Tuesday, March 12, 2013

Kicking Kinetosis

Kicking Kinetosis

By: Lesley Stein

It was a dark, chilly, and windy morning in November.  I arrived at Morro Bay to fish for the Collaborative Fisheries Project.  The night before, I checked the swell report, as I am prone to motion sickness, or kinetosis, and unfortunately, it appeared as though rough seas were ahead.  But, with high hopes of somehow overcoming my seasickness with a motion sickness pill and some ginger root tablets, I boarded the boat the following morning.  After departing from the peaceful bay, I began to feel a little warm inside. My mouth began to salivate and my body began to sweat while my stomach started churning, and I was extremely nauseous.  My motion sickness had come back with a vengeance.  All I wanted to do was lay down and close my eyes, until the boat docked.  Not only was this desire to remain unsatisfied, but I furthermore still had to tag, weigh, measure and release the catch soon to be reeled in.  My miraculous concoction of over-the-counter motion sickness medication and ginger tablets did not live up to my expectations and without a moment to find a trash can or even a fishing bucket, I rushed to the side of the boat and, well, fed the fish.   Although I knew everyone was disgusted watching me hurl over the side of the boat every five minutes, I must say, they were highly impressed with my multi-tasking skills of projectile vomiting while gripping a flailing 20-pound lingcod in my hands! 

How and why does this happen?
So what role does the inner ear (vestibular system) play in all of this, you ask?  Well, just as, your muscles, eyes, and skin receptors detect motion or a lack of motion, so too, does your inner ear.  The vestibular system (see Figure 2) consists of a semicircular canal system, conveying rotational movements, and otoliths, expressing linear accelerations.  Within the semicircular ducts are tiny hair cells called crista, which detect the movement of fluid inside the ear.  

In a nutshell, it is caused by the inner ear (see Figure 1). Overstimulations of the labyrinthine canals of the ear initiate motion sickness.  Motion sickness occurs when the inner ear, the eyes and other parts of the body that distinguishes motion, send contradictory messages to the brain.


Figure 1. The three main parts of the ear: external, middle, and inner.  The inner ear plays a role in motion sickness.

When we move our bodies intentionally, for example, when we run or jump, the input from all three of these pathways to our brain is in sync.  However, when we experience unintentional movement, as occurs when aboard a moving fishing vessel, the input to the brain does not coordinate.  During motion sickness, the brain receives conflicting messages from these numerous interpreters that express contradictory states of the body’s physical status.  For example, on a boat, your feet are not physically moving, so your joint sensory receptors say to your brain, “I am still.”  However, your eyes perceive the vanishing shoreline and flowing wake behind the boat indicating movement, telling your brain, “I am moving.”  Similar to reading a book in the car—your eyes are focused on a stationary page, while your body registers the movement of the car.  And your skin receptors feel wind, as experienced during a fast paced run, telling your brain, “I am moving.”  But your legs and arm muscles are not moving, thus tell your brain, “I am still.”  In other words, you feel motion, but you don’t see it.  Or, you see motion, but you don’t feel it.  Imagine how you would feel trying to decode these conflicting messages!

Figure 2. The anatomy of the inner ear.

Figure 3.  (a) The head is positioned straight, the, therefore the cristae are also straight.  (b)  When the head turns the cristae flex in the opposite direction.  Note: fluid inside the inner ear is moving the cristae. 

Motion sickness occurs when our brain receives these contradictory messages.  My personal encounter with motion sickness was specific to seasickness, which is just one type of motion sickness.  Many people experience the symptoms of motion sickness traveling in a car, train, airplane, bus, subway or while watching video games, IMAX movies, or riding roller coasters.  While I was on the boat, my inner ears and skin receptors sent signals to my brain indicating motion.  However, my muscle receptors registered my motionless status as I was standing still, or at times, sitting still.  My eyes were glued to the floor that wasn’t moving, but as soon as my eyes met the horizon or shoreline, my eyes sent an opposing signal indicating motion—conflicting with the one sent just moments ago from the same receptor. 

