This is from one of my crewmembers
Would love to talk with the astronaut/doctor about his experiences with space motion sickness or SMS. His comments on the etiology of motion sickness in terms of mismatch between vestibular motion detection signals and brain state regarding other detectors of motion is the leading theory among vestibular scientists. As I told you, that is what my specialty is, vestibular neuroscientist. We study not just motion detection, best motion perception, inner ear disfunction, eye movement control during motion, balance, spatial orientation, and navigation.
I can tell you that as of today’s date, we only have theory about what produces motion sickness in it’s many forms, not a known physiology base that has a pharmacological intervention that works for everyone, certainly not a cure. We (vestibular scientists) have gained a great deal of information over many decades on the subject but it remains an enigma. We do know quite a bit about how the brain processes motion information and how multisensory integration signals in the brain and their functional imbalance is the root cause of motion perception dysfunction. There are priors (effects of vision, proprioception, balance motor command efferent feedback) that are all individualized through experience and developmental variances that lead to differences in one person’s susceptibility over another’s. What I personally am working on for many years is the brain’s multisensory integration capacity and what happens when that integration is disrupted.
His comments are correct as I understand it regarding SMS. Of course, he has personal experience as an astronaut. I have only worked with the astronaut and cosmonaut core in the past, but not recently. As I understand it through current scientific literature and discussion with my colleagues who do human spaceflight work at JSC, MIT, and some other places the guided use of promethazine by the astronaut core is under continual flight doc supervision, and as Bill states, it is supplemented by amphetamine to offset the drowsiness side effect of promethazine. I am familiar with scope/dex and it’s use early in the space program, mostly at the beginning of the space station era, and we have used it in our monkey vestibular studies. As he states, it was replaced by the current regime of promethazine and amphetamine/ephidrine. As I understand it, use of promethazine for SMS is usually given before a sleep cycle, to diminish the drowsiness side effects for awake mission performance.
Currently, in our scientific understanding, we know that SMS is mainly produced by an acute substantial change in the gravