Facial nerve tests

tests of facial nerve

1. Tests of facial nerve function Dr. Rajendra Singh Lakhawat

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

3. 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.

4. 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.

5. 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.

6. 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.

7. House- Brackmann Facial Nerve Grading System

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

9. 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.

10. 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.

11. 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.

12. 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.

13. 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.

14. 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.

15. 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.

16. 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.

17. 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.

18. 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.

19. 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.

20. 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).

21. 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.

22. 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.

23. 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.

24. 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%.

25. 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.

26. 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.

27. 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.

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

29. 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.”

30. 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 .

31. 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 .

32. 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 .

33. 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.

34. 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

35. 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.

36. 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.

37. 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.

38. 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 .

39. 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.

40. 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).

41. 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.

42. 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.

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

44. 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.

45. 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 .

46. 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 day s—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.

47. 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

48. 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.

49. 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.

50. 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.

51. 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.

52. 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.

53. 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.

54. 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.

55. 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

56. 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 .

57. 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 .

58. 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.

59. 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.

60. 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.

61. 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.

62. 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

63. 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.

64. 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).

65. 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.

66. 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

67. 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.

68. 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 f ailure , and another operation should be considered (e.g., hypoglossal-facial anastomosis ).

69. 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.

70. 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.

71. 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.

72. 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.

73. 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.

74. 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.

75. 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.

76. 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).

77. 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.

78. 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, 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)

79. 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.

80. 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).

81. 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.

82. 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.

83. 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 ).

84. 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.

85. 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.

86. 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.

87. 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.

88. 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.

89. 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.

90. 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.

91. 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.

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