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INSIGHTS in practice SPECIAL COLLECTION Five selected articles that supports your clinical approach to VNG/ENG INSIGHTS IN PRACTICE Clinical Topics in Otoneurology
Hearing assessment Fitting & Testing Balance assessment Best Practices for the Evaluation and Management DIRECTIONAL PREPONDERANCE REVISITED Baseline Shift and Gain Stephen P. Cass, M.D., M.P.H.
Kamran Barin, Ph.D. and Charles W. Stockwell, Ph.D. Asymmetry in the Caloric Test Stephen P. Cass, M.D., M.P.H., is Associate Professor in the Department
In the bithermal caloric test, each ear is irrigated twice— Each response starts about 20 seconds after onset of the of Otolaryngology at the University of Colorado Health Science Center. He isfellowship trained in Neurotology, specializing in disorders of the ear, hearing once with cool water (or air) and once with warm water irrigation, reaches peak intensity about 60 seconds later, and balance. His research interest involves basic and clinical studies of the Kamran Barin, Ph.D. (or air). Each irrigation stimulates the horizontal and then declines. Responses to right cool and left warm vestibular system. Dr. Cass is co-author with Dr. Joseph Furman of Vestibular semicircular canal of the irrigated ear and provokes a irrigations have rightward slow phases. Responses to right Disorders: A Case-Study Approach. nystagmus response. Cool stimulations provoke nystagmus warm and left cool irrigations have leftward slow phases.
responses with slow phases toward the irrigated ear. Warm The intensities of all four responses are exactly equal. We held a two-day course, "Best Practices for the Evaluation and Managementof Dizziness: A Workshop with Leading Clinicians." in Chicago on June 25- Kamran Barin, Ph.D., is Director of In the standard bithermal caloric test, right warm and left cool stimulations provoke nystagmus responses with slow Kamran Barin, Ph.D., is
In real life, the intensities of all four caloric are rarely 26, 2004. The course was presented by the Department of Otolaryngology, Balance Disorders Clinic at the Ohio irrigations are expected to generate right-beating nystagmus phases away from the irrigated ear. University of Colorado School of Medicine and sponsored by the University of Director of Balance Disorders exactly equal, because caloric stimuli are rarely exactly INSIGHTS IN PRACTICE State University Medical Center and while left warm and right cool irrigations are expected to Colorado School of Medicine, Office of Continuing Medical Education.
Clinic at the Ohio State Caloric stimuli are uncalibrated. Even though all patients equal and also because response intensity is affected by Educational support was provided by GN Otometrics, North America. I Assistant Professor, Department generate left-beating nystagmus. In a normal individual, the University Medical Center receive the same external stimulus, we know that some extraneous factors, such as alertness, eye position, and Clinical Topics in Otoneur
s course director.This is the second course in this series. The first of Otolaryngology, Department of intensities of all four caloric responses are approximately the course was held in Chicago on October 11-12, 2002. A copy of these pro- Fig. 1. Normal horizontal canal system at rest.
and Assistant Professor, patients receive stronger semicircular canal stimulation recording artifacts. For clarity of presentation, the caloric February
Speech and Hearing Sciences, The same and therefore, there is no significant difference between s was published as an Insights in Practice article that can be accessed on than others, presumably because their external ear canals responses shown in Fig. 1 (as well as in the figures that It is essential to understand the response of the vestibular system to injury. Ohio State University, Columbus, right-beating and left-beating responses. Some patients however, Fig. 1 shows a normal horizontal semicircular canal system, viewed from
Interpretation of Static Position are larger and straighter. We do make the key assumption follow) are idealized responses generated by computer, not In the first course we heard from clinicians in the specialties of primary care, have directional preponderance (DP) in which responses in one above. When the head is at rest, tonic neural input comes from the two hori- of Speech and Hearing that all four caloric stimulations of a given patient are actual responses recorded from patients.
neurotology, neurology, audiology, physical therapy, and psychiatry. We learned zontal canals and the level of input from the two canals is exactly the same.
Testing in VNG/ENG direction are significantly greater than the responses in the Sciences, The Ohio State equally strong. Thus we expect some patients to have THE FIXATION SUPPRESSION TEST that there is little controversy about management, but a great deal more con- opposite direction. DP is defined as the normalized (scaled) troversy about evaluation. Dizzy patients usually see a primary care physician University, Columbus, Ohio.
stronger caloric responses than others, but expect all four first. Most of them have benign disorders that can be successfully managed by difference between the peak nystagmus slow-phase velocities caloric responses to be of equal strength in a patient with Kamran Barin, Ph.D., and Laurie R. Davis, M.N.S. the primary care physician, but a few have serious disorders that require referral Kamran Barin, Ph.D.
(SPVs) from irrigations that are expected to generate right- normal vestibular function. The primary purpose of the bithermal caloric test is to to a specialist. Most of us agreed that the specialist who accepts dizzy patient The caloric test is quantified using two parameters: unilateral beating nystagmus and those from irrigations that are expected Charles W. Stockwell, Ph.D.,
detect a unilateral lesion of the horizontal semicircular 1 Sometimes moving the head from one position to another The fixation suppression test is part of the standard ENG From these data, the examiner then calculates should be prepared to take a comprehensive history and perform a weakness (UW) and directional preponderance (DP). The clinical to generate left-beating nystagmus. Mathematical formulas for is President of Charles W.
An example of normal caloric responses is shown in Fig. 1.
thorough physical examination, but we disagreed about which clinical observa- canal (or its afferent pathway). We can say that such a provokes a transient nystagmus, either immediately or examination. It tests the patient's ability to suppress Index (FI) by the formula, tions are required. Sometimes the history and physical examination fail to yield usefulness of UW, also known as canal paresis, is well established calculating DP and other caloric parameters are provided in the Stockwell & Associates, Inc., after a short delay. As the purpose of the static position Right Cool SPV = 40o/sec Left Warm SPV = 40o/sec lesion exists when caloric responses of one ear are a definite diagnosis and we need additional information provided by laboratory Kamran Barin, Ph.D. is the Director of but there is considerable debate about the value of DP. Some vestibular nystagmus during fixation upon a visual target.
a consulting firm based in Fix / SPVNoFix * 100.
tests. We disagreed about which tests should be ordered for which patients.
test is to detect the steady-state nystagmus that is present significantly weaker than those of the other ear.
Balance Disorders Clinic at the Ohio laboratories choose not to include DP in the interpretation of the The most commonly used test procedure is one described Caro, Michigan.
as long as the head remains in the critical head position, FI is a measure of nystagmus intensity durinIg econd course, I wanted to get closer to a clear definition of best prac- Interpretation of DP State University Medical Center and caloric test. One reason for the low clinical value of abnormal by Alpert (1974). For at least one right-beating and one An example is shown in Fig. 2. The responses of the right transient nystagmus should not be included in the tices for the evaluation and management of the dizzy patient. I assembled a fixation expressed as a percentage of nystagmus intensity Assistant Professor, Department of DP may be the fact that it can be caused by two distinct left-beating caloric response, the patient's nystagmus is ear are noticeably weaker than those of the left ear. faculty of experts in the specialties of neurotology, neurology, and vestibular interpretation of this test. Instead, the examiner should The normal limits reported for DP from different studies have just before opening the eyes. If nystagmus is completely Otolaryngology - Head and Neck pathologies. The first is a static asymmetry in the peripheral or recorded with eyes closed until shortly after the peak of testing. I asked them to describe their methods, to present the evidence under- Right Cool SPV = 20o/sec amr 40o/sec
an Barin, Ph.D., is
perform the appropriate maneuver and interpret the ranged from as low as 20% to as high as 50%. Currently, most suppressed by fixation, FI will be 0%. If nystagm decision-making, and to indicate where the evidence is weak. I Right Warm SPV = 40o/sec Surgery, Department of Speech and central vestibular pathways and the second is a gain asymmetry the response. At that time the examiner tells the patient Left Cool SPV = 40o/sec Director of the Balance allowed plenty of time for discussion among faculty members and the audi- results as a part of the dynamic position testing.
laboratories consider DP of less than 30% to be within normal incompletely suppressed by fixation, FI will be between to open the eyes and fixate upon a small stationary target Hearing Science, and Biomedical in the secondary vestibular neurons within the vestibular nuclei. ence. In this manner, I hoped to identify areas of consensus and to hear various Disorders Clinic at the Ohio 0% and 100%. If nystagmus is enhanced by fixation, FI Engineering Program. Because the current formula for calculating DP combines both limits (Sills et al., 1977).
Figure 1.
for about 10 seconds. Then the examiner computes the Normal caloric responses. The two responses of the right viewpoints in areas of disagreement.
Fig. 2. Normal horizontal canal system during angular acceleration to
State University Medical ear (RC and RW) are on the left side of the chart, and the two will be greater than 100%. The normal range for FI is 60% average slow phase velocity of three nystagmus beats just abnormalities into a single parameter, it is possible that important I began the course with a quick review of vestibular anatomy
responses of the left ear (LW and LC) are on the right side of the Center and Assistant 2 Traditionally, static position testing has been limited to There has been a controversy about the interpretation and clinical or less, which means that, in 95% of normal individuals, Dr. Barin has taught national and international courses and information is being lost. This article reviews the abnormalities before opening the eyes (SPV and physiology. I described the anatomy of the vestibular labyrinth and ori-
Fig. 2 shows what happens when the head undergoes angular acceleration to
chart. Vertical axis: slow phase eye velocity (deg/sec). Values NoFix) and the average slow Professor, Department of the interpretation of horizontal eye movements. The main Right Warm SPV = 20o/sec Left Cool SPV = 40o/sec visual fixation suppresses vestibular nystagmeus n of the labyrinth in the head, and explained the structure and function the person's left (counterclockwise in our view). Endolymph movement sla value of abnormal DP. Initially, abnormal DP was considered above zero denote rightward velocities, and values below zero phase velocity of three nystagmus beats during fixation minars in different areas of vestibular assessment and that can cause DP and offers computational methods for Otolaryngology and of the sensory receptors in the ampullae of the semicircular canals and the behind head movement. In the left horizontal canal, this lag deflects the cupu- reason for this is that the vertical channel in ENG is often denote leftward velocities. Horizontal axis: time (seconds) after a central finding but this conclusion was reached based on rehabilitation. He serves as a consultant for Otometrics. separating the contribution of each abnormality.
Fix), as shown in Figure 1.
maculae of the utricle and saccule. I traced the neural pathways of the vestibu- onset of irrigation. la upward (in our view), causing an increase in the level of neural input. In the Figure 2. Unilateral weakness.
Department of Speech and noisy and contaminated by eye blinks. In VNG, the caloric responses that were obtained in the presence of fixation lar nerve, vestibular nuclei, and the vestibulo-ocular and vestibulo-spinal sys- right horizontal canal, this lag deflects the cupula downward (in our view), Hearing Sciences, The Ohio differences in the noise level and resolution between (Fitzgerald and Hallpike, 1942). Therefore, what was considered IXATION SUPPRESSION AND SMOOTH PURSUIT
continues , .Columbus,
horizontal and vertical channels are relatively insignificant.
There is strong experimental and clinical support for the Therefore, VNG users should consider vertical nystagmus idea that the pursuit system is responsible for The purpose of static position testing, also known as the in the interpretation of the static position test. ENG users vestibular nystagmus (Chambers and Gresty, 1982; positional test, in the video- and electro-nystagmography may wish to skip this step because of the high level of Laurie R. Davis, M.N.S., is
Halmagyi and Gresty, 1979). The pursuit system is designed (VNG/ENG) test battery is to determine the presence and artifacts in the vertical channel. The flow charts in a clinical audiologist at to keep the image of a small moving target on the fovea— characteristic of nystagmus when the patient's head is placed Figures 2 and 3 show the interpretation for horizontal and Mayo Clinic Scottsdale in the most sensitive part of retina. Movement of the in different orientations with respect to gravity. Although the vertical nystagmus, respectively.
target's image across the retina causes retinal slip. When test procedure is relatively simple (see Barin, 2006, for the pursuit system detects retinal slip, it triggers an eye details), the interpretation of the results may not be When nystagmus has both horizontal and vertical movement that tracks the target. This tracking eye straightforward to inexperienced VNG/ENG examiners. This components, the examiner must make sure that it movement minimizes retinal slip and tends to keep the article provides a basic step-by-step algorithm for the represents true eye movements and is not due to crosstalk.
Figure 1. Calculating average slow phase velocity of nystagmus
target's image on the fovea. When a person with vestibular Crosstalk occurs when eye movements in one channel with eyes closed (SPV interpretation of static position testing.
