Choroba lokomocyjna
Patofizjologia i mechanizm
Choroba lokomocyjna to zespół objawów wynikających z konfliktu sensorycznego pomiędzy układem przedsionkowym, wzrokowym i proprioceptywnym, prowadzący do aktywacji ośrodka wymiotnego w pniu mózgu. Patomechanizm opiera się na teorii niedopasowania neuronalnego, gdzie rozbieżność między rzeczywistymi a oczekiwanymi bodźcami sensorycznymi wywołuje objawy ze strony układu pokarmowego, ośrodkowego układu nerwowego i autonomicznego. Kluczową rolę odgrywają neurotransmitery: histamina (receptory H1), acetylocholina (receptory muskarynowe) oraz noradrenalina. Mechanizm przechowywania prędkości (velocity storage mechanism, VSM) w ośrodkowym układzie przedsionkowym jest istotny dla podatności na chorobę, a jego parametry, takie jak stała czasowa VSM i maksymalna prędkość wolnej fazy oczopląsu (SPV), korelują z nasilenie objawów. Podatność jest indywidualna i zależy od czynników genetycznych, płci (większa u kobiet), wieku (szczyt w wieku 9-10 lat), migreny oraz ciąży.
Mechanizm choroby lokomocyjnej
Choroba lokomocyjna (ang. motion sickness) to zespół objawów występujących w odpowiedzi na rzeczywisty lub postrzegany ruch. Charakteryzuje się objawami ze strony układu pokarmowego, ośrodkowego układu nerwowego oraz objawami autonomicznymi, które występują z różnym nasileniem u poszczególnych osób. Podatność na chorobę lokomocyjną jest zróżnicowana indywidualnie – niektórzy cierpią przy minimalnej prowokacji, podczas gdy u innych trudno wywołać objawy.12
Teoria konfliktu sensorycznego
Najszerzej akceptowaną teorią wyjaśniającą patomechanizm choroby lokomocyjnej jest teoria konfliktu sensorycznego (sensory conflict theory) lub inaczej teoria niedopasowania neuronalnego (neural mismatch theory). Teoria ta tłumaczy chorobę lokomocyjną jako rezultat konfliktu pomiędzy rzeczywistymi a oczekiwanymi bodźcami sensorycznymi pochodzącymi z różnych układów.34
Konflikt sensoryczny pojawia się, gdy występuje rozbieżność między informacjami docierającymi do mózgu z trzech głównych systemów sensorycznych:56
- Układu przedsionkowego (błędnika) w uchu wewnętrznym, który wykrywa ruch i pozycję głowy
- Układu wzrokowego, który dostarcza informacji o otoczeniu i ruchu
- Układu proprioceptywnego (czucia głębokiego), który informuje o pozycji ciała i ruchu poszczególnych części ciała
Do konfliktu sensorycznego dochodzi najczęściej, gdy informacje z jednego z tych źródeł wykrywania ruchu nie są zgodne z pozostałymi. W większości przypadków to dane wzrokowe nie pokrywają się z danymi przedsionkowymi i proprioceptywnymi. Teoria konfliktu sensorycznego (neural mismatch) wyjaśnia te zjawiska rozbieżnością między trwającym doświadczeniem sensorycznym a długoterminową pamięcią dotyczącą oczekiwanych wzorców bodźców.910
Mechanizm neurofizjologiczny
Bodźce aferentne z narządu przedsionkowego docierają do jąder przedsionkowych w pniu mózgu, które jednocześnie otrzymują sygnały z układu wzrokowego i proprioceptywnego. Następnie projekcje eferentne docierają do kory skroniowo-ciemieniowej poprzez tylno-boczny wzgórze, co wyzwala reakcje autonomiczne i aktywuje ośrodek wymiotny.31
Mechanizm przetwarzania ruchu angażuje:211
- Kanały półkoliste – odpowiedzialne za wykrywanie ruchu kątowego (obrotowego)
- Narządy otolitowe (woreczek i łagiewka) – wykrywające przyspieszenie liniowe i siłę grawitacji
Kiedy występuje niezgodność między rzeczywistymi a oczekiwanymi wzorcami bodźców przedsionkowych, wzrokowych i kinestetycznych, uruchamia to kaskadę objawów choroby lokomocyjnej. Badania wykazały, że choroba lokomocyjna występuje tylko wtedy, gdy VIII nerw czaszkowy (przedsionkowo-ślimakowy) i móżdżkowe drogi przedsionkowe są nienaruszone. Osoby pozbawione funkcjonalnego układu przedsionkowo-ślimakowego są odporne na chorobę lokomocyjną.1213
Rola neuroprzekaźników
W rozwoju choroby lokomocyjnej biorą udział złożone struktury ośrodkowego układu nerwowego i regiony jądrowe z udziałem wielu neuroprzekaźników. Kluczową rolę odgrywają trzy neurotransmitery:148
- Histamina – receptory histaminowe H1 uczestniczą w rozwoju objawów choroby lokomocyjnej, w tym wymiotów. Sygnał niedopasowania neuronalnego aktywuje neurony histaminergiczne w podwzgórzu, a zstępujące impulsy histaminergiczne stymulują receptory H1 w ośrodku wymiotnym pnia mózgu
- Acetylocholina – skuteczność skopolaminy, antagonisty receptorów muskarynowych acetylocholiny, potwierdza znaczenie acetylocholiny w patogenezie choroby lokomocyjnej. Model cholinergiczny pamięci asocjacyjnej sugeruje, że skopolamina zapobiega chorobie lokomocyjnej poprzez zmniejszenie sygnału niedopasowania neuronalnego i ułatwienie procesów adaptacji/habituacji
- Noradrenalina – układ neuronów noradrenergicznych w miejscu sinawym jest hamowany przez sygnał niedopasowania neuronalnego. Amfetamina przeciwdziała wywołanemu przez niedopasowanie zahamowaniu transmisji noradrenergicznej, co zapobiega chorobie lokomocyjnej
Typy konfliktów sensorycznych
Choroba lokomocyjna może być podzielona na trzy kategorie w zależności od rodzaju konfliktu sensorycznego:17
- Choroba lokomocyjna wywołana ruchem, który jest odczuwany, ale nie widziany – np. choroba morska w kabinie statku bez widoku na horyzont (konflikt przedsionkowo-wzrokowy)
- Choroba lokomocyjna wywołana ruchem, który jest widziany, ale nie odczuwany – np. choroba symulatorowa lub choroba lokomocyjna w przestrzeni kosmicznej
- Choroba lokomocyjna wywołana, gdy oba systemy wykrywają ruch, ale nie odpowiadają sobie wzajemnie – np. podczas korzystania z rzeczywistości wirtualnej, gdy bodźce wzrokowe i przedsionkowe są sprzeczne
Inny mechanizm konfliktu może obejmować niezgodność między ruchem kątowym a przyspieszeniem liniowym lub grawitacją, jak ma to miejsce w środowisku zerowej grawitacji podczas obrotów (przyspieszenie kątowe). Również wzorzec ruchu, który różni się od oczekiwanego wzorca (np. w środowisku zerowej grawitacji, unoszenie się zamiast spadania) może być czynnikiem wyzwalającym.12
Teoria ewolucyjna i inne teorie
Poza teorią konfliktu sensorycznego istnieją również inne hipotezy wyjaśniające mechanizm choroby lokomocyjnej:1019
- Teoria ewolucyjna – sugeruje, że choroba lokomocyjna mogła rozwinąć się jako mechanizm obronny przeciwko neurotoksynom. Obszar postrema w mózgu odpowiedzialny jest za wywoływanie wymiotów, gdy wykrywane są toksyny, oraz za rozwiązywanie konfliktów między widzeniem a równowagą. Gdy występuje niezgodność między bodźcami sensorycznymi, mózg może błędnie interpretować to jako halucynacje wywołane przez toksyny, co prowadzi do wymiotów w celu usunięcia domniemanej toksyny
- Hipoteza oczopląsu – oparta na stymulacji nerwu błędnego wynikającej z rozciągania lub pociągania mięśni pozagałkowych występujących jednocześnie z ruchami oczu wywołanymi stymulacją przedsionkową
- Teoria niestabilności postawy – głosi, że długotrwałe ruchy powodują niestabilność postawy, co prowadzi do choroby lokomocyjnej
- Teoria asymetrii narządów otolitowych – zakłada, że główną przyczyną choroby lokomocyjnej jest nierównowaga w sygnałach przedsionkowych faworyzująca kanały półkoliste (nauzogenne) względem narządów otolitowych (anty-nauzogenne)
Neuroanatomia choroby lokomocyjnej
Choroba lokomocyjna angażuje specyficzne struktury mózgu i szlaki neuronalne, które są odpowiedzialne za przetwarzanie sygnałów sensorycznych i wywoływanie objawów.7
Główne struktury zaangażowane w chorobę lokomocyjną
Komponenty ośrodkowego układu nerwowego, które pośredniczą w chorobie lokomocyjnej obejmują:7
- Układ przedsionkowy – główny system sensoryczny zaangażowany w patogenezę
- Jądra pnia mózgu – przetwarzają sygnały z układu przedsionkowego
- Podwzgórze – zaangażowane w autonomiczne aspekty choroby lokomocyjnej
- Moduł i języczek móżdżku – uczestniczą w integracji sygnałów przedsionkowych
- Drogi wymiotne, w tym:
- Chemoreceptorowa strefa wyzwalająca w obszarze postrema
- Ośrodek wymiotny
- Drogi eferentne wymiotne
Mechanizm przechowywania prędkości
Mechanizm przechowywania prędkości (velocity storage mechanism, VSM) jest kluczowym elementem w patogenezie choroby lokomocyjnej. Jest to integrator neuronalny zlokalizowany w ośrodkowym układzie przedsionkowym, którego główną funkcją jest przedłużanie stałej czasowej wolnej fazy prędkości gałki ocznej (SPEV TC) i postrzeganego czasu trwania obrotu (PRD) w odniesieniu do ruchu. Ma to na celu kompensację niedostatecznej wrażliwości układu przedsionkowego w wykrywaniu ruchów o niskiej częstotliwości.22
Badania wykazały istotne korelacje między stałą czasową VSM a podatnością na chorobę lokomocyjną. Efektywność VSM w modulowaniu SPEV TC i PRD prawdopodobnie determinuje skłonność do występowania konfliktów sensorycznych. Zdolność do łatwej modyfikacji stałej czasowej przechowywania prędkości przedsionkowej jest potencjalnym markerem skutecznej habituacji choroby lokomocyjnej.2322
Neurobiologia odpowiedzi autonomicznej
Szlaki pośredniczące w zaangażowaniu autonomicznego układu nerwowego w chorobie lokomocyjnej nie zostały w pełni wyjaśnione. Badania sugerują, że sygnał niedopasowania neuronalnego aktywuje neurony histaminergiczne w podwzgórzu, a impuls zstępujący stymuluje receptory H1 w ośrodku wymiotnym pnia mózgu.1413
Ostatnie badania wykazały, że receptory neurokininowe 1 dla substancji P (NK1) w ośrodku wymiotnym odgrywają główną rolę w chorobie lokomocyjnej i są ważniejsze niż receptory w chemoreceptorowej strefie wyzwalającej. Blokowanie tych receptorów jest skuteczniejsze niż hamowanie chemoreceptorowej strefy wyzwalającej.24
Badania na myszach zidentyfikowały neurony glutaminergiczne w jądrach przedsionkowych pośredniczące w odpowiedzi na hipergrawację i rotację. Jedna z subpopulacji tych neuronów wyraża cholecystokininę (CCK), peptyd związany z nudnościami i zmniejszeniem przyjmowania pokarmu. Optogenetyczna stymulacja tych neuronów odtwarza wiele objawów choroby lokomocyjnej.25
Czynniki wpływające na podatność na chorobę lokomocyjną
Podatność na chorobę lokomocyjną jest zróżnicowana indywidualnie i zależy od wielu czynników.26
Czynniki genetyczne
Badania sugerują, że podatność na chorobę lokomocyjną ma częściowo podłoże genetyczne. Jedno z badań porównało warianty genetyczne u dużej liczby osób z podatnością i bez podatności na chorobę lokomocyjną. Badacze zidentyfikowali powszechne warianty genetyczne w pobliżu 35 genów, które mogą być związane z tym schorzeniem.2728
Obiecującym kierunkiem badań jest ostatnio zgłoszony związek polimorfizmu genetycznego receptora α2-adrenergicznego ze zwiększoną autonomiczną odpowiedzią na stres i chorobę lokomocyjną.29
Predyspozycje fizjologiczne
Istnieje kilka czynników fizjologicznych zwiększających podatność na chorobę lokomocyjną:3031
- Płeć – kobiety są bardziej podatne niż mężczyźni, częściowo z powodu wpływu hormonów. Estrogen, główny żeński hormon płciowy, może przyczyniać się do objawów nudności i zawrotów głowy
- Wiek – dzieci w wieku 2-12 lat są szczególnie podatne, z największą częstością występowania około 9-10 roku życia
- Migrena – osoby cierpiące na migrenę mają około 5-krotnie większą częstość występowania choroby lokomocyjnej niż osoby bez migreny, z około 50% częstością występowania
- Ciąża – badania sugerują, że istnieje wspólny mechanizm przedsionkowy między chorobą lokomocyjną a wymiotami i nudnościami podczas ciąży
Czynniki związane z charakterystyką ruchu
Charakterystyka mechanicznego ruchu pojazdów, która prowokuje chorobę lokomocyjną, została precyzyjnie określona:3233
- Częstotliwość ruchu – ruchy o niskiej częstotliwości (0,2-0,4 Hz) są szczególnie nauzogenne
- Rodzaj ruchu – ruchy obrotowe, pionowe i o niskiej częstotliwości wywołują więcej objawów niż ruchy liniowe, poziome i o wysokiej częstotliwości
- Przewidywalność ruchu – badania wykazały, że osoby, które nie wiedzą, kiedy i jak nastąpi ruch, mogą mieć większe trudności
- Nagłe, szarpane ruchy – są bardziej nauzogenne niż wolniejsze, płynne ruchy, ponieważ bardziej zaburzają równowagę płynów
Adaptacja i habituacja
Jeśli osoba jest narażona na ruch przez dłuższy czas (na przykład podczas długiej podróży morskiej) lub ma powtarzające się ekspozycje, jej mózg może się z czasem dostosować do stałego ruchu i może nie doświadczać już choroby lokomocyjnej. Ten proces adaptacji i habituacji jest ważnym mechanizmem obronnym.1835
Z tej perspektywy behawioralne środki zaradcze, takie jak uzyskanie widoku horyzontu i unikanie zadań wzrokowych, opierają się na zmniejszeniu niedopasowań wzrokowo-przedsionkowych, podczas gdy habituacja, desensytyzacja nabyta w wyniku wielokrotnych ekspozycji, aktualizuje „model wewnętrzny” w celu zaakceptowania nowych wzorców relacji sensorycznych.4
Biomarkery i obiektywne wskaźniki choroby lokomocyjnej
Badania koncentrują się na identyfikacji obiektywnych biomarkerów podatności na chorobę lokomocyjną, które mogłyby pomóc w lepszym zrozumieniu jej mechanizmów i opracowaniu bardziej ukierunkowanych metod prewencji i leczenia.36
Parametry odruchu przedsionkowo-ocznego
Badania wykazały, że następujące parametry związane z odruchem przedsionkowo-ocznym (vestibulo-ocular reflex, VOR) mogą służyć jako obiektywne wskaźniki podatności na chorobę lokomocyjną:3738
- Maksymalna prędkość wolnej fazy oczopląsu (SPV) – obiektywny pomiar odpowiedzi układu przedsionkowego na przyspieszenie
- Stała czasowa kopułki – parametr wewnętrzny układu przedsionkowego, odzwierciedlający czas reakcji receptorów kopułki i wskazujący na szybkość, z jaką układ przedsionkowy postrzega i przywraca równowagę
- Stała czasowa przechowywania prędkości – reprezentuje czas, przez który sygnały przedsionkowe są przechowywane i przedłużane w pniu mózgu
- Czas trwania oczopląsu – koreluje z podatnością na chorobę lokomocyjną
Asymetria przedsionkowa
