Mechanism Of Balance

ByDr. Utkal Mishra

Introduction The main function of the mammalian

vestibular system is to

Provide general orientation of the body with respect to gravity

Enable balanced locomotion and body position Readjust autonomic functions after body

reorientation Ensure gaze stabilization.

Introduction

Physiology of equilibrium

Balance of body during static or dynamic positions is

maintained by 4 organs:

1. Vestibular apparatus

2. Eye

3. Posterior column of spinal cord

4. Cerebellum

Vestibular apparatus

Semicircular canals - Angular acceleration & deceleration

Utricle - Horizontal linear acceleration & deceleration

Saccule - Vertical linear acceleration & deceleration

Relevant Anatomy

Orientation of semicircular canals

RALP PlaneLARP Plane

Motion Decomposition Every motion in space can be

broken down into

3 Rotational degrees of freedom – 1. Yaw

(SCC) 2. Pitch 3. Roll

3 Translational degrees of freedom – 1. Left–Right

(U & S) 2. Up–Down

3. For–Aft

Physiology of head movement HEAD MOVEMENT SEMICIRCULAR CANAL

STIMULATED

YAW LATERAL

PITCH POSTERIOR + SUPERIOR

ROLL SUPERIOR + POSTERIOR

Cristae Location – Ampullated ends

of 3 SCC.

Elevated sensory area containing sensory hair cells

Tips of cilia are embedded in a gelatinous mass composed of polysaccharide called – CUPULA

Cupula functions as a water tight partition & displacement occurs in one direction at a time as a swing door.

Macula Located in utricle – floor

(horizontal) & saccule – posterior

wall (vertical) The hair cells are embedded in a

gelatinous layer impregnated with crystals of CaCO3 called OTOLITH MEMBRANE.

A filamentous network connects the lower surface of otolithic membrane with sensory epithelium called SUBCUPULAR MESHWORK .

A virtual curved line called STRIOLA divides utricular hair cells into medial & lateral groups & sacuular hair cells into ventral & dorsal groups with opposite orientation

Vestibular Sensory Cells Vestibular sensory epithelium consists

of 2 types of hair cells –

TYPE 1 – Flask shaped sorrounded by cup shaped thick myelinated single afferent nerve terminal

TYPE 2 – Cylindrical with multiple thin afferent nerve terminals at its base

The apex of hair cells is bathed in endolymph and is sorrounded by nonsensory supporting cells & dark cells.

Hair Cells Hair cell consists of a

hair bundle at the apical end.

Each HAIR BUNDLE consists of 1 large knobed KINOCILLIUM & 20 - 300 STEREOCILLIA

Stereocillia Have a cytoskeleton made up of

actin filament crosslinked by fibrin

Arranged in a HEXAGONAL configuration

With shortest steriocillia at one end & tallest at other end like a staircase.

The ion channel involved in mechanoelectrical transduction are located in steriocillia.

Connected to each other by fibrillary strands called TIP LINKS

The upper end of each tip link is anchored to the stereocilium at a point called INSERTIONAL PLATE or PLAQUE.

Tension in the tip link controls the opening or closing of the ion channels.

Kinocillium

It is a true cillium consisting of an axoneme (9+2).

Only function of kinocillium is - transmission of stimulus forces to stereocillia.

Displacement of stereocillia towards kinocillium causes depolarization.

Hair Cell Physiology

Mechanotransduction

Displacement of stereocillia towards kinocillium

Stretches Tip links

Influx of K+ & Ca+

Depolarization

Gating Compliance An intrinsic property of direct

mechano-electrical transduction that enhances hair cell sensitivity.

Hair bundle displacement in the positive direction opens transduction channels.

Channel opening decreases the stiffness of the hair bundle

This in turn promotes further movement in a positive direction resulting in a positive feedback mechanism

Adaptation It prevents saturation of mechano-transductor

response from large sustained stimuli > 25ms. It also allows a cell to detect small stimuli in the

presence of an enormous background input.

