3 Computerized Testing of the Vestibular Patient

There is no single diagnostic test that will definitively determine the source of a patient’s complaints of dizziness.1 Often, a battery of tests is ordered to help render a diagnosis. Computerized testing of the dizzy patient may not be indicated for all patients, but should be used for patients whose diagnosis is not evident from history or bedside testing alone. An appropriate diagnostic work-up of the dizzy patient will allow the clinician to document any abnormalities, as well as guide the physician to the proper medical or rehabilitative treatment for the patient.

The primary purpose of computerized vestibular testing is to determine the presence or absence of a lesion. If abnormal test results are obtained, the examination then must determine if the origin is peripheral or central, if the lesion is unilateral (and which side) or bilateral, and whether the results indicate which end-organ (site of pathology) may be contributing to the symptoms. The interpretation of vestibular test results depends on integrating the findings from examinations specific to all six semicircular canals and four otoliths.²

The structures of the vestibular system that are assessed during computerized testing include the following: horizontal semicircular canal (HSCC), posterior semicircular canal (PSCC), anterior semicircular canal (ASCC), otoliths (saccule and utricle), and the vestibular nerve (inferior and superior portions).

Before 1990, assessment of peripheral vestibular structures was limited to only the HSCCs and the superior portion of the vestibular nerve.³ Currently, computerized testing can assess the function of each of the structures mentioned. Each test assesses a different part of the vestibular system and also examines various frequencies of movement (Fig. 3.1). Computerized vestibular tests include videonystagmography (VNG) with bithermal caloric testing (BCT), sinusoidal harmonic acceleration (SHA) testing and step testing via the rotational chair test (RCT), vestibular evoked myogenic potential (VEMP) testing, video head impulse testing (vHIT), and computerized dynamic platform posturography (CDP). It must also be remembered that not all patients with vestibular signs and symptoms have abnormal electrophysiologic test results.

Balance disorders are often accompanied by otologic symptoms, including changes in hearing, tinnitus, or aural fullness. A comprehensive evaluation of hearing should accompany and, if possible, precede any additional testing.

Fig. 3.1 Frequency progression of computerized vestibular tests.

Similar to the bedside evaluation, some computerized vestibular tests use eye movement as a method of assessing vestibular function. The vestibulo-ocular reflex (VOR) is one of three vestibular reflexes, along with the vestibulospinal reflex (VSR) and the vestibulocolic reflex (VCR), that can be assessed with computerized testing. We evaluate the VOR with VNG, RCT, and the vHIT. The VSR is assessed with platform posturography. Vestibular evoked myogenic potential (VEMP) will evaluate the VCR.

A large number of medications may affect the results of many computerized tests. Any central nervous system (CNS) depressant may result in abnormal eye movements, decreased alertness, and findings that may mimic vestibular hypofunction. CNS stimulants may increase vestibular responses. Apparently, the VEMP is the only computerized vestibular test whose results are not influenced by medication or hearing loss.4 No medication should be stopped or started without the permission of the patient’s physician.

Computerized Tests of Vestibular Function

Videonystagmography with Bithermal Caloric Testing

The VOR functions to create compensatory eye movements that are equal to, but opposite to, head movement, to maintain a steady visual image. Videonystagmography is a direct measure of VOR function. The VOR is directly measured via infrared goggles during VNG testing. Historically, electronystagmography (ENG) was used to record eye movements; surface electrodes recorded changes in the corneoretinal potential, assessing the eyes’ movement. VNG is now the preferred method.

Videonystagmography uses digital and infrared recording technology to record eye movements and allows for both subjective and objective analysis of changes in eye position.⁵ Because of its many clinical advantages over ENG, VNG yields a more accurate analysis and interpretation of eye movements.^5,6 Both ENG and VNG consist of a series of subtests that may vary from center to center, but generally fall into three categories: oculomotor testing, positional testing, and BCT.

