tests of Facial nerve Function

Diagnostic tests of Facial nerve
M.Rogha M.D.
Isfahan university of medical sciences
In facial paralysis, as in most medical problems, history and physical examination usually provide
more useful information than laboratory tests. Sometimes, however, a more objective evaluation of
facial nerve function is indicated to detect a facial nerve lesion to:
measure its severity
localize it to a particular intracranial, intratemporal, or extratemporal site
assess the prognosis for recovery
assist in treatment decisions
detect and avoid surgical injury.
Useful diagnostic tests add information to what is already known, influence the
choice of therapy, and ultimately improve clinical outcome.
Physical Examination
facial motor paralysis
Facial weakness can be extremely subtle. Rapid repetitive blinking can
unmask a mild facial weakness.
Attempts have been made to standardize measurement of facial function,
using techniques as simple as measurements with hand-held calipers and as
complex as digital photographic and videographic documentation.
Several systems of clinical measurement of facial nerve function have been
devised, such as House-Brackmann grading system.
Topognostic Tests
Topognostic tests were intended to reveal the site of lesion by use of a simple
Lesions below the point at which a particular branch leaves the facial nerve
subserved by that branch.
trunk will spare the function
Topognostic tests are not reliable in inflammatory diseases of the nerve.
Lacrimal Function (Schirmer’s test )
A defect in the afferent (the trigeminal nerve a long the opthalmic division,
or V1) or efferent (the facial nerve by way of the greater superficial petrosal
nerve) limb of this reflex may cause a reduced flow.
when a sensory deficit is present, presence of bilateral corneal anesthesia
should be considered, and stimulation of lacrimation by other noxious stimuli
(e.g., inhalation of ammonia) should be performed instead of the
conventional Schirmer’s test.
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.
May added Schirmer’s test to the salivary flow test and MST (under
“Electrodiagnostic Testing”) in a battery of prognostic tests. A decrease to
25% of normal in any of these was associated with a 90% chance of a poor
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 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. The prognostic value of this test
therefore seems limited.
chorda tympani carries fibers subserving taste from the Anterior two thirds of the
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, which is named
electrogustometry (EGM).
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 to 4 mA . 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. In healthy persons, the two sides of
the tongue have similar thresholds for electrical stimulation, rarely differing by
greater than 25%.
Taste function appears to recover before visible facial movement in some cases,
so if the results of electrogustometry are normal in the second week or later,
clinical recovery may be imminent.
Physical Examination
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, especially if performed
Reduced submandibular flow implies a lesion at or proximal to the point at
which the chorda tympani nerve leaves the main facial trunk.
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 90%
May and Hawkins noted that salivary flow decreases sooner than do threshold
changes in NET in idiopathic facial paralysis. They argued that a flow rate of
25% or less of that on the contralateral unaffected side, is an indication for
Salivary ph
At least one report showed that 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 in this study, all of
the control sides had pH levels of 6.4 or more. The overall accuracy of
prediction was 91%. Unfortunately, the reported experience with salivary pH
is very limited.
it is still unknown whether this test gives an earlier prognosis than other
Magnetic resonance imaging (MRI) with intravenous gadolinium contrast 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
oticus, usually in the perigeniculate portions of the nerve.
This enhancement may persist for more than1 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.
Sunderland histopathologic classification of
peripheral nerve injury.
Sunderland histopathologic classification
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. During 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. An example of a Sunderland class I injury is the
neurapraxia of an arm or leg that has“gone to sleep.”
Sunderland histopathologic classification
Class II:
lass 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. In a class II injury, 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
Sunderland histopathologic classification
Class III:
If the lesion disrupts the endoneurium, wallerian degeneration occurs
as in a class II injury, but the regenerating axons are free to enter the wrong
endoneurial tubes or may fail to enter an endoneurial tube at all. 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.
Sunderland class III to V nerve injuries, in which aberrant regeneration can
occur, are neurotmesis injuries.
Sunderland histopathologic classification
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
Sunderland histopathologic classification
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.
Sunderland histopathologic classification
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.
Sunderland histopathologic classification
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. The twitch can be
observed visually, or the electrical response of the facial muscles may be
recorded. Because no wallerian degeneration occurs, this electrical
stimulability distal to the site of lesion is preserved indefinitely in isolated
class I injury.
Sunderland histopathologic classification
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. However, before axonal degeneration, the distal segment is still electrically
stimulable. Wallerian degeneration begins immediately after injury but progresses slowly.
