last updated: 2017-05-11


This text is an adaptation of my inaugural lecture at the VU University, Amsterdam, the Netherlands, presenting a personal view, though largely based on what I have learnt from others.





Standing and walking erect on two legs is an Art requiring a control system with adequate sensors, ample redundancy, and smart adaptive integration of available information.  This is something humans normally do pretty well. Normally, because there are conditions in which this fails.  After prolonged rotation we generally feel dizzy and may even fall, which may also happen after the intake of alcohol.  Also we may get sick of motion, even by only looking at motion pictures while sitting still, do we abort simulator trainings due to simulator sickness, and have complete naval battles been lost due to seasickness.  Furthermore we may lose sharp sight due to vibrations, do we fall more often after the age of 70, and do some of us suffer from vestibular diseases such as Ménière's disease [1].  Lastly, pilots may get disoriented ultimately resulting in a controlled flight into terrain.


To understand self-motion perception, some knowledge on kinematics (which is about motion per se) and kinetics (which is about the causes of motion, typically forces) may be helpful.







Object motion, i.e., that of an infinitesimal small point, can generally be described by position (x, defined in three dimensions (x,y,z) relative to some point in space, it's velocity (v = dx/dt), and/or it's acceleration (a = dv/dt = d2x/dt2). Higher order derivatives may also be defined, such as jerk (j = da/dt = d3x/dt3), snap (s = dj/dt = d4x/dt4), cracle (c = ds/dt = d5x/dt5) and pop (p = dc/dt = d6x/dt6).  The latter three are also onomatopoeic mascots used by Kellogg's, referring to the sound of chewing cornflakes.  To define the state of an object in time, either all it's time derivatives should be known at one particular moment, or one of them should be known over a certain interval.




A body, moreover, generally consists of several (infinitesimal small) points.  If these points are rigidly connected, the motion of the body as a whole can be described by the linear motion of its centre of mass, and the way all the points rotate about that centre.  The state of a (rigid) body in the 3D world is then given by six degrees of freedom: three (linear) translations (along, e.g., the x-, y-, and z-axis), and three angular motions about these axes.  Note that, although all points within the body may have different linear motions, the angular motion of all points within a rigid body are equal!




Motion is furthermore largely determined by the laws of physics, in particular Newton's laws of motion.  These roughly state that


1.  An object moves with a constant velocity (v, characterized by direction and magnitude, the latter possibly being zero), unless perturbed by an external force (F).  This law was, in fact, already formulated by Galilei before Newton.

2.  If perturbed, the change of velocity, i.e., its acceleration (a = dv/dt) of the body is directly proportional to (and in the same direction as), that external force (F=ma, with m the mass of the object).

3.  If one object exerts a force (F1) on a second object, the latter will exert a reaction force (F2) equal in magnitude and opposite in direction to that of the first (F2= -F1).




In addition, Newton's law of universal gravitation states that gravity is the phenomenon that two masses attract each other by a force (Fg) directly proportional to both masses (m1 and m2) and inversely proportional to the square of their mutual distance (r) according Fg = k×m1m2/r2×r (with r here denoting a unit vector along the line connecting the two masses).  This also gives weight to masses according Newton's second law, i.e., Fg = mg, with g = 9.81 m/s2 the average free-fall or gravitational acceleration at the Earth's surface.  The relationship between gravity and inertia will be detailed below.





Our central nervous system (CNS), however, does not always seem to be aware of all these time derivatives and laws, why the laws of perception may differ from the laws of physics.  For example, perceived velocity not necessarily equals the time derivative of (perceived) position, and perceived acceleration does not need to equal the time derivative of (perceived) velocity, nor does it need to be proportional to (perceived) acceleration as given by Newton's second law.  Moreover, in our 3D world we have to deal with six degrees of freedom, three translations and three rotations.  On Earth, we have to deal with gravity in addition, which by Newton's second and third laws gives rise to an acceleration, the free-fall acceleration (g=-Fg/m), theoretically adding three more degrees of freedom.  The latter, however, are dependent on the other degrees of freedom by the laws of physics, i.e., when we tilt our body, for example, gravity rotates with respect to our body unambiguously prescribed by that body-tilt.  Here again, our CNS not always to reckons this relationship. The ambiguities left by the CNS may all together already explain why we are facing illusions, postural instabilities and motion sickness.




