VERTIGO AND ITS MANAGEMENT

CONETENTS

Introduction

Epidemiology

Definition

History

Vestibular System

Causes of vertigo

Bedside evaluation of Vestibular System

1. History
2. Examination
3. Management

References

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Introduction

Vertigo is not a separate disease process, but a multisensory and sensorimotor syndrome with
various etiologies and pathogeneses. It is among the commonest symptoms presented to doctors,
with a lifetime prevalence of around 20% to 30%.

It is one of the types of dizziness with dysequilibrium, presyncope and lightheadedness.

Dizziness is one of the most common complaints among patients presenting to primary
healthcare physicians, neurologists, cardiologists and otolaryngologists. ‘Dizziness’ and
‘Giddiness’ are common terms used by the patients to describe their condition when they feel
unsteady, off balance, rocking, swimming, walking on cotton wool, clumsy on their feet or dizzy
in their head. These symptoms are nonspecific and cover broad differential diagnosis which
includes disorders like light headedness, disequilibrium, ataxia, syncope and the true vertigo.

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Vertigo’ has been derived from Latin words ‘Vertere’ meaning ‘to turn’ and ‘igo’ meaning
‘condition of turning about’.

Epidemiology
Approximately 30% people - experience moderate to severe dizziness at some point in their life
(Neuhauser et al. 2005).

Dizziness - Females > Males and older people

Though most people report nonspecific forms of dizziness, nearly 25% of these people report
true vertigo

The incidence of vertigo in general population is about 20 to 30 % (Sonawale S et al. 2018).

Definition
A sensation of rotation or imbalance of one’s self or of one’s surrounding in any plane.

History
Prosper Meniere (1861) - first to recognize the association of vertigo with hearing loss and to
localize the symptom to the inner ear.

Robert Barany (1906) - First clinical description of BPPV (Benign paroxysmal positional
Vertigo) in 1921. Introduced Caloric testing - most widely used test of the Vestibulo-ocular
reflex (VOR). Nobel Prize for mechanism of caloric stimulation.

Neuroimaging in 1970s greatly expanded understanding of causes of dizziness/vertigo - prior to

which, stroke was considered an exceedingly rare cause of vertigo (Fisher 1967).

In a classic paper, Drachman and Hart (1972) described four subtypes of dizziness: Vertigo,
Presyncopal lightheadedness, Disequilibrium and other dizziness.

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Over the past 25 years - understanding of the mechanisms for the common neuro-otological
disorders has increased.

BPPV – now readily identified and cured bedside.

The Head-Thrust test – bedside test to identify a vestibular nerve lesion, and has particular
utility in helping distinguish vestibular neuritis from a posterior circulation stroke (Halmagyi
and Curthoys 1988; Kattah et al. 2009; Newman- Toker et al. 2008; Nuti et al. 2005)

The Vestibular System

Vestibular system

Peripheral Central

Peripheral system is bilaterally composed of three semicircular canals (posterior, superior,

lateral) and the otolithic organs (saccule and utricle). The semicircular canals detect rotational
head movement while the utricle and saccule respond to linear acceleration and gravity,
respectively. These vestibular organs are in a state of symmetrically tonic activity, that when
excited stimulate the central vestibular system. This information, along with proprioceptive and
ocular input, is processed by the central vestibular pathways (e.g. vestibular nuclei) and
maintains our sense of balance and position

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The plane in which the eyes deviate as a result of vestibular stimulation depends on the
combination of canals that are stimulated.
Once vestibular signals leave the vestibular nuclei - divide into vertical, horizontal, and torsional
components.
So a lesion of central vestibular pathways can cause a pure vertical, pure torsional or pure
horizontal nystagmus.

Causes of Vertigo

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Peripheral – A disordered generation of the nerve impulses by vestibule.

Intermediate – Faulty transmission of impulses along the 8th cranial nerve (vestibulo cochlear
nerve)
Central – Misinterpretation of impulses by vestibular nuclei in brain

Peripheral Intermediate Central

Meniere’s disease Vestibular neuronitis Vertebrobasilar insufficiency
Benign paroxysmal positional Acoustic neuroma Posterior inferior cerebellar
vertigo Drugs called ototoxic artery syndrome.
Labyrinthitis drugs eg : antibiotics such Basilar migraine
Vestibulotoxic drugs as streptomycin, Cerebellar disease
Head trauma kanamycin, neomycin Multiple sclerosis
Perilymph fistula Tumours of brainstem and 4th
Syphilis ventricle
Epilepsy
Cervical vertigo

Zatonoski T (2014)

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Red flags” suggestive of a Central vestibular lesion :-

