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Current Otolaryngology  > XV. Facial Nerve > Chapter 67. Anatomy, Physiology, & Testing of the Facial Nerve  >

Facial Nerve Anatomy

The facial nerve is involved in numerous pathologic conditions affecting the temporal bone, ranging from congenital anomalies to degenerative disorders and from infectious to neoplastic conditions. In each instance, a solid understanding of its complex anatomy and physiology is crucial to the physician 's ability to both diagnose and treat disorders of the facial nerve with an awareness of future prognosis .

Embryology

Intratemporal Development

The facial nerve (Figure 671; Table 671) first develops near the end of the first month of gestation, when the acousticofacial primordium, giving rise to both the facial and acoustic nerves, develops adjacent to the primordial inner ear, the otic placode. Anlagen of the geniculate ganglion appear early in the second month of gestation. Adjacent to the developing geniculate ganglion, the acousticofacial primordium differentiates into a caudal trunk, becoming the main trunk of the facial nerve, and a rostral trunk, eventually developing into the chorda tympani nerve. The complex, tortuous course of these two nerves is explained by their separate origin and subsequent intersection. During the sixth week of gestation, the motor division of the facial nerve establishes its position in the middle ear between the membranous labyrinth (an otic placode structure) and the developing stapes (a second arch structure). During this time, the chorda tympani nerve becomes associated with the trigeminal nerve, which carries the chorda tympani on its way to the tongue via the lingual nerve. The greater superficial petrosal nerve, which carries preganglionic parasympathetic fibers toward the pterygopalatine ganglion, also develops during this time period.

Table 671. Facial Nerve Development.


Gestational Month Development
1 Acousticofacial (AF) primordium gives rise to both the facial and acoustic nerves
2 Geniculate ganglion develops
Caudal trunk of AF primordium develops into main trunk of facial nerve (FN)
Rostral trunk of AF primordium develops into chorda tympani nerve
Motor division of FN establishes position between labyrinth and stapes
Chorda tympani nerve becomes associated with trigeminal nerve
Greater superficial petrosal nerve develops
5 extratemporal branches develop
Facial muscles develop independently
3 FN elongates
Fallopian canal develops, continuing through birth
Parotid bud engulfs extratemporal FN
Facial musculature is identifiable and functional
4Birth FN elongates
Fallopian canal continues to develop
Postnatal FN axon myelination, continuing through age 4 years
Lateral location of extratemporal facial nerve gradually medializes under developing mastoid tip

Anatomic relationships of the facial nerve are established by the end of the second gestational month. In subsequent development, the nerve elongates as the temporal bone grows, while the fallopian canal, the bony canal that transmits the facial nerve through the temporal bone, begins to form. Although the fallopian canal begins its development in the fifth gestational month, it is not complete until several years after birth. Incomplete development of the fallopian canal is responsible for the natural dehiscences identified in temporal bone specimens, and may contribute to facial palsies associated with otitis media.

Extratemporal Development

During the sixth gestational week through the end of the second gestational month, all five divisions of the extratemporal nervethe temporal, zygomatic, buccal, mandibular, and cervical branchesare present. During the third month, the parotid bud enlarges and engulfs the facial nerve. The facial muscles (Figure 672), developing independently, are formed at 78 weeks' gestation and must be innervated by the distal facial nerve branches or else the muscle will degenerate , although this critical time period before degeneration is not currently known. By the end of the third gestational month, a majority of the facial musculature is identifiable and functional.

Postnatal Development

At birth, the facial nerve is located just beneath the skin near the mastoid tip as it emerges from the temporal bone, and is vulnerable to the postauricular incision in a young child. As the mastoid tip forms and elongates during childhood however, the facial nerve assumes its more medial and protected position. Individual axons of the facial nerve also undergo myelination until the age of 4 years, an important consideration during electrical testing of the nerve during this time period.

Central Neuronal Pathways

Supranuclear Pathways

The primary somatomotor cortex of the facial nerve, controlling the complex motor function of the face, is located in the precentral gyrus, corresponding to Brodmann areas 4, 6, and 8 (Figure 673). Neural projections from this area making up the corticobulbar tract descend through the internal capsule and then through the pyramidal tracts within the basal pons. In the caudal pons, most of the facial nerve fibers cross the midbrain to reach the contralateral facial nucleus. A small number of facial nerve fibers innervate the ipsilateral facial nucleus, a majority of which are destined for the temporal branch of the nerve. This innervation pattern explains why central nervous system lesions spare the forehead muscle, since they receive input from both cerebral cortices, whereas peripheral lesions involve all branches of the facial nerve.

In addition to these voluntary neural projections to the facial nerve, there is also an extrapyramidal cortical input to the facial nucleus from the hypothalamus, the globus pallidus, and the frontal lobe, all of which control involuntary facial expression associated with emotion. Additional projections to the facial nuclei from the visual system are involved in the blink reflex. Projections from the trigeminal nerve and nuclei contribute to the corneal reflex, whereas those from the auditory nuclei help the eye close involuntarily in response to loud noises.

Facial Nucleus & Brainstem

The efferent projections from the facial motor nucleus emerge dorsomedially to form a compact bundle that loops over the caudal end of the abducens nucleus beneath the facial colliculus or internal genu (or turn ). The neurons then pass between the facial nerve nucleus and the trigeminal spinal nucleus, emerging from the brainstem at the pontomedullary junction (Figure 674).

Nervus Intermedius

The nervus intermedius, or Wrisberg's nerve, mediates taste, cutaneous sensation of the external ear, proprioception, lacrimation, and salivation. The nervus intermedius exits the brainstem adjacent to the motor branch of the facial nerve (Table 672; Figure 675). The nerve commonly clings to the adjacent cochleovestibular nerve complex rather than the facial nerve and crosses back to the seventh nerve as it approaches the internal auditory meatus.

Table 672. Subdivisions and Functions of the Facial Nerve.


