Учебники / Otolaryngology - Basic Science and Clinical Review

The vestibular system can be thought of as a system that senses and controls motion. Its functions begin with the detection of head position and motion by the vestibular end-organs.The vestibular hair cells transduce the mechanical stimuli into neural signals and convey them to the brainstem. The brainstem processes the signals to generate secondary neuron messages appropriate to specific reflex tasks. Here we examine in particular two of the brainstem’s tasks: integration and velocity storage. These tasks have important effects on our tests of vestibular function. The brainstem then distributes its secondary vestibular neuron signals to other areas of the central nervous system (CNS) to generate vestibular reflexes and sensation. Specifically, neuronal signals are sent to the oculomotor nuclei to generate the vestibulo-ocular reflex (VOR), which stabilizes our gaze (eye position in space). Other neurons go to the cervical spinal motor neurons to generate the vestibulocolic reflex (VCR), and to the lower spinal motor neurons to generate the vestibulospinal reflexes (VSRs). These reflexes stabilize both our posture and our gait.There are cortical pathways to provide us with a conscious sense of motion. Autonomic pathways have long been known, but only recently have we begun to

appreciate their function. Vestibular input, particularly otolith information about our posture with respect to gravity, is used here to adjust hemodynamic parameters to maintain cerebral perfusion. Finally, vestibular input to the cerebellum is critical to coordination of the vestibular motor reflexes and to the ability to adapt those reflexes when changes occur, such as injury to a vestibular end-organ or alteration in vision (e.g., a new pair of glasses).

THE VESTIBULAR PERIPHERY

The three semicircular canals with their associated ducts are sensors of angular head acceleration. Each begins and ends in the utricle.The business end of the semicircular duct within the canal is the ampulla, a swelling near the utricle that houses the sensory receptor apparatus. The horizontal (or lateral) canal is actually pitched up 20 degrees from the horizontal when the head is upright. There are two vertical canals: the posterior (or inferior) and the anterior (or superior).These three semicircular canals lie at almost right angles to each other, so that any angular motion in three-dimensional space can be detected.

There are two otolith organs (maculae) located in the utricle and saccule.These are sensors of linear acceleration, whether it is either a to-and-fro movement of the head or gravity acting on the stationary head. The macula of the utricle lies approximately in the horizontal plane, and the macula of the saccule lies approximately in the vertical, parasagittal plane. The superior vestibular nerve supplies the receptor epithelium of the horizontal and anterior canal cristae, the macula of the utricle, and part of the saccular macula. The inferior vestibular nerve supplies afferent innervation to the receptor epithelium of the posterior canal crista and most of the macula of the saccule.

ADEQUATE STIMULI FOR

VESTIBULAR RECEPTOR

EPITHELIUM

All vestibular hair cells sense shearing forces. When the hair bundle composed of stereocilia is deflected toward the kinocilium, the hair cell is excited. Its receptor potential goes up, it releases more neurotransmitter, and the firing rate of the underlying afferent nerve increases from its baseline-level firing rate, which is already high ( 90 spikes per second). Conversely, if the sensory hair bundle is deflected away from the kinocilium, the process is reversed, and the firing rate of the afferent nerve goes down. However, the responses of the vestibular system are not symmetrical.There is a greater increase in firing for a given excitatory deflection than there is a decrease for the same magnitude inhibitory deflection. Incredibly, Flourens and Ewald figured this out in the nineteenth century. By cannulating individual ducts of the semicircular canals in pigeons, they showed that the nystagmus produced by endolymph displacement in one direction was greater than in the other direction.This observation was codified as Ewald’s second law.

The advantage of having a high baseline-level firing rate for the vestibular nerve is twofold. First, there is a very low threshold to sensation.The stimulus does not have to reach some high level before the afferents respond. Rather, a very small stimulus will be detected as a modulation in the firing rates of already-active afferent nerves. So, for example, the perceptual threshold to angular acceleration is as low as 0.1 degree/sec2. Moving at that speed in a swivel chair, it would take an individual almost 90 seconds to go one revolution. Linear accelerations as small as 5 10 4 g can be detected. It would take an elevator moving at this acceleration 40 seconds to travel one floor.

