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PATHOPHYSIOLOGY
MOTION SICKNESS/
KINETOSIS
Кини Бхаргав 313
Other names
Kinetosis, travel sickness, seasickness, airsickness,
carsickness, simulation sickness, space motion
sickness, space adaptation
syndrome.
Motion sickness or kinetosis, also
known as travel sickness, it occurs
when accelerations effect on the
body.
The cause of motion sickness is
either real or perceived motion. This
may include from car travel, air
travel, sea travel, space travel, or
reality simulation. Risk factors
include pregnancy, migraines, and
Meniere’s disease.The diagnosis is
based on symptoms.
Symptoms commonly include nausea,
vomiting, cold sweat, headache,
sleepiness, yawning, loss of appetite,
and increased salivation. Occasionally
tiredness can last for hours to days an
episode of motion sickness, known as
"sopite syndrome".Rarely severe
symptoms such as the inability to
walk, ongoing vomiting, or social
isolation may occur.
Motion sickness can be divided into three
categories:
1)Motion sickness caused by motion that is
felt but not seen, as in terrestrial motion
sickness;
2)Motion sickness caused by motion that is
seen but not felt, as in space motion
sickness;
3)Motion sickness caused when both
systems detect motion but they do not
correspond, as in either terrestrial or space
motion sickness.
Motion felt but not seen:
In these cases, motion is
sensed by the vestibular system
and hence the motion is felt,
but no motion or little motion
is detected by the visual
system, as in terrestrial motion
sickness.
Carsickness:
A specific form of terrestrial motion sickness, being carsick is
quite common and evidenced by disorientation while
reading a map, a book, or a small screen during travel.
Carsickness results from the sensory conflict arising in the
brain from differing sensory inputs. Motion sickness is
caused by a conflict between signals arriving in the brain
from the inner ear, which forms the base of the vestibular
system, the sensory apparatus that deals with movement
and balance, and which detects motion mechanically. If
someone is looking at a stationary object within a vehicle,
such as a magazine, their eyes will inform their brain that
what they are viewing is not moving. Their inner ears,
however, will contradict this by sensing the motion of the
vehicle.
Varying theories exist as to cause. The sensory
conflict theory notes that the eyes view motion
while riding in the moving vehicle while other
body sensors sense stillness, creating conflict
between the eyes and inner ear. Another
suggests the eyes mostly see the interior of the
car which is motionless while the vestibular
system of the inner ear senses motion as the
vehicle goes around corners or over hills and
even small bumps. Therefore, the effect is
worse when looking down but may be lessened
by looking outside of the vehicle.
In the early 20th century, Austro-
Hungarian scientist Róbert Bárány
observed the back and forth
movement of the eyes of railroad
passengers as they looked out the side
windows at the scenery whipping by.
He called it "railway nystagmus". Also
called "optokinetic nystagmus". It
causes nausea and vomiting. His
findings were published in the journal
Laeger, 83:1516, Nov.17, 1921.
Airsickness:
Air sickness is a kind of terrestrial motion sickness
induced by certain sensations of air travel. It is a
specific form of motion sickness and is considered a
normal response in healthy individuals. It is
essentially the same as carsickness but occurs in an
airplane. An airplane may bank and tilt sharply, and
unless passengers are sitting by a window, they are
likely to see only the stationary interior of the plane
due to the small window sizes and during flights at
night. Another factor is that while in flight, the view
out of windows may be blocked by clouds, preventing
passengers from seeing the moving ground or passing
clouds.
Seasickness:
Seasickness is a form of terrestrial motion sickness
characterized by a feeling of nausea and, in extreme
cases, vertigo experienced after spending time on a
boat. It is essentially the same as carsickness, though
the motion of a watercraft tends to be more regular. It
is typically brought on by the rocking motion of the
craft or movement while the craft is immersed in
water.As with airsickness, it can be difficult to visually
detect motion even if one looks outside the boat since
water does not offer fixed points with which to visually
judge motion. Poor visibility conditions, such as fog,
may worsen seasickness.
The greatest contributor to seasickness is the
tendency for people being affected by the
rolling or surging motions of the craft to seek
refuge below decks, where they are unable to
relate themselves to the boat's surroundings
and consequent motion. Some sufferers of
carsickness are resistant to seasickness and
vice versa. Adjusting to the craft's motion at
sea is called "gaining one's sea legs"; it can
take a significant portion of the time spent at
sea after disembarking to regain a sense of
stability "post-sea legs".
