716 Aviation, Space, and Environmental Medicine x Vol. 84, No. 7 x July 2013
Space Motion Sickness and Motion Sickness:
Symptoms and Etiology
William E. Thornton and Frederick Bonato
This manuscript was received for review in June 2012 . It was
accepted for publication in January 2013 .
Address correspondence and reprint requests to: William E. Thornton,
M.D., 7640 Pimlico Lane, Boerne, TX 78015; firstname.lastname@example.org .
Reprint & Copyright © by the Aerospace Medical Association,
begins without premonition and with one or two heaves
of projectile vomiting after tens of minutes to several
hours of weightlessness (usually in 1 to 2 h) ( 30 , 41 ).
Similar episodes typically follow hours later. Ingested
foods and liquids will typically be regurgitated after a
short time ( 15 ). Initial vomiting may be preceded by, but
is usually followed by, some of the following: malaise,
loss of appetite, stomach awareness, and individually
variable nausea. There is a marked antipathy to physical
or mental activity, marked somnolence, loss of initiative,
lassitude, and irritability. Headache is common but vari-
able. There is little change in skin temperature or pallor,
although fl ushing is sometimes seen ( 12 , 42 ).
Symptoms typically increase over the fi rst few hours
before stabilizing, irrespective of activity, sleep, or immo-
bilization ( 42 ). Well-trained crewmembers have success-
fully performed trained-for tasks while experiencing
SMS, including complex manual manipulations ( 42 ).
However, there have been a few disabling cases, per-
haps the most severe case documented being that of
Senator Jake Garn, who fl ew aboard STS-51-D in 1985
( 24 ). SMS resolution typically occurs within 24-72 h,
with symptoms dissipating in about 1 to 2 h. One author
who reviewed the signs that were recorded during
Garn ’ s recovery (available in Johnson Space Center
archives) can attest that even Garn ’ s severe symptoms
subsided after 2 d in orbit. SMS typically does not recur,
although there have been rare reports of recurrence
on extended missions ( 6 ).
Compared to SMS, MS onset is often more insidious.
MS signs and symptoms typically progress to possible
vomiting, whereas SMS is likely to start with vomiting
without premonition. According to well-accepted diag-
nostic criteria for grading motion sickness ( 18 ), MS symp-
toms can include nausea, dizziness, increased salivation,
pallor, flushing, drowsiness, retching, and sweating.
Hence, there is some overlap of SMS and MS symptoms,
but also clear distinctions.
T HORNTON WE, B ONATO F. Space motion sickness and motion
sickness: symptoms and etiology. Aviat Space Environ Med 2013;
84:716 – 21.
The adverse symptoms of space motion sickness (SMS) have remained
problematic since the beginning of manned spacefl ight. Despite over 50 yr
of research SMS remains a problem that affects about half of all space
travelers during the fi rst 24-72 h of a spacefl ight. SMS has been treated
as another form of motion sickness (MS) despite distinct differences in
symptomology. In this review SMS and MS differences are examined and
documented based on available data. Vestibular biomechanics that oc-
cur during weightlessness coupled with theoretical assertions regarding
human evolution have led us to propose a two-component model of
SMS. The fi rst component involves confl icting sensory signals inherent to
the otolith organs that occur during weightlessness. The second compo-
nent is a bimodal confl ict between the otoliths and semicircular canals
that can occur during normal head movements in weightlessness. Both
components may inadvertently, and mistakenly, signal that a vestibular
malfunction has occurred, hence initiating a protective mechanism that
may produce symptoms that discourage activity.
Keywords: motion sickness , space medicine , vestibular .
manned (second orbital) spacefl ight ( 44 ). Symptoms
can include periodic projectile vomiting, hypersensitiv-
ity to head motion, malaise, loss of appetite, stomach
awareness, nausea, headache, emesis, antipathy to activ-
ity, somnolence, loss of initiative, lassitude, and irritabil-
ity ( 39 ). SMS has an incidence rate of about 50% during
the 24-72 h of most spacefl ights ( 31 ). After a half century
of studies and attempted countermeasures, SMS re-
mains an unresolved problem ( 25 ).
