Evaluation of the Dizzy Patient (Sep.1996)

EVALUATION OF THE DIZZY PATIENT
SOURCE: UTMB Department of Otolaryngology Grand Rounds
DATE: September 25, 1996
RESIDENT PHYSICIAN: Jim C. Grant, M.D.
FACULTY PHYSICIAN: Jeffrey T. Vrabec, M.D.
SERIES EDITOR: Francis B. Quinn, Jr., M.D.

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"This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion."

INTRODUCTION

For the otolaryngologist, the dizzy patient often presents a diagnostic challenge. The initial clinical evaluation of the dizzy patient has ,as the basic objectives, the following:

(1) to identify as quickly as possible cases requiring emergent care;

(2) to identify the location of the lesion causing symptoms to the peripheral or vestibular systems or to systemic changes in the body as a whole;

(3) to identify the specific pathology causing the symptoms; and

(4) to control the symptoms while the evaluation is being done.1

In identifying the cause of the symptoms, the evaluation of the patient must be done meticulously with a thorough history and physical examination, augmented with laboratory, radiographic, or specialized vestibular testing as deemed necessary.

In an article by Baloh (1995), he describes several types of "dizziness", vestibular versus non-vestibular. He notes that while some patients will use key words in their history that indicate true vertigo, yet others describe "unsteadiness," "light-headedness," or "floating" which generally indicates a non-vestibular reason for their subjective sensation of dizziness.2 The types of dizziness and common causes have been divided into categories which includes

(1) vertigo (BPPV, Meniere's disease, vertebrobasilar insufficiency, etc),

(2) pre-syncopal light headedness (orthostatic hypotension, vasovagal episode, cardiac arrhythmia, hyperventilation),

(3) psychophysiological dizziness (anxiety, panic attacks, phobias),

(4) disequilibrium (peripheral neuropathy, stroke, cerebellar atrophy causing a loss of vestibulospinal, proprioceptive, or cerebellar function),

(5) ocular dizziness (impaired vision causing visual-vestibular mismatch),

(6) multisensory dizziness (diabetes mellitus / aging causing partial loss of multiple sensory systems),

(7) physiologic dizziness (motion sickness, height vertigo).3

It is the examiner's task to define which type of dizziness the patient is experiencing and translate this into a diagnosis with a treatment plan. The difficulty in this task arises from the overall complexity involved in keeping the person balanced with different stimulus constantly altering the environment.

Balance is a highly integrated network that is organized to receive stimulus which is interpreted centrally and translated to controlled movements of the ocular and spinal motor systems. Information regarding rotatory stimulation and linear acceleration are supplied by the vestibular system, proprioceptive information is supplied by sensory input from the feet, ankle, hip, and neck, and visual perception of spatial orientation is supplied by the ocular system.4 The information supplied by the systems is integrated by the central nervous system and translated to fine motor movements. The supranuclear portion of the oculomotor system coordinates vestibular, saccadic, pursuit, optokinetic, vergence, and fixation reflexive movements; whereas, the nuclear and infranuclear control the cranial nuclei II, III, IV, VI responsible for eye movements.5 The spinal motor system is essential in making limb / axial skeleton changes required for proper balance. Any disturbances within this system can make the patient feel "dizzy". For the otolaryngologist, vestibular dysfunction is of particular interest.

The clinician must keep in mind the basic clincal manifestations of vestibular dysfunction while performing the arduous tasks of history taking, physical examination, and interpreting objective test data.

HISTORY

Sudden Unilateral Vestibular Loss.

