Optimizing the sensitivity of the head thrust test for identifying vestibular hypofunction.

Individuals who sustain damage to their vestibular systems may experience vertigo, disequilibrium, gait ataxia, postural instability, and blurred vision during head motion (oscillopsia). One cause of oscillopsia is a deficient vestibulo-ocular reflex (VOR). The deficient VOR can reduce visual acuity during head rotation. (1) Because of the direct relationship between function of the vestibular receptors in the inner ear and eye movements produced by VORs, the bedside examination of eye movements can be of great importance in defining and localizing vestibular pathology. (2)

The head thrust test (HTT) has been widely accepted as a clinical test that is used to assess the angular vestibulo-ocular reflex. (3-7) During the HTT, the patient is asked to focus his or her eyes on a target. Next, the patient's head is gently grasped, and a small-amplitude (5[degrees]-10[degrees]) but high-acceleration (3,000-4,000[degrees]/s/s) thrust is applied by the examiner. Once the head stops moving, the eyes are observed for a corrective saccade. The corrective saccade is a rapid eye motion that returns the eyes toward the target and indicates a decreased gain (eye velocity/head velocity) of the VOR. Individuals with normal vestibular function do not use corrective saccades after the HTT (the eyes stay fixed on the target) (Figure, photographs A and B). People with vestibular hypofuncfion may use a corrective saccade after the head is thrust toward the side of the hypofunction (Figure, photographs C-E).

[FIGURE OMITTED]

The specificity of the HTT for identifying lateral semicircular canal pathology for patients with unilateral vestibular hypofunction (UVH) is high (95%-100%) (3,8-11) yet the sensitivity is variable. For patients with complete UVH due to nerve section, the sensitivity and specificity are 100%. (3,8) For patients with nonsurgically induced unilateral hypofunction, a group that more accurately reflects a clinical population, the HTT has a sensitivity of 34% to 39% and a specificity' of 95% to 100%. (9-11)

We believe the technique used to perform the horizontal HTT may be the cause of the low sensitivity in patients with UVH due to causes other than nerve section. We reasoned that position of the head and the unpredictability of the stimulus (random direction and random onset of head rotation) would be important components in identifying a peripheral vestibular lesion using the HTT. In none of the prior studies investigating the validity of data obtained with the HTT (3,8-11) did the authors state that the head was placed in a starting position of 30 degrees pitched down, a position that might optimize the acceleration signal being induced exclusively through the lateral semicircular canal. We hypothesized that if the horizontal HTT is done without initially pitching the head 30 degrees down, the head acceleration signal may not be isolated within the lateral semicircular canals. The vertical semicircular canals (anterior and posterior semicircular canals), therefore, may detect the head rotation signal and prevent cutoff of inhibitory input from the contralesional horizontal vestibular afferents. (12-14) Cutoff of the inhibitory input has been offered as an explanation for the positive HTT. (3,4)

Some researchers (9,10) administered the HTT with predictable timing. We have shown that when subjects with UVH made a predictable (volitional) head thrust, they generated a unique type of saccade more often than during an unpredictable (passive) head thrust. (15) This saccade occurred during the head thrust and was in the opposite direction of the moving head (preprogrammed saccade). The preprogrammed saccade returned the eye to the center of the orbit, often eliminating the need for a corrective saccade. This behavior, in part, also might explain the reduced sensitivity of the HTT.

The primary purpose of our study was to examine sensitivity and specificity of the horizontal HTT to identify patients with UVH when the test was done in a manner attempting to induce the acceleration signal through the lateral semicircular canals and to limit the effects of prediction (head pitched in 30[degrees] of cervical flexion and moved unpredictably). In addition, we report the sensitivity and specificity of the HTT to identify patients with bilateral vestibular hypofunction (BVH), which has not been previously reported.

Method

Subjects

Subjects were individuals complaining of dizziness or imbalance who were initially seen in a tertiary care facility from 1995 to 2001 by a neurologist specializing in dizziness and balance disorders. The neurologist was experienced in administering the HTT. Subjects were selected based on a retrospective chart review, and all data were obtained from their medical records. Inclusion criteria consisted of the subjects complaining of dizziness or imbalance and having undergone vestibular function testing. Exclusion criteria consisted of having a history of benign paroxysmal positional vertigo, anxiety disorders, cervical spine pathology, ocular malalignment, central nervous system pathology, or excessive alcohol use (greater than 59.13 mL [2 oz] of 100% alcohol per day).