But, there is more, as may already be exemplified by the well-known, but ever striking visual illusion [2] shown by the turning face right.  And here again the CNS plays a crucial role.  Yet, some knowledge on our senses themselves is essential too, most importantly the organs of balance and the eyes.





Just behind our ears, embedded by the skull, there is a cavity (also called the vestibule), containing two sensor: the cochlea by which we hear, and the organs of balance by which we feel motion.  The organs of balance, in turn, consist of two parts: a set of three semi-circular canals by which we feel angular motion, and two sets of otoliths by which we feel linear motion.




Semicircular canals

The semi-circular canals contain fluid (endolymphe) which lags the head due to inertia when the head moves.  Within each canal, a little valve (the cupula), connected to the head by hair cells, moves with the endolymphe, thus signalling angular motion.  If the head rotates with a constant velocity, the endolymphe will move with the head because that cupula restricts the flow of endolymphe and because of friction between the endolymphe and the wall of the canals. Due to elastic properties, the cupula will then return to its resting position, thus signalling no motion anymore. You may experience this yourself while being rotated carefully by a friend on a desk chair, with your eyes closed, of course.  If you would then stop abruptly, the endolymphe will  keep on moving, due to inertia again, thus giving you a sense of rotation in the opposite direction.  This sensation will die out for the same reasons as mentioned above.  This illusory motion is also called the somatogyral illusion.  People in whom the organs of balance are not functioning, this somatogyral illusion is absent.  This is often the case in totally deaf people, because the endolymphe of the cochlea is shared by the organs of balance, and dysfunction of the one is also shared by a dysfunction of the other.  You may find a nice demonstration in the (Dutch) educative children's programme klokhuis.
To only sense angular and not linear motion (see the otoliths below) the cupula should be as heavy as the endolymphe (i.e., having the same specific mass), which is the case indeed.  Perhaps nice to know is that alcohol has a lower specific mass than endolymphe.  If there is sufficient alcohol in your blood, the blood vessel containing cupula of the most vertically oriented canal will then float upwards, thus giving a spinning sensation you may recognize.


Within the sacs connecting the canals, each ear also contains two layers of hair cells with calcium-carbonate crystals on top.  These layers are also called otoliths, and are sensitive to linear motion.  The most horizontally oriented layer (in an upright head orientation) is called the utricule (or utriculus in Latin) and is mostly sensitive to horizontal motion.  The other, most vertically oriented layer is called the saccule (or sacculus) and is mostly sensitive to vertical motion.  Different from the utricles, the saccules are assumed to also have an auditory function.  The brushes shown in the image above [
3], only exemplify the function of the otoliths, rather than showing an anatomically correct image.  This function, is about as follows.



In the image shown here, one of the crystals is represented by a little blue ball, and is attached to the head, the big orange ball, by means of a string, the gray line in between.  If then the head is accelerated upwards in space, if not attached to the head, the crystal would remain in place if not attached to the head.  But because it is, it will be pulled upward by the string, and because that string is flexible, that string bends.  Moreover, in case of a static acceleration, the deflection thereof is constant.  The larger the acceleration, the larger the deflection, and the cell from which the string originates, will signal accordingly.  The otoliths therefore function as pretty good accelerometers.  However, on Earth, these crystals are also attracted by the mass of the Earth, i.e., by gravity (see above), where the gravitational force is proportional to the masses and inversely proportional to their mutual distance squared.  Because the mass of the Earth is huge, this force is considerable at the Earth's surface.  The problem, however, is that although gravity is physically different from inertia, the acceleration associated with it, i.e., the gravitational acceleration, is indistinguishable from inertial acceleration, a phenomenon also referred to as Einstein's equivalence principle [4].


As a consequence, I am in favour of drawing the gravitational acceleration as a vector pointing upward, despite the gravity (force) vector pointing downward.