NoFix) and during visual fixation (SPVFix).
nystagmus fixates upon a stationary target, the slow generate activities in the other channel. Those activities EO indicates the point at which the patient opened the eyes.
phases of the nystagmus move the target's image across do not represent true eye movements and are usually the retina, thus generating retinal slip. The pursuit system The flow chart in Figure 1 is a summary of the interpretation caused by the misalignment of the electrodes in ENG or reacts by moving the eyes in the direction opposite the process. Additional information is provided below for the continues nystagmus slow phases, thus suppressing the nystagmus.
numbered items on the flow chart. INSIGHTS in practice SPECIAL COLLECTION Benefit from "The Chartr Experience"
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INSIGHTS in practice SPECIAL COLLECTION INSIGHTS IN PRACTICE Clinical Topics in Otoneurology
DIRECTIONAL PREPONDERANCE REVISITED Kamran Barin, Ph.D. and Charles W. Stockwell, Ph.D. In the bithermal caloric test, each ear is irrigated twice— Each response starts about 20 seconds after onset of the once with cool water (or air) and once with warm water irrigation, reaches peak intensity about 60 seconds later, (or air). Each irrigation stimulates the horizontal and then declines. Responses to right cool and left warm semicircular canal of the irrigated ear and provokes a irrigations have rightward slow phases. Responses to right nystagmus response. Cool stimulations provoke nystagmus warm and left cool irrigations have leftward slow phases.
responses with slow phases toward the irrigated ear. Warm The intensities of all four responses are exactly equal. stimulations provoke nystagmus responses with slow Kamran Barin, Ph.D., is
In real life, the intensities of all four caloric are rarely phases away from the irrigated ear. Director of Balance Disorders exactly equal, because caloric stimuli are rarely exactly Clinic at the Ohio State Caloric stimuli are uncalibrated. Even though all patients equal and also because response intensity is affected by University Medical Center receive the same external stimulus, we know that some extraneous factors, such as alertness, eye position, and and Assistant Professor, patients receive stronger semicircular canal stimulation recording artifacts. For clarity of presentation, the caloric than others, presumably because their external ear canals responses shown in Fig. 1 (as well as in the figures that are larger and straighter. We do make the key assumption follow) are idealized responses generated by computer, not of Speech and Hearing that all four caloric stimulations of a given patient are actual responses recorded from patients.
Sciences, The Ohio State equally strong. Thus we expect some patients to have University, Columbus, Ohio.
stronger caloric responses than others, but expect all four caloric responses to be of equal strength in a patient withnormal vestibular function. The primary purpose of the bithermal caloric test is to Charles W. Stockwell, Ph.D.,
detect a unilateral lesion of the horizontal semicircular is President of Charles W.
An example of normal caloric responses is shown in Fig. 1.
canal (or its afferent pathway). We can say that such a Stockwell & Associates, Inc., Right Cool SPV = 40o/sec Left Warm SPV = 40o/sec lesion exists when caloric responses of one ear are a consulting firm based in significantly weaker than those of the other ear.
Caro, Michigan.
An example is shown in Fig. 2. The responses of the right ear are noticeably weaker than those of the left ear. Right Cool SPV = 20o/sec Left Warm SPV = 40o/sec Right Warm SPV = 40o/sec Left Cool SPV = 40o/sec Figure 1. Normal caloric responses. The two responses of the right
ear (RC and RW) are on the left side of the chart, and the two responses of the left ear (LW and LC) are on the right side of the chart. Vertical axis: slow phase eye velocity (deg/sec). Values Right Warm SPV = 20o/sec Left Cool SPV = 40o/sec above zero denote rightward velocities, and values below zero denote leftward velocities. Horizontal axis: time (seconds) after onset of irrigation. Figure 2. Unilateral weakness.
INSIGHTS in practice SPECIAL COLLECTION Is this weakness outside normal limits? The preferred direction are weaker than those in the other direction.
measure of caloric response intensity is peak slow phase When we provoke two responses from each ear—one in velocity, that is, slow phase velocity of nystagmus at the each direction—and sum these two responses when point of strongest response. To calculate unilateral calculating unilateral weakness, then any directional weakness, we insert these peak slow phase velocity values preponderance cancels out. into a formula first proposed by Jongkees and Philipszoon Over the years, the phenomenon of directional (1964). First we find the difference between ears by preponderance has been the source of much controversy summing the peak slow phase velocities of the two and confusion. Originally, Fitzgerald and Hallpike (1942) responses of the right ear and, from this sum, subtracting said that directional preponderance is a sign of central the sum of the peak slow phase velocities of the two nervous system dysfunction, but they were observing responses of the left ear. Then, because unilateral caloric nystagmus with the patient's eyes open and so weakness is proportional to caloric response strength and what they called directional preponderance was actually caloric stimuli are uncalibrated, we normalize this asymmetric fixation suppression of caloric nystagmus.
difference between ears, that is, we divide it by the sum of Nevertheless this interpretation of directional the peak slow phase velocities of all four responses.
preponderance persisted for many years, despite the fact Finally we multiply the result by 100. In other words, that later investigators (for example, Stahle, 1958; Coats, (RW + RC) – (LW + LC) 1965; Baloh et al., 1977) recorded caloric responses with Eq. 1 X 100 = UW (in percent), visual fixation denied and found directional preponderance to be associated with a variety of vestibular disorders,both peripheral and central.
where RW is peak slow phase velocity of the right warmresponse, RC is peak slow phase velocity of the right cool To compound the confusion, it turns out that directional response, LW is peak slow phase velocity of the left warm preponderance is comprised of two different abnormalities.
response, LC is peak slow phase velocity of the left cool The first is gain asymmetry, in which responses in one response, and UW is unilateral weakness. A positive UW direction are weaker than those in the other direction.
denotes a unilateral weakness in the left ear, and a The second is bias, in which caloric responses are equally negative UW denotes a unilateral weakness in the right ear.
strong in both directions, but the baseline of the responses A UW greater than about 25 percent is generally considered outside the normal limit. Inserting peak slow phase velocity values from Fig. 2 into An example of gain asymmetry is shown in Fig. 3.
(20 + 20) – (40 + 40) Right Cool SPV = 40o/sec X 100 = -33 percent, Left Warm SPV = 40o/sec which is outside the normal limit. This result is localizing.
It indicates a lesion of the right horizontal semicircular canal or its afferent pathway. Right Warm SPV = 10o/sec Left Cool SPV = 10o/sec Figure 3. Gain asymmetry.
If all caloric tests yielded responses like those shown in Responses with leftward slow phases are clearly weaker Fig. 1 or Fig. 2, then we would not have to irrigate each than those with rightward slow phases.
ear twice. A single irrigation of each ear, either warm or Is this gain asymmetry outside normal limits? To calculate cool, would suffice. Unfortunately, some patients have a gain asymmetry, we use a formula that was also first directional preponderance, that is, caloric responses in one proposed by Jongkees and Philipszoon (1964). First we INSIGHTS in practice SPECIAL COLLECTION find the difference between the two directions of 15,542 patients who underwent bithermal caloric testing.
nystagmus by summing the peak slow phase velocities of All of these patients had DP's of at least 40 percent and the two responses with leftward slow phases and, from this none had significant unilateral weaknesses or significant sum, subtracting the sum of the peak slow phase velocities spontaneous nystagmus. About half of them had Meniere's of the two responses with rightward slow phases. Then disease or benign paroxysmal positional vertigo, and most because gain asymmetry is proportional to caloric response of the others received no diagnosis. Halmagyi et al. said strength, we normalize this difference by dividing it by the that gain asymmetry is generally a transient, benign sum of the peak slow phase velocities of all four responses.
abnormality. In a companion paper (Cartwright et al., Then we multiply the result by 100. In other words, 2000), they postulated that it is due to an asymmetricdynamic response of neurons in the medial vestibular (RW + LC) – (LW + RC) nuclei on either side of the brain. We have never seen a Eq. 2 X 100 = DP (in percent), convincing case of gain asymmetry in our own laboratories (Stockwell, 1987; Barin & Bahram, 2001), but the report of where RW, RC, LW, and LC are the same as in Eq. 1, and DP Halmagyi et al. indicates that it does in fact exist.
is directional preponderance. A DP greater than about 30percent is generally considered to be outside the normal limit. A positive DP denotes a directional preponderanceto the right, and a negative DP denotes a directional An example of bias is shown in Fig. 4. There is no preponderance to the left.
Right Cool SPV = 60o/sec Left Warm SPV = 60o/sec A note on nomenclature: It is customary to designate directional preponderance according to the direction of stronger fast phases. Thus when it is said that there is a directional preponderance to the left, it is meant that responses with leftward fast phases are stronger than those Right Warm SPV = 20o/sec Left Cool SPV = 20o/sec with rightward fast phases. However we think it makes more sense to designate directional preponderance Figure 4. Bias.
according to the direction of weaker slow phases, since unilateral weakness and no gain asymmetry, but the slow phases are being displayed in the chart. Thus when baseline of all responses is shifted upward, that is, to the we say there is a directional preponderance to the left, we right, by about 20 deg/sec. This patient also has mean that responses with leftward slow phases are weaker spontaneous nystagmus with rightward slow phase than those with rightward slow phases.
velocities of about 20 deg/sec with eyes closed.
Inserting peak slow phase velocity values from Fig. 3 into Spontaneous nystagmus and bias are both due to a static baseline shift in the horizontal vestibulo-ocular system, (10 + 10) – (40 + 40) and they always occur together. Like gain asymmetry, bias X 100 = -60 percent, (and spontaneous nystagmus) occurs in patients with a wide variety of vestibular disorders, both peripheral andcentral.
which is outside the normal limit. This result indicatesthat the gain of responses with leftward slow phases is Many normal individuals have a small amount of bias and significantly lower than the gain of responses with spontaneous nystagmus, so how much is outside the rightward slow phases, which is a nonlocalizing normal limit? It is generally agreed that the normal limit is about 6 deg/sec, so the bias of 20 deg/sec seen in Fig.
4 is abnormal.
Gain asymmetry is extremely rare. In fact, for many yearswe did not believe it even existed, but recently Halmagyi What happens when we calculate directional preponderance et al. (2000) said they found this abnormality in 114 of in this patient? Inserting peak slow phase velocity valuesfrom Fig. 4 into Eq. 2 yields INSIGHTS in practice SPECIAL COLLECTION (20 + 20) – (60 + 60) UNILATERAL WEAKNESS AND GAIN ASYMMETRY
X 100 = -50 percent.
The three abnormalities described above can exist alone or in any combination. Fig. 5 shows an example of two This is a mistake. We cannot use Eq. 2 to calculate bias.
Right Cool SPV = 20o/sec This formula normalizes the difference between the two Left Warm SPV = 40o/sec directions of nystagmus under the presumption that the difference is proportional to response strength. Bias is not proportional to response strength, so the formula is inappropriate when the difference is due to bias. Right Warm SPV = 5o/sec Left Cool SPV = 10o/sec Eq. 2 is appropriate for calculating gain asymmetry, because gain asymmetry is proportional to response Figure 5. Unilateral weakness and gain asymmetry.
strength. However we must first eliminate the bias. To dothis, we simply subtract the bias from the peak slow phase coexisting abnormalities—unilateral weakness and gain velocities of caloric responses in the same direction and asymmetry. First we calculate unilateral weakness using add it to the peak slow phase velocities of responses in the opposite direction and then calculate gain asymmetry (5 + 20) – (40 + 10) using the new values. In other words, X 100 = -33 percent.
(RW' + LC') – (LW' + RC') Eq. 3 X 100 = GA (in percent), Then we calculate gain asymmetry using Eq. 3, RW' + LC' + LW' + RC' (5 + 10) – (40 + 20) where GA is gain asymmetry and RW', LC', LW', and RC' are X 100 = -60 percent.
RW, LC, LW, and RC, respectively, after eliminating any Note that the presence of gain asymmetry has no effect To illustrate, if we eliminate the bias from peak slow phase whatsoever on the value we get for unilateral weakness, velocity values in Fig. 4, we get and vice versa. Note also that since there was no bias, we could have used either Eq. 2 or Eq. 3 to calculate gain UNILATERAL WEAKNESS AND BIAS
and when we insert these new values into Eq. 3, we get Fig 6. shows an example of two coexisting abnormalities— (40 + 40) – (40 + 40) Right Cool SPV = 40o/sec Left Warm SPV = 60o/sec X 100 = 0 percent.
This result indicates no gain asymmetry, which is correct. Right Warm SPV = 0o/sec Left Cool SPV = 20o/sec Figure 6. Unilateral weakness and bias.
INSIGHTS in practice SPECIAL COLLECTION unilateral weakness and bias. The bias is about 20 (10 + 10) – (40 + 40) deg/sec, and the patient has spontaneous nystagmus with X 100 = -60 percent.
rightward slow phase velocities of about 20 deg/sec with eyes closed. We calculate unilateral weakness using Eq. 1, Note that the normal limit of 30 percent for directional (0 + 40) – (60 + 20) preponderance is based on studies that lumped together X 100 = -33 percent.
gain asymmetry and bias. We do not have a normal limit for gain asymmetry by itself, but it is probably somewhatless than 30 percent. We need new normative studies to Note that the presence of bias has no effect on the value establish a correct normal limit for gain asymmetry.
we get for unilateral weakness, so we do not have toeliminate it first.
UNILATERAL WEAKNESS, GAIN ASYMMETRY, AND BIAS
This combination of unilateral weakness and bias ischaracteristic of a sudden and recent unilateral peripheral Fig. 8 shows an example of three coexisting vestibular lesion. Over time, the bias (and the patient's abnormalities—unilateral weakness, gain asymmetry, and spontaneous nystagmus) decline due to vestibular Right Cool SPV = 40o/sec Left Warm SPV = 60o/sec compensation, although the unilateral weakness may AIN ASYMMETRY AND BIAS
Fig. 7 shows an example of two coexisting abnormalities— Right Warm SPV = -15o/sec Left Cool SPV = -10o/sec Right Cool SPV = 60o/sec Left Warm SPV = 60o/sec Figure 8. Unilateral weakness, gain asymmetry, and bias.
bias. The bias is about 20 deg/sec, and the patient has spontaneous nystagmus with rightward slow phase velocities of about 20 deg/sec with eyes closed. The right warm and left cool caloric responses failed to overcome the Right Warm SPV = -10o/sec Left Cool SPV = -10o/sec patient's spontaneous nystagmus, so RW and LC are expressed as negative numbers. First we calculate Figure 7. Gain asymmetry and bias.
unilateral weakness using Eq. 1, gain asymmetry and bias. The bias is about 20 deg/sec, (-15 + 40) – (60 - 10) and the patient has spontaneous nystagmus with rightward X 100 = -33 percent.
slow phase velocities of about 20 deg/sec with eyes closed. Note that the right warm and left cool caloricresponses failed to overcome the spontaneous nystagmus We must eliminate the bias before calculating gain completely, so RW and LC are opposite the expected direction. When this happens, their values are expressed as negative numbers.