Oculomotor Testing

Oculomotor testing helps differentiate between peripheral vestibular end-organ and the central vestibular system. Oculomotor testing includes gaze stability testing, saccadic tracking, smooth pursuit tracking, and optokinetic tracking.

Gaze Stability

Gaze stability testing is accomplished under two conditions—with vision, and with vision denied—for at least 20 to 30 seconds in each eye gaze direction. The patient is asked to fixate on a target, typically displayed on a light bar located 4 feet from the patient. Based on center gaze, left gaze, and right gaze, the clinician will determine if nystagmus is present. If nystagmus is present with vision denied, the examiner will have the patient fixate on the target to determine if the nystagmus diminishes or abates with vision. Nystagmus is defined as rapid movement of the eyes, with two distinct phases: the slow phase, which results from vestibular input, and the quick, corrective phase, in which the eyes move in the opposite direction. The direction of the nystagmus is defined by the direction of the quick component, but is usually measured by the slow phase (slow phase velocity).

Horizontal nystagmus that is diminished by at least 50% with vision is considered peripheral, whereas nystagmus that is not reduced or abolished with vision may be indicative of a central pathology.⁷ Peripheral nystagmus should follow Alexander’s law,^7,8 which states that the slow phase of nystagmus caused by a unilateral peripheral vestibular pathology increases when the patient stares in the direction of the fast phase.⁸ Vertical nystagmus may occur in a normal patient, but it can indicate central pathology.

Saccadic Tracking

Saccadic tracking measures the ability of the patient to coordinate eye movement with visual target movement. In the VNG test battery, eye velocity, latency, and accuracy are measured. An abnormal finding in saccadic tracking may be due to an oculomotor pathology or a central dysfunction once technical error (drowsiness, inattentiveness, drugs, anticonvulsants, sedatives, antidepressants, etc.) has been ruled out. Abnormal results in both directions are of lesser clinical value and may be due to an oculomotor/visual acuity problem.⁹ Significant asymmetric smooth pursuit (between rightward and leftward) may be due to a structural disorder, degenerative disorders, or medication or alcohol intake.¹⁰ Test results may also be affected by a strong spontaneous nystagmus.

Smooth Pursuit (Pendular Tracking)

Optokinetic testing, as assessed on the VNG, is not a true test of the entire optokinetic system, which requires full field visual stimuli (these results could be obtained if OPK is assessed using the RC). In the VNG, OPK measures the eye movement elicited by the tracking of a moving field leftward and rightward on a light bar; a normal response is symmetric. Optokinetic asymmetry, if noted, may be a sign of a nonlocalizing CNS dysfunction.9 Patients who demonstrate normal smooth pursuit should also demonstrate normal and symmetric OPK. For an optokinetic test to be judged abnormal, drugs, inattentiveness, poor vision, uncooperativeness, and congenital nystagmus must also be ruled out.

Positional Testing

Static Positional Testing

Nystagmus provoked by head or body position is assessed as part of the VNG battery. Positional testing is performed with vision and with vision denied (mental alerting tasks are used whenever the patient is denied vision). The patient is tested in at least four head positions (head left, head right, supine flat, supine head ventroflexed 30°).⁹ Nystagmus observed in the head right or head left position may be caused by neck rotation. This can be ruled out by testing the patient in the body left or body right position. If body rotations do not elicit nystagmus, the nystagmus may be cervicogenic in origin.¹¹

In each position, eye movements are observed for at least 20 to 30 seconds with vision denied to determine the presence of nystagmus. If nystagmus is observed, it will be described by the direction of the fast phase, the degree of the slow phase, and whether or not it can be fatigued with visual fixation. If the observed nystagmus is diminished with fixation, the nystagmus is identified as peripheral in nature, possibly indicating a unilateral peripheral pathology; this will often be corroborated by peripheral findings on other subtests of the VNG.¹¹ Nystagmus that cannot be fatigued with fixation, whether direction fixed or direction changing in any position or in multiple head positions, may be indicative of CNS pathology (usually in the cerebellar system).¹¹

If the slow phase velocity of horizontal nystagmus is equal to or exceeds 6° per second in any single head position with ENG and is equal to or exceeds 4° per second in any single head position with VNG, it is considered a significant finding.¹¹ Vertical nystagmus without visual fixation may be considered abnormal if it is equal to or exceeds 6° per second in any single head position. Vertical nystagmus that is not fatigued with visual fixation is a central finding.