Facial Nerve Subdivision Function
Branchial motor Muscles of facial expression
  Posterior belly of digastric muscle
  Stylohyoid muscle
  Stapedius muscle
Visceral motor Salivationlacrimal, submandibular, and sublingual
  Nasal mucosa or mucous membrane
General sensory Sensory to auricular concha
  External auditory canal
  Tympanic membrane
Special sensory Chorda tympani nervetaste to anterior two- thirds of the tongue


General visceral efferent fibers of the nervus intermedius are preganglionic parasympathetic neurons that innervate the lacrimal, submandibular, sublingual, and minor salivary glands. The cell bodies of these nerves arise in the superior salivatory nucleus and join the facial nerve after it has passed the abducens nucleus. They travel together until reaching the geniculate ganglion in the temporal bone. At this point, the greater superficial petrosal nerve branches off, composed of neurons destined for the pterygopalatine ganglion. The greater superficial petrosal nerve ultimately innervates the lacrimal, minor salivary, and mucosal glands of the palate and nose. Remaining fibers form part of the chorda tympani nerve, proceed to the submandibular ganglion, and eventually proceed to the submandibular and sublingual salivary glands.

The special visceral afferent fibers, which also form a portion of the chorda tympani nerve, receive input from the taste buds of the anterior two thirds of the tongue, as well as the hard and soft palates (Figure 676). These sensory afferents for taste have their cell bodies in the geniculate ganglion and will eventually synapse in the medulla, in the nucleus solitarius.

The general sensory afferent neurons of the nervus intermedius are responsible for cutaneous sensory information from the external ear canal and postauricular region. These cutaneous sensory fibers enter the spinal trigeminal tracts without synapsing in the geniculate ganglion.

Cerebellopontine Angle

The facial nerve leaves the brainstem at the pontomedullary junction (see Figure 674), where it lies in close approximation to the vestibulocochlear nerve. This intimate relationship takes on critical importance when lesions such as a vestibular schwannoma arise in the region of the cerebellopontine angle, a common location for central nervous system tumors . In this location, the facial nerve is placed in jeopardy both during the growth of the tumor and during attempted surgical resection in this area.

During its lateral course through the cerebellopontine angle and internal auditory canal, the relative positions of the facial and cochleovestibular nerves change by rotating 90. In the cerebellopontine angle, the facial nerve is covered with pia, is bathed in cerebrospinal fluid, and is devoid of epineurium, leaving it susceptible to manipulation trauma during intracranial surgery.

Intratemporal Nerve Pathways

After traversing the cerebellopontine angle, the facial nerve enters the temporal bone along the posterior face of the petrous bone. Within the temporal bone, the facial nerve successively passes through four regions before its exit out of the stylomastoid foramen: (1) the internal auditory canal, (2) the labyrinthine segment, (3) the intratympanic segment, and (4) the descending segment (Figures 677, 678, and 679). From the lateral end of the internal auditory canal to its exit out the stylomastoid foramen, the nerve travels approximately 3 cm within the fallopian canal.



Internal Auditory Canal

The facial nerve enters the temporal bone along the posterior face of the petrous bone, piercing the internal auditory meatus. At the lateral end of the internal auditory canal (IAC), the traverse crest divides the IAC into superior and inferior portions. The superior portion is in turn further divided by the smaller and more laterally located vertical crest or "Bill's bar." At this lateral portion of the IAC, the anatomy is most consistent: The superior portion is occupied by the facial nerve anteriorly and the superior vestibular nerve posteriorly (see Figure 678). Within the IAC, the dural covering of the facial nerve is transformed to epineurium.

Labyrinthine Segment

At the lateral portion of the IAC, the facial nerve pierces the meatal foramen to enter the labyrinthine segment. The labyrinthine segment is notable in that it is the narrowest portion of the fallopian canal, where it averages < 0.7 mm in diameter, occupies the canal to the greatest proportional extent, and is lined by a fibrous annular ligament. As a result, it is believed that infections or inflammations causing edema of the facial nerve within this region can lead to temporary or permanent paralysis of the nerve, such as in Bell palsy.

The geniculate ganglion is considered the end of the labyrinthine segment of the nerve and lies just superior to the nerve. Arising from the geniculate ganglion is the greater superficial petrosal nerve, containing preganglionic parasympathetic fibers destined for the lacrimal gland, as well as for the nasal and palatine mucosal glands. The nerve also contains some minor taste neurons that supply the posterior palate.

Tympanic Segment

At the geniculate ganglion, the facial nerve makes its first genu and becomes the tympanic segment of the facial nerve, so called because it travels within the middle ear space. This portion of the nerve is approximately 10 mm long. Landmarks for the nerve at this location include the cochleariform process, which gives rise to the tensor tympani muscle, and the "cog," a small bony prominence projecting from the roof of the epitympanum. The facial nerve then travels posteriorly, just superior to the oval window and stapes. The nerve then curves inferiorly at its second genu, just posterior to the oval window, pyramidal process, and stapedial tendon, and anterior to the horizontal semicircular canal. It is this portion of the nerve that is most susceptible to injury during surgery because processes such as cholesteatoma frequently erode the bone covering the facial nerve in this region, leaving it precariously exposed.

In addition to bony dehiscence from pathology, natural fallopian canal dehiscences have also been described in cadaver specimens, a majority of which occurred in the tympanic segment. In more than 80% of cases, the dehiscences involved the portions of the canal adjacent to the oval window.

Vertical, Descending, or Mastoid Segment

After the second genu, the nerve traverses the synonymously named vertical, descending, or mastoid segment en route to the stylomastoid foramen. As the facial nerve descends inferiorly in this portion, it gradually assumes a more lateral position. Important branches of the nerve in this segment include the nerve to the stapedius muscle and the chorda tympani nerve. As it arises from the facial nerve, the chorda tympani nerve makes an approximately 30 angle and delineates a triangular space known as the "facial recess," an important surgical route of entry into the middle ear space.

