PHYSIOLOGY of EquilibriumDr Herman Mulijadi MS.SpKP

Lesson ObjecitvesExplain the component of organs and system that participate in the maintenance of body balanceExplain the component of vestibular systemDraw the receptors in each component of the vestibular system and explain how they workDifferentiate the angular and linear accelerationExplain the component of the vestibular system that sensitive to angular and linear accelerationExplain the mechanism of sea sicknessExplain some experiment to test body balanceDefine nystagmus and explain its mechanism

**Balance:It is :the ability to maintain equilibrium

Orthe ability to maintain your center of mass/gravity over your base of support in any given sensory environment .

BalanceBalance 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.

Response Action

Balance is a highly integrated networkocular system - visual perception of spatial orientation is supplied by the eyesvestibular system -rotatory stimulation and linear acceleration Informationproprioceptive system - information input from the feet, ankle, hip, and neck central nervous system - integrated these information and translated to fine motor movements

Balance System ElementsVestibulo-ocular SystemCoordinate head and eye movements to maintain stable gaze and visual acuity while actively moving aboutPosture Control (vestibulo-spinal) SystemMaintain postural stability while actively moving about

Physiological CharacteristicsVestibulo-ocular SystemHorizontal semicircular canal & visual inputsResponses dominated by short pathway reflexesSimple movement geometry & biomechanicsPosture Control SystemVertical canal, otolithic, visual & proprioceptive inputsResponses mediated by complex central pathwaysResponses influenced by task & environmentComplex movement geometry & biomechanics

SomatosensoryOrgans and system that participate in the maintenance of body balanceSense body position relative to the base of supportExecute coordinated body movements Central AdaptationUse sensory inputs and body movements appropriate to the task conditions

*

*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.Input from the muscles and joints2) This information will assist in:Coordinating eye, head & neck movements to stabilize the visual system.In maintaining posture, muscle tone, & stiffness in the muscles.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.

Integration of sensory inputBalance 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 Brain1. Brainstem Vestibular NucleiPrimary input comes from the vestibular portion of CN VIII (vestibular-cochlear)There are 4 Vestibular Nuclei:superior division: utricle, anterior part of saccule, and horiz & anterior canalsinferior division: posterior part of saccule, and posterior canalto vestibular nucleito cerebellum

Other inputs to vestibular nuclei:Cerebellum: primarily inhibitorySpinal cordPontine reticular formationContralateral vestibular nuclei

FunctionLateral/Deiters NucleusHelp the body maintain a desired posture (ie. vestibulospinal reflexes)Medial/SuperiorCoordinates eye, head, and neck movements InferiorIntegrate information from the cerebellum and other sensory systems

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 cordMedial V-S-cervical & thoracicReticulospinal tract-via brainstem reticular formation

*

Maintenance of Equilibrium - balance, posture, eye movement Monitors vestibular performanceReadjusts central vestibular processing of static & dynamic postural activityCoordination of half-automatic movement of

walking and posture maintenace - posture, gait Adjustment of Muscle Tone Motor Learning Motor Skills Cognitive FunctionCerebellumMidline (vermal) regions regulate balance and eye movementsLateral 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 CentersThalamusConnection with vestibular cortex and reticular formation arousal and conscious awareness of body; discrimination between self movement vs. that of the environment

Vestibular CortexJunction of parietal and insular lobeTarget for afferents along with the cerebellum

Both process vestibular information with somatosensory and visual input

Motor outputAs 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 eyesThe 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 jointsThe 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 systemThe human balance system involves a complex set of sensorimotor-control 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

Importance of Vestibular SystemBalance, equilibrium, posture, head, body, eye movementIt enables us to recognize our static position, velocity, and acceleration.Vestibular LabyrinthOtolith organs - gravity and tiltSemicircular canals - head rotationUse hair cells, like auditory system, to detect changes

The Vestibular SystemThe 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 SystemVestibular NerveCentral Nervous System ConnectionsMotor Output - Vestibular Ocular Reflex (VOR) - Vestibulospinal Reflex (VSR)- Vestibulo-colicPeripheral 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 gravityThe semicircular canals enable us to be aware of our three-dimensional dynamic position.

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 reflexThe 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 velocityVestibulospinal reflexMaintains vertical alignment of the trunkWhen the head tips in one direction, the body elongates to that side and shortens on the other Postural changes in response to vestibular signalsVestibulo-colic reflex

- Activates the neck musculature to stabilize the head in space Compensates for displacements of the head that occur during gaitHead position maintained despite body movements

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

Macular hair cells responding to tiltHair cells project into gelatinous type mixture that has calcium carbonate crystals (otoconia) embedded within.Otoconia are gravity sensitiveUtricle senses horizontal linear accelerationSaccule senses vertical linear acceleration

The Vestibular System

*

The Semicircular Canal sense head rotations - Angular accelerationsStructure

The Vestibular System

*

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.Linear acceleration

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.

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.

Angular acceleration

Response to Angular Acceleration

Direction of Head Movement

Endolymph soon catches up with direction and velocity of rotation. Cupula no longer deflected.Hair cells no longer stimulated.Post-RotationalHead stops moving, but endolymph keeps on moving (again, because of inertia). Cupula deflected in opposite direction.CupulaBeginning of RotationMiddle of Rotation

*

Figure 14.8. Functional organization of the semicircular canals. The position of the cupula without angular acceleration. 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. 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.

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.

The Vestibulo-Ocular Reflex (VOR)

*

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. Vestibulospinal Reflex (VSR)Generates compensatory body movement to maintain head and postural stability, thereby preventing falls

Lateral Vestibulospinal TractLateral 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.

Lateral Vestibular nucleus

Medial Vestibulospinal TractMedial 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. Lateral Vestibular nucleus

Sensory OrganizationMotor ControlInitiate Automatic/Voluntary MovementsEnvironmentalInteractionVisualSystemVestibularSystemSomato-SensationCompare, Select& Combine SensesDetermineBody PositionSelect & AdjustMuscle Contractile PatternsAnkleMusclesGenerateBody MovementsTrunkMusclesThighMusclesBalance Control

Erect Standing Posture & the Gravity Line (Sagittal Analysis)Gravity line falls:Forward of ankleThrough or forward of the kneeThrough of behind the hip (common hip axis)Behind or through thoracic spineThrough acromiumThrough or forward of atlanto-occipital jt.

Erect Standing Posture & the Gravity Line (Frontal Analysis)Gravity line falls:Symmetrically between two feetThrough the umbilicusThrough the xiphoid processThrough the chin & noseBetween the eyes

The Gravity Line and Anti-gravity Muscles (Sagittal Plane)Gravity line falls:Forward of ankleThrough or forward of the kneeThrough of behind the hip (common hip axis)Behind or through thoracic spineThrough acromiumThrough or forward of atlanto-occipital

Anti-gravity muscle:Gastroc-soleusQuadriceps

Hip extensors

Paraspinals

Neck extensors

Limits of Stability

Vestibular SystemVestibuleSemicircular CanalsLinear AccelerationAngular AccelerationSacculeUtricleSensory Epithelium: MaculaMacula in Horizontal PlaneMaximally stimulated when head bent side to sideMacula in Vertical PlaneMaximally stimulated when head bent forward-backward.Anterior, Posterior, LateralSpecialized Epithelium: Crista ampularis

Hair Cells

Otolithic Membrane

CupulaKinocilium

Vestibular Ganglion (Scarpas Ganglion)Vestibular NerveSuperiorInferiorMedialLateralVestibular Nuclei

MLFLateral Vestibulospinal TractCerebellumFastigial NucFlocculonodular lobeVermis

*

Vestibular Function TestsPosturography Static & dynamicCaloric testRotary Chair test

*

Vestibulospinal Reflexes testROMBERGS TEST is screening test for standing balance

Patient stands with feet together, arms by the side with eyes open then closedPeripheral vestibular lesions- the bodys centre of gravity is displaced to the side of the labyrinthine lesionCentral disturbances- pattern of unsteadiness of gait and direction of fall are irregular.

Cerebellar function:The midline cerebellar structure, the vermis are concerned with posture, gait, and truncal equilibrium

Test hemispheric functionPast pointing is a vestibulo spinal test of upper extrimities

Test hemispheric functionPOSITIONAL TESTS ( cerebellar lesions) Finger-nose pointing- overshooting indicates cerebellar lesion

Test hemispheric function

POSITIONAL TESTS ( cerebellar lesions) Dysdidokinesia- central cerebellar lesion

Vestibulospinal ReflexesUNTERBERGERS Stepping TestStepping on the spot with the eyes closed and arms outstretched for 30 secPeripheral disorders- rotation of body axis to the side of the labyrinthine lesionCentral disorders the deviation is irregularOnly deviations of > than 30o is significant

The stepping test evaluates te vestibulo spinal response of lower extrimities to labyrinthine stimuli

NystagmusInvoluntary 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 )

NystagmusPrimary diagnostic indicator in identifying vestibular lesionsPhysiologic nystagmusvestibular, visual, extreme lateral gaze

Pathologic nystagmusspontaneous, positional, gaze evoked

Labeled by the direction of the fast componentCentral vs. peripheral cause differentiated by duration

Type NystagmusPendular nystagmus : an equal speed of eyes in boh direction, extra vestibular origin e.g congenital ocular nystagmusJerk 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 clockwiseForm NystagmusHorizontal, vertical, rotary, diagonal or mix

Nystagmus IntensityAnderson,s classification:First degree- appear with the patient gazing in the direction of fast componentSecond degree- appears with gaze in the neutral positionThird degree- appears in all direction of the gaze

Unilateral or mono ocular versus binocular. Mono ocular typer is rareSpontaneous or induced NystagmusThe spontaneous type appears with no external presented to the patientThe 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 NystagmusFirst Degree nystagmus present only when the eyes deviate to the side of the lesionSecond Degree nystagmus present when patient looks straight aheadThird 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/second2. Vestibular: has fast and slow component, decreased with fixation, conjugate, horizontal3. Ocular : sinusoidal suppressed by convergence and enhanced by fixation, Congenital, occupational4. Central : by exclusion e.g paroxymal alternating nystagmus; a jerky type present in neutral position but shift direction spontaneously

Positional NystagmusNystagmus in which was caused by a particular head position.Classification;Type I is direction-changing nystagmus, the direction of fast component change as the subject change the head position.Type II is direction fixed nystagmus. There is no change the direction of the fast component as the subject chnges head positionType 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 / BPPVNystagmus 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 / BPPVHallpike ManouvrePatient 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 positionRepeat with head to other side

Neck torsion ( cervical) nystagmus and vertigoNystagmus 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 reflexROTATIONAL TESTSNystagmus Induced by accelerating and decelerating rotating chair, tests both labyrinths simultaneouslyCALORIC TESTSCOWS- cold water opposite side, warm water same side, direction of nystagmusExtent of caloric response indicates function of labyrinth

Vestibulo-ocular ReflexElectronystagmograghyPositive potential between the cornea and retina recorded as eyes move from straight ahead gazeTest includes different head positions, eyes open, closed and caloric tests

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 ADAPTEDMOTION SICKNESS

MOTION STIMULIRETINAVESTIBULER APPARATUSSOMATO SENSORIS RECEPTORVESTIBULER NUCLEIVESTIBULER CEREBELLUMHIPOTALAMUSPITUITRYAUTONOMIC CENTREVOMITING CENTRECTZ CEREBRAL CORTEX SIGN & SYMPTOMNAUSEA, DIZZINESS, SOMNOLENCE, HEADACHE, DEPRESSION, PERFORMANCE DCREAMENTINCREASED SECRETION ADH,ACTH,GH,PRLSWEATING, PALLOR, DECREASED GASTRIC MOTILITY, CARDIOVASCULER & RESPIRATORY CHANGESVOMITINGCENTRAL NERVOUS SYSTEMNEURAL STRUCTUR OF MOTION SICKNESS, BENSON 1977NEURAL STRUCTUR OF MOTION SICKNESS

TEORI TERJADINYA MABUK GERAKTEORI KONFLIK SENSORIS ; INPUT ERROR;

2. TEORI NEURAL MISMATCH ; CENTRAL ERRORNAUSEA : GREEK = NAUXIA = SEA - SICKNESSISTILAH MOTION SICKNESS / MABUK GERK KDG-KDG TIDAK TEPAT KRN TIDAK SELALU DISEBABKAN RANGSANG GERAK SPT SIMULATOR SICKNESS, CINERAMA SICKNESS DAN BUKAN SUATU PENYAKITISTILAH LAIN : MOTION MALADAPTATION SYNDROM

Neural mismatch / central error*Motion sickness :

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

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

*

NEURAL MISMATCH HYPOTHESISSTIMULUS ( INPUT )RECEPTORBRAIN MECHANISMERESPONS ( OUTPUT )ACTIVE MOVEMENTPASSIVE MOVEMENTMOTION STIMULIEYESSEMI CIRCULAR CANALOTOLITH & OTHER GRAVI RECEPTORCOMPERATORMOTOR CONTROL SYSTEMMOTION SICKNESS SYNDROM NEURAL CENTRES MEDIATING SIGN & SYMPTOMS OF MOTION SICKNESS LEAKY INTEGRATORMISMATCH SIGNALVOLITIONAL AND REFLEX MOVMENT THRESHOLDINTERNAL MODEL NEURAL STORE OF EXPECTED SIGNAL

UPDATES INTERNAL MODEL (ADAPTATION)

*

*

TYPE & CATAGORIES OF SENSORY CONFLICT*

TYPE OF CONFLICTCATEGORY OF CONFLICTVISUAL (A) VESTIBULER(B)CANAL(A) OTOLITH(B)TYPE I SIMULTANT DIFFWATCHING WAVE FROM SHIP, USE BINOCULAR IN MOVING VEHICLE, MAKING HEAD MOVEMENT WHEN VISION IS DISTORTED BY OPTICAL DEVICE, PSEUDO CORIOLIS STIMULATIONTYPE II* a A+ &B-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,MENIERSCINERAMA SICKNESS , SIMULATOR SICKNESS, HAUNTED SWING, CIRCULAR VECTIONPOSISTIONAL ALCOHOL NYSTAGMUS, CALORIC STIMULATION OF SEMICIRCULARIS, VESTIBULAR DISSORDER/e.g PRESSURE VERTIGO, CUPULO LITHIASIS, BPPVTYPE II b A- &B+LOOKING IN SIDE A MOVING VEHICLE WITHOUT EXTERNAL VISUAL REFRENCE (e.g BELOW DECK IN BOAT) READING IN MOVING VEHICLELOW FREQUENCY (

*Antihistamin me (-) severity motion sickness dengan c menghambat sinyal pada neural mismatch dan bekerja langsung , efektif untuk diberikan sebelum atau sesudah muntah. Efek anti emetik : kombinasi efek peripheral (gastrokinetik) dan antagonis terhadap reseptor Dopamin D2 Antagonis di CTZ (chemoreceptor Trigger Zone): Domperidone dan Metoklopramide

OndansetronBlokade sentral di CTZ pada area post rema dan nucleus traktus solitaries sebagai kompetitif selektif reseptor 5-HT3Memblok 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

*

Thanks for your attentionAny Question?

**

*

*

*

*

*

*

*

*

*

*