Based on patient data obtained from the charts, which included the results of vestibular function testing, subjects were categorized as belonging to 1 of 3 groups: (1) subjects with UVH, (2) subjects with BVH, and (3) subjects with nonvestibular dizziness. This was done to determine the effectiveness of the clinical head thrust based on severity of hypofunction. Subjects with a diagnosis of UVH had a difference in slow component eye velocity of greater than 25% between the right and left sides on the caloric test (>25% unilateral weakness). Subjects with a diagnosis of BVH demonstrated a slow component eye velocity of less than 5[degrees]/s to cold, warm, and ice water irrigation in each ear and a gain of less than 0.1 on the rotary chair test (240[degrees]/s constant velocity). Typically, only subjects with BVH underwent both rotary chair and caloric testing. Subjects assigned to the nonvestibular dizziness group had complaints of dizziness but normal vestibular function test results.

Subjects with vestibular hypofunction were assigned to subcategories based on whether they exhibited incomplete or complete hypofunction as determined by caloric examination. Based on their medical records, patients with incomplete vestibular hypofunction demonstrated reversal of nystagmus between cold and warm water caloric irrigations. Patients with complete vestibular hypofunction showed neither reversal nor a response to ice water irrigation.

Data for a total of 176 subjects in all 3 groups were included in the overall analysis. The group characteristics are shown in Table 1. No difference in age was found across the groups (analysis of variance [ANOVA] F = 2.4, P = .64).

Procedure

Data were obtained retrospectively from medical records from the Dizziness and Balance Centers of Emory University and the University of Miami. The rights of the patients were protected by 1 of 2 means: (1) Patient data were tabulated from a de-identified database (n = 170), or (2) informed consent was obtained (n = 6). The term "de-identified" means that the health information was stripped of all identifiers so that the health information does not identify an individual and does not present any reasonable basis by which the information can be used to identify the individual. Data from the de-identified database were originally collected before our intent to investigate sensitivity and specificity of the HTT.

All data were de-identified. Data collected included information regarding diagnoses, vestibular function test results, HTT results, and subject age. Individuals with the following peripheral vestibular diagnoses were included in the study: vestibular neuritis, vestibular ototoxicity, Meniere disease, vestibular nerve section due to vestibular schwannoma or Meniere disease, labyrinthitis, and idiopathic vestibular hypofunction.

For the purposes of clarity, all references to the HTT in this report refer to testing in the horizontal plane. Based on medical records, one investigator routinely did the HTT as part of the initial clinical examination before vestibular function testing was performed. This investigator was experienced in administering the HTT. The subjects were instructed to look at the investigator's nose (distance of 38 cm [15 in]). The investigator's nose was chosen because it provided a convenient near target. Individuals with vestibular hypofunction have more difficulty generating an adequate response for a near target because vergence of the eyes requires the gain of the VOR to be larger. (16-18)

A typical head thrust test was administered by first placing a subject's head into 30 degrees of cervical flexion. This was done using anatomical landmarks (imaginary line between the inferior rim of the ocular orbit through the external acoustic meatus) to match the lateral semicircular canal in situ. The subject's head would then be moved unpredictably to the right or left from center. The examiner attempted to keep the head thrust unpredictable by moving the head in a manner that was random in direction and timing of onset. Total amplitude of head rotation was approximately 5 to 10 degrees. After each HTT, the head was slowly moved back to center. The test was repeated in each direction 3 times. Individuals with a positive head thrust were identified as having a corrective saccade in at least 2 of the 3 thrusts (toward one ear if the subject had a diagnosis of UVH and toward both ears if the subject had a diagnosis of BVH).

Sensitivity, specificity, positive and negative predictive values, likelihood ratios, and accuracy were calculated using the following formulas (19):

(1) Sensitivity = (True positives/[True positives + False negatives]) x 100 = %

(2) Specificity = (True negatives/[True negatives + False positives]) x 100 = %

(3) Positive predictive value = (True positives/ [True positives + False positives]) x 100 = %

(4) Negative predictive value = (True negatives/ [True negatives + False negatives]) x 100 = %

(5) Accuracy = (True negatives + True positives)/Total x 100 = %

(6) Positive likelihood ratio = Sensitivity/(1 - Specificity)