Histopathologic degeneration of the distal segment becomes apparent approximately 1
week after insult and continues for the ensuing 1 to 2 months. In the case of the facial
nerve, this delay in degeneration results in continued electrical stimulability of the distal
segment for up to 3 to 5 days after injury.
Thus, during these first days after an insult, electrodiagnostic testing of any form cannot
distinguish between neurapraxic and neurodegenerative injuries.
Electrodiagnostic Testing
Tests based on two principles of, electrical stimulation and recording of the
electromyographic response, are useful in determining prognosis and
sometimes in stratifying patients for nonsurgical versus surgical management.
However, they are rarely useful in differential diagnosis.
Limitations of facial nerve electrical testing
After wallerian degeneration, electrical testing can distinguish axonally intact but
neurapraxic lesions (class I) from axonally disrupted and neurodegenerative lesions
(classes II to V). It cannot, however, 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).
Majority of insults to the facial nerve, whether compressive, inflammatory, or traumatic
(except for complete transections), probably are class VI, with a variable threshold of
electrical stimulability commensurate with the proportion of neural degeneration across
the nerve trunk.
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, 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. Next, 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. the paralyzed
nerve is as easy to stimulate distal to the site of lesion as the healthy nerve. After a more severe
injury (Sunderland classes II to V) in which distal axonal degeneration occurs, electrical
excitability is gradually lost, over a period of 3 to 5 days even after a total section of the nerve.
Therefore, NET (and all other electrical tests involving distal stimulation), always lag several
days behind the biologic events themselves.
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.
The NET is useful only during the first 2 to 3 weeks of complete paralysis, before complete
degeneration has occurred.
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, however, maximal stimuli (current levels at which the greatest
amplitude of facial movement is seen) current are used.
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.
According to May and coworkers, when MST results remained normal in Bell’s
palsy, 88% of patients recovered completely. Reduced movement presaged
only a 27% chance of complete recovery.
An absence of electrically stimulated movement was always associated with
incomplete recovery.
In ENoG, the facial nerve is stimulated
transcutaneously at the stylomastoid
foramen. Responses to maximal electrical
stimulation of the two sides are compared,
but they are recorded in a more objective
fashion by measuring the evoked compound
muscle action potential (CMAP) with a
second bipolar electrode pair placed
(usually) in the nasolabial groove. A supra
maximal stimulus often is used, and peakto-peak amplitude is measured in millivolts
(mV). The average difference in response
amplitude between the two sides in healthy
patients has been said to be only 3%. The
term “electroneuronography” is actually a
misnomer, because it is the facial muscle
CMAP that is measured and recorded. Some
workers use the term evoked electromyography synonymously with
the amplitude of response on the paralyzed side can be expressed as a precise
percentage of that on the healthy side.
Patients reaching 90- 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.
Most proponents of ENoG use it mainly to obtain an early prognosis in acute
facial paralysis (Bell’s or post-traumatic) or to select patients for
decompression surgery.
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.
ENoG also has demonstrated some success in preoperative detection of facial
nerve infiltration by malignant parotid tumors, even when no paresis is seen
on clinical examination.
EMG is the recording of spontaneous and voluntary muscle potentials using
needles introduced into the muscle.
it does not permit a quantitative estimate of the extent of nerve
degeneration (the percentage of degenerated fibers).
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.
After loss of excitability, tests requiring electrical stimulation such as NET
and ENoG are no longer useful. However, EMG may give prognostically useful
information during this phase of the illness.
After10 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 poly-phasic 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.
It may be helpful in the assessment of long-standing facial paralysis, along
with muscle biopsy, to determine the possible success of substitution
anastomosis or cross facial anastomosis as a mechanism of restoring facial
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 15-18 months, the anastomosis should
be considered a failure, and another operation should be considered
(e.g.,hypoglossal-facial anastomosis).
Facial Nerve Monitoring
Direct visualization of facial contractures is the simplest form of facial nerve
monitoring during surgeries.
By applying needle electrodes to the facial muscles (orbicularis oculi and
orbicularis oris ) and recording CMAPs the activity of the facial nerve can be
monitored in a more standardized, precise, and sensitive fashion. facial muscle
movement is activated only with direct mechanical, stretch, caloric, or other
nonelectrical stimulation of the facial nerve.