Motion seen but not felt:
In these cases, motion is detected by
the visual system and hence the
motion is seen, but no motion or little
motion is sensed by the vestibular
system. Motion sickness arising from
such situations has been referred to
as "visually induced motion sickness"
(VIMS)
Space motion sickness:
Zero gravity interferes with the vestibular
system's gravity-dependent operations, so that
the two systems, vestibular and visual, no
longer provide a unified and coherent sensory
representation. This causes unpleasant
disorientation sensations often quite distinct
from terrestrial motion sickness, but with
similar symptoms. The symptoms may be more
intense because a condition caused by
prolonged weightlessness is usually quite
unfamiliar.
Motion that is seen and felt:
When moving within a rotating
reference frame such as in a
centrifuge or environment where
gravity is simulated with centrifugal
force, the coriolis effect causes a
sense of motion in the vestibular
system that does not match the
motion that is seen
Pathophysiology.
There are various hypotheses that
attempt to explain the cause of the
condition.
Sensory conflict theory:
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 this
theory, when the brain presents the mind with
two incongruous states of motion; the result is
often nausea and other symptoms of
disorientation known as motion sickness. Such
conditions happen when the vestibular system
and the visual system do not present a
synchronized and unified representation of one's
body and surroundings.
According to sensory conflict theory, the
cause of terrestrial motion sickness is the
opposite of the cause of space motion
sickness. The former occurs when one
perceives visually that one's surroundings are
relatively immobile while the vestibular
system reports that one's body is in motion
relative to its surroundings.The latter can
occur when the visual system perceives that
one's surroundings are in motion while the
vestibular system reports relative bodily
immobility (as in zero gravity.)
Neural mismatch:
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. This theory emphasizes "the limbic
system in the integration of sensory information
and long-term memory, in the expression of the
symptoms of motion sickness, and the impact of
anti-motion-sickness drugs and stress hormones
on limbic system function. The limbic system
may be the neural mismatch center of the
brain."
Defense against poisoning:
It has also been proposed that motion
sickness could function 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 the
cabin of a ship with no portholes), 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 incongruity, the brain
concludes that the individual is
hallucinating and further concludes that
the hallucination is due to poison
ingestion. The brain responds by
inducing vomiting, to clear the supposed
toxin. Treisman's indirect argument has
recently been questioned via an
alternative direct evolutionary
hypothesis, as well as modified and
extended via a direct poison hypothesis.
The direct evolutionary hypothesis
essentially argues that there are plausible
means by which ancient real or apparent
motion could have contributed directly to
the evolution of aversive reactions, without
the need for the co-opting of a poison
response as posited by Treisman.
Nevertheless, the direct poison hypothesis
argues that there still are plausible ways in
which the body's poison response system
may have played a role in shaping the
evolution of some of the signature
symptoms that characterize motion sickness.
Nystagmus hypothesis:
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. There are
three critical aspects to the theory: first is the
close linkage between activity in the vestibular
system, i.e., semicircular canals and otolith
organs, and a change in tonus among various
of each eye's six extra-ocular muscles.
Thus, with the exception of voluntary eye
movements, the vestibular and oculomotor
systems are thoroughly linked. Second is the
operation of Sherrington's Law describing
reciprocal inhibition between agonist-
antagonist muscle pairs, and by implication
the stretching of extraocular muscle that must
occur whenever Sherrington's Law is made to
fail, thereby causing an unrelaxed (contracted)
muscle to be stretched. Finally, there is the
critical presence of afferent output to the
Vagus nerves as a direct result of eye muscle
stretch or traction.
Thus, 10th nerve stimulation resulting from
eye muscle stretch is proposed as the cause
of motion sickness. The theory explains why
labyrinthine-defective individuals are
immune to motion sickness;why symptoms
emerge when undergoing various body-head
accelerations; why combinations of
voluntary and reflexive eye movements may
challenge the proper operation of
Sherrington's Law, and why many drugs that
suppress eye movements also serve to
suppress motion sickness symptoms.
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). This theory attempts to integrate
previous theories of motion sickness. For example,
there are many sensory conflicts that are
associated with motion sickness and many that are
not, but those in which canal stimulation occurs in
the absence of normal otolith function (e.g., in free
fall) are the most provocative. The vestibular
imbalance theory is also tied to the different roles
of the otoliths and canals in autonomic arousal
(otolith output more sympathetic).