If our central nervous system (CNS) would not reckon this equivalence principle, it might assume the free-fall acceleration to be inertial, thus being caused by motion.  It is then easy to calculate by integrating the free-fall acceleration (9.81m/s2) twice over an interval of 5 minutes, we would have travelled over a vertical distance of approximately 440km, which is about the height at which the International Space Station is circling around us.  Though it may seem trivial, the observation that most of us generally do not experience this, is by far trivial.  Moreover, it leads to the conclusion that our CNS, despite Einstein's equivalence principle, apparently is capable of making the distinction between inertial and gravitational acceleration.  This extraordinary capability seems to be based on the genetical capacity of our CNS to learn that gravity is constant (at least in our life), while inertial self-motion is either variable or of short duration.  Although I wonder whether Einstein has given this a thought, the first to explicitly mention and elaborate on this idea was Mayne [5].  He assumed our CNS applies a kind of low-pass filtering of otolith signals to estimate gravity and high-pass filtering to estimate motion.  This normally seems to work quite well, but there are circumstances in which this mechanism fails.


Somatogravic illusion


In case of an aircraft increasing its speed on the runway before it can take-off, the inertial acceleration lasts for several (tens) of seconds.  In that case, the vector addition of the gravitational (pointing up) and inertial (pointing forward) accelerations tilts forward.  Due to the mentioned neuronal filter, that resultant acceleration will be assumed to be the free-fall acceleration after some seconds, and because we have learnt that gravity is Earth vertical, we then "think" we are tilted instead.  This is called the somatogravic illusion, and may also be experienced in a civil aircraft accelerating on the runway.  Because vision may suppresses this illusion (see also below) it is essential not to look outside, or just to close your eyes.




Especially in military aviation, this illusion is life threatening.  If, for example, a pilot accelerates at low altitude in bad visual (night) conditions, intending to fly straight and level, he should not compensate for this illusion.  If yet done so, this would, and actually does so, so now and then, result in what may be called a controlled flight into terrain.







Self-motion is not only perceived by the organs of balance, but by our eyes as well.  If we move, head and eyes all together, the image of the world will move on our retinas, and this information is added in our CNS to that of the organs of balance to improve the estimate of self-motion.  This addition can nicely be observed when in a train at a station looking at a train leaving from the opposite platform, often giving rise to a strong feeling of self-motion.  This illusion is called "vection" and may also be experienced in (IMAX) theatres with big projection screens [6,7,8].




Frame and polarity


With vection, motion is essential.  In getting information about gravity, static visual cues are essential too.  Although visual cues do not provide information about the magnitude of gravity, they do so about its orientation.  Walls, ceilings, floors, trees, all provide information about what we have learnt to be horizontal, vertical, up and down.  Whenever these structures are slanting, either by accident or deliberately, in virtual environments or in real, we may get sick and have trouble keeping balance.  In Japan, for example, Earth quake proof buildings sometimes get slanted as a whole, after which its inhabitants suffer from instabilities and nausea [9,10].  For esthetical reasons or for fun, ignorant architects may also incorporate slanted structures in their designs, and that too may not always be appreciated by the general public for the same reasons.   I would say: think twice or ask advice.




Gaze stabilisation (VCR and VOR)


Where vision plays an important role in determining our orientation with respect to gravity and keeping balance, or organs of balance play an important role in orienting our eyes at objects of interest.  In that respect it is essential to understand that we can only see colours with the centre of our retinas, and this center also has the highest density of photoreceptors and hence the largest resolving power.  Moreover, only in this central region we can see colours.  Whenever we are moving, the image of what we are focusing at may then get out of this high resolution region.  The chicken, solves this problem by keeping the head as still in space as possible, while moving the body under that, until so now and then the head makes a fast movement forward, as can be seen in the animation, the real time video and the same slow motion video







Something comparable happens when you take up a chicken and make her roll, for example, as shown below.  A more amusing version with music can be found in a commercial by Mercedes, referring to this as magic body control.  More scientifically speaking it is called the vestibulo-collic reflex (VCR).




We, humans, do something comparable, but by moving the eyes in the head, rather than moving the head on the body.  The basic problem here is that if this would be controlled by vision, (left image 1) light must first be converted into neural signals by the retina, (2) these signals be relayed to the visual cortex for processing (3, say, the graphical card in the back of our head), after which (4) the appropriate signals have to be relayed back to the eyes again, i.e., to the muscles (5) that can position the eyes such that they image the object of interest onto that central retinal part again.  This, however, is a rather complex and hence slow process, easily resulting in a blurred image.  You may observe that yourself by keeping your head still, while looking at your hand waving at arm-length.  If, however, you would then keep your hand still while shaking your head, the image of your hand will most probably keep in focus.