Before calculating gain asymmetry, we have to eliminate Then we calculate gain asymmetry by inserting the new values into Eq. 3, (5 + 10) – (40 + 20) X 100 = -60 percent.
Then we use the new values to calculate gain asymmetry INSIGHTS in practice SPECIAL COLLECTION Coats, A.C., (1965). Directional Preponderance and In the bithermal caloric test, each ear receives two Unilateral Weakness As Observed in the irrigations—a warm irrigation that provokes a response in Electronystagmographic Examination. Ann Otol Rhinol one direction and a cool irrigation that provokes a Laryngol 74: 655.
response in the other direction. From these four Fitzgerald G., and Hallpike, C.S., (1942). Studies in Human responses, we can distinguish between unilateral weakness, Vestibular Function. I: Observations on the Directional in which the responses of one ear are weaker than those of Preponderance (‘Nystagmusbereitschaft') of Caloric the other ear, and directional preponderance, in which Nystagmus Resulting from Cerebral Lesions. Brain 62 (part responses in one direction are weaker than those in the other direction. Directional preponderance has two Halmagyi, G.M., Cremer, P.D., Anderson, J., Murofushi, T, components. The first is gain asymmetry, which is and Curthoys, I.S., (2000). Isolated Directional proportional to caloric response strength. The second is Preponderance of Caloric Nystagmus. I. Clinical bias, which is independent of caloric response strength.
Significance. Am J Otol 21: 559.
Before calculating gain asymmetry, it is first necessary to Jongkees, L.B.W., and Philipszoon, A.J., (1964).
eliminate bias from the responses. Electronystagmography. Acta Otolaryngol (Suppl. 189).
Unilateral weakness is highly localizing. It denotes a Stahle, J., (1958). Electro-nystagmography in the caloric lesion of the horizontal semicircular canal or its afferents and rotary tests. Acta Otolaryngol (Suppl.) 137: 5.
on the side of the weaker response. Gain asymmetry and Stockwell, C.W., (1987). Directional Preponderance. ENG bias are nonlocalizing. Both abnormalities denote a Report, ICS Medical, 37.
vestibular lesion, either peripheral or central.
A NOTE TO ICS MEDICAL CUSTOMERS
The elimination of bias described in this article cannot be Baloh, R.W., Sills, A. W., and Honrubia, V., (1977). Caloric performed by current ICS Medical software and must be Testing: Patients with Peripheral and Central Vestibular done by hand. This feature will be included in our next Lesions. Ann Otol Rhinol Laryngol (Suppl.) 43: 24.
software release.
Barin, K., and Bahram, V., (2001). Clinical Significance ofDirectional Preponderance in Bithermal Caloric Testing.
Presentation at ARO Annual Meeting.
Cartwright, A.D., Cremer, P.D., Halmagyi, G.M., andCurthoys, I.S., (2000). Isolated Directional Preponderanceof Caloric Nystagmus: II. A Neural Network Model. Am JOtol 21: 568.
An Exclusive Publication of ICS Medical
125 Commerce Drive Schaumburg, IL 60173-5329 2002 ICS Medical 913-002 022000 Printed in USA INSIGHTS in practice SPECIAL COLLECTION INSIGHTS IN PRACTICE Clinical Topics in Otoneurology
THE FIXATION SUPPRESSION TEST Kamran Barin, Ph.D., and Laurie R. Davis, M.N.S. The fixation suppression test is part of the standard ENG From these data, the examiner then calculates a Fixation examination. It tests the patient's ability to suppress Index (FI) by the formula, vestibular nystagmus during fixation upon a visual target.
The most commonly used test procedure is one described Fix / SPVNoFix * 100.
by Alpert (1974). For at least one right-beating and one FI is a measure of nystagmus intensity during visual left-beating caloric response, the patient's nystagmus is fixation expressed as a percentage of nystagmus intensity recorded with eyes closed until shortly after the peak of just before opening the eyes. If nystagmus is completely Kamran Barin, Ph.D., is
the response. At that time the examiner tells the patient suppressed by fixation, FI will be 0%. If nystagmus is Director of the Balance to open the eyes and fixate upon a small stationary target incompletely suppressed by fixation, FI will be between Disorders Clinic at the Ohio for about 10 seconds. Then the examiner computes the 0% and 100%. If nystagmus is enhanced by fixation, FI State University Medical average slow phase velocity of three nystagmus beats just will be greater than 100%. The normal range for FI is 60% Center and Assistant before opening the eyes (SPV or less, which means that, in 95% of normal individuals, Professor, Department of NoFix) and the average slow phase velocity of three nystagmus beats during fixation visual fixation suppresses vestibular nystagmus by at Otolaryngology and Department of Speech and Fix), as shown in Figure 1.
Hearing Sciences, The Ohio FIXATION SUPPRESSION AND SMOOTH PURSUIT
State University, Columbus,Ohio.
There is strong experimental and clinical support for theidea that the pursuit system is responsible for suppressingvestibular nystagmus (Chambers and Gresty, 1982; Laurie R. Davis, M.N.S., is
Halmagyi and Gresty, 1979). The pursuit system is designed a clinical audiologist at to keep the image of a small moving target on the fovea— Mayo Clinic Scottsdale in the most sensitive part of retina. Movement of the target's image across the retina causes retinal slip. Whenthe pursuit system detects retinal slip, it triggers an eyemovement that tracks the target. This tracking eyemovement minimizes retinal slip and tends to keep the Figure 1. Calculating average slow phase velocity of nystagmus
target's image on the fovea. When a person with vestibular with eyes closed (SPVNoFix) and during visual fixation (SPVFix).
nystagmus fixates upon a stationary target, the slow EO indicates the point at which the patient opened the eyes.
phases of the nystagmus move the target's image acrossthe retina, thus generating retinal slip. The pursuit systemreacts by moving the eyes in the direction opposite thenystagmus slow phases, thus suppressing the nystagmus.
INSIGHTS in practice SPECIAL COLLECTION Some investigators (e.g., Barnes, et al., 1978) have saidthat if the pursuit system is responsible for fixationsuppression of vestibular nystagmus, then the fixationsuppression test is really a test of the pursuit system,which means that the fixation suppression test isredundant, because the pursuit system is already beingtested by two other ENG tests—the tracking test and theoptokinetic test. On the other hand, Tomlinson andRobinson (1981) have said that a different system—thevestibular cancellation system—is primarily responsible forfixation suppression of vestibular nystagmus. They havesaid that the vestibular cancellation system reducesnystagmus intensity and places the image of the targetnear the fovea, and then the pursuit system eliminates anyresidual nystagmus. If so, then the fixation suppressiontest evaluates a different system and is therefore notredundant. It may reveal abnormalities not detected bythe tracking and the optokinetic tests (and vice versa). Let us examine this issue by comparing the results of thefixation suppression test with those of the tracking andoptokinetic tests.
Figure 2. Test results from a patient with normal tracking (A),
optokinetic responses (B), and fixation suppression (C).
NORMAL FIXATION SUPPRESSION WITH NORMAL
TRACKING AND OPTOKINETIC RESPONSES
In the optokinetic test (Figure 2B), the patient tracks a Figure 2 shows a patient with normal tracking, optokinetic series of small targets moving first to the right and then to responses, and fixation suppression. the left at a constant velocity of 40º/sec. Nystagmus In the tracking test (Figure 2A), the patient follows a small responses are considered normal if slow phase velocities target oscillating back and forth in the horizontal plane.
are at least 30º/sec in both directions. In this patient, Frequencies of target motion range from 0.2 to 0.7 Hz with average slow phases velocities are 38º/sec for rightward peak-to-peak amplitudes of 30º at all frequencies. Peak moving targets and 33º/sec for leftward moving targets.
target velocities range from 20 to 70º/sec. The ratio of Both values are within normal limits. (Note that the peak eye velocity to peak target velocity is determined for optokinetic test, despite its name, is not a test of the each target frequency and compared with age- and sex- optokinetic system; it is a test of the pursuit system. A matched normative values. The top panel shows a sample true test of the optokinetic system would require targets of target motion and superimposed eye motion at 0.2 Hz.
that subtend the full visual field.) The bottom panel shows tracking gains for rightward and In the fixation suppression test (Figure 2C), FI is equal to leftward tracking at each target frequency. Tracking is 20% for nystagmus with rightward slow phases and 24% within normal limits for both directions of target motion at for nystagmus with leftward slow phases. Both values are all frequencies.
within normal limits.
INSIGHTS in practice SPECIAL COLLECTION ABNORMAL FIXATION SUPPRESSION WITH ABNORMAL
ABNORMAL FIXATION SUPPRESSION WITH NORMAL
TRACKING AND OPTOKINETIC RESPONSES
TRACKING AND OPTOKINETIC RESPONSES
Figure 3 shows a patient with abnormal tracking, Figure 4 shows a patient with abnormal fixation optokinetic responses, and fixation suppression. In the suppression, but normal tracking and optokinetic Figure 3. Test results from a patient with abnormal tracking (A),
Figure 4. Test results from a patient with normal tracking (A)
optokinetic responses (B), and fixation suppression (C).
and optokinetic responses (B) and with abnormal fixationsuppression (C).
tracking test (Figure 3A), the patient has saccadic pursuitand tracking gains are abnormally low for both directions responses. In the tracking test (Figure 4A), the patient of target motion. In the optokinetic test (Figure 3B), follows the target smoothly and tracking gains are within average slow phase velocity of optokinetic nystagmus is normal limits at all target frequencies. In the optokinetic 3º/sec for rightward moving targets and 6º/sec for leftward test (Figure 4B), average slow phase velocity of moving targets. In the fixation suppression test (Figure optokinetic nystagmus is 31º/sec for rightward moving 3C), FI is 200% for nystagmus with rightward slow phases targets and 37º/sec for leftward moving targets. In the and 100% for nystagmus with leftward slow phases. These fixation suppression test (Figure 4C), the patient fails to abnormalities indicate a CNS lesion. They are seen in suppress the caloric nystagmus adequately. FI is patients with a variety of neurological disorders involving approximately 64% for nystagmus with rightward slow the cerebellum, brainstem, or cerebral cortex.
phases and 75% for nystagmus with leftward slow phases.
This result is uncommon. It denotes a lesion in the centralnervous system, most likely in the flocculus of thecerebellum.
INSIGHTS in practice SPECIAL COLLECTION Abnormal fixation suppression with normal pursuit supportsthe hypothesis of Tomlinson and Robinson (1981) thatfixation suppression and pursuit are mediated by separateneural mechanisms, but there are other possibleexplanations. First, tracking and fixation suppression areunder voluntary control, so perhaps the patient simplyfailed to fixate on the visual target during the fixationsuppression test. Second, the stimuli used in the trackingand optokinetic tests have predictable trajectories, whereasthe timing of nystagmus fast phases is less predictable.
Predictable targets are easier to track than unpredictabletargets (Leigh and Zee, 1991). Third, the velocity limit ofthe pursuit system is approximately 30-40º/sec for younghealthy persons and closer to 20º/sec for persons over theage of 60. Therefore a patient could have normal pursuitand yet display abnormal fixation suppression if theintensity of to-be-suppressed nystagmus exceeds thepatient's pursuit velocity limit. (It should be noted thatthis third explanation is implausible in the case shownhere, since slow phase velocity of caloric nystagmus just Figure 5. Test results from a patient with abnormal tracking (A)
before opening the eyes is only about 24-25º/sec.) and optokinetic responses (B) and with normal fixationsuppression (C).
NORMAL FIXATION SUPPRESSION WITH ABNORMAL
TRACKING AND OPTOKINETIC RESPONSES
This result is also uncommon. It also supports the Figure 5 shows a patient with abnormal tracking and hypothesis of separate pursuit and vestibular cancellation optokinetic responses, but normal fixation suppression. In systems, because then it would be possible for a patient the tracking test (Figure 5A), the patient has saccadic with defective pursuit to suppress vestibular nystagmus pursuit and lower than normal tracking gains in both using the vestibular cancellation system. But again there directions. The tracking defect is asymmetric, being much might be another explanation. Weak caloric nystagmus worse when the target moves to the right. In the does not pose much of a challenge to the pursuit system.
optokinetic test (Figure 5B), average slow phase velocity Thus a patient who has a mild pursuit defect and weak of optokinetic nystagmus is 16º/sec for rightward moving caloric responses may be able to suppress caloric targets and 27º/sec for leftward moving targets. In the nystagmus, yet be unable to generate normal tracking and fixation suppression test (Figure 5C), nystagmus is virtually optokinetic responses. eliminated during fixation and the FI is equal to 0% forboth directions of nystagmus.