The second advantage of the high baseline-level firing rate of vestibular nerve is that we can sense movement in the off direction. If the nerve were silent at rest, there would be no way of knowing when the hair bundle was

being deflected in this “off ” direction (i.e., the firing rate cannot become some negative number). Instead, this high baseline-level firing rate gives us a bidirectional response from each ear.

Thus the labyrinth has an incredible dynamic range of head velocities that can be detected. But the range is not infinite, a fact that becomes very important in interpreting vestibular test findings in the presence of unilateral hypofunction. With sufficiently high head accelerations in the off direction, some afferent nerves eventually do reach zero firing, or “cutoff.” When this cutoff occurs, the system exhibits what we call “nonlinearity.” Up to that point, if we doubled the acceleration in the off direction, we saw that the firing rate on that side would go down by half. Now, if we double the acceleration again, nothing happens to the firing rate; it remains at zero.Thus the linear relationship is lost.

Nonlinearity is not a problem if both sides of the vestibular system are functioning. The excitatory signal from the side toward which the head is turning continues to inform the brainstem about the motion (and can do so up to very high rates, i.e., 400 spikes per second). If the labyrinth on that side is not functioning, and we have attained a high enough acceleration to silence afferents on the intact, inhibited side, then the brainstem sees no further change in firing from afferents on either side. It therefore loses the ability to detect any movements of higher acceleration.

How do shearing forces actually develop in the vestibular end-organs? In the maculae of the utricle and saccule, the hair cells are arrayed in a horizontal or vertical sheet, respectively. The hair bundles insert into a gelatinous layer called the otoconial membrane. On top of this lie the otoconia or otoliths (i.e., crystals of calcium carbonate). The otoconial membrane is therefore denser than the surrounding endolymph, and tilting the head results in a kind of “slab-avalanche” movement that carries the hair bundles with it. In the semicircular canals, the hair cells are arrayed on a crest, the crista ampullaris, which extends across the ampulla perpendicular to the orientation of the canal. Another gelatinous membrane, the cupula, extends from this crest up to the roof of the ampulla, sealing the canal side off from the utricular side.When relative endolymph motion occurs in the canal, the cupula puckers in the center like a sail, and the attached hair bundles are deflected with it.

DIRECTIONAL SENSITIVITY AND SEMICIRCULAR CANAL PLANES

The exact geometry of hair cell orientation determines the directions of forces to which a given end-organ will

respond.Again, the direction of the kinocilium determines the “on” direction for the hair cell. In the semicircular canal cristae all of the kinocilia point in the same direction. In the horizontal canals, they point toward the utricle, and movement of endolymph toward the utricle (utriculopetal) excites the end-organ.This is what occurs in the right ear, for example, when the head turns to the right. In the vertical canals, however, the polarization is reversed. All of the kinocilia point away from the utricle, and utriculofugal flow of endolymph excites the sensory cells of these canals. This is what occurs, for example, in the superior canal when the head is pitched down, and in the posterior canal when the head is pitched up.

One of the important consequences of these arrangements is that canals work in “push-pull” pairs, and the six canals form three canal planes. The horizontal canals (HCs) are paired in the horizontal plane, and a yaw movement that excites one horizontal canal always inhibits the other.The vertical canals pair as follows: the right anterior (RA) canal works in conjunction with the left posterior (LP), forming the RALP plane, which lies 45 degrees off the sagittal plane; at almost a right angle to this plane, the left anterior (LA) canal pairs with the right posterior (RP), forming the LARP plane. Mixed vertical-torsional head movements stimulate these vertical canals. Remember that each canal is excited by turning the head toward the side of that canal in the plane of that canal.Thus the left HC is excited by leftward rotation in the HC plane. Pitching the head down and rolling it to the right in the RALP plane excites the RA canal and inhibits the LP canal. Pitching the head up and rolling it to the left in the RALP plane reverses the pattern: the LP canal is excited, and the RA inhibited.