(7) Negative likelihood ratio = (1 - Sensitivity)/Specificity

"True positives" were those subjects with confirmed vestibular hypofunction (UVH or BVH) based on abnormal caloric or rotary chair test results and who had a positive HTT. "True negatives" were those subjects with normal vestibular function based on caloric or rotary chair test results and who had a negative HTT. "False negatives" were those subjects with confirmed vestibular hypofunction who had a negative HTT. "False positives" were those subjects with confirmed normal vestibular function who had a positive HTT. Sensitivity and specificity for subjects with vestibular hypofunction was assessed using subjects with nonvestibular dizziness as the criterion reference point. We chose subjects with complaints of dizziness and normal vestibular function as the criterion for comparison (instead of subjects with normal vestibular function and no complaints of dizziness) to provide what we believe is a more clinically appropriate assessment of test validity. Analysis of variance was used to assess differences in age (P<.05).

Results

Sensitivity and Specificity to Identify, Peripheral Vestibular Hypofunction

Unilateral vestibular hypofunction. The contingency table for tabulating the sensitivity and specificity of the HTT to identity peripheral vestibular hypofunction according to the patient's HTT and diagnostic classification is presented in Table 2. Fifty-six of 79 subjects with UVH had a positive ipsilesional HTT, resulting in a combined sensitivity of 71% (incomplete and complete lesions). Of the 23 subjects with UVH who had a negative HTT, only 4 had a complete loss of vestibular function unilaterally. The difference in sensitivity for subjects with incomplete and complete UVH was 58% versus 88% (Tab. 3).

Bilateral vestibular hypofunction. Twenty-seven of 32 subjects with BVH had a bilaterally positive HTT, resulting in a combined sensitivity of 84% (incomplete and complete lesions). The other 5 subjects with BVH had a positive HTT in one direction only and were found to have incomplete loss of vestibular function. Similar to the sensitivity of the HTT for subjects with UVH, sensitivity improved depending oil extent of the hypofunction (76% for incomplete BVH and 100% for complete BVH) (Tab. 3).

All subjects. Eighty-three of 111 subjects with peripheral vestibular hypofunction (UVH and BVH) had a positive HTT in at least one direction. No subjects with nonvestibular dizziness were found to have a positive HTT and a positive vestibular function test. As a result, the overall sensitivity of the HTT in identifying subjects with vestibular hypofunction was 75% (Tab. 3). Twelve subjects with nonvestibular dizziness were found to have a false positive HTT. As a result, the overall specificity of the HTT to rule out vestibular hypofunction was 82%.

Discussion

Sensitivity and Specificity of the HTT

The method we used for administering the HTT to identify subjects with varying degrees of UVH had a sensitivity of 71%, as compared with sensitivity values of 34% to 39% previously reported. (9-11) We believe the improved sensitivity may be due to 2 factors. First, performing the HTT with the head pitched 30 degrees down places the lateral semicircular canals in the plane of rotation. If the HTT is done with the neck in a neutral position (no cervical flexion), the head acceleration may be distributed among the vertical semicircular canals. (14) We believe that, as a result, peripheral vestibular afferents and central vestibular neurons of the intact lateral semicircular canals are exposed to less acceleration and therefore are less likely to reach inhibitory cutoff. Second, ensuring that the head thrust is unpredictable in timing and direction may prevent preprogrammed saccades and the effects of prediction. When a head rotation is predictable, the gain of the VOR is greater compared with an unpredictable head rotation. (20-23) These phenomena have been suggested to be due, in part, to the central nervous system's ability to generate an appropriate VOR once the brain is able to predict the intended head rotation. (22-24) Some researchers (9,10) have done the HTT with predictable timing. Patients with vestibular hypofunction can generate preprogrammed eye movements during predictive head movements to stabilize gaze. (15) Preprogrammed eye movements may eliminate the need of corrective saccades, which can decrease the sensitivity of the HTT. Preprogrammed saccades have been shown to occur during predictable head thrusts as well as during pseudorandom whole-body rotations. (15,25) The effects of central preprogramming also have been suggested as the mechanism for improved visual acuity during predictable head rotation in patients with vestibular hypofunction. (26) We believe making the HTT unpredictable improves sensitivity of the HTT, in part, because the effects of central preprogramming are reduced.