In general, this type of patient experiences intense vertigo, nausea, vomiting, and diaphoresis following the episode of damage / ablation of the vestibular end organ. Examples of this type of loss include inner ear trauma, suppurative or viral labyrinthitis, or labyrinthectomy. The symptoms become maximal within one hour and remain so for 12 - 36 hours. Over the ensuing few days, the vertigo gradual decreases but reappears on head motion. Vertigo with head motion also decreases within 2 - 4 days, but motion of the patient or perception of rapid movement in the environment may cause the symptoms to recur. Typically, the most disturbing problems are with station and gate, which may cause staggering or falling because of the decreased ability to alter the body's position. Although there is considerable patient variability especially regarding the older person, most are almost symptom free within 2 - 3 months with the residual symptoms becoming more prominent with fatigue, loss of visual orientation (i.e. dark room), or altered proprioceptive influences (i.e non-level ground).

Gradual Unilateral Vestibular Loss.

Because of the gradual loss of vestibular function, this type of patient typically does not complain of vertigo. This scenario is seen in the patient with a space occupying lesion of the vestibular nerve or internal auditory canal. There may be gait and station difficulties as with the patient months after an acute unilateral loss, but the general patient is not intensely disabled.

Gradual Symmetric Vestibular Loss.

As usually caused by vestibulotoxic medication, the gradual loss of both vestibular organs does not typically cause vertigo but causes permanent gait and station problems. Most patients are able to ambulate with a wide based gait and compensate for most situations; however, the older, less healthy patient, may require assistance devices for walking and have significant disability. Fixed objects appear to jump with any head movements (oscillopsia).

A careful and thorough history is paramount in evaluating the possible cause of the patient's symptoms. While dizziness is a relatively nonspecific symptom that may be caused by several different pathological events, true vertigo indicates a lesion within the vestibular system. Vertigo is defined as the "hallucination of movement, either of self (subjective) or the environment (objective)".6 As discussed earlier, there are certain catch phrases that the patient uses that provides valuable information to the examiner in distinguishing vestibular from nonvestibular causes of dizziness. The patient who relays a message of a spinning sensation internally and feeling as though they are leaning to one side will often have vestibular related disorder explaining their symptoms.

Once a basic description of how the patient perceives their dizziness, several areas must be addressed in detail in taking the history.

1. Duration of the Attacks.

Is it measurable in seconds, minutes, hours, days, or variable. Delineating the duration of the attacks often proves invaluable in defining the cause. For instance, BPP causes vertiginous episodes lasting seconds while in vestibular neuronitis causes vertigo to last for days.

2. Frequency of the Attacks.

3. Effect of Head Position / Movement on the Vertigo Attacks.

Typically, in the peripheral vestibular disorders head movement or position incites or augments an episode.

4. Associated Otologic Symptoms.

Is there a hearing loss, tinnitus, or aural fullness? Flucuating hearing loss / tinnitus / aural fullness is seen in idiopathic endolymphatic hydrops; whereas, these may not be present in a central cause such as vertebrobasilar insufficiency.

5. Associated Vegetative / Constitutional Symptoms.

In peripheral vestibular disorders vegetative symptoms are common (i.e. nausea and vomiting), but not so in central vestibular disorders. The patient with prior complaints of visual, sensory, or motor losses are suggestive of a central lesion like a neoplasm.

6. Concomitant Ear Disease.

Is there a history of otorrhea, prior otological surgery, or head trauma? Positive histories may indicate infection, perilymphatic fistula, labyrinthe concussion, etc. as the cause.

7. Systemic Factors.

Does the patient give a history of ototoxic medication exposure (aminoglycosides, cisplatin, diuretics, etc.)? Is there a history of systemic disease (connective tissue disorder, syphilis)? Is there a strong cardiac history?

8. Family History.

This is valuable in the familial ataxia sub-population.