The explanation is that just behind our ears, (right image, 1) the organs of balance detect the motion of the head, and (2) send the information more or less directly, i.e., in a  short reflex arc, back to the eye muscles (3).  If we move the head 10 degrees left, the eyes will more or less move ten degrees right.  This, in first instance [11], does not need complex processing by that graphical card, why this reflex is simple and fast, resulting in a sharp image, even when the head moves relatively fast.  This vestibulo-ocular reflex (VOR) is simple, fast and involuntary, which implies it also exists when the eyes are closed, whether you want it or not.


As explained above, the headshaking is mainly detected by the semi-circular canals, and these do not respond to a constant angular motion.  Moreover after abruptly stopping a constant rotation, the fluid flow within the canals will last for some while, and this too can nicely observed when looking at the eyes. Especially, when using lenses that give an enlarged view on the eys, and prevent a clear vision by the subject and thus prevent visual suppression of the VOR, this is fun.  Here, the relatively slow phases are driven by the canals, while the fast resetting jumps act comparable to the fast forward motion of the chicken's head.  All together the lsow and fast phases are called nystagmus.  This reflex allows doctors to test the function of the organs of balance without the need of invasive examination.




Altogether, our organs of balance thus play a major role by controlling our eye movements for gaze stabilisation.  Moreover, this may even be an evolutionary explanation why they are so close to our eyes.  The other way round, because vision is important for keeping balance, one might say that we keep balance by our eyes, and look with our organs of balance [12].  In the following, I will elaborate on the mechanism by which we keep balance.





Servo system


To keep balance, we need a control mechanism.  A simple example, a so called servo system, is shown below.  Left in this illustration, the desire to reach or maintain a certain condition or state is represented.  Though not too important for the following, you may think of this state as a certain position or orientation in space, a certain walking speed or acceleration or any other kinematic descriptor.  Our brain has to convert this desire into signals controlling our muscles to realise the desired state as indicated in the centre.  In addition to what we want, there may also be external perturbations, as caused by wind, for example.  This is also where gravity comes into play.  At the right of the illustration, the estimated state based on sensory information is shown.  When this estimate is then compared with what we originally wanted, and there would still be a difference, the control loop will continue to readjust the state of the body until the estimated is just what we wanted.




Unfortunately, this control system is too easy for three major reasons.  Firstly, the sensory system, e.g., our eyes and organs of balance, should be perfect.  As shown above, however, they are not.  The semi-circular canals, for example, are insensitive to constant angular motion.  Secondly, the control loop should be fast, while one-fifth of a second due to neuronal delays within our CNS are no exception.  When chasing a prey, or even more so when being chased by a predator, this may be too much.  And last but not least, the estimate of acceleration should be perfect as well.  This estimate, however, is impeded by gravity, as shown by the somatogravic illusion, for example.


Internal model


That is why our CNS is in need of another mechanism to contol our body motion.  One mechanism that may do the job is shown below this paragraph.  Somewhat based on the servo mechanism shown above, the dark blocks that have been added represent "knowledge" our CNS seems to have about how our body reacts to the muscles activation and how our sensors react again to that.  This knowledge is also termed a neural store, observer, or internal model, and the signal tapped from the muscle activation an efference copy.  If that internal model would be up to date, its estimate of the sensory estimated state, would be equal to what the latter actually is.  Further analysis then shows that also the estimated state of the body equals the actual state of the body.  In this way, the CNS can create the best possible estimate to be compared with what we want, thus closing the feedback loop controlling our body motion.  If, however, the output of the internal model would not be equal to what the estimated sensory information is, due to, e.g., an external perturbation, the difference may be fed back to the internal model of the body.  This makes a secondary control loop driving the difference as yet to zero, and again creating a perfect estimate of the actual state of the body.




The elegancy of this control mechanism is that it allows for sensory imperfections, neuronal delays, and the problem caused by Einstein's equivalence principle, as long as all inadequacies are included in the internal model.  It then not only enables an optimal control of self-initiated body motion and to correct for external perturbations (including gravity), but a better understanding of our motion and attitude perception, including the way our eyes are moving [8,13,14].  Moreover, it also is capable of explaining why and how we suffer from motion sickness.





