Учебники / Otolaryngology - Basic Science and Clinical Review

must be corrected by central processing. Initial asymmetries are introduced by the mechanical properties of the cupula, as already discussed. Next, there is an asymmetry of rate sensitivity between the left and right side. Again, looking at the horizontal semicircular canal, each hair cell on each side has a baseline firing rate.A positive stimulus will enhance the firing rate of one side while decreasing the firing rate of the other side.The increase of firing is ultimately limited by the refractory period of the vestibular neurons. However, inhibition is possible only to a lesser degree because a hair cell cannot decrease its spontaneous discharge rate below zero. The asymmetry is overcome by having the system function in a push-pull fashion and by introducing significant central integration of bilateral signals. This makes the phase measurement particularly sensitive to unilateral abnormalities of the peripheral vestibular system. Partial or complete loss of information from one side creates progressively enlarged phase abnormalities that are not completely corrected by central compensation.

Comparison of peak eye velocity to peak chair velocity yields the gain. Gain is initially decreased in a peripheral vestibular lesion. Studies have shown that spontaneous firing rates of the vestibular nucleus increase after labyrinthectomy, thus allowing gain to return to normal after a peripheral vestibular lesion.Thus test results showing a decrease in gain and an increase in phase imply an acute or uncompensated lesion, whereas test results showing normal gain and increased phase imply that compensation has taken place. Symmetry can be determined by comparing the leftward and rightward eye movement velocities by the following formula:

((Vr V l)/(Vr V l) 100)

A graphical representation of gain, phase, and symmetry is then produced over a range of frequencies (Fig. 34-3). As can be seen in Fig. 34-3, phase retains a linear relationship over midto high-range frequencies and increases at low frequencies. This is due to the mechanical properties of the cupula and the effect of central processing. The frequency at which the phase loses its linear relationship and increases is called the corner frequency and is the frequency at which the phase lead is equal to 45 degrees.The time constant ( ) is a measure of the relationship between the stimulus, deflection of

the cupula, and the effect of central processing. The value of may be determined by taking the inverse of the corner frequency times 2 ( 1/2 f). The time constant is a sensitive indicator of vestibular dysfunction because, as already discussed, aberrations of peripheral input affect the symmetry of central processing, thereby altering the phase and time constant.

Compared with the caloric test, which essentially checks only one frequency, the rotation test looks at a range of values, just like an audiogram tests a range of hearing frequencies. Interpretation of test results requires normative data for various age groups. Overall, using a battery of tests that include both caloric testing and rotation yields the greatest diagnostic sensitivity. Several different patterns of findings and their interpretations are reviewed in Table 34-3.

VISUAL-VESTIBULAR INTERACTION

Combining rotation testing with visual stimuli generates a sensitive test of central balance disorders. The test subject is exposed first to standard rotation testing to determine the VOR gain, phase, and symmetry.The fixation test considers the ability to suppress nystagmus by focusing on a fixed target.This allows one to determine the fixation index, which is a sensitive indicator of central nervous system dysfunction. Optokinetic nystagmus is tested by exposing the subject to a rotating pattern of vertical stripes that surround the patient’s entire visual field. The visual VOR (VVOR) is tested by performing harmonic sinusoidal rotation of the patient with eyes open and a stationary optokinetic drum.

POSTUROGRAPHY

Because balance is a combination of vestibular, visual, and proprioceptive sensations, several forms of posturography have been designed to evaluate global balance function. The most commonly used today is computed dynamic posturography. Patients with dysequilibrium of unknown etiology, a history of recurrent falls, a history of head trauma, or persistent dizziness despite a negative workup, as well as suspected malingerers, are candidates for this test.The test subject stands on a “force plate” that is able to detect motion and weight distribution. A