9. Psychiatric History.

Does the patient suffer from anxiety, phobias, frequent panic attacks? This is valuable in the psychogenic patient.7

There are certain characteristics based on the history that allow the examiner to distinguish between vestibular versus. non-vestibular causes of dizziness. In the patient with vertigo secondary to vestibular (mainly peripheral) dysfunction, they typically have episodic attacks which may worsen with head movement or be provoked by certain head positions; have associated nausea and vomiting; and may have associated auditory symptoms.8 Continuous vertigo is not characteristic of a vestibular lesion.9 In the psychophysiologic dizzy patient, they may often have associated history of acute and chronic anxiety problems, while the cardiac patient may give a solid history of syncopal or pre-syncopal episodes. The patient with cardiac-related dizziness may also complain of palpitations. During the exam, the psychogenic patient may have difficulty providing a good description of the dizziness and may show frank affective abnormalities during the interview. For systemic causes of dizziness, it is important to ask about current medications, including street drug use. Certain drug classes cause dizziness as a side effect (i.e. neuroleptic) that may be missed if history taking is not thorough.10

For the patient whose history indicates vertigo secondary to a disturbance in the vestibular system, the task in the history taking is now directed at distinguishing a peripheral from a central lesion. Patient's with central lesions may have other neurological complaints such as visual, sensory, or motor loss that manifest. In general, the patient with central vestibular lesion typically has less severe vertigo than peripheral as well as less symptoms of nausea and vomiting. Tinnitus is more often related to a peripheral dysfunction.11

In the history, exploring the duration of the episodes is especially helpful in directing the physician to the diagnosis. This can be divided into symptoms lasting from seconds, minutes, hours, days, or variable. The patient with benign positional vertigo will complain of the severe episodes of vertigo lasting seconds, experienced with specific head positions.12 Characteristic of vertebrobasilar insufficiency and migraine attacks (with or without headache) are those episodes that occur abruptly and last in duration for minutes.13 In the patient who complains of vertiginous attacks lasting for hours, typically 2 - 3, may have Meniere's syndrome (idiopathic endolymphatic hydrops) or secondary endolymphatic hydrops (caused by otic syphilis, Cogan's disease, delayed endolymphatic hydrops, or recurrent vestibulopathy).14 The diagnosis of idiopathic endolymphatic hydrops may be further supported if there ar complaints of fluctuating hearing loss, tinnitus, and aural fullness.15 Finally, the patient who gives a history of vertigo lasting in the order of days may indicate vestibular neurolabyrinthitis, labyrinth trauma, or infarction of either the labyrinth, the brain stem, or the cerebellum. Vertigo of variable duration may indicate inner ear fistula or may also be related to inner ear trauma.

PHYSICAL EXAMINATION

Following the exhaustive history, the physical examination should cover all organ systems with an obvious focus on the ear, mastoid, and nervous system. Of note, supine, sitting, erect blood presuure is important to rule-out orthostatic hypotension, as well as pulse to examine for palpalble arrthymias. The carotid arteries should be asucultated which may explain the vertigo on vertebrobasilar insufficiency. Likewise, bruits may indicate advanced atherosclerosis and possibility of vascular injury (infarct) is the cause. Neck torsion examines for vertebral artery compression (i.e vertebral bony spur). Obviously, a careful otological exam is warranted. Similarily, the neurological exam covers mentation, sensory and motor systems. Below are special focuses that are used in the examination of the dizzy patient.

1. Tests of Balance.

The Romberg test is extremely useful in patients with an acute unilateral labyrinthine lesion, with the patient swaying toward the diseased side. This test is insensitive, however, in the patient with a chronic unilateral vestibular lesion (i.e. acoustic neuroma). 16 In the normal Romberg test, the patient stands with feet together, arms folded, and eyes closed while the observer watches for swaying or movement of the feet to attain balance. The tandem Romberg test is then attempted which will allow detection of more subtle balance deficiencies that will otherwise be missed on the standard test. The difference in this test is that the patient stands heel to toe rather than with feet together.17 Tandem gait testing is also performed. In tandem (heel to toe) gait, the visual clues obtained from keeping the eyes open allow for compensation for any chronic vestibular defects or proprioceptive deficits. In acute vestibular lesions, however, even the visual clues are not adequate for complete compensation and the patient is unable to perform the test without unsteadiness, staggering, or broad based gait.18 When the visual stimulus is removed (eyes closed), however, the patient with either acute or chronic vestibular defects will fail the test.

