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CLINICAL EXAMINATION OF VERTIGO DR.B.BHUVANESHWARI

Clinical examination of vertigo

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Page 1: Clinical examination   of vertigo

CLINICAL EXAMINATION

OF VERTIGO

DR.B.BHUVANESHWARI

Page 2: Clinical examination   of vertigo

NYSTAGMUS

IT IS INVOLUNTARY OSCILLATION OF ONE OR BOTH EYE S ABOUT ONE OR MORE

AXES.

IT IS EITHER PHYSIOLOGICAL OR PATHOLOGICAL

PHYSILOGICAL

a)congenital

b)induced(OKN)

PATHOLOGICAL

In heath,to maintain a steady gaze these mechanisms are important

,VOR and gaze holding mechanism,problem in any of these will lead to

nystagmus.

Page 3: Clinical examination   of vertigo

NYSTAGMUS

PERIPHERAL CENTRAL

TYPE COMBINED HORIZONTAL

AND TORSIONAL

PURELY VERTICAL(MOST

COMMON),HORIZONTAL

OR TORSIONAL

DIRECTION ONE DIRECTION MAY CHANGE DIRECTION

VISUAL FIXATION INHIBITS NO CHANGE

FATIGABLE YES NO

LATENCY PRESENT ABSENT

Page 4: Clinical examination   of vertigo
Page 5: Clinical examination   of vertigo

LAWS OF NYSTAGMUS

ALEXANDER’S LAW

The first element says that spontaneous nystagmus after an acute vestibular

impairment has the fast phase directed toward the healthy ear. The direction

of the nystagmus, by convention, is named for the fast phase, so the

spontaneous nystagmus is directed toward the healthy ear.

the second element says nystagmus is greatest when gaze is directed toward

the healthy ear, is attentuated at central gaze and may be absent when gaze

is directed toward the impaired ear.

The third element says that spontaneous nystagmus with central gaze is

augmented when vision is denied. This became apparent with the

implementation of electrographic testing.

Page 6: Clinical examination   of vertigo

EWALD’S LAW

Ewald's first law: "The axis of nystagmus parallels the anatomic axis of the

semicircular canal that generated it".

Ewald's second law: "Ampullopetal endolymphatic flow produces a stronger

response than ampullofugal flow in the horizontal canal".

Page 7: Clinical examination   of vertigo

EAVLUATION OF VERTIGO

EXAMINATION OF EYE MOVEMENTS

SPONTANEOUS AND GAZE EOKED NYSTAGMUS

CONVERGENCE

SMOOTH PURSUIT

SACCADE

VESTIBULO-OCCULAR REFLEXS

POSITIONAL MANOEUVRES

Page 8: Clinical examination   of vertigo

SPONTANEOUS NYSTAGMUS

CONGENITAL SQUINT

NYSTAGMUS APPEARS DURING CONVERGENCE

WHILE IN PRIMRY GAZE SPONTANEOUS LATENT NYSTAGMUS SHOULD BE ELICITED WITH COVER TEST.

THESE SUBJECTS ARE ASSYMPTOMATIC WITH LATENT NYSTAGMUS

WHILE SPONTANEOUS NYSTAGMUS IN PRIMARY GAZE IN ACUTE SYMPTOMATIC PATIENTS(WITH ACUTE VERTIGO,SEVERE UNSTEADINESS,NAUSEA) INDICATES SOME PERIPHERAL VESTIBULAR PATHOLOGY LIKE VESTIBULAR NEURITIS,MENIERES,RECENT LABYRINTHINE SURGERY,TRAUMA.

THESE PERIPHERAL NYSTAGMUS ARE PREDOMINANTLY HORIZONTAL WITH MINOR TORSIONAL COMPONENT.FAST PHASE TOWARDS CONTRALATERAL SIDE OFLESION

Page 9: Clinical examination   of vertigo

WHILE THESE KIND OF NYSTAGMUS CAN OCCUR IN CENTRAL LESIONS IN THE 8TH

NERVE ROOT ENTRY ZONE OR VESTIBULAR NUCLEI BUT THEY HAVE ASSOCIATED

BRINSTEM SYMPTOMS AND SIGNS.