computer program then changes the position of the floor or the visual horizon. Using sets of normative data, the patient’s response to adverse balance situations can be determined. Depending on the combination of stimulus conditions, testing can suggest whether a balance disorder is due to proprioceptive, visual, vestibular, or a combination of problems. This portion of the test is known as the sensory organization test (SOT). Overall, six conditions are tested, combining platform fixed or moving with eyes open or closed and fixed or moving platform with moving visual surround. Conditions 5 and 6 (eyes closed, platform moving, and platform and visual surround moving) test for vestibular dysfunction. Posturography does not provide diagnostic or localizing (e.g., peripheral vestibular vs cerebellar) information, only an assessment of balance function. Additional tests are used to evaluate the patient’s center of gravity and whether balance is maintained using movements of the ankle or hip.The CDP setup is able to sense the speed of response to a forward or backward translation or tilt, allowing a calculation of reflex speed. Again, using normative data, abnormal reflex times can be identified, suggesting neuropathies of central motor disorders.

SELF-TEST QUESTIONS

For each question select the correct answer from the lettered alternatives that follow.To check your answers, see Answers to Self-Tests on page 716.

1.Normal electronystagmography electrodes are unable to detect

A.Direction-changing nystagmus

B.Vertical nystagmus

C.Horizontal nystagmus

D.Rotatory nystagmus

2.Posturography allows localization of vestibular disease to

A.The cerebellum

B.The otolith organs

Falls and failure of various components of the test occur in repeatable patterns.This has allowed the testing to be used to identify functional patients.

TESTS UNDER DEVELOPMENT

TraditionalVOR testing is limited to examination of the horizontal semicircular canal.The maculae of the utricle and saccule contribute significantly toward balance function, acting as accelerometers and gravity sensors. Saccular function is currently being investigated using a sound stimulus that triggers contraction of the sternocleidomastoid muscle. Other tests have focused on factors such as perception of the visual vertical and measuring the influence of otolith function on theVOR.

SUGGESTED READINGS

Baloh R, Halmagyi M, eds. Disorders of theVestibular System. New York: Oxford University Press; 1996

Baloh R, Honrubia V. Clinical Neurophysiology of the Vestibular System. Philadelphia: FA Davis; 1990

Barber H, Stockwell C. Manual of Electronystagmography. St. Louis: CV Mosby; 1976

C.The visual system

D.None of the above

3.Which of the following tests has the highest test–retest reliability?

A.Caloric irrigation with air

B.Caloric irrigation with a closed loop system

C.Caloric irrigation with an open loop system

D.All of the above

Knowledge of the facial nerve—its course, function, and rehabilitation—influences decision making in multiple clinical subspecialties, including otology, facial plastic surgery, and head and neck oncology. Therefore, it is important to understand, the complex anatomy and physiology of this nerve in health and disease.

By convention, the facial nerve is divided into intracranial, intracanalicular, labyrinthine, geniculate, tympanic (horizontal), mastoid (vertical), and extracranial segments. The main trunk of the extracranial segment is then subdivided first at the pes anserinus and then further as it divides into the frontal, zygomatic, buccal, marginal mandibular, and cervical branches.

CENTRAL ANATOMY

The facial nerve has sensory, motor, and autonomic components. The 10,000 axons of the facial nerve roughly correspond to the 7000 cell bodies in the facial motor nuclei and 3,000 fibers arising from efferents in the salivatory and lacrimal nuclei, and afferents to the nucleus tractus solitarius. Corticobulbar fibers originating in somatomotor cortex cell bodies project through the internal capsule to caudal pons, where they decussate before synapsing with both ipsilateral and contralateral facial nerve motor nuclei.The dorsal portion of the facial motor nucleus receives both ipsilateral and contralateral innervation and supplies the superior facial mimetic musculature; the ventral facial motor nucleus receives

only contralateral fibers, innervating the lower portion of the face: this is the basis for the sparing of forehead function seen with a unilateral upper motor neuron lesion. The superior salivatory and lacrimal nuclei are also located in the caudal pons, and it is from these nuclei that parasympathetic general visceral efferent nerve fibers originate. These fibers supply the lacrimal gland and extraparotid salivary glands.