INSIGHTS in practice SPECIAL COLLECTION fixation. Avoid beats that occur within one secondbefore and after opening the eyes, since these beats Should we perform the fixation suppression test as part of often contain artifact.
the standard ENG examination? We think the answer is"yes." The procedure is simple and benign and does not 5. When interpreting the fixation suppression test, take additional testing time. Two test results presented recognize that nystagmus intensities between 20 and above (Figures 4 and 5) support the hypothesis that 40º/sec are optimal for testing fixation suppression.
pursuit and fixation suppression are mediated by separate Intensities above 40º/sec may overwhelm even a neural mechanisms. However, such results do not prove normal pursuit (or cancellation) system and yield false the hypothesis, since other possible explanations exist.
positive results, especially in elderly patients.
Nevertheless it is a fact that the fixation suppression test Intensities below 20º/sec may not pose a sufficient sometimes detects abnormalities in patients who have challenge to the pursuit (or cancellation) system and normal tracking and optokinetic responses and vice versa.
yield false negative results.
The fixation suppression test has a major shortcoming—thedifficulty of the test depends upon how strong caloric nystagmus happens to be when the patient opens the eyes.
Alpert, J.N., (1974). Failure of fixation suppression: A If the nystagmus is very weak, even a patient with pathologic effect of vision on caloric nystagmus.
defective pursuit (or cancellation) can suppress it. If it is very strong, even a person with normal pursuit (or Barnes, G.R., Benson, A.J., and Prior, A.R.J., (1978).
cancellation) cannot suppress it. There are other Visual-vestibular interaction in the control of eye shortcomings as well. Therefore the test must be conducted movement. Aviat Space Environ Med, 49:557-564.
with care and the results interpreted with caution. Werecommend that attention be paid to the following details: Chambers, B.R., and Gresty, M.A. (1983). The relationshipbetween disordered pursuit and vestibulo-ocular reflex 1. Perform the test during all four caloric responses. Then suppression. J Neurol Neurosurg Psychiatr, 46:61-66.
you will have two opportunities to observe fixationsuppression for each direction of nystagmus.
Halmagyi, G.M., and Gresty, M.A. (1979). Clinical signs ofvisual-vestibular interaction. J Neurol Neurosurg Psychiatr, 2. Closely watch the tracing and ask the patient to open the eyes immediately after the response reaches peakintensity, which usually occurs between 60 and 90 Leigh, R.J., and Zee, D.S. (1991). The Neurology of Eye seconds after the onset of the irrigation.
Movements. F.A. Davis Company, Philadelphia.
3. When testing fixation suppression, make sure the Tomlinson, R.D., and Robinson, D.A. (1981). Is the patient is actually fixating on a small visual target. It is vestibulo-ocular reflex cancelled by smooth pursuit? In not enough for the patient simply to open the eyes.
Fuchs, A. and Becker W. (eds.): Progress in Oculomotor Some patients are reluctant to fixate, especially if Research, New York, Elsevier/North-Holland, 533-539.
distressed by the dizziness that is part of the caloricresponse.
4. When measuring nystagmus slow phase velocities, select beats from a 5 second time period just beforeopening the eyes and a 5 second time period just after INSIGHTS in practice SPECIAL COLLECTION COMMENTS/QUESTIONS ON ARTICLE
DIZZINESS DIAGNOSTIC FORUM AND CALORIC TEST
We would welcome any comments or questions you mayhave regarding this article. Please e-mail us at: These are two valuable educational opportunities offered [email protected] or send a fax to ICS Medical through the ICS Medical website. The Forum on Diagnosis Educational Services at 847/534-2151. Be sure to give us and Management of Dizziness includes a complete list of your contact details so the authors may respond to you.
disorders that cause dizziness and information about each. The Caloric Test Course is an hour-long course on ENG COURSES 2003
administration and interpretation of the Caloric Test. Please look on our website: www.icsmedical.com for datesand locations. These two-day courses are invaluable forprofessionals looking to gain more knowledge onadministration and interpretation of ENG's.
NEW VIDEO CLIPS CASE STUDIES CD
We're pleased to make available a CD containing fourinteresting Case Studies, which feature video clips ofabnormal eye movements gathered on the ICS CHARTR VNGsystem. The Case Studies are presented by Preston C.
Calvert, M.D., Dept. of Neurology, Johns Hopkins UniversitySchool of Medicine. The CD sells for $10. For moreinformation, please visit our website.
An Exclusive Publication of ICS Medical
125 Commerce Drive Schaumburg, IL 60173-5329 2002 ICS Medical 913-002 022000 Printed in USA INSIGHTS in practice SPECIAL COLLECTION Hearing assessment Fitting & Testing Balance assessment Best Practices for the Evaluation and Management of Dizziness
Stephen P. Cass, M.D., M.P.H.
Biography
Stephen P. Cass, M.D., M.P.H., is Associate Professor in the Department
of Otolaryngology at the University of Colorado Health Science Center. He is
fellowship trained in Neurotology, specializing in disorders of the ear, hearing
and balance. His research interest involves basic and clinical studies of the
vestibular system. Dr. Cass is co-author with Dr. Joseph Furman of Vestibular
Disorders: A Case-Study Approach. We held a two-day course, "Best Practices for the Evaluation and Managementof Dizziness: A Workshop with Leading Clinicians." in Chicago on June 25-26, 2004. The course was presented by the Department of Otolaryngology,University of Colorado School of Medicine and sponsored by the University ofColorado School of Medicine, Office of Continuing Medical Education.
Educational support was provided by GN Otometrics, North America. Iserved as course director.This is the second course in this series. The firstcourse was held in Chicago on October 11-12, 2002. A copy of these pro- Fig. 1. Normal horizontal canal system at rest.
ceedings was published as an Insights in Practice article that can be accessed on www.bsure4balance.com.
It is essential to understand the response of the vestibular system to injury.
Fig. 1 shows a normal horizontal semicircular canal system, viewed from
In the first course we heard from clinicians in the specialties of primary care, above. When the head is at rest, tonic neural input comes from the two hori- neurotology, neurology, audiology, physical therapy, and psychiatry. We learned zontal canals and the level of input from the two canals is exactly the same.
that there is little controversy about management, but a great deal more con-troversy about evaluation. Dizzy patients usually see a primary care physicianfirst. Most of them have benign disorders that can be successfully managed bythe primary care physician, but a few have serious disorders that require referralto a specialist. Most of us agreed that the specialist who accepts dizzy patientreferrals should be prepared to take a comprehensive history and perform athorough physical examination, but we disagreed about which clinical observa-tions are required. Sometimes the history and physical examination fail to yielda definite diagnosis and we need additional information provided by laboratorytests. We disagreed about which tests should be ordered for which patients.
In the second course, I wanted to get closer to a clear definition of best prac-tices for the evaluation and management of the dizzy patient. I assembled afaculty of experts in the specialties of neurotology, neurology, and vestibulartesting. I asked them to describe their methods, to present the evidence under-lying their decision-making, and to indicate where the evidence is weak. Iallowed plenty of time for discussion among faculty members and the audi-ence. In this manner, I hoped to identify areas of consensus and to hear variousviewpoints in areas of disagreement.
Fig. 2. Normal horizontal canal system during angular acceleration to
I began the course with a quick review of vestibular anatomy
and physiology. I described the anatomy of the vestibular labyrinth and ori-
Fig. 2 shows what happens when the head undergoes angular acceleration to
entation of the labyrinth in the head, and explained the structure and function the person's left (counterclockwise in our view). Endolymph movement lags of the sensory receptors in the ampullae of the semicircular canals and the behind head movement. In the left horizontal canal, this lag deflects the cupu- maculae of the utricle and saccule. I traced the neural pathways of the vestibu- la upward (in our view), causing an increase in the level of neural input. In the lar nerve, vestibular nuclei, and the vestibulo-ocular and vestibulo-spinal sys- right horizontal canal, this lag deflects the cupula downward (in our view), continues INSIGHTS in practice SPECIAL COLLECTION causing a decrease in the neural input. Thus the level of neural input from the vestibular abnormalities for many years after the event. Some patients compen- left ear is greater than the level of neural input from the right ear. As a result, sate better than others, and those who compensate poorly usually receive bene- the person has a sensation of leftward rotation, left-beating nystagmus, and a fit from vestibular rehabilitation therapy.
tendency to fall to the right.
Then I described how I take a history from the dizzy patient. It is
Fig. 3 shows what happens when a person suffers an acute lesion of the right
often said that history taking is the most important part of the evaluation of horizontal canal. Neural input from the right canal is abolished, whereas tonic the dizzy patient. I agree. Dizziness can be caused by an unusually large num-ber of diseases and it is important to develop a working knowledge of all themedical conditions and disorders associated with dizziness. A good place tostart with this task is the Compendium of Vestibular Disorders that can beaccessed on www.bsure4balance.com. The patient's history offers an impor-tant opportunity to gain information needed to distinguish among them andto create a working list of potential diagnoses.
I take a comprehensive (Level V) history from every new dizzy patient—adaunting task. To make it easier, I use an electronic patient records system. Inthe waiting room, the patient fills out an eight-page questionnaire that asksquestions in a forced-choice format. An optical character recognition systemreads the patient's responses and inserts them into a custom-designed templatethat yields a finished chart note. I take my laptop into the exam room andreview my chart note with the patient, correcting and amplifying as needed.
A complete list of the items on my questionnaire can be accessed onwww.bsure4balance.com.
Fig. 3. Acute lesion of right horizontal canal.
David Solomon, M.D., Ph.D., Assistant Professor of Neurology at the
Johns Hopkins University School of Medicine, described how he conducts a
neural input from the left horizontal canal remains. Thus the level of neural physical examination of the dizzy patient. input from the left ear is greater than the level of neural input from the rightear. This asymmetry is the same as the one that occurs when a person rotates Dr. Solomon performs a thorough examination of eye movements, as follows: leftward and the reaction is also the same—a sensation of leftward rotation 1. Eye movement exam. He examines the patient's eye movements with eyes (which we now call "vertigo"), left-beating nystagmus (which we now call open in the light and with vision denied using Frenzel lenses, or video-ocu- "spontaneous nystagmus"), and a tendency to fall to the right (which we can lography. He looks for spontaneous (horizontal) nystagmus, vertical nystag- detect with postural tests). Acute lesions in other parts of the vestibular system mus, torsional nystagmus, gaze-evoked nystagmus, and dissociated nystag- cause similar (but not identical) signs and symptoms, and as we will see later, we can often localize the exact site of lesion by carefully noting the features ofthese signs and symptoms.
2. Head thrust test. He asks the patient to look straight ahead and then jerks the patient's head quickly rightward and leftward, looking for "catch up" The lesion may be permanent, but nevertheless the patient's signs and symp- saccades that denote a weak vestibulo-ocular response when the head is toms abate over a period of days and weeks due to vestibular compensation. A jerked toward the side of a labyrinthine loss.
major part of the compensation process is a reduction of the asymmetry due tothe gradual reappearance of tonic neural activity in the vestibular nuclei on the 3. Head-shaking test. He shakes the patient's head rapidly back and forth 15 side of the damaged horizontal canal, as shown in Fig. 4. Compensation is
times and then looks for nystagmus while the patient's head is held never complete, however. Our physical exam and tests still can detect subtle motionless. Head-shaking nystagmus usually (but not always) beats awayfrom the side of a labyrinthine loss.
4. Hyperventilation test. Hyperventilation sometimes induces nystagmus in patients with a fistula or a compressive lesion (such as acoustic neuroma,cholesteatoma, or blood vessel) or an inflammatory lesion (such as multiplesclerosis) that causes demyelination in peripheral or central vestibular path-ways.
5. Valsalva maneuver. The Valsalva maneuver sometimes induces nystagmus in patients with Arnold-Chiari malformation, perilymphatic fistula, orsuperior semicircular canal dehiscence.
6. Ocular tilt reaction (OTR). A unilateral otolithic lesion sometimes caus- es tonic ocular torsion and skew deviation when the head is tilted towardthe side of the lesion.
7. Dix-Hallpike maneuver. He starts with the patient seated on the exami- nation table with legs extended and the head turned 45 deg rightward.
Then he brings the patient back rapidly to the supine position with the Fig. 4. Chronic lesion of right horizontal canal.
head still turned rightward and hanging backward over the end of the INSIGHTS in practice SPECIAL COLLECTION examining table, as shown in Fig. 5. After performing the maneuver, he
Dr. Barin described five commonly used laboratory vestibular tests: looks for a nystagmus response, noting its latency, direction, duration, and 1. ENG/VNG is a battery of eye movement tests. For decades, we have performed ENG (electronystagmography), in which eyemovements are monitored with electrodes placed on the skinaround the eyes. In recent years, ENG has been largely supplant-ed by VNG (videonystagmography), in which eye movements aremonitored by infrared video cameras mounted inside lightproofgoggles.