THE CENTRAL NYSTAGMUS DIFFERS FROM PERIPHERAL IN THAT

WAVEFORMS(PENDULAR,QUASI-SINUSOIDAL)

CENTRAL LESIONS PREDOMINANTLY HAVE DOWNBEATING NYSTAGMUS

Page 10: Clinical examination   of vertigo

GAZE EVOKED NYSTAGMUS

IN PERIPHERAL LESIONS AFTER ACUTE PHASE NYSTAGMUS CANNOT BE ELICITED

IN PRIMARY GAZE

IN SUCH CASES NYSTAGMUS CAN BE ELICITED ONLY BY GAZE DEVIATION TO THE

OPPOSITE SIDE OF LESION i.e in the direction of fast phase

GAZE PARETIC NYSTAGMUS

This occurs in central lesion where patient unable to hold gaze in the

eccentric position of the orbit , this nystagmus is usually of larger amplitude

nystagmus usually results from ipsilateral brainstem and cerebellar lesion

Page 11: Clinical examination   of vertigo

Smooth pursuit

The slow phase eye movement on a moving target (<10-15*per second) is

smooth pursuit.

When the target moves at velocities of 40-50 degree per second or more

pursuit becomes abnormal or broken pursuit.

Abnormal pursuit indicates central vestibular disorder

EXAMINATION

examiner should hold a solid target like pen,key that is visible to the

subject

The target has to b moved slowly taking 4 to 5 seconds to travel from left

to right and vice versa

Page 12: Clinical examination   of vertigo

INTERPRETATION

WHEN THE PURSUIT IS BROKEN TO THE RIGHT,THE LESION IS LIKELY TO

BE IN THE IPSILATERAL CEREBELLUM OR PARIETAL LOBE.

IN BRAINSTEMLESIONS IPSILATERAL ABNORMAL PURSUIT NOTED.IF VESTIBULAR

NUCLEUS INVOLVES THIS CAUSES NYSTAGMUS.

LIMITATIONS

AGE

VISUAL PROBLEMS

Page 13: Clinical examination   of vertigo

Saccadic eye movement

Saccades are fast movement of eyes (200-500 degree per second) which

allows us to shift the gaze from one object to another.

Unlike smooth pursuit target need not be necessarily moving they can be

generated with commands

Properties of saccade

saccadic velocity

saccadic accuracy

saccadic conjugacy

Page 14: Clinical examination   of vertigo

Saccadic velocity

Saccadic slowing takes longer time to travel from one object to another.

Saccadic slowing is intermediate staging between normal saccade and absent

saccade (i.e gaze palsy)

Saccadic slowing indicates some neurodegenerative disorder that reduces

saccadic velocity

Page 15: Clinical examination   of vertigo

Saccadic accuracy

Saccadic hypometria

Here where the patient takes two or three corrective saccades to

fix the target.these occurs in lesions of cortex ,basal

ganglia,brainstem,cerebellum,oculomotor nucleus.

SACCADIC HYPERMETRIA

Here patients saccade too large initially and travels past the target

so patient makes corrective saccade in opposite direction.this indicates

cerebellar abnormality.

Page 16: Clinical examination   of vertigo

SACCADIC CONJJUGACY

It is the conjugate movement of eyes to fix the target

Patient should not have any 3,4,6 cranial nerve palsy to demonstrate this.

Abnormal saccadic conjugacy in horizontal plane indicates internuclear

opthalmoplegia due to lesion in medial longitudinal fasciculus.

Page 17: Clinical examination   of vertigo

OPTOKINETIC NYSTAGMUS

PROCEDURE

A ROATING STRIPED DRUM PLCED IN FRONT OF THR PATIENT THE SLOW

IPSILATERAL EYE MOVEMENT(SMOOTH PURSUIT) AND FAST CONTRALATERAL EYE

MOVEMENT (SACCADES) PRODUCES OKN.

ABNORMALITY IN OKN INDICATES CORTICAL AND SUBCORTICAL LESION.SS

Page 18: Clinical examination   of vertigo

Vestibular ocular reflex

It is reflex to maintain gaze stability during head movements, this function is

responsible for gaze stability during walking, running, while turning our head.

Clinical manoeuvers available to detect VOR

a)DOLL’S EYE MANOEUVRE

b)HEAD IMPULSE OR HEAD THRUST MANOEUVRE

Page 19: Clinical examination   of vertigo

DOLLS EYE MANOEUVRE

THIS CAN BE ASSESD BY

a) direct observation of eyes

b)measurement of visual acuity

c) opthalmoscope

Page 20: Clinical examination   of vertigo

Observation of eyes

Procedure

Patient made to sit in front of the examiner, pt asked to fixate a

feature in examiners face. the examiner then oscillates the head from side to

side at a frequency of 0.5 to 1 Hz.

In the absence of VOR pt eye movements will not be smooth and interrupted

by a catch-up saccade.

This occurs because at 0.5 -1 Hz frequency head oscillation produces peak

velocities of 94-188 degree per second this velocity is too high for the pursuit

to compensate so catch-up saccades occurs.

