Menu Close

Vestibular Function test

Vestibular Function test. The central nervous system receives information’s from vestibular system, visual and proprioceptive sensory inputs. Human brain uses all of this information and regulates the equilibrium and body posture by coordinating the eyes, head, and body during movements. The equilibrium and body posture system is like a two-sided push and pull system, which is equal on both sides during neutral position. As a result, any lesion causing disturbances in these sensory inputs, is likely to cause dizziness. 

Assessment of vestibular functions can be divided into two groups:

  1. Clinical tests
  2. Laboratory tests

1. CLINICAL TESTS OF VESTIBULAR FUNCTION

A. Spontaneous Nystagmus

Nystagmus is an important tell-tale sign in the evaluation of vestibular function. Nystagmus is defined as rhythmical, involuntary, oscillatory movement of eyes without a cognitive, visual or vestibular stimulus. The direction of nystagmus may be horizontal, vertical or rotatory. Typically, nystagmus is horizontal from horizontal canal, rotatory from the superior (anterior) canal and vertical from the posterior canal.

Diagram: Types of Nystagmus

Vestibular nystagmus has a slow and a fast component. The ‘slow phase’ is due to the abnormality in the vestibular system while the ‘fast phase’ is due to the corrective central mechanism. However, while only the slow phase plays a part in image stabilization, it is the fast phase which is actually detected, and hence by convention, the direction of the nystagmus is attributed to that of its fast phase.

For example; The past-pointing and falling occur toward the slow component of nystagmus, which indicates the side of vestibular weakness. In case of right side acute vestibular failure, fast component of the nystagmus is to the left but the past-pointing and falling will be towards the right (side of the slow component). 

Diagram: Showing machanism of nystagmus

DEGREES OF NYSTAGMUS. Intensity of nystagmus is indicated by its degree.

1stdegree It is a weak nystagmus and is visible when patient looks in the direction of fast phase
2nddegree It is stronger than 1st degree, visible when patient looks straight ahead.
3rddegree It is stronger than 2nd degree, visible even when patient looks in the opposite direction of fast phase

*These degrees of nystagmus are according to Alexander’s law and may not hold true in case of nystagmus of central origin.

How to look for nystagmus.

Patient is asked to sit on the examination chair or patient may lie supine on the bed. The clinician keeps his finger about 30 cm centrally in front of the patient’s eyes. The clinician moves his finger in all four directions and ask patient to follow his finger. The finger should not move beyond 30 degrees from the initial central position as it will lead to gaze nystagmus.

If spontaneous nystagmus is present, it generally indicates towards an organic lesion which can be peripheral or central in origin.

Nystagmus of peripheral origin Nystagmus of central origin
1.Due to lesion of labyrinth or VIIIth nerve  1.Due to lesion in central neural pathways (vestibular nuclei, brainstem, cerebellum). 
2.Peripheral nystagmus is fatiguable but reproducible.   2. Peripheral nystagmus is non-fatiguable but non-reproducible.
3.Nystagmus of peripheral origin can be suppressed by optic fixation by looking at a fixed point, and enhanced in darkness or by the use of Frenzel glasses (+20 dioptre glasses) both of which abolish optic fixation. 3.Nystagmus of central origin cannot be suppressed by optic fixation.
4.Irritative lesions e.g serous labyrinthitis cause nystagmus to the side of lesion.
Paretic lesions (purulent labyrinthitis, trauma to labyrinth, section of VIIIth nerve) cause nystagmus to the healthy side.    
4. Torsional nystagmus indicates lesion of the brainstem/vestibular nuclei and is seen in syringomyelia. 
Vertical downbeat nystagmus indicates lesion at craniocervical region such as Arnold–Chiari malformation or degenerative lesion of the cerebellum.
Vertical up-beat nystagmus is seen in lesions at the junction of ponsand medulla or pons and midbrain.  
Pendular nystagmus is either congenital or acquired. The latter is seen in multiple sclerosis. Pendular nystagmus may also be disconjugate, i.e. vertical in one eye and horizontal in the other.

B. Corneal reflex (Blink reflex).

Normally there is an involuntary bilateral blinking (closure) of the eyelids elicited by touching the cornea. 