Some features of SMS are similar to motion sickness
(MS); hence, the term ‘ space motion sickness ’ ( 12 ).
Another early term that had been sometimes used synony-
mously for SMS is space adaptation syndrome; however,
this term has since given way to SMS. Early investiga-
tions and SMS treatments were based on MS, including
symptoms that can occur during parabolic fl ight ( 25 ).
While SMS was recognized as a transient disorder, MS
countermeasures were not effective enough to be used
( 11 ) and MS drugs were only partially effective ( 7 ). These
fi ndings called into question the idea that SMS is simply
another form of MS.
PACE MOTION sickness (SMS) is an ill effect of
weightlessness that was fi rst reported on the fourth
SMS and MS Symptomology Compared
A comparison of SMS and MS symptoms is shown in
Table I . The following description of SMS is based on
in-fl ight observations and measurements and validated
reports from a limited number of cases. SMS usually
Peer review and editorial oversight for this article were conducted
by Sarah A. Nunneley, M.D., M.S., Editor Emerita of this journal.
From Boerne, TX, and Montclair State University, Montclair, NJ.
Aviation, Space, and Environmental Medicine x Vol. 84, No. 7 x July 2013
SMS VS. MOTION SICKNESS — THORNTON & BONATO
Angular motion hypersensitivity is invariably present
in SMS ( 17 , 42 , 44 ). Pitching head movements provoke
the most disturbing sensations, followed in severity
by roll and then yaw movements ( 3 ). Such motions can
exacerbate SMS symptoms, including the usual nausea
to vomiting progression often seen in MS. Not surpris-
ingly, provocative angular head motions are typically
avoided during SMS ( 6 ).
On STS-7, Norman Thagard observed the absence of
bowel sounds in SMS ( 41 ). Recordings on subsequent
fl ights confi rmed the rapid disappearance of bowel
sounds and their reemergence in the hour coincident
with symptom resolution ( 42 ). This may be a reliable ob-
jective indication of SMS ( 41 ) and a topic that should
perhaps be studied more rigorously. We note here that
gastrointestinal (GI) motility seems to differ in SMS and
MS. Whereas GI motility at least based on limited data
appears to cease when SMS occurs, some investigators
have reported that during visually induced MS GI
motility actually increases from a normal baseline of
3 cpm to 4-9 cpm ( 37 ). In short, SMS and MS symptoms,
although overlapping to some degree, are different in
some notable ways. It seems logical to infer from these
symptom differences that the causes of SMS and MS are
Origin and Function of SMS and MS
Several theories of SMS have been proposed and
described in detail in other available reviews ( 26 ).
Hence, these theories will only briefl y be mentioned
here; they include the following suppositions. Sensory
confl ict theories assert that incongruent signals from
two or more sensory modalities can lead to symptoms
( 34 ) both for SMS and MS. Otolith asymmetry is a postu-
lated difference in bilateral otoconia layer mass that
several investigators asserted could contribute to SMS
( 14 , 19 ). The otolith tilt translation theory asserts that
otolith sensors must respond identically to gravity and
inertia ( 47 ). However, during weightlessness, only inertia
will be present, leading to the prediction that transient
acceleration/deceleration signals from the otolith sen-
sors resulting from head rotations would be mistakenly
sensed by the brain as translations ( 3 ). It has also been
proposed that gravity transitions can lead to a sensed
vertical that is inconsistent with the subjective vertical
based on previous experience ( 4 , 5 ) and this vertical
mismatch in turn leads to SMS. Fluid shifts have also
been considered as a possible cause of SMS after it was
discovered during Skylab IV that liters of fl uid were
rapidly shifted from the extremities to the torso and
head ( 40 ) and then lost over the next several days ( 43 ).
Here we propose an SMS theory based on evolution
with the understanding that such theories are often criti-
cally viewed because they do not lend themselves to
empirical investigation. We speculate that evolution and
natural selection are the only scientifi cally acceptable
explanation of the presence of the vestibular system and
its pathways to gut and brain. The reconstruction of
evolutionary developments that led to the presence of
these systems today is diffi cult and incomplete, but our
interpretation is consistent with the information that is
available. Whereas the value of positing an SMS theory
based on evolution can be debated, we present the the-
ory here for those who wish to contemplate the “ why ”
in addition to the “ how, ” an evolutionary context hope-
fully adding to a fuller understanding.