One finds the termini of afferent fibers in the nucleus tractus solitarius (NTS) and the spinal trigeminal tract. The chorda tympani nerve is composed of special visceral afferent fibers whose cell bodies are located in the geniculate ganglion and which project to the NTS. Sensation from the skin of the external auditory canal and postauricular area is conveyed via general sensory afferents terminating in the spinal trigeminal tract.

CEREBELLOPONTINE ANGLE

The facial nerve traverses the cerebellopontine angle in close association with the cochleovestibular nerve and the intermediate nerve of Wrisberg, which carries parasympathetic, general visceral efferents to the salivary and lacrimal glands, as well as special visceral afferent fibers from the chorda tympani and general sensory afferents from the external auditory canal and postauricular area.This segment of the nerve derives its vascular supply from the labyrinthine artery off the anterior inferior cerebellar artery.As the facial and cochleovestibular nerves enter the internal auditory canal, the vestibular and cochlear nerves rotate 90 degrees such that the cochlear nerve, which leaves the pons posterior to the facial nerve, ultimately assumes an inferior and

Figure 35-1 Rotation of the facial nerve in relationship to the eighth nerve in the cerebellopontine angle (CPA). Cochlear nerve (CN); fifth cranial nerve (CNV); seventh cranial nerve (CNVII andVII); eighth cranial nerve (VIII); internal auditory canal (IAC); inferior vestibular nerve (IVN); singular nerve (SN); superior vestibular nerve (SVN); vestibular nerve (VN). (From May M, Schaitkin BM.The Facial Nerve, May’s 2nd ed. New York: Thieme Medical Publishers; 2000:33, Fig. 2–12. Reprinted with permission.)

slightly anterior relationship to the facial nerve as it progresses laterally (Fig. 35-1).

INTERNAL AUDITORY CANAL

Fibers of the nerve of Wrisberg, frequently called the nervus intermedius when visible in the internal auditory canal (IAC), fuse to form a single bundle with the motor fibers as they move laterally. Near the lateral extreme of the IAC, the vertical crest (Bill’s bar) marks an anterior and posterior division of this canal; the transverse crest, located anteriorly, divides the canal into superior and inferior divisions. Superior to the transverse crest one finds the facial nerve anteriorly, and the superior vestibular nerve is separated posteriorly by Bill’s bar. Inferiorly, the transverse crest marks a separation of the facial nerve from the cochlear nerve, which are both anterior structures (see Chapter 22). The facial nerve’s narrowest portion occurs as it exits the IAC at the meatal foramen, which is on average no wider than 0.68 mm.

INTRATEMPORAL COURSE

OF THE FACIAL NERVE

Within the temporal bone, the facial nerve courses through the fallopian canal, measuring 30 mm in length between the meatal and stylomastoid foramina. The labyrinthine segment of the facial nerve originates distal to the meatal foramen and is the shortest segment, 3 to 4 mm in length, before reaching the geniculate ganglion (the so-called first genu). At the geniculate ganglion, there is a dehiscence in the floor of the middle cranial fossa called the facial hiatus, through which the greater superficial petrosal nerve (GSPN) emerges (Fig. 35-2).

Cell bodies for the chorda tympani and for the sensory nerves of the GSPN are found in the geniculate ganglion. In addition, preganglionic secretory fibers pass through the geniculate ganglion on their way to the sphenopalatine ganglion via the GSPN.

The tympanic segment spans the 12 to 13 mm between the first and second genu of the facial nerve. Making a sharp posterior and lateral bend at the geniculate ganglion, it maintains a superior relationship to the canal of the tensor tympani muscle and cochleariform process. In 30 to 50% of temporal bone specimens, the segment in the medial wall of the middle ear cavity can be dehiscent. Continuing, the nerve passes medial to the incus and inferior to the horizontal semicircular canal, where it gives off a branch that innervates the stapedius muscle. Posterior to the oval window, the tympanic segment of the facial nerve enters the sinus tympani and turns inferiorly at the second genu, forming the mastoid segment of this nerve.