The reflex is mediated by:

  • Afferents: via the ophthalmic branch (V1) of the trigeminal nerve (CN V) sensing the stimulus on the cornea only.
  • Efferent: via the facial nerve (CN VII) initiating the motor response (efferent fiber) to oculi orbicularis
  • Center: (nucleus) is located in the pons of the brainstem.

Method: A small wisp of cotton wool is touched on the cornea on the lateral aspect without touching eyelashes and conjunctiva while the patient is asked to look forward and straight. Look for blinking and tearing in both the eyes.

Interpretations. The corneal reflex may be slowed or absent in disorders which affects the trigeminal nerve, facial nerve, or brain stem nuclei such as posterior fossa and cerebellopontine angle tumours such as acoustic neuroma.

C. Fistula test

Normally pressure changes produced in the external canal are not transmitted to the labyrinth. The basis of this test is to detect the existence of an abnormal communication between the middle and inner ear. 

Method. The test is performed by applying intermittent pressure on the tragus or by using Siegel’s speculum, in order to produce pressure changes in the ear canal. If there is existence of an abnormal communication between the middle and inner ear, the pressure changes are transmitted to the labyrinth.  Stimulation of labyrinth results in nystagmus and vertigo. The direction of nystagmus is observed. The direction of nystagmus will be to the opposite side in positive fistula test.

Interpretations.

Negative test (i.e. No fistula).

  1. Normally the pressure changes in the external auditory canal cannot be transmitted to the labyrinth
  2. When labyrinth is dead.

Positive test (i.e. fistula present connecting inner ear to middle ear) when there is 

  1. Erosion of horizontal (lateral) semi-circular canal as in cholesteatoma or a surgically created window in the (horizontal)lateral semi-circular canal (following fenestration operation).
  2. Abnormal opening in the oval window (poststapedectomy fistula) or the round window (rupture of round window membrane). 

In other way, Positive fistula also implies that the labyrinth is still functioning.

False negative fistula (i.e. negative fistula test but fistula is present) test is also seen when fistula is there but is covered by cholesteatoma or granulation tissue and does not allow pressure changes to be transmitted to the labyrinth.

False positive fistula test (i.e. positive fistula test with-out the presence of a fistula) is seen in

  1. Congenital syphilis. Annular ligament is lax and mobile causing stapes footplate is hyper-mobile.
  2. 25% cases of Meniere’s disease. It is due to the fibrous bands connecting utricular macula to the stapes footplate. 

It is called as Hennebert’s sign and is associated with both congenital syphilis and Meniere’s disease. In both these conditions, movements of stapes result in stimulation of the utricular macula (membranous labyrinth). When giddiness is produced more by loud noise rather than pressure it is known as Tullio’s phenomenon, which is seen in association with labyrinthine fistula and following fenestration surgery.

D. Romberg’s Test

Method. The patient remove his shoes and stands with feet together and arms by the side. Patient will stand quietly, first with eyes open, and subsequently with eyes closed. Examiner must stand close to the patient to prevent the person from falling over and hurting himself. With the eyes open, patient can still compensate the imbalance because of visual input but with eyes closed, visual input is lost and vestibular system is at more disadvantage. 

If patient can perform this test without sway, “Sharpened Romberg test” is performed, which is a variation of the original test. In this the patient stands with his feet in heel-to-toe position, with one foot directly in front of the other. The arms are folded across the chest with hand lies on the opposite shoulders. 

Interpretations. 

  • In peripheral vestibular lesions, the patient sways to the side of lesion. Inability to perform the sharpened Romberg test indicates vestibular impairment.
  • In central vestibular disorder, patient shows swaying or instability even with eyes open.
  • A ‘wooden soldier’ fall straight backwards is often non-organic.

E. Gait Test

Method. The patient is asked to walk along a straight line in normal speed for 5 metres to a fixed point, first with eyes open and then closed. The examiner walks alongside to prevent the person from falling over and hurting himself. 

Interpretation. In case of recent vestibular hypofunction, with eyes closed, the patient tends to deviate to the affected side. 

F. Tandem Gait Test

Method. The patient is asked to take 10 heel-to-toes steps in a straight line in normal speed with arms folded on the chest, first with eyes open and then closed. The examiner walks alongside the patient for safety reasons and looks out for deviation towards the side of the lesion.

