SCREENING TESTS FOR VESTIBULAR DYSFUNCTION

INTRODUCTION:

The goal of the initial office examination is to determine whether the probable site of the lesion is peripheral or central. A directed case history and brief physical examination often allow a more direct route to diagnosis and treatment. The examiner is responsible for determining on initial contact whether the patient’s complaints suggest a neurologic emergency such as brain stem stroke (Baloh, 1998). Once the examiner is comfortable that the patient’s symptoms and

physical signs are of a nonurgent nature, an examination to categorize the patient’s ‘‘type’’ of dizziness follows. Patients with chronic balance disorders typically see several different physicians without a diagnosis or resolution to their complaint. Many are treated symptomatically with vestibular suppressant medication even though a diagnosis of vestibular dysfunction has not been made. In many cases, patients with a chronic history of symptoms report that a thorough history was never taken (Linstrom, 1992). To quote Dr. Joel Goebel, ‘‘The accuracy and quality of the history is directly related to the patience and skill of the examiner’’ (personal communication). It is therefore important to spend sufficient time with individual patients to understand their history and complaints thoroughly before attempting to make a diagnosis.

Role of the Case History Interview

A thorough history is critical for three main reasons:

1.      Many patients have difficulty articulating their symptoms beyond simply describing themselves as being ‘‘dizzy.’’

2.      Additional evaluation and treatment will differ depending on the suspected site of the lesion.

3.      Some vestibular disorders cannot be differentiated solely on the results of vestibular evaluation (e.g., Meniere’s disease versus labyrinthitis) (Shepard, 1999

The value of a thorough history should not be underestimated. This is reflected in the result of one study in which a provisional diagnosis based only on case history and screening examinations proved correct for 76% of patients seen (Kroenke et al., 1992).

Preexamination Preparations

Before the initial patient appointment, it is important that the patient be sent a questionnaire with instructions to complete it before arriving for the appointment. The questionnaire is not intended to be a substitute for a comprehensive case history interview but rather as a motivation for the patient to think about how to articulate the symptoms. The questionnaire should focus not only on current symptoms but also on the patient’s recalling the first episode of dizziness. It should also include questions about associated symptoms that the patient may not consider part of the ‘‘dizziness problem’

Quality

The key to a preliminary diagnosis is determining whether the patient’s complaints are of vertigo. Vertigo is described as a sensation or illusion of spinning or rotation, continuing with the eyes closed. Vertigo indicates the strong likelihood of peripheral vestibular disease, but central disease cannot be ruled out. Motion-provoked dysequilibrium and nausea are frequently associated witha nonacute vestibular loss. Other frequent descriptions of symptoms include lightheadedness, dysequilibrium while stationary, or ‘‘feeling drunk.’’ These complaints are often associated with systemic or central nervous system (CNS) disease.

Temporal Course

Temporal course includes information regarding the onset, duration, and frequency of symptoms. In general, dizziness lasting for less than 1 minute when the patient is lying down is associated with benign paroxysmal positional vertigo (BPPV), whereas dizziness lasting less than 1 minute when the patient is standing is associated with orthostatic hypotension. Dizziness lasting several minutes is most often associated with peripheral vestibular disorders, but it can be associated with vascular etiology, such as migraines or transient ischemic attacks. Dizziness lasting hours with a gradual decrease of symptoms is associated with unilateral peripheral vestibular disease, such as labyrinthitis, neuronitis, or hydrops (Meniere’s syndrome). Dizziness of more than 24-hours’ duration without a gradual decrease of symptoms may be associated with CNS or psychiatric disease.

Dizziness History Questionnaire Sample:

Precipitating, Exacerbating, or Relieving Factors

Symptoms that are brought on or increased by a change in head position, or with eyes closed, suggest peripheral disease. Symptoms noticed only while standing, but never when sitting or lying, suggest vascular or orthopedic disease. Symptoms that are constant and are unaffected by position change are suggestive of central pathology.

Associated Symptoms

Symptoms such as tinnitus, hearing loss, otalgia, or aural fullness, particularly unilateral complaints, suggest the probability of peripheral vestibular disease. Symptoms such as slurred speech, syncope or presyncope, numbness or tingling of the face or extremities, or ‘‘spots before eyes’’ suggest a more central etiology.