Normally, we do not get sick when moving ourselves.  We only get sick from unnatural motions forced upon us, like by a car, aircraft or ship [15,16,17].  An important detail concerns the observation that people without functioning organs of balance do not suffer from motion sickness [18,19].  Moreover, this observation can nicely be taken into account in the observer model shown above [20], assuming that the conflict between the sensed and predicted sensory state of the body provokes our gastrointestinal system.  The larger the conflict, the sicker we get.  If every disadvantage has its advantage, the advantage of sickness is that it probably incites adaptation or habituation.  In the model shown above, the conflict (between the sensed and predicted states) plays a major role in making and keeping the internal model up-to-date, allowing for an ecological explanation of motion sickness.




Another pleasant incidental circumstance of assuming the above model, is that we can calculate with it.  Then, this model may be simplified by only considering external motions, thus assuming a passive passenger.  All blocks dealing with the control of self-motion may then be eliminated.  Another limitation may be that to vertical sinusoidal motion.  This leaves a relatively simple model of which all blocks can be approximated with known mathematical (transfer) functions, resulting in the predicted amount of motion sickness as a function of motion amplitude and frequency [16].




The coloured 3D graph show the predicted motion sickness incidence (MSI, on the applicate or z-axis) as a function of the motion frequency (f, on the abscissa or x-axis) and amplitude (A, on the ordinate or y-axis).  Somewhat trivial may be the prediction that we get sicker with more motion.  What may be surprising is the prediction that we hardly get sick from motions varying with a frequency of over 0.6 Hz and below 0.06, but are very sensitive to motions varying with a frequency of 0.16 Hz, i.e., with a period of about 6 seconds.  This graph may thus also explain why sailing on the (Dutch) IJsselmeer may be more provocative with respect to seasickness than the North Sea.  At the latter the waves may be higher, but will generally also be longer and slower, the net effect being less.  Even more surprising, at least to me, is the observation that these predictions seem to be very close to what has been observed.  To that end, the inset on the top-right of the above picture shows the results of an experiment in which more than 500 subjects have been exposed to vertical periodic motion in a simulator for up to 2 hours each, or less when they had to vomit [21].  All axes in this graph are equal to that of the predicted values, thus showing a remarkable resemblance.  Though not the ultimate proof of the pudding, this resemblance, stated carefully, at least does not speak against the framework presented here.


Sickness and performance


With respect to sickness, it may be worth mentioning that this not only concerns a luxury problem.  Anarchasis, in the 6th century BC, for example, already divided humans into three categories: the living, the dead, and the seasick.  Also the reservists shown left below [22] suggest, if I may say so, not being capably of winning a war right after the depicted transport.  Although this picture may look like a caricature (which it yet isn't), the observational data shown right further substantiate this problem [23].  Moreover, from other studies, we now also know that the effect of seasickness on crew performance can even be larger than the effect of the ship motion per se [24].






So far, the above considerations on sickness only concerned physical motion, thus concerning our organs of balance.  As may be assumed from the considerations on vision, what we see may also affect sickness.  And this indeed is the case, in a positive as well as negative sense.  It is, for example, common sense among sailors that looking at the horizon has a positive (alleviating) effect on seasickness [25,26].  The other way round, looking at motion pictures can be sickening [27], even when being immobile oneself.  The latter is then generally referred to as visually induced motion sickness or more specifically cybersickness in case of computer gaming, for example.  With these games getting better, computer screens getting bigger, and 3D getting more common, cybersickness may get a serious issue (see also below).  A special fact of interest may be (and for me it certainly is) that people without functioning organs of balance do not only suffer from (physical) motion sickness, but also not from visually induced motion sickness [28].  Sickness, furthermore, not only is an issue with respect to gaming, with flight and driving simulators it is an issue too.  50% drop-out due to sickness has been shown not to be an exception [29,30].  Then, it may be essential to make an explicit distinction between motion sickness and simulator sickness, the latter only referring to sickness in case the simulated real condition would not give rise to sickness.  The way all different kinds of motion sickness are related is shown in the Venn diagram below.  Here, I deliberately drew space motion sickness separate from the others, because of the rare condition of the virtual absence of gravity.