2. Evaluation of Basic Eye Movements.

In the vestibuo-ocular reflex, the afferent limb begins in the labyrinthe and travels through the peripheral nerve to the central nervous system where a highly integrated connection between the vestibular nuclei, oculomotor nuclei, and cerebellum exist.19 The efferent limb is the oculomotor nuclei to the ocular muscles in which eye movement is elicited. This reflex is vital in balance, as is other reflexive pathways such as the vestibulo-spinal. In addition, the eye movements themselves in response to vestibular stimulation provide important information to the examiner, especially when looking at patterns consistent with central or peripheral disease. In addition to assessment of the supranuclear oculomotor systems, the infranuclear system must also be adequately evaluated.20 There are several functional classes of eye movements which includes vestibular, optokinetic (separate system from the vestibulo-ocular system), smooth pursuit, nystagmus, saccade, and vergence. "The vestibular and optokinetic movements act to keep an image stationary on the retina during head rotation by producing compensatory slow phases in the in the orbit that are equal and opposite to head movements. Saccade, pursuit, and vergence eye movements change gaze so that the [images] brought to or kept on the fovea, where visual resolution is the highest. Saccades rapidly bring onto the fovea the image of an object directed at the peripheryan object into focus when detected in the periphery while smooth pursuit movement [while] puruit movements maintain [n already moving object on the fovea]. Vergence movements cause the eyes to move in opposite direction so that an image can be placed simultaneously on both foveas."21 Finally, the function of the physiolog nystagmus eye movement is to allow the eye to reset and redirect gaze on the object of interest when there is prolonged rotation, while the visual fixation system allows the person to focus on a stationary object without moving the eye.22 The testing battery encompassed in electronystagmography (ENG) allows a formal measurement these supranuclear eye movements (except for vergence) through the vestibulo-ocular reflex; however, these can also be assessed in a clinical based physical exam.

In assessing visual fixation, the patient is instructed to fixate on stationary targets placed directly in front, at 20 - 30 degrees right and left of central gaze, and 20 - 30 degrees above and below central gaze while the examiner looks for abnormal spontaneous nystagmus.23 In the normal patient, the eyes can remain fixated on a non-moving object indefinitely. Spontaneous nystagmus, when detected, has a fast beating phase (saccadic movement) which defines its direction followed by a slow phase. In addition, the nystagmus may be horizontal, vertical, or rotary in nature and may also change its direction (fast beating phase) when the patient changes the direction of gaze, or else it may remain fixed. By defining whether the gaze-evoked nystagmus is direction changing versus direction fixed as well as horizontal, vertical or rotary, the anatomic site of the lesion is narrowed. For instance, peripheral vestibular disorders (end organ or nerve) will usually exhibit direction-fixed horizontal nystagmus with the fast phase opposite the affected ear.24 Clinically, a patient with an acute (evaluated within days of the inciting event) right peripheral weakness will have a left beating horizontal nystagmus regardless of where the gaze is directed (right or left).25 Additionally, the velocity of the nystagmus increases with eye deviation away from the weak ear (in the same direction of the fast phase). Direction-changing horizontal nystagmus (i.e. rightward gaze producing right beating nystagmus / leftward gaze producing left beating nystagmus) indicates a central lesion, either in the brainstem or the cerebellum.26 Vertical nystagmus also indicates a central lesion with upward beating gaze nystagmus suggesting brainstem or cerebellar lesion, while downward beating gaze nystagmus indicating a lesion in the cerebellum or cervicomedullary junction (i.e. in Arnold-Chiari malformation).27 Brain stem pathology affecting the vestibular nuclei may also have spontaneous nystagmus in a rotary fashion.