Badania z wykorzystaniem przedsionkowych miogennych potencjałów wywołanych (VEMP) wykazały, że u osób podatnych na chorobę lokomocyjną występuje zmiana w międzyusznym współczynniku asymetrii (IAAR) zarówno w przypadku szyjnych VEMP (cVEMP), jak i ocznych VEMP (oVEMP). Wskazuje to na możliwą zmienność w asymetrii funkcjonalnej narządów otolitowych.3940
Teoria opracowana przez kompleks przemysłowo-wojskowo-kosmiczny sugeruje, że choroba lokomocyjna zależy od asymetrii masy otokonii. Ta asymetria może prowadzić do konfliktów w sygnałach przedsionkowych i zwiększać podatność na chorobę lokomocyjną.21
Szlaki molekularne
Badania z wykorzystaniem fosfoprotomiki zidentyfikowały szlaki molekularne zaangażowane w mechanizm choroby lokomocyjnej i działanie substancji przeciwdziałających jej objawom. Białka różnicowo fosforylowane wpływają na gęstość postsynaptyczną, synapsy glutaminergiczne i inne miejsca oraz są zaangażowane w różne szlaki chorób neurodegeneracyjnych, szlaki endocytozy, szlaki sygnalizacyjne cAMP i szlaki sygnalizacyjne MAPK.41
Badania molekularne sugerują, że substancje przeciwdziałające chorobie lokomocyjnej, takie jak izoramnetyna, najpierw regulują synapsy glutaminergiczne, a następnie zmniejszają pobudliwość jądra przedsionkowego poprzez hamowanie szlaku sygnalizacyjnego NMDAR1/CaMKII/CREB, ostatecznie łagodząc serię objawów choroby lokomocyjnej.41
Implikacje kliniczne i terapeutyczne
Zrozumienie patomechanizmu choroby lokomocyjnej ma istotne implikacje dla jej zapobiegania i leczenia.3
Mechanizm działania leków
Leki stosowane w zapobieganiu i leczeniu choroby lokomocyjnej działają poprzez wpływ na różne neuroprzekaźniki zaangażowane w jej patogenezę:4243
- Leki przeciwhistaminowe (np. dimenhydrynat, znany jako Dramamine) – blokują receptory histaminowe H1 w mózgu, zmniejszając aktywność histaminy w układzie przedsionkowym, co zmniejsza percepcję ruchu przez mózg i łagodzi związane z nim objawy
- Skopolamina – antagonista receptorów muskarynowych acetylocholiny, zakłóca transmisję sygnałów, które wyzwalają nudności i wymioty w pniu mózgu i układzie przedsionkowym
- Amfetamina – mechanizm przeciwdziałania chorobie lokomocyjnej nie jest do końca jasny, ale prawdopodobnie związany jest ze zwiększeniem stężenia dopaminy w ośrodkowym układzie nerwowym
Blokada etapów rozwoju choroby lokomocyjnej
Rozwój choroby lokomocyjnej obejmuje trzy etapy: przetwarzanie sensoryczne, generowanie sygnału niedopasowania neuronalnego i połączenie wymiotne. Blokada któregokolwiek z tych etapów może być wykorzystana do zapobiegania lub leczenia choroby lokomocyjnej.16
Badania nad nowymi klasami środków farmakologicznych, takimi jak antagoniści N-metylo-D-asparaginianu (NMDA) i agoniści receptorów 5HT1a wykazują obiecujące rezultaty u zwierząt, ale oczekują na badania u ludzi.23
Behawioralne środki zaradcze
Behawioralne autogenne środki zaradcze przeciwko rozwojowi choroby lokomocyjnej, takie jak kontrolowane oddychanie, które można łatwo wdrożyć, wykazują znaczące łagodzące działanie na nudności i są wartościowe przy krótkotrwałych, umiarkowanych ekspozycjach.23
Z perspektywy teoretycznej, zachowania takie jak uzyskanie widoku horyzontu i unikanie zadań wzrokowych opierają się na zmniejszeniu niedopasowań wzrokowo-przedsionkowych, podczas gdy habituacja aktualizuje „model wewnętrzny” w celu zaakceptowania nowych wzorców relacji sensorycznych.4
Nowe kierunki badań
Ostatnie badania koncentrują się na dokładniejszym zrozumieniu mechanizmów neuronalnych choroby lokomocyjnej i opracowaniu bardziej skutecznych, opartych na nauce metod zapobiegania i leczenia:46
- Odkrycie podklasy neuronów w jądrach przedsionkowych i głębokich jądrach móżdżku, które reagują preferencyjnie na pasywne ruchy głowy
- Identyfikacja neuronów konfliktu sensorycznego przedsionkowego i ich potencjalnej roli w kontroli postawy i chorobie lokomocyjnej
- Badanie nieskompensowanego komponentu (egzaferencji) wynikającego z biernego ruchu, który normalnie pomaga kompensować nieoczekiwane zaburzenia postawy
- Określenie mechanizmu, za pomocą którego utrzymująca się aktywność tych neuronów lub ich celów stymuluje pobliskie ośrodki wymiotne pnia mózgu
Dokładniejsza charakterystyka tych mechanizmów i ich potencjalnej roli w chorobie lokomocyjnej może prowadzić do skuteczniejszego, naukowo uzasadnionego zapobiegania i leczenia choroby lokomocyjnej.46
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Materiały źródłowe
- #1 Motion Sickness (Nursing) Articlehttps://www.statpearls.com/articlelibrary/nursingarticle/25279
Motion sickness is a common and complex syndrome that occurs in response to the real or perceived motion. Its presentation can be diverse, including the gastrointestinal, central nervous system, and autonomic symptoms. There is considerable individual variability in motion sickness susceptibility, as some individuals may suffer from minimal provocation and in others, it may be very difficult to elicit symptoms. […] Motion sickness occurs when there is a mismatch between actual versus expected sensory inputs. Although the exact neurobiological mechanism is unclear, many countermeasures have been developed to prevent and alleviate this condition. […] The sensory conflict and neural mismatch theory is the most widely accepted theory for explaining motion sickness. It describes the conflict that occurs between the visual, vestibular and somatosensory systems resulting from real or virtual motion. Afferents from the vestibular apparatus arrive at the vestibular nuclei of the brainstem, which also receives inputs from the visual and proprioceptive systems. Efferent projections then reach the temporoparietal cortex via the posterolateral thalamus, triggering autonomic reactions and the vomiting center. When there is a discrepancy between actual versus expected patterns of vestibular, visual, and kinesthetic inputs, it initiates the cascade of motion sickness symptoms.
- #2 Motion sickness – UpToDatehttps://www.uptodate.com/contents/motion-sickness
Motion sickness is a syndrome that occurs in response to real or perceived motion, which can include gastrointestinal, central nervous system, and autonomic symptoms. […] Motion sickness is considered a physiologic form of dizziness, since it is not indicative of a disease process and can be induced in nearly all normal human subjects. […] This topic discusses the pathogenesis, epidemiology, clinical presentation, diagnosis, prevention, and treatment of motion sickness. […] PATHOGENESIS […] The brain receives numerous inputs that are used to estimate the motion and spatial orientation of the head. The principal sensory signals that contribute to this process are vestibular cues from the labyrinth, visual information, and somatosensory cues. Afferent information derived from the labyrinth encodes both angular motion (sensed by the semicircular canals) and linear acceleration and gravitational force (sensed by the otolith organs).