Sensitivity of the HTT Related to Extent of Pathology

We found that the HTT was more sensitive in identifying subjects with complete versus incomplete loss of vestibular function. The HTT was more sensitive in categorizing subjects with complete BVH (100%) than in categorizing subjects with complete UVH (88%). Subjects with either UVH or BVH might be expected to have similar occurrences of corrective saccade use (and therefore similar sensitivities using the HTT), considering each group had a complete lesion as defined by caloric and rotary chair testing. One explanation may be the extent of the lesion. Because patients with BVH have a more extensive injury than those with UVH, (27) the response range of the VOR for head acceleration may be smaller for people with BVH. In contrast, people with UVH have intact contralateral peripheral vestibular afferents that we believe can respond to a broader range of head accelerations.

Limitations of Studies Comparing Results of the HTT and the Caloric Test

Twenty-two percent (12/53) of our subjects with dizziness not associated with vestibular dysfunction had a positive HTT but negative caloric or rotary chair testing results. This finding reduced the overall specificity of the HTT to 82%. One explanation is that these 12 individuals may have a high acceleration detect in their VOR that could not be detected by the caloric testing. In our clinical experience, a small number of people with normal vestibular function based on caloric and rotary chair examinations have a positive head thrust test and complain of dizziness or imbalance only during rapid head motion. We have used the term "high acceleration defects of the VOR" to identify these individuals with normal vestibular function tests yet reduced performance of the VOR during rapid head accelerations. A more complete battery of vestibular tests (ie, one that includes accelerations at middle and high frequencies) may be needed to test this hypothesis.

An additional explanation for the reduced specificity of the HTT relates to differences with the caloric test. Although, the caloric test is recognized as the most useful test for identifying individuals with suspected peripheral UVH, (28,29) the information provided by caloric testing is dissimilar to the information provided by the HTT. The caloric test generates nystagmus as a result of an unnatural stimulation of the semicircular canals that is equivalent to a very-low-frequency head rotation. In contrast, the HTT represents a natural and high-acceleration head rotation. The caloric test, therefore, does not test the lateral semicircular canals with a stimulus equivalent to the HTT. As a result, factors other than technique used to perform the HTT likely contribute to the variability of the sensitivity of the HTT to identify individuals with UVH.

Importance of Training and Experience in Performing the HTT

In our study, a clinician with more than 20 years of experience administered the HTTs. We believe that proper training is necessary in order to perform the HTT correctly. Proper technique includes correct head position, inducing a rapid head thrust through a small amplitude, and making sure the head thrust is unpredictable both in direction and timing. We encourage all practitioners to study with someone who is skilled in performing the test.

Limitations of the Study

We did not examine the reliability of our examiner's findings or whether differences would have been found with multiple examiners. Similarly, we did not investigate whether proper training is necessary to perform the head thrust correctly. We believe, however, that performing the head thrust test is a learned skill.

Conclusion

The sensitivity of the HTT for identifying individuals with UVH is good when the head is thrust unpredictably in the plane of the lateral semicircular canals (keeping the head in 30[degrees] of cervical flexion). This degree of sensitivity is considerably improved compared with previous established values, although it is not sensitive enough to replace vestibular function testing. The HTT is more sensitive in patients with BVH. Correctly assessing the VOR with the HTT is an essential component of the clinical examination of the peripheral vestibular system. Proper position of the head, ensuring that the head thrust is unpredictable, and experience of the clinician are likely the most critical components for administering the HTT.

Table 1.
Group Characteristics (a)

                                          Subjects With Unilateral
                                          Vestibular Hypofunction

                          Subjects With
                          Nonvestibular
                          Dizziness       All     iUVH    cUVH

N                         65              79      45      34
Age (y)
  [bar]X                  64.4            65.3    60.6    64.7
  SD                      16.8            16.2    14.1    17.6
  Range                   29-87           29-87   29-85   30-87
Sex ratio (male:female)   21:44           33:46   21:24   13:21

                          Subjects With Bilateral
                          Vestibular Hypofunction

                          All     iBVH    cBVH

N                         32      21      11
Age (y)
  [bar]X                  66.7    66.3    66.1
  SD                      13.3    18.7     6.5
  Range                   29-91   29-91   53-75
Sex ratio (male:female)   15:17   11:10   5:6

(a) i = incomplete (nystagmus reversal with a change in caloric
temperature), c = complete (no response to ice water irrigation),
UVH = unilateral vestibular hypofunction (ipsilesional).
BVH = bilateral vestibular hypofunction.