The facial nerve during its descent through the mastoid gives off two more branches: the sensory auricular branch supplying the external ear and the chorda tympani nerve (Fig. 35-3).The mastoid segment continues vertically for a distance of 12 to 20 mm where the facial

Figure 35-2 Intratemporal course of the facial nerve. (From Fisch H et al. Microsurgery of the Skull Base. NewYork:Thieme Medical Publishers; 1988. Reprinted with permission.)

A

Figure 35-3 Surgical anatomy of the mastoid portion of the facial nerve. (A) Macroscopic photograph of a left human temporal bone after dissection of the mastoid cavity and the facial recess with identification of the facial nerve (FN) and the chorda tympani (CT) and auricular (AU) branches of this cranial nerve. (B) Diagram of the course of the facial nerve through the mastoid region of the temporal bone, with identification of the tip of the

B

short process of the incus (I); the chorda tympani nerve, origin at the fallopian canal (C); the origin of the auricular branch of the facial nerve (B); and the point of intersection between the chorda tympani and the auricular branch of the facial nerve (B’). HSCC, horizontal semicircular canal. (From Eshraghi AA et al. Sensory auricular branch of the facial nerve. Otol Neurotol 2002;23: 393–396. Reprinted with permission.)

nerve exits at the stylomastoid foramen. In children younger than 2 years, the facial nerve can be dangerously superficial at its exit because it is not yet protected from lateral damage by either the tympanic ring or the mastoid tip. With growth of the temporal bone, the stylomastoid foramen comes to lie between the mastoid tip laterally and the styloid process medially.

EXTRACRANIAL COURSE

OF THE FACIAL NERVE

As the facial nerve exits the stylomastoid foramen, it gives nerve branches to the posterior belly of the digastic, stylohyoid, and postauricular muscles. The main trunk of the facial nerve immediately plunges into the parenchyma of the parotid gland, dividing it into superficial and deep lobes. It courses for approximately 2 cm before bifurcating at the pes anserinus. Distal to the

bifurcation, the frontal, zygomatic, and buccal branches interconnect in a highly variable plexus composed of thin nerve filaments. The marginal mandibular and cervical branches of the facial nerve are less likely to form such interconnections (Fig. 35-4).

MOTOR END PLATE

Facial nerve fibers interface with striated mimetic musculature at the motor end plate in an acetylcholinedependent synapse. This neuromuscular junction resembles a synapse at the nerve terminal, but the distal portion is a specialized muscle structure. Acetylcholine molecules, on leaving the nerve terminal, cross the primary synaptic cleft (which is continuous with the basal lamina) to activate acetylcholine receptors in the secondary synaptic cleft, consisting of invaginated channels of the nerve fiber’s sarcolemma.

While acetylcholine molecules travel through the primary synaptic cleft, they are subject to metabolism by acetylcholinesterase. The cholinergic nature of the facial neuromuscular junction forms the basis for botulinum toxin (Botox) treatment of facial muscle hyperfunction (for additional information and applications of Botox, see Chapter 57). Botulinum toxin (trade names Oculinum and Botox) is a neurotoxin produced by Clostridium botulinum, a soil anaerobe.This neurotoxin acts by blocking the release of acetylcholine at the nerve terminal.

PATHOPHYSIOLOGY OF

THE FACIAL NERVE

RESPONSE OF THE NEUROMUSCULAR

UNIT TO INJURY

The axon’s metabolic demands make it reliant on continuity with the neuron’s cell body, its source of nutrients. Likewise, normal structure and function of muscle fibers rely on intact innervation. Electrodiagnositic testing of the facial nerve is based on knowledge of the immediate and delayed events of neuromuscular injury; treatment and prognosis of facial nerve pathology are informed by the results of electrodiagnostic testing.