- #3 Motion Sickness – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK539706/
Motion sickness occurs when there is a mismatch between actual versus expected sensory inputs. […] Although the exact neurobiological mechanism is unclear, many countermeasures have been developed to prevent and alleviate this condition. […] The sensory conflict and neural mismatch theory is the most widely accepted theory for explaining motion sickness. […] It describes the conflict that occurs between the visual, vestibular and somatosensory systems resulting from real or virtual motion. […] Afferents from the vestibular apparatus arrive at the vestibular nuclei of the brainstem, which also receives inputs from the visual and proprioceptive systems. […] Efferent projections then reach the temporoparietal cortex via the posterolateral thalamus, triggering autonomic reactions and the vomiting center. […] When there is a discrepancy between actual versus expected patterns of vestibular, visual, and kinesthetic inputs, it initiates the cascade of motion sickness symptoms. […] Motion sickness tends to occur when the input from the proprioceptive, vestibular and visual are mixed or in conflict.
- #4 Motion Sickness | Yellow Book | CDChttps://www.cdc.gov/yellow-book/hcp/travel-air-sea/motion-sickness.html
The most widely accepted explanation for motion sickness is the sensory conflict or neural mismatch theory. The sensory conflict or mismatch is between incoming patterns of vestibular, visual, and kinesthetic (perception of motion) inputs versus the expected patterns as predicted by an „internal model.” […] If inconsistencies in the patterns are detected, centers in the brain are activated that mediate the signs and symptoms of motion sickness. […] From this perspective, behavioral countermeasures, such as obtaining a horizon view and avoiding visual tasks, are based on reducing visual-vestibular mismatches, whereas habituation, desensitization acquired over multiple exposures, updates the „internal model” to accept new patterns of sensory relationships.
- #5 The Neurophysiology and Treatment of Motion Sicknesshttps://pmc.ncbi.nlm.nih.gov/articles/PMC6241144/
Individuals vary in their susceptibility to autonomic symptoms, ranging from fatigue to massive vomiting, induced by passive movement at relatively low frequencies (0.2 to 0.4 Hz) in situations without any visual reference to the horizontal plane. […] The various types of motion sickness are adequately explained by the intersensory conflict model, incorporating the vestibular, visual, and proprioceptive systems and extended to include consideration of postural instability and asymmetry of the otolith organs. […] The term motion sickness (also called kinetosis) describes a set of symptoms that occur in association with motion of a person or his or her surroundings, triggering a stress reaction that results in autonomic symptoms. […] The sensory conflict model is widely accepted as explaining the pathogenesis of motion sickness. Incongruent sensory information results in conflict between the vestibular, optic, and proprioceptive systems.
- #6 Motion sickness | MedLink Neurologyhttps://www.medlink.com/articles/motion-sickness
Motion sickness is a normal response to complex motion stimuli of sufficient intensity and duration that is thought to be due to a mismatch of signals from vestibular, visual, and proprioceptive receptors as integrated in the brainstem and cerebellum. […] Motion sickness is thought to be due to a mismatch of signals from vestibular, visual, and proprioceptive receptors as integrated in the brainstem and cerebellum. […] The pathogenesis of motion sickness remains incompletely understood, and several different pathogenetic models have been proposed. […] Motion sickness results from a mismatch of signals from vestibular, visual, and proprioceptive receptors as integrated in the brainstem and cerebellum. […] Sensory conflict is important in the development of motion sickness and, more specifically, a conflict between incoming sensory information from position and motion senses and what is expected from prior experience.
- #7 Motion Sickness – Injuries; Poisoning – Merck Manual Professional Editionhttps://www.merckmanuals.com/professional/injuries-poisoning/motion-sickness/motion-sickness
Motion sickness is a symptom complex that usually includes nausea, often accompanied by vague abdominal discomfort, vomiting, dizziness, pallor, diaphoresis, and related symptoms. It is induced by specific forms of motion, particularly repetitive angular and linear acceleration and deceleration, or as a result of conflicting vestibular, visual, and proprioceptive inputs. […] Excessive stimulation of the vestibular apparatus by motion is the primary cause. This stimulation may be due to actual physical motion or perceived motion. […] Vestibular stimulation can result from angular motion (sensed by the semicircular canals) or linear acceleration or gravity (sensed by the otolithic organs [utricle and saccule]). Central nervous system (CNS) components that mediate motion sickness include the vestibular system and brainstem nuclei, the hypothalamus, the nodulus and uvula of the cerebellum, and emetic pathways (eg, medullary chemoreceptor trigger zone, vomiting center, and emetic efferents).
- #8 The Neurophysiology and Treatment of Motion Sickness (12.10.2018)https://di.aerzteblatt.de/int/archive/article/201532
Individuals vary in their susceptibility to autonomic symptoms, ranging from fatigue to massive vomiting, induced by passive movement at relatively low frequencies (0.2 to 0.4 Hz) in situations without any visual reference to the horizontal plane. […] The various types of motion sickness are adequately explained by the intersensory conflict model, incorporating the vestibular, visual, and proprioceptive systems and extended to include consideration of postural instability and asymmetry of the otolith organs. […] The sensory conflict model is widely accepted as explaining the pathogenesis of motion sickness. Incongruent sensory information results in conflict between the vestibular, optic, and proprioceptive systems. […] The development of symptoms involves complex central brain structures and nuclear regions with many neurotransmitters participating, including histamine.
- #9 Understanding Motion Sicknesshttps://www.uspharmacist.com/article/understanding-motion-sickness
Humans detect motion through three sources of input to the nervous system. One is the vestibular system. Movement is detected in this system by stimulation of hair cells in the semicircular canals and in the maculae of the utricle and sacculus. Movement is registered in all three dimensions when endolymph moves through the semicircular canals or when small particles known as otoliths impact on hair cells. […] Motion sickness may occur when one of the sources of motion detection does not agree with the other two. In the majority of cases, visual input does not coincide with vestibular/proprioceptive input. The theory that encompasses and explains these concepts are known as the „neural mismatch” or „sensory conflict” theory. […] The hypothesized etiology of motion sickness explains why patients with a bilateral loss of the vestibular system are seemingly immune to the condition in normal circumstances. On the other hand, patients with vertigo, Meniere’s disease, or migraine are more prone to motion sickness.
- #10 Motion sickness – Wikipediahttps://en.wikipedia.org/wiki/Motion_sickness
A variation of the sensory conflict theory is known as neural mismatch, implying a mismatch occurring between ongoing sensory experience and long-term memory rather than between components of the vestibular and visual systems. […] It has also been proposed that motion sickness could function as a defense mechanism against neurotoxins. […] Yet another theory, known as the nystagmus hypothesis, has been proposed based on stimulation of the vagus nerve resulting from the stretching or traction of extra-ocular muscles co-occurring with eye movements caused by vestibular stimulation. […] A recent theory argues that the main reason motion sickness occurs is due to an imbalance in vestibular outputs favoring the semicircular canals (nauseogenic) vs. otolith organs (anti-nauseogenic).
- #11 Motion sickness – UpToDatehttps://www.uptodate.com/contents/motion-sickness/print
Motion sickness is a syndrome that occurs in response to real or perceived motion, which can include gastrointestinal, central nervous system, and autonomic symptoms. […] Motion sickness is considered a physiologic form of dizziness, since it is not indicative of a disease process and can be induced in nearly all normal human subjects. […] This topic discusses the pathogenesis, epidemiology, clinical presentation, diagnosis, prevention, and treatment of motion sickness. […] The brain receives numerous inputs that are used to estimate the motion and spatial orientation of the head. The principal sensory signals that contribute to this process are vestibular cues from the labyrinth, visual information, and somatosensory cues. Afferent information derived from the labyrinth encodes both angular motion (sensed by the semicircular canals) and linear acceleration and gravitational force (sensed by the otolith organs).