Table 2.
Contingency Table for All Subjects (a)

                       Positive        Negative
                       Dx              Dx               Total

Positive head thrust   Nonvestibular   Nonvestibular    95
                         dizziness=0     dizziness=12
                       UVH=56          UVH=0
                         iUVH=26         iUVH=0
                         cUVH=30         cUVH=0
                       BVH=27          BVH=0
                         iBVH=16         iBVH=0
                         cBVH=11         cBVH=0

Negative head thrust   Nonvestibular   Nonvestibular    81
                         dizziness=0     dizziness=53
                       UVH=23 (b)      UVH=0
                         iUVH=19         iUVH=0
                         cUVH=4          cUVH=0
                       BVH=5           BVH=0
                         iBVH=5 (c)      iBVH=0
                         cBVH=0          cBVH=0
Total                  111             65               176

(a) i = incomplete (nystagmus reversal with a change in caloric
temperature). c = complete (no response to ice water irrigation),
UVH = unilateral vestibular hypofunction (ipsilesional),
BVH = bilateral vestibular hypofunction, positive Dx = positive
diagnosis (positive caloric test [UVH and BVH] and rotary chair
test [BVH]), negative Dx = negative diagnosis (negative caloric
test [all 3 groups] and rotary chair test [BVH]), positive head
thrust = corrective saccade observed after heard movement stopped.

(b) No subject with UVH had a positive head thrust in both
directions.

(c) Subjects with iBVH had a positive head thrust in both
direction and a positive head thrust in opposite direction.

Table 3.
Validity of the Data Obtained With the Head Thrust Test (HTT)
for Identifying Subjects With Peripheral Vestibular Hypofunction
Based on Extent of Lesion (a)

                      All        All Subjects   All Subjects
Validity Measures     Subjects   With UVH       With BVH

Sensitivity (%)       75         71             84
Specificity (%) (b)   82
  PV+                 87         82             69
  PV-                 65         70             91
  LR+                  4.16
  LR-                  0.30
Accuracy (%)          77         76             82

                      Incomplete   Complete

Validity Measures     UVH   BVH    UVH   BVH

Sensitivity (%)       58    76     88    100
Specificity (%) (b)
  PV+                 68    57     71     48
  PV-                 74    91     93    100
  LR+
  LR-
Accuracy (%)          55    71     58     66

(a) Incomplete = nystagmus reversal with a change in caloric
temperature, complete = no response to ice water irrigation,
UVH = unilateral vestibular hypofunction (ipsilesional),
BVH = bilateral vestibular hypofunction, PV+ = positive
predictive value. PV- = negative predictive value, LR+ = positive
likelihood ratio, LR- = negative likelihood ratio.

(b) Only subjects with nonvestibular dizziness (n = 12) were
found to have false positive HTT, resulting in overall
specificity of 82%.

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MC Schubert, PT, PhD, is Post-doctoral Fellow, Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University, Baltimore, MD 21205 (USA) ([e-mail]). Address all correspondence to Dr Schubert.

RJ Tusa, MD, PhD, is Professor, Department of Neurology, Emory University, Atlanta, Ga.

EL Grine, PT, MSPT, is Physical Therapist, Spine & Sport Physical Therapy, Manassas, Va. He was a student in the Division of Physical Therapy at the University of Miami, Coral Gables, Fla, when this project was initiated.

SJ Herdman, PT, PhD, FAPTA, is Professor, Department of Rehabilitation Medicine, Emory University.

Each of the authors contributed to concept/research design and writing of the manuscript. Dr Schubert and Mr Grine performed data collection and analysis. Dr Tusa and Dr Herdman provided subjects, project management, and facilities/equipment. Dr Schubert. Dr Tusa, and Dr Herdman provided fund procurement. Dr Tusa, Mr Grine, and Dr Herdman provided consultation (including review of manuscript before submission). The authors thank John P Carey, MD, for assistance in generating the Figure.

Informed consent was obtained for a subset of the subject population from the Institutional Review Board of Emory University.

Preliminary findings of this work were presented at the Combined Sections Meeting of the American Physical Therapy Association, February 14-18, 2001, San Antonio, Tex, and at the American Academy of Neurology meeting, April 13-20, 2002, Denver, Colo.

This study was supported by the Foundation for Physical Therapy (MCS) and by National Institute on Deafness and Other Communication Disorders grant 03196 (SJH, RJT).

This article was received April 4, 2003, and was accepted & September 4, 2003.