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PHYSIOLOGY

of
Equilibrium
Dr Herman Mulijadi MS.SpKP

Lesson Objecitves

1. Explain the component of organs and system that participate


in the maintenance of body balance
2. Explain the component of vestibular system
3. Draw the receptors in each component of the vestibular
system and explain how they work
4. Differentiate the angular and linear acceleration
5. Explain the component of the vestibular system that sensitive
to angular and linear acceleration
6. Explain the mechanism of sea sickness
7. Explain some experiment to test body balance
8. Define nystagmus and explain its mechanism

Balance:

It is :
the ability to maintain equilibrium
Or
the ability to maintain your center of
mass/gravity over your base of support in
any given sensory environment .

03/03/15

Balance
Balance is very complex involving multiple systems that
interact flawlessly and automatically to coordinate input
from our environment and the central nervous system
to produce a motor output and keep you upright/vertical.
Postural control is related to balance in the dynamic mode.

Balance is a highly integrated network


the position of the
head relative to the
environment & orients
the head to maintain
posture

orientation of
the head in
space and on
accelaration

EMOTION,PERSONALITY,
BEHAVIOUR,ANXIETAS,

LIMBIC SYSTEM
(HIPOCAMPUS-MEMORY)

the perception of
the static position
& the position
during
movements.

central nervous
system - integrated
these information
and translated to
fine motor
movements

PARIETAL ASSOCIATON
CORTEX
( POSTERIOR PARIETAL )

PARIETAL LOBE OF
CEREBELLAR CORTEX
( CEREBELLUM )

VISUAL CORTEX
CHIASMA
OPTICUM

N OPTICUS

INFORMASI

THALAMO
MOTOR
CORTICO
CENTER MID
PROJECTION
BRAIN
MEDIAL
LEMNISCI
SUPERIOR, MEDIAL,
LATERAL, INFERIOR
GANGLION VESTIBULAR

OF EYES

OF INNER
EAR

CORTICO
ASSOCIATIO
N AREAS
BASAL
GANGLIA

DORSAL
CEREBELLAR
TRACT

SPINAL
CORD

MOTOR
CORTEX

CEREBELLUM

BRAIN STEM

SPINAL MOTOR
NEURON

OF SKIN,JOINTS,
SUPPORTING
TISSUE

From
environment

ocular system - visual


perception of spatial
orientation is supplied
by the eyes

SENSORY RECEPTOR

vestibular system
-rotatory stimulation and
linear acceleration
Information

proprioceptive
system information input
from the feet, ankle,
hip, and neck

Response Action

Balance System Elements

Vestibulo-ocular System
Coordinate head and eye movements to maintain stable gaze
and visual acuity while actively moving about
Posture Control (vestibulo-spinal) System
Maintain postural stability while actively moving about

Physiological Characteristics
Vestibulo-ocular

System
Horizontal semicircular canal & visual inputs
Responses dominated by short pathway reflexes
Simple movement geometry & biomechanics
Posture Control System
Vertical canal, otolithic, visual & proprioceptive inputs
Responses mediated by complex central pathways
Responses influenced by task & environment
Complex movement geometry & biomechanics

Organs and system that participate in the maintenance of body balance


Central

Sense body
position
relative to the
base of
support

Somatosensory

Adaptation
Use sensory
inputs and body
movements
appropriate to the
task conditions

Execute
coordinated
body
movements

Input from the muscles and joints


1)

The somato-sensory system provides information about the


relative location of the body parts/

Proprioception reflects the perception of the static position.

Kinesthesia refers to the position during movements.


Information arises from peripheral sources (muscles, jt. capsule,
soft tissues):
Sensory receptors information to vestibular system & the
medulla & brainstem through the dorsal colummedial lemniscal
pathway.
2) This information will
assist in:
1) Coordinating eye,
head & neck
movements to
stabilize the visual
system.
2) In maintaining
posture, muscle
tone, & stiffness in
the muscles.
3) Coordinate
movement patterns

2) Input from the eyes / The visual system :


Through the retina, the optic nerve and thalamus provide information
about the position of the head relative to the environment & orients the
head to maintain posture.

Sensory receptors in the retina are called


rods and cones.
When light strikes the rods and cones,
they send impulses to the brain that
provide visual cues identifying how a
person is oriented relative to other objects.
For example, as a pedestrian walks along
a city street, the surrounding buildings
appear vertically aligned, and each
storefront passed first moves into and then
beyond the range of peripheral vision.

3) Input from The vestibular system:


Provides information on orientation of the head in space and on
accelaration.
Any movement, including weight shifts to adjust posture stimulate the
vestibular receptors vestibular nerve cerebellum spinal cord
for postural control.
Sensory information about
motion, equilibrium, and spatial
orientation is provided by the
vestibular apparatus,
which in each ear includes the
utricle, saccule, and three
semicircular canals.
The utricle and saccule detect
gravity (vertical orientation) and
linear movement.
The semicircular canals, which
detect rotational movement, are
located at right angles to each
other and are filled with a fluid
called endolymph.
10

Integration of sensory input


Balance information provided by the peripheral sensory organseyes,
muscles and joints, and the two sides of the vestibular systemis sent to
the brain stem. There, it is sorted out and integrated with learned information
contributed by the cerebellum (the coordination center of the brain) and the
cerebral cortex (the thinking and memory center).
The cerebellum provides information about automatic movements that have
been learned through repeated exposure to certain motions.
For example, by repeatedly practicing serving a ball, a tennis player learns to
optimize balance control during that movement.
Contributions from the cerebral cortex include previously learned information;
for example, because icy sidewalks are slippery, one is required to use a different
pattern of movement in order to safely navigate them

The Brain
1. Brainstem Vestibular Nuclei
Primary input comes from the vestibular portion of CN VIII (vestibular-cochlear)
There are 4 Vestibular Nuclei:
Lateral/Deiters
Nucleus

Function
Help the body maintain a desired posture (ie.
vestibulospinal reflexes)

Medial/Superior

Coordinates eye, head, and neck movements

Inferior

Integrate information from the cerebellum and other


sensory systems

superior division: utricle, anterior part of saccule, and horiz & anterior canals
inferior division: posterior part of saccule, and posterior canal
to vestibular nuclei
to cerebellum

Other inputs to vestibular nuclei:


Cerebellum: primarily inhibitory
Spinal cord
Pontine reticular formation
Contralateral vestibular nuclei

From the Vestibular Nuclei:

Vestibulo-Oculomotor Pathways:
Direct: to oculomotor nuclei.
Indirect: via reticular formation to oculomotor nuclei (III IV and VI)
Vestibulo-Spinal Pathways:
Lateral V-S-throughout spinal cord
Medial V-S-cervical & thoracic
Reticulospinal tract-via brainstem reticular formation

Cerebellum
Maintenance of Equilibrium
- balance, posture, eye movement
Monitors vestibular performance
Readjusts central vestibular processing of static &
dynamic postural activity
Coordination of half-automatic movement of
walking and posture maintenace
- posture, gait
Adjustment of Muscle Tone
Motor Learning Motor Skills
Cognitive Function
Midline (vermal) regions regulate balance
and eye movements
Lateral regions control muscles of the
extremities.
The cerebellum plays a central role in
modulating ocular motor reflexes with the
goal of maximizing visual performance

Relay Centers
Thalamus
Connection with vestibular cortex and reticular formation
arousal and conscious awareness of body; discrimination between
self movement vs. that of the environment
Vestibular Cortex
Junction of parietal and insular lobe
Target for afferents along with the cerebellum
Both process vestibular information with somatosensory and
visual input

Motor output
As sensory integration takes place, the brain stem transmits impulses to the
muscles that control movements of the eyes, head and neck, trunk, and legs, thus
allowing a person to both maintain balance and have clear vision while moving.

Motor output to the eyes


The vestibular system sends motor control signals via the nervous system to
the muscles of the eyes with an automatic function called the vestibulo-ocular
reflex- gaze stability.

Motor output to the muscles and joints


The motor impulses that are sent from the brain to the other muscles of
the body control their movement so that balance is maintained whether a
person is sitting, standing, or turning cartwheels posture control /
vestibulo-spinalis reflex

The coordinated balance system


The human balance system involves a complex set of sensorimotorcontrol systems.
Its interlacing feedback mechanisms can be disrupted by damage to
one or more components through injury, disease, or the aging process.
Impaired balance can be accompanied by other symptoms such as
dizziness, vertigo, vision problems, nausea, fatigue, and concentration
difficulties.
The complexity of the human balance system creates challenges in
diagnosing and treating the underlying cause of imbalance.
Vestibular dysfunction as a cause of imbalance offers a particularly
intricate challenge because of the vestibular systems interaction with
cognitive functioning,2 and the degree of influence it has on the control of
eye movements and posture

The Vestibular System


Importance of Vestibular System
Balance, equilibrium, posture,
head, body, eye movement
It enables us to recognize
our static position,
velocity, and acceleration.
Vestibular Labyrinth
Otolith organs - gravity and tilt
Semicircular canals - head
rotation
Use hair cells, like auditory
system, to detect changes

The vestibular system is the basis of our three-dimensional model of


the world.
It is the unifying system in our brain that coordinates information
received from other systems.

Main Components of the Vestibular System


Peripheral End Organs
Located in the inner ear, it is composed of five organs: the utricle
and saccule (otolith organs), and the three semi-circular canals.
The otolith organs sense the heads linear acceleration and
Orientation of the head with respect to gravity or position relative to
gravity
The semicircular canals enable us to be aware of our threedimensional dynamic position.
Vestibular Nerve
Central Nervous System
Connections
Motor Output
- Vestibular Ocular Reflex (VOR)
- Vestibulospinal Reflex (VSR)
- Vestibulo-colic

The function of the vestibular system can be


simplified by remembering some basic
terminology of classical mechanics.
All bodies moving in a three-dimensional
framework have six degrees of freedom: three
of these are translational and three are
rotational. The translational elements refer to
linear movements in the x, y, and z axes (the
horizontal and vertical planes).
Translational motion in these planes (linear
acceleration and static displacement of the
head) is the primary concern of the otolith
organs.
The three degrees of rotational freedom refer to
a body's rotation relative to the x, y, and z axes
and are commonly referred to as roll, pitch, and
yaw. The semicircular canals are primarily
responsible for sensing rotational accelerations
around these three axes.

Vestibular outputs very rapidly influence eye, head, and


postural reflexes

Vestibulo-ocular reflex
The VOR generates compensatory eye movements in order to
stabilize gaze during head motion (i.e. Rotation of head to the
left results in rightward compensatory eye movement) Eye
velocity compensates for head velocity
Vestibulospinal reflex
Maintains vertical alignment of the trunk
When the head tips in one direction, the body elongates to that
side and shortens on the other
Postural changes in response to vestibular signals
Vestibulo-colic reflex
- Activates the neck musculature to stabilize the head in space
Compensates for displacements of the head that occur during gait
Head position maintained despite body movements

The Vestibular System


The Otolith Organs: Detect changes in head angle, linear acceleration,gravity

Macular hair cells responding to tilt


Hair cells project into gelatinous type mixture that has calcium carbonate crystals (otoconia) embedded within.
Otoconia are gravity sensitive
Utricle senses horizontal linear acceleration
Saccule senses vertical linear acceleration

The Vestibular System


The Semicircular Canal sense head rotations - Angular accelerations
Structure

Linear acceleration

Figure 14.2. The morphological polarization of vestibular hair cells and the polarization maps of the vestibular organs. (A) A
cross section of hair cells shows that the kinocilia of a group of hair cells are all located on the same side of the hair cell. The
arrow indicates the direction of deflection that depolarizes the hair cell. (B) View looking down on the hair bundles. (C) In the
ampulla located at the base of each semicircular canal, the hair bundles are oriented in the same direction. In the sacculus
and utricle, the striola divides the hair cells into populations with opposing hair bundle polarities.

The mechanisms underlying the depolarization and


hyperpolarization of vestibular hair cells depend,
respectively,
on the potassium-rich character of endo lymph and the
potassium-poor character of the perilymph that bathes
the basal and lateral portions of the hair cells.
Deflection of the stereocilia toward the kino cilium
causes potassium channels in the apical portions of the
stereocilia and kinocilium to open. K+ flows into the cell
from the endolymph, depolarizing the cell membrane (see
Fig. 7).
This depolarization in turn causes voltage-gated calcium
channels at the base of the hair cells to open, allowing
Ca++ to enter the cell.
The influx of Ca++ causes synaptic vesicles to release
their transmitter (aspartate or glutamate) into the
synaptic clefts, and the afferent fibers respond by under
going depolarization and increasing their rate of firing.

.
When the stimulus subsides, the stereocilia and
kinocilium return to their resting position, allowing most
calcium channels to close and voltage-gated potassium
channels at the base of the cell to open.
K+ efflux returns the hair cell membrane to its resting
potential (see Fig. 7).
Deflection of the stereocilia away from the kino cilium
causes potassium channels in the basolateral portions of
the hair cell to open, allowing K+ to flow out from the cell
into the interstitial space.
The resulting hyperpolarization of the cell membrane
decreases the rate at which the neurotransmitter is released
by the hair cells and consequently, decreases the firing
rate of afferent fibers.
Almost all vestibular primary afferent fibers have a
moderate spontaneous firing rate at rest (approximately 90
spikes per second). Therefore, it is likely that some hair cell
calcium channels are open at all times, causing a slow,
constant release of neurotransmitter.
The ototoxic effects of some aminoglycoside antibiotics
(e.g., streptomycin, gentamicin) may be due to direct
reduction of the transduction currents of hair cells.

Figure 14.5. Forces acting on the


head and the resulting displacement
of the otolithic membrane of the
utricular macula. For each of the
positions and accelerations due to
translational movements, some set
of hair cells will be maximally
excited, whereas another set will be
maximally inhibited. Note that head
tilts produce displacements similar to
certain accelerations.

Angular acceleration

Figure 14.7. The ampulla of the posterior semicircular canal showing the
crista, hair bundles, and cupula. The cupula is distorted by the fluid in the
membranous canal when the head rotates.

Response to Angular
Acceleration

Beginning of Rotation
Direction of Head Movement

Middle of Rotation

Post-Rotational

Cupula

Relative Direction of
Endolymph
Inertia makes
endolymph initially
drag behind
when head starts to
rotate. Cupula
deflected.

Endolymph soon
catches up with
direction and velocity of
rotation. Cupula no
longer deflected.
Hair cells no longer
stimulated.

Head stops moving,


but endolymph keeps
on moving (again,
because of inertia).
Cupula deflected in
opposite direction.

Figure 14.8. Functional organization of


the semicircular canals.
(A)The position of the cupula without
angular acceleration.
(B)Distortion of the cupula during
angular acceleration. When the head is
rotated in the plane of the canal (arrow
outside canal), the inertia of the
endolymph creates a force (arrow
inside the canal) that displaces the
cupula.
(C) Arrangement of the canals in pairs.
The two horizontal canals form a pair;
the right anterior canal (AC) and the left
posterior canal (PC) form a pair; the left
AC and the right PC form a pair.

The Vestibulo-Ocular Reflex (VOR)

Figure 14.10. Connections underlying


the vestibulo-ocular reflex. Projections
of the vestibular nucleus to the nuclei
of cranial nerves III (oculomotor) and
VI (abducens).
The connections to the oculomotor
nucleus and to the contralateral
abducens nucleus are excitatory ,
whereas the connections to ipsilateral
abducens nucleus are inhibitory .
There are connections from the
oculomotor nucleus to the medial
rectus of the left eye and from the
adbucens nucleus to the lateral rectus
of the right eye. This circuit moves the
eyes to the right, that is, in the
direction away from the left horizontal
canal, when the head rotates to the
left. Turning to the right, which causes
increased activity in the right
horizontal canal, has the opposite
effect on eye movements. The
projections from the right vestibular
nucleus are omitted for clarity.

Vestibulospinal Reflex (VSR)


Generates compensatory body movement to maintain head and
postural stability, thereby preventing falls
Figure 14.11. Descending
projections from the medial and
lateral vestibular nuclei to the spinal
cord.
The medial vestibular nuclei
project bilaterally in the medial
longitudinal fasciculus to reach the
medial part of the ventral horns and
mediate head reflexes in response
to activation of semicircular canals.
The lateral vestibular nucleus
sends axons via the lateral
vestibular tract to contact anterior
horn cells innervating the axial and
proximal limb muscles. Neurons in
the lateral vestibular nucleus receive
input from the cerebellum, allowing
the cerebellum to influence posture
and equilibrium.

Lateral Vestibulospinal Tract


Lateral
Vestibular
nucleus

Lateral Vestibulospinal Tract:


The inputs from the otolith organs project mainly
to the lateral vestibular nucleus, which in turn
sends axons in the lateral vestibulospinal tract to
the spinal cord.
The input from this tract exerts a powerful
excitatory influence on the extensor (antigravity)
muscles. When hair cells in the otolith organs are
activated, signals reach the medial part of the
ventral horn. By activating the ipsilateral pool of
motor neurons innervating extensor muscles in the
trunk and limbs, this pathway mediates balance
and the maintenance of upright posture.
Decerebrate rigidity, which is characterized by
rigid extension of the limbs, arises when the
brainstem is transected above the level of the
vestibular nucleus. The tonic activation of extensor
muscles in this instance suggests that the
vestibulospinal pathway is normally strongly
suppressed by descending projections from higher
levels of the brain, especially the cerebral cortex.

Medial Vestibulospinal Tract


Lateral
Vestibular
nucleus

Medial Vestibulospinal Tract:


Axons from the medial vestibular
nucleus descend in the medial
longitudinal fasciculus to reach the upper
cervical levels of the spinal cord.
This pathway regulates head position
by reflex activity of neck muscles in
response to stimulation of the
semicircular canals from rotational
accelerations of the head.
For example, during a downward pitch
of the body (e.g., tripping), the superior
canals are activated and the head
muscles reflexively pull the head up. The
dorsal flexion of the head initiates other
reflexes, such as forelimb extension and
hindlimb flexion, to stabilize the body and
protect against a fall.
2001 by Sinauer Associates, Inc.

Balance Control

Sensory Organization

Initiate Automatic/
Voluntary Movements

Determine
Body Position

Compare, Select
& Combine Senses

Visual
System

Vestibular
System

Environmental
Interaction

Motor Control

Select & Adjust


Muscle Contractile Patterns

SomatoSensation

Ankle
Muscles

Thigh
Muscles

Generate
Body Movements

Trunk
Muscles

Erect Standing Posture & the Gravity Line


(Sagittal Analysis)
Gravity line falls:
Forward of ankle
Through or forward of the knee
Through of behind the hip
(common hip axis)
Behind or through thoracic spine
Through acromium
Through or forward of atlantooccipital jt.

Erect Standing Posture & the


Gravity Line (Frontal Analysis)
Gravity line falls:
Symmetrically between two feet
Through the umbilicus
Through the xiphoid process
Through the chin & nose
Between the eyes

The Gravity Line and Anti-gravity Muscles (Sagittal Plane)


Gravity line falls:

Forward of ankle
Through or forward of
the knee
Through of behind
the hip (common hip
axis)
Behind or through
thoracic spine
Through acromium
Through or forward of
atlanto-occipital

Anti-gravity muscle:
Gastroc-soleus
Quadriceps
Hip extensors
Paraspinals

Neck extensors

Limits of Stability

Vestibular System
Linear Acceleration
Vestibule

Angular Acceleration

Otolithic Membrane

Cupula

Semicircular Canals
Anterior, Posterior, Lateral

Kinocilium

Utricle
Saccule
Sensory Epithelium: Macula

Hair Cells

Specialized Epithelium: Crista ampularis


Vestibular Ganglion (Scarpas Ganglion)
Vestibular Nerve

Macula in Horizontal Plane


Maximally stimulated when
head bent side to side

Macula in Vertical Plane


Maximally stimulated when
head bent forward-backward.
Cerebellum
Fastigial Nuc
Flocculonodular lobe
Vermis

Superior
Inferior Vestibular
Medial Nuclei
Lateral

Lateral
Vestibulospinal
Tract

MLF

Vestibular Function Tests


Posturography Static &
dynamic
Caloric test
Rotary Chair test

Vestibulospinal Reflexes test


Cerebellar function:
The midline cerebellar structure, the vermis are concerned with
posture, gait, and truncal equilibrium
ROMBERGS TEST is screening test for standing balance
Patient stands with feet together, arms by the side with eyes open then closed
Peripheral vestibular lesions- the bodys centre of gravity is displaced to the
side of the labyrinthine lesion
Central disturbances- pattern of unsteadiness of gait and direction of fall are
irregular.

Test hemispheric function


Past pointing is a vestibulo spinal test of upper extrimities

Test hemispheric function


POSITIONAL TESTS ( cerebellar lesions)
Finger-nose pointing- overshooting indicates cerebellar lesion

Test hemispheric function

POSITIONAL TESTS ( cerebellar lesions)

Dysdidokinesia- central cerebellar lesion

Vestibulospinal Reflexes
The stepping test evaluates te vestibulo spinal response of
lower extrimities to labyrinthine stimuli
UNTERBERGERS Stepping Test
Stepping on the spot with the eyes closed and arms outstretched for 30 sec
Peripheral disorders- rotation of body axis to the side of the labyrinthine lesion
Central disorders the deviation is irregular
Only deviations of > than 30o is significant

Nystagmus
Involuntary rhythmical oscillation of eyes
away from the direction of gaze, followed
by return of eyes to their original position.
The direction of the fast component
determines the direction of the
nystagmus
( towards the
dominant vestibular centre, inhibitory
impulses are suppressed i.e the side of
the lesion )

Nystagmus
Primary diagnostic indicator in
identifying vestibular lesions
Physiologic nystagmus
vestibular, visual, extreme lateral gaze

Pathologic nystagmus
spontaneous, positional, gaze evoked

Labeled by the direction of the fast


component
Central vs. peripheral cause
differentiated by duration

Type Nystagmus
1.Pendular nystagmus : an equal speed of eyes in boh
direction, extra vestibular origin e.g congenital ocular
nystagmus
2.Jerk nystagmus: biphasic quality with fast and slow
component, usualy response to vestibular stimulation such as
caloric testing

Direction Nystagmus
Right, left, up and down or rotary clockwise or counter
clockwise

Form Nystagmus
Horizontal, vertical, rotary, diagonal or mix

Nystagmus Intensity
Anderson,s classification:
1.First degree- appear with the patient gazing in the direction
of fast component
2.Second degree- appears with gaze in the neutral position
3.Third degree- appears in all direction of the gaze

Unilateral or mono ocular versus binocular.


Mono ocular typer is rare

Spontaneous or induced Nystagmus


1.The spontaneous type appears with no external presented to the
patient
2.The induced type may appear secondary to pathologic process
or due to a stimulus applied for diagnostic purpose e.g. positional
or thermal induced nystagmus

Spontaneous Nystagmus

First Degree nystagmus present only when the eyes deviate to the
side of the lesion
Second Degree nystagmus present when patient looks straight
ahead
Third Degree nystagmus present in both directions

Classification of spontaneous nystagmus


1. Normal : vertical with eyes closed, horizontal with eyes coles
voluntary, less than 6 degress to 10 degress/second
2. Vestibular: has fast and slow component, decreased with fixation,
conjugate, horizontal
3. Ocular : sinusoidal suppressed by convergence and enhanced by
fixation, Congenital, occupational
4. Central : by exclusion e.g paroxymal alternating nystagmus; a jerky
type present in neutral position but shift direction spontaneously

Positional Nystagmus
Nystagmus in which was caused by a particular head position.
Classification;
1.Type I is direction-changing nystagmus, the direction of fast component
change as the subject change the head position.
2.Type II is direction fixed nystagmus. There is no change the direction of
the fast component as the subject chnges head position
3.Type III is irregular. The response may alternate between types I and II or
may change direction even though the subject doesnot change the head

Paroxymal positional Nystagmus / BPPV


Nystagmus in which was caused by change in position such as looking up
to a ceiling or turning over the bed, The vertigo typically is brought on by
sudden change in head position, but subsides as the subject maintain the
provocative position. The vertigo is usually transient and frequently
associated with nusea and vomiting.

Paroxymal positional Nystagmus / BPPV

Hallpike Manouvre
Patient sits on bed, head turned 45 degrees to left or right.
Patient is rapidly laid back with head over edge of bed 30 degrees below
the horizontal. Eyes open look for nystagmus.
After 30 sec return patient to upright position
Repeat with head to other side

Neck torsion ( cervical) nystagmus and vertigo


Nystagmus is a form of positional nystagmus. The stimulus is a neck
torsion induced by turning the head on the body with nech twisting to
produce and alteration in the head body relationship.
Patients with the cervical or neck torsion nystagmus displays myriad of
symptomp

Vestibulo-ocular reflex
ROTATIONAL TESTS
Nystagmus Induced by accelerating and
decelerating rotating chair, tests both
labyrinths simultaneously
CALORIC TESTS
COWS- cold water opposite side, warm
water same side, direction of nystagmus
Extent of caloric response indicates
function of labyrinth

Vestibulo-ocular Reflex
Electronystagmograghy
Positive potential between the
cornea and retina recorded as eyes
move from straight ahead gaze
Test includes different head positions,
eyes open, closed and caloric tests

MOTION SICKNESS
MOTION SICKNESS IS A CONDITION CHARACTERIZED
PRIMARILY BY NAUSEA,VOMITING, PARLOR, AND
COLD SWEATING, THAT OCCUR WHEN A MAN IS
EXPOSED TO REAL OR APPARENT MOTION STIMULI
WITH WHICH HE IS UN FAMILIAR AND HENCE UN
ADAPTED

NEURAL STRUCTUR OF MOTION SICKNESS


CENTRAL NERVOUS SYSTEM

SIGN & SYMPTOM

CEREBRAL
CORTEX

HIPOTALAMUS
RETINA

VESTIBULER
CEREBELLUM
PITUITRY

MOTION
STIMULI

VESTIBULER
APPARATUS

SOMATO
SENSORIS
RECEPTOR

VESTIBULER
NUCLEI

CTZ

AUTONOMIC
CENTRE

VOMITING
CENTRE

NEURAL STRUCTUR OF MOTION SICKNESS, BENSON 1977

NAUSEA,
DIZZINESS,
SOMNOLENCE,
HEADACHE,
DEPRESSION,
PERFORMANCE
DCREAMENT
INCREASED
SECRETION
ADH,ACTH,GH,
PRL
SWEATING,
PALLOR,
DECREASED
GASTRIC
MOTILITY,
CARDIOVASCUL
ER &
RESPIRATORY
CHANGES

VOMITING

NAUSEA : GREEK = NAUXIA = SEA - SICKNESS


ISTILAH MOTION SICKNESS / MABUK GERK KDG-KDG TIDAK TEPAT
KRN TIDAK SELALU DISEBABKAN RANGSANG GERAK SPT
SIMULATOR SICKNESS, CINERAMA SICKNESS DAN BUKAN SUATU
PENYAKIT
ISTILAH LAIN : MOTION MALADAPTATION SYNDROM
TEORI TERJADINYA MABUK GERAK

1.

TEORI KONFLIK SENSORIS ; INPUT ERROR;

2.

TEORI NEURAL MISMATCH ; CENTRAL ERROR

Konflik Sensoris
Ketidakcocokan sensorik dari berbagai reseptor sensorik
perifer yaitu antara mata/visus, propioseptif
Benson membagi Beberapa tipe

Neural mismatch / central error


Motion sickness :
informasi dari mata, telinga, sist vestibuler
dengan
informasi yang diharapkan oleh tubuh pengalaman masa lalu
Bila rangsangan gerak memberikan informasi SAMA DENGAN
pengalaman yang diterima
di masa lalu motion
sickness
TEORI MEMORI DAPAT MENERANGKAN ADANYA ADAPTASI
WALAUPUN KONFLIK TETAP TERJADI
65

NEURAL MISMATCH HYPOTHESIS


STIMULUS
( INPUT )

RECEPTOR

BRAIN MECHANISME

MOTOR CONTROL
SYSTEM

EYES

OTOLITH &
OTHER
GRAVI
PASSIVE
MOVEMENT RECEPTOR

UPDATES INTERNAL
MODEL (ADAPTATION)

COMPERATOR
MISMATCH
SIGNAL

MOTION
STIMULI

SEMI
CIRCULAR
CANAL

VOLITIONAL
AND REFLEX
MOVMENT

INTERNAL MODEL
NEURAL STORE OF
EXPECTED SIGNAL

LEAKY
INTEGRATOR

THRESHOLD

ACTIVE MOVEMENT

RESPONS
( OUTPUT )

NEURAL
CENTRES
MEDIATING
SIGN &
SYMPTOMS
OF MOTION
SICKNESS

MOTION
SICKNESS
SYNDROM

67

TYPE & CATAGORIES OF SENSORY CONFLICT*


TYPE OF CONFLICT

CATEGORY OF CONFLICT
VISUAL (A) VESTIBULER(B)

TYPE I
SIMULTANT DIFF
TYPE 1 : BOTH SYSTEM
CONCURRETLY SIGNAL
CONTRADICTING OR
UNCORRELATED
INFORMATION

TYPE II* a
A+ &BTYPE 2 (i): VISUAL CUES
WITHOUT THE EXPECTED
AND NORMALLY
CORRELATED VESTIBULAR
SIGNAL

TYPE II b
A- &B+

TYPE 2 (ii) : THE


VESTIBULAR CUES NOT
ACCOMPANIED BY THE
EXPECTED VISUAL CUES

* BENSON 1984

CANAL(A) OTOLITH(B)

WATCHING WAVE FROM SHIP, USE


BINOCULAR IN MOVING VEHICLE,
MAKING HEAD MOVEMENT WHEN
VISION IS DISTORTED BY OPTICAL
DEVICE, PSEUDO CORIOLIS
STIMULATION

CORIOLIS , MAKING HEAD


MOVEMENT IN ABNORMAL
ACCELERATION ENVIRONMENT
WHICH MAY BE CONSTANT (e.g
HYPER OR HYPO GRAVITY OR
FLUCTUATING ( LINIER
OSCILATIONSPACE SICKNESS,
VESTIBULAR
DISSORDER,MENIERS

CINERAMA SICKNESS ,
SIMULATOR SICKNESS,
HAUNTED SWING, CIRCULAR
VECTION

POSISTIONAL ALCOHOL
NYSTAGMUS, CALORIC
STIMULATION OF SEMICIRCULARIS,
VESTIBULAR DISSORDER/e.g
PRESSURE VERTIGO, CUPULO
LITHIASIS, BPPV

LOOKING IN SIDE A MOVING


VEHICLE WITHOUT EXTERNAL
VISUAL REFRENCE (e.g BELOW
DECK IN BOAT) READING IN
MOVING VEHICLE

LOW FREQUENCY (<0.5 Hz)


TRANSLATION OCCILATION,
ROTATING LINEAR ACCELERATOR
VECTOR (e.g BARBEQUE-SPIT
ROTATION, ROTATION ABOUT AN
OFF VERTICAL AXIS

* TYPE 2 : ONE SYSTEM SIGNAL INFORMATION IN THE ABSENCE


OF THE EXPECTED SIGNAL FROM OTHER SYSTEM

Efek anti emetik : kombinasi efek


peripheral (gastrokinetik) dan
antagonis terhadap reseptor Dopamin
D2 Antagonis di CTZ (chemoreceptor
Trigger Zone)
: Domperidone dan Metoklopramide

Antihistamin me (-) severity


motion sickness dengan c
menghambat sinyal pada neural
mismatch dan bekerja langsung ,
efektif untuk diberikan sebelum
atau sesudah muntah.

Ondansetron
Blokade sentral di CTZ pada area
post rema dan nucleus traktus
solitaries sebagai kompetitif selektif
reseptor 5-HT3
Memblok reseptor 5-HT3 di perifer
pada ujung nervus saraf vagal di sel
enterokromafin di traktus
gastrointestinal
Scopolamin mencegah
terjadinya motion sickness
dengan mengurangi sinyal
neural mismatch dan
memfasilitasi proses
adaptasi

69

Thanks for your attention

Any Question?