- #12 Motion Sickness – Injuries; Poisoning – Merck Manual Professional Editionhttps://www.merckmanuals.com/professional/injuries-poisoning/motion-sickness/motion-sickness
The exact pathophysiology is undefined, but motion sickness occurs only when the 8th cranial nerve and cerebellar vestibular tracts are intact; those lacking a functional vestibulo-cochlear system are immune to motion sickness. […] The trigger may involve conflicting vestibular, visual, and proprioceptive inputs. For example, visual input that indicates being stationary may conflict with the sensation of movement (eg, looking at an apparently unmoving ship cabin wall while sensing the ship rolling). Alternatively, moving visual input may conflict with lack of perception of movement, eg, viewing a rapidly moving slide with a microscope or watching a virtual reality game while sitting still (also termed pseudomotion sickness or pseudokinetosis, given the lack of actual acceleration). […] Another possible trigger is a conflict in inputs between angular motion and linear acceleration or gravity, as can occur in a zero-gravity environment when turning (angular acceleration). Also, a pattern of motion that differs from the expected pattern (eg, in a zero-gravity environment, floating instead of falling) can be a trigger. […] In space adaptation syndrome (motion sickness during space travel), weightlessness (zero gravity) is an etiologic factor. This syndrome reduces the work efficiency of astronauts during the first few days of space flight, but adaptation occurs over several days.
- #13 Motion sickness | MedLink Neurologyhttps://www.medlink.com/articles/motion-sickness
Vestibular inputs are felt to be fundamental as deaf-mute individuals with bilateral vestibular hypofunction do not become seasick. […] The pathways mediating autonomic nervous system involvement in motion sickness have been incompletely elucidated. […] The mechanism proposed by Reason and Brand for adaptation to a provocative stimulus (sensory conflict) was detailed in their neural mismatch model using motor control modeling concepts from Von Holst. […] There has been widespread, though not universal, acceptance of this sensory conflict theory, and available experimental data support the general framework and the specific proposition that sensory conflict causes motion sickness.
- #14 Neural mechanisms of motion sicknesshttp://medical.med.tokushima-u.ac.jp/jmi/vol48/text/v48_n1-2_p044.html
Three kinds of neurotransmitters: histamine, acetylcholine and noradrenaline, play important roles in the neural processes of motion sickness, because antihistamines, scopolamine and amphetamine are effective in preventing motion sickness. […] Histamine H1-receptors are involved in the development of the symptoms and signs of motion sickness, including emesis. […] On provocative motion stimuli, a neural mismatch signal activates the histaminergic neuron system in the hypothalamus, and the histaminergic descending impulse stimulates H1-receptors in the emetic center of the brainstem. […] The neural mismatch hypothesis in the development of motion sickness is the most plausible. […] The essential components of the neural mismatch model of motion sickness are illustrated in Fig. 1. […] If there is a discrepancy between the expected patterns and current inputs, the mismatch signal is generated, triggering the neural mechanisms mediating autonomic nervous symptoms.
- #15 Neural mechanisms of motion sicknesshttp://medical.med.tokushima-u.ac.jp/jmi/vol48/text/v48_n1-2_p044.html
These findings that FMH prevents motion sickness suggest that the histaminergic neuron system is specifically involved in the development of motion sickness. […] The histaminergic input to the emetic center through H1-receptors is independent of dopamine D2-receptors in the chemoreceptor trigger zone in the area postrema and serotonin 5HT3-receptors in the visceral afferent, which are also involved in the emetic reflex. […] The efficacy of scopolamine, an antagonist of acetylcholine muscarinic receptors, has been shown to prevent motion sickness in humans. […] Accordingly, acetylcholine has been considered to be one of the most important neurotransmitters involved in motion sickness. […] The cholinergic model of associative memory suggests that scopolamine prevents motion sickness by reducing the neural mismatch signal and by facilitating the adaptation/habituation processes.
- #16 Neural mechanisms of motion sicknesshttp://medical.med.tokushima-u.ac.jp/jmi/vol48/text/v48_n1-2_p044.html
Amphetamine antagonizes mismatch-induced suppression of noradrenergic neural transmission, resulting in preventing motion sickness. […] The noradrenergic neuron system in the locus coeruleus is suppressed by the neural mismatch signal. […] The findings suggest transmission from cholinergic to histaminergic processes in the development of motion sickness. […] Therefore, it is suggested that the neural mismatch signal activates the VML, leading to inhibition of noradrenaline-containing LC neurons via GABAA-receptors. […] The suppression of the noradrenergic neuron system during vestibular stimulation may account for the sopite syndrome. […] The development of motion sickness involves the three steps of sensory processing, generation of the neural mismatch signal, and the emetic linkage. […] Blockade of any step can be used to prevent or treat motion sickness.
- #17 Motion sickness – Wikipediahttps://en.wikipedia.org/wiki/Motion_sickness
Motion sickness occurs due to a difference between actual and expected motion. […] The cause of motion sickness is either real or perceived motion. […] Motion sickness can be divided into three categories: Motion sickness caused by motion that is felt but not seen i.e. terrestrial motion sickness; Motion sickness caused by motion that is seen but not felt i.e. space motion sickness; Motion sickness caused when both systems detect motion but they do not correspond i.e. either terrestrial or space motion sickness. […] Contemporary sensory conflict theory, referring to „a discontinuity between either visual, proprioceptive, and somatosensory input, or semicircular canal and otolith input”, is probably the most thoroughly studied. […] According to sensory conflict theory, the cause of terrestrial motion sickness is the opposite of the cause of space motion sickness.
- #18 Motion sickness | Better Health Channelhttps://www.betterhealth.vic.gov.au/health/healthyliving/motion-sickness
Motion sickness may occur in response to certain types of movement, whether it is the person or what they are looking at (for example, a movie screen) that is moving. […] In part, motion sickness is thought to take place when there is a mismatch between the information that the brain receives from the inner ear balance mechanism (vestibular system) and what the eyes see. […] For example, if the eyes tell the brain that a person is stationary (such as looking at the interior of a cabin on a ship), but the vestibular system senses head movements (due to motion of the ship), then this is thought to cause a mismatch of messages to the brain and leads to motion sickness. […] If a person is exposed to motion for an extended period (for example, during a long journey at sea) or has repeated exposures, their brain may adapt in time to the constant motion and they may no longer experience motion sickness. […] Medications either calm the nerves of the inner ear or soothe the brains vomiting centre. However, nearly all motion sickness pills are most effective if they are taken before you feel sick.
- #19 A review on motion sickness of autonomous driving vehicles – Extricahttps://www.extrica.com/article/23947
The objective of this study is to investigate the symptoms, types, etiology, and assessment methods of motion sickness in autonomous vehicles in order to gain a comprehensive understanding of its occurrence mechanism and emphasize the significance of enhancing autonomous vehicle algorithms for improved ride comfort. […] Motion sickness was first documented over 2,000 years ago by the Greek physician Hippocrates, who observed that motion disturbs the body when sailing at sea. […] Currently regarded as a natural response to an unnatural environment, motion sickness is commonly explained by theories such as sensory conflict theory, evolutionary theory, and postural instability theory. […] According to the sensory conflict theory, motion sickness arises from a discrepancy between the internal sensory system and the external visual system.
- #20 Motion sickness pathophysiology – wikidochttps://www.wikidoc.org/index.php/Motion_sickness_pathophysiology
Motion sickness on the sea can result from being in the berth of a rolling boat without being able to see the horizon. Sudden jerky movements tend to be worse for provoking motion sickness than slower smooth ones, because they disrupt the fluid balance more. A „corkscrewing” boat will upset more people than one that is gliding smoothly across the oncoming waves. […] The most common hypothesis for the cause of motion sickness is that it evolved as a defense mechanism against neurotoxins. The area postrema in the brain is responsible for inducing vomiting when poisons are detected, and for resolving conflicts between vision and balance. When feeling motion but not seeing it (for example, in a ship with no windows), the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the disconcordance, the brain will come to the conclusion that one of them is hallucinating and further conclude that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin.