A stereotypical sequence of events follows interruption of axonal continuity, whether the interruption occurs from compression or transection. Chromatolysis, or dispersal of Nissl substance within the neuron’s cell body, is a classic finding first described in the facial nerve nucleus. A general increase in cellular metabolism is reflected in increased numbers of organelles and unregulated oxidative metabolism. Damming of anterograde axoplasmic transport causes the proximal axon stump to swell. Growth cones form within 3 days and extend axon sprouts into the periphery, growing at a rate of 1 mm per day.

The distal axon stump swells transiently as a result of retrograde axoplasmic damming; within the initial 24 to 48 hours, physiological processes such as axoplasmic transport and nerve conductivity remain largely intact. Thereafter, the effects of wallerian degeneration act to compromise first axoplasmic flow and then myelinization of the affected nerve. Schwann’s cells proliferate, some of which perform a phagocytic function and some of which enter endoneural tubes to form Büngner’s bands.

Denervation of muscle fibers is manifested as loss of muscle mass and voluntary control. In the initial weeks following such injury, the rate of atrophy is steep but then stabilizes. Fibrillation of the nerve begins within 2 to 3 weeks.With chronic denervation, muscle tissue is

eventually replaced by fibrous tissue that contributes to sequelae such as contractures. New motor end plates that are formed after an injury are more numerous than those present before the injury.

SUNDERLAND CLASSIFICATION

OF NEURAL INJURY

Injury to the facial nerve, commonly caused by inflammatory, neoplastic, or iatrogenic processes, can occur at any point in its course. Sunderland (1978) described five degrees of injury in peripheral nerves (Fig. 35-5) The first three degrees of injury can be produced by inflammatory entities such as Bell’s palsy and herpes zoster oticus, and the fourth and fifth degrees of injury involve disruption of the nerve as produced by traumatic, neoplastic, or iatrogenic mechanisms. It should be remembered that a single given nerve can exhibit mixed degrees of injury.

First-degree injury, also called neuropraxia, is the loss of conduction across a point of compression or increased intraneural pressure. The nerve is otherwise intact, with no disruption of endoneurium, axons, or axoplasmic flow. With removal of the source of compression, a full return of function occurs.

Second-degree injury, also called axonotmesis, occurs when the endoneurium is intact, but there is axoplasmic damming of nutrients, which results in axonal disruption. This type of injury can occur when there is a more chronic compressive insult to the nerve, and, although the nerve can recover when this compression is relieved, recovery generally takes longer than with neuropraxia. Wallerian degeneration of the distal axon segment occurs.

Third-degree injury, or neurotmesis, results from interruption of endoneurial tubules.When the endoneurium is disrupted, regenerating nerve fibers lose the ability to rejoin corresponding distal segments. During recovery, this cross-wiring of neural projections leads to aberrant regeneration and can cause phenomena such as synkinesis, facial spasm, and gustatory lacrimation. Recovery of full muscle strength is incomplete.

Fourth-degree injury, or partial transection, disrupts the perineurium as well as the endoneurium. The opportunity for regenerating axons to enter incorrect fascicles of a degenerated nerve is therefore increased, and sequelae such as synkinesis are more severe and more frequent. Recovery of full muscle strength is seldom seen.

Fifth-degree injury is complete transection with a disruption of both the epineurium and perineurium. No spontaneous recovery can be expected; therefore, surgical intervention is required. Unrepaired injuries

exhibit total paralysis of deinnervated areas, and synkinesis is not found.

ABERRANT REGENERATION

An intact endoneural tube allows a regenerating axon to reestablish communication with the appropriate distal stump. With discontinuity of the endoneural tube, Schwann’s cells of Büngner’s bands act as a scaffolding for axonal regeneration, but often the proximal axons can reconnect with the wrong distal stump. This “cross-wiring” leads to the phenomena of aberrant regeneration, which include but are not limited to muscle spasticity, synkinesis, gustatory lacrimation, and Frey’s syndrome.