In its most inferior portion, the facial nerve takes on a close proximity to the digastric ridge and muscle, where the nerve is consistently medial and anterior to these structures. On exiting the stylomastoid foramen, the nerve becomes encased in the thick fibrous tissue of the cranial base periosteum and digastric muscle.

Although the facial nerve most commonly descends in its vertical segment as a single nerve, bifurcations, trifurcations, and hypoplasia of the facial nerve have been found within the mastoid segment. In addition, the chorda tympani nerve has been noted to arise from the facial nerve anywhere from the stylomastoid foramen to the geniculate ganglion.

Peripheral Facial Nerve Anatomy

The facial nerve exits the skull base through the stylomastoid foramen, between the mastoid tip laterally and the styloid process medially (Figure 6710). At the stylomastoid foramen, the facial nerve passes into the parotid gland, typically as a single large trunk. The nerve then divides within the parotid gland into its temporofacial and cervicofacial branches. Rarely, this division can occur within the temporal bone and exit the stylomastoid foramen as separate branches.

Within the parotid gland, the nerve can assume numerous configurations, with frequent anastomoses between branches. However, generally five main branches of the nerve can be identified: (1) the temporal, (2) the zygomatic, (3) the buccal, (4) the mandibular, and (5) the cervical. The temporal branch innervates the frontalis muscle, which allows for the voluntary raising of eyebrows . The zygomatic branch innervates the orbicularis oculi muscle and is critical for proper eye closure. The buccal nerve innervates the buccinator and orbicularis oris, allowing for proper mouth closure and cheek muscle activity. The mandibular branch innervates the platysma. The posterior auricular nerve, arising just after the exit of the facial nerve from the stylomastoid foramen, sends branches to the occipitalis muscle posteriorly on the skull.

Baxter A. Dehiscence of the fallopian canal: an anatomical study. J Laryngol Otol. 1971;85:587. (An anatomic study describing naturally occurring dehiscences of the facial nerve.) [PMID: 5581361]

Courbille J. The nucleus of the facial nerve: the relation between cellular groups and peripheral branches of the nerve. Brain. 1966;1:338. (A classic study of the anatomy of the facial nerve nucleus.) [PMID: 5961910]

Fowler E. Variations in the temporal bone course of the facial nerve. Laryngoscope. 1961;91:937.

Gasser RF. The development of the facial nerve in man. Ann Otol Rhinol Laryngol. 1967;76:37. (A classic manuscript on the embryologic development of the facial nerve.) [PMID: 6020340]

Gasser RF. The development of the facial nerve muscles in man. Am J Anat. 1967;120:357. (A classic manuscript on the development of the muscles of facial expression.) [PMID: 5447369]

Gasser RF. The early development of the parotid gland around the facial nerve and its branches in man. Anat Rec. 1970;167:63. (A classic manuscript on the development of the parotid gland in relation to the facial nerve.) [PMID: 5447369]

Gasser RF, May M. Embryonic development of the facial nerve. In: May M, ed. The Facial Nerve. New York: Thieme, Inc., 1987:3.

Ge XX, Spector GJ. Labyrinthine segment and geniculate ganglion of facial nerve in fetal and adult human temporal bones. Ann Otol Rhinol Laryngol Suppl. 1981;90(4 Pt 2):1. (A classic study of the intratemporal portion of the facial nerve.) [PMID: 6792965]

Nager GT, Proctor B. Anatomic variations and anomalies involving the facial canal. Otolaryngol Clin North Am. 1991;24:531. (A classic, comprehensive study of the anatomy of the facial canal.) [PMID: 1762775]

Proctor B, Nager GT. The facial canal: normal anatomy, variations and anomalies. II. Anatomical variations and anomalies involving the facial canal. Ann Otol Rhinol Laryngol Suppl. 1982;97:45. (A classic study of the anatomy of the facial canal.) [PMID: 6814329]

Rhoton AL Jr, Kobayashi S, Hollinshead WH. Nervus intermedius. J Neurosurg. 1968;29:609. (A classic study of the anatomy of the nervus intermedius.) [PMID: 5708034]

Sherwood CC. Comparative anatomy of the facial motor nucleus in mammals, with an analysis of neuron numbers in primates. Anat Rec A Discov Mol Cell Evol Biol. 2005;287(1):1067. (A contemporary study of the central motor pathways of the facial nerve.) [PMID: 16200649]

Toth M, Moser G, Patonay L, Olah I. Development of the anterior chordal canal. Ann Anat. 2006;188(1):7. (A contemporary study of the chorda tympani nerve pathway.) [PMID: 16447906]

Vidic B, Wozniak W. The communicating branch of the facial nerve to the lesser petrosal nerve in human fetuses and newborns. Arch Anat Histol Embryol. 1969;52(5):369. (A classic anatomic study of the communicating branch of the facial nerve.) [PMID: 4926584]

Facial Nerve Physiology

Anatomic Considerations

The facial nerve trunk consists of approximately 10,000 nerve fibers, approximately 7000 of which are myelinated motor fibers. The facial nerve sheath consists of several layers . The endoneurium, closely adherent to the layer of Schwann cells of the axons, surrounds each nerve fiber. The perineurium, which is the intermediate layer surrounding groups of fascicles, provides tensile strength to the nerve and is believed to represent the primary barrier to the spread of infection. The outermost layer of the nerve is the epineurium. This outer layer contains the vasa nervorum, which provides the blood supply to the nerve.