• Other central signs or symptoms
• Direction-changing nystagmus
• Vertical nystagmus
• A negative head-thrust test
• A skew deviation or
• Substantial stroke risk factors (Kattah et al. 2009)

Drugs that induce vertigo

Recurrent positional Vertigo

• Positional vertigo - symptom being triggered, not simply worsened, by certain positional
changes.
• Most likely BPPV - but this is not the only possibility.
• Strong suspicion of BPPV when the positional vertigo is brief (<1 minute), has typical triggers,
and is unaccompanied by other neurological symptoms.
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• A burst of vertical torsional nystagmus - specific for BPPV of the posterior canal (Aw et al.
2005).
Central positional nystagmus - disorders affecting the posterior fossa, including tumors,
cerebellar degeneration, Chiari malformation, or MS.
• Nystagmus typically downbeating and persistent, though a pure torsional nystagmus may occur
as well.

Bedside Evaluation for Vestibular System

History

1. Nature of sensation.
2. Timing of initial spell.
3. Duration and frequency of symptoms:
Short term spells: BPPV, Perilymph fistula, LSSC fistula.
Medium length spells: Meniere’s disease, hypoglycemia, arrythmias.
Longer spells: Vestibular migraine

4. Precipitating factors:
• Rolling over bed/Tilting backwards: BPPV
• Sound or pressure stimuli: Superior canal dehiscence syndrome.
• Exposure to light or sound/certain food: Vestibular migraine.

5. Associated symptoms:
• Aural fullness and tinnitus: Meniere’s Disease.
• Headache or visual symptoms: Vestibular migraine.
• Other cranial nerve involvement: CP angle tumour.
• Ataxia: Cerebellar Dysfunction.
• Sweating, dyspnoea, palpitations: Panic attacks.
• Otosclerosis : Hearing loss.

6. Medical condition: CVA, Head Trauma

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7. Drug history
8. 8. Family history : Osteosclerosis/Meniere’s disease /Migraine

Examination
Complete head and neck examination
Otoscopy & audiology
Cranial nerve assessment
Visual acuity
Vestibular function test.
Cerebellar function test.

Vestibular Function Test

• Examination of eye movements
• Examination of postural balance
• Otolith function test

Examination of eye movement

Clinical test Laboratory test

NYSTAGMUS OCULOGRAPHY
• Spontaneous nystagmus • Electro-nystagmography
• Gaze evoked nystagmus • Video-Oculography
• Pursuit Movements
• Saccadic Movements
DOLL’S EYE MANOEUVRE CALORIC TEST

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• Modified Kobrak Test

• Fitzgerald Hallpike Test
(Bithermal Caloric Test)
FISTULA TEST ROTATIONAL TEST
HEAD THRUST TEST
POSITIONAL MANOEUVRE
• Dix Hallpike

Examination of Postural balance

Clinical test Laboratory test
EXAMINATION OF GAIT, POSTUROGRAPHY
POSTURE AND BALANCE
ROMBERG TEST

UNTERBERGER’S STEPPING
TEST
WOFEC TEST

Otolith Testing

• Linear acceleration test

• Subjective visual vertical
• Click – evoked vestibular myogenic potential

Nystagmus
• To-and-fro beating of the eyes with slow and fast component.
• Caused by disorder in the physiology of vestibulo-ocular reflex.
• VOR is a three-neuron arc; vestibular afferent neuron, interneuron, oculomotor neuron.
• Fastest reflex in the body, latency 7ms, <5% error rate.

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• Alexander’s law.
• Ewald’s law.

EWALD’S LAW
• E.J. Richard Ewald(1892), German physiologist.
• Experiments on SCC of pigeons.
• 1ST LAW: The axis of nystagmus parallels the anatomic axis of semi-circular canal that
generated it.
• 2ND LAW: Ampullopetal endolymphatic flow produces a stronger response than
ampullofugal flow, in the horizontal canal

ALEXANDER’S LAW:
• Gustav Alexander (1912), Austrian otolaryngologist.
• FIRST LAW: After an acute vestibular impairment, spontaneous nystagmus has the first
phase directed towards healthy ear.
• SECOND LAW: Nystagmus is maximum when gaze is directed towards healthy ear,
attenuated at central gaze and may be absent at gaze towards impaired ear.
• THIRD LAW: Spontaneous nystagmus with central gaze is augmented, when vision is
denied

Spontaneous nystagmus
Nystagmus in the primary, straight ahead position of the eyes.
Usually seen during acute vertigo attack.
Waveform, direction of beat, site of lesion.
Severity of nystagmus
-1st degree: weak nystagmus, present only when patient look in direction of fast component.
- 2nd degree: moderate nystagmus, present when pt. looks straight ahead.
- 3rd degree: strong nystagmus, present when pt. looks in direction of slow component.

