanically stimulated at some point
between its cell body and its synapse on a
muscle fiber, action potentials will be
propagated in two directions:
An orthodromic or antegrade impulse will
travel distally toward the muscle.
An antidromic or retrograde impulse will
travel proximally toward the cell body.

82. The orthodromic impulse will cross the
neuromuscular junction, resulting in
an observable muscle contraction and a
recordable compound muscle action
potential. This M-wave is the same
potential recorded in ENoG.
The antidromic impulse will not cross a
synapse, it can be recorded by
electrodes on the proximal nerve (near
field) or at a distance (far field).

83. The antidromic impulse will not travel
farther “upstream” than the facial
nucleus motor neuron, but it can be
reflected back along that neuron’s axon
in an orthodromic direction.
eventually reaching the muscle and
stimulating a muscle action potential—
the F-wave—that is delayed relative to
the initial M-wave.

84. These F-waves are unusually large in
hemifacial spasm,96 suggesting that facial
nucleus hyperexcitability plays a role in that
disorder.
F-waves are easily disrupted by even the
mildest degree of facial paresis.
They often are abnormal with delayed
latency or decreased amplitude or are
absent in patients with acoustic tumors,
even when clinical examination of facial
nerve function yields normal findings.

85. 3. 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.
Studies found blink reflex abnormalities
(recorded by EMG) in many patients with
acoustic tumors (far more than were found
by ENoG).

86. 4. Magnetic Stimulation
A rapidly varying magnetic field
produced by a surge of current in a coil
placed over the skin will induce
electrical currents in underlying tissue
and can be used to stimulate nerves.

87. Two potential advantages over conventional
electrical stimulation of the facial nerve:
(1) the nerve can be maximally stimulated
without pain or discomfort, and
(2) if the coil is placed in the
temporoparietal area (transcranial
stimulation), the nerve seems to be
stimulated in the region of the geniculate
ganglion or the internal auditory canal.

88. This functionality, when coupled with
electrical stimulation of the facial
nerve at the stylomastoid foramen,
could obviously be useful for siteof-
lesion determination, at least in the
earliest phases of paralysis before
electrical excitability distal to a lesion
is lost.

89. Patients with magnetically stimulable
nerves, when tested up to 4 days after onset
of Bell’s palsy, had a better prognosis than
those whose responses had been lost.
This technique may not be useful for
prognostic purposes after the first few days.
Magnetic stimulation offered no unique
prognostic information in acoustic tumor
cases once tumor size (the best predictor of
facial nerve outcome) is considered.

90. 5. Optical Stimulation
Another method of stimulating the facial
nerve without direct tissue contact is by
optical excitation.
Contact-free optical excitation provides the
important potential benefit of neural
stimulation without mechanical trauma.

91. Unfortunately, early efforts at optical nerve
stimulation using ultraviolet-wavelength
excimer laser were successful only at energy
densities comparable to the photoablation
threshold.
Such optical excitation techniques would have
an obvious advantage for use in locations in
which mechanical dissection of the facial
nerve must be kept to a minimum, such as at
the CP angle, where the nerve does not yet
have a protective layer of epineurium for
support. This specific application has not yet
been reported.

92. 6. Transcranial Electrical
Stimulation Induced Facial Motor
Evoked Potentials
Test the integrity of the nerve proximal to
dissection, which may be vital to know
during dissection of a large cranial base
tumor, when the facial nerve root entry
zone is not readily identified.

93. MEP (motor evoked potentials)
recordings are performed before tumor
microdissection (baseline), at regular
intervals 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.

94. THANK YOU