2 distinct models of adaptation –

Active Motor Model

Calcium Dependent Closure Model

Active Motor Model Myosin 1b

Hair bundle deflection towards kinocilium increases tension in tip links with opening of transduction channels

DEPOLARIZATION

Motor cannot resist the increased tension & slips down the stereocillium

Tip link tension reduced & channels closedHYPERPOLARIZATION

Stereocillia returns to resting stage

Calcium Dependent Closure ModelOpening of transduction

channel

Calcium enters & binds to channel protein

Closure of channel

Vestibulo-Ocular Reflex• It is a reflex eye movement due to stimulation of cristae of

SCC during head rotation

• It helps in Gaze Stabilization by producing eye movements in the directionopposite to head movement, thus preserving the image on the fovea.

• Movement of head to left left horizontal canal stimulated & right horizontal canal inhibited

• To keep eyes fixed on a stationary point, both eyes move to right side bystimulating right lateral rectus & left medial rectus muscles.

Principle Of VOR Generation (PUSH- PULL)HEAD ROTATION TO LEFT STIMULATES LEFT

HORZ. CANAL

SIGNAL GOES TO MVN

AXONS DECUSSATE TO CONTRALATERAL ABDUCENS NUCLEUS

RT. LATR. RECTUS CONTRACTION

INTERNEURONS FROM RT. ABDUCENS NUCLEUS AGAIN CROSSES TO LEFT BY MLF & PROJECTS TO LEFT

OCCULOMOTOR NUCLEUS

LEFT MEDIAL RECTUS CONTRACTION

HYPERPOLARIZATION OF RIGHT SCC

RELAXATION OF LEFT LATERAL RECTUS & RIGHT MEDIAL RECTUS

PUSH

PULL

Right

Vestibulospinal reflex Effector organs - Extensor muscles of neck, trunk,

arms and limbs.

The driving input here is mainly Gravity detected by the otolith system.

These reflexes are mediated through projections of the vestibular nuclei on to the Medial and Lateral Vestibulospinal tract.

Similar to the VOR, the same push–pull mechanisms are used for controlling the balance between extensor and flexor muscles.

Cervicoocular reflex

When the head is fixed but the body is rotated, nystagmus may be observed.

This reflex is based on the stimulation of neck receptors.

In humans, this reflex is very unreliable and unpredictable

Only in subjects with congenital peripheral vestibular loss, does this alternative strategy for gaze stabilization become helpful.

Central Projections Of Vestibular System In the brain stem there are 4 vestibular nuclei

Superior Lateral Medial Descending

From there several projections are found to Occulomotor Nuclei Lateral & Medial Vestibulospinal Tract Parapontine Reticular Formation Vestibulocerebellum- Floculus, Nodulus Nucleus Tractus Solitarius Cingulate Gyrus

VESTIBULAR FUNCTION TESTS

Dr Utkal Mishra

Vestibular Function Tests

Assessment of vestibular function can be divided into 2 groups –

1. CLINICAL TESTS 2. LABORATORY TESTS

Clinical Tests Of Vestibular Function 1. Clinical examination of eye

movements 2. Fistula Test 3. Romberg Test 4. Gait 5. Tests Of Cerebellar Dysfunction

Clinical Examination of Eye MovementsThe oculomotor examination should include: Nystagmus Convergence; Smooth pursuit; Saccades; Vestibulo-ocular reflexes; Positional manoeuvres.

Nystagmus It is defined as involuntary rhythmic

oscillatory movement of eyes. Described under headings –

1. Plane – Horizontal, Vertical, Torsional 2. Waveform – Saw tooth / Jerk – Contains a fast &

slow phase Pendular- Quasisinusoidal

No fast or slow phase 3. Direction – Indicated by direction of fast component 4. Intensity – ALEXANDERS LAW

1st degree – Nystagmus present when looks in direction of fast component.

2nd degree - Nystagmus present when looks straight ahead.

3rd degree – Nystagmus present when looks in direction of slow component.

Types of Nystagmus

DIFFERENCEPeripheral Central

Latency 2-20 s No latency

Duration < 1 min > 1 min

Direction Direction fixed Direction changing

Fatiguability Fatiguable Non fatiguable

Symptoms Severe Vertigo None

Suppressed by Visual fixation None

Enhanced by Darkness or by using Frenzel’s glasses

None

Vestibular nystagmus is of 2 types

Peripheral - Due to lesions of Labyrinth or VIIIth Nerve.

Central – Due to lesions of Vestibular Nuclei, Brain stem, Cerebellum.