General Health Status

Patients with advanced diabetes may exhibit dysequilibrium and postural instability secondary to peripheral neuropathy or may experience postural hypotension secondary to autonomic neuropathy. Patients with a history of cardiovascular disease may experience reduced blood volume to the brain. Patients with a history of migraine headache are prone to vestibular migraine.

Medications

A review of the patient’s current and past medications is useful in the case history interview. Not only does this provide the examiner insight as to possible medication-related dizziness or vertigo, it also provides a second chance to review any health conditions that the patient may have omitted from the history interview.

Examination of the Vestibular Ocular Reflex

For most peripheral labyrinthine or ‘‘central’’ neurologic diseases, the eyes are the windows to the vestibular system. Inspection of eye movements can provide considerable information to assist in preliminary diagnosis. The two categories of eye movement are

(1)         reflexive eye movements generated by stimulation of the peripheral vestibular apparatus and  

(2)         voluntary eye movements controlled by the cerebellum. Certain patterns of nystagmus are associated with either peripheral labyrinthine or central site of lesion.

Static Evaluation

Static evaluation of vestibular dysfunction primarily involves inspection for spontaneous or gaze nystagmus. These are best viewed through Frenzel lenses or infrared video oculography, but can be viewed directly with the help of a penlight, otoscope, or ophthalmoscope. Spontaneous or gaze nystagmus represents a tonic imbalance in the vestibular system. Peripheral vestibular nystagmus is horizontal rotary, whereas pure vertical or pure torsional nystagmus is considered a sign of central etiology. Peripheral vestibular nystagmus diminishes with visual fixation, whereas central nystagmus is not affected by fixation and may even increase. Peripheral vestibular nystagmus is mostly conjugate, whereas central nystagmus may be more intense in one eye. Peripheral vestibular nystagmus will increase in intensity when gaze is directed toward the fast phase (typically away from the lesion side) and will decrease with gaze away from the fast phase. Central nystagmus may have a change in the direction of the fast phase when gaze is shifted (Busis, 1993).

Dynamic Evaluation

®    HEADSHAKE NYSTAGMUS

Headshake nystagmus (HSN) is believed to be a result of dynamic asymmetry within the vestibular ocular reflex (VOR). As the head is shaken back and forth in a horizontal fashion, the intact labyrinth is generating a stronger response than the lesioned side. This increase in activity on the intact side builds up and is stored in a ‘‘central velocity storage mechanism.’’ When the headshaking ceases, this stored energy discharges, causing a slow-phase response away from the

intact labyrinth, resulting in a brief period of nystagmus beating away from the lesioned labyrinth. Evaluation for HSN can be done through direct visualization, electrooculography,

or infrared video monitoring. Goebel and Garcia (1992) report that HSN can be easily documented using Frenzel lenses. The patient is instructed to tilt his or her head down at 30 degrees and then to shake the head back and forth as quickly as possible for a period of 30 seconds. This can also be done manually by the examiner. Immediately following cessation of movement, the eyes are opened and observed for nystagmus. A brief period of horizontal nystagmus may be noted. Three patterns of post-HSN have been identified. The most common is a brief horizontal nystagmus beating away from the lesioned labyrinth, which occurs within the first several seconds following headshake. A second pattern involves a horizontal nystagmus beating toward the lesioned side and occurring about 20 seconds after the headshake. This is felt to be a central compensatory response and is termed recovery nystagmus.A third pattern involves both the aforementioned types with an initial burst of nystagmus away from the lesioned side, then a reversal in direction toward the lesioned side. Again, this is believed to be the

result of a compensatory response to peripheral vestibular asymmetry (Jacobson, Newman, & Safadi, 1990). The presence of HSN correlates well with peripheral vestibular function; however, HSN has been identified in patients with cerebellar dysfunction. HSN secondary to central lesions may exhibit a vertical component following a horizontal headshake maneuver (Zee & Fletcher, 1996). Jacobson et al. (1990) report that HSN testing has a low sensitivity (27%) but fairly good specificity (85%) for identifying patients with vestibular dysfunction. They note that a potential weakness of their study is the fact that their ‘‘gold standard’’ for identifying patients with vestibular dysfunction was through caloric and rotary chair testing. Neither of these tests evaluates the high-frequency area (]/1 to 2 Hz) of the VOR thought to be involved in the generation of headshake nystagmus.