Treisman appears to have been the fi rst to suggest ( 45 )
that MS is the inadvertent result of an evolutionary sys-
tem triggered by the vestibular nuclei. He proposed that
the GI detection and emesis system for ejection of in-
gested poisons could be triggered by blood-borne toxins
generated by vestibular activity. While in general his
evolutionary concept may be correct, in 1983 it was dem-
onstrated that the proposed mechanism in this scheme
does not exist ( 29 ).
In 2010, an ancient species adaptation for protection
against vestibular malfunction inadvertently triggered
by some motions and by weightlessness was described
( 39 ). This protective mechanism (PM) is based on known
or accepted neuroanatomy and functions that collectively
trigger autonomic GI and brain protective responses in
the case of confl icting signals from the vestibular system
produced by injury, malfunction, or environment. Phy-
logenetic and functional features of this “ fail safe ” sys-
tem will be briefl y described here, and the operational
features in the etiology section.
Two systems essential to advanced animal life are
those that deal with nutrition and orientation ( 32 ). To
facilitate nutrition, primitive ocean dwellers developed
a one-way digestive tract with neurological control of its
motility ( 38 ). A second neural connection could produce
vomiting when gut pressure became abnormal. Sensing
body orientation progressed to the development of hair
cells that indicated the direction of the local gravito-
inertial vector ( 46 ). At some point during evolution,
tracts establishing communication between gut and oto-
lith sensors bridged the tiny gap between GI and ves-
tibular neurons in the brain stem.
A primary activity of our ancestral fi sh was fi nding
food while avoiding being eaten. Any malfunction of its
vestibular system could compromise its ability to swim
and maneuver, making it vulnerable. Causes of vestibu-
lar dysfunction were and still are varied, but often tran-
sient. A GI/vestibular connection that produces paresis
of the GI tract would in turn produce symptoms that
would discourage activity. An affected fi sh could simply
“ lie-up ” for some time, increasing survival odds. When
some fi sh left the sea for dry land approximately 375 mil-
lion years ago ( 36 ), the PM was propagated into many
vertebrate species, including Homo sapiens , where it re-
Unfortunately, when we are placed in some moving
environments, real or simulated, the vestibular system
also triggers the PM, producing MS. In weightlessness
the PM can lead to SMS. Both sets of conditions may
inadvertently, and mistakenly, signal that a vestibular
malfunction has occurred. In summary, a logical and
supportable answer to why MS and SMS occur is that
under some contrived circumstances they are unfortu-
nate byproducts of a valuable PM normally activated
718 Aviation, Space, and Environmental Medicine x Vol. 84, No. 7 x July 2013
SMS VS. MOTION SICKNESS — THORNTON & BONATO
by vestibular failure that can also be falsely triggered
by environmental conditions.
An Evidence-Based Etiology of SMS
Our SMS model is based on a biophysical analysis of
known vestibular organ characteristics and connections.
This model has two components. The fi rst component is
unique to weightlessness and involves confl icted sen-
sory signals that occur in a single sensory modality; spe-
cifi cally, the hairs cells of the otilith organs. The second
component involves head movements and the semicir-
cular canals. Although the fi rst component may be all
that is required for SMS to occur, unless head move-
ments are prevented, the second component will nor-
mally serve to exacerbate symptoms.
It has been speculated that the gravito-inertia depen-
dent otolith sensors must play a role in SMS ( 8 , 16 ), but
the mechanism has never been fully described. To un-
derstand the otolith organs ’ role in SMS, and the fi rst
component of our theory, we begin with the vestibular
hair cell ( 16 ) that is present in many species ( 23 ). In
humans there are 30-40 thousand otolith hair cells, each
having cilia on their apical surfaces. Two aspects of the
cilia are important to SMS: 1) they are “ spring loaded ”
to a neutral position ( 22 ); and 2) in this position they
produce a constant frequency discharge through their
associated neurons ( 28 ).