With the eyes open this primarily tests cerebellar function as the visual components compensate for chronic vestibular and proprioceptive deficits. However, tandem walking with closed eyes is a good test of vestibular function assuming that the visual and proprioceptive functions are intact. 

Interpretation. 

Patients with peripheral vertigo may have some impaired balance but are still able to walk. But patients with central vertigo often cannot walk or even stand without falling.

G. Unterberger Stepping Test

Unterberger described the tendency of patients having vestibular imbalance to turn while walking. 

Method. The patient is asked to march on the spot 50 times with the arms extended and eyes closed. Repetition of test is essential for consistency. 

Interpretation. 

  • A positive test is indicated by rotational movement of the patient towards the side of the lesion. 
  • Patients having unilateral paralytic labyrinthitis, will rotate to the side of lesion. 
  • Patients having active irritative lesion will not be able to perform the test

H. Past-pointing test

Past pointing means the movement of a pointing finger that goes beyond the intended mark. This is called overshooting and is a manifestation of dysmetria. 

Method. The patient stands in front of the clinician. The clinician extend his arms and points both of his index fingers approximately 15cm (6 inches) apart. The patient is asked to lift the both arms over the head and then bring the arms down to touch his index fingers to the clinician’s index fingers. 

Interpretation. 

  • Normally, the test can be performed without difficulty. 
  • Patients with vestibular disease have problems to line up with the clinician’s fingers. 
  • The past-pointing, falling, slow component of nystagmus and turn in unterberger test are all in the same direction. 

I. Dix Hallpike Maneuver (Positional test)

This test should be conducted when patient complains of vertigoprovoked by head–neck movements or in certain head positions. Typical symptoms are brief intense spells of rotatory vertigo which usually precipitates during an abrupt change in head position, getting out of bed, turning over in bed, bending over, looking up or when extending or flexing the neck. 

Positional test is done to elicit vertigo and the patient should be informed and warned beforehand. Careful examination of the patient’s eyes is essential during the test.

It also helps to differentiate a peripheral from a central lesion.

Method. 

  • Patient sits on a couch. 
  • Examiner holds the patient’s head, turns it to approximately 45° horizontally to the right.
  • During complete procedure patient is required to keep his eyes open and should look at one point on the examiner’s face (i.e. the nose or bridge of the nose). 
  • Then patient quickly lies in a supine position so that his head hangs over the edge of the couch, approximately 30° below the horizontal. 
  • Keep the patient in the head-down position for a few (20-30) seconds
  • Patient’s eyes are observed for nystagmus and can use his right hand to keep eyes wide open.
  • The test is repeated from initial sitting position with head turned to left and then again in straight head-hanging position. 

Four parameters of nystagmus are observed: 

  1. Latency, 
  2. Duration, 
  3. Direction
  4. Fatiguability 
  Peripheral Central
Latency 2–20 s No latency
Duration Less than 1 min More than 1 min
Direction of nystagmus Direction fixed,  towards the under-most ear Direction changing
Fatiguability Fatiguable Non-fatiguable
Accompanying symptoms Severe vertigo None or slight
Intensity of vertigo Severe Mild
Reproduciblity Non-reproducible Reproducible
Incidence Common Rare 

Positional nystagmus in peripheral and central lesions of vestibular system. Positional nystagmus is elicited by hallpike manoeuvre.

II. LABORATORY TESTS OF VESTIBULAR FUNCTION

These tests helps to confirm the diagnosis and allows quantitative evaluation of peripheral vestibular function and the vestibular-ocular reflex. 

A. CALORIC TEST

The principal of caloric test is to induce nystagmus by making changes in temperature in the external auditory canal through thermal or cold water or air (in patients having perforation in eardrum). It is an important test where clinician can assess each ear’s vestibular function, while rotational tests assess both ear’s simultaneously. Meanwhile due to local discomfort and induced vertigo, few patients cannot tolerate the caloric test. If the induced vertigo is similar to one patient experience, it proves labyrinthine origin of vertigo.

Principle. Irrigation with water at 30 or 44°C (37 ± 7°C) with each irrigation lasting 40 seconds is the standard procedure, which causes nystagmus in the normal patients. There should be a 5 minutes gap between consecutive irrigations, allowing normalization of temperature of the temporal bone.