®    HEAD THRUST (HEAD IMPULSE) TEST:

The VOR in response to head movement may be evaluated by rotating the patient’s head in the YAW plane (as in shaking the head ‘‘no’’), first at slower speeds to allow the patient time to become familiar with the procedure and relax the muscles in the neck. Start with the patient’s head 15 to 30 degrees lateral from center. The patient’s eyes should be focused on a centered target, typically on the examiner’s nose. Then apply brief, high-acceleration head thrusts of about 15 to 30 degrees back to center (Fig.). The examiner should monitor the patient’s eye movements to see whether visual fixation is maintained or whether the patient loses visual contact and must make quick corrective eye movements (catch-up saccades) to gain visual contact with the target (Harvey, Wood, & Feroah, 1997). Horizontal head movement tests the horizontal semicircular canal, whereas the anterior and posterior canals can be tested by rotating the head in a diagonal

direction (Cremer et al., 1998). A lack of visual fixation and subsequent catch-up saccade during rapid head acceleration suggest a loss of function in the corresponding ipsilateral semicircular canal (Aw et al., 1999). For example, a loss of visual fixation with a rapid horizontal head thrust to the right would be consistent with decreased sensitivity in the right horizontal semicircular canal, as shown in 

®    DYNAMIC VISUAL ACUITY

Another simple test of the VOR is to have the patient read a Snellen eye chart (Fig.) and establish visual acuity. This is followed by the examiner rotating the patient’s head back and forth at a speed of 1 and 2 Hz horizontally while reading the chart. Loss of one line is considered normal. Loss of three lines indicates possible VOR deficit (Longridge & Mallinson, 1987). static visual acuity.

Figure:  Snellen eye chart: The patient reads the letters in descending order to establish

 Scoring visual acuity is usually determined by noting the lowest line on which the patient cannot correctly identify at least 50% of the optotypes (characters). Sensitivity and specificity in testing dynamic visual acuity may be improved using recently developed computerized measurement techniques. Using these techniques, static visual acuity is measured, and the patient is then instructed to rotate his or her head in a sinusoidal back and forth motion in the YAW plane.

Speed or velocity of head motion is measured using the same type of motion sensor used in active head rotation testing (see Fig. 3_/4). The characters on the screen are visible only when the patient’s head is moving above a preset speed. To evaluate effectively the contribution of the VOR to dynamic visual acuity, the speed of head movement must exceed the limits of the voluntary pursuit system, typically the upper limit of which approaches 2 Hz. To provide additional information to help lateralize vestibular dysfunction, the software can be adjusted to allow the characters to be visible only when the head is moving in a single direction. Herdman et al. (1998) reports that this technique is highly sensitive and specific for differentiating normal patients from patients with vestibular dysfunction.

Figure. Dynamic visual acuity: The patient moves his head back and forth while viewing the computer screen. When the speed of head movement exceeds a predetermined level, a character appears on the screen. If the head slows down to below the predetermined speed, the character disappears

®    Eye-Movement Tests

These tests of voluntary control of eye movements provide information about the patient’s ability to perform efficient and accurate eye movements that are controlled by the cerebellum (Leigh & Zee, 1991). Although the age of the patient must be taken into consideration when assessing what is ‘‘normal,’’ gross abnormalities on eye-movement tests indicate the possibility of CNS disease and referral for neurologic evaluation.

Saccadic tracking can be assessed by having the patient quickly shift the gaze from one point to another, typically the examiner’s nose and a finger held out to the side. Accuracy, speed, and initiation time should be judged. Smooth pursuit can be tested by having the patient follow the examiner’s finger as it moves slowly through the field of vision. Age, medications, and inattention can influence smooth pursuit ability; however, asymmetric or grossly abnormal responses indicate the possibility of cerebellar dysfunction.