It should be noted that visual fixation inhibits spontaneous nystagmus in the patient with an acute peripheral vestibular lesion; therefore, unless the patient is evaluated within days of the acute episode, nystagmus will not be present with fixation. In fact, in the course of the exam, fixation must then be removed by the use of Frenzel glasses (+30 diopter) which markedly blurs the vision thereby alowing the detection of spontaneous nystagmus. In central lesions, visual fixation does not inhibit spontaneous nystagmus.28

Saccadic eye movement can be evaluated by having the patient look back and forth between two spots separated by about 20 degrees while observing the eyes for undershooting or overshooting the target.29 Ocular dysmetria refers inaccurate saccadic eye movement; more specifically, hypometric saccade refers to consistently undershooting the target while hypermetric saccade refers to consistently overshooting the target.30 Bilateral ocular dysmetria is seen in both cerebellar or brain stem lesions, while unilateral ocular dysmetria may be seen in cerebellopontine angle lesions in the same side as the dysmetria; whereas, the patient with decrease saccadic velocity may hav extroculor muscle weakness, peripheral nerve palsy, or various progressive neurological deteriorating states.31

Testing smooth pursuit can be performed by having the patient follow pendular movements of the examiner's fingers in the center of the visual fields. With an impaired visual pursuit system, the patient is unable to smoothly track the moving object. Instead, rapid corrective eye movements replace the pursuit movements resulting in an overall "breaking up" pattern. Typically, visual pursuit abnormalities are seen in brainstem or cerebellar lesions. 32 It should be noted, however, in the patient with intense sponatneous nystagmus the smooth pursuit test may be affected.

The optokinetic system complements the vestibular system in maintaining visual fixation when the head is in motion, typically for more sustained head movements.33 For the short-lived, quick head movements, however, the vestibular system maintains visual fixation through the vestibulo-ocular reflex. Abnormalities in the optokinetic system are generally seen in lesions affecting the ocular motor pathway in the brainstem and cerebral cortex. Optokinetic eye movement testing may be grossly tested by having the patient fixate on a horizontal and vertically moving stripes as can be found on an optokinetic drum or a banded cloth. Testing the optokinetic system in actuality may be difficult as the patient's entire visual field must be filled with the drum or banded cloth; otherwise, the patient will pursue the moving stimulus in relation to fixed point at the periphery of the target which is actually a test of the smooth pursuit system.34 If performed correctly, a nystagmus is created which should appear symmetrically regarding evaluation of the right beating and left beating nystagmus (depending on the direction the drum is turning). Generally, abnormal testing indicates a cerebral lesion; however, a brain stem lesion or a unilateral peripheral vestibular lesion may produce an asymmetric nystagmus secondary to the presence of spontaneous nystagmus.35

3. Position Testing.

There are two types of position related testing--static and dynamic--that are used in the evaluation of the vertiginous patient. Static positional testing determines if a change in the head position creates nystagmus or alters an existing spontaneous nystagmus. To remove visual suppression on nystagmus, the testing occurs with eyes closed or Frenzel glasses in place. The patient is then placed in the following positions--sitting, supine-head straight, supine-head right, supine-head left, and supine-head hanging. This test is non-localizing in regards to central versus peripheral, but it does indicate organic disease. A patient may have spontaneous nystagmus only (present in sitting position only), nystagmus present only in head positions besides sitting which is referred to as positional nystagmus, or may have spontaneous and positional nystagmus which means that head positions alter the nystagmus (i.e intensifies or changes direction).36 The nystagmus may be direction changing or direction fixed in regards to alterations of head positions. The dynamic positioning test is especially useful in diagnosing paroxysmal positional vertigo.