  • Hot water heats the endolymph in the duct, which tends to rise as its specific gravity decreases. This sets flow of endolymph towards the ampulla deflecting cupula, as if the head were rotated. A nystagmus occurs, lasting approximately 2 minutes with fast phase to the side which is irrigated.
  • Cold water or air produces opposite effects, causing fast phase to the opposite side. 

Procedures.

1. Fitzgerald–Hallpike  Test (bi-thermal  caloric test). The patient reclines on the couch at 30 degrees (so that horizontal SCC comes in vertical position). After examination of ears for wax, debris and TM, ears are alternatively irrigated for 40 seconds alternately with water at 30 °Cand at 44 °C (37 ± 7°C). Patient’s eyes are observed for nystagmus during whole procedure. The time is recorded from the start of irrigation to the end of nystagmus and charted on a calorigram.  Sometimes nystagmus is not elicited in any ear, in such cases before diagnosing dead labyrinth, the test should be repeated with 20 °C water at for 4 min. Cold irrigation induces nystagmus to opposite side and warm irrigation to the same side. A mnemonic expression that can help in remembering the direction of the nystagmus in the caloric test is COWS (“cold opposite, warm same”). Therefore, left cold and right warm irrigation induce right-beating nystagmus, and vice versa. 

Most common findings are canal paresis and directional preponderance (or combination of both). Both canal paresis and directional preponderance must be greater than 15 to 20% to be clinically significant. 

Interpretations

Canal paresis It denotes that the response (measured as duration of nystagmus) elicited from one side to cold and warm stimuli is less as compared with the opposite side. It can also be expressed as percentage of the total response from both ears. Less or no response from a particular side invariably implies depressed function of the ipsilateral labyrinth, vestibular nerve or vestibular nuclei of that side. The condition can be unilateral or bilateral.Canal Paresis is usually seen in Meniere’s disease, vestibular schwannoma, post-labyrinthectomy or vestibular nerve section.  
Directional preponderance It takes into consideration the total duration of right beating nystagmus, which is produced by cold water in left ear and warm water in right ear, is compared with the left beating nystagmus that is generated by cold water in right ear and warm water in left ear. It is seen in both central and peripheral lesions and further investigations like BERA and CT/MRI scan are required to differentiate between the two. Directional preponderance occurs towards the side of a central lesion, away from the side in a peripheral lesion; however, it can only suggest pathology and usually not able to localise the lesion in central vestibular pathways. Therefore, if the nystagmus is 25–30% or more on one side than the other, it is called directional preponderance to that side.
Ipsilateral canal paresis and contralateral directional preponderance Seen in Meniere’s disease.
Ipsilateral canal paresis and directional preponderance Seen in acoustic neuroma. 
No nystagmus with cold and warm water Seen in dead labyrinth.

2. Cold-air Caloric (Dundas grant’s) Test. Cold air is introduced in the ear by pouring ethyl chloride in Dundas grant tube, which is a coiled copper tube wrapped in cloth. This test is used when there is perforation in eardrum.

B. ELECTRONYSTAGMOGRAPHY

It detects and records of spontaneous or induced nystagmus which is not seen with the naked eye. A pair of disposable surface electrodes are placed around the orbit which records the difference in potential between the cornea and the retina (corneo-retinal potentials).It is a relatively easy, non-invasive test and allows a proper permanent documented record of nystagmus for future reference and medicolegal cases. It cannot record torsional eye movements.

C. OPTOKINETIC TEST

This test is used to diagnose a central lesion.

Principle. In response to repetitive visual pattern such as a series of moving stripes or large striped curtain in front of our eyes. The eyes follow one object with a slow-phase movement. The eyes are reset in the orbit by a fast component. This sequence of slow ipsilateral and fast contralateral eye movements forms optokinetic nystagmus.

Method. Patient is instructed to look straight ahead rather than followat a series of vertical stripes on a drum or open magazine moving slowly in both direction and the results analyzed.

Interpretation.

  • Normal nystagmus. Nystagmus with slow component in the direction of moving stripes and fast component in the opposite direction. 
  • Abnormal nystagmus. It is usually seen in brainstem and cerebral or other central disorders. 