- #21 Motion Sicknesshttps://www.dizziness-and-balance.com/disorders/central/motion.htm
Another situation where motion sickness is common is in outer space. […] A partial vestibular loss (for a subset of otolithic input) is supposedly associated with strong motion sickness. […] The essence of this theory is that it is just eye movement produced by retinal slip (i.e. relative movement of the world with respect to retina), that provokes motion sickness. […] This theory suggests that body movement, rather than eye movement or sensory conflict is the dominant influence on motion sickness. […] Acquired susceptibility to motion sickness is rare. […] Migraine is a definite risk factor for motion sickness, with roughly a 5 fold greater incidence than non-migraineurs, and a roughly 50% prevalence (Marcus et al, 2005). […] The space-military industrial complex has developed a theory of motion sickness that depends on asymmetry in otoconial mass (Scherer et al, 1997). […] Motion sickness is sometimes associated with prolonged vestibular responses (Hoffer et al. 2003), implying that these individuals simply appreciate motion more than others. […] There is also less motion sickness in patients with vestibular loss (Paillard et al, 2013).
- #22 A Preliminary Study: Central Vestibular Sensitivity Affects Motion Sickness Susceptibility through the Efficacy of the Velocity Storage Mechanismhttps://www.mdpi.com/2039-4349/10/2/245
Aby wyodrÄbniÄ zdania, akapity i twierdzenia dotyczÄ ce „Motion sickness Pathogenesis, mechanism”, oto odpowiedni tekst: […] It has long been suggested that Motion sickness Susceptible (MSS) individuals are inclined to possess vestibular systems that are more sensitive as compared to individuals less prone to motion sickness. […] The sensitivity of the Central Vestibular System (CVS) plays a critical role in the production of motion sickness. […] While the etiology of motion sickness remains elusive, the theory of sensory conflict is widely accepted as the most common cause for motion sickness. […] Sensory conflict results from the mismatched integration of multiple sensory inputs (proprioceptive, visual and vestibular) at the level of neural integrators. […] Among the many neural integrators in the brain, sensory conflict is known to result from one integrator, which is called the Velocity Storage Mechanism (VSM), located at the central vestibular system. […] While the VSM functions to integrate sensory information from multiple inputs, its primary function is to prolong the Slow-Phase Eye Velocity Time Constant (SPEV TC) and Perceived Rotational Duration (PRD) in relation to motion, to compensate for the vestibular systemâs lack of sensitivity in detecting low frequency movements. […] Although the exact relationship between SPEV TC, PRD, and MSS has yet to be characterized, it is postulated that the efficiency of the VSM in modulating SPEV TC and PRD determines the propensity for sensory conflicts to occur. […] The role of the CVS in the production of motion sickness is understood from several habituation studies that have assessed the correlation between SPEV TC and MSS after exposure to habituation training. […] However, unlike SPEV TC, significant differences for post-rotatory CW and CCW PRD were observed at fast-speed rotations. […] This is likely due to the velocity storage playing a greater role in the post-rotatory experience as compared to per-rotation. […] For fast speed rotations, both per and post-rotatory PRD were significant predictors of motion sickness susceptibility. […] The prediction of MSS using regression analysis seemed to be consistent for SPEV TC, since between groups, no significant difference was noted. […] However, PRD on the other hand could be a more reliable measure of habituation training efficacy and should be concurrently recorded with SPEV TC in future studies on habituation and motion sickness susceptibility.
- #23https://journals.lww.com/co-neurology/fulltext/2005/02000/motion_sickness.7.aspx?generateEpub=Article%7Cco-neurology:2005:02000:00007%7C%7C
Ability to modify readily the time constant of vestibular velocity store has emerged as a potential candidate marker of successful motion sickness habituation. […] Behavioural autogenic countermeasures to the development of sickness, such as controlled breathing, which can be implemented readily, are shown to have significant ameliorating effects on nausea and are of value for short term moderate exposures. […] New classes of pharmacological agents such as N-methyl-D-aspartate antagonists and 5HT1a receptor agonists show promise in animals but await trials in humans.
- #24 Motion Sickness in Animals – Nervous System – Merck Veterinary Manualhttps://www.merckvetmanual.com/nervous-system/motion-sickness/motion-sickness-in-animals
Motion sickness is characterized by signs referable to stimulation of the vestibular and autonomic nervous systems, including excessive salivation and vomiting. […] The principal causative mechanism involves stimulation of the vestibular apparatus in the inner ear, which has connections to the emetic center in the brain stem. […] Recent evidence has revealed that the neurokinin 1 substance P receptors (NK1) in the emetic center play a major role in motion sickness in both dogs and cats and are more important than the receptors in the CRTZ. […] NK1 receptors are located in the emetic center of the brain stem, which is the source most responsible for the vomiting and nausea of motion sickness. Blocking these receptors is more effective than inhibiting the CRTZ. Therefore, maropitant is probably the drug of choice to treat motion sickness in dogs.
- #25https://www.the-scientist.com/the-culprits-behind-motion-sickness-71570
Scientists identified neurons that drive the disagreeable symptoms of motion sickness in mice. […] Despite its prevalence, motion sickness mechanisms are incompletely understood, and many available treatments cause problematic drowsiness. Now, a team of neuroscientists, including Albert Quintana and Elisenda Sanz at the Autonomous University of Barcelona and Richard Palmiter at the University of Washington, have pinpointed the neurons that control motion sickness symptoms in mice, suggesting new therapeutic avenues. […] Building on previous research showing that glutamatergic neurons in the vestibular nuclei (VN) mediated responses to hypergravity, the neuroscientists demonstrated the importance of these neurons in rotation-induced physiological responses as well. […] One subpopulation expressed cholecystokinin (CCK), a peptide implicated in nausea and reduction in food intake. When researchers stimulated these neurons optogenetically, they recapitulated many symptoms of motion sickness. […] A CCK antagonist blocked some of the rotation-induced symptoms. […] We have identified a different mechanism to prevent motion sickness that doesnt seem to affect the alertness circuitry in the brain.
- #26 The Pharmacologic Management of Motion Sicknesshttps://www.uspharmacist.com/article/the-pharmacologic-management-of-motion-sickness
Motion sickness is a common malady in the general population; however, the exact mechanism through which it occurs is not completely known. […] Motion sickness occurs when the motion perceived visually does not match that sensed by the brain. […] Susceptibility to motion sickness varies among individuals. […] Additionally, motion sickness may be caused by certain medications, including but not limited to macrolides, metronidazole, morphine, digoxin, and some selective serotonin reuptake inhibitors. […] The mechanism by which sympathomimetics like amphetamine prevent motion sickness is unclear. […] Initially, it was thought that these agents increased the amount of norepinephrine in the central nervous system (CNS), which in turn countered the increased acetylcholine activity responsible for motion sickness.
- #27 Motion sickness: MedlinePlus GeneticsLockhttps://medlineplus.gov/genetics/condition/motion-sickness/
Motion sickness is a common condition characterized by a feeling of unwellness brought on by certain kinds of movement. […] The factors that contribute to motion sickness are not well understood, but susceptibility to the condition does seem to be partly genetic. When motion sickness occurs, it likely results from a mismatch in signals about movement coming from different parts of the body. […] Researchers believe it is this sensory conflict that triggers the symptoms of motion sickness. The mechanism by which a sensory mismatch could lead to dizziness, nausea, and related symptoms is unclear, and other explanations for motion sickness are also being explored. […] Common, complex conditions such as motion sickness are often polygenic, which means they involve variations in many genes.
- #28 Motion sickness: MedlinePlus GeneticsLockhttps://medlineplus.gov/genetics/condition/motion-sickness/
One study compared genetic variations in a large number of people with and without a susceptibility to motion sickness. The researchers found common genetic variations in or near 35 genes that may be associated with the condition. […] Additional research will be necessary to confirm the association between variations in specific genes and motion sickness susceptibility.