The steps in the Dix-Hallpike test are

(1) patient is in an erect sitting position with head forward;

(2) the head is turned to the side (right or left) with the side of the suspected lesion tested first,

(3) then the patient moved to a supine position with the head below the horizontal plane of the body.37

The classical response of a positive Dix-Hallpike test for paroxysmal positional vertigo is

(1) subjective vertigo,

(2) transient nystagmus burst,

(3) a gradual lessening in the severity of the nystagmus and vertigo when the maneuver was repeated (fatigue),

(4) the response begins following a latency period of 1 to 10 seconds once the head reaches the final position.38 The nystagmus has been classically described as rotary in nature; however, Baloh, et al (1987) describes vertical components of the nystagmus on testing.39 In general, the response is elicited with the head positioned to the side of the affected ear.

4. Oculo-cephalic Response Testing.

This test is easily performed by rapidly turning the patient's head in a vertical and horizontal plane while carefully noted the eye movements. The oculo-cephalic response, a.k.a doll's eye response, has been shown to be a function of the vestibulo-ocular reflex. In an alert patient, the vestibulo-ocular reflex and visuomotor systems provide information allowing smooth compensatory eye movements when the head is turned in a horizontal or vertical plane; therefore, the eyes can remain fixed on a target.40 In a comatose patient, the visuomotor system is not intact and upon turning the head the eyes will deviate, conjugately, in the opposite direction if the brain stem is intact; while, an abnormal response occurs when the eyes do not deviate or deviate to the same side as the head turn.41 An abnormal test in the comatose patient is ominous. While this test has been used primarily in the unconscious, comatose patient to assess brain stem functioning, it has recently gained interest in the evaluation of the alert patient with a vestibular disorder. It has been noted that patients with loss of peripheral vestibular function will have ocular drift to the same side of the rapid head deviation followed by compensatory refixation saccade to reset gaze on the stationary target, where the initial ocular drift is to the weakened peripheral system.42

5. Fistula Tests.

A high index of suspicion of inner ear fistula needs to be given for the vertiginous patient who gives a past medical history of trauma to the temporal bone (blunt, penetrating, or barotrauma), otological surgery (stapedectomy), or heavy physical exertion. Hennebert's test consists of introducing positive pressure (i.e. using a pneumatic otoscope) into the ear and observing for slow conjugate contralateral deviation of the eyes followed by ipsilaterally directed nystagmus beats.43 Frenzel glasses should be placed on the patient. This test has questionable clinical applications as the this test is only positive in approximately 25% of proven fistulas.44 Another test for detecting perilymph fistulas is the turning test in which the patient walks in a straight line with eyes closed and then turns 180 degrees, either to the right or left. If a fistula is present, the patient will sway or stagger to the side of the lesion. This test has been shown to be positive in 90% of those patients with a proven fistula.45

There are several tests that are particularly helpful in evaluating the dizzy patient, including the basic audiogram test battery, the ENG, rotation related tests, posturography, and laboratory/radiographic tests.

6. Auditory Function Testing.

In addition to tuning fork testing during the basic otological physical examination, the vertiginous patient should undergo audiological testing, evaluating pure tone, speech discrimination, tympanometry, and tympanic membrane reflexes. The auditory brainstem response testing may be further indicated for those patients having speech discrimination scores that appear inconsistent with the sensorineural hearing loss (i.e. in the patient with an acoustic neuroma). The ABR in these patients will typically illustrate a prolonged I - III and I - V wave interval; whereas, in the patient with suspected multiple sclerosis, the ABR will typically show a prolongation of III - V wave intervals.46

7. Electronystagmography.

The basis of the ENG battery of testing is to monitor eye movements through electrode detection of corneoretinal potentials that are generated through stimulation of the vestibular system. During the battery of tests that construe the ENG evaluation, the central vestibular, peripheral vestibular, and ocular motor pathways are examined. The ENG test is limited to only one major vestibular tract, specifically the vestibulo-ocular reflex. It does not address the vestibulospinal tract which is important in maintaining balance and posture. Additionally, in bithermal caloric testing as well as rotary chair testing, the horizontal semicircular canal and corresponding superior branch of the vestibular nerve are directly evaluated, not the remaining semicircular canals, otolith organs, or inferior branch of the vestibular nerve.47

The usual subtests include :

(1) gaze (fixation) test,

(2) ocular pursuit test,

(3) optokinetic test,

(4) static positional test,

(5) dynamic positioning test, and

(6) bithermal caloric test.