Classification of Facial Nerve Degeneration

If the facial nerve is injured, various degrees of injury may result. The most widely used model of clinical-pathologic classification of nerve injury is the classification originally proposed by Sunderland (Figure 6711):

(1) First-degree injuries, also referred to as neuropraxia , are characterized by the blockage of axoplasm flow within the axon. Although an action potential cannot be propagated across the lesion site, a stimulus applied distal to the lesion will conduct normally to produce an evoked response.
(2) Second-degree injuries entail axonal and myelin disruption distal to the injury site as a result of the progression of a first-degree injury. Such injuries eliminate the propagation of an externally applied stimulus as wallerian degeneration of the axon ensues.
(3) Third-degree injuries involve complete disruption of the axon, including its surrounding myelin and endoneurium.
(4) Fourth-degree injuries entail the complete disruption of the perineurium.
(5) Fifth-degree injuries entail the disruption of the epineurium.
(6) Sixth-degree injuries, a proposed addition to the Sunderland classification by later authors, takes into account the observed patterns of blunt and penetrating injuries of the nerve. These injuries are characterized by normal function through some fascicles and varying degrees of injury (first-degree through fifth-degree injuries), differentially involving fascicles across the nerve trunk.

Central to Sunderland's classification is the notion that axonal recovery depends on the integrity of the connective tissue elements of the nerve trunk. This model predicts a high likelihood for the complete recovery of peripheral innervation when endoneurial tubules remain intact to support reinnervation, as is the case with first- and second-degree injuries. In contrast, disruption of the endoneuriuma third-degree injury or worse in this model increases the likelihood of irreversible axonal injury and aberrant patterns of regeneration.

An example of abnormal neural regrowth is "crocodile tears," or increased lacrimation associated with eating . It occurs when efferent fibers normally targeted to travel with the chorda tympani nerve to the submandibular and sublingual glands are misdirected through the greater superficial petrosal nerve to the lacrimal gland. This results in parasympathetic innervation of the lacrimal gland as well as the normal target, the salivary glands.

Moran LB, Graeber MB. The facial nerve axotomy model. Brain Res Brain Res Rev. 2004;44(2-3):154. (Contemporary, scientific study of facial nerve injury and repair.) [PMID: 15003391]

Myckatyn TM, Mackinnon SE. The surgical management of facial nerve injury. Clin Plast Surg. 2003;30(2):307. (Review of the management of injuries to the facial nerve based on clinical presentation.) [PMID: 12737358]

Sunderland S, Cossar DF. The structure of the facial nerve. Anat Rec. 1953;116(2):147. (A classic study of the structure of the facial nerve that helped lead to Sunderland's classification of facial nerve injury.) [PMID: 13065751]

Facial Nerve Testing

The impaired transmission of neural impulses can result from physiologic blockage (in the absence of nerve fiber degeneration) and axonal discontinuity with wallerian degeneration. Because the clinical presentation of a facial paralysis does not distinguish between simple conduction block and axonal disruption, investigators have explored an array of testing procedures designed to define the extent of nerve injury (Table 673).

Table 673. Tests of Facial Nerve Function.


Test Measure Advantages Disadvantages
Minimal excitability test The lowest stimulus intensity that consistently excites all branches on the uninvolved side

Portability

Patient comfort

Easy to perform

Subjective

Relies on visual detection

Maximal excitability test Compares response on involved vs. uninvolved side of face

Portability

Patient comfort

Easy to perform

Subjective

Relies on visual detection

Electroneuronography and evoked electromyograph (EMG)

Assesses the facial motor response to a supramaximal stimulus

Records the compound muscle action potential

Reflects % motor fibers of the facial nerve that have undergone degeneration

< 90% denervation prognosticates excellent recovery

Repeated every other day to detect ongoing degeneration beyond the 90% critical level

Useful early in the course of facial paralysis

Some measures useful in predicting the ultimate level of spontaneous recovery

Patient discomfort
Electromyography

Measures postsynaptic membrane potentials

Motor unit potentials in five muscle groups in the first 3 days after onset of palsy associated with good outcome in > 90% of patients

Precision characterization of motor units

Possible pitfalls with early testing

Sparse residual motor units that suggest a favorable outcome may be evident despite severe injury to large portions of fibers that are at risk for degeneration

Antidromic conduction

F wave represents activity in facial muscles generated by antidromically activated motor neurons

In Bell palsy, F wave seen only after recovery begun

Can provide direct and immediate assessment of facial nerve function

Limited dynamic range and prognostic value

Primarily animal testing, research

Magnetic simulation Electromagnetic coil to produce neural activation Intensity of the stimulus is minimally attenuated by intervening tissue

Limited clinical utility

Difficult to interpret results

Trigeminofacial reflex

EMG recording of the blink reflex

Compares responses between the affected and normal sides

Abolished R1 reflex associated with little chance of recovery in the first 2 months after onset of paralysis

Easy to perform May be limited by small response amplitude

In an initial evaluation of patients with acute facial paralysis, the clinician should aim to determine the prognosis for recovery as well as the cause of the paralysis. Early determination of the prognosis for recovery may permit intervention both to minimize nerve injury and to optimize regeneration.

Topognostic Testing

Topognostic test batteries are intended to determine the level of facial nerve injury by testing peripheral facial nerve function. The underlying hypothesis is that injury to the facial nerve at a particular location will affect all branches proximal to the lesion, yet leave distal branches with normal function. For example, if tearing is diminished (Schirmer test), the lesion is assumed to be proximal to the point at which the greater superficial petrosal nerve branches from the geniculate ganglion. Additional testing includes immittance testing (abnormal stapedial muscle function reflecting nerve impairment above the stapedial motor branch), and salivary secretion and taste testing (chorda tympani nerve function). Although attractive in theory, topognostic modalities have often provided inconsistent information on the level of neural injury, since lesions of the nerve can affect the motor, sensory, and autonomic portions of the nerve differently.

For example, the Schirmer tear test has been shown to have an accuracy rate of only 60% using intraoperative electrical stimulation to specify the site of nerve conduction block in Bell palsy. However, the Schirmer test does have great practical value in assessing tear production and the need for adjunctive measures for eye care.