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Gaze evoked nystagmus

Patient is asked to look 30 degree from the primary position, in any direction.

Smooth pursuit movements

-Tracking movement of the eye, when the target moves slowly (<10-15 deg/sec).
-Velocity limited.
-Normal pursuit rules out central vestibular disorder.

Saccadic eye movements

-Fast movements of eyes (200-500 deg/sec) which allows to shift gaze from one object of
interest to another.

DOLL’S EYE TEST

Patient in sitting position
↓
Asked to fixate on nose of examiner
↓
Examiner oscillates patient’s head from side to side (0.5-1Hz).
↓
1) Absence of VOR - Eye movement will not be smooth and interrupted by catchup saccades
towards fixation target.
2) Decrease in dynamic visual activity.
3) On opthalmoscopy, small amplitude nystagmus can be seen

FISTULA TEST

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• Stimulus – intermittent pressure on tragus or with use of Siegle’s speculum.

• Response :
Normal- No vertigo and nystagmus.
Positive- vertigo and nystagmus.
Mechanism – in presence of fistula or vestibulofibrous bands, applied pressure causes deviation
of cupula. Positive in HSC fistula, Meniere’s disease etc

HEAD THRUST TEST

To make VOR deficit more apparent.
Sudden discrete brisk and unpredicatable head turn (10- 15deg)
↓
Catchup Saccades seen
Useful for identifying acute U/L peripheral vestibular deficits

POSITIONAL MANOEUVRE
Dix-Hall pike manoeuvre:
Used for identification of posterior canal BPPV
Features of Nystagmus:
1.Latency of 2-10sec
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2. Increase in amplitude in 10s and decline in 30s.

3. Fatigability present.
4. Direction of Nystagmus-Vertical torsional nystagmus.
HC Variant of BPPV- Exclusively horizontal, lasts longer.
AC Variant of BPPV- Rare, vertical torsional nystagmus.

LABORATORY TESTS OF EYE MOVEMENTS

ELECTRONYSTAGMOGRAPHY
PRINCIPLE:
• Retina is negatively charged as compared to cornea, creating an electric field k/a corneoretinal
potential

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• Movement of eye → Movement of electric field → Change in electric potential detected by

surface electrodes

Indications
• Assessment of eye movements in dark (avoid visual suppression).
• Nystagmus waveform (to d/b congenital and acquired).
• Quantification to monitor progression and recovery from vestibular disorders.

OTHER TECHNIQUES
• Video nystagmography
-Small video camera mount on goggles used.
-2D Systems record horizontal and vertical nystagmus.
-3D Records torsional nystagmus.
• Infrared oculography.
• Scleral search coil technique

CALORIC TEST
Principle: Changes in temperature in external auditory canal influence the activity of vestibular
labyrinth.
Position of Patient: Supine with head raised 30 degree above horizontal-which places HSC in
vertical position.
Mechanism: Thermal changes induce convection currents in horizontal canal when placed
vertically and thus, cupular deflections and change the discharge rate of vestibular nerves.
• Caloric test are highly sensitive for unilateral lesion because each ear is stimulated separately.
• Nystagmus produced by this is analyzed and assess the activity of vestibular system
• 3 types:
1. Modified Kobrak test

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2. Bithermal caloric test

3. Cold air caloric test

Bithermal caloric test

Fitzgerald – Hallpike test.
• Pt. lies supine with head tilted 30 degree forward so that HSCC is vertical.
• Ear is irrigated for 40 sec, with water at 30 degree and 44 degree and nystagmus are noted till
its end point.
• If no nystagmus appeared from any ear, test is repeated with water at 20 degree water for 4
minute before labeling the labyrinth dead.

Modified kobrak test

• Pt. seated with head tilted 60 degree backwards to place H S C C in vertical position.
• Ear irrigated by ice cool water for 60 sec with 5/ 10/20/40 ml.
• Response seen with 5ml of water towards opposite ear - Normal
• Response seen with 5 to 40 ml water – Hypoactive labyrinth.
• No response seen with 40 ml – Dead labyrinth.

Cold air caloric test

• Test done in perforated TM because irrigation is contraindicated.
• Done with DUNDAS GRANT TUBE, coiled copper tube wrapped in cloth, air is cooled by
mixing with ethyl chloride and then blown to ear.
• “Varioair” is used these days which has precise control over amount and temperature of air.

Rotational tests
Head rotation is natural stimulus for VOR
Position: Seated in rotational chair with head tilted forward, in a dark room with head
immobilised to decrease proprioceptive impulses

EXAMINATION OF POSTURAL BALANCE

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Unterberger’s stepping test:

• Visual and proprioceptive inputs are cut off
• Pt deviate/rotate to side of weaker hypoactive vestibule.
• Parameters evaluated in test:
1. Displacement
2. Angular deviation
3. Angular rotation
4. Breadth of lateral sway
Romberg test:
Pt. blind folded and stands erect with feet close together for 1 minute.
Max. breadth of sway is 10 cm .
>10cm - abnormal - indicates a central lesion.

