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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
THANK YOU
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