Facial nerve tests

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

Quantitative tests of facial nerve
function are used
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.

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

Rapid repetitive blinking can unmask a
mild facial weakness.
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.

Several systems of clinical
measurement of facial nerve function
have been devised, but 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.

House-Brackmann Facial Nerve
Grading System

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

Limitation of this System
Is in the evaluation of ACUTE 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.

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.

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.

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.

Lacrimal function
place a folded strip of sterile filter
paper into the conjunctival fornix of
each eye and compare the rate of tear
production of the two sides.
the filter paper acts as an irritant,
stimulating an increased flow of tears,
which are then wicked along the filter
paper strip by capillary action.

The length of the wetted portion
(usually after 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.

The reflex is consensual.
Schirmer’s test usually considered
positive if the affected side shows less
than one-half the amount of
lacrimation seen on the healthy side.

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.

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.

An absent reflex or a reflex that is
less than one-half the amplitude of
the C/L 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.

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.

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.

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.
⤓ed S.M. 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.

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.

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 as per a study, all of the control
sides had pH levels of 6.4 or more. The
overall accuracy of prediction was 91%.

IMAGING
Gd enhanced MRI has revolutionized tumor
detection in the CP 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 oticus, usually
in the perigeniculate portions of the nerve.

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.
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.

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

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

Class I
Pressure on nerve trunk, 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 insult (e.g., local anesthetic
infiltration) is removed, the nerve can
recover quickly.
e.g. an arm or leg that has “gone to sleep.”

Class II
A more severe lesion, 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.

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.

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.

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.

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

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.

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.

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.

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.

Histopathologic degeneration of the distal
segment becomes apparent approx 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 bw neurapraxic and
neurodegenerative injuries.

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 b/w 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).

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.

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.

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

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.

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.

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.

A difference of 3.5 mA or more in
thresholds b/w 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

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.

In total paralysis, the test can
determine whether a pure conduction
block exists or whether
degeneration is occurring, as
indicated by progressive loss of
excitability.
Total paralysis for >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 useless, because
clinically evident recovery always begins
before any apparent electrical excitability
returns.
because the regenerating axons are smaller,
more irregular in size, and fewer in number
than before the lesion occurred.

Therefore 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.

Partial degeneration and a bad outcome are
not synonymous.
Laumans and Jonkees state that even
patients who show degeneration 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.

Maximum Stimulation Test
The MST is similar to the NET in that it
involves visual 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.

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 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.

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

Electroneuronography (ENoG)
The facial nerve is stimulated
transcutaneously at the stylomastoid
foramen, 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.

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.

advantage - objective registration of
electrically evoked responses, and the
amplitude of response on the paralyzed
side can be expressed in percentage.
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 have degenerated on the paralyzed
side.

Abnormal – if 30% or greater asymmetry.
Electrical recording of the muscle response
also offers the possibility of measuring
latency, which is the time elapsed between
stimulus and response.
increased latency in the first 72 hours is a
reliable predictor of a poor outcome.

Limitations are similar to NET and MST.
 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.

In 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.

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 obtain early prognosis in
acute facial paralysis or to select
patients for decompression surgery

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.

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).

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.

After loss of excitability, NET and ENoG
are no longer useful.
but EMG may give prognostically
useful information during this phase.
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

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.

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).

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.

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.

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.

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.

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.

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.

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.

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).

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.

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)

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.

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).

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.

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.

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).

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.

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.

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.

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.

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.

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.

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.

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.

Facial nerve tests

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