The standard ENG/VNG test battery consists of a. four oculomotor tests (saccade test, tracking test, optokinetic test, and gaze test with fixation), which detect CNS lesions, b. two vestibular tests (static positional test and gaze test without fixation), which detect lesions of the peripheral or central vestibular system, Fig. 5. Right Dix-Hallpike maneuver. Position of the patient at the
start of the maneuver (A) and at the end of the maneuver (B).
c. two tests (Dix-Hallpike maneuver and pressure test), which (Courtesy of Dr. Parnes). identify specific etiologies, d. the caloric test, which detects and lateralizes lesions of the presence or absence of accompanying vertigo. Then he returns the patient horizontal semicircular canal or its afferent pathways.
to the sitting position and repeats the maneuver with the patient's headturned leftward. This test detects posterior and anterior canal BPPV, which ENG/VNG has more clinical value than any other laboratory vestibular is denoted by a vertical-torsional nystagmus response that is delayed in test. Dr. Barin recommends that it be used in the evaluation of all dizzy onset, transient, and accompanied by vertigo. The direction of the nystag- patients, except that it should be deferred pending treatment outcome in mus specifies the involved canal.
patients with BPPV. ENG/VNG detects one or more abnormalities in 8. Nylen-Barany positional test about 50 % of dizzy patients and about 75 % of these abnormalities speci- (also called the "roll test"). With the patient fy the site of lesion. Other laboratory tests detect few of these abnormali- in the supine position, he rapidly turns the head 90 deg rightward and ties. A skilled clinician can detect most of them during physical examina- then 90 deg leftward. This test detects nonlocalizing positional nystagmus tion, although physical examination does not permit quantitative analysis (either geotropic or ageotropic) and horizontal canal BPPV.
or yield a permanent record.
Dr. Solomon also conducts vestibulospinal tests. While the patient is sitting, 2. Rotary chair testing consists of recording horizontal eye movements as he looks for head tilt, past pointing, and axial postural asymmetry. With the the patient is rotated about a vertical axis with the horizontal semicircular patient standing, he first performs one or more static tests (Romberg, sharp- canals in the plane of rotation. The patient is usually tested under three ened Romberg, stance on a foam cushion, and Valsalva maneuver) and then conditions: (a) in complete darkness, (b) while viewing an earth-fixed visu- performs one or more dynamic tests (tandem gait, the Fukuda stepping test, al surround, and (c) while viewing a head-fixed visual target. Under each of and the circular walking test).
these conditions, the patient undergoes a series of sinusoidal oscillations at He also conducts a general neurological examination, which includes evalu- frequencies from about 0.01 Hz at octave intervals to about 1 Hz. Phase, ation of cranial nerves, deep tendon reflexes, distal vibration sensation, and gain, and symmetry of eye velocity re head velocity is computed for each cerebellar function (finger to nose, rapid alternating hand movements, heel to test frequency.
shin). He looks for dysarthria, dysphagia, dysmetria, diplopia, Horner's syn- Rotary chair testing has only fair clinical value. It is useful in documenting drome, loss of pin prick or temperature sensation on one side of the face bilateral vestibular loss, although the ice water caloric test, the active head and/or the other side of the body, intractable hiccups, visual inversion, visual rotation test, and the head thrust test also detect this condition. Otherwise loss, oculopalatal tremor, and mental confusion.
rotary chair abnormalities are nonlocalizing.
In addition, he performs an orthostatic blood pressure screening test, a dynamic visual acuity test, 3. Active head rotation consists of asking the patient to shake his or her and a headache evaluation as indicated by the presenting history and symptoms. head in the horizontal and vertical planes at frequencies from about 0.5 Hzto about 6 Hz while viewing an earth fixed visual target. Head movement Kamran Barin, Ph.D., Assistant Professor, Dept. of Otolaryngology and
is monitored by a head-mounted velocity sensor and eye movement is Dept. of Speech and Hearing Science, The Ohio State University, discussed monitored by electrodes. Phase, gain, and symmetry of eye velocity re head laboratory vestibular testing. He said that laboratory vestibular tests provide an velocity are computed at each test frequency.
independent assessment of the peripheral vestibular system, the vestibular Active head rotation has about the same clinical usefulness as rotary chair test- nerve, and central vestibular pathways. They detect lesions, differentiate ing. It costs less and tests both horizonal and vertical vestibulo-ocular responses between peripheral and central lesions, and lateralize peripheral lesions or fur- at higher frequencies, although head and eye movements at high frequencies ther localize central lesions. They also help with devising treatment plans, are difficult to measure accurately.
monitoring the progress of treatment, and planning for acoustic neuroma,vestibular ablation, and cochlear implantation surgeries.
INSIGHTS in practice SPECIAL COLLECTION 4. Computerized dynamic posturography (CDP) is comprised of two test Labyrinthitis/vestibular neuronitis is often accompanied or preceded by an batteries. The first is the Sensory Organization Test (SOT), in which the upper respiratory infection. It is characterized by vertigo lasting for days, nys- patient's postural stability is measured as visual and somatosensory cues are tagmus beating away from the affected ear, and nausea and vomiting. Cochlear manipulated. The second is the Movement Coordination Test (MCT), in symptoms are present with labyrinthitis and absent with vestibular neuronitis; which the patient's postural stability is measured as the supporting surface otherwise signs and symptoms are identical. Dr. Parnes treats this disorder is tilted or translated.
symptomatically with antiemetics and vestibular sedatives. He treats with oralsteroids if he sees the patient within 72 hours after onset of acute vertigo.
The diagnostic value of CDP is limited. Malingering patients tend to show There is no evidence that anti-virals are efficacious.
an aphysiologic pattern of responses, so the test is sometimes used in med-ical-legal cases. Some physical therapists use it to design vestibular rehabili- Recurrent vestibulopathy is characterized by Meniere's-like spells of vertigo.
tation therapy and monitor its progress.
There are no cochlear or other localizing symptoms and no diagnostic teststhat specify this disorder. A few patients with recurrent vestibulopathy go on 5. Vestibular-evoked myogenic potentials (VEMP) is a new vestibular test.
to develop typical Meniere's disease. Treatment is symptomatic, and symptoms The patient is presented with loud monaural clicks or tone bursts and resolve spontaneously over 2-3 years in most patients.
short-latency EMG responses are recorded from surface electrodes placedover the ipsilateral sternocleidomastoid muscles. These responses are ampli- Dehiscent superior semicircular canal syndrome (DSSCS) is characterized fied, filtered, and averaged over at least 100 repetitions of the stimulus.
by vertigo and oscillopsia in response to loud sounds (the Tullio phenomenon) Animal studies indicate that they arise from the saccule.
or maneuvers that change middle ear or intracranial pressure. Eye movementsevoked by these stimuli align with the plane of the dehiscent superior canal.
It has been shown that VEMP identifies the symptomatic ear in patients with The patient may also have pulsatile tinnitus, sensitivity to body sounds, and Tullio phenomenon. Initial reports suggest that it also detects various other hearing loss. Treatments are avoidance of symptom-inducing situations, middle fossa resurfacing of the affected canal, or middle fossa or transmastoid occlu- Dr. Barin says that he performs laboratory vestibular testing according to the sion of the affected canal.
protocol shown in Fig. 6. Each new dizzy patient first receives a Dix-Hallpike
BPPV is usually caused by free-floating particles in the endolymph of the pos- maneuver and if the test is positive, the patient receives canalith repositioning terior semicircular canal (posterior canalithiasis). Dr. Parnes performs the Dix- treatment. If treatment is successful and the patient has no other unexplained Hallpike maneuver to identify the affected canal and then administers canalith
repositioning treatment, as shown in Fig. 7. His success rate after a single
treatment is 80%. If the patient still has BPPV at the next visit, he repeats the
treatment. His success rate after three treatments is 95%.
Fig. 6. Protocol for laboratory vestibular testing.
signs or symptoms, the patient receives no further laboratory vestibular testing.
Fig. 7. Diagnosis and treatment of right posterior canalithiasis. Position
If the Dix-Hallpike maneuver is negative or treatment is unsuccessful, the of patient and canaliths before right Dix-Hallpike maneuver (A), after
patient receives ENG/VNG. If ENG/VNG shows a bilateral caloric weakness, right Dix-Hallpike maneuver (B), during canalith repositioning treat-
the patient receives either a rotary chair test or active head movement test to ment (C), and after canalith repositioning treatment (D).
confirm this abnormality. If aphysiologic behavior is suspected, the patientreceives CDP to confirm this suspicion. Dr. Barin does not yet perform He treats intractable BPPV with posterior semicircular canal occlusion. He has VEMP in his laboratory, but is following research in this area with interest.
performed this operation on 46 patients (in both ears of two patients). BPPVwas completely relieved in every case. One patient had a hearing loss with ver- Lorne S. Parnes, M.D., Professor of Otolaryngology and Clinical
tigo three months after surgery. Six patients had protracted periods of imbal- Neurology, Dept. of Otolaryngology, University of Western Ontario, discussed ance after surgery and one patient developed horizontal canal BPPV. He has the diagnosis and treatment of five peripheral vestibular disorders—labyrinthi- seen free-floating particles in 13 of 40 operated ears.
tis/vestibular neuronitis, recurrent vestibulopathy, dehiscent superior semicir-cular canal syndrome, BPPV, and Meniere's disease.
Dr. Parnes says he rarely sees cases of horizontal canal BPPV and has neverseen a case of anterior canal BPPV.
INSIGHTS in practice SPECIAL COLLECTION Meniere's disease is characterized by multiple attacks of vertigo (each lasting Dr. Solomon then discussed specific diseases, as follows: more than 20 minutes), unilateral fluctuating sensorineural hearing loss, and 1. Vertebrobasilar insufficiency presents initially as an attack of vertigo in ipsilateral tinnitus or aural fullness (or both). When one or more of these crite- 19% of patients, and 62% of patients experience at least one isolated ria is missing, the diagnosis is called "probable" or "possible" Meniere's disease.
attack of vertigo at some time during the course of the disease. These Dr. Parnes administers the following medical treatments for Meniere's disease: attacks are usually accompanied by nausea and vomiting. Patients with ver- low salt diet, avoidance of caffeine, nicotine, and stress, diuretics, benzodi- tebrobasilar insufficiency nearly always have other brainstem or visual com- azepines, antihistamines, histamine (betahistine), vasodilators, and corticos- plaints, such as visual loss, diplopia, drop attacks, unsteadiness, incoordina- tion, extremity weakness, or confusion. When vertebrobasilar insufficiencyis first suspected, the patient is treated with daily aspirin and attention to If medical treatment fails, he treats with intratympanic gentamicin titration.
risk factors. If episodes persist, aspirin /dipyridamole or clopidogrel may be He injects 1 ml of 40 mg/ml stock IV gentamicin solution through a myringo- substituted. If significant stenosis is found or episodes are frequent and dis- tomy once a week. Treatments are discontinued if the audiogram shows a sig- abling, treatment is anticoagulation with heparin followed by wayfarin, nificant hearing drop for two successive weeks, if a new onset of persistent titrating to an international normalized ratio of 2-3.
dizziness or imbalance occurs, if a new onset of spontaneous or head-shakenystagmus occurs, or when four treatments have been given. This treatment 2. Lateral medullary syndrome (or Wallenberg's syndrome) is caused by yields excellent control of vertigo and a low incidence of hearing loss (and no occlusion of the posterior inferior cerebellar artery (PICA). This artery sup- cases of severe hearing loss) and does not preclude further treatment if it fails.
plies the dorsal lateral medullary plate and portions of the posterior medialcerebellum. Occlusion of the PICA at its origin causes the full-blown syn- David Solomon, M.D., Ph.D., discussed the diagnosis and management
drome—vertigo, spontaneous nystagmus, skew deviation, altered subjective of common neurological vestibular disorders. He finds it useful to distinguish visual vertical, ipsilateral limb ataxia, ipsilateral facial hemianesthesia, ipsi- among three types of dizziness—presyncope, vertigo, and dysequilibrium with- lateral Horner's syndrome, ipsilateral vocal cord paresis, ipsilateral gag, ipsi- lateral palatal weakness, gait ipsipulsion, saccade ipsipulsion, and contralat- Presyncope implies insufficient central nervous system blood flow.
eral body pain and temperature sensory loss. Occlusion of distal branches Common causes are hyperventilation, orthostatic hypotension, vasovagal of PICA can produce a syndrome that mimics a labyrinthine disorder— attacks, decreased cardiac output (arrhythmia, myocardial infarction, con- vertigo, dysequilibrium, and spontaneous nystagmus. gestive heart failure, aortic stenosis), anxiety or panic disorders, hypo- 3. Pontine syndrome is caused by occlusion of the anterior inferior cerebellar glycemia, and drug toxicity (alcohol, barbiturates, benzodiazepines, anticon- artery (AICA). This artery supplies the lateral pons and part of the middle vulsants, cardiovascular drugs).
cerebellar peduncle. It also gives off the labyrinthine artery, which provides Vertigo implies either peripheral or central nervous system disease. A single exclusive blood supply to the inner ear, as shown in Fig. 8. Occlusion of
attack of vertigo that lasts more than 24 hours may be due to the AICA causes vertigo, nystagmus, ipsilateral tinnitus, ipsilateral hearing labyrinthitis/vestibular neuronitis, posterior circulation infarction, cerebellaror brainstem hemorrhage, or multiple sclerosis. Recurrent attacks of vertigothat lasts for a few seconds may be due to uncompensated vestibular loss,crisis of Tumarkin, or drop attacks. Recurrent attacks that last for minutesmay be due to TIAs. Recurrent attacks that last for hours may be due toMeniere's disease or migraine. Recurrent attacks that last for days may bedue to labyrinthitis/vestibular neuronitis, stroke, or multiple sclerosis.
Positional vertigo is usually caused by BPPV (the attacks are severe andbrief), but can also be caused by central disorders, such as posterior fossatumors and infarction, Chiari malformation, cerebellar degeneration, andmultiple sclerosis (the attacks are usually mild and persistent).
Disequilibrium without vertigo implies a bilateral vestibular loss (cis-platin or gentamicin), peripheral neuropathy (diabetes), a spinal cord dorsalcolumn lesion (compressive, B12 deficiency, syphilis), cerebellar atrophy,white matter disease, normal pressure hydrocephalus, or an extrapyramidaldisorder (Parkinson's disease, progressive supranuclear palsy).