- #29 (PDF) Motion sickness: advances in pathogenesis, prediction, prevention, and treatmenthttps://www.academia.edu/19940255/Motion_sickness_advances_in_pathogenesis_prediction_prevention_and_treatment
Motion sickness has a major influence on modern traveling activities and the rapidly spreading engagement in virtual reality immersion. Recent evidence emphasizes the role of the otoliths in the pathogenesis of motion sickness, and several new theories may help explain its occurrence beyond the traditional sensory conflict theory. A promising new direction is the recently reported association of genetic polymorphism of the alpha2-adrenergic receptor with increased autonomic response to stress and motion sickness. […] The sensory conflict hypothesis is the most widely accepted theory for MS. […] It has long been suspected that genetic and/or evolutionary factors govern motion sickness susceptibility. […] The main causes in adulthood are still unknown, but it has been suggested that this condition can be related to the hormonal cycle. […] Numerous studies have investigated the neurobiological mechanism and the control measures of MS. […] The aim of this review is to remind the current knowledge about pathogenesis, epidemiology, diagnosis and treatment methods of the special issue: motion sickness.
- #30 Motion Sickness: Surprising Causes and Symptomshttps://www.verywellhealth.com/seven-things-you-dont-know-about-motion-sickness-1192151
Motion sickness (kinetosis) causes symptoms that include dizziness, nausea, and headache. It occurs when you’re moving (in a car, for example) and your brain receives mixed signals from your body, inner ear, and eyes about its surroundings. […] Studies have shown that essentially everyone has the potential to get motion sickness because it’s related to the vestibular system (and its ear-related role in motion, balance, and coordination). […] Females are more likely than males to get motion sickness, partly because of hormones. Estrogen, the primary female sex hormone, can contribute to symptoms of nausea and dizziness. […] A small study has shown that people who don’t know when or how motion will occur may have more difficulty. […] The precise cause remains unclear, but it’s possible another mechanism (including ear-related) is at work.
- #31 Azthena logo with the word Azthenahttps://www.news-medical.net/health/Risk-of-motion-sickness.aspx
Motion sickness is an unpleasant sensation commonly seen in some vulnerable individuals when they are subjected to unnatural motion. […] Motion sickness can be caused by travelling in cars, boats, ships, trains, aeroplanes, submarines, space ships, riding amusement rides that spin, swinging on park or play ground swings etc. […] Research suggests that there is a common underlying vestibular mechanism of causation between motion sickness and vomiting and nausea during pregnancy. […] Studies show that frequent blood vessel constrictions lead to ischemia or lack of blood supply to the vestibular apparatus and the labyrinth especially during an attack of migraine. This raises the susceptibility to motion sickness. […] In addition, those with migraine have a lower triggering threshold for nausea and vomiting at the brain center called the vomiting center which makes migraine sufferers more at risk of motion sickness and its associated symptoms of nausea and vomiting. […] Anxiety and stress regarding fears of developing motion sickness often gives rise to actual development of motion sickness.
- #32https://journals.lww.com/co-neurology/fulltext/2005/02000/motion_sickness.7.aspx?generateEpub=Article%7Cco-neurology:2005:02000:00007%7C%7C
The public’s longstanding resigned tolerance to motion sickness threatens to change, due to the widespread introduction of nauseogenic tilting trains and the increasing use of virtual reality immersion. […] Scientific effort over the last 5 years has focused on precise evaluation of the stimuli that provoke sickness and on the development of behavioural and new pharmacological interventions to suppress sickness. […] The precise mechanical ride characteristics of vehicles that provoke sickness have been identified and this will lead to guidelines for future engineering design, especially for suspension systems that compensate for inertial tilt, and recommendations for passengers at risk. […] The frequency characteristics of motion provoking sickness have been defined with greater precision and identified with shifts in perception of motion versus orientation, and changes in the quality of reflex eye movements.
- #33 Prevention and Treatment of Motion Sickness | AAFPhttps://www.aafp.org/pubs/afp/issues/2014/0701/p41.html
Motion sickness is a common syndrome that occurs upon exposure to certain types of motion. It is thought to be caused by conflict between the vestibular, visual, and other proprioceptive systems. […] The pathogenesis of motion sickness is not clearly understood, but it is thought to be related to conflict between the vestibular, visual, and other proprioceptive systems. Rotary, vertical, and low-frequency motions produce more symptoms than linear, horizontal, and high-frequency motions. […] Although nausea may be the first recognized symptom of motion sickness, it is almost always preceded by other subtle symptoms such as stomach awareness (i.e., a sensation of fullness in the epigastrium), malaise, drowsiness, and irritability. Failure to attribute early symptoms to motion sickness may lead to delays in diagnosis and treatment.
- #34 A review on motion sickness of autonomous driving vehicles – Extricahttps://www.extrica.com/article/23947
The evolutionary theory posits that motion sickness is a natural response developed through human evolution. […] Postural instability theory states that prolonged movements cause postural instability which leads to motion sickness. […] Motion sickness is a significant concern in the field of vehicle engineering due to its substantial interindividual variability and potential impact on the comfort and safety of vehicle occupants. […] The close correlation between low-frequency vibration and motion sickness has been widely acknowledged by scholars. […] Autonomous vehicles bring about changes in the drivers role to passengers, especially driving behaviors such as rapid acceleration, rapid deceleration, and sharp turns, making passengers experience unaccustomed motion stimuli. […] In the journey of autonomous vehicles, motion sickness is not only affected by vehicle acceleration and low-frequency vibration.
- #35 Summer traveler or astronaut, motion sickness is a real problem, say MIT space program researchers | MIT News | Massachusetts Institute of Technologyhttps://news.mit.edu/2000/motion
The past 25 years of the space program has uncovered more than has ever been known about the physical basis for motion sickness. […] Motion sickness, they say, results from conflicting information reaching the brain from your eyes and your inner ear, and from different parts of the inner ear itself. […] They point out that motion sickness has affected virtually every astronaut and that virtually everybody with normal inner-ear balance function can be made motion sick. […] Understanding and remedying motion sickness becomes particularly relevant when planning a manned space flight to Mars. […] Young’s and Oman’s research indicates that astronauts and regular folks become accustomed to unnatural or nauseating movements over time, with or without medication.
- #36 Quantitative study on objective indicators for assessing motion sickness susceptibility based on Vestibulo-Ocular Reflex experiments | Scientific Reportshttps://www.nature.com/articles/s41598-024-80233-4
Motion sickness (MS) is a common physiological response that often occurs when individuals are exposed to environments with repeated acceleration stimuli. MS results from a mismatch between the vestibular system and visual and proprioceptive inputs. […] The vestibular system, responsible for sensing acceleration stimuli, is closely related to the onset of MS. Some studies indicated that subjects without vestibular labyrinth function did not develop MS, and even those with impaired vestibular labyrinth function exhibited some immunity to MS. Therefore, a normally functioning vestibular system in the inner ear is necessary for the development of MS. […] The physiological significance of sensory conflict and neural mismatch lied in promoting the perception of sensory organs of motion information, facilitating continuous self-learning and adjustment, and ultimately forming an adaptation to abnormal motion.
- #37 Quantitative study on objective indicators for assessing motion sickness susceptibility based on Vestibulo-Ocular Reflex experiments | Scientific Reportshttps://www.nature.com/articles/s41598-024-80233-4
The cupula time constant is an intrinsic parameter of the vestibular system, reflecting the response time of the cupula receptors and indicating the speed at which the vestibular system perceives and restores balance. The velocity storage time constant represents the duration for which vestibular signals are stored and prolonged in the brainstem. The nystagmus SPV serves as an objective measure of the vestibular systems response to acceleration. […] The significant correlation between the MSAQ scores and the maximal nystagmus SPV suggested that SPV could serve as an objective measure of MS susceptibility, further confirming the close relationship between the vestibular system and MS. […] Correlation analysis revealed a significant relationship between the cupula time constant and MSAQ scores among the 65 volunteers, indicating that the cupula time constant could be directly used to measure MS susceptibility.