Electrophysiologic Testing

The interpretation and validity of electrophysiologic testing of an acute facial palsy rests on two tenets with regard to nerve fiber function:

(1) Segmentally demyelinated fibers maintain the capacity to propagate a stimulus, albeit at a higher threshold, than that of normal fibers. Anatomically intact fibers will therefore continue to propagate an applied stimulus, whereas those that have become disrupted and subsequently degenerated will not.
(2) By estimating the proportion of degenerated motor fibers, a clinician may distinguish palsies that will fail to recover spontaneously and will produce long- term sequelae.

Ideally, electrophysiologic testing provides an index of the severity of injury to the nerve trunk by reflecting the proportion of motor fibers that have progressed beyond a first-degree injury. Correlation of the ultimate level of recovery with early electrophysiologic findings determines the prognostic value of the test in identifying the subset of facial palsy patients who will not obtain satisfactory, spontaneous recovery.

Electrophysiologic tests can only indirectly assess the severity of injury to the intratemporal facial nerve; because this portion of the nerves lies entirely within the temporal bone, electrical stimulation proximal to the site of conduction blockade is possible only when the nerve is activated intracranially. For this reason, clinical tests of facial nerve function rely on measures of nerve stimulation distal to the stylomastoid foramen. Even in the presence of severe neural injury, conduction distal to a lesion continues until its axoplasm is consumed and wallerian degeneration ensues. This process requires 4872 hours to progress from intratemporal to extratemporal segments, thereby rendering electrical stimulation tests falsely normal during this period. Routine electrophysiologic tests therefore fail to detect nerve conduction as it occurs, thereby delaying the differentiation of neuropraxia from degeneration.

Nerve Excitability Testing

Minimal excitability testing with the Hilger nerve stimulator has provided a readily accessible method of facial nerve assessment. The test is indexed according to the thresholds for visually detectable activity generated by surface stimulation of a facial nerve branch. The test reflects elevated thresholds for neuromuscular stimulation produced by axonal disruption and degeneration. The lowest stimulus intensity that consistently excites all branches on the uninvolved side establishes the normal threshold. A 2.03.5 mA difference between the uninvolved and involved sides is considered abnormal and suggests impending denervation. Additional advantages of the test include the portability of the equipment and less patient discomfort compared with other tests (such as the maximal stimulation test).

A disadvantage of the test is the subjective nature of the measured response, relying on the visual detection of a limited number of facial muscles. In addition, current threshold levels for peripheral branches are likely to selectively activate large nerve fibers with lower thresholds and those fibers closer to the stimulating electrode, thereby excluding an unknown proportion of motor fibers from the assessment.

Dumitru D, Walsh NE, Porter LD. Electrophysiologic evaluation of the facial nerve in Bell's palsy. A review. Am J Phys Med Rehabil. 1988;67(4):137. (Comprehensive review of electrophysiologic facial nerve testing that is still timely .) [PMID: 3041998]

Gantz BJ, Gmur A, Fisch U. Intraoperative evoked electromyography in Bell's palsy. Am J Otolaryngol. 1982;3(4):273. (The technique of intraoperative evoked electromyography is described in detail. The limited extent of the blocked motor fibers suggests that segmental, rather than total, intratemporal decompression is needed in Bell palsy.) [PMID: 7149140]

Gates GA. Nerve excitability testing: technical pitfalls and threshold norms using absolute values. Laryngoscope. 1993;103(4 Pt 1):379. (Practical review of nerve excitability testing.) [PMID: 8459745]

Ikeda M, Abiko Y, Kukimoto N, Omori H, Nakazato H, Ikeda K. Clinical factors that influence the prognosis of facial nerve paralysis and the magnitudes of influence. Laryngoscope. 2005;115(5):855. (Contemporary study evaluating the factors resulting in facial nerve recovery outcomes using clinical and electrophysiologic testing.) [PMID: 15867653]

Lewis BI, Adour KK, Kahn JM, Lewis AJ. Hilger facial nerve stimulator: a 25-year update. Laryngoscope. 1991;101(1 Pt 1):71. (Review of the impact of the Hilger nerve stimulator on facial nerve assessment.) [PMID: 1984555]

Maximal Stimulation Test

A test of maximal electrical stimulation can be used to determine whether nerve degeneration has developed in the course of an acute facial paralysis. It involves a transcutaneous electrical impulse designed to saturate the nerve with current, activating all functioning fibers. The response on the involved side is characterized as being (1) equal to the contralateral side, (2) minimally diminished (50% of normal), (3) markedly diminished (< 25% of normal), or (4) absent.

When the response is markedly diminished or absent within the first 2 weeks of the clinical paralysis, it has been found that there is a 75% chance of incomplete facial nerve recovery. When the response completely disappeared within the first 10 days, recovery was typically incomplete and significant sequelae ensued. Conversely, if responses were symmetric during the first 10 days of a clinical paralysis, complete return was found in more than 90% of patients tested . The use of supramaximal stimulation provides sensitivity and consistency in testing when used early in the course of an acute facial paralysis. However, the interpretation of the maximal stimulation test relies on a subjective evaluation of the visually graded evoked response.

Gates GA. Nerve excitability testing: technical pitfalls and threshold norms using absolute values. Laryngoscope. 1993;103(4 Pt 1):379. (Practical review of nerve excitability testing.) [PMID: 8459745]

Ikeda M, Abiko Y, Kukimoto N, Omori H, Nakazato H, Ikeda K. Clinical factors H, Nakazato H, Ikeda K. Clinical factors that influence the prognosis of facial nerve paralysis and the magnitudes of influence. Laryngoscope. 2005; 115(5):855. (Contemporary study evaluating the factors resulting in facial nerve recovery outcomes using clinical and electrophysiologic testing.) [PMID: 15867653]

May M. Nerve excitability test in facial palsy: limitations in its use based on a study of 130 case. Laryngoscope. 1972;82:2122. (This study describes the usefulness and drawbacks of the facial nerve excitability test based on the author's personal experience.) [PMID: 5081746]

May M, Blumenthal F, Klein S. Acute Bell's palsy: prognostic value of evoked electromyography, max stimulation and other electrical tests. Am J Otol. 1983;5:107. (Evoked electromyography and maximal stimulation tests were the most accurate electrical tests for predicting the course of acute facial paralysis when performed serially within the first 10 days after onset.) [PMID: 6881304]

Evoked Electromyography & Electroneuronography

Similar to the maximal stimulation test, evoked electromyography (EEMG) or electroneuronography (ENoG) assesses the facial motor response to a supramaximal stimulus. In contrast to maximal stimulation testing, the EEMG technique records the compound muscle action potential (CMAP) with surface electrodes placed in the nasolabial fold. The CMAP can be graphically displayed for quantitative analysis and printed for the medical record (Figure 6712). Waveform responses are analyzed to compare peak-to-peak amplitudes between normal and involved sides.

