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Pro Otology
Balkan Journal of Otology & Neuro-Otology, Vol. 3, No 1:30-34 © 2003
All rights reserved. Published by Pro Otology Association

Vestibular Screening

Nuri Özgirgin

Baskent University Hospital, Ankara, Turkey

ABSTRACT

Objective: The aim of the study is to built a consecutive plan for investigating the vestibular system. It reveal the advantages and disadvantages of the existing methods.
Data sources: The study is based on the results obtained during author”s practice and through comparative examinations. The literature used is from the last thirteen years in English, Turkish languages.
Conclusions: There are enough opportuniyies for diagnosing and locating the pathologies that cause vertigo and dizziness in almost all cases. The comparatively new method – videonystagmography is able to overcome some of the diagnostic deficiencies of electronystagmography which is a traditional instrumental study with proved properties.
Key words: Nystagmus, Electronystagmography, Videonystagmography.
Pro Otology 1: 30-34, 2003

INTRODUCTION

Vestibular tests gain importance in diagnosing the peripheral and central vestibular disorders. Electronystagmography (ENG), based on recording of corneo-retinal potentials, served on screening the vestibular system for several years. Disadvantages of ENG such as recording the eye movements on electrophysiological basis, which the rotatory and some forms of positional nystagmus cannot be evaluated, motivated the lookouts for new devices. A new device was introduced in 1993 that fulfils the lacks of the system having no mechanical interference with the eye and recording the eye movements under different visual conditions. The patient’s movements are not restricted. With this instrument eye movements are recorded by using a CCD video camera mounted on light tight masks or goggles.

Videonystagmography (VNG) plays an important role in diagnosis by providing simultaneous subjective observation of eye movements as well as objective collection and analysis of the eye movement waveforms.

The system enables recording of torsional components in BPPV (Benignenal Paroxismal Positional Vertigo); it allows digital recordings of eye movements that is conveniently stored in the database that is ready to retrieve. The components of the nystagmus are more accessible with this system and even low values of SPV can be managed. Real-time observation and control of the patient’s status and eye movements are possible.

The basics of vestibular system pathologies and its evaluation by using videonystagmography will be discussed. The article presents the advantages of the method.

SHORT ANATOMY

As it is well known the peripheral vestibular system is composed of the vestibule and three semicircular canals as called as the labyrinth. Medial to the labyrinth there is internal auditory meatus that hosts the inferior and the superior vestibular nerves. The cochlear acqueduct which connects the perilymphatic space to subdural compartments is situated in halfway between the internal auditory canal and the sigmoid sinus and the vestibular aqueduct that drains the endolymph to the sac is located on the inferior side of the pyramid.

Each semicircular canal has a membranous tube having a cross sectional diameter of 0,4 mm. The plane of the LSCC (lateral semicircular canal) makes a 30-degree angle with the horizontal plane. The two other canals are in vertical positions and share a common opening on the posterior side of the utriculus. Each canal has an ampulla that covers the sensory epithelium which, is attached on the crista. The hair cells are located on the surface of the crista with their cilia and protrude into the cupula (1).

PHYSIOLOGY OF THE PERIPHERAL VESTIBULAR SYSTEM

The peripheral vestibular system, the labyrinth is sensitive to both linear and angular accelerations. The semicircular canals sense angular accelerations, The otoliths; the utricle and the saccule, sense linear acceleration. As the stereocilia bend toward the kinocilium the action potentials increase and when the hairs gets away from the kinocilium the action potentials decrease.

NYSTAGMUS

The slow phase of the nystagmus is triggered by the labyrinthine stimulus and the quick phase is initiated in the paramedian reticular formation and are organized in the brainstem (2). Components of a typical beat of nystagmus:

History

A careful history of attack of dizziness should be received. The physician has to determine the status of the patient at the onset of the first and subsequent attacks. The medicines that the patient was taking have to be reported. It is important to note, what the patients were doing at the onset of the symptoms and what they felt and how they reacted to it. The position of the body and the head and if they were stationary or at motion is important. The level of consciousness and the presence of tinnitus or pressure in the ears has to be noted. The duration of the attack is important. The type of rotation sensation (true vertigo?) has to be asked and the degree of inability has to be noted. Weakness or numbness of the arms has to be noted if present. The position of the body that cause vertigo to become worse has to be asked, the best and worse positions for producing or alleviating vertigo should be noted. The blurr of vision is important. The subsequent attacks if present has to be clarified as being same or less severe. The frequency of attacks has to be recorded (3).