Diagnosis
The diagnosis is based on
symptoms.Other conditions that
may present similarly include
vestibular disorders such as benign
paroxysmal positional vertigo and
vestibular migraine and stroke.
Treatment
Treatment may
include
behavioral
measures or
medications.
Behavioral measures:
Behavioral measures to decrease
motion sickness include holding the
head still and lying on the
back.Focusing on the horizon may
also be useful. Listening to music,
mindful breathing, being the driver,
and not reading while moving are
other techniques
Medication:
Three types of medications are useful:
antimuscarinics such as scopolamine, H1
antihistamines such as dimenhydrinate, and
amphetamines such as
dexamphetamine.Benefits are greater if used
before the onset of symptoms or shortly
after symptoms begin.Side effects, however,
may limit the use of medications. A number
of medications used for nausea such as
ondansetron and metoclopramide are not
effective in motion sickness.
Scopolamine is the most effective
medication. Evidence is best for when it is
used preventatively.It is available as a skin
patch.Side effects may include blurry vision.
Other effective first generation
antihistamines include meclizine,
promethazine, cyclizine, and cinnarizine.In
pregnancy meclizine and dimenhydrinate
are generally felt to be safe. Side effects
include sleepiness. Second generation
antihistamines have not been found to be
useful.
Dextroamphetamine may be used
together with an antihistamine or an
antimuscarinic. Concerns include their
addictive potential.
Those involved in high-risk activities,
such as SCUBA diving, should evaluate
the risks versus the benefits of
medications.Promethazine combined
with ephedrine to counteract the
sedation is known as "the Coast Guard
cocktail".
Alternative medicine:
Acupuncture has not been found to
be useful. Ginger root is commonly
thought to be an effective anti-
emetic, but it is ineffective in
treating motion sickness. Providing
smells does not appear to have a
significant effect on the rate of
motion sickness.
Epidemiology:
Roughly one-third of people are highly
susceptible to motion sickness, and most of the
rest get motion sick under extreme conditions.
Around 80% of the general population is
susceptible to cases of medium to high motion
sickness. The rates of space motion sickness have
been estimated at between forty and eighty
percent of those who enter weightless orbit.
Several factors influence susceptibility to motion
sickness, including sleep deprivation and the
cubic footage allocated to each space traveler.
Studies indicate that women are more likely to be
affected than men,and that the risk decreases
with advancing age.
THANK YOU!!!
Спасибо!!!!

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PATHOPHYSIOLOGY-MOTION SICKNESS.pptx

  • 2. Other names Kinetosis, travel sickness, seasickness, airsickness, carsickness, simulation sickness, space motion sickness, space adaptation syndrome.
  • 3. Motion sickness or kinetosis, also known as travel sickness, it occurs when accelerations effect on the body.
  • 4. The cause of motion sickness is either real or perceived motion. This may include from car travel, air travel, sea travel, space travel, or reality simulation. Risk factors include pregnancy, migraines, and Meniere’s disease.The diagnosis is based on symptoms.
  • 5. Symptoms commonly include nausea, vomiting, cold sweat, headache, sleepiness, yawning, loss of appetite, and increased salivation. Occasionally tiredness can last for hours to days an episode of motion sickness, known as "sopite syndrome".Rarely severe symptoms such as the inability to walk, ongoing vomiting, or social isolation may occur.
  • 6. Motion sickness can be divided into three categories: 1)Motion sickness caused by motion that is felt but not seen, as in terrestrial motion sickness; 2)Motion sickness caused by motion that is seen but not felt, as in space motion sickness; 3)Motion sickness caused when both systems detect motion but they do not correspond, as in either terrestrial or space motion sickness.
  • 7. Motion felt but not seen: In these cases, motion is sensed by the vestibular system and hence the motion is felt, but no motion or little motion is detected by the visual system, as in terrestrial motion sickness.
  • 8. Carsickness: A specific form of terrestrial motion sickness, being carsick is quite common and evidenced by disorientation while reading a map, a book, or a small screen during travel. Carsickness results from the sensory conflict arising in the brain from differing sensory inputs. Motion sickness is caused by a conflict between signals arriving in the brain from the inner ear, which forms the base of the vestibular system, the sensory apparatus that deals with movement and balance, and which detects motion mechanically. If someone is looking at a stationary object within a vehicle, such as a magazine, their eyes will inform their brain that what they are viewing is not moving. Their inner ears, however, will contradict this by sensing the motion of the vehicle.