ELECTROPHYSIOLOGY

Although the single most important prognostic indicator for the return of facial function after injury is the presence of voluntary movement, numerous electrodiagnostic tests have been developed for the assessment of facial nerve motor function. These tests, especially

Figure 35-5 Sunderland classification of the degree of nerve injury and the estimated potential for the recovery of neural function. (From Sunderland, S: Nerve and Nerve Injuries. 2nd ed. London: Churchill Livingstone; 1978:88, 89, 96, 97, 133. Reprinted with permission.)

electroneuronography (ENOG), have largely replaced topognostic testing, which used measures of lacrimation (Schirmer’s test) and stapedial reflex to establish the site of lesion.The majority of the electrophysiological assays rely on comparisons between the paralyzed and normal sides of the face and therefore can be inaccurate in the presence of preexisting or congenital facial nerve disorders on the “normal” side.

The nerve excitability test, maximal stimulation test, and ENOG are all evoked response tests, in that they apply a stimulus in the form of a square-wave electrical pulse. Electromyography (EMG), in the setting of facial nerve testing, is a measure of volitional muscle action: the patient is asked to move a muscle group, and resulting motor potentials are recorded. The four tests described above are the most frequently relevant to facial nerve disorders encountered by the otolaryngologist. Although the field of neuromuscular electrophysiology offers other measures of motor nerve function, such as nerve conduction velocity, the majority of facial nerve disorders seen by otolaryngologists are evaluated by the four aforementioned tests.

NERVE EXCITABILITY TEST

The nerve excitability test (NET) measures the minimal current required to cause a detectable movement in the face. A reference electrode from a stimulator such as the Hilger nerve stimulator is placed between the mastoid tip and the mandible.The stimulating electrode is placed over the approximate location of the pes anserinus. Starting at 0 mA, the threshold current required (normal range 1–4 mA) is found first on the normal side; these thresholds are then compared with the thresholds obtained from the paralyzed side of the face. A difference of 2.0 mA or greater between the normal and paralyzed sides of the face is considered significant.

MAXIMAL STIMULATION TEST

The maximal stimulation test uses an approach similar to the NET, but grades facial function based on a scale that an observer applies to movements elicited by the highest stimulus intensity the patient can comfortably tolerate (usually 8–10 mA). Movement of the paretic side of the face is described as normal, slightly decreased, greatly decreased, or absent in comparison to the unaffected (normal) side of the face.

ELECTRONEURONOGRAPHY

ENOG is a measure of a muscle compound action potential (CAP) that uses a paradigm similar to the maximal stimulation test, but that quantifies the response to stimulation. The ENOG employs a stimulating electrode placed between the mastoid tip and the mandible. Maximal stimulus intensity is applied, but it is limited by the patient’s pain threshold.This generates a biphasic muscle potential, the sum of many individual motor unit potentials, which is detected by skin surface electrodes. A peak-to-peak amplitude measure of this biphasic CAP is calculated and compared with responses obtained from the intact side (Fig. 35-6). This measure, expressed as percent excitability, correlates to the degree of muscle degeneration on the deinnervated side.

Because nerve conduction can remain intact until a sufficient degree of wallerian degeneration has occurred, the ENOG can be unreliable in the initial 48 to 72 hours after a nerve injury. The prognostic utility of ENOG is greatest within 3 weeks of injury; patients manifesting less than 10% excitability within 2 weeks of paralysis onset are classified as having sustained a severe injury. In the face of this degree of injury, the chances of complete recovery are less than 50%, and surgical decompression must be contemplated.

Figure 35-6 Electroneuronography: muscle compound action potentials from monitoring of patients with a normal facial nerve (bottom trace) and an injured facial nerve (top trace).