Central NystagmusType of Nystagmus Cause RemarksPendular Nystagmus Multiple Sclerosis Can be disconjugate – vertical

in one eye & horizontal in other eye.

Purely Torsional Syringomyelia

Vertical Downbeat Arnold Chiari Malformation

Vertical Upbeat Pontomedullary juncn. lesions

Congenital Nystagmus Jerk Nystagmus with slow phase velocity exponentially increasing.

Seasaw Nystagmus Mid-brain lesions One eye goes up other goes down

Dissociated Nystagmus Internuclear Opthalmoplegia Only abducting eye shows nystagmus

Periodic Alternating Nystagmus

Lesions in Nodulus of Cerebellum

Changes direction every 2 minutes

Perverted Nystagmus Multiple Sclerosis Nystagmus occuring in a a plane other than that of vestibular stimulation.

Vestibulo-Occular Reflex VOR stabilizes gaze in space during head

movements By generating slow phase eye movements of an

equal velocity but in opposite direction to head movement.

Clinical Tests for VOR are –

1. Doll’s Head Manoeuvre

2. Dynamic Visual Acuity

3. Head Impulse Test

Doll’s Head Manoeuvre

Examiner oscillates the patients head from side to side at a

frequency of approx. 0.5-1Hz.

Maintain fixation(Normal

VOR)

Interrupted Eye movements with catch up saccades towards

fixation target(Abnormal VOR)

Post Meningitis / Ototoxicity

Patient sits in front of examiner & fixates a part of

examiners face(nose)

Dynamic Visual AcuityPatient reads a visual acuity

chart6/6

Standing behind the patient Examiner oscillates the

patient’s head at approx. 1Hz. While a new visual

acuity is taken

Gross reduction of VOR

Deterioration of Two lines

No change in Visual Acuity

NORMAL

Head Impulse TestPatient seats in front of

Examiner & fixate a target across the room

Head is turned briskly by 15 degree across midline

by the examiner

Fixation maintainedNORMAL

Acute Vestibular Neuronitis

Eyes moves with head & refixate with catch up

saccades.

Positional Manoeuvre (Hallpike)Patient sits on a couch & looks

straight ahead at one point on the examiner’s face

Examiner holds the patient head & turns it 450 to right

Patient placed in supine position with head hangs 300 below

horizontal

Patient eyes are observed for nystagmus for minimum 20 sec

Nystagmus appearing after a latent period of 2-20 s

Last for < 1 min & is always in one direction

On subsequent repetitions nystagmus disappears

(Fatiguable)

Nystagmus appearing immediately, changing direction

& non fatiguable

BPPV

CENTRAL LESIONS

Fistula test Intermittent pressure on tragus induces nystagmus by

pressure changes in EAC which is transmitted to labyrinth. Results - Negative Normal

Positive Erosion of Horz. SCC Fenestration Operation Post-Stapedectomy Fistula Rupture of round window

False Negative Cholesteatoma covering the fistula Dead Labyrinth

False Positive Hypermobile stapes (Congenital Syphilis) Stapes connected to Utricular macula by fibrous bands (Meniere’s disease)

Romberg’s Test

Sways to the side of lesion (Peripheral Lesion)

Shows instability(Central Lesion)

No sway or instability

Sharpened Romberg’s Test

Pt. stands with one heel in front of toes

& arms folded across the chest

Patient stands with feet together & arms

by the sidewith eyes open then

closed

Unterberger’s Test

Turns towards theHypoactive side(Peripheral Lesion)

Shows instability(Central Lesion)

Patient asked to walk on the spot with eyes

closed & keeping the arm & index fingers

pointing towards examiners index fingers

Gait

Sways to the side of lesion (Peripheral Lesion)

Shows instability(Central Lesion)

Paradoxical Improvement with fast walking

Acute Vestibular Neuronitis

Patient is asked to walk along a straight line

to a fixed point, first with eyes open then

closed

Tests of Cerebellar DysfunctionDISEASE OF SIGNSCEREBELLAR HEMISPHERE Asynergia

Dysmetria Adiadochokinesia Rebound Phenomenon

MIDLINE OF CEREBELLUM Wide base Gait Falling in any direction Inability to make sudden turns while walking Truncal ataxia

Laboratory Tests of Vestibular Function Caloric Test

Modified Kobrak Test Fitzgerald-Hallpike Test Cold Air Caloric Test

Electronystagmography Optokinetic Test Rotation Test Galvanic Test Posturography

Caloric Test Principle- Changes in temperature in Extn. Auditory canal

induces convection currents in endolymph of Lateral SCC causing vertigo & nystagmus

Advantage – Only test available to test each labyrinth separately.