Central nervous system dysfunction is implied by physical findings of direc-tion changing or purely vertical nystagmus, sustained or non-fatigable posi- Fig. 8. Labyrinthine arterial supply.
tional nystagmus, disconjugate nystagmus, abnormal posture when seated, loss, ipsilateral gait and limb ataxia, ipsilateral facial hemianesthesia, ipsilat- inability to stand, focal motor deficit, dysarthria, dysphagia, diplopia, limb eral facial paralysis, ipsilateral Horner's syndrome, and contralateral hemi- ataxia, Horner's syndrome, loss of pin prick or temperature sensation on one body sensory loss.
side of the face and/or on the other side of the body, or intractable hiccups.
ENG findings of defective saccades, pursuit, or gaze holding also imply central 4. Cerebellar infarction sometimes occurs without brainstem involvement.
nervous system dysfunction. Spontaneous nystagmus with normal calorics sug- Since brainstem signs are absent, a mistaken diagnosis of labyrinthine gests (but does not prove) central dysfunction.
pathology might be made. Key differentiating findings are normal respons-es on the head thrust test combined with gaze-evoked or vertical nystag-mus and/or ataxia. A cerebellar infarction may affect only the inferior andmedial cerebellum, causing nystagmus without ataxia, or it may affect onlythe cerebellar hemispheres, causing ataxia without nystagmus.
INSIGHTS in practice SPECIAL COLLECTION 5. Migraine is present in about 11 million Americans, with 18% of females may be present. Paraneoplastic disease occurs when an immune response is and 6% of males affected. The highest prevalence is at 30-45 years of age.
triggered by a tumor that is usually remote from the nervous system. Anti- It has been shown that migraine is undiagnosed in 41% of females and Yo antibodies cause a loss of Purkinje cells in the cerebellum, resulting in a 29% of males who meet strict diagnostic criteria. Most cases of "sinus" syndrome of ataxia, dysarthria, and nystagmus. This may be the presenting headache are migraine. Some patients with migraine also have dizziness, picture, and when antibodies are detected, a search for the tumor must either true vertigo or imbalance and motion sensitivity. Dizziness may occur before or during the headaches or it may occur independently.
10. Wernicke's encephalopathy is caused by thiamine deficiency and can be Dizziness is often accompanied by photophobia, phonophobia, or visual or brought on by poor nutrition, prolonged vomiting, alcoholism, eating dis- other auras. Acute attacks usually last for minutes to hours, seldom longer orders, or chemotherapy. Signs include vertical nystagmus, gaze-evoked than 24 hours. Migraine may be indistinguishable from Meniere's disease, nystagmus, and bilateral abducens palsies. Ataxia and mental changes are except that accompanying hearing loss is uncommon. Treatment is both usually present as well. Signs may reverse within hours of thiamine admin- behavioral and pharmacological. Behavioral treatment includes regular sleep patterns, stress reduction, migraine diet (avoiding chocolate, cheese,red wine), and eliminating caffeine and habitual analgesic use.
11. Normal pressure hydrocephalus is characterized by dementia, inconti- Pharmacological treatment to abort attacks includes combinations of caf- nence, and gait disorder. MRI shows enlarged ventricles out of proportion feine, aspirin, acetaminophen and butalbital or a non-steroidal anti-inflam- to atrophy. Ventriculography is not helpful. Response to prolonged CSF matory (such as ibuprofen or naproxyn sodium). Prophylactic treatments drainage is the best predictor of improvement with a shunting procedure.
include beta blockers (propranolol), tricyclic antidepressants (nortripty-line), calcium channel blockers, and valproic acid. Acetazolamide and other 12. Epileptic vertigo is rare. It is characterized by episodes of vertigo lasting anticonvulsants have also been used.
minutes, sometimes with associated ictal nystagmus, dysphagia, amnesia,disorientation, and visual field abnormalities.
6. Sporadic adult-onset ataxia can be caused by a variety of disorders, including vitamin deficiency, glutin sensitivity, thyroid disorder, paraneo- Finally, I presented management of psychological and
plastic syndrome, and multiple system atrophy (Shy-Drager syndrome).
psychiatric aspects of dizziness. More than one-third of patients with
The diagnostic evaluation includes testing for thyroid function, B12, mag- vestibular dysfunction have anxiety symptoms. These symptoms cause nesium and vitamin E levels, antigliadin and antiendomysium antibody, decreased functioning, decreased quality of life, and prolonged recovery from Hashimoto's antibodies- thyroglobulin and thyroid peroxidase antibodies, antineuronal antibodies, trinucleotide repeats for autosomal dominant I disagree with the traditional criteria for psychogenic dizziness—vague spinocerebellar ataxias, anti-GAD antibodies, and TATA-binding protein.
description of symptoms, exacerbation of symptoms in certain environments, In many cases, no cause is found and even if a cause is found, no effective reproduction of symptoms by hyperventilation, and normal physical exam.
treatment exists.
While dizziness can be a symptom of a psychiatric disorder, dizziness without 7. Multiple sclerosis typically begins between 20-40 years of age. It usually other psychiatric symptoms is insufficient for the diagnosis of psychiatric dis- presents with optic neuritis, but presents with vertigo in 5% of patients.
ease. Panic disorder may cause lightheadedness, but also causes palpitations Vertigo is a symptom sometime during the course of the disease in about and shortness of breath. Panic, general anxiety, acute stress, and post-traumatic 50% of patients. Bilateral internuclear ophthalmoplegia is the hallmark of stress disorders may cause an "unreal" feeling, but also cause anxiety, numb- multiple sclerosis, but various types of central nystagmus may also be seen.
ness, and flashbacks. Depression may cause a vague "swimming" feeling, but An attack of multiple sclerosis may mimic a peripheral vestibular lesion also causes poor appetite and insomnia. Conversion disorder may cause imbal- with a unilateral caloric weakness. An IV pulse of high-dose steroids may ance, but also causes tremors and other nonphysiologic behaviors.
shorten an attack. Acquired pendular nystagmus may respond to Vestibular disorders commonly induce symptoms of anxiety or panic, especial- gabapentin. Vertical nystagmus may respond to gabapentin or baclofen.
ly in patients with vulnerable temperaments. Anxiety is part of the response to 8. Arnold Chiari malformation (Type 1) is characterized by unexplained vestibular dysfunction, just as heart palpitations are part of the response to sensorineural hearing loss, headache, vertigo, ataxia, dysequilibrium, dys- physical exercise. Concerns about future attacks of vertigo, possible embarrass- phagia or other lower cranial nerve dysfunction. Gaze-evoked nystagmus, ment, serious medical illness, mental illness, and disability further increase the downbeat nystagmus, and defective pursuit are typical ocular motor find- patient's anxiety. There is a subset of patients with both panic disorder and ings. Treatment is suboccipital decompression of the foramen magnum.
vestibular dysfunction. These patients have vestibular symptoms between panicattacks, agoraphobia or height phobia, and discomfort in malls or supermar- 9. Neoplastic diseases can cause dizziness. Infratentorial ependylomas arise kets. Patients with chronic dizziness must pay more attention to maintaining from the lining of the fourth ventricle. Protracted nausea and vomiting are their balance and have less time for attention to other tasks. They often com- often present, and the classical headache is positional, with pain present plain of "brain fog" or a "spacey" feeling. Patients with chronic dizziness may while supine and relieved by sitting up. Brainstem gliomas may occur at also have symptoms of depression—trouble concentrating, poor sleep, fatigue, any age, but are most common in children. Cerebellar signs, trigeminal and social withdrawal.
and lower cranial nerve involvement occurs. In children, medulloblatomamay cause non-fatiguing paroxysmal positional nystagmus, which is usually Dismissive behavior by the clinician adversely affects the outcome of treat- purely vertical and accompanied by vertigo and generalized dysequilibri- ment. Such behavior includes: (a) failing to acknowledge that there is a prob- um. Vestibular schwannomas (or acoustic neuromas) account for 85-90% lem, (b) minimizing the seriousness of the problem, (c) suggesting that the of all schwannomas. Presentation of vestibular schwannomas is usually problem is "mental," and (d) spending too little time with the patient.
insidious, with unilateral progressive hearing loss and vestibular loss (with- Dismissive behavior makes the patient anxious and angry. The opposite of dis- out vertigo). Tinnitus, headache, mastoid pain, facial weakness or otalgia missive behavior is validating behavior. Such behavior includes: (a) evaluating INSIGHTS in practice SPECIAL COLLECTION both vestibular and psychiatric symptoms, (b) assessing temperament, (c) Infants with Hearing Loss: avoiding suggestion of psychogenicity, (d) explaining vestibular mechanisms,(e) explaining somatopsychic mechanisms, and (f) identifying sources of sec- Assessment and Intervention ondary anxiety and providing corrective information. Validating behavior usu-ally means spending more time with the patient.
This exciting new course will be held in Chicago on June 9 & 10. Three lead-ing clinicians will present it: Dr Robert Margolis, Dr Sandra Gabbard and Dr Useful treatments are vestibular rehabilitation therapy and medication Lisa Hunter. All have made major contributions to the knowledge of assess- (Clonzepam 0.5 mg PO BID is drug of choice). If evaluation reveals a true ment and intervention for childhood hearing loss.
psychiatric disorder, the patient should be referred to a psychiatric professionalwho is knowledgeable about vestibular disorders. Such a referral should be Day I will cover physiologic and behavioral audiologic assessment. Day II will made after counseling the patient and should not be made on the first visit.
cover an integrated family-centered approach, including counseling, audiologicintervention and perspectives from parents.
After hearing these presentations, we broke up into small groups for
practical demonstrations of diagnostic and treatment techniques. Dr. Solomon
The course is intended for all hearing healthcare professionals who assess and demonstrated the head thrust test; Dr. Parnes demonstrated the Dix-Hallpike manage hearing loss in the pediatric population.
and canalith repositioning maneuvers; Dr. Barin demonstrated the interpreta- Contact GN Otometrics directly at [email protected] or download tion of ENG/VNG tracings; and Timothy C. Hain, M.D., Chicago Dizziness the brochure at www.gnotometrics.com for additional information and and Balance and Associate Professor of Neurology at Northwestern University, to register.
demonstrated the interpretation of video eye movement recordings. Dr. Parnes wrapped up the course with a presentation of difficult cases.
Summary. Most dizzy patients have benign disorders that can be successfully
VNG/ENG Courses 2005 managed by a family physician, but some have serious disorders that requireevaluation and management by a specialist. As specialists who see dizzy Our leading, comprehensive 21⁄2 day course covering Test Administration, patients, we must be able to distinguish among many possible diagnoses, Interpretation and Hands-on VNG/ENG testing, will be held in three including some outside our own areas of specialty. We must be prepared to locations as follows: take comprehensive histories and perform thorough physical examinations, as Atlanta: May 12-14
outlined in this course. Sometimes our evaluations yield definite diagnoses, butmore often they yield lists of possible diagnoses, and to distinguish among Seattle: September 8-10
them, we must seek information provided by laboratory testing. We rely pri- Chicago: October 20-22
marily upon imaging studies and laboratory analyses of blood and other bodyfluids to help confirm or refute possible diagnoses. Audiometric and vestibular Contact GN Otometrics directly at [email protected] or download tests are also useful, especially for determining the functional state of the the brochure at www.gnotometrics.com for additional information and vestibular system, but rarely crucial for diagnosis. Our goal is to make the to register.
correct diagnosis and treat accordingly. However, in a subset of patients weneed to treat without a definite diagnosis.
It has been a terrific privilege to organize these conferences and interact withour outstanding faculty. Our attendees have been highly motivated learnersand active participants. No one left early; in fact, we had to be asked to leaveby the hotel staff as they anxiously readied for an evening wedding. For ourfaculty, and me, the reward is in seeing and feeling the intense attention, inter- GN Otometrics is the world's leading manufacturer of hearing and balance est, and urge to learn of our participants, all with the goal to better care for assessment instrumentation and software. Our extensive product portfolio ranges their patients with dizziness. I invite you to consider joining us for the 3rd from infant screening applications, audiologic diagnostics, and office management such conference planned for June 2006.
software, to balance testing and hearing instrument fitting.
As an organization, we are committed to developing innovative, integrated solutions that help healthcare professionals make the best possible decisions. This, in turn, helps our customers improve the overall standard of patient carewherever they are located.
Based in Copenhagen, Denmark, we maintain marketing and development centers in both the United States and Germany. GN Otometrics is part of GN Store Nord.
GN Otometrics, Denmark. +45 72 111 555 [email protected] Otometrics, North America. 1-800-289-2150 [email protected] INSIGHTS in practice SPECIAL COLLECTION INSIGHTS in practice SPECIAL COLLECTION Interpretation of Static Position Testing in VNG/ENG Kamran Barin, Ph.D.
1 Sometimes moving the head from one position to another provokes a transient nystagmus, either immediately or Kamran Barin, Ph.D. is the Director of after a short delay. As the purpose of the static position Balance Disorders Clinic at the Ohio test is to detect the steady-state nystagmus that is present State University Medical Center and as long as the head remains in the critical head position, Assistant Professor, Department of transient nystagmus should not be included in the Otolaryngology - Head and Neck interpretation of this test. Instead, the examiner should Surgery, Department of Speech and perform the appropriate maneuver and interpret the Hearing Science, and Biomedical results as a part of the dynamic position testing.