This test is positive in bilateral vestibular loss (gentamycin toxicity, meningitis

or idiopathic)

Page 21: Clinical examination   of vertigo

DYNAMIC VISUAL ACUITY

Patient visual acuity is noted priorly eg(6/6).patient is made to read the

visual acuity chart while examiner behind the patient oscilates the head at a

frequency of 1Hz.

Normal persons visual acuity does not changes with the test or one line

difference is fond(eg 6/9)

Patient VOR is said to b abnormal when two or three line detoriation noted.

False positive in patients with spontaneous nystagmus.

False negative if the patient themselves control the head movement

Page 22: Clinical examination   of vertigo

HEAD IMPULSE TEST

Principle of head impulse test:

It is based on the fact that excitation of canal can shoot up the

discharge rate in sensory epithelium from resting rate of 90 to sudden spike of

300.

Whereas inhibition of primary and secondary vestibular neurons cannot produce

these spikes

So when a normal scc is stimulated it can produce enough discharge to carry out

the VOR,disinhibition by the contralateral semicircular cannal for the excited

side type 1 vestibular neurons constitutes minimal for VOR.

Page 23: Clinical examination   of vertigo

procedure

Patient asked to fixate a target across the room. The head is turned in

discrete steps 10-15degree across midline , briskly, By the examiner this

produces velocity of several hundred degrees per second.

A fast right side thrust will produce one or more catch-up saccade towards

left to the target in acute unilateral vestibular loss ( vestibular neuritis,

labyrinthitis)

Page 24: Clinical examination   of vertigo

Head thrust test

Page 25: Clinical examination   of vertigo

VESTIBULO-OCCULAR REFLEX

SUPRESSION

PATIENT ASKED TO FIXATE THE FIXATE THE OBJECT AND HAS TO MOVE HIS HEAD

SIDE TO SIDE HIMSELF OR BY THE EXAMINAER ANY BREAKTHROUGH NYSTAGMUS

INDICATES CENTRAL PATHOLOGY.IT IS NORMAL IN PERIPHERAL LESION.

Page 26: Clinical examination   of vertigo

POSITIONAL MANOEUVRES

TEST FOR POSTERIOR CANNAL AND ANTERIOR CANNAL BPPV

DIX-HALPIKE MANOEUVRE

TEST FOR HORIZONTAL CANNAL BPPV

SUPINE HEAD ROLL TEST

Page 27: Clinical examination   of vertigo

DIX HALPIKE TEST

Page 28: Clinical examination   of vertigo

SUPINE ROLL TEST

Page 29: Clinical examination   of vertigo

REPOSITIONING MANOEUVERS

FOR P-BPPV

EPLEY’S MANOEUVRE

BRANDT DAROFF POSITIONAL EXERCISE

SEMONT’’S LIBERATORY MANOEVURE

FOR H-BPPV

BBQ ROLE TEST

GUFONI TEST

YAW ROTATION

FORCED PROLONGED POSITION ON HEALTHY SIDE

Page 30: Clinical examination   of vertigo

EPLEY’S MANOEUVRE

Page 31: Clinical examination   of vertigo

SEMONTS TEST

Page 32: Clinical examination   of vertigo

BBQ ROLL TEST

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GUFONI TEST

Page 34: Clinical examination   of vertigo

CALORIC TEST

PRINCIPLE: CHANGES IN THE TEMPERATURE OF EAC influences the vestibular

activity

Procedure

patients head end elevated to 30 degree to make the horizontal

semicircular cannal vertical.

Water irrigation at 30 and 44 degree celcius in the order left cold,right

cold,left warm,right warm.

Normal response: nystagmus for cold water occurs on the opposide side of

irrigation.nystagmus due to warm water occurs on the same side (COWS)

Page 35: Clinical examination   of vertigo
Page 36: Clinical examination   of vertigo

INTERPREATION

B/L absence of caloric nystagmus in case of aminoglycoside toxicity or

postmeningitis.

U/L absence in U/L vestibular schwannoma or vestibular neuritis

Directional preponderance in case of peripheral lesions for eg left vestibular

neuritis causes right directional preponderance ie right beatin nystagmus is

stronger than the left beating nystagmus.

Perverted nystagmus:this indicates nystagmus occurring in all planes instead

of normal horizontal plane this indicates central pathology

Page 37: Clinical examination   of vertigo

ROTATIONAL TESTS

VELOCITY STEP OR IMPULSIVE ROTATIONAL TEST

THE STIMULUS CONSIST OF SUDDEN INCRESSE IN CHAIR VELOCITY FROM 0 TO 60 OR 90 DEGREE.THE TIME TAKEN TO REACH THIS VELOCITY IS CALLED ACCELERATIN TIME IT IS BOUT 1 TO 2 SECONDS.TE TEST IS CARRIED OUT IN A DARK ROOM.