Patients with incomplete paralyses due to Bell palsy invariably recover function to normal or near-normal levels and do not require EEMG evaluation. The reappearance of facial movement within 34 weeks after onset also predicts an excellent prognosis for functional recovery. EMG sampling of motor activity to detect visually imperceptible facial function is advised.

When assessed within a critical time window, reductions in the amplitude of the EEMG response of the affected side are considered to reflect the percentage of motor fibers of the facial nerve that have undergone degeneration. Facial EEMG is most reliable during the initial phase of accelerated denervation when reliable results can be obtained (ie, in the first 23 weeks after the onset of a paralysis due to Bell palsy or herpes zoster oticus). When neuropraxic fibers become "de-blocked" either in the recovery phase or later as axons regenerate peripherally, stimulated nerve fibers discharge asynchronously. Because regenerated fibers do not discharge in synchrony , the response is disorganized and consequently diminished. This phenomenon imposes a time constraint on the reliability of EEMG testing that must be considered in interpreting the test results.

ENoG is most useful early in the course of facial paralysis. More than 50% of patients with complete paralysis who exhibit a 90% reduction in CMAP amplitude have less than a satisfactory, spontaneous return of facial function. When results demonstrate < 90% denervation (> 10% in CMAP amplitude relative to the normal side), excellent recovery has been uniformly observed.

It is recommended that EEMG testing should be repeated on an every-other-day basis to detect ongoing degeneration beyond the 90% critical level. The time span of reduced electrical excitability (ie, the velocity of denervation as demonstrated by repeated testing) and the degree of degradation of the CMAP response (ie, the nadir of the response) are most useful in predicting the ultimate level of spontaneous recovery. The earlier the EEMG response drops to 10% of normal, the worse the prognosis is. Some surgeons have advocated a decompression of the facial nerve proximal to the geniculate ganglion if the 90% level is reached, although this decompression must be performed within 2 weeks of the onset of the facial palsy.

Chung WH, Lee JC, Cho Do Y, Won EY, Cho YS, Hong SH. Waveform reliability with different recording electrode placement in facial electroneuronography. J Laryngol Otol. 2004;118(6):421. (Examining four parameters of facial nerve electroneuronography, the authors found that with the electrode placed on the nasal ala, the threshold was significantly lower, thus concluding that placement of the recording electrode on the nasal ala is the preferred method.) [PMID: 15285858]

Coker NJ. Facial electroneuronography: analysis of techniques and correlation with degenerating motoneurons. Laryngoscope. 1992;102:747. (Comprehensive review of electroneuronography.) [PMID: 9226049]

Fisch U. Maximal nerve excitability testing vs electroneuronography. Arch Otolaryngol. 1980;106:352.

Fisch U. Surgery for Bell's palsy. Arch Otolaryngol. 1981;107:1. (This study shows that the advantage of electroneuronography vs maximal nerve excitability test (NET) is the quantitative analysis of the number of degenerated fibers and the assessment of an accurate degeneration profile in Bell palsy.) [PMID: 6246866]

Gantz BJ, Rubinstein JT, Gidley P, Woodworth GG. Surgical management of Bell's palsy. Laryngoscope. 1999;109(8):1177. (The study showed that electroneurography in with voluntary EMG successfully predicts that surgical decompression within 2 weeks of onset medial to the geniculate ganglion significantly improves the chances of normal or near-normal return of facial function in the group that otherwise has a high probability of a poor result.) [PMID: 10443817]

May M, Blumenthal F, Klein S. Acute Bell's palsy: prognostic value of evoked electromyography, max stimulation and other electrical tests. Am J Otol. 1983;5:107. (Evoked electromyography and maximal stimulation tests were the most accurate electrical tests for predicting the course of acute facial paralysis when performed serially within the first 10 days after onset.) [PMID: 6881304]

Sillman JS, Niparko JK, Lee SS, Kileny PR. Prognostic value of evoked and standard electromyography in acute facial paralysis. Otolaryngol Head Neck Surg. 1992;107:377. (The findings from this study support previous reports of the prognostic value of evoked electromyography in idiopathic facial paralysis, but suggest that this test may have less predictive value in the evaluation of facial paralysis as a result of trauma.) [PMID: 1408222]

Thomander L, Stalberg E. Electroneurography in the prognostication of Bell's palsy. Acta Otolaryngol. 1981;92:221. (Using electroneurography, the prognosis for recovery for the individual patient can be judged with relatively high accuracy on day 4 [70%].) [PMID: 7324892]

Electromyography

The electromyographic (EMG) response reflects postsynaptic membrane potentials that may be either initiated at the neuromuscular junction with voluntary activation or generated spontaneously across the muscle membrane. These potentials are easily recorded with either bare-tip (monopolar) or concentric (coaxial) needle electrodes.

Voluntarily and spontaneously generated facial motor responses can help to characterize the condition of motor units with precision. However, the results obtained with testing in any single field should be buttressed with testing in adjacent fields. Motor unit potentials in four of five muscle groups in the first 3 days after the onset of an acute facial paralysis is associated with a satisfactory outcome in more than 90% of patients. Motor units in two of three muscle groups predicted a satisfactory outcome in 87% of patients. When motor units were either limited to one muscle group or abolished, satisfactory recovery was found in only 11% of cases.

