Diagnostic tests of Facial nerve

1. Diagnostic tests of Facial nerve M.Rogha M.D. Isfahan university of medical sciences

2. 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.

3. Physical Examinationfacial 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 videographicdocumentation. • Several systems of clinical measurement of facial nerve function have been devised, such as House-Brackmann grading system.

5. 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. • Topognostic tests are not reliable in inflammatory diseases of the nerve.

6. 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’stest. • 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 recovery.

7. 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.

8. Taste • chorda tympani carries fibers subserving taste from the Anterior two thirds of the tongue. • 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 electrogustometryare normal in the second week or later, clinical recovery may be imminent.

9. Physical ExaminationTaste

10. 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 repeatedly. • 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% accuracy. • 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 surgery.

11. 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 tests.

12. Imaging • Magnetic resonance imaging (MRI) with intravenous gadolinium contrast has revolutionized tumor detection in the cerebellopontineangle 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.

14. Pathophysiology Sunderland histopathologic classification of peripheral nerve injury.

15. 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“goneto sleep.”

16. 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 axonotmesis.

17. 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 endoneurialtube 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 neurotmesisinjuries.

18. Sunderland histopathologic classification Class IV: Perineurialdisruption implies an even more severe injury, in which the potential for incomplete and aberrant regeneration is greater. Intraneuralscarring may prevent most axons from reaching the muscle, resulting in not only greater synkinesis but incomplete motor function recovery.

19. 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.

20. 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 neurodegenerationhas been advocated as an additional class of injury.

21. 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.

22. 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.

23. 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.

24. Limitations of facial nerve electrical testing • After wallerian degeneration, electrical testing can distinguish axonallyintact but neurapraxic lesions (class I) from axonallydisrupted 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 stimulabilitycommensurate with the proportion of neural degeneration across the nerve trunk.

25. 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 perineuraltissues 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 severedegeneration 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.

26. 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.

27. electroneuronography • 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 peak-to-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 electro-myography synonymously with electroneuronography.

28. electroneuronography • 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. • Kartushpointed out that ENoG also can document subclinical facial nerve involvement by tumors, especially acoustic neuromas. Patients with acoustic tumors who had ENoGevidence 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.

30. electromyography • 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 prognosticallyuseful 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.

33. electromyography • 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 motion. • 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 polyphasicreinnervation potentials at 15-18 months, the anastomosis should be considered a failure, and another operation should be considered (e.g.,hypoglossal-facial anastomosis).

34. 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.

35. 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. Prasstermed 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.

36. 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.

37. Unconventional Tests of Facial Nerve Function AntidromicPotentials • 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 orthodromicimpulse will travel distally toward the muscle, whereas an antidromic or retrograde impulse will travel proximally toward the cell body. • Near-field antidromicresponses 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 hemifacialspasm, 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.

38. 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.

39. 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 temporoparietalarea (transcranialstimulation), 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 stylomastoidforamen, could obviously be useful for site-of-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.

40. 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 examination. • 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.

41. Unconventional Tests of Facial Nerve Function transcranial electrical stimulation–induced Facial Motor evoked Potentials • Another more recently developed method involves transcranialelectrical 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 ipsilateralto 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 technique. • It is necessary to use nonvolatile anesthesia for transcranial electrical stimulation (only propofoland narcotic infusions are used for maintenance of anesthesia, as volatile agents adversely affect corticobulbarstimulability). • 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).