  • 9. Varying theories exist as to cause. The sensory conflict theory notes that the eyes view motion while riding in the moving vehicle while other body sensors sense stillness, creating conflict between the eyes and inner ear. Another suggests the eyes mostly see the interior of the car which is motionless while the vestibular system of the inner ear senses motion as the vehicle goes around corners or over hills and even small bumps. Therefore, the effect is worse when looking down but may be lessened by looking outside of the vehicle.
  • 10. In the early 20th century, Austro- Hungarian scientist Róbert Bárány observed the back and forth movement of the eyes of railroad passengers as they looked out the side windows at the scenery whipping by. He called it "railway nystagmus". Also called "optokinetic nystagmus". It causes nausea and vomiting. His findings were published in the journal Laeger, 83:1516, Nov.17, 1921.
  • 11. Airsickness: Air sickness is a kind of terrestrial motion sickness induced by certain sensations of air travel. It is a specific form of motion sickness and is considered a normal response in healthy individuals. It is essentially the same as carsickness but occurs in an airplane. An airplane may bank and tilt sharply, and unless passengers are sitting by a window, they are likely to see only the stationary interior of the plane due to the small window sizes and during flights at night. Another factor is that while in flight, the view out of windows may be blocked by clouds, preventing passengers from seeing the moving ground or passing clouds.
  • 12. Seasickness: Seasickness is a form of terrestrial motion sickness characterized by a feeling of nausea and, in extreme cases, vertigo experienced after spending time on a boat. It is essentially the same as carsickness, though the motion of a watercraft tends to be more regular. It is typically brought on by the rocking motion of the craft or movement while the craft is immersed in water.As with airsickness, it can be difficult to visually detect motion even if one looks outside the boat since water does not offer fixed points with which to visually judge motion. Poor visibility conditions, such as fog, may worsen seasickness.
  • 13. The greatest contributor to seasickness is the tendency for people being affected by the rolling or surging motions of the craft to seek refuge below decks, where they are unable to relate themselves to the boat's surroundings and consequent motion. Some sufferers of carsickness are resistant to seasickness and vice versa. Adjusting to the craft's motion at sea is called "gaining one's sea legs"; it can take a significant portion of the time spent at sea after disembarking to regain a sense of stability "post-sea legs".
  • 14. Motion seen but not felt: In these cases, motion is detected by the visual system and hence the motion is seen, but no motion or little motion is sensed by the vestibular system. Motion sickness arising from such situations has been referred to as "visually induced motion sickness" (VIMS)
  • 15. Space motion sickness: Zero gravity interferes with the vestibular system's gravity-dependent operations, so that the two systems, vestibular and visual, no longer provide a unified and coherent sensory representation. This causes unpleasant disorientation sensations often quite distinct from terrestrial motion sickness, but with similar symptoms. The symptoms may be more intense because a condition caused by prolonged weightlessness is usually quite unfamiliar.
  • 16. Motion that is seen and felt: When moving within a rotating reference frame such as in a centrifuge or environment where gravity is simulated with centrifugal force, the coriolis effect causes a sense of motion in the vestibular system that does not match the motion that is seen
  • 17. Pathophysiology. There are various hypotheses that attempt to explain the cause of the condition.
  • 18. Sensory conflict theory: 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 this theory, when the brain presents the mind with two incongruous states of motion; the result is often nausea and other symptoms of disorientation known as motion sickness. Such conditions happen when the vestibular system and the visual system do not present a synchronized and unified representation of one's body and surroundings.
  • 19. According to sensory conflict theory, the cause of terrestrial motion sickness is the opposite of the cause of space motion sickness. The former occurs when one perceives visually that one's surroundings are relatively immobile while the vestibular system reports that one's body is in motion relative to its surroundings.The latter can occur when the visual system perceives that one's surroundings are in motion while the vestibular system reports relative bodily immobility (as in zero gravity.)
  • 20. Neural mismatch: 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. This theory emphasizes "the limbic system in the integration of sensory information and long-term memory, in the expression of the symptoms of motion sickness, and the impact of anti-motion-sickness drugs and stress hormones on limbic system function. The limbic system may be the neural mismatch center of the brain."