Neurological examination

A detailed neurological examination including the cranial nerve functions has to be performed.

Balance function tests should include Rhomberg test, past pointing tests to screen vestibulo-spinal imbalance, ataxia examination that is specific for central nervous system (CNS) involvement. Electronystagmography (ENG) (based on recording of corneo-retinal potentials, oriented in the direction of long axis of the eye) is a must on screening the vestibular system (4).

However ENG has some disadvantages.

-It records the eye movements in pair electrodes only; so, rotatory and some forms of positional nystagmus cannot be evaluated by ENG.

- Small eye movements that can be identified under direct vision of the eyes can be masked by extraneous oscillation of the ENG line due to electric noise.

However an ideal nystagmographic system should be simple, there would be no mechanical interference with the eye. It should be able to record eye movements under different visual conditions. The patient’s movements should not be restricted. A recording instrument should be included in the system (5).

Videonystagmography (VNG) fulfils these conditions. It was first introduced in 1993. Eye movements are recorded by using a CCD video camera mounted on light tight masks or goggles. A hardware and software PC-based system analyzes the video images for the different components of eye movements (6).

Advantages of VNG are:

-The components of the nystagmus are more accessible.

-Even low values of SPV can be managed (2°/s).

-Real-time observation & control of the patient’s status and eye movements is possible.

-It is more comfortable in respect to ENG (no electrodes, no wiping).

-We gain time (the technique is easier).

-Recording of torsional components in BPPV is only possible with VNG.

-It allows digital recordings of eye movements that is conveniently stored and ready to retrieve.

-Tracings are cleaner, no interference is observed because of the electrode drift or other artifact.

-It needs no electrodes, so there is no cost.

-It is possible to see eye movements by video monitoring that cannot otherwise be observed.

-Video monitoring is easier to use, and it is more sensitive than Frenzel’s glasses.

-In most cases of vestibular dysfunction, conjugate eye movements are the norm. Disconjugate eye movements (vestibular or ocular motor disturbances) can only be detected by IR cameras.

-It allows quantitative measuring of eye movements.

-Evaluation of the eye movements is possible in darkness and records exactly special forms of the various eye movement patterns.

-It provides a permanent record that can be revised or compared later.

Safety of infrared illuminations

IR cameras are used in VNG. The power of the infrared emissions should be less than 1mW/cm2, Values above, can eventually lead to seriously damage tissues of the eyes. The possible physiological effects from the infrared rays emitted by its system concerns the cytological changes resulting from this stress that is related with the power of the illumination system.

Special Conditions

VNG cannot be used effectively in cases with a partially sighted or blind person, or someone with one eye only (artificial eye), hardly seeing or totally blind patient.

Eyes open versus eyes closed in nystagmography. There are four different fixation conditions for nystagmographic testing. Eyes open fixating is used to observe the suppressive effect of the CNS. Eyes open behind the Frenzel glasses / Eyes open in total darkness / Eyes closed (ENG only) are the conditions that remove the suppressive effects of the CNS on nystagmus.

When the eyes are closed (in ENG) the lid has a mechanical interference on eye movements (doll’s eyes phenomenon).

In this condition the nystagmic responce may be reduced.

The eyes open in total darkness or behind Frenzel’s do not vary significantly among each other. When the eyes are open in the IR/Video goggle (in total darkness) the nystagmic response becomes more evident and recorded without any loss. Thus the eyes open in total darkness (without fixation) is an important advantage of IR/Video NG system. This is created by the goggle and the illumination is maintained with invisible infrared light.

See through lenses with two miniature video cameras allows the patient to fix the eyes on the light bar. If there is spontaneous nystagmus with fixation during the first two weeks of acute symptoms, it supports peripheral vestibular lesion. Otherwise spontaneous nystagmus with fixation is in favor of central pathologies.