THIS ELICITS PER-ROTATIONAL NYSTAGMUS WHICH SLOWLY DECAYS AND EVENTUALLY STOPS.FULL CHAIR VELOCITY TO BE MAINTAINED FOR 60-90SECONDS OR UNTIL NYSTAGMUS DISAPPEARS.AT THIS POINT CHAIR IS SUDDENLY STOPPED AND SIMILAR NYSTAGMIC RESPONSE APPEARS IN OPPOSITE DIRECTION.THIS NYSTAGMUS IS TERMED S POS ROTATIONAL NYSTAGMUS.

CLOCKWISE OR RIGHTWARDS ROTATION INDUCES RIGHT BEATING NYSTAGMUSBASED ON THE PRINCIPLE THAT EYEMOVEMENT IS OPPOSITE TO HEAD ROTATION.POST ROTATIONAL NYSAGMUS OCCURS TOWARDS LEFT

Page 38: Clinical examination   of vertigo

Sinusoidal rotation test

In this test chair is sinusoidally modulated.usually,a range of frequencies from

0.005-1 Hz while peak velocity is kept constant.

The results are given as gain (ratio of slow phase eye velocity to chair

velocity) strength of vestibular response and

Phase(difference in degrees between maxima and minima pf chair and eye

velocity waveforms) measures degree of asymmetry.

Page 39: Clinical examination   of vertigo

INTERPRETATION

B/Lreduction or absence of response in case of B/L vestibular failure.

Assymetry indicates vestibular system disorder.

Loss of VOR suppression,investigated by chair-fixed target indicative of

central disease.

Page 40: Clinical examination   of vertigo

EXAMINATION OF POSTURE, BALANCE

AND GAIT

POSTURE

ABNORMAL TITLTS ROTATION-DYSTONIA,

FLEXED- PARKINSONISM

HYPEREXTENDED-PROGRESSIVE SUPRANUCLEAR PALSY

TITUBATION – CEREBELLAR DISEASE

IPSILATERAL EAR DOWN HEAD TILT,WITH SKEW EYE DEVIATION,IPSILATERAL

BODY PULSION– WALLENBERG SYNDROME (LESION OF VESTIBULAR NUCLEI)

Page 41: Clinical examination   of vertigo

ROMBERGS’S TEST

PATIENT SHOWS A TENDENCY TO FALL ON THE IPSILESIONAL SIDE ON EYE

CLOSURE.

ONLY IN ACUTE PHASE OF VESTIBULAR DISEASE THIS BECOMES POSITIVE.

POSTURAL REFLEXES ARE EXAMINED BY GENTLE PUSHING AND PULLING OF

UPPER TRUNK.

IN AKINETIC PATIENTS LIKE PARKINSONISM THIS RESPONSE IS COMPLETELY

ABSENT.

IN PERIPHERAL VESTIBULAR LESIONS THIS RESPONSE IS PESERVED.

Page 42: Clinical examination   of vertigo

WALKING

Drsal column lesion – tabeic gait

Sensory ataxia – raises the feet high from the ground and places the feet on

the ground under intense visual control.

Cerebellar lesion- drunken gait

Parkinsonian disease- gait stuck with loss of arm swing on the same side.

Utenbergs test- in unilateral pheripheral when patient is asked to walk on the

spot with eyes closed.patient turns towards the hypoactive side.

Page 43: Clinical examination   of vertigo

POSTUROGRAPHY

Computer dynamic posturography is a test for vestibule-spinal tract.it evaluates

overall balance function and the capacity of the body to maintain erect [osture

and gait.

METHODS OF POSTUROGRAPHY

a)Sensory organisation test –this tests capacity of patient to maintain equilibrium

during variety of changing sensory inputs

b)Motor co-ordination

Page 44: Clinical examination   of vertigo

SENSORY ORGANISATION TEST

Page 45: Clinical examination   of vertigo

THIS TESTS DEMONSTRATES CNS FUNCTION IN CORRECTLY PICKING THE

CONTRADICTORY INPUTS AND INDENTIFYING THE CORRECT INPUT FOR

MAINTAING EQUILIBRIUM.

IN THE ABOVE TESTABNORMALITY IN SITUATION 5,6 SUGGEST DISORDER OF

VESTIBULAR INPUT.

4,5,6 SUGGEST DISORDER OF VISUAL AND VESTIBULAR INPUTS.

Page 46: Clinical examination   of vertigo

THANK YOU