If the cilia are displaced in a direction from the
shortest stereocilia toward the long kinocilium neu-
ron, discharge frequency is increased. Reverse the di-
rection of the displacement and frequency is decreased.
Displacements from other directions or pressure changes
TABLE I. CHARACTERISTICS OF MOTION SICKNESS AND PRIMARY SPACE MOTION SICKNESS.
Motion Sickness in 1 g Space Motion Sickness *
Onset Ramps up, adding symptoms in sequence:
salivation, pallor, cold sweating, stomach
awareness, nausea, vomiting. Rate
depends on stimulus intensity.
Depends on duration and intensity of
stimulus. Most adapt with continued
stimulus in days to weeks. Some
Trapezoidal; height and slope depend
on intensity of stimulus.
Stomach awareness, anorexia, nausea,
and vomiting, which may become
continual and severe with retching.
Skin pallor, cold sweating. GI system
has abnormal activity.
Variable. Some develop “ sopite syndrome ”
with somnolence, lethargy. Often
physically and mentally disabled.
Decreasing symptoms over many hours.
Symptoms of nausea and vomiting may
recur after cessation of very long stimulus.
Mal de embarkment (MS on leaving
ship after long voyage).
Highly variable with intensity.
Typically, sudden projectile vomiting
without warning, minutes to hours
after weightlessness begins.
Duration 8 to 72 h, typically 24 to 36.
Time profi le Similar to step function; constant
unless provoked by motion stimuli.
Stomach awareness, anorexia.
Nausea, usually mild if present.
Brief, few heaves, periodic (hours).
No change or sometimes fl ushing,
warmth. GI system: constant ileus.
Somnolence, lethargy, variable headache,
averse to all physical and mental activity.
Can perform trained tasks.
Once begun, recovery is rapid (1 to 3 h).
Can recur in a few individuals on return
to g loads.
Gastrointestinal (GI) symptoms
Autonomic nervous system activity
Central nervous system
* These characteristics are based on the single modality otolithic (primary) component of SMS. The secondary bimodal SSC/otolithic confl ict is hyper-
sensitive to normal head motions, but appears to produce symptoms similar to 1-g MS.
have little or no effect. Connection of the cilia to a mass
creates a single axis accelerometer. The fi brous reticular
membrane covers a layer of hair cells with passages for
the cilia to make mechanical connections to the gelati-
nous membrane that supports a layer of dense otoco-
nia ( 23 , 33 ). When this arrangement is tilted, the weight
of the otoconia displaces the gel and cilia, producing a
signal proportional to the angle of tilt.
Rows of sensors with a common orientation are de-
picted in Fig. 1A ( 20 ). Examining a single plane of this
arrangement in 1 g ( Fig. 1B ) and then in weightless-
ness ( Fig. 1C ) reveals what we think is the primary
cause of SMS. Although it is acknowledged that the
otolith organs respond to force, responding equiva-
lently to gravity and linear acceleration, we have used
‘ weight ’ in Fig. 1 for the purpose of illustration. The
sensor arrangements in Fig. 1A are shown with the
head upright in 1 g. The combined output of a row of
sensors in the almost vertically mounted saccule indi-
cates a g vector, but its polarity is ambiguous. When
this is combined with orientation of the utricular vec-
tor, the ambiguity is resolved into a vector pointing
down. This process will go on in all the other vectors
that are combined into a single congruent orientation
In Fig. 1C the otoliths are in weightlessness and the
cilia of all hair cells return to their neutral position,
generating signals that would normally indicate that
all the cilia were perpendicular to a gravity vector with
two possible polarities. This can only happen during
weightlessness. While the fi rst order signals from sen-
sors with a common orientation are congruent, their
Aviation, Space, and Environmental Medicine x Vol. 84, No. 7 x July 2013
SMS VS. MOTION SICKNESS — THORNTON & BONATO
combined signals in weightlessness will produce mul-
tiple confl icts and a meaningless output. This confl icted
signal may trigger the GI and other “ fail safe ” protec-
tive mechanisms and hence the primary symptoms of
SMS that will continue until the confl ict is resolved via
adaptation. This confl ict: 1) is induced only by weight-
lessness and hence is unique to SMS; 2) occurs within a
single sensory modality (otolith organs); and 3) is pro-
duced by an intrinsic functional failure in the modali-
ty ’ s sensor.