Postural (in)stability


Another reason why research on cybersickness may be of interest, concerns the observation that most of us are more instable after watching motion pictures than before watching [31].  This not only has been observed in the lab, but also in a normal (3D) cinema audience [32], and it makes sense to assume that after several hour (or even days) of gaming this effect is even more obvious.  An intriguing thought concerns the possibility that the more we get used to watching motion pictures with respect to sickness (see below), the more instable we (seem to) get.  Another provoking thought may be the observation that a comparable instability as observed after watching motion pictures is known from taking alcohol.  Although comparing apples with oranges, the following graph in combination with the fact that in some countries postural stability is taken as a criterion for safe driving, is telling [31].






Back to basic it seems to make sense assuming that perception is is not the direct effect of sensory information.  Instead, it seems likely that perception is the result of a process aiming at making an optimal estimate of what reality is, and this process takes certain knowledge into account, assumed predictive for the future.  This knowledge may, furthermore, be made more concrete by an internal model.  Perception, stated differently, thus seems to be the result of an interpretation made by our CNS, only using indirect information from our senses.  This will then have certain consequences, like the effect of watching a manipulated passport photograph shown above.  There are, however, many more examples, some of which I will touch on in the remainder of this text.




Babies, for example, do not suffer from motion sickness.  They may throw up, doing that even regularly, but they do not do that due to motion.  Given the sketched frame of mind, the idea seems to be that babies are only moved passively, no motion control mechanism being active yet.  As soon as they start moving themselves, especially when standing up, however, they are in need of such a control mechanism, and creating or filling up the internal model or neural store is then at issue.  That process, however, is then troubled by the fact that both the body and the nervous system are continuously growing, i.e., liable to changes.  Until the age of about 20 years, the internal model therefore lags reality continuously, and only after that it can really "settle".  This, accordingly, should, and according the grafph below apparently is the period of life in which most conflicts between sensed and predicted signals are present, and we are also most susceptible to motion sickness.  For the same reason, the preservation and further fine tuning of the internal model results in habituation, 80 year olds being about four times less susceptible to seasickness than 20 year olds, for example [33].  Just getting old therefore seems to be a fair advice against motion sickness, at least seasickness.





Another example, though not completely different.  Apart from age, there are several reasons why the functioning of our senses may vary over time.  An inflammation of the vestibular nerve (called a vestibular neuritis by the ENT doctor), for example, may cause an acute problem.  The way the endolymphe within behaves in our semi-circular canals may change, seems to be the cause of the longer lasting Ménière's disease.  The nice thing about the sketched framework is that these changes do not necessarily need to cause a permanent problem.  As long as the internal model is capable of adapting to the new condition, the conflict between sensed and predicted signals can be kept small, thus also minimising the associated problems like sickness and postural instabilities.  The problems will then mainly be evident in the acute phase when either the senses are instable, or the internal model not yet up-to-date.  The process of getting this internal model up-to-date also refers to adaptation, habituation, or vestibular compensation, and may even be the major reason for our CNS to apply an internal model anyway.




The last example I would like to mention here again concerns motion sickness.  Especially sailors are familiar with the fact that we get used to ship motion within hours to days, also accompanied with a reduction in sickness.  After debarking, they also know about a motion sensation like still bein on the boat, and this motion can also be accompanied by sickness again.  Normally the latter disappears within hours to days. In some, however, it does not.  This is referred to as mal-de-debarquement, or when it lasts for more than days, sometimes even years, mal-de-debarquement syndrome.  Intriguingly, it has been observed that in most of these cases the organs of balance are still functioning normally, why it seems likely that the internal model got disorganised, not being able to get organised again.  From a mathematical point of view, one may then think of optimisation of the internal model transfer functions by minimising the mentioned conflict as the cost function, the process being caught in a local minimum, far off the optimal solution.





If our CNS does indeed apply an internal model to optimise the control of body motion, and if indeed it does so by keeping that up-to-date using a conflict related to motion sickness, this also offers possibilities for cure of diseases often assumed untreatable so far.  To further validate the framework presented here and then to find out how a malfunctioning internal model can best be cured, I consider a major challenge for the coming years.  The results may then be rewarding, not only for patients suffering from vertigo, dizziness and nausea.  It may also be of benefit for the treatment of elderly who keep afraid of falling after an unlucky fall.