In the caloric test, a single end-organ is stimulated by a thermal event on the horizontal canal; where cold stimulus produces a contralateral directed nystagmus and a warm stimulus produces an ipsilateral directed nystagmus.48 Directional preponderance (differences greater than 30%) and unilateral weaknesses (interear differences greater than 20%) are evaluated for the calorics; furthermore, fixation suppression is also examined with the ability to suppress caloric induced nystagmus in the peripheral vestibular dysfunctioned patient.49 The patient who fails to supress the nystagmus has a strong likelihood of a central nervous system disease, specifically in the cerebellum.

8. Rotational Tests.

By stimulation of the horizontal canal through head rotation, the rotary chair test allows for electrooculographic (EOG) recordings of the compensatory nystagmus eye movements over a range of acceleration frequencies. Unlike the nystagmus produced caloric stimulation of a unilateral horizontal semicircular canal / superior vestibular nerve, the rotary chair stimulates both canals and both superior vestibular nerves. While the advantage of bilateral stimulation of bilateral peripheral vestibular systems is that it allows the evaluation of the brainstem integration of simultaneous labyrinth response to stimuli, it also requires that caloric testing is performed to determine the relative strengths of the horizontal canals.50 The normal response as the chair is rotated is slow compensatory eye movement in the direction opposite the rotation with a fast saccade to return the eye in the forward position.51 The test has three parameters--phase (time for the slow phase eye movement in relationship to the head rotation velocity), gain (ratio of maximum eye velocity to maximum chair velocity), and symmetry (compares the slow-phase eye velocity when rotating right versus left).52

9. Posturography.

The ENG battery and rotation test evaluate vestibuloocular reflex in the vertiginous patient without addressing the effects of somatosensory (i.e. proprioceptive) and visual influences on equilibrium and patient. Essentially, the vestibulospinal tract is not evaluated. Basically, the test addresses two major areas:

(1) motor control test which examines the patient's motor system and the ability of the CANS to adapt to changing conditions, and

(2) sensory organization test which examines proprioceptive, visual, and vestibular systems working as an integrated whole.53

Clinically, the types of patient that would be candidates for posturography are:

(1) those in whom history indicates imbalance or unsteadiness rather than straightforward vertigo,

(2) children with delayed motor development,

(3) those patients in whom the impact a lesion has on the patient's balance and posture for rehabilitation planning, and

(4) in whom there is suspected organic vestibular pathology and VOR testing is non-contributory.54

10. Laboratory Tests.

Occasionally laboratory tests are valuable in diagnosing the cause of vertigo. A syphilis screening test (RPR) supports the diagnosis of otic syphilis, while an anti-nuclear antibody titer and / or sedimentation rate may help with the diagnosis of a systemic connective disease. In general, however, the history and physical examination are more valuable in diagnosing vestibular disorders.

11. Radiographic Exams.

Radiographic exams may be useful in diagnosing the vertiginous patient. Computed tomography has several clinical applications especially for evaluation of the temporal bone (i.e in trauma situation). MRI is superior for evaluation of acoustic neuromas (especially intracanilcular), for clearly defining arteries and veins (i.e. vertebral artery tortuosity), and the brain (infarcts, ischemia).55

BIBLIOGRAPHY

1. Bailey, Byron J. Head and Neck Surgery - Otolaryngology, 1993. pg 1870.

2 . Baloh, Robert W. Approach to the evaluation of the dizzy patient. Otolaryngology -Head and Neck Surgery. Vol 112 (1), pg. 3.

3 . Ibid, pg 3-4.

4 . Bailey, Byron J. Head and Neck Surgery - Otolaryngology, 1993. pg 1483.