Engineering Program. Dr. Barin has taught national and international courses and Traditionally, static position testing has been limited to seminars in different areas of vestibular assessment and the interpretation of horizontal eye movements. The main rehabilitation. He serves as a consultant for Otometrics. reason for this is that the vertical channel in ENG is oftennoisy and contaminated by eye blinks. In VNG, thedifferences in the noise level and resolution betweenhorizontal and vertical channels are relatively insignificant.
Therefore, VNG users should consider vertical nystagmus The purpose of static position testing, also known as the in the interpretation of the static position test. ENG users positional test, in the video- and electro-nystagmography may wish to skip this step because of the high level of (VNG/ENG) test battery is to determine the presence and artifacts in the vertical channel. The flow charts in characteristic of nystagmus when the patient's head is placed Figures 2 and 3 show the interpretation for horizontal and in different orientations with respect to gravity. Although the vertical nystagmus, respectively.
test procedure is relatively simple (see Barin, 2006, fordetails), the interpretation of the results may not be When nystagmus has both horizontal and vertical straightforward to inexperienced VNG/ENG examiners. This components, the examiner must make sure that it article provides a basic step-by-step algorithm for the represents true eye movements and is not due to crosstalk.
interpretation of static position testing.
Crosstalk occurs when eye movements in one channelgenerate activities in the other channel. Those activitiesdo not represent true eye movements and are usually The flow chart in Figure 1 is a summary of the interpretation caused by the misalignment of the electrodes in ENG or process. Additional information is provided below for the continues numbered items on the flow chart. INSIGHTS in practice SPECIAL COLLECTION INSIGHTS in practice SPECIAL COLLECTION the misalignment of cameras or goggles in VNG.
consistent with a central lesion. If the nystagmus intensity Crosstalk can be recognized when the patient is asked to increases significantly without fixation, the nystagmus with make purely horizontal or vertical eye movements. Any fixation should be considered "leak through" of the strong activities in the other channel represent crosstalk. The nystagmus without fixation. Therefore, the interpretation examiner should either repeat the test or subtract the should follow the same path as that of nystagmus without effect of the crosstalk from the tracings.
3 Static position testing should include examining the eye 6 Horizontal nystagmus that changes direction in a single movements in at least four different positions: sitting, head position is always abnormal. This type of nystagmus, supine, head right, and head left. If fewer head positions called periodic alternating nystagmus, is usually present are tested, a partial interpretation is still possible according both with and without fixation and changes direction to the guidelines of the flow chart. The examiner should about every 2-4 minutes. This finding is consistent with a be aware that the position testing for some head positions central lesion.
may be embedded in other parts of VNG/ENG. Forexample, the results from the spontaneous nystagmus test Detection of periodic alternating nystagmus is hampered or the gaze test may be used in place of the position test in by the fact that typical recording of eye movements in the sitting position as long as the fixation conditions are each head position is much shorter than 2-4 minutes.
taken into account.
Instead, the examiner must look for inconsistencies in thedirection of nystagmus for parts of the VNG/ENG test Sometimes it is necessary to include other head positions battery that provide equivalent test conditions. For such as body right, body left, or head hanging. Some example, the nystagmus direction in the gaze or laboratories routinely include those and other head spontaneous nystagmus test without fixation is expected to positions. The interpretation algorithm is also applicable be the same as the nystagmus direction in the sitting position. When such inconsistencies are observed, theduration of the recording for the suspected head positionshould be extended to determine if the nystagmus changes 4 The static position test is typically performed in the absence of fixation. However, the effect of fixation is thesingle most useful factor in differentiating nystagmus thatis generated by central lesions from other types of 7 Horizontal nystagmus without fixation does not always nystagmus. Therefore, some laboratories routinely test the indicate an abnormality. A number of studies have shown patient with and without fixation. The algorithm allows that some form of nystagmus without fixation is present in for this possibility. However, even when position testing many individuals without a history of dizziness or other with fixation is not available, the effect of fixation for the balance disorders (Barber and Wright, 1973). The most sitting position can be determined from the gaze test or important characteristic that differentiates normal from the spontaneous nystagmus test.
abnormal nystagmus without fixation is the nystagmusintensity. Other criteria, such as the number of headpositions in which the nystagmus is persistent or 5 Horizontal nystagmus with fixation is always abnormal. No intermittent, are outdated and should not be used. The other criterion, such as nystagmus intensity, is needed and presence and intermittency of nystagmus are related to the simple presence of nystagmus with fixation is enough.
technical issues such as the patient's level of alertness or To localize the lesion, the nystagmus with fixation should gaze direction. Therefore, it does not seem logical to be compared to the nystagmus without fixation. If the include those factors in identifying abnormal nystagmus nystagmus intensity does not increase significantly (at least without fixation. To avoid such technical issues and to double) when the fixation is eliminated, the results are obtain a valid static position test, it is important for the INSIGHTS in practice SPECIAL COLLECTION INSIGHTS in practice SPECIAL COLLECTION examiner to maintain a steady level of patient alertness or ageotropic nystagmus depending on the elapsed time throughout the test. since the ingestion of alcohol.
Nystagmus intensity is defined as the velocity of the As a result, abnormal horizontal nystagmus without nystagmus slow-phase. Traditionally, a threshold of 6º/sec fixation, including all of its variations of spontaneous, has been used for pathologic nystagmus without fixation positional, geotropic, and ageotropic, is a non-localizing (Barber and Stockwell, 1980). This limit has been derived finding that can originate from the peripheral vestibular based on ENG testing and there is a question whether the system in either ear or central vestibular pathways. same limit should apply to VNG (Hain, 2008). In a yetunpublished study of 40 normal individuals in ourlaboratory, we found the normal limit using VNG to be 9 The overall interpretation of static position testing for about 4º/sec. However, until this finding is confirmed by horizontal nystagmus is based on the combination of more large-scale studies of VNG findings in the normal findings for each head position. For example, the overall population, we continue to use the normal limit of 6º/sec interpretation indicates a central lesion if a central finding for both ENG and VNG.
is identified for any head position. In the absence of acentral finding, all other abnormalities indicate a non-localizing finding.
8 Abnormal horizontal nystagmus without fixation does not provide localizing information. It can be caused by lesionsin the peripheral as well as central vestibular pathways.
10 When horizontal nystagmus is not present in the sitting or supine positions but appears in the head right or head left Horizontal nystagmus without fixation can be classified position, the effect of neck rotation should be examined based on its direction and intensity in different head by testing the patient in the body right or body left positions. For example, nystagmus that has the same positions. If the nystagmus disappears in the body right direction and intensity in different head positions is or body left position, it should be attributed to the neck usually classified as spontaneous nystagmus whereas rotation. Otherwise, neck rotation has no effect.
nystagmus that has the same direction but differentintensity in different head positions is classified aspositional nystagmus. At times, nystagmus can beat in 11 Vertical nystagmus with fixation is always abnormal different directions in the head right and head left (Baloh and Honrubia, 1990). No other criterion is needed positions. When the nystagmus beats toward the ground and the simple presence of nystagmus with fixation is (right-beating in head right and left-beating in head left), enough. This type of nystagmus, either down-beating or it is classified as geotropic nystagmus. When the nystagmus up-beating, is consistent with a central lesion.
beats away from the ground (left-beating in head right andright-beating in head left), it is classified as ageotropic orapogeotropic nystagmus.
12 Vertical nystagmus without fixation has been reported in both healthy individuals with no prior history of dizziness Over the years, different classes of nystagmus without or balance disorders as well as in patients with various fixation have been associated with lesions in the peripheral abnormalities (Barber and Wright, 1973; Kim et al, 2000).
or central vestibular pathways. For example, ageotropic Currently, there are no established normal limits for nystagmus has been considered a central finding by some vertical nystagmus without fixation. In the previously laboratories. However, there are many counter-examples mentioned study, we found vertical nystagmus without to such assumptions. For example, positional alcohol fixation to be common in our sample of 40 normal nystagmus, which is caused by the change of the cupula individuals. The 95% confidence limit of this sample was density with respect to the endolymph density within the about 7º/sec. This limit was established using VNG but peripheral vestibular system, can result in either geotropic we currently use the normal limit of 7º/sec for vertical INSIGHTS in practice SPECIAL COLLECTION INSIGHTS in practice SPECIAL COLLECTION nystagmus without fixation for both ENG and VNG.
Even when vertical nystagmus without fixation is Baloh, R.W., and Honrubia, V. Clinical Neurophysiology of the abnormal, currently there is not enough information to Vestibular System. Philadelphia: F A Davis, 1990; 112-129. determine its localization and clinical significance. In ourlaboratory, we report presence of abnormal vertical Barber, H.O., and Stockwell, C.W. Manual of nystagmus without fixation and state that its clinical Electronystagmography. St Louis: C V Mosby, 1980; 142-152. significance is unknown at this time.
Barber, H.O., and Wright, G. Positional Nystagmus in Normals. Adv. in Otorhinolaryngol. 19:1973; 276-283. 13 The overall interpretation of static position testing for Barin, K. Current State of Static Position Testing. vertical nystagmus is based on the combination of findings for each head position. For example, the overall interpretation indicates a central lesion if a central finding is identified for any head position. In the absence of a central finding, the localization and clinical significance ofall other abnormal findings for vertical nystagmus are Kim J.I., Somers J.T., Stahl J.S., Bhidayasiri R., and Leigh R.J. Vertical Nystagmus in Normal Subjects: Effects of Head Position,Nicotine and Scopolamine. J Vestib Res. 2000 10(6); 291-300. 14 The report for static position testing should include descriptions of all types of abnormal horizontal andvertical nystagmus and their clinical significance. Thereport should also include a description of any nystagmusthat is present even when it is within normal limits.
When applicable, the report should describe the effect ofneck rotation on the nystagmus that is absent in the ICS Chartr 200 software 6.2 and higher implement a sitting and supine positions but appears in the head right version of the above algorithm in the Interpretation or head left position. Finally, the report should include a Assistant. To use the algorithm, the user must record the description of any transient nystagmus that is provoked as eye movements during tests that are specifically identified a result of moving from one position to another.
as "w/ vision" and "w/o vision".
Otometrics is the world's leading manufacturer of hearing and GN Otometrics, North America. Phone: 800-289-2150 balance instrumentation and software – innovative concepts designed to help healthcare professionals make the best possible Our solutions range from infant screening applications andaudiologic diagnostics, to balance testing and hearing instrumentfitting. As an industry leader, we are committed to developinginnovative, integrated solutions that help healthcare professionalsmake the best possible decisions.
INSIGHTS in practice SPECIAL COLLECTION INSIGHTS in practice SPECIAL COLLECTION Baseline Shift and Gain Asymmetry in the Caloric Test Kamran Barin, Ph.D. Kamran Barin, Ph.D., is Director of In the standard bithermal caloric test, right warm and left cool Balance Disorders Clinic at the Ohio irrigations are expected to generate right-beating nystagmus State University Medical Center and while left warm and right cool irrigations are expected to Assistant Professor, Department generate left-beating nystagmus. In a normal individual, the of Otolaryngology, Department of intensities of all four caloric responses are approximately the Speech and Hearing Sciences, The same and therefore, there is no significant difference between Ohio State University, Columbus, right-beating and left-beating responses. Some patients however, have directional preponderance (DP) in which responses in one direction are significantly greater than the responses in the opposite direction. DP is defined as the normalized (scaled) difference between the peak nystagmus slow-phase velocities (SPVs) from irrigations that are expected to generate right- The caloric test is quantified using two parameters: unilateral beating nystagmus and those from irrigations that are expected weakness (UW) and directional preponderance (DP). The clinical to generate left-beating nystagmus. Mathematical formulas for usefulness of UW, also known as canal paresis, is well established calculating DP and other caloric parameters are provided in the but there is considerable debate about the value of DP. Some laboratories choose not to include DP in the interpretation of the caloric test. One reason for the low clinical value of abnormal Interpretation of DP DP may be the fact that it can be caused by two distinct pathologies. The first is a static asymmetry in the peripheral or The normal limits reported for DP from different studies have central vestibular pathways and the second is a gain asymmetry ranged from as low as 20% to as high as 50%. Currently, most in the secondary vestibular neurons within the vestibular nuclei. laboratories consider DP of less than 30% to be within normal Because the current formula for calculating DP combines both limits (Sills et al., 1977).
abnormalities into a single parameter, it is possible that important information is being lost. This article reviews the abnormalities There has been a controversy about the interpretation and clinical that can cause DP and offers computational methods for value of abnormal DP. Initially, abnormal DP was considered separating the contribution of each abnormality.
a central finding but this conclusion was reached based on caloric responses that were obtained in the presence of fixation (Fitzgerald and Hallpike, 1942). Therefore, what was considered INSIGHTS in practice SPECIAL COLLECTION to be abnormal DP was actually related to asymmetric failure of Different types of DP fixation suppression. Subsequent studies in which the caloric test was performed in the absence of fixation found DP in both Figure 1 shows two different types of DP. In Figure 1A, caloric
peripheral and central pathologies (Coats, 1966; Baloh et al., responses are shifted in one direction indicating presence of 1977). Therefore, abnormal DP in its current form is considered nystagmus at the beginning of all four irrigations. The caloric a non-localizing finding. Abnormal DP has also been reported in stimulus in an ear with an intact tympanic membrane does not normal individuals, which further casts doubt on its clinical value reach the labyrinth for at least 10 seconds from the onset of the (Coats, 1965).
irrigation. Therefore, this baseline shift represents a pre-existing nystagmus in the standard caloric position. That is, this patient Due to its low sensitivity to pathologies and lack of specificity to has some form of spontaneous nystagmus. This nystagmus is central versus peripheral abnormalities, some laboratories do not added to the caloric-induced nystagmus when they are in the include DP in the interpretation of the caloric test. However, it same direction and subtracted from it when they are in opposite has now become clear that DP can be caused by two different directions. As a result, significant DP is generated because the types of abnormalities. Therefore, the low clinical value of DP peak caloric responses for two irrigations (right cool and left should not come as a surprise because the current method warm, in this case) are greater than those for the other two of calculating DP does not distinguish between these two irrigations (right warm and left cool, in this case). This type of DP abnormalities. It seems worthwhile to define new parameters is called Bias or Baseline Shift (BS).
that can separately quantify these abnormalities.