As may be clear from this text, motion sickness is not a disease.  Moreover, it seems to be inherent to a normal, i.e., healthy life, especially when unnatural motion is at issue.  To explain motion sickness in all of its manifestations, an internal model seems to be of particular use.  Hence, here too the further elaboration of how our CNS may apply this approach will likely also reveal solutions not thought of before.


Another challenge is the optimising of motion simulators.  With the aimed reduction of costs, training on the job is often replaced by training in a simulator.  If motion would then be a factor of importance in real, it should also be in the simulation.  A problem with the simulation of motion is that most often, the vehicle to be simulated is capable making much larger motions than the simulator can.  An aircraft can go all over the world, a flight simulator should generally stay in its building.  Although from a technical point of view it then makes sense to minimise the difference(s) between the motion parameters (kinematic and kinetic) of the real vehicle and the simulator, from a human perspective it makes more sense to minimise the difference between the perceptions of both.  A motion perception model would then be helpful, especially when not only taking our senses into account but also what is sometimes referred to as mental set, or cognition.  To do so, an internal model may also be of benefit.


And, who knows, one day we may even be able to show neuronal structures actually operating like an internal model.  Up to that moment the challenge is to make its use by our CNS not only plausible as done in this text, but also probable.  For scientific reasons it might as well be good if it could be proven not to exist.




1.      Not "meunière", for that relates to the way of preparing, e.g., trout.

2.      Thanks to Eric Groen and Walter van Dijk, Soesterberg.

3.      Thanks to Bernd de Graaf and Peter Schep, Soesterberg.

4.      Einstein A (1907).  On the relativity principle and the conclusions drawn from it.  Jahrbuch der Radioaktivitat und Elektronik 4:411-462.

5.      Mayne R (1974).  A systems concept of the vestibular organs.  In: H.H. Korn­hu­ber (ed), Handbook of sensory physiology. IV-2 Vestibular system,  (Springer Verlag, Berlin, pp 493-580.

6.      It may be interesting to know that the time it takes to experience vection is about the time it takes for the endolymphe to stand still in the semicircular canals.  When rotating with the eyes open, the addition of visual and vestibular signals thus gives a fair estimate of self-rotation.

7.      By presenting optic flow rotating in roll (i.e., about an axis through our cyclopean eye), one might experience head-over-heels rotation. Might, because our otoliths tell us we are still upright.  It appears that our CNS combines information from the eyes and the otoliths, finally resulting in a sense of static tilt.  This illusion is so strong that it may easily lead to falling.  It is a rewarding to have sufficient knowledge to mathematically describe this integration, as described in note 8.

8.      Bos JE, Bles W (2002).  Theoretical considerations on canal-otolith interaction and an observer model.  Biological Cybernetics 86:191-207.

9.      Kitahara M, Uno R (1967).  Equilibrium and vertigo in a tilting environment.  Annals Oto-Rhino-Laryngology 76:166-177.

10.   De Wit G (1973).  The Flying Enterprise symptom.  Oto-Rhino-Laryngology 35:248-251.

11.   This reflex, however, is affected by the so called “velocity storagemechanisme, resulting in a longer lasting sensation of rotation as can be explained on the function of the semicircular canals only (see also note 13).

12.   Wit G de, Vente PEM, Bos JE, Bles W.  (1999) Het snelle labyrint ten dienste van het trage oog / The fast labyrinth for the benefit of the slow eye.  Nederlands Tijdschrift KNO-Heelkunde 5:7-10.

13.   Merfeld DM, Young LR, Oman CM, Shelhamer MJ (1993).  A multidimensional model of the effect of gravity on the spatial orientation of the monkey.  Journal of  Vestibular Research 3:141-161.

14.   An observer model like this can also explain other phenomena.  The internal model of people missing an arm, for example, needs time to get rid of that arm as well.  In the meantime, a spontaneous burst of neural signals can be taken by the internal model, resulting in a sensed output just as real as when the arm was still present, thus explaining phantom pain.  With tickling, something comparable happens.  In case of tickling oneself, the sensory signals will be equal to the predicted signals based on the efference copy.  No conflict no error signal, no unusual condition.  Being tickled, however, there is no efference copy, and the difference between the sensed and predicted signals do provoke an odd feeling.