Disadvantage – Anatomic abnormality of Extn. Or Middle ear interfere with results

Types – 3 types 1. Modified Kobrak Test 2. Fitzgerald-Hallpike Test 3. Cold Air Caloric Test

Modified Kobrak TestPatient is seated with head tilted 600

backwards(Horz. Canal in vertical position)

Ear irrigated with ice water for 60 sec

Start with 5ml NO RESPONSE

Nystagmus beating towards opposite ear 10 ml

NORMAL

20 ml

40 ml

DEAD LABYRINTH

Fitzgerald- Hallpike TestPatient lies supine with head tilted 300

forward(Horz. Canal in vertical position)

Procedure follows order LEFT COLD>>RIGHT COLD>>LEFTWARM>>RIGHT

WARMGap of 5 minutes

Cold water induces nystagmus to opposite side

& warm water to same side of irrigation

Time taken from the start of irrigation to end of nystagmus recorded in a chart called

CALORIGRAM

Irrigation for 4 min with water at 200C

Ear is irrigated for 40 sec alternately with water at 300C & 440 C

NO RESPONSE

NO RESPONSE

DEAD LABYRINTH

Cold Air Caloric Test

It is done when there is Tympanic membrane perforation.

Test is done with Dundas – Grant tube which is a coiled copper tube wrapped in cloth.

Air in the tube is cooled by pouring ethyl chloride & blown into ear

This is only a rough qualitative test.

Interpretations of Caloric Test There are 3 main abnormalities of caloric

response- 1. Bilateral Absence of Caloric Response 2. Unilateral Canal Paresis 3. Directional Preponderance

Bilateral Absence of Caloric Nystagmus Occurs in –

Post- Meningitis Ototoxic drugs Meniere’s Disease Head Trauma Idiopathic

Unilateral Canal Paresis

It indicates a reduced or absent response from one ear.

Causes are – Acoustic neuroma Post labyrinthectomy Vestibular nerve section

Can be expressed as percentage as

Response from Left ear = L30 + L44 × 100

L30 + L44 + R30 + R44

Directional Preponderance It indicates that the Duration of nystagmus to

one side is 25-30% more than other side irrespective of whether it is elicited from right or left labyrinth.

DP occurs towards the side of central lesion &

away from the side of peripheral lesion

Right beating nystagmus =

L30 + R44

L30 + L44 + R30 + R44

× 100

Electro/Video nystagmography It is a method of detecting &

recording of nystagmus. It depends on the presence of

corneoretinal potentials recorded by surface electrodes placed around orbit.

Advantage – 1. Detect fine nystagmus not

visible to naked eye 2. To keep a permanent

record 3. To detect nystagmus in

dark. Disadvantage –

1. Cannot record torsional eye movement

2. Other biological potentials can be picked up as artifact (EEG)

Optokinetic test

Patient is asked to follow a series of vertical stripes on a rotating drum.

Normally it produces nystagmus with slow component in the direction of moving stripes & fast component in opposite direction.

Abnormality indicates central

lesion.

Rotational Tests Patient is seated in a Barany’s

revolving chair with head tilted 300 forward rotated 10 turns in 20 s.

The chair is stopped abruptly & nystagmus is observed towards the side of rotation.

2 types of rotation- Velocity Step/ Impulsive

Rotation Sinusoidal Rotation

Normally nystagmus lasts for 25-40s.

Advantage – Test can be performed in cases of congenital abnormalities where SCC failed to develop

Disadvantage- Both the labyrinths are simutaneously stimulated.

Galvanic Test Only test which differentiates an end

organ lesion from that of vestibular nerve.

Patient stands with his feet together eyes closed & arms outstretched & then a current of 1mA is passed to one ear.

Normally patient sways towards the side of anodal current. (Intact vestibular nerve)

Posturography It is a method to evaluate vestibular

function by measuring postural stability.

2 main types Static Posturography- Fixed platform Computerized Dynamic Posturography –

Movable platform

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