ELECTROMYOGRAPHY

EMG frequently employs needle electrodes to detect striated muscle activity in response to volitional movement. Muscle responses are graded from 1 to 4 , with 4 being a normal response and 1 an absent response. Normal muscle will discharge a short burst of activity with needle insertion, followed by relative electrical silence when the muscle is at rest. Deinnervated muscle exhibits spontaneous fibrillation potentials, a characteristic random firing pattern, when at rest. It will not produce a voluntary motor unit action potential. Fasciculation, a spontaneous firing of an entire motor unit, also can be recorded from deinnervated muscle. Again, the accuracy of EMG is dependent on the time course of wallerian degeneration, and a deinnervated muscle may not exhibit fibrillation potentials until a time period of 48 to 72 hours has elapsed following the initial injury. Reinnervation is heralded by the return of voluntary polyphasic motor unit action potentials.

FACIAL NERVE MONITORING DURING SURGERY

Facial nerve monitoring (FNM) is beneficial during procedures that carry a high risk for facial nerve injury. (e.g., cochlear implantation, revision tympanomastoidectomy,

surgery to remove an invasive cholesteatoma, and repair of external auditory canal bony stenosis). FNM is used regularly in otolaryngology, which makes it a state-of-the-art adjunct for advanced ear surgery and lateral skull base surgery. It is also very useful in training centers where residents perform some portions of otologic or parotid operations. However, FNM should never be used as a replacement for anatomical knowledge, technical skill, and clinical judgment of the surgeon.

PHYSIOLOGY

Electrical, mechanical, or thermal stimulation results in depolarization of the facial nerve and a compound muscle action potential (CMAP). This CMAP is the composite electrical activity within the target muscle resulting from synchronous activation of a group of motor neurons. FNM using EMG monitoring essentially measures this electrical activity in the portion of the muscle nearest the recording electrodes and converts the electrical activity to sound via a loudspeaker with or without a visual oscilloscope display of neural activity.

Synchronous activity initiated by electrical stimulation produces a biphasic and well-defined waveform, whereas asynchronous activity related to mechanical stimulation produces a polyphasic pattern. When these FNM response patterns are converted to sound, electrical stimulation results in a well-defined train of pulsed sounds, whereas mechanical stimulation yields a rough burst of acoustic energy.

ELECTROMYOGRAPHY MONITORING

Monitoring of more than one muscle provides additional sensitivity. A typical montage of two-channel bipolar recording includes a pair of needle electrodes in the orbicularis oculi muscle 3 mm apart and another pair of electrodes in the orbicularis oris muscle. The ground electrode is placed in the musculature of the forehead, and the anode for the monopolar nerve stimulator is inserted at a site in the ipsilateral shoulder.

Neuromuscular blocking agents should not be employed following induction of anesthesia if the facial nerve is to be monitored. It is also crucial that patients be adequately grounded to the monopolar electrocautery unit to permit a safe path for current return. If proper grounding is not achieved, the electrocautery current could potentially find a route through

Figure 35-7 A typical configuration of electrode placement for the two-channel bipolar facial nerve monitoring electrodes. Recording electrodes are placed in two distinct facial muscle groups, indicated by the double arrows in recording sites A and B. The arrows at C and D represent the areas where reference and ground electrodes are placed, respectively.

the nerve-monitoring electrodes and result in severe burns to the patient (Fig. 35-7).

STIMULATION

The parameters for safe nerve stimulation are 100 to 250 sec pulses with a current range of 0.05 to 0.5 mA. Most normal facial nerves should be stimulated by direct contact of the probe using a 1100 sec pulse of 0.05 mA. Settings of 0.05 to 0.1 mA are recommended when working close to the nerve.A higher level of stimulation may be required when bone, connective tissue, or granulation tissue covers the nerve.

Burst Activity

Burst activity occurring with gentle manipulation of the nerve is indicative of a healthy facial nerve. During the course of surgery, many burst potentials may be observed, and they are usually not associated with significant trauma to the nerve. Lack of burst activity during dissection may indicate minor manipulation of a healthy nerve, significant manipulation of an already injured nerve, or a problem with the monitoring connections and instrumentation. Electrical stimulation of the nerve at this point can be used to verify the