VNG STUDIES

Oculographic studies are performed by using the see through lenses. These are saccade, smooth pursuit, optokinetic, spontaneous and fixation (gaze) nystagmus. Positionals, Dix Halpike and Calorics are done by using goggles. These tests are classified under nystagmogarphy.

Before testing

It is advised that not take sleeping pills, tranquilizers, antihistamines, anti-dizzy medications, anti-depressants, pain medications, diuretics, sedatives, muscle relaxants, barbiturates, anti-anxiety medications for a minimum of 48 hours. Before any evaluation of occulomotor function visual acuity must be evaluated and noted. Poor eyesight can affect all of the tests for occulomotor function, especially gaze, pursuit, optokinetic and saccade.

The nystagmus is induced either by spontaneously (triggered by vestibular system pathology) or by stimulation (optically, caloric and postural changes) Vestibular nystagmus having a fixed direction (vertical, oblique, horizontal or rotational) is caused by lesions at any point between the vestibular nuclei and the thalamus. This nystagmus does not compensate but persists indefinitely if the lesion is irreversible. It always has slow and fast phases. The intensity increases if visual fixation prevented (7). The spontaneous nystagmus increases on looking in the direction of the fast component confirms Alexander’s law (8).

Primary gaze

Patient looks at the light bar in neutral gaze for 10 seconds. Examiner looks for nystagmus or abnormal saccadic intrusions, which interfere with gaze stabilization. The patient should be able to fixate the eyes when shifted 30 degrees from the mid position in four cardinal directions.

If nystagmus is seen with attempted fixation, abnormal central gaze stabilization and strong vestibular nystagmus should be probable. It should be noted that the mechanism of gaze nystagmus is quite different from that of spontaneous nystagmus and the two should not be confused.

In gaze nystagmus the eyes are held voluntarily in a position of fixation. In this condition the eyes are unable to hold the position of fixation and drift back towards the midposition and as the target is moved from the fovea, a saccade is made to bring the eyes back to the eccentric target once again. It is often seen with lesions of the CP angle. The lesion is usually on the side of the larger amplitude nystagmus.

Saccade

Saccadic eye movements are induced with a series of lights separated by known angular degrees, and moved through a series of stepwise jumps of different amplitudes. In normal conditions the eyes reach the new position rapidly, without detectable oscillation or correction.

Saccade parameters are velocity (varies linearly according to the angle of displacement of the saccade), accuracy (saccade amplitude/target displacement amplitude x 100. Mean for normal is 88%) and latency.

Saccade in normal subjects

Normal subjects consistently undershoot the target of jumps larger than 20 degrees. Overshoots of the target are rare. A characteristic delay time (latency) of approximately 200 milliseconds occurs between each target jump and induced saccade.

Abnormal saccades

Accuracy: Dysmetric saccades (Overshooting – hypermetric or Undershooting - Hypometric) show cerebellar disorders, disorders of the cortical subcortical or supranuclear centers.

Tremor: Small frequent movements with a magnitude less than one degree and frequency of 215-50 Hz appearing over the whole tracing.

Slowing: Lesions anywhere in the diffuse central pathways (pretectal and paramedian pontine gaze centers, early lesions of the medial longitudinal fasciculus (MLF), the occulomotor neurons, and the extra ocular muscles)

Dysmetric glyssadic saccades occurs in cerebellar dysfunction.

In paretic saccade the new position is reached more slowly but still similar to normal saccade and it occurs in diffuse brainstem insults (9).

Smooth pursuit

The patient is asked to follow slowly moving target that is moving smoothly on the light bar as well as possible. The tracing forms a regular sinus wave, with occasional small inconsistent rapid movements. A comparison is made between eye and target velocity. The slope of this eye / target velocity relationship represents the gain of the smooth pursuit system. The mean gain in normal subjects is 0.95.

Frequent corrective saccades to keep up the target, produce saccadic pursuit. The gain of the smooth pursuit system is markedly decreased in such patients. The trace shows a step pattern. If they are attentive or fatigued this can be observed in normal subjects. In case of the velocity exceeds the limit of their pursuit system (faster than 20-30 degrees per second) saccadic pursuits may occur. Elderly normal subjects (>70 years) may also exhibit saccadic pursuit.