®    Positioning:

The Dix-Hallpike maneuver is performed to elicit nystagmus and vertigo commonly associated with BPPV. The patient is seated on an examining table and then, with the head turned 45 degrees to the side, is brought backwards rapidly into the supine position (Fig.). Most BPPV involves the posterior semicircular canal, and a positive response to this maneuver is the elicitation of vertigo and nystagmus that is rotary and beats upward and toward the undermost ear. There is usually a short latency (2 to 15 seconds) before the vertigo and nystagmus occur, and the duration of the signs is usually 15 to 45 seconds. On having the patient rise quickly to the sitting position, a milder vertigo may be appreciated with nystagmus typically opposite that noted in the supine position. Repeated maneuvers result in reduced vertigo and nystagmus response.

The examiner must be careful to note whether the nystagmus is purely vertical or persistent because these are indications of possible central nystagmus. BPPV can occur in the horizontal or anterior semicircular canals, and the duration and direction of the nystagmus will vary accordingly (Lempert & Tiel-Wick, 1996).

Figure. Dix-Hallpike maneuver: With the head turned and extended over the end of the examining table, the head should be turned both to the right and the left. (Reprinted with permission from Desmond, A. L., & Touchette, D. (1998). Balance disorders: Evaluation and treatment: a short course for primary care physicians . Chatham, IL: Micromedical Technologies.)

Other Screening Examinations

ü  Romberg Testing

The Romberg is a screening test for standing balance and is performed by having the patient stand with the feet together, arms either folded across the chest or at the sides. If the patient is able to maintain this position with minimal swaying, the patient is then asked to continue standing with eyes closed. Excessive sway with eyes closed relative to open may indicate a vestibular lesion, most often on the side to which the patient sways the most. Equal but excessive sway in the eyes open and eyes closed condition indicates possible proprioceptive weakness.

A tandem or sharpened Romberg can be performed by having the patient stand heel to toe and evaluating the postural stability with eyes open versus closed. This is simply a more difficult version of the Romberg test, and the interpretation would be similar. Patients with compensated vestibular dysfunction will often perform normally on the Romberg test, whereas patients with

proprioceptive loss will exhibit the greatest difficulty. It is imperative to provide assurance that the examiner will not let the patient fall.

ü  Dysdiadochokinesis Testing

Dysdiadochokinesis is the inability to make finely coordinated antagonistic movements. It is frequently seen in patients with cerebellar dysfunction. Testing for dysdiadochokinesis can be performed by having the patient perform rapid supination and pronation of the hands against the knees (rapid alternating hand movements). Poor performance on this test is believed to be the result of inappropriate timing of muscle activity disabling the patient from quickly stopping movement. This becomes visibly apparent when attempting to perform rapid alternating movements requiring efficient initiation and cessation ofmovement (Urbscheit & Oremland, 1995).

ü  Tandem Gait Test

Tandem gait (walking heel to toe) in a tight figure eight or circular pattern requires an intact cerebellar function. An ataxic gait has been reported as the most common symptom of cerebellar dysfunction and is felt to be a result of the patient’s inability to estimate the amount of muscle movement required to make a step (Urbscheit & Ormland, 1995). Because there are many causes other than cerebellar dysfunction for poor performance on tandem walking tasks, the specificity of this examination is understandably low.

ü  Fukuda Stepping Test

This test involves having the patient march in place, with the eyes closed, for 100 steps. According to Fukuda (1959), normal patients are able to complete the task without moving more than 1 m or rotating more than 45 degrees. Patients with vestibular dysfunction reportedly deviate from center and frequently rotate in the direction of the affected labyrinth. Fukuda recommends that a grid be drawn on the floor, but simple observation can provide information about the patient’s ability to remain oriented when visual and somatosensory feedback is diminished (Allison, 1995).

References

Ø  Allison, L. (1995). Balance disorders. In: D. Umphred (Ed.), Neurologic rehabilitation , 3rd ed. (pp. 802_/ 837). St. Louis: Mosby-Year Book.

Ø  American Academy of Neurology. American Autonomic Society, Consensus Committee. (1996). Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. Neurology, 46, 1470.

Ø  Aw, S. T., Halmagyi, G. M., Black, R. A., Curthoys, I. S., Yavor, R. A., & Todd, M. J. (1999). Head impulses reveal loss of individual semicircular canal function. J Vestib Res , 9 , 173_/180.