This mismatch of neural signals ultimately, activates the postrema in the brain, which controls emesis (vomiting), as illustrated in the figure below (Figure 4).  The vomiting-reflex is controlled in the vomiting center, or the lateral reticular formation, located in the medulla oblongata at the base of your brain.  The link between motion sickness and vomiting is not wholly understood, but one theory includes the toxin theory.  According to this theory, vomiting is a defense mechanism against neurotoxins.  Due to the conflicting signals sent to the brain, the brain interprets one of them as a hallucination, triggered by poison or drugs.  The brain, in turn, instructs the body to purge itself of these toxins through emesis.

Figure 4. The pathway of the postrema area in the brain, controlling vomiting

So, we now know why we get motion sickness, but what do we do about it?  

There are several different remedies to help alleviate the symptoms, but there is no “cure” per sue.  One of the most popular methods, includes the one that failed to come to my rescue that Saturday morning, over-the-counter medication.  These include drugs like Dramamine or Bonine.  These are antiemetics, or drugs that inhibit vomiting.  These drugs work by blocking the messages of certain neurotransmitters like serotonin, acetylcholine, dopamine, and histamine.  If the brain does not receive information from these neurotransmitters, it is unable to respond.  These antiemetics block the transmission of information from the vestibular apparatus to the lateral reticular formation (vomiting or emetic center) in the medulla oblongata.   See the figure below (Figure 5) to see the where the antiemetics can block neurotransmitters’ signal to the vomiting center.  

Figure 5. Different pathways of antiemetics blocking neurotransmitters' signals in the vomiting center

But these antiemetics also tend to pack another punch—extreme drowsiness.  The reason being is because some antiemetics are also antihistamines, like Dramamine.  The main ingredient in antihistamines that causes drowsiness is called diphenhydramine that fights histamine (as seen above) by binding to the receptors of specific cells in the body that histamine would typically bind to otherwise, blocking them from relaying their message.   If histamine does not have access to these receptors, it cannot react on the body.  But antihistamines are not solely responsive to histamine receptors, but acetylcholine receptors as well.  If diphenhydramine clocks an acetylcholine receptor, acetylcholine reuptake no longer occurs, causing an excess of acetylcholine, and thus drowsiness.  The only medication that I have taken (and I have take a lot) that did not cause this unfavorable side effect is Triptone, which is unfortunately, no longer being manufactured. Scopolamine patches, placed behind the ear, as well as, wristbands applying pressure to specific pressure points believed to alleviate motion sickness, has been successful for many.  Ginger root pills or chews can also diminish the side effects of motion sickness, phenols in ginger also help relax the stomach muscles, including the pyloric valve; therefore, reducing the activity of the stomach.  Ginger also promotes the stomach to secrete digestive juices or enzymes, furthermore, neutralizing stomach acids. Other than these more medicinal aids, a few words of personal advice...Always have food in your stomach before you travel, it may help you not get sick and if you do get sick, at least you will not be throwing up bile..  And lastly, carry a barf bag to avoid some embarrassment.


Bles, W., J.E. Bos, B.D. Graaf, E. Groen, and A.H Wertheim. 1998. Motion sickness: Only one provocative con´Čéict? Brain Research Bulletin 47: 481-487.

Brad Bowins. Motion sickness: A negative reinforcement model. 2010. Brain Research Bulletin 81:7-11.

Charles Oman. 1998. Sensory conflict in motion sickness: an observer theory approach. NASA, Ames Research Center, Spatial Displays and Spatial Instruments 16-54.

Huang, Y.D., S.W. Xia, P. Dai, and D.Y. Han. 2011. Role of AQP1 in inner ear in motion sickness. Physiology & Behavior 104: 749-753

Karen Naifeh. 1986. Exploratory Studies of Physiological Components of Motion Sickness: Cardiopulmonary Differences Between High and Low Susceptibles. National Aeronautics and Space Administration ARC 275a.

Theeuwes, J., A.F. Kramer, S. Hahn, and D.E. Irwin. 1998. Our eyes do not always go where we want them to go: capture of the eyes by new objects. Psychological Science September 9: 379-385.










  1. Could jumping up & down like a crazy person while on the boat correct these contradictory messages to the brain? If your moving around a lot then not only will your eyes sense movement but the rest of your body will as well. Although, this technique may be just as embarrassing as personally chumming the waters!

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