In short, the otolith organs did not evolve to function
in weightlessness. When placed in a weightless environ-
ment, otolithic output becomes functionally meaning-
less. Afferent vestibular signals instead indicate to the
brain that some vestibular malfunction has occurred.
These signals in turn activate a set of protective failsafe
mechanisms that are ancestral in nature and serve to im-
mobilize the subject. This single modality confl ict can-
not happen on Earth and hence cannot be a cause of
terrestrial motion sickness; it only applies to SMS.
The second component to our model involves a bi-
modal confl ict between the semicircular canals and the
otiliths that can contribute to symptoms when head
movements occur. To understand this confl ict it is im-
portant to note that in addition to sensing orientation
per se, otolith organs also sense angular motion or
changes in orientation. Some otolith hair cells become
active during orientation changes and produce a signal
proportional to the rate of change ( 1 ). Semicircular
canals (SSC) are involved only in change of orienta-
tion or angular motion ( 2 ). Signals from the otolith sen-
sors and SSCs are normally congruent. However, during
weightlessness there will be no meaningful otolithic
output and head motions will lead to incongruent oto-
lith and canal signals. This confl ict may be the cause of
hypersensitivity to head motion for those with SMS.
Even though this confl ict involves motion, it is essen-
tially caused by otolithic malfunction due to weightless-
ness and hence is unique to spacefl ight and SMS.
This bimodal confl ict was experienced in an unforget-
table way on STS 8. Gardner and Thornton were string-
ing wire for an EOG study in the fi rst hour on orbit
when Gardner had two or three heaves of projectile
vomiting. Both were careful to avoid rapid head move-
ments. Thornton began a focused neuro on Gardner that
was unremarkable until Gardner was pitched forward
with eyes closed at a nominal rate. Thornton was forci-
bly shoved away to the shout of “ Don ’ t do that! ” Thorn-
ton had his own projectile vomiting 15 min later and, on
normal head tilt, experienced the virtually indescribable
confl ict that had provoked Gardner ’ s atypical outburst.
It seems reasonable to assume that this bimodal confl ict
is processed along the same pathway through the che-
moreceptor trigger zone that may be used by ordinary
(1 g) MS, triggering nausea and vomiting.
In short, our model of SMS contains two components
as can be seen in Fig. 2 . This etiology asserts a new and
unique intramodal otolith sensor confl ict, whose stimu-
lus is weightlessness. In addition, a motion-dependent
bimodal confl ict between otolith sensors and the SSCs is
included in the model. Despite our assertion of two sep-
arate components to this etiology, there is the potential
for overlapping symptoms.
Resolution of SMS symptoms typically occurs after
8 to 72 h (typically 24-48 h) of weightlessness ( 35 ).
Resolution is remarkably rapid, occurring completely
in a few hours. This requires signifi cant change in the
vestibular system. Conceivably the changes could be
accommodated within the functional limits of neuronal
signal processing, given the extent and complexity of
the vestibular system, but that is still largely unknown.
How do neurons adapt to confl icting sensory inputs?
There is ample clinical evidence that adaptation to even
severe vestibular damages or loss occurs in surprisingly
In the case of SMS, suppression of the otolith signals
may be adequate to remove both single and bimodal
confl icts and their symptoms. A functional suppression
by the existing nerve circuits demonstrates some perma-
nence as indicated by disturbed function during entry
and on return to 1 g. Although not statistically signifi -
cant, some reports suggest that SMS may be reduced on
subsequent fl ights ( 27 ). This would indicate architec-
tural and circuit adaptation. Moreover, there is accumu-
lating evidence from in-fl ight animal studies of neural
systems receiving vestibular signals showing that neural
Fig. 1. Otolith sensor function in 1 g and weightlessness. A) Saccu-
lar and utricular maculae geometry very generally consists of otoconia
membrane sheets for each organ. The saccular sheet is mounted almost
vertically and normal to most of the utricular macula, which is raised at
the anterior end so that all 1-g axes can be detected. Orientations of the
hair cells’ polarities are shown by the arrows. BA indicates body/head
vertical axis. B) Tilting from head upright in 1 g stimulates response of
the hair cells in the plane through the saccules. The signal from the sac-
cule (S) indicates that the g vector is down. The otoconia membrane of
the utricles (U) is only slightly affected by small head tilts. Signals from
S and U are combined in the associated second order neuron (N 2 ) that
produces a sensed orientation of a downward g vector parallel with the
head’s vertical axis. C) In weightlessness all hair cells move to their neu-
tral position, indicating a g vector parallel to their cilia with all possible
polarities. When these multiple g vector signals are combined at N 2 , as
shown in the example, a confusing signal is produced.