The canals drive eye movements in these planes.This is Ewald’s first law. A pure stimulation of one of the horizontal canals, for example, will drive the eyes conjugately in the horizontal plane. Likewise, pure stimulation of the left posterior canal, as occurs in benign paroxysmal positional vertigo (BPPV), will drive the eyes in the RALP plane.

The relationship of the two maculae is even more complicated.There is a prominent dividing curve going through the middle of each macula.This plane of separation in each macula is called the striola. Hair cells on opposite sides of the striola have an opposite polarization of the relationship of their stereociliary bundle to the kinocilium. In the macula of the saccule, all of the polarization vectors point away from the striola. In the utricular macula, they all point toward the striola. However, the net result is not a null vector. In fact, in the utricle there is a 3:1 predominance of vectors pointing

ipsilaterally. This becomes important in explaining the skew and tilt reactions seen in patients with unilateral labyrinthine hypofunction.

SEMICIRCULAR CANALS

AFFERENT PHYSIOLOGY

We now move out of the end-organs and consider the signals carried to the brainstem. One might suppose that the semicircular canals would act like simple tubes of fluid with inertia, and that the fluid, sitting still in the canals as they moved around with the head, would faithfully inform the brain about the acceleration of the head. After all, by Newton’s laws, force (F ) mass (m)acceleration (a) (F ma), so the acceleration of the head should result in a proportional force on the endolymph and the cupula of the ampulla. One of the remarkable things that Steinhausen predicted in the 1930s, however, was that the canals instead would sense velocity. This is because he included in his calculations the very significant elastic restoring force of the gelatinous cupula. This force dominates the system, and the result of his “torsional pendulum” model is that the canals act as mechanical integrators, converting an acceleration signal into a velocity signal. In panel A of Fig. 33-1, we see this manifested as we record the firing rate of a horizontal canal afferent. At the top, the stimulus given is a step of acceleration in the “on” direction. Just below that in panel B of Fig. 33-1 is shown the mathematical integration of this step. It is a ramp, and, by definition, is the velocity of the stimulus. Now look at the firing rate and see that it rises more like a ramp than a step.We say that this afferent is encoding velocity.

What is the significance of this to the VOR? The eye muscles do not need an acceleration and position signals. Rather, their actions can be derived from a velocity signal. Thus the semicircular canals perform the first and positions signal processing necessary to match the input signal characteristics to the reflex output needs. In fact, the integration performed by the semicircular canals is incomplete. As we shall discuss on this section, the brainstem further processes the signals to complete the integration needed for the control of eye movements.

Another manifestation of this integration appears in responses to sinusoidal rotations, which play an important role in vestibular testing. When we differentiate a sine wave, we get the cosine.This has all the same values as the sine wave, but they occur 90 degrees earlier in the cycle. When the two (sine input and cosine output) are plotted together, however, it appears that the output is lagging behind the input by 90 degrees.We say that the response lags the stimulus by 90 degrees.The phase lag which is

shown in panel C of Fig. 33-1, actually is smaller than 90 degrees, so the integration is incomplete. Panel D of Fig. 33-1 summarizes the behavior of many canal afferents seen in many species, including primates. Some fibers do show a 90-degree phase lag over the frequencies of head movements that we commonly encounter, but most have a smaller phase lag. Indeed, some can more appropriately be said to encode the input acceleration.As we learn more about the other vestibular reflexes (vestibulocolic, vestibulospinal), we may find the role that these acceleration signals play in the sense of balance.

THE BRAINSTEM AND BEYOND: THE VESTIBULO-OCULAR REFLEX

We now consider the means by which the vestibular signals reach the target areas of the brainstem that control eye movements. Primary afferents project almost exclusively to the ipsilateral four vestibular nuclei on the floor

of the fourth ventricle at the pontomedullary junction. These are the superior, medial, lateral, and descending vestibular nuclei. As a rough rule, canal inputs project to the more rostral parts of the superior, medial, and lateral nuclei. The maculae otolith inputs project most heavily to the caudal medial and descending nuclei.