Dynamic Positional Testing: Dix-Hallpike Diagnostic Maneuver

Following tests of static positioning, where nystagmus is recorded while the patient’s head remains in various positions, as a subtest of VNG, a Dix-Hallpike diagnostic maneuver is performed to determine if there is any nystagmus during the actual positioning of the head. During the maneuver, the patient’s eyes are observed and recorded and the patient is asked to report any vertiginous symptoms.

Hallpike is performed to document the presence of benign paroxysmal positional vertigo (BPPV). In some centers, in the presence of a positive Hallpike, the clinician will immediately perform the maneuver to treat the BPPV.

By far the most common location of the BPPV is the PSCC, followed by HSCC BPPV; however, BPPV may be present in the ASCC or concurrently in multiple canals.¹² Patients with PSCC BPPV display the normal few beats of nystagmus during the movement followed by a burst of intense nystagmus after the movement is completed. The nystagmus rapidly builds up in intensity, reaches a crescendo, slowly diminishes, and finally disappears, usually within 10 to 15 seconds, while the head is held in position. The nystagmus has a primarily upward component with a torsional component toward the lower ear.¹³

Subjective vertigo is the absence of recordable nystagmus during the diagnostic positioning maneuvers. It does not preclude a diagnosis of BPPV, especially in the presence of a very suggestive history.¹² The reported subjective vertigo should follow a pattern similar to expected nystagmus: latency, a transient crescendo-decrescendo nature, and fatigability.

Head-Shake Nystagmus (HSN)

A head-shake test, performed with the VNG goggles, with vision denied, may also be included (and recorded) as part of the VNG battery to determine the presence or absence of post-HSN. Eye movement is recorded prior to, during, and after the head-shake stimulus, with the head tilted 30° forward. HSN may be the result of peripheral as well as central vestibular lesions.14 The recording of three or more beats of horizontal nystagmus after horizontal head shake, if contralesional, may suggest a (unilateral) peripheral vestibular imbalance.^14. Typically, if the origin is peripheral, other subtests of the VNG will support this diagnosis. A diagnosis of peripheral vestibular dysfunction cannot be ruled out based solely on a negative head-shake test.¹⁵

Post-HSN may also be due to central pathology and patterns may vary. It may be purely vertical, purely horizontal, mixed horizontal–vertical, or mixed horizontal–vertical–torsional.¹⁶ Post-HSN may be the result of a central velocity storage abnormality.

Bithermal Caloric Testing

Bithermal caloric testing (BCT) is used to stimulate the HSCC of both the right and left ear. Each ear is stimulated separately with water or air, allowing the examiner to assess the function of the right and left systems independently. Bithermal caloric testing is a very useful computerized test and has many advantages, including the ability to aid in identifying the site of dysfunction and lateralizing a lesion. The equipment for BCT is also readily available in most areas, which makes the test readily accessible for evaluation of the dizzy patient. However, BCT does not examine the entire right and left peripheral system. During BCT, only low-frequency (0.003 Hz) stimulation is presented to the HSCC (innervated by the superior portion of the vestibular nerve). This leaves the functioning of other neural structures of the vestibular system, such as the PSCC, ASCC, utricle, saccule, and inferior vestibular nerve, unknown.

Bithermal caloric testing also takes a relatively long time to perform when compared with the rest of the VNG battery. It requires a minimum of four stimulations: right cool (RC), right warm (RW), left cool (LC), and left warm (LW). Four stimulations can take ~ 30 minutes to complete. The process may be longer depending on the patient. Lastly, BCT does not give any information about vestibular compensation; therefore, BCT is best used as part of a battery of tests to aid a physician in diagnosis.