Although these findings suggest a role for early EMG testing in prognosticating functional recovery, others have noted potential pitfalls of early EMG testing that may mislead the examiner . Sparse residual motor units that suggest a favorable outcome may be evident despite severe injury to large portions of fibers that are at risk for degeneration. The clinical evidence of this was noted as an unsatisfactory recovery despite voluntary motor potentials in 38% of Bell palsy patients. These observations suggest that EMG assessment should be performed within at least two muscle groups to more accurately assess the degree of denervation.

Early in the course of an acute facial paralysis, preserved facial motor activity may escape clinical inspection and yet provide prognostic information when combined with other testing modalities. For example, subclinical motor activity that is still detectable by the EMG may complement the use of evoked electromyography in the early phase of a clinical paralysis. EMG monitoring is of limited use in detecting early degeneration, since electrical evidence of nerve degeneration is absent in the first 10 days of the paralysis. Ten to fourteen days after the onset of a clinical paralysis, EMG recordings reflect the dynamic resting membrane potentials of postsynaptic elements. In this phase, muscle membrane, deprived of "trophic" substances that are normally transported through the axon, undergoes changes that destabilize the resting potential. These changes produce spontaneous depolarizations reflected in the EMG as fibrillation potentials. Such changes are interpreted as indicative of persistent denervation.

Substantial axonal loss and impaired reinnervation yield fibrillation potentials as long as postsynaptic membranes remain electrically active. With persistent denervation, EMG recordings are silent and the short burst of discharges normally found on needle insertion is absent. Conversely, successful reinnervation generates high-frequency polyphasic potentials that increase in amplitude and duration and replace fibrillation potentials. In rare cases of protracted paralysis due to Bell palsy, longitudinal EMG evaluations detect persistent nerve degeneration or reinnervation.

Bozorg Grayeli A, Kalamarides M, Fraysse B et al. Comparison between intraoperative observations and electromyographic monitoring data for facial nerve outcome after vestibular schwannoma surgery. Acta Otolaryngol. 2005;125(10):1069. (A four-channel facial EMG device was shown to be an excellent indicator of good immediate facial function outcome during vestibular schwannoma surgery.) [PMID: 16298788]

Cronin GW, Steenerson RL. The effectiveness of neuromuscular facial retraining combined with electromyography in facial paralysis rehabilitation . Otolaryngol Head Neck Surg. 2003; 128(4):534. (This study demonstrates that neuromuscular facial retraining exercises and electromyography are effective for improving facial movements in patients with recovering facial nerve paralysis.) [PMID: 12707657]

Dumitru D, Walsh NE, Porter LD. Electrophysiologic evaluation of the facial nerve in Bell's palsy: a review. Am J Phys Med Rehabil. 1988;67(4):137. (Comprehensive review of electrophysiologic facial nerve testing that is still timely.) [PMID: 3041998]

Gordon AA, Friedberg MD. Current status of testing for seventh nerve lesions. Otolaryngol Clin North Am. 1978;11:301. (Electromyography may assist in prognosticating a functional return, determining neural conduction across the site of injury and following reinnervation in the recovery period.) [PMID: 3041998]

Granger C. Prognosis in Bell's palsy. Arch Phys Med Rehabil. 1976; 57:33. (Using clinical and electromyographic methods , it should be possible to forecast recovery within 3 days after onset to preselect patients in need of any proposed curative treatment program designed to salvage the facial nerve.) [PMID: 1247374]

May M, Blumenthal F, Klein S. Acute Bell's palsy: prognostic value of evoked electromyography, max stimulation and other electrical tests. Am J Otol. 1983;5:107. (Evoked electromyography and maximal stimulation tests were the most accurate electrical tests for predicting the course of acute facial paralysis when performed serially within the first 10 days after onset.) [PMID: 6881304]

Sillman JS, Niparko JK, Lee SS, Kileny PR. Prognostic value of evoked and standard electromyography in acute facial paralysis. Otolaryngol Head Neck Surg. 1992;107:377. (The findings from this study support previous reports of the prognostic value of evoked electromyography in idiopathic facial paralysis, but suggest that this test may have less predictive value in the evaluation of facial paralysis as a result of trauma.) [PMID: 1408222]

Facial Nerve Assessment with Central Activation

The previously described electrodiagnostic tests indirectly assess the severity of injury to the intratemporal segment of the facial nerve. Investigators have explored alternate testing procedures in which the facial nerve is activated central to the presumed site of involvement within the temporal bone.

Antidromic Conduction

Testing via antidromic (retrograde) conduction provides an alternative to electrodiagnostic testing of peripheral fibers that, at least theoretically, can provide a direct and immediate assessment of facial nerve function. Antidromic conduction of electrical activity in the facial nerve can be measured with near- and far-field techniques in animals (Figure 6713) and clinically with middle ear recording electrodes. It has been demonstrated that the far-field response to antidromic stimulation represented composite activity along the facial pathway and did not appear to reflect stimulation of the facial nerve at a specific site along the intracranial segment.

The F wave represents activity in facial muscles generated by antidromically activated motor neurons and contains no reflex components . For electrodiagnostic purposes, F waves evoked by electrical stimulation may be recorded with intramuscular needle electrodes. This response has a long latency and is normally small in amplitude, thereby limiting its dynamic range and prognostic value. In patients with Bell palsy, electrical stimulation of the nerve reliably produces F-wave responses only after recovery has begun.