  • 21. Defense against poisoning: It has also been proposed that motion sickness could function 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 the cabin of a ship with no portholes), the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still.
  • 22. As a result of the incongruity, the brain concludes that the individual is hallucinating and further concludes that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin. Treisman's indirect argument has recently been questioned via an alternative direct evolutionary hypothesis, as well as modified and extended via a direct poison hypothesis.
  • 23. The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent motion could have contributed directly to the evolution of aversive reactions, without the need for the co-opting of a poison response as posited by Treisman. Nevertheless, the direct poison hypothesis argues that there still are plausible ways in which the body's poison response system may have played a role in shaping the evolution of some of the signature symptoms that characterize motion sickness.
  • 24. Nystagmus hypothesis: 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. There are three critical aspects to the theory: first is the close linkage between activity in the vestibular system, i.e., semicircular canals and otolith organs, and a change in tonus among various of each eye's six extra-ocular muscles.
  • 25. Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of Sherrington's Law describing reciprocal inhibition between agonist- antagonist muscle pairs, and by implication the stretching of extraocular muscle that must occur whenever Sherrington's Law is made to fail, thereby causing an unrelaxed (contracted) muscle to be stretched. Finally, there is the critical presence of afferent output to the Vagus nerves as a direct result of eye muscle stretch or traction.
  • 26. Thus, 10th nerve stimulation resulting from eye muscle stretch is proposed as the cause of motion sickness. The theory explains why labyrinthine-defective individuals are immune to motion sickness;why symptoms emerge when undergoing various body-head accelerations; why combinations of voluntary and reflexive eye movements may challenge the proper operation of Sherrington's Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.
  • 27. 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). This theory attempts to integrate previous theories of motion sickness. For example, there are many sensory conflicts that are associated with motion sickness and many that are not, but those in which canal stimulation occurs in the absence of normal otolith function (e.g., in free fall) are the most provocative. The vestibular imbalance theory is also tied to the different roles of the otoliths and canals in autonomic arousal (otolith output more sympathetic).
  • 28. Diagnosis The diagnosis is based on symptoms.Other conditions that may present similarly include vestibular disorders such as benign paroxysmal positional vertigo and vestibular migraine and stroke.
  • 30. Behavioral measures: Behavioral measures to decrease motion sickness include holding the head still and lying on the back.Focusing on the horizon may also be useful. Listening to music, mindful breathing, being the driver, and not reading while moving are other techniques
  • 31. Medication: Three types of medications are useful: antimuscarinics such as scopolamine, H1 antihistamines such as dimenhydrinate, and amphetamines such as dexamphetamine.Benefits are greater if used before the onset of symptoms or shortly after symptoms begin.Side effects, however, may limit the use of medications. A number of medications used for nausea such as ondansetron and metoclopramide are not effective in motion sickness.
  • 32. Scopolamine is the most effective medication. Evidence is best for when it is used preventatively.It is available as a skin patch.Side effects may include blurry vision. Other effective first generation antihistamines include meclizine, promethazine, cyclizine, and cinnarizine.In pregnancy meclizine and dimenhydrinate are generally felt to be safe. Side effects include sleepiness. Second generation antihistamines have not been found to be useful.
  • 33. Dextroamphetamine may be used together with an antihistamine or an antimuscarinic. Concerns include their addictive potential. Those involved in high-risk activities, such as SCUBA diving, should evaluate the risks versus the benefits of medications.Promethazine combined with ephedrine to counteract the sedation is known as "the Coast Guard cocktail".
  • 34. Alternative medicine: Acupuncture has not been found to be useful. Ginger root is commonly thought to be an effective anti- emetic, but it is ineffective in treating motion sickness. Providing smells does not appear to have a significant effect on the rate of motion sickness.
  • 35. Epidemiology: Roughly one-third of people are highly susceptible to motion sickness, and most of the rest get motion sick under extreme conditions. Around 80% of the general population is susceptible to cases of medium to high motion sickness. The rates of space motion sickness have been estimated at between forty and eighty percent of those who enter weightless orbit. Several factors influence susceptibility to motion sickness, including sleep deprivation and the cubic footage allocated to each space traveler. Studies indicate that women are more likely to be affected than men,and that the risk decreases with advancing age.