720 Aviation, Space, and Environmental Medicine x Vol. 84, No. 7 x July 2013
SMS VS. MOTION SICKNESS — THORNTON & BONATO
plasticity is remarkable and rapid ( 13 ). Other in-fl ight
animal studies have found rapid changes in genetic ex-
pression in select vestibular areas ( 10 ). Similar rapid
changes have been found in otolithic sensors with both
increases in the number of hair cell synapses as well as
apparent degeneration of other synapses ( 9 ). Existence
of equivalent change and their signifi cance in humans
remain to be demonstrated. However, it is reasonable
to assume that both neurological accommodation and
adaptation occurs in all humans on exposure to weight-
lessness for more than a few hours, and that a signifi -
cant fraction of them will have a variety of symptoms,
beginning with return of g loading on reentry and con-
tinuing for various individual postfl ight periods ( 21 ).
It is beyond the scope of this paper to examine these
Prior to SMS, MS had been studied and, although the-
ories differed somewhat, it was generally agreed that its
cause was a confl ict between different sensory modali-
ties. However, its origin remained a question, for while
a phylogenetic protection against endogenous toxins
had been proposed ( 45 ), the existence of this specifi c
mechanism was not supported. When SMS symptoms
began to occur during orbital fl ight it was assumed that
SMS was another member of the MS family and the prob-
lem was investigated and treated accordingly. Numerous
etiologies were proposed and investigated but none cov-
ered all aspects of SMS.
By considering SMS and MS as inadvertent byproducts
of an ancient phylogenetic protective mechanism and
by examining the biophysical effects of weightlessness,
we have proposed an etiology of SMS. Weightlessness is
a singularity in the range of gravito-inertial forces and
produces a singular confl icted response in the otolith
sensors. This confl ict only occurs for SMS and is absent
for MS. Hence, the etiologies of SMS and MS are different
in this way. A second component contributing to SMS is
a bimodal confl ict between otolith sensors and angular
motion sensors that can occur during head movements.
This second component appears to produce GI and other
symptoms consistent with the known pathways in MS.
This etiology for SMS appears to strain long held hopes
of prefl ight adaptation, but it may offer a basis for more
Authors and affi liations: William E. Thornton, M.D., no affi liation,
Boerne, TX, and Frederick Bonato, Ph.D., Montclair State University,
1. Baloh RW, Kerber KA . Clinical neurophysiology of the vestibular
system. New York: Oxford University Press; 2011:45 .
2. Beliz TA . Brief review of vestibular system anatomy and its
higher order projections . Neuroanatomy 2005 ; 4 : 24 – 7 .
3. Benson AJ . Modifi cation of the response to angular accelerations
by linear accelerations. In: Kornhuber HH, ed. Handbook of
sensory physiology, volume VI. Vestibular system, part 2:
psychophysics, applied aspects and general interpretations.
Berlin: Springer; 1974:281 – 320 .
4. Bles W, Bos JE, de Graaf B, Groen E, Wertheim AH . Motion
sickness: only one provocative confl ict? Brain Res Bull 1998 ;
47 : 481 – 7 .
5. Bles W, de Graaf B . Postural consequences of long duration
centrifugation . J Vestib Res 1993 ; 3 : 87 – 95 .
6. Bryanov II, Gorgilzadze GI, Kornilova LN . Vestibular function.
In: Gazenko OG, ed. Results of medical research performed
on the Salyut 6-Soyuz Orbital Scientifi c-Research Complex.