Magnetic Stimulation

Transcranial magnetic stimulation uses an electromagnetic coil to produce neural activation. This method of neural activation is unique in that the intensity of the stimulus is minimally attenua ted by intervening tissue. This feature enables central activation via a transcranial application of induced current. Animal studies have demonstrated that transcranial magnetic stimulation can be used to activate the facial nerve centrally , although the precise site of stimulation is difficult to determine. Observations suggest that the evoked response is likely due to excitation of the facial nerve intratemporally or intracranially rather than via cortical or brainstem excitation .

Clinical experience with electromagnetic stimulation in pathologic states, including Bell palsy, is in keeping with observations that localize the lesion intratemporally. In 11 patients with recent onset of Bell palsy, none demonstrated evoked CMAPs with magnetic stimulation. The lack of response is attributed to the elevation in threshold associated with segmental demyelination and the inability of the current generated by the electromagnetic field to reach the threshold.

Further refinement in the application and interpretation of transcranial magnetic stimulation for prognosticating facial nerve lesions awaits further understanding of the actual site of activation. The development of coils that facilitate a more focused current offers the possibility of site-specific stimulation of the central facial motor tract and intracranial segment of the facial nervesites proximal to the typical sites of nerve injury for most acute facial paralyses.

Trigeminofacial Reflex

The blink reflex can be tested clinically to assess the efferent arc contributed by cranial nerve VII. Electromyographic recording of the trigeminofacial reflex provides a quantitative assessment of facial nerve conduction via activation of the facial nucleus centrally. This technique records action potentials reflexively generated in the orbicularis oculi muscle in response to an electrical stimulus applied to the supraorbital area (V1 branch). Responses between the affected and normal sides are compared to provide quantitative assessment of the reflex, thereby providing a measure of the functional integrity of the facial nerve. Trigeminofacial reflex testing of acute facial paralysis may be limited by small response amplitudes.

An abolished R1 trigeminofacial reflex response is associated with little chance of recovery in the first 2 months after onset of paralysis. Preserved, early R1 responses predicted return to normal facial nerve function within the first month. The performance of this test in selecting those patients with an absent R1 response who have a poor long-term prognosis is yet to be evaluated.

Hallett M, Cohen LG. Magnetism: a new method for stimulation of nerve and brain. JAMA. 1989;262:538. (Describes the use of magnetic stimulation as a means of activating cortical regions of the brain.)

Kartush JM, Bouchard KB, Graham MD, Linstrom C. Magnetic stimulation of the facial nerve. Am J Otol. 1989;10:14. (Normal volunteers and one patient with acute facial paralysis were studied with both magnetic and electric stimulation of the facial nerve.) [PMID: 2719085]

Kartush JM, Garcia P, Telian SA. The source of far-field antidromic facial nerve potentials. Am J Otolaryngol. 1987;8:199. (This study identifies the generator sites of the far-field antidromic facial nerve response in dogs and shows that complete transection of the facial nerve at the CPA has little effect on the responses.) [PMID: 3631416]

Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice. Philadelphia: FA Davis, 1983.

Maccabee PJ, Amassian VE, Cracco RQ, Cracco JB, Anziska BJ. Intracranial stimulation of the facial nerve in humans with the magnetic coil. Electroencephalogr Clin Neurophysiol. 1988;70:350. (This noninvasive technique may be useful in evaluating patients with peripheral facial nerve disorders, including Bell palsy.) [PMID: 2458243]

Nakatani H, Iwai M, Takeda T, Hamada M, Kakigi A, Nakahira M. Waveform changes in antidromic facial nerve responses in patients with Bell's palsy. Ann Otol Rhinol Laryngol. 2002; 111(2):128. (This study demonstrates that monophasic or flat waves with a low facial score strongly suggest nerve degeneration and that antidromic facial nerve response is recommended as a method of diagnosing paralysis and monitoring the progression of intratemporal facial nerve damage during its early stages.) [PMID: 11860064]

Niparko JK, Kartush JM, Bledsoe SC, Graham MD. Antidromically evoked facial nerve response. Am J Otolaryngol. 1985;6:353. (Results of antidromic conduction testing suggest that the recorded potentials measured represent antidromic activation of the facial nerve, further suggesting that antidromic testing may provide a useful means of assessing proximal facial nerve function in pathologic states.) [PMID: 4073377]

Nowak DA, Linder S, Topka H. Diagnostic relevance of transcranial magnetic and electric stimulation of the facial nerve in the management of facial palsy. Clin Neurophysiol. 2005;116(9):2051. (The authors demonstrate that transcranial magnetic stimulation in the early diagnosis of Bell palsy is less specific than previously thought, although transcranial magnetic stimulation may be capable of localizing the site of lesion within the fallopian canal.) [PMID: 16024292]

Sawney BB, Kayan A. A study of the F wave from the facial muscles. Electromyography. 1970;3:287. [PMID: 5509973]

Schriefer TN, Mills KR, Murray NMF, Hess CW. Evaluation of proximal facial nerve conduction by transcranial magnetic stimulation. J Neurol Neurosurg Psych. 1988;51:60. (A magnetic stimulator was used for direct transcutaneous stimulation of the intracranial portion of the facial nerve in patients with a variety of facial nerve pathologies.) [PMID: 3351531]

Stennert E, Frentup KP, Limberg CH. Modern recording technique of the trigeminofacial reflexes. In: Fisch U, ed. Facial Nerve Surgery. Birmingham, AL: Aesculapius, 1977.

Wigand ME, Bumm P, Berg M. Recordings of antidromic nerve action potentials in the facial nerve. In Fisch U, ed. Facial Nerve Surgery. Birmingham, AL: Aesculapius, 1977:101.

Zealar D, Kurago Z. Facial nerve recording from the eardrum. Otolaryngol Head Neck Surg. 1985;93:474. (Noninvasive technique described for recording from the facial nerve within the fallopian canal using electrodes placed on the eardrum.) [PMID: 3931021]


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Current Diagnosis and Treatment in Otolaryngology
Current Diagnosis and Treatment in Otolaryngology
ISBN: 0735623031
EAN: 2147483647
Year: 2004
Pages: 76

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