Pathologic pursuits occur frequently with administration of drugs, with degenerative cerebellar disease, cerebral vascular occlusions, and cerebellopontine angle tumors. It may be transiently observed in acute lesions of the peripheric labyrinth or vestibular nerve (10).

Qualitative abnormalities

Nystagmic pursuit (saw tooth shape) occurs with congenital nystagmus.

Ataxic pursuit is sparse rapid movements. Posterior fossa tumors, degenerative diseases of the cerebellum and brainstem, cerebral vascular diseases are the causes.

Abolished tracking is defined as complete absence of tracking and occurs with brainstem infarct, tumors and viral mesencephalitis.

Optokinetic Nystagmus (OKN)

OKN is induced in response to movement of the visual surround. It is a reflex oscillation of the eyes induced by movement of large areas in the visual field. The eyes are able to follow a smoothly moving target in the visual field because of the functioning of the smooth-pursuit system (< 30 deg/sec). The eyes beat into the direction of the quick phases. Deficits in pursuit are associated with deficits in OKN.

Classification of abnormalities

Distortion of direction: Nystagmus contains oblique or rotational components. This suggests brainstem lesions

Inversion of direction: The fast phase is in the same direction as the stimulus.

Asymmetry: Shows greater amplitude frequency or fatigue on one side and seen with cerebral, cerebellar or labyrinthine pathologies.

Depression: The nystagmus is obviously depressed or absent. Manifest I brainstem lesions.

Micrography: The amplitude is small and the frequency is high and it is observed in vertebral-basillary artery insufficiency.

Headshake test for nystagmus

When the head is shaken repeatedly an increased tension occurs in the vestibular system and this tension probably persists transiently following the motion of the head is discontinued giving rise to the nystagmus. The patient’s head is rotated in 90º for 20 seconds at 2 Hz or more with eyes closed and examined for nystagmus with eyes open and head still with and without Frenzel’s glasses. Post head shaking nystagmus, is a vestibular nystagmus. It is always pathological under Frenzel’s glasses (Reflects decompensation of asymmetrical vestibular input), with fixation the nystagmus is expected to be controlled, otherwise a CNS pathology is likely to be present (11).

Head Thrust

A dynamic deficit in vestibular function? Decreased sensitivity into the vestibular nucleus.

Positional nystagmus

Positional nystagmus is evaluated by Dix-Halpike maneuver, Roll maneuvers and positional tests. The nystagmus proves its properties such as type, duration, latency, and fatigability with repeated testing.

Dix Halpike Maneuver

The patient’s head is turned 45 degrees towards one side. The examiner stands behind, pulls the patients briskly backward. The patient lies supine with the head still turned to that side and hanging over the end of the examining table. The head is hold at least 20 seconds and the eyes monitored. Then the patient is turned to the sitting position The nystagmus is pure torsional, it can be clearly observed, and recorded, with video monitoring. Differentiating canalithiasis from cupulolithiasis is also possible. While monitoring or recording eye movement, the asymptomatic side is tested first and then the symptomatic side. The torsional and vertical components occur because of the anatomy of the semicircular canals and their connections to the extraocular muscles (12).

Positional Test

Spontaneous nystagmus is a reflection of tonic left-right vestibular asymmetry. It is typically seen after a recent unilateral peripheral vestibular lesion and has fast phases away from the side of the lesion. It is performed to determine if different head positions (sitting, supine, right ear down and left ear down) induce or modify vestibular nystagmus. It generally appears in only one position and has a clearly marked latency with short duration. The nystagmus is horizontal, or horizontal rotatory, toward the lower ear. The repetition of the test produces fatigue.

Roll maneuver

The head is rotated 90 degrees to right and left in supine position. This is performed to examine the horizontal canal for canalithiasis.

It is possible to diffrentiate differentiate between semicircular canals and canalithiasis vs. cupulolithiasis. In cupulolithiasis the otoconia are stuck to the cupula and in canalithiasis the otoconia float in the canal (13).

In posterior SCC canalithiasis the nystagmus is latent, transient, upbeating torsional, fatigable on repeat testing.