Ø  Baloh, R. (1998). Dizziness: Neurological emergencies. Neurol Clin North Am, 16(2), 305_/321.

Ø  Busis, S. N. (1993). Office evaluation of the dizzy patient. In: I. K. Arenberg (Ed.), Dizziness and balance disorders (pp. 159_/173). New York: Kugler Publications.

Ø  Cass, S., & Furman, J. (1993, Nov). Medications and their effects on vestibular function testing. In: ENG report (pp. 81_/84). Chicago: ICS Medical.

Ø  Cremer, P., Halmagyi, G. M., Aw, S. T., Curthoys, I. S., McGarvie, L.A., Todd, M.J., et al. (1998). Semicircular canal plane head impulses detect absent function of individual semicircular canals. Brain , 121, 699_/716.

Ø  Desmond, A. L. (2000). Vestibular rehabilitation. In: M. Valente, H. Hosford-Dunn, & R. J. Roeser (Eds.), Audiology treatment (pp. 639_/676). New York: Thieme Medical Publishers.

Ø  Desmond, A. L., & Touchette, D. (1998). Balance disorders: Evaluation and treatment: A short course for primary care physicians . Chatham, IL: Micromedical Technologies.

Ø  Drachman, D. A., & Hart, C. W. (1972). An approach to the dizzy patient. Neurology, 22, 323_/333.

Ø  Ell, J. (1992). Dizziness*/organic or functional? Aust Fam Physician , 21(10), 1431_/1436.

Ø  Faye, E. E. (1976). Clinical low vision . Boston: Little, Brown and Company.

Ø  Fukuda, T. (1959). The stepping test: Two phases of the labyrinthine reflex. Acta Otolaryngol , 50, 95.

Ø  Goebel, J., & Garcia, P. (1992). Prevalence of post-headshake nystagmus in patients with caloric deficits and vertigo. Otolaryngol Head Neck Surg, 106(2), 121_/127.

Ø  Hanashiro, P. (1990). Hyperventilation: Benign symptom or harbinger of catastrophe? Postgrad Med, 88(1), 191_/196.

Ø  Harvey, S., Wood, D., & Feroah, T. (1997). Relationship of the head impulse test and head-shake nystagmus in reference to caloric testing. Am J Otol , 18, 207_/213.

Ø  Herdman, S., Tusa, R. J., Blatt, P., Suzuki, A., Venuto, P.J., & Roberts, D. (1998). Computerized dynamic visual acuity test in the assessment of vestibular deficits. Am J Otol , 19, 790_/796.

Ø  Hornsveld, H., & Garssen, B. (1996). The low specificity of the hyperventilation provocation test. J Psychosom Res , 41(5), 435_/449.

Ø  Hornsveld, H., Garssen, B., Dop, M. F., & Van Speigel, P. (1990). Symptom reporting during voluntary

Ø  hyperventilation and mental load: Implications for diagnosing hyperventilation syndrome. J Psychosom Res , 34(6), 687_/697.

Ø  Jacob, R. G. (1988). Panic disorder and the vestibular system. Psychiatr Clin North Am, 11 (2), 361_/374.

Ø  Jacobson, G., Newman, C., & Safadi, I. (1990). Sensitivity and specificity of the head-shaking test for detecting vestibular system abnormalities. Ann Otol Rhinol Laryngol, 90, 539_/542.

Ø  Kroenke, K., Lucas, C. A., Rosenberg, M. L., Sherokman, B., Herbers, J. E., Wehrle, P. A., et al. (1992). Causes of persistent dizziness: a prospective study of 100 patients in ambulatory care. Ann Intern Med, 117 (11), 898_/905.

Ø  Leigh, R. J., & Zee, D. S. (1991). The neurology of eye movements, 2nd ed. Philadelphia: F.A. Davis.

Ø  Lempert, T., & Tiel-Wick, K. (1996). Positional maneuver for treatment of horizontal-canal benign positional vertigo. Laryngoscope , 106, 476_/478.

Ø  Linstrom, C. (1992). Office management of the dizzy patient. Otolaryngol Clin North Am, 25(4), 745_/ 780.

APPENDIX: