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PathophysiologyandTreatmentofMotion
Sickness
JohnF.GoldingMichaelA.Gresty
CurrOpinNeurol.201528(1):8388.

AbstractandIntroduction
Abstract

PurposeofreviewMotionsicknessremainsbothersomeinconventionaltransportandisanemerginghazardin
visualinformationtechnologies.Treatmentremainsunsatisfactorybutadvancesinbrainimaging,neurophysiology,
andneuropharmacologymayprovideinsightsintomoreeffectivedrugandbehaviouralmanagement.Wereview
thesemajordevelopments.
RecentfindingsRecentprogresshasbeeninidentifyingbrainmechanismsandlociassociatedwithmotion
sicknessandnauseaperse.Thetechniqueshaveincludedconventionalneurophysiology,pathwaymapping,and
functionalMRI,implicatingmultiplebrainregionsincludingcortex,brainstem,andcerebellum.Understandingofthe
environmentalandbehaviouralconditionsprovocativeofandprotectiveagainstmotionsicknessandhowvestibular
diseasemaysensitizetomotionsicknesshasincreased.Theproblemofnauseogenicinformationtechnologyhas
emergedasatargetforresearch,motivatedbyitsubiquitousapplications.Increasedunderstandingofthe
neurophysiologyandbrainregionsassociatedwithmotionsicknessmayprovideformoreeffectivemedicationinthe
future.However,thepolysymptomaticnatureofmotionsickness,highinterindividualvariability,andtheextensive
brainregionsinvolvedmayprecludeasingle,decisivetreatment.
SummaryMotionsicknessisanemerginghazardininformationtechnologies.Adaptationremainsthemost
effectivecountermeasuretogetherwithestablishedmedications,notablyscopolamineandantihistamines.
Neuropharmacologicalinvestigationsmayprovidemoreeffectivemedicationintheforeseeablefuture.
Introduction

Aresurgenceofinterestinmotionsicknessinrecentyearshasbeenattributabletotheuseofnauseogenicvisual
displaysandrealizationoftheinvolvementofthevestibularsystem,thekeymechanisminmotionsickness,with
clinicaldisordersincludingmigraine.Nonetheless,characteristicofthehistoryofmotionsicknessstudies,progress
hasbeenslow.Someofthecentralneuronalpathwaysinvolvedinprocessingofprovocativestimulihavebeen
identified.Thereisgreaterunderstandingoftheenvironmentalandbehaviouralcircumstancesandmedical
conditionsthatmodulatemotionsickness,butlittleadvanceintreatments.

Symptomatology
Motionsicknessispolysymptomatic.Nauseaandvomitingmaybeaccompaniedbyahostofsignificantsymptoms
includingheadache,sopite(drowsiness),sweating,facialpallor,coldsweating,increasedsalivation,sensationsof
bodilywarmth,dizziness,and,unsurprisingly,lossofappetiteandincreasedsensitivitytoodors. [1]Theimportance
andnegativeimpactonperformanceofsopiteisunderestimated, [2]andyawninghasbeenshowntobea
behaviouralmarker. [3]Theheadacheprovokedcanbemigrainousanddisabling. [1]Gastricdysrhythmiasmay
provideamarkerofnauseainmotionsickness, [4]anddropinstomachfundusandsphincterpressurecorrelates
withnausea. [5]

ProvocativeCircumstances
Inanextensivesurveyofacruiseship,motionsicknesswasthemostcommonreasonforphysicians'consultations,
theincidenceof4.2per1000person/daysbeinghigherthanforinfectionsorinjuries. [6]Uptoaquarterofcodrivers
becamemotionsickinrallycarsiftheywerereadingabookorsittinginthebackseat. [7]Althoughmotion
perceptionsensitivitytooffverticalaxisrotationincreasedimmediatelyafterreturnfromspaceflightcomparedto
prespaceflight,motionsicknesssusceptibilitydecreased.
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[8]Vectioncanbeinducedusingauditorycues,although

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prespaceflight,motionsicknesssusceptibilitydecreased. [8]Vectioncanbeinducedusingauditorycues,although
weakerthanvisuallyinducedvection,andunlikevisualmotion,auditorycuesformotionfailtoproducesickness. [9]
Theadditionofbodyloadswhilestandingcanmodulatebothposturalswayandmotionsicknessinducedbyvisual
motion. [10]Watching3Dstereoscopicvideofilmsprovokesmoremotionsicknessthan2Dvideos. [1113]By
contrast,anotherstudyinbothadultsandchildrenfoundonlylowlevelsofsickness,withnocleardifferences
between2Dversus3D,andconcludedthatuseofastereoscopic3Dsystemforupto2hourswasacceptablefor
mostusersregardlessofage. [14]
Withvehicularmovement,nauseogenicitypeaksatamechanicalfrequencyofaround0.2Hz,andthishasalso
beenshowntrueforexposuretooscillatingvisualfieldmotion. [15]Hypothesesforthefrequencydependenceof
nauseogenicityincludeaphaseerrorinsignallingmotionbetweencanalotolithandsomatosensorysystems,ora
frequencydependentphaseerrorbetweenthesensedverticalandthesubjectiveorexpectedvertical.Ithasalso
beenproposedthatazoneofperceptuomotorambiguityaround0.2Hztriggerssickness,becauseathigher
frequencies,imposedaccelerationsareusuallyinterpretedastranslationoftheselfthroughspace,whereasat
lowerfrequencies,imposedaccelerationsareusuallyinterpretedasatiltinthegravitoinertialforce(GIF)vector. [1]
Theregionof0.2Hzwouldbeacrossoverbetweenthesetwointerpretationsand,thus,afrequencyregionof
maximaluncertaintyconcerningtheappropriateframeofreferencefororientation.Arelated'ecological'explanation
hasbeenproposedthatthisfrequencytuningisrelatedtomechanicallimitationsonhumanbodymotion.This
proposesthatacauseofmotionsicknessmaybethedifficultyinselectingappropriatetacticstomaintainbody
stabilityatvehiclemotioncirca0.2Hz,betweenwholebodyGIFalignment,seenatlowerfrequencies,versus
lateropulsion,seenathigherfrequencies. [1]

MechanismsandTheories
Thegenerallyacceptedexplanationofthe'how'ofmotionsicknessisbasedonsomeformofsensoryconflictor
sensorymismatchbetweenactualversusexpectedinvariantpatternsofvestibular,visual,andkinaestheticinputsas
predictedbyan'internalmodel'. [1]OmanandCullen[16]haveidentifiedbrainstemandcerebellarneuronswhose
activitycorrespondstowhatmightbeexpectedofputative'sensoryconflict'neurons.Thepathwaysthatintegrate
vestibularandemeticgastrointestinalsignalsthatproducenauseaandvomitingarebeingelucidated. [17]Galvanic
vestibularstimulationinthecatproducespatternsofneuralactivationrevealedbycfoslabelling,someofwhich
correlatewithovertsignsofmotionsickness,othersofwhichshownosuchrelationshipbutmayrelatetocovert
affectiveaspectssuchasnausea. [18]Theonsetofvisuallyinducednauseainhumanswasstudiedwithfunctional
MRI.Increasedactivityprecedingnauseawasfoundintheamygdala,putamen,anddorsalpons/locuscoeruleus,
whereas,withonsetofnausea,activitywasobservedinabroadernetworkincludinginsular,anteriorcingulate,
orbitofrontal,somatosensory,andprefrontalcortices.Strongnauseawasassociatedwithsustainedanteriorinsula
andmidcingulateactivation,suggestingacloselinkagebetweenthesespecificregionsandnauseaperception. [19]
Bycontrastwiththe'how'ofmotionsickness,(i.e.,themechanisms),thereisavarietyofopinionconcerningthe
'why'.Themostpopulartheoryisthatmotionsicknesscouldhaveevolvedfromasystemdesignedtoprotectfrom
potentialneurotoxiningestionbyinducingvomitingwhenunexpectedcentralnervoussysteminputsaredetected
thatmightindicatepoisoning(the'toxindetector'hypothesis). [1]Thisevolutionarilyancientsystemisinadvertently
activatedbymotionthatcausesmismatch.Alternativehypothesesproposethatmotionsicknesscouldbetheresult
ofaberrantactivationofvestibularcardiovascularreflexesitmaybeanunfortunateconsequenceofthephysical
proximityofthemotiondetector(vestibular)andvomitingcircuitryinthebrainstemororiginatefromawarning
systemthathasevolvedtodiscourageselfexposuretocircumstancescausingdisorientationormotorinstability. [1]
Recentvariantsofthelastideapostulatethatmotionsicknessevolvedtodiscourageriskyactivityintheancestral
fishthatweresufferingvestibularmalfunction[20]orprotohominidswouldavoidlookingforfoodinswayingtrees
thatmightthreatensecurity,thustendingtosurvive. [21]

MarkersforIndividualSusceptibility
Monozygoticanddizygotictwinstudiesindicatehumanheritabilityofmotionsicknesshavingaconcordanceof70%
inchildhooddecreasingto55%inadulthood,probablybecauseofhabituationtodifferentialenvironmentaleffects.
[1]Inshrews,selectivebreedingforhighversuslowmotionsicknesssusceptibilitystrainshasshowntheimportance
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ofgeneticdeterminantsandthatthisextendstoanaesthesiainducedemesis,indicatingsomecommon
mechanisms. [22]Veryyoungchildrenarerelativelyimmunetomotionsickness,susceptibilitythenincreasingand
peakingataround9years. [23]Susceptibilitythenprogressivelydeclinesthroughadolescence,adulthood,andold
agealthoughtherearegreatindividualdifferences. [24]Femalestendtobemoresusceptiblethanmalesalthough
thishasasmallereffectsizethanage.Ataroundmenopause,femalesusceptibilityappearstoshowatransient
increaseversustheirageequivalentmalecontemporaries. [24]Thereasonforthisisunknownbuttheremaybe
contributionfromchangesinmigraineheadachestomore'vertigolike'symptomsthatpeakaroundmenopausein
women,aneffectthatisnotseeninmenoverthesameageperiod(ThomasLempert,Berlin,Germany,personal
communication).Personalitytraitssuchashigheranxietyonlyshowverysmallrelationshipswithmotionsickness
susceptibility. [1,24]
Somespecialgroupsareatlowerorhigherriskformotionsicknessasrevealedbystudiesusingbothvalidatedself
reportmotionsicknesssusceptibilityquestionnairesandnauseogenicoffverticalaxisrotation[24,25](Fig.1).
Comparedwithcontrols,patientswithbilateralvestibularloss(BVL)areeithercompletelyresistanttomotion
sicknessorhaveverylowsymptomscores.TheobservationthatsomepatientswithBVLcanstillexhibitsome
degreeofmotionsicknessisreminiscentofearlyreportsthatpseudocoriolismotioncouldelicitmotionsicknessin
somepatientswithBVL[1]perhapsindicatingthatothertypesofsensoryconflictwithoutvestibularinputare
sometimespossible.Unilateralvestibularloss(UVL)alsodecreasessusceptibilitybuttoalesserextentthanBVL
however,itshouldbenotedthatthesewere'compensated'patientswithUVL,thatis,whohaveadaptedtosensory
conflictcausedbythelossofvestibularfunctionononeside,sinceintheacutephase,theusualobservationisthat
patientswithUVLmaybemoresensitivetomotion.Patientswithvestibularneuritisandbenignparoxysmal
positionalvertigoshownooveralldifferenceinsusceptibilitycomparedwithcontrolsbutwithinthisbroadpicture
manyindividualshaveupordownregulatedtheirsensitivitytomotioninresponsetotheirdisease.Vestibular
migraineleadstogreatlyelevatedsusceptibilityandpatientsattendingmigraineclinics,butwithoutvestibular
migraine,haveequivalentelevationsofsusceptibility.Otherrecentstudieshaveshownthatvestibularsymptoms
includingmotionsicknessaregreaterinpatientsdiagnosedwithmigraineasopposedtotensiontypeheadache. [26]
Somepatientswithvestibulardiseasemayshowhighermotionsicknesssusceptibilitytoopticflow. [27]Atelephone
surveysuggestedthatpatientswithMeniere'sdiseasehadelevatedmotionsicknesssusceptibilitycomparedwith
controlsbutnotaselevatedaspatientswithvestibularmigraine. [28]

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Figure1.

MSsusceptibilityscoresareshownforpatientgroupstogetherwithsignificancesofcomparisonwithageequivalent
healthycontrols.The95%CIissmallerforcontrolsasaconsequenceoflargernumbers.MSsusceptibilityfor
Meniere'sdiseaseisnotshownbecauseofsmallnumbersbutisprobablysimilartomigrainegroups.BPPV,benign
paroxysmalpositionalvertigoBVL,bilateralvestibularlossCI,confidenceintervalMS,motionsicknessUVL,
unilateralvestibularloss[24,25].
Physiologicalmarkersforpredictingmotionsicknesssusceptibilityhaveprovedelusive.Althoughmotionsickness
producesprofoundautonomicchanges,baselineautonomiccharacteristicsareunlikelytoprovideusefulpredictors.
[29]Theevidencethatindividualdifferencesinposturalstabilityorperceptualstylearegoodpredictorsofmotion
sicknesssusceptibilityseemslimitedandcontradictory. [1,15,30]Shortertimeconstantsofthecentralvestibular
velocitystorehavebeensuggestedtocorrelatewithreducedmotionsicknesssusceptibility, [30]butthereis
sufficientcontraryevidencetoquestionifthisisareliablepredictorithasbeensuggestedthatitisnottheduration
ofthetimeconstantperse,buttheabilitytomodifyreadilythetimeconstantthatmaybeacandidatemarkerfor
successinmotionsicknesshabituation. [1]Inasimilarvein,reducedthresholdsforcervicalvestibularevoked
myogenicpotentialspredictfuturehabituationtoseasickness,thesuggestionbeingthatcervicalvestibularevoked
myogenicpotentialsatlowerthresholdsindicatesthattheindividualhasbroaderdynamicrangeinwhichthereflex
canrespondandadapttoawiderarrayofstimulusamplitudes. [31]Individualdifferencesinbrainwhitematter
structurerevealedbyfunctionalMRImayrelatetonauseasusceptibility. [32]PatientswithpersistentMalde
debarquementsyndromeexhibitimpairedposturalstabilitybutdonotexhibitdifferencesinintracorticalexcitability
comparedwithcontrols. [33]

BehaviouralTreatmentsandOtherCountermeasures
Habituationoffersthesurestcountermeasuretomotionsicknessbeingfreeofsideeffectsandsuperiortodrug
treatmentsbut,bydefinition,isalongtermapproach.
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[34]Optokinetictraininggaveimprovementsinreducing

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treatmentsbut,bydefinition,isalongtermapproach. [34]Optokinetictraininggaveimprovementsinreducing
seasicknessin71%ofthosetreatedversus12%ofcontrols. [35]Motionsicknessdecreaseswithrepeatedexposures
toahighGflightsimulator. [36]Morecomprehensivemotionsicknessdesensitizationprogrammesarehighly
effectiveandlongtermsuccessratesof85%havebeenachieved. [37]Visualvestibulosomatosensoryconflict
inducedbyvirtualrealityincreasesposturalinstabilityandmotionsicknesslikesymptoms.Subsequently,the
contributionofvisualinputsisreducedandsuchsensoryreweightingmayreflectadaptationtoreducetheimpactof
suchvisuallyprovocativeenvironments. [38]
Beingincontrol,asdriverorpilotratherthanbeingthepassenger,affordssomeprotectionagainstmotion
sickness. [1]Similarly,enhancedperceptionsofcontrolandpredictabilityappeartoreducemotioninducednausea.
[39]Exertionofcontrolreducedmotionsicknessinducedbyplayingvideogamesonatabletcomputer. [40]Lying
supine,oraligningthebodywithchangesintheGIFenvironment,oravoidingheadmovementscanreducemotion
sickness. [1]Consistentwiththelatterobservation,passiverestraintofhead,shoulders,hips,andkneesreduced
motionsicknessinducedbyplayingavideogamewhilestanding. [41]
Ithaslongbeenknownthatviewofastablehorizonreferencecanincreaseresistancetomotionsickness[1]but
provisionofanartificialhorizonfailedtohaveanyeffectonMaldedebarquement. [42]Standingwithawiderstance
widthandviewofthehorizonmayreduceposturalinstabilityandmotionsicknessatsea. [43]Stroboscopic
illuminationprotectedagainstmotionsicknessforbackseatmilitaryhelicopterpersonnel,perhapsbyreducing
retinalslip. [44]
Controlledregularbreathinghasbeenshowntoprovideincreasedmotiontolerance,andmayinvolveactivationof
theknowninhibitoryreflexbetweenrespirationandvomiting. [34]Acupressurebandsorelectroacupuncturehave
producedconflictingfindingsastotheireffectivenessagainstmotionsickness. [34]Althoughgalvanicvestibular
stimulation(GVS)cancausevertigoandnausea,theoppositeeffecthasbeenproposedthatitmayprovidea
novel,modulatorycountermeasureformotionsickness. [45]GVSsynchronouswiththevisualfieldmaynormalize
electrogastrographicandautonomicresponsesandreducemotionsicknessduringflightsimulation. [46]Repetitive
transcranialmagneticstimulationcanreducesymptomsforMaldedebarquementsyndrome. [47]
Providingpleasant(orunpleasant)scentshadnoeffectonmotionsicknesssensitivity,althoughmotionsickness
doesenhancesensitivitytoodors. [48]Listeningtopleasantmusiccanreducevisuallyinducedmotionsickness. [49]
Positiveverbalinstructionsandplacebocanpromotereductionsinmotionsickness. [50]