In horizontal SCC Dix-Halpike test may be negative. The roll test is the optimal test for this type of BPPV. In canalithiasis the nystagmus is purely horizontal (left or right) geotropic, latent and persists for several minutes, reverses direction when the head is turned to the opposite side.

Anterior SCC canalithiasis is the least common. The nystagmus is torsional, with down beat vertical component and it is transient.

Central positional nystagmus

The nystagmus has no latency in all test positions. It has a long duration and the direction is fixed in relation to the head and it does not show fatigue. There is little or no vertigo. It occurs due to a lesion of cerebellum or cerebello-vestibular pathways. It is present in all of posterior fossa lesions but 26% of supratentorial lesions. Positional downbeat nystagmus with vertigo is due a central problem MRI scan with gadolinium shows a small mass in the cerebellar nodulus that was found to be a low-grade glioma.

Caloric tests

The caloric test is the most widely used clinical test of the vestibulo-ocular reflex. Each labyrinth is stimulated individually. The stimulus is easy to apply without requiring complex equipment.

Test methodology

In bithermal caloric test (Fitzgerald and Halpike) the irrigation is applied with a constant flow rate of water at 30 and 44º degrees for 30-40 seconds. At least 5 minutes intervals are applied between the stimulations. The LSSC is the mostly affected structure (14).

The results are interpreted according to the Jongkees formula. If spontaneous nystagmus is present its SPV is added to that of the caloric induced nystagmus in the same direction or it is subtracted from that of the caloric induced nystagmus in the opposite direction. In bilateral peripheral vestibular lesions, there is no use of calculations.

The test is resumed as vestibular paresis if there is more than 20 % asymmetry between left and right-sided responses and as directional preponderance in case of having more than 25 % asymmetry between left and right beating nystagmus. Fixation suppression index is 50 %.

CLASSIFICATION OF ABNORMALITIES

Vestibular paresis reflects the diminished response in one ear. It is due to a lesion of the labyrinth or the nerve. CNS lesions may exhibit CP if the lesion involves the root entry one of the vestibular nerve. Acoustic tumors produce CP by direct lesion of the nerve.

Directional preponderance occurs when the nystagmus towards one side is more intense. It shows an asymmetry in the vestibular tonus by lesion of the facilitating elements on one side or of the inhibiting nervous elements on the other side. Peripheral endorgan and eighth nerve lesions as well as CNS lesions (from brainstem to cortex) may induce DP. If present without spontaneous nystagmus a central lesion is more likely.

The posterior semicircular canal can be tested by Kobrak stimulation. In this case the nystagmus is rotatory and cannot be recorded with ENG. Frenzel lenses do not allow documentation so VNG is necessary.

Qualitative findings

Dysrhythmia is the variation of amplitude and frequency of the elements of the nystagmus over short periods. This can be present in posterior fossa midline tumors.

In micrography the SPV is normal, but the individual movements are in small amplitude and the frequency is increased. This can be observed with the aging process.

If the visual fixation is less than <50%, central pathology should be suspected. The eyes are fixed by opening the front panel of the goggle or turning on, an embedded light in the goggle (during 90-110 seconds of stimulation). The SPV should be suppressed more than 50%. It is calculated with the formula: MSCV with fixation / MSCV without fixation x 100. Caloric testing with fixation Pathologic data The suppression fixation index > 50%. With this approach two separate systems, vestibulo-ocular reflex and the smooth pursuit system are being evaluated. The procedure should be performed during the maximum response of SPV. This test may reflect the lesions of the midline cerebellum.

Perverted nystagmus

Caloric stimulation of the LSSC also exhibits oblique or vertical nystagmus. This can be found in normal subjects in smaller magnitudes. If the amplitude of vertical nystagmus is higher than the horizontal nystagmus, it is called as perverted nystagmus and suggests both peripheral and central lesions especially on the floor of the fourth ventricle.

CONCLUSION

The vestibular work up is capable of diagnosing and locating the pathologies that cause vertigo and dizziness in almost all cases. Until now electronystagmography has been the gold standard in evaluation of vestibular disorders. However it still has some diagnostic deficiencies that can be fulfilled by videonystagmography.

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