D. ROTATIONAL TESTS

The rotational chair is used for analyzing horizontal canal vestibulo-ocular reflex (VOR).

Method. The patient is asked to sit in a motorized and computer-con- trolled chair (Barany’s revolving chair) without optical fixation. The revolving chair delivers desired velocity and rotational waveforms. Patient’s head is comfortably immobilized and kept in tilted 30° forward position. The chair is rotated in either direction and is stopped suddenly and the resulting nystagmus is carefully monitored and recorded using either ENG or VNG. Normally nystagmus lasts for 25–40 s. The test is useful as it can be performed in cases of congenital abnormalities where ear canal has failed to develop and it is not possible

Further it can be performed in two methods.

  1. Sinusoidal rotation stimulation. The chair is rotated sinusoidally over a range of frequencies, e.g. from approximately 0.05Hz to 1Hz, while the peak velocity of the stimulus is kept constant
  2. Velocity step or ‘impulsive’ rotational test. There is abrupt increase in chair velocity, say from stationary position to 60 or 90 degrees per second, measuring the per- and post- rotation responses to clockwise and anti-clockwise.This complete procedure is then repeated in the opposite direction.

These tests are generally available higher centres and provide a less provocative alternative to the caloric test. This test provides an alternative to caloric test and is tolerated well by children. However, both labyrinths are tested simultaneously and does not give information of site of lesion and is relatively expensive.

Interpretation. There are three main abnormalities seen.

Response Disorder
Bilateral reduced or No Response Seen in bilateral vestibular failure, ototoxicity, post-meningitis and idiopathic.
Asymmetric response or Directional preponderance. Seen in vestibular system disorder.
Loss of VOR suppression Seen in central disorder.

e. CUPULOMETRY

F. GALVANIC TEST

G. POSTUROGRAPHY

H. VESTIBULAR EVOKED MYOGENIC POTENTIALS (VEMP)

 

III. CEREBELLAR FUNCTION TESTS

  1. Asynergia (abnormal finger-nose test). The patient touches his tip of nose with his forefinger and then touches the clinician’s finger, held within the reach of outstretched arm of the patient. The test is repeated as fast as patient can. Position of clinician finger can be changed to make test more sensitive. Patients having cerebellar dysfunction will not be able to touch the nose on first attempt (dysmetria). Reason is intention tremors are more pronounced as the hand approaches the face.
  2. Dysmetria (inability to control range of motion). i.e. movements are incorrect in range, direction and force. The movements may overshoot their intended mark (hypermetria) or fall short of it (hypometria). 
  3. Adiadochokinesia (inability to perform rapid alternating movements). e.g. supination and pronation, of the forearm or patting the palm of one hand to the palm and back of the other hand.
  4. Rebound phenomenon (inability to control movement of extremity when opposing forceful restraint is suddenly released). When the patient attempts to do a movement against a resistance, and if the resistance is suddenly removed, the limb moves forcibly in the direction towards which the effect was made. This is called rebound phenomenon. It is due to the absence of breaking action of antagonistic muscles.

———— End of the chapter ————

Learning resources.

  • Scott-Brown, Textbook of Otorhinolaryngology Head and Neck Surgery.
  • Glasscock-Shambaugh, Textbook of  Surgery of the Ear.
  • Logan Turner, Textbook of Diseases of The Nose, Throat and Ear Head And Neck Surgery.
  • Rob and smith, Textbook of Operative surgery.
  • P L Dhingra, Textbook of Diseases of Ear, Nose and Throat.
  • Hazarika P, Textbook of Ear Nose Throat And Head Neck Surgery Clinical Practical.
  • Mohan Bansal, Textbook of Diseases of Ear, Nose and Throat Head and Neck surgery.
  • Anirban Biswas, Textbook of Clinical Audio-vestibulometry.
  • W. Arnold, U. Ganzer, Textbook of  Otorhinolaryngology, Head and Neck Surgery.
  • Salah Mansour, Textbook of Comprehensive and Clinical Anatomy of the Middle Ear.

Author:

Dr. Rahul Kumar Bagla
MS & Fellow Rhinoplasty & Facial Plastic Surgery.
Associate Professor & Head
GIMS, Greater Noida, India
msrahulbagla@gmail.com

Leave a Reply

Your email address will not be published. Required fields are marked *