15.   Bles W, Bos JE, Graaf B de, Groen E, Wertheim AH (1998).  Motion sickness: only one provocative conflict?  Brain Research Bulletin 47:481-487.

16.   Bos JE, Bles W (1998).  Modelling motion sickness and subjective vertical mismatch detailed for vertical motions.  Brain Research Bulletin 47:537-542.

17.   Motion sickness can thus be compared with being tickled (see note 14).  Here too, the sensation only occurs due to an external perturbation.  The major difference here is the way the conflict is transformed into sensation, just an odd feeling, or something that can accumulate and finally resulting in vomiting.

18.   Irwin JA (1881).  The pathology of seasickness.  The Lancet 2:907–909.

19.   James W (1882).  The sense of dizziness in deaf-mutes.  Am. J. Otol. 4:239–254.

20.   Here I assume that the neuronal filter making the distiction between inertia and gravity, only operates on the (afferent) signals coming from the otoliths within the organs of balance.  Because this process also takes time within the internal model, there will always be a difference between the actually sensed signals of people with functioning organs of balance and the prediction thereof by the internal model.  In people without functioning organs of balance there are no afferent otolith signals, and with an accordingly adapted internal model there can also be no conflict (see also note 16).

21.   O'Hanlon JF, McCauley ME (1974).  Motion sickness incidence as a function of the frequency and acceleration of vertical sinusoidal motion.  Aerospace Medicine 45:366-369.

22.   Thanks to Michael McCauley, California.

23.   Bos JE, Colwell JL, Wertheim AH (2002). A focus on motion sickness regarding the 1997 NATO performance assessment questionnaire (PAQ) data.  TNO-Report, TNO Human Factors, Soesterberg, the Netherlands. TM-02-A017.

24.   Bos JE, Valk PJL, Hogervorst MA, Munnoch K, Perrault D, Colwell JL (2008).  TNO contribution to the Quest 303 trial - Human performance assessed by a vigilance and tracking test, a multi-attribute task, and by dynamic visual acuity.  TNO report, TNO Human Factors, Soesterberg, the Netherlands TNO-DV 2008 A267.

25.   Bos JE, MacKinnon SN, Patterson A (2005).  Motion sickness symptoms in a ship motion simulator: effects of inside, outside, and no view. Aviation Space and Environmental Medicine 76:1111–1118.

26.   Bos JE Houben MMJ, Lindenberg J. (2012).  Optimising human performance by reducing motion sickness and enhancing situation awareness with an intuitive artificial 3D Earth-fixed visual reference.  Proc. Maritime Systems and Technology Conference, Malmö, Sweden, 11-13 September. pp. 1-10.

27.   Bos JE, Bles W, Groen EL (2008).  A theory on visually induced motion sickness.  Displays 29:47-57.

28.   Cheung BSK, Howard IP, Money KE (1991).  Visually-induced sickness in normal and bilaterally labyrinthine-defective subjects.  Aviation Space and Environmental Medicine 62:527-531.

29.   It furthermore makes sense to assume that those feeling so bad that they quit, only make up the tip of the iceberg.  Most often nausea is preceded by other symptoms also known to affect performance but do not give rise to quitting.  Because also these people will not benefit from a simulator training as intended, simulator sickness can be a significant economic issue (see also notes 23 and 30).

30.   Reed N, Diels C, Parkes AM (2007). Simulator sickness management: enhanced familiarisation and screening processes. Proceedings 1st International Symp­osium on Visually Induced Motion Sickness, Hong Kong, 10-11 December pp. 156-162.

31.   Emmerik ML van, Vries SC de, Bos JE (2011).  Internal and external fields of view affect cybersickness.  Displays 32:169–174.

32.   Bos JE, Ledegang WD, Lubeck AJA, Stins, JF (2013).  Cineramasickness and postural instability.  Ergonomics 56:1430-1436.

33.   Bos JE, Damala D, Lewis C, Ganguly A, Turan O (2007).  Susceptibility to sea­sickness.  Ergonomics 50:890–901.