Moscow: Meditsina; 1986:169-85, 248 – 56 .
7. Buckey J . Space physiology. New York: Oxford University Press;
8. Budelman BU . Morphological diversity of equilibrium receptor.
In: Atema J, Fay RR, Popper AN, Tavolga WN, eds. Sensory
biology of aquatic animals. New York: Springer-Verlag; 1988:
757 – 82 .
9. Cheung B, Vasitkus P . Perspectives of electrogastrography and
motion sickness . Brain Res Bull 1998 ; 47 : 421 – 31 .
10. Cheung CC, Hecht H, Jarchow T, Young LR . Threshold-based
vestibular adaptation to cross-coupled canal stimulation .
J Vestib Res 2007 ; 17 : 171 – 81 .
11. Clément G, Deguine O, Parant M, Costes-Salon MC, Vasseur-
Clausen P, Pavy-LeTraon A . Effects of cosmonaut vestibular
training . Eur J Appl Physiol 2001 ; 85 : 539 – 45 .
12. Clement G, Reschke M . Neuroscience in space. New York:
Springer-Verlag; 2008:72 .
13. Crampton G , ed. Motion and space sickness. Boca Raton, FL: CRC
Press; 1990 .
14. Egorov B, Samarin G . Possible changes in the paired operation
of the vestibular apparatus during weightlessness . Kosm Biol
Aviakosm Med 1970 ; 4 : 85 – 6 .
15. Gibson EG . Skylab 4 crew observations. In: Johnston R, Dietlein L,
eds. Biomedical results from Skylab. Washington, DC: Scientifi c
and Technical Information Offi ce, National Aeronautics and
Space Administration, 1977:22 – 6 .
16. Gray O . A brief survey of the phylogenesis of the labyrinth .
J Laryngol Otol 1955 ; 69 : 151 – 79 .
17. Graybiel A, Lackner JR . A sudden-stop vestibulovisual test for
rapid assessment of motion sickness manifestations . Aviat
Space Environ Med 1980 ; 51 : 21 – 3 .
Fig. 2. Function diagram of SMS. The primary confl ict is intrinsic to
the otoliths and produces the episodic projectile vomiting of SMS by
constant inhibition of GI motility. The second is between the otolith or-
gans and semicircular canals during angular motion and follows the usu-
al pathway in motion sickness through the chemoreceptor trigger zone
to the vomiting center. If motion stimulus is continued, the usual nausea
and vomiting of motion sickness occurs. Confl ict signals also trigger the
Aviation, Space, and Environmental Medicine x Vol. 84, No. 7 x July 2013 Download full-text
SMS VS. MOTION SICKNESS — THORNTON & BONATO
18. Graybiel A, Wood C, Miller E, Cramer D . Diagnostic criteria for
grading the severity of acute motion sickness . Aerosp Med
1968 ; 39 : 453 – 5 .
19. Gurovskiy NN, Bryanov II, Yegorov AD . Changes in the vestibular
function during space fl ight . Acta Astronaut 1975 ; 2 : 207 – 16 .
20. Guyton AC . Textbook of medical physiology, 8h ed. Philadelphia:
W.B. Saunders; 1991 .
21. Hammer LR . Aeronautical Systems Division studies in weight-
lessness: 1959-1960. Wright-Patterson Air Force Base, OH:
Aeronautical Systems Division, Air Force Systems Command,
United States Air Force; 1961. Wadd Technical Report 60-715 .
22. Hoagland H . Impulses from sensory nerves of catfi sh . Proc Natl
Acad Sci U S A 1932 ; 18 : 701 – 5 .
23. Hunter-Duvar I . Vestuble: sensory epithelia. In: Friedmann I,
Ballantyne J, eds. Ultrastructural atlas of the inner ear. Boston:
Butterworths; 1984:214 – 16 .
24. Johnson Space Center . Oral history project. Houston, TX: NASA
Johnson Space Center; May 13, 1999:13 – 35 .
25. Lackner JR, Di Zio P . Space motion sickness . Exp Brain Res 2006 ;
175 : 377 – 99 .