We know that stimulation of the right horizontal canal (as by head turning to the right) must result in compensatory conjugate eye movements to the left.This requires activation of the left lateral rectus and right medial rectus. We can trace here a three-neuron reflex arc going to the left lateral rectus and a three-neuron reflex arc to the right medial rectus. Simultaneously, the right lateral and the left medial recti must be inhibited. These pathways can be traced as well. Thus each canal gives rise to two excitatory and two inhibitory pathways, for a total of 12 pathways. Note that eight of these travel in the medial longitudinal fasciculus. Lesions here, like the classic occurrence of a multiple sclerosis plaque

causing internuclear opthalmoplegia, will disrupt the machinery that produces the normal conjugate eye movements of the VOR.

We have considered the “hardware,” or the wiring of the system. But what does the “software” do? That is, what sort of signal processing occurs in these secondary and higher order neurons that is of clinical importance? Recall that we found that afferents carried an incompletely integrated signal. If one supposed that eye movements needed to be generated from these signals, then it becomes clear that one of the tasks for the brainstem is to complete the integration.Thus the brainstem acts as a velocity to position integrator.There are more circuitous pathways for vestibular input to reach the ocular motor centers than the simple three-neuron arcs we have seen. Some of these go through the reticular formation and the nucleus prepositus hypoglossi, where the integrator function may lie. However, this integrator function is not unique to vestibular reflexes, and it is shared with other eye movement systems. For example, when we move and hold our gaze to one side, the integrator takes a pulse signal to move the eye and integrates it to get a prolonged signal that holds the eye in the new position.

One of the consequences of integrator dysfunction is the inability to hold eccentric gaze.The failing or “leaky” integrator allows the eye to drift slowly back to the neutral position from wherever it is in the orbit. This explains Alexander’s law, which states that nystagmus (vertigo) will be augmented when looking in the direction of the fast phase. When looking toward the fast phase, the slow drift in the opposite direction adds to the slow phase, augmenting the nystagmus.When looking toward the slow phase, however, the drift is in the opposite direction and subtracts from the slow-phase velocity.

Another failing of the afferent input is that it dies away too quickly.The time constant of the cupula, a measure of how fast it returns to its resting position after a displacement, is 13 seconds. A VOR based on this would do fine during high-frequency head movements, but at lower frequencies it would cause the eye to complete its motion too quickly, giving it a large phase lead at low frequencies. We will see this when we discuss rotary chair testing.

The brainstem makes up for this deficit by prolonging the vestibular input signal, an operation known as velocity storage. This may be accomplished by recurrent loops in the VOR circuitry that add up the signal and “store” it over time. Note: This is not the same as the velocity to position integrator we discussed previously, a common misconception, but like

the integrator, velocity storage is shared with other eye movements. So, for example, optokinetic nystagmus dies away slowly as an “afternystagmus” because of the effect of velocity storage. Velocity storage is commonly crippled on the side of a unilateral labyrinthine hypofunction.Thus a prolonged sinusoidal input will be stored on the intact side, but not on the lesioned side. This is the origin of post-headshaking nystagmus.

THE VESTIBULOCOLIC AND VESTIBULOSPINAL REFLEXES

The vestibular system also keeps us upright with respect to gravity. Linear acceleration signals from the otolith organs are processed in the medial and lateral vestibular nuclei, which give rise to the medial and lateral vestibulospinal tracts (MVST and LVST, respectively). The MVST provides input to the neck muscles, and this explains why vestibular lesions can cause a head tilt.The LVST descends to the thoracic and lumbar spinal cord to drive the extensor (antigravity) muscles of the lower limbs.

THE CEREBELLUM AND

THE VESTIBULAR SYSTEM

We have seen how the vestibular system acts like a machine to drive eye movements in the canal planes. There may be circumstances when we wish to turn off theVOR, as, for example, when we are following a moving target by moving our head. If the VOR stayed on in this circumstance, the eyes would be driven off in the wrong direction. Control of the VOR for these situations is provided by the cerebellum, in particular by the flocculus.