PharmacologicalCountermeasures
Drugscurrentlyusedagainstmotionsicknesswereidentifiedover40yearsago. [1]Theymaybedividedintothe
followingcategories:antimuscarinics(e.g.,scopolamine),H1antihistamines(e.g.,dimenhydrinate),and
sympathomimetics(e.g.,amphetamine).Combinationsforexamplescopolamineanddexamphetaminearehighly
effectivesincebothdrugscombinetheirdifferentantimotionsicknesspropertiesandtheirrespectivesideeffectsof
sedationandstimulationcanceleachotherout.However,suchcombinationsarelessusedbecauseoftheabuse
potentialofamphetamine.Themainpracticaladvanceshavebeenindrugdelivery,suchasthetransdermal
scopolaminepatchtoprovideextendedprotectionbutwithslowonset,andtheongoingdevelopmentofrapidacting
intranasalscopolamine.Otherclassesofpotentantiemeticsarenoteffectiveagainstmotionsickness,includingD2
dopaminereceptorantagonistsand5HT3antagonistsusedforsideeffectsofchemotherapy.Thisisprobably
becausetheirsitesofactionmaybeatvagalafferentreceptorsorthebrainstemchemoreceptortriggerzone,
whereasantimotionsicknessdrugsactelsewhere. [1]
Approachestodevelopingnewantimotionsicknessdrugsincludereexaminationof'old'drugssuchasphenytoin,
aswellasthedevelopmentofneweragentssuchasneurokinin1antagonists.Suchdrugsincludephenytoin,
betahistine,chlorpheniramine,cetirizine,fexofenadine,benzodiazepinesandbarbiturates,theantipsychotic
droperidol,corticosteroidssuchasdexamethasone,tamoxifen,opioidssuchastheopiatereceptoragonist
loperamide,neurokininNK 1receptorantagonists,vasopressinV 1areceptorantagonists,NmethylDaspartate
antagonists,3hydroxypyridinederivatives,5HT1areceptoragonistssuchastheantimigrainetriptanrizatriptan,and
selectivemuscarinicM3/M5receptorantagonistssuchaszamifenacinanddarifenacin. [1]Sofar,noneofthese
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drugshaveanyadvantageoverthosecurrentlyavailableformotionsickness.Thereasonsvaryandincludelackof
efficacyandcomplexpharmacokineticsor,inthosethatareeffective,unacceptablesideeffects.
Research,however,continuesondrugtreatment.Dexamethasonealleviatesmotionsicknessinratsinpartby
enhancingtheendocannabinoidsystem. [51]Cannabidiolicacidpreventsbothmotionortoxininducedvomitingin
shrewsandnauseainducedbehaviourinrats. [52]Therelativeeffectsonsemicircularcanalandotolithfunctionsby
variousantimotionsicknessdrugsincludingmeclizine,dimenhydrinatecombinedwithcinnarizine,andpromethazine
combinedwithDamphetaminemayprovideinsightsintotheirmechanismofaction. [53]Ginger(activeingredient
gingerol)mayhaveantiemeticeffectsformotionsicknessbutconflictingreportsindicatethatsucheffectsareweak.
[54]

Conclusion
Mainadvancesinrecentyearshavebeeninidentifyingbrainmechanismsandlocithatareassociatedwithmotion
sicknessand/ornausea.Similarly,althoughmotionsicknessispolysymptomatic,pharmacotherapeuticresearchhas
mainlytargetednauseaandvomiting,sofar,withlittleadvantageoverestablishedantimotionsicknessdrugs.
Futuredevelopmentofdrugswithhighlyselectiveaffinitiestoreceptorsubtypesrelevanttomotionsicknessmay
produceanantimotionsicknessdrugofhighefficacywithfewsideeffects.However,thepolysymptomaticnatureof
motionsicknesswithitshighinterindividualvariabilitymayprecludeasingledecisivetreatment.Inthisrespect
motionsicknessissimilartomigraine,withwhichmotionsicknessisfrequentlycompounded.

Sidebar
KeyPoints

Habituationremainsthemosteffectivetreatmentformotionsickness.
Therehavebeenveryfewpracticaladvancesinantimotionsicknessmedicationoverthestandard
treatmentssuchasscopolamineorantihistamines.
Visuallyinducedmotionsicknessthroughnewtechnologiessuchas3Ddisplayshasemergedasa
significantnewsourceofmotionsickness.
Therehasbeensignificantprogressinmappingneurophysiologicalpathwaysassociatedwithnauseaand
motionsickness,whichmayprovideamorerationalbasisforfuturetreatments.
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Acknowledgements
None.
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