Figure 1. Different types of DP: A) BS, B) GA. For clarity of presentation, simulated caloric responses are used instead of
actual patient test results.
INSIGHTS in practice SPECIAL COLLECTION Figure 1B shows a different type of DP in which the caloric
The formula for DP can be partitioned into two components responses in one direction are truly stronger than the responses in with the first component related to spontaneous nystagmus the opposite direction. There is no spontaneous nystagmus as the and BS and the second component related to GA. However, SPVs at the onset of all four caloric irrigations are zero. This type the representation of BS in this form has a major shortcoming of DP has been described in the literature but it is an extremely as the intensity of spontaneous nystagmus is divided by the sum rare finding (Sills et al., 1977). Halmagyi et al. (2000) found this of four caloric responses (Barin and Stockwell, 2002). Because type of DP in less than 1% of patients who underwent vestibular spontaneous nystagmus is independent of the caloric irrigations, testing whereas BS constituted the remaining 99% of the cases it does not seem logical to scale or normalize its intensity based with clinically-significant DP. They termed this type of DP, Gain on the caloric responses. The consequence of normalizing the intensity of spontaneous nystagmus is shown in Figure 2. The
same level of spontaneous nystagmus can generate a wide range
of values for DP that can be normal (Figure 2A) or abnormal
Quantification of BS and GA (Figure 2B). That is, the caloric test parameters are different
despite the fact that underlying abnormality is the same in
Although the caloric responses in Figure 1A and 1B represent
Figures 2A and 2B.
two different abnormalities, UW and DP parameters are the same. In order to differentiate between these two cases, new parameters are needed to quantify BS and GA. Figure 2. The effect of normalizing the intensity of spontaneous nystagmus or BS on DP: A) Strong caloric responses, B) Weak
caloric responses. For clarity of presentation, simulated caloric responses are used instead of actual patient test results.
INSIGHTS in practice SPECIAL COLLECTION The most appropriate method for quantifying BS appears to be The intensity of spontaneous nystagmus (and by extension, BS) the SPV of spontaneous nystagmus. This can be accomplished depends on the gaze position and the level of alertness. That is in different ways. First, the intensity of spontaneous nystagmus the reason in actual patient testing (Figure 3) the BS levels from
can be calculated from the supine position in the static position different irrigations are approximately the same but they are not testing because this position is similar to the standard caloric test exactly the same as in the idealized responses (Figure 1 and 2).
position (Figure 3B). A better alternative is averaging of the
Using a best-fitting line or averaging of the SPVs addresses nystagmus SPVs from the first few seconds of each irrigation. this issue. On the other hand, the direction of spontaneous This will account for any potential calibration change from the nystagmus does not change in a single head position. Therefore, position test to the caloric test. The averaging of SPVs can be any difference in the direction of BS from one irrigation to done computationally but a graphical approach simplifies the another usually represents a technical error (such as not waiting process. It involves finding a best-fitting horizontal line that long enough between irrigations). In very rare cases, periodic passes through the SPV points at the beginning of each irrigation alternating nystagmus, which represents a central abnormality, (Figure 3A). The intersection of this line with the vertical axis
can cause changing of nystagmus direction in a single head position. If the direction of BS is different in different irrigations and technical errors have been ruled out, the presence of periodic Figure 3. A) Graphical method for estimating BS. The green line represents a best-fitting horizontal line for the SPV points
within the first few seconds of each irrigation (dotted black boxes). B) The static position test result for the same patient
showing left-beating nystagmus in the supine position with an average SPV of 10 deg/sec.
INSIGHTS in practice SPECIAL COLLECTION alternating nystagmus can be verified by repeating the position Abnormal GA is an extremely rare finding. Halmagyi et al (2000) test in a single head position and recording the nystagmus for an found less than 1% of the patients who underwent vestibular extended period of time (typically, 5 minutes or longer).
testing demonstrated abnormal GA. Baloh and Honrubia (2001) have suggested that abnormal GA denotes a central lesion. The true asymmetry in the intensity of right-beating versus left- Halmagyi et al (2000) did not address this issue directly but beating nystagmus can be quantified using the same formula found abnormal GA in a variety of both central and peripheral for the DP after removing the contribution of the spontaneous lesions. In their study of patients with abnormal GA, the majority nystagmus from each of the peak caloric responses. This is of those with peripheral vestibular lesions had a diagnosis of indeed the definition of GA. Note that dividing of the difference either benign paroxysmal positional vertigo or Meniere's disease. between right-beating and left-beating nystagmus intensities by In a companion paper, Cartwright et al (2000) suggested that the total caloric responses is appropriate because after removing abnormal GA was due to a dynamic asymmetry in the secondary the contribution of the spontaneous nystagmus, all of the vestibular neurons. They further suggested that such an parameters in the formula for GA represent caloric-induced SPVs. asymmetry in peripheral vestibular lesions was brought on by a faulty compensation mechanism in response to fluctuations One more note on the somewhat confusing terminology for of vestibular function. If we accept this notion, the concept of expressing BS and GA. BS is usually expressed with respect to the abnormal GA representing a central lesion is still plausible because direction of stronger slow phases whereas GA is usually expressed both the secondary vestibular neurons and the compensation with respect to the direction of stronger fast phases. For example, mechanisms reside within the central vestibular pathways. BS in Figure 1A is to the right whereas GA in Figure 1B is to the
However, further studies are needed to determine the value of GA in identifying the site of lesion.
Interpretation of BS and GA Because BS and GA are independent parameters, they should be There are two distinct abnormalities that can cause a significant interpreted separately. BS and spontaneous nystagmus represent DP in the caloric test. Because the current method of calculating the same abnormality and therefore, their normative limits and DP does not distinguish between these two abnormalities, new interpretation are the same. Most laboratories use SPVs of less parameters were defined that can separately quantify these than 4-6 deg/sec as the normal limit for spontaneous nystagmus, abnormalities. Further studies are needed to determine whether which can be used directly as the normal limit for BS.
GA and BS are clinically more useful than DP. Nonetheless, identifying the distinct components of DP is a logical step and In many cases, abnormal BS occurs concurrently with abnormal addresses major shortcomings of DP.
UW, which indicates an acute or uncompensated peripheral vestibular lesion. In the absence of an abnormal UW, abnormal BS and spontaneous nystagmus indicate a non-localizing finding involving peripheral or central vestibular pathways.
The normative values and the interpretation of GA are not well-established because there are very few studies that have examined GA independent of DP. Halmagyi et al (2000) used values of greater than 40% for abnormal GA but again, that limit was based on their normal limits for DP. In our laboratory, we use a somewhat arbitrary limit of less than 25% for normal GA. More studies are needed to establish the normal limits of GA in a more definitive manner.
INSIGHTS in practice SPECIAL COLLECTION Note that the above formulas are algebraic operations and peak values are signed numbers with positive numbers representing The method for quantifying GA is presented here. The rightward slow-phase or left-beating nystagmus and negative conventional formula for DP is: numbers representing leftward slow-phase or right-beating
nystagmus (Figure 4). Sometimes caloric irrigations produce
TotRB – TotLB nystagmus in the opposite direction of what is expected (usually DP = _ x 100, due to presence of strong spontaneous nystagmus). The above TotRB + TotLB formulas are still applicable as long as the correct signs are used for the peak values of those responses. The common terminology where TotRB represents total responses from the irrigations that for DP is to express it with respect to the direction of stronger fast are expected to generate right-beating nystagmus and TotLB represents total responses from the irrigations that are expected to generate left-beating nystagmus. The parameters in the above When there is spontaneous nystagmus, the caloric response formula are determined from the peak nystagmus SPVs for right is a combination of the caloric-induced nystagmus and the warm (PeakRW), left warm (PeakLW), right cool (PeakRC), and left spontaneous nystagmus. That is, cool (PeakLC) irrigations: PeakXX = CalXX + SN, TotRB = – PeakRW – PeakLC, TotLB = PeakRC + PeakLW where Cal is the maximum SPV of caloric-induced nystagmus, SN is the average SPV of spontaneous nystagmus and XX stands for RW (right warm), LW (left warm), RC (right cool), and LC (left cool) irrigations. If we apply this concept to UW, the contribution of spontaneous nystagmus completely disappears from the formula for UW. That is, UW is defined as the relative difference Figure 4. Signed values of SPV: A) Positive numbers for rightward slow-phase or left-beating nystagmus, B) Negative
numbers for leftward slow-phase or right-beating nystagmus.
INSIGHTS in practice SPECIAL COLLECTION between the peak caloric responses of the right and left ears and Replacing the peak values in the formula for DP yields: TotRE – TotLE TotRB = – PeakRW – PeakLC = – CalRW – CalLC – 2 x SN , UW = x 100. TotRE + TotLE TotLB = PeakRC + PeakLW = CalRC + CalLW + 2 x SN, TotRE represents total responses from the right ear and TotLE represents total responses from the left ear: – 4 x SN DP = ( _ + (– CalRW – CalLC) +( CalRC + CalLW) TotRE = PeakRC – PeakRW, TotLE = PeakLW – PeakLC. (– CalRW – CalLC) – (CalRC + CalLW) Replacing the peak values: (– CalRW – CalLC) + (CalRC + CalLW) TotRE = PeakRC – PeakRW = CalRC + SN – CalRW – SN = The first component in the DP formula is related to spontaneous CalRC – CalRW, nystagmus and was discussed earlier. The second component represents the true asymmetry in the intensity of right-beating TotLE = PeakLW – PeakLC = CalLW + SN – CalLC – SN = versus left-beating nystagmus after removing the contribution CalLW – CalLC. of the spontaneous nystagmus. Therefore, the appropriate quantification for GA is: Therefore, UW is appropriately based on the caloric-induced nystagmus alone without any contamination by spontaneous nystagmus: (– CalRW – CalLC) – (CalRC + CalLW) (– CalRW – CalLC) +( CalRC + CalLW) (CalRC – CalRW) – (CalLW – CalLC) UW = _ x 100. (CalRC – CalRW) + (CalLW – CalLC) where CalXX can be calculated by subtracting the BS from the corresponding PeakXX. Note that dividing of the difference between right-beating and left-beating nystagmus intensities In fact, the rationale for performing bithermal caloric testing is by the total caloric responses is appropriate because all of the to cancel out the effect of spontaneous nystagmus in calculating parameters in the above formula represent caloric-induced SPVs.
UW. In the above formula, the difference between the responses of right and left ears is divided by the total of all four caloric responses to scale or normalize UW. This is logical in view of the fact that there is considerable variability among the individual caloric responses from one person to another.
INSIGHTS in practice SPECIAL COLLECTION Baloh, R.W. and Honrubia, V. (2001). Clinical Neurophysiology of the ICS Chartr software versions 6.0 and higher are capable of Vestibular System. New York: Oxford University Press. calculating BS and GA.
Baloh, R.W., Sills, A. W., and Honrubia, V., (1977). Caloric Testing: Patients With Peripheral and Central Vestibular Lesions. Ann Otol Rhinol Laryngol (Suppl.) 43: 24. Barin, K. and Stockwell, C.W. (2002) Directional Preponderance Revisited. Insights in Practice, February 2002, 1. Cartwright, A.D., Cremer, P.D., Halmagyi, G.M., and Curthoys, I.S., (2000). Isolated Directional Preponderance of Caloric Nystagmus: II. A Neural Network Model. Am J Otol 21: 568. Coats, A.C., (1965). Directional Preponderance and Unilateral Weakness as Observed in the Electronystagmographic Examination. Ann Otol Rhinol Laryngol 74: 655. Coats, A.C. (1966). Directional Preponderance and Spontaneous Nystagmus as Observed in the Electronystagmographic Examination. Ann Otol Rhinol Laryngol 75: 1135. Fitzgerald G., and Hallpike, C.S., (1942). Studies in Human Vestibular Function. I: Observations on the Directional Preponderance (‘Nystagmusbereitschaft') of Caloric Nystagmus Resulting from Cerebral Lesions. Brain 62 (part 2): 115. Halmagyi, G.M., Cremer, P.D., Anderson, J., Murofushi, T, and Curthoys, I.S., (2000). Isolated Directional Preponderance of Caloric Nystagmus. I. Clinical Significance. Am J Otol 21: 559. Sills, A.W., Baloh, R.W., and Honrubia, V. (1977). Caloric Testing 2. Results in Normal Subjects. Ann Otol Rhinol Laryngol (Suppl.) 43: 7. GN Otometrics, Europe. +45 45 75 55 55. [email protected]
GN Otometrics, North America. 1-800-289-2150. [email protected]
www.otometrics.com
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