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 commensurate in
size with the delivered current intensity, and modulation of current intensity can
provide the surgeon with good sensitivity for locating and mapping the facial
nerve. Early in the dissection before the facial nerve has been visually identified,
initial stimulation with higher current levels allows the surgeon to stimulate the
nerve from a far, without the need for direct contact on the nerve. As dissection is
carried closer to the nerve, lowering the current level allows for more precise
determination of nerve location. As dissection is continued and the facial nerve (or
its candidates) are identified, low level current stimulation directly on the nerve
provides confirmation that the nerve has been positively identified.
Facial Nerve Monitoring
When the surgeon stimulates the nerve electrically, a CMAP is recorded from the
monitored facial muscles and can be plotted on an oscilloscope (if visual display is
being used), 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 termed these two
characteristic sounds bursts and trains, respectively. Learning to identify these
sounds is easy, providing instant feedback regarding the location of the facial
nerve and concomitant surgical manipulation. Bursts imply near-instantaneous
nerve stimulation; trains signify ongoing stimulation of the nerve, which can be
potentially more damaging.
excessive intraoperative train activity predicts poor outcome.
if at the end of the surgical procedure the nerve can be stimulated successfully
with low currents (0.05 to 0.1 mA), all investigators agree that the prognosis for
postoperative function is excellent.
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. So Electrode position should always be checked before operation.
Unconventional Tests of Facial Nerve Function
Acoustic Reflex evoked Potentials
a scalp-recorded potential at 12- to 15-msec latency in response to acoustic
stimulation contralateral to the recording site and attributed this to facial
motor pathway activation. The response persisted after paralysis during
anesthesia, and these workers proposed its use for intraoperative monitoring
of facial nerve function.
the response is extremely small (much lower in amplitude than that of the
auditory brainstem response), which would make it difficult and slow to
record, requiring prolonged averaging.
Unconventional Tests of Facial Nerve Function
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 impulse will travel distally toward the muscle, whereas an antidromic or
retrograde impulse will travel proximally toward the cell body.
Near-field antidromic responses were reliably altered by surgical lesions placed between the
stimulating and the recording electrodes.
Far-field antidromic potentials have been recorded from the scalp after electrical
stimulation near the stylomastoid foramen. However, these responses are difficult to record
and interpret.
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, suggesting that facial nucleus hyperexcitability plays a role in that disorder. F-waves
are easily disrupted by even the mildest degree of facial paresis.
Antidromic stimulation of peripheral branches of the facial nerve has been introduced into
intraoperative monitoring, with continuous recording of either near-field potentials from the
facial nerve near the brainstem or F-waves from facial musculature. F-wave monitoring
provides earlier and better prognostic information to the surgeon than that obtained with
continuous EMG monitoring.
Unconventional Tests of Facial Nerve Function
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
Although this finding suggests that subclinical facial nerve involvement is
more common than has been clinically appreciated, neither study offered
evidence that blink reflex testing added any prognostic information to that
available from tumor size.
Unconventional Tests of Facial Nerve Function
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.
This method offers two potential advantages over conventional electrical
stimulation of the facial nerve:
(1) the nerve can be maximally stimulated without pain or discomfort
(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
Unconventional Tests of Facial Nerve Function
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.
short-wavelength infrared pulsed laser light is used to successfully stimulate
the extra temporal facial nerve without neural damage seen on histologic
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 cerebellopontine angle, where the nerve does
not yet have a protective layer of epineurium for support.
Unconventional Tests of Facial Nerve Function
transcranial electrical stimulation–induced Facial Motor evoked Potentials
Another more recently developed method involves transcranial electrical stimulation of
the cortical facial motor pathway and measurement of the corresponding facial motor
evoked potentials (MEPs), in order to evaluate the integrity of entire nerve.
In intraoperative transcranial electrical stimulation, spiral electrodes are placed
overlying the facial motor cortex contralateral to the side of the lesion being removed.
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. Lower motor neuron stimulation propagates to the facial musculature, where a
muscle action potential is recorded in the standard fashion; this corticobulbar-derived
CMAP is the MEP. Thus, the integrity of the entire facial motor tract is tested by this
It is necessary to use nonvolatile anesthesia for transcranial electrical stimulation (only
propofol and narcotic infusions are used for maintenance of anesthesia, as volatile
agents adversely affect corticobulbar stimulability).
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 HouseBrackmann grades III to VI).

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