26. Lackner JR, DiZio P . Angular displacement perception modulated
by force background . Exp Brain Res 2009 ; 195 : 335 – 43 .
27. Lapayev EV, Vorobyev OA . The problem of vestibular physiology
in aerospace medicine and prospects for its solution. . In:
Proceedings of Space Biology and Aerospace Medicine: 8th
All-Union Conference; Kaluga, 1986. Moscow, Russia: Nauka;
1986:85 – 6 .
28. Lundberg YW, Zhao X, Yamoah EN . Assembly of the otoconia
complex to the macular sensory epithelium of the vestibule .
Brain Res 2006 ; 1091 : 47 – 57 .
29. Money KE, Cheung BS . Another function of the inner ear:
facilitation of the emetic response to poisons . Aviat Space
Environ Med 1983 ; 54 : 208 – 11 .
30. Mullane M . Riding rockets. New York: Scribner; 2006:171 .
31. Putcha L, Younker D, Daniels V . Space motion sickness: analysis
of medical debriefs data for incidence and treatment [Abstract] .
Aviat Space Environ Med 2012 ; 83 : 303 – 4 .
32. Peusner KD . Development of the gravity sensing system . J
Neurosci Res 2001 ; 63 : 103 – 8 .
33. Purves D, Augustine GJ, Fitzpatrick D, Hall WC, LaMantia A,
et al. , eds. Neuroscience, 3rd ed. Sunderland, MA: Sinauer
Associates; 2004:317 – 9 .
34. Reason J, Brand J . Motion sickness. London: Academic Press;
35. Reschke MF, Harm DL, Parker DE, Sandoz GR, Homick JL,
Vanderpoeg JM . Neurophysiologic aspects: space motion
sickness. In: Nicogosbian, AE, Huntoon, CL., Pool, SL, eds.
Space physiology and medicine, 3rd ed. Philadelphia: Lea and
Febiginger; 1994:228 – 60 .
36. Shubin N . Your inner fi sh. New York: Vintage Books; 2009 .
37. Stern RM, Koch KL, Leibowitz HW, Lindblad IM, Shupert CL,
Stewart WR . Tachygastria and motion sickness . Aviat Space
Environ Med 1985 ; 56 : 1074 – 7 .
38. Stevens CE, Hume IP . Comparative physiology of vertebrate
digestive systems, 2nd rev. ed. Cambridge: Cambridge University
Press; 1995: 288 – 320 .
39. Thornton WE . A rationale for space motion sickness . Aviat Space
Environ Med 2011 ; 82 : 467 – 8 .
40. Thornton WE, Hoffl er GW, Rummel JA . Anthropometic changes
and fl uid shifts. In: Johnston R, Dietlein L, eds. Biomedical
results from Skylab. Washington, DC: Scientifi c and Technical
Information Offi ce, National Aeronautics
Administration; 1977:330 – 8 .
41. Thornton WE, Linder BJ, Moore TP, Pool SL . Gastrointestinal
motility in space motion sickness. Aviat Space Environ Med
1987; 58(9, Pt. 2):A16 – 21 .
42. Thornton WE, Moore TP, Pool SL, Vanderploeg J . Clinical
characterization and etiology of space motion sickness. Aviat
Space Environ Med 1987; 58(9, Pt. 2):A1-8 .
43. Thornton WE, Ord J . Physiological mass measurements in
Skylab. In: Johnston R, Dietlein L, eds. Biomedical results from
Skylab. Washington, DC: Scientifi c and Technical Informa-
tion Offi ce, National Aeronautics and Space Administration;
44. Titov G, Caiden M . I am eagle. Indianapolis: Bobbs-Merrill; 1962 .
45. Treisman M . Motion sickness: an evolutionary hypotheses . Science
1977 ; 197 : 493 – 5 .
46. Wetzig J . Will man need the vestibular system in generations
to come? A slightly heretical review . Physiologist 1993 ; 36 ( 1,
Suppl .) S9 – 12 .
47. Young LR . Perception of the body in space: mechanisms. In:
Darian-Smith I, ed. Handbook of physiology; section 1, the
nervous system; volume III, sensory processes, part 2. Bethesda:
American Physiological Society; 1984:1023 – 66 .