5. Ibid, pg 1483.

6. Cummings, Charles W. Otolaryngology - Head and Neck Surgery, 1993. pg. 3184.

7. Ibid, pg 3154.

8. Baloh, Robert W. Approach to the evaluation of the dizzy patient. Otolaryngology - Head and Neck Surgery. Vol 112 (1), pg. 3.

9. Ibid, pg 3.

10. Ibid, pg 4.

11. Ibid, pg 4.

12. Cummings, Charles W. Otolaryngology - Head and Neck Surgery, 1993. pg. 3164.

13. Baloh, Robert W. Approach to the evaluation of the dizzy patient. Otolaryngology - Head and Neck Surgery. Vol 112 (1), pg. 3.

14. Cummings, Charles W. Otolaryngology - Head and Neck Surgery, 1993. pg. 3154.

15. Ibid, pg 3154 - 3160.

16. Baloh, Robert W. Approach to the evaluation of the dizzy patient. Otolaryngology - Head and Neck Surgery. Vol 112 (1), pg. 4.

17. Ibid, pg 5.

18. Bailey, Byron J. Head and Neck Surgery - Otolaryngology, 1993. pg 1873. 19. Ibid, pg 1483.

20. Ibid, pg 1484.

21. Cummings, Charles W. Otolaryngology - Head and Neck Surgery, 1993. pg. 2683.

22. Ibid.

23. Ibid, pg. 2654.

24. Ibid, pg. 2656.

25. Ibid.

26. Ibid.

27. Ibid.

28. Baloh, Robert W. Approach to the evaluation of the dizzy patient. Otolaryngology - Head and Neck Surgery. Vol 112 (1), pg. 5.

29. Cummings, Charles W. Otolaryngology - Head and Neck Surgery, 1993. pg. 2657.

30. Ibid, pg. 2655.

31. Ibid, pg. 2659.

32. Ibid, pg. 2661.

33. Bailey, Byron J. Head and Neck Surgery - Otolaryngology, 1993. pg 1487.

34. Cummings, Charles W. Otolaryngology - Head and Neck Surgery, 1993. pg. 2601 - 2602.

35. Ibid.

36. Ibid, pg. 2663 - 2664.

37. Ibid, pg 2665.

38. Ibid.

39. Baloh, RW, Honrubia V, Jacobson K. Benign postional vertigo: clinical and oculographic features in 240 cases. Neurology, 1987, pg 371.

40. Harvey, SA, Wood, DJ. The oculocephalic response in the evaluation of the dizzy patient. Laryngoscope (106), 1996. pg 6.

41. Foster CA, Foster BD, Spindler J. Functional loss of the horizontal doll's eye reflex following unilateral vestibular lesions. Laryngoscope (104), 1994, pf 473 - 474.

42. Harvey, SA, Wood, DJ. The oculocephalic response in the evaluation of the dizzy patient. Laryngoscope (106), 1996. pg 6 - 9.

43. Bailey, Byron J. Head and Neck Surgery - Otolaryngology, 1993. pg 1873.

44. Ibid.

45. Ibid.

46. Ibid, pg. 1875.

47. Cummings, Charles W. Otolaryngology - Head and Neck Surgery, 1993. pg. 2655.

48. Ibid, pg 2667.

49. Ibid, pg. 2670.

50. Bailey, Byron J. Head and Neck Surgery - Otolaryngology, 1993. pg 1485.

51. Cummings, Charles W. Otolaryngology - Head and Neck Surgery, 1993. pg. 2671.

52. Ibid, pg. 2671.

53. Bailey, Byron J. Head and Neck Surgery - Otolaryngology, 1993. pg 1485.

54. Cummings, Charles W. Otolaryngology - Head and Neck Surgery, 1993. pg. 2679.

55. Bailey, Byron J. Head and Neck Surgery - Otolaryngology, 1993. pg 82 - 90.