.
Posturography
• Quantitative measurements of processes that maintain upright stance under static and
dynamic conditions.
• The most commonly used posturography paradigm is sensory organization test.
• Equilibrium score measures patient’s sway when standing upright in 6 conditions

Result:

• Eyes closed, stable surface (2): Loss of proprioceptive functions.

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• Eyes open, sway referenced surface (4): Loss of visual contribution to balance.
• Eyes closed, sway referenced surface (5): Loss of Vestibular function

EVALUATION OF OTOLITH FUNCTION

Vestibular Evoked Myogenic Potential Responses

Short latency responses measured from tonically contracting SCM that relax in response to I/L
presentation of loud click.
VEMP responses probably originate in saccule.
Each ear can be tested separately.
Aapplications of this test are still developing, main diagnostic value in SSC dehiscence
syndrome.

MANAGEMENT
Pharmacological treatment.
Vestibular rehabilitation.
Surgical treatment.
Adjunctive treatment.

Pharmacological treatment
Suppress symptoms during acute vestibular attack i.e vestibular sedatives.
Specific treatment of condition that causes vestibular symptoms i.e. Meniere, migraine.
General medical t/t of other coexisting or underlying condition.
Experimental drugs- accelerate compensation

VESTIBULAR SEDATIVES
ANTI-CHOLINERGICS
Targets efferent feedback from brainstem to vestibular labyrinth and muscarinic receptor
antagonist, increases motion tolerance.
Hyoscine: most effective drug for t/t of motion sickness.
Scopolamine.

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S/E: Dry mouth, dilated pupils, sedation.

ANTI-HISTAMINICS
Competitive antagonists at H1 receptors, increases firing of MVN through H2 receptors.
PHENOTHIAZINES: Promethazine.
PIPERAZINES: Cyclizine, dimenhydrinate.

DOPAMINE ANTAGONISTS
D2 receptor antagonist, acts through its anti-emetic action.
Prochlorperazine( STEMETIL)
S/E: Sedation, extrapyramidal side effects.

CALCIUM CHANNEL BLOCKERS

Mechanism of action- unclear
Inhibits influx of Ca2+ intracellularly
Flunarizine, nimodipine.

VESTIBULAR REHABILITATION
Based on the concept of capacity of vestibular system for adaptation, habituation and
plasticity for recalibration of vestibular reflexes by substitution of sensory input, motor
responses and strategies, in order to achieve symptomatic recovery following a vestibular
lesion.
Includes:
• Repositioning exercises.
• Adaptation exercises.
• Habituation exercises.
• General exercises to increase muscle force, balance and gait.

GENERAL PRINCIPLES OF VRT

• Decrease centrally sedating or vestibular suppressant drugs

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• Exercise must provoke vertigo

• Initiate as early as possible
• Exercise should simulate real life situations
• Maintenance exercises to recurrence of symptoms

KEY COMPONENTS OF VRT

• Explain the rationale behind the exercises and patient motivation.
• Choice of exercise.
• Graded approach, to facilitate learning.
• Diligence and perservance.

PHYSICAL EXERCISE REGIMENS

Targets adaptation, sensory substitution, habituation and balance retraining.
Includes:
• Systematic preset exercise programmes.
• Cawthorne-Cooksey exercises.
• Vestibular habituation exercises: Norre’s approach.
• Customized exercise programmes.
• University of Michigan’s approach.
• The John Hopkins/University of Miami programme

REFERENCES
• Writer, HS & Arora, RD. (2012). Vestibular Rehabilitation: An Overview.
Otorhinolaryngology Clinics - An International Journal. 4. 54-69. 10.5005/jp-journals-
10003-1088.
• Thompson, Timothy & Amedee, Ronald. (2009). Vertigo: A Review of Common
Peripheral and Central Vestibular Disorders. The Ochsner journal. 9. 20-6
• Strupp, Michael & Brandt, Thomas. (2008). Diagnosis and Treatment of Vertigo and
Dizziness. Deutsches Ärzteblatt international. 105. 173-80. 10.3238/arztebl.2008.0173.

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• Kameshwaran, Mohan & Sarda, Kushal. (2017). Therapeutic interventions in vertigo

management. International Journal of Otorhinolaryngology and Head and Neck Surgery.
3. 777. 10.18203/issn.2454-5929.ijohns20174311.
• Collie, M.H. (2013). Vertigo diagnosis and management. Clin Rev. 23. 46-53.

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