- #38 Quantitative study on objective indicators for assessing motion sickness susceptibility based on Vestibulo-Ocular Reflex experiments | Scientific Reportshttps://www.nature.com/articles/s41598-024-80233-4
The significant correlation between nystagmus duration and MSAQ scores further supported the close relationship between the velocity storage effect and the onset of MS. […] In this study, we identified that the maximal nystagmus SPV, the cupula time constant, the velocity storage time constant, and the nystagmus duration could serve as objective indicators of MS susceptibility.
- #39 Thieme E-Journals – Annals of Otology and Neurotology / Full Texthttps://www.thieme-connect.com/products/ejournals/html/10.1055/s-0043-1764173
The otolith of vestibular system in the human body helps in maintaining the static balance. Travelling can cause defect in static balance that may lead to motion sickness. […] The review indicates a significant change in the interaural asymmetry ratio of both cVEMP and oVEMP results in individuals with motion sickness. This shows that there might be a variation in the functional asymmetry in the otoliths. […] It was believed that motion sickness had major contributions from the visual system, causing alterations in the vestibular system. However, later it was found that even a blind person could develop motion sickness. This shows that it is not the visual system, but that the vestibular system plays a major role in motion sickness susceptibility. […] Studies have shown that VEMP can be utilized to identify susceptibility to motion sickness.
- #40 Thieme E-Journals – Annals of Otology and Neurotology / Full Texthttps://www.thieme-connect.com/products/ejournals/html/10.1055/s-0043-1764173
There is evidence that the amplitude asymmetry ratios between the VEMP results of people vulnerable to motion sickness are distinct from normal. […] The study by Singh et al was the only study where the threshold of both cVEMP and oVEMP was observed. […] The IAAR of both cVEMP and oVEMP in Singh et al and Neupane et al was found to be reduced in the experimental group. […] This shows that there might be a variation in the functional symmetry in the otoliths, because of sensory conflict in space and due to weight variability that is seen in them. From this, it can be derived that there might be otolith changes due to motion sickness. […] A significant change was seen in the IAAR compared to amplitude and latency in individuals susceptible to motion sickness. From the review, it is clear that there might be otolith changes due to motion sickness that can have a smaller impact on the VEMP.
- #41 Deep insights into the mechanism of isorhamnetin’s anti-motion sickness effect based on photoshoproteomics – Food & Function (RSC Publishing)https://pubs.rsc.org/en/content/articlehtml/2024/fo/d4fo02761b
Isorhamnetin has recently been found to exhibit a remarkable anti-motion sickness effect, yet the underlying mechanism is still unclear. […] In particular, protein phosphorylation, protein serine/threonine/tyrosinase activity and signal transduction might play a role in isorhamnetin’s anti-motion sickness effect. […] Results showed that differentially phosphorylated proteins have an effect on postsynaptic density, glutamatergic synapses and other sites and are involved in various neurodegenerative disease pathways, endocytic pathways, cAMP signaling pathways and MAPK signaling pathways. […] Two key differentially phosphorylated proteins in glutamatergic synapses, namely, DLGAP and EPS8, might play key roles in isorhamnetin’s anti-motion sickness process. […] The final molecular experimental verification results from qRT-PCR and western blot analyses indicated that isorhamnetin firstly regulates glutamatergic synapses and then reduces the excitability of the vestibular nucleus through inhibiting the NMDAR1/CaMKII/CREB signaling pathway, ultimately alleviating a series of symptoms of motion sickness in mice.
- #42 Neural mechanisms of motion sicknesshttp://medical.med.tokushima-u.ac.jp/jmi/vol48/text/v48_n1-2_p044.html
The neural mismatch hypothesis explains many of the known characteristics of motion sickness, including space motion sickness and visually-induced motion sickness. […] Antihistamines, which block histamine H1-receptors, are effective in preventing motion sickness in humans. […] Therefore, the histaminergic neuron system in the brain has been suspected to play an important role in the neural processes of motion sickness. […] These findings demonstrate that rats, like humans, suffer from motion sickness due to the neural mismatch signal generated by the vestibular information passed through the inner ear. […] The double rotation-induced pica is suppressed by diphenhydramine, an antagonist of H1-receptor, showing that the histaminergic mechanisms involved in human motion sickness are apparently also involved in the development of motion sickness in rats.
- #43 What is the mechanism of Dimenhydrinate?https://synapse.patsnap.com/article/what-is-the-mechanism-of-dimenhydrinate
Dimenhydrinate, commonly known as Dramamine, is a medication widely used to prevent and treat motion sickness and nausea. Understanding its mechanism involves delving into how this compound interacts within the human body to alleviate symptoms of motion-induced discomfort. The primary action of dimenhydrinate revolves around its antihistamine component, diphenhydramine. This substance works by blocking histamine receptors, specifically the H1 receptors, in the brain. In the context of motion sickness, histamine plays a crucial role in the vestibular system, which is responsible for maintaining balance and spatial orientation. When a person experiences motion sickness, the vestibular system sends conflicting signals to the brain about the body’s position and movement. This confusion triggers a series of responses, including nausea, vomiting, and dizziness. By inhibiting the H1 receptors, diphenhydramine reduces the activity of histamine in the vestibular system, thus diminishing the brain’s perception of motion and alleviating the associated symptoms. In addition to its antihistamine properties, diphenhydramine also has anticholinergic effects. It blocks acetylcholine receptors in the central nervous system, which can further help to reduce nausea and vomiting. By dampening the action of acetylcholine, diphenhydramine provides a dual mechanism for combating motion sickness. Dimenhydrinate operates through a combination of antihistamine and anticholinergic actions to mitigate the symptoms of motion sickness. The diphenhydramine component blocks histamine and acetylcholine receptors in the brain, reducing the perception of motion and alleviating nausea and vomiting. Understanding this mechanism provides insight into how dimenhydrinate effectively addresses the discomfort associated with motion sickness, allowing individuals to travel with greater ease and comfort.
- #44 What is the mechanism of Scopolamine?https://synapse.patsnap.com/article/what-is-the-mechanism-of-scopolamine
Scopolamine is particularly effective in preventing motion sickness and postoperative nausea and vomiting. […] This effect is attributed to its action on the vestibular system and the vomiting center in the brainstem. […] By blocking muscarinic receptors in these areas, scopolamine interferes with the transmission of signals that trigger nausea and vomiting. […] Scopolamine operates through its antagonistic action on muscarinic acetylcholine receptors, leading to both central and peripheral effects. […] Its ability to inhibit parasympathetic activity makes it a valuable therapeutic agent for conditions like motion sickness, postoperative nausea, and spasms.
- #45 Motion Sickness – Wandr Healthhttps://www.travelwithwandr.com/treatments/motion-sickness/
Motion sickness is a common condition that occurs when there is a disconnect between the sensory signals received by the brain. […] Meclizine works by blocking histamine receptors in the brain, which helps reduce the symptoms of nausea and dizziness associated with motion sickness. […] Motion sickness can significantly disrupt travel experiences, but meclizine provides an effective option for prevention and treatment.
- #46 Brainstem processing of vestibular sensory exafference: implications for motion sickness etiologyhttps://dspace.mit.edu/handle/1721.1/87071?show=full
The origin of the internal sensory conflict stimulus causing motion sickness has been debated for more than four decades. […] Recent studies show a subclass of neurons in the vestibular nuclei and deep cerebellar nuclei that respond preferentially to passive head movements. […] The un-cancelled component (exafference) resulting from passive movement normally helps compensate for unexpected postural disturbances. […] Notably, the existence of such vestibular sensory conflict neurons had been postulated as early as 1982, but their existence and putative role in posture control, motion sickness has been long debated. […] We propose that conditions producing persistent activity of these neurons, or their targets, stimulates nearby brainstem emetic centers via an as yet unidentified mechanism. […] Finally, we propose that fuller characterization of these mechanisms, and their potential role in motion sickness could lead to more effective, scientifically based prevention and treatment for motion sickness.