During BCT, the patient is supine with the head ventroflexed 30° while the ear canal is stimulated (via air or water) to create a temperature gradient across the HSCC, which causes a change in the density of endolymph.¹⁷ (It should be noted that the nystagmus created is measured via the slow phase, but it is named by the fast phase.) Warm stimulation causes the endolymph to become lighter, creating ampullopetal deflection of the cupula, generating nystagmus, with a fast phase beating toward the stimulated ear.¹⁷ The opposite occurs with cool stimulation. Cool stimulation causes the endolymph to increase in density and become heavier, creating an inhibitory response, causing nystagmus that beats away from the stimulated ear.¹⁷

The acronym COWS (cool opposite and warm same) is used for the above response pattern. For example, cool air stimulation of the right ear will create a left-beating nystagmus, and warm stimulation of the right ear will create a right-beating nystagmus. The nystagmus is recorded via infrared VNG goggles that deny vision, while the patient is alerted. Mental alerting is needed to ensure that central suppression does not occur, reducing the obtained nystagmus (Fig. 3.2).¹⁸

The peak response of nystagmus is recorded from all four stimulations and is then analyzed. The sum total of both right stimulations and both left stimulations is compared using Jongkee’s formula (first described in 1962), to determine if a significant reduced vestibular response (RVR) is present.¹⁹ RVR may also be referred to as a unilateral weakness (UW). UW of 20% or 25% (depending on the laboratory) is generally judged to be a significant finding and can be calculated using the following formula¹⁹:

UW = (RC + RW) – (LC + LW)/(RW + RC + LW + LC)

A UW of 20 to 25% is judged to be significant for peripheral dysfunction on the ipsilateral side of the reduced response, indicating significant horizontal canal dysfunction on that side. For example, a 37% UW in the right ear would be reported as a significant right UW, suggestive of right peripheral vestibular dysfunction.

Directional preponderance (DP) is computed to determine if caloric responses create more right-beating nystagmus than left-beating nystagmus. A value of 30% to 35% is typically judged to be a significant DP, but the value may vary by laboratory. The following formula is used¹⁹:

DP = (RW + LC) – (LW + RC)/(RW + RC + LW + LC)

A DP is typically seen in the presence of a spontaneous nystagmus. In this scenario, the eyes are already moving prior to caloric stimulation; hence, there is a tendency for the eyes to move farther in one direction. A significant DP is typically indicative of an acute peripheral vestibular disorder. DP is sometimes found in isolation (without spontaneous nystagmus or UW). An isolated significant DP is generally due to a benign transient disorder, which 50% of the time is BPPV or Meniere’s disease.²⁰ Approximately 5% of patients with an isolated significant DP will have a central nervous system (CNS) lesion. If present, the CNS lesion should be apparent to the clinician during physical examination.²⁰

In addition to calculation of UW and DP, all four calorics are evaluated to determine if hypoactive or hyperactive responses are present. Responses are considered hypoactive if the sum of both irrigations on each side is less than 12° per second.¹⁷ The authors of this chapter recommend that the presence of bilateral weakness be confirmed with a RCT, as RCT is not dependent on the stimulus travelling through the outer and middle ear.

Fig. 3.2 This graphic representation is commonly referred to as “pods” and is used to display results obtained during bithermal caloric testing (BCT). (a) Results of BCT exhibiting normal responses. The peak slow phase velocity was identified during each stimulation and used for calculation of unilateral weakness (UW) and directional preponderance (DP); both are nonsignificant. The four small boxes below are a visual representation of the obtained nystagmus for each stimulation. (b) Results of BCT exhibiting a significant right UW. Peak slow phase velocities of nystagmus were identified during each stimulation and used to calculate UW and DP; UW is 68% in the right ear, indicating dysfunction on the right side. The graphic representation of obtained responses shows an obvious difference between right and left stimulations.

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