The canal input is sent not only to the interneuron in the reflex arc but also to the cerebellum. The Purkinje’s cells of the cerebellum provide a copy of the signal, but now as an inhibitory signal, to the same interneuron. The result is a cancellation of the VOR. Probably the most common situation in which this occurs is when we move our head to shift our gaze. Here we do not want the eye to remain stationary in space, but to move along with the head. (In actuality, the eye gets on target before the head, and the VOR is turned back on at the end of the head movement to keep the eye there.)

The cerebellum is critical to vestibular adaptation. When there is a loss of vestibular function, leading to a decreased input from one side, the cerebellum adjusts the central circuits to cancel the imbalance. The cerebellum

also adjusts the system to compensate for changes in our vision (e.g., presbyopia, new eyeglasses), so that theVOR does not cause the image to overshoot or undershoot the fovea because of the magnification change.

SUGGESTED READINGS

Baloh RW and Halmagyi GM. Disorders of the Vestibular System. NewYork, Oxford University Press; 1996

Carey JP and Della Santina CC. Principles of applied vestibular physiology. In Cummings C.W., Otolaryngology-Head and

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.Which vestibular organ has its kinocilia located closest to the utricle?

A.Saccule

B.Posterior canal

C.Superior canal

D.Horizontal canal

2.The vestibular system in one labyrinth works

A.As an isolated sensor of movement

B.In conjuction with the matched sensory organs in the opposite labyrinth

Neck Surgery, Fourth Edition, 2005. Philadelphia, Elsevier Mosby 2005; 3115–3159

Ewald JR. Physiologische Untersuchungen uber das Endorgan des Nervus Octavus. In Wiesbaden, Germany. Bergmann; 1892

Highstein SM, Fay RR, Popper AN, eds. The Vestibular System (Springer Handbook of Auditory Research, Vol 19). New York, Springer-Verlag; 1995

Steinhausen W. Über die Beobachtung der Cupula in den Bogengängsampullen des Labyrinths des lebenden Hechts. Pflügers Arch Ges Physiol 1933; 232, 500–512

C.Primarily to sense velocity

D.As a high-frequency movement sensor

3.Ewald’s first law postulates that

A.Nystagmus is generated in the plane of the semicircular canal being stimulated.

B.Nystagmus is strongest when gazing in the direction of the fast phase of nystagmus.

C.Only vertical nystagmus is nontorsional.

D.Unilateral weakness may be detected by the presence of nystagmus.

Testing balance is a complex subject due to the variety of sensory systems involved in the perception of balance. Testing falls into two main groups: tests that rely on the activation of the vestibulo-ocular reflex (VOR; i.e., electronystagmogram and rotation testing) and tests of global balance (posturography). The electronystagmogram (ENG) is actually a test battery that screens for central as well as peripheral vestibular dysfunction. Finally, there are a variety of experimental vestibular test procedures that test otolith function and cervical vertigo and attempt to test directly activation of the central vestibular system.The basic principles that underlie vestibular testing are the evaluation of the VOR (see Chapter 33), through the assessment of the output response induced by stimulation of the horizontal semicircular canal. The basics of the VOR response are shown in Fig. 34-1.

THE ELECTRONYSTAGMOGRAM

The fundamental test of balance is the ENG. The ENG test battery relies on the recording of nystagmus (vertigo) after a variety of stimuli. This is most frequently accomplished by placing electrodes that measure the shift in the corneoretinal potential. The cornea has a positive (+) charge, and the retina has a negative ( ) charge.The movement of the eye creates a

movement of the dipole that can be recorded and amplified. Calibration is accomplished by comparing the electrode output to eye movement induced by looking at a target point. By knowing the angle of eye movement divergence and recording the change in the eye dipole on a fixed speed chart recorder, the eye movement speed can be calculated (Fig. 34-2). By convention, an upward deflection on the chart recorder represents a rightward deviation, and a downward - deviation represents a leftward eye deflection. Standard electrode placement also allows placement of a vertical electrode that records upward or downward eye movement. ENG electrodes do not record torsional eye movements because the dipole does not shift. This makes it difficult to record nystagmus that has a torsional component, such as benign paroxysmal positional vertigo (BPPV). Recording of eye movement with infrared video cameras allows the recording of nystagmus in all directions. Assessment of vestibular defects using ENG consists of three phases. Initially, the presence of spontaneous nystagmus with eyes open and closed is tested, looking for congenital nystagmus as well as suppressible and nonsuppressible nystagmus. Testing of pursuit, saccade testing, and optokinetic testing are then done to check for central dysfunction (Table 34-1). Positional and positioning nystagmus are then evaluated. A review of expected eye movements

induced by stimulation of the various canals is given in Table 34-2.

THE CALORIC TEST

The caloric test evaluates the function of the horizontal semicircular canals. A variety of stimuli (open loop, closed loop, air) are used to change the temperature of the external auditory canal (EAC). Open-loop water calorics are considered the most reliable, with the lowest test–retest variability. The test is performed with the patient lying at a 30-degree angle, which places the horizontal semicircular canal perpendicular to the ground. Because the horizontal canal is closest to the EAC, the change in EAC temperature during irrigation with water is transmitted to the horizontal canal.The change in temperature induces a change in density of the endolymph, resulting in flow of endolymph and displacement of the cupula. The stimulus provided by calorics is approximately equivalent to a rotational stimulus of 0.025 Hz. Normal walking and head turns yield stimuli in the 4 to 8 Hz range. Alternating warm (44°C) and cool (30°C) stimuli result in endolymph flow in opposite directions, yielding nystagmus in opposite directions. A cold irrigation causes an ampullofugal flow, deflecting the kinocilium away from the utricle and inhibiting the spontaneous firing rate of the hair cells. A warm irrigation causes

Figure 34-1 A schematic representation of eye movement in response to a rotational stimulus. Seen from above, a clockwise or rightward head movement results in deflection of the horizontal canal kinocilium toward the utricle on the right and away from the utricle on the left.The right hair cells are excited and increase their firing rate, whereas the left hair cells are inhibited and decrease their firing rate.The firing rate of the right vestibular nucleus increases, whereas the firing rate of the left vestibular nucleus decreases. This leads to signals to the oculomotor nuclei of the III and VI nerves (discussed in greater detail in Chapters 27 and 33). Essentially, the left lateral rectus and the right medial rectus are stimulated to contract, whereas the left medial and right lateral rectus muscles are allowed to relax.This results in a slow eye movement to the left and a fast saccadic movement to the right. Because nystagmus is defined by the fast phase, this results in a right-bearing nystagmus.Warm water irrigation on the right side would have a similar effect.

ampullopetal flow, thereby deflecting the kinocilium toward the utricle and exiting and increasing the firing rate of the hair cells. This increase in the rate of firing results in stimulation of the ipsilateral III nerve and contralateralVI nerve nucleus.This induces a deviation of the eyes toward the opposite ear (slow phase of nystagmus) and a saccadic correctional movement of the eyes toward the stimulated ear (fast phase of nystagmus). By convention, the direction of nystagmus is defined by the fast phase.Therefore, a warm irrigation in the right ear will produce a right-bearing nystagmus, which is shown on the chart recorder as an upward deflection. The mnemonic COWS describes the direction of nystagmus response after a caloric stimulus: cold water irrigation nystagmus bears toward the opposite ear; warm water irrigation nystagmus bears toward the same side ear.The normal rate of nystagmus after caloric stimulation ranges from 8 to 80 degrees per second. When both ears are alternately irrigated with warm and cold water, nystagmus rates can be determined, and the function of one horizontal canal with relationship to the other can be determined.The Jongkees formula

[(L30 L44) (R30 R44)]/ (L30 L44 R30 R44),

where L is left, R is right, 30 is 30°C irrigation, and 44 is 44°C, describes the presence of unilateral weakness;

Figure 34-2 A basic electronystagmography tracing shows one channel of a recording. Upward deflections represent rightward eye movement, and downward deflections represent leftward eye movement.The more perpendicular deflections represent fast eye movement, whereas the shallow sloped deflections represent the slow component of eye movement.The equipment is calibrated such that 1 degree of eye displacement equals 1 mm of pen displacement. Given a known paper speed (usually 10 mm per second), one can determine the slow-phase velocity of the nystagmus.

that is, there is less nystagmus produced by one ear, which represents a peripheral vestibular weakness. A second formula

[(L30 R44) (R30 L44)]/ (L30 L44 R30 R44)

describes directional preponderance (i.e., the nystagmus tends to bear more to the right or left).This is a nonlocalizing finding. In the absence of a caloric response, an ice water caloric irrigation can determine if there is any residual function in the labyrinth.

ROTATIONAL TESTING

An alternate way of testing the VOR is to stimulate the horizontal canal by rotation. By rotating a patient in a motorized chair and measuring the compensatory eye movements over multiple rotations at different frequencies, a graph of vestibular function (horizontal canal) at more physiological stimulus frequencies can be

TABLE 34-1 SUMMARY OF ENG TESTING AND CLINICAL

SIGNIFICANCE

BPPV, benign paroxysmal positional vertigo; ENG, electronystagmography

obtained.This test can be performed in several different ways, but most commonly it is done with a clockwise and counterclockwise rotational stimulus. The stimulus can be described as a sine wave with a known frequency and angle of displacement.The time it takes to complete one cycle of clockwise and counterclockwise rotation is the period (T).The stimulus frequency is the number of oscillations of the chair per second and is measured in Hertz (i.e., a 1 Hz stimulus is a 1 cycle per second stimulus). As the frequency increases, the time it takes to complete a cycle decreases; thus frequency is inversely related to period. For a given period, changing the maximum angle of chair displacement will change the chair acceleration and velocity; thus displacement is usually kept constant. Frequencies tested range from 0.01 to

TABLE 34-2 STIMULUS PATTERNS OF THE VESTIBULAR

END-ORGANS

1 Hz and include those frequencies that are harmonics (multiples) of the fundamental test frequency.This tests response over the lowto midfrequency range within the linear range of the system’s dynamic range. For each frequency point, testing must be performed over an extended time period to allow the eye movement response to reach a steady state.Alternate testing protocols include sum of sines, which combines multiple frequencies, pseudorandom, and velocity trapezoids, all of which have distinct advantages and disadvantages. Testing is performed with eyes open and in the dark, which yields

stronger and more reliable responses. Subject attention is important for collecting accurate data.

The nystagmus response is recorded either with ENG electrodes or with an infrared video camera averaged and transformed into a sinusoid and can be described in terms of position, velocity, and acceleration. As shown in Fig. 34-1, the slow eye movement should be in the opposite direction of chair movement.The speed of the slow component of nystagmus can then be measured in several different ways. Phase describes the temporal difference between the stimulus waveform (chair movement) and the output waveform (eye movement), and gain describes the ratio of stimulus to eye movement output.At high frequencies the eye velocity matches the chair velocity (therefore, there is little difference between timing of the stimulus and response), the phase is low, and gain approaches one. At lower frequencies this relationship breaks down. (This is demonstrated in the plot of a normal rotation test seen in Fig. 34-3.) To understand why this occurs, we must briefly review the VOR in greater detail.The processing of theVOR can be broken down into two segments. Initially, angular acceleration is mechanically detected by the deflection of the cupula. Mathematical models have shown that deflection of the cupula is proportional to the velocity of head movement at frequencies greater than 0.1 Hz.This relationship breaks down at lower frequencies, requiring the addition of central processing to allow accurate eye movements. The stimulation of each vestibular endorgan results in a change in activity of the vestibular nucleus; this yields stimulation of agonist muscles and inhibition of antagonist muscles produced by each side. Several asymmetries are introduced to the system that

Figure 34-3 The results of a rotation test using sinusoidal harmonic stimulation at a frequency range of 0.01 to 0.64 Hz. The results are shown within 2 and 2.5 standard deviations. Both gain and phase have a linear pattern between 0.1 and 1 Hz. At lower frequencies the phase lead increases. Gain represents the

relationship between maximum stimulus and maximum eye velocity, whereas phase represents the timing difference between the stimulus and the output wave (see text). Symmetry of eye movement (predominance of rightward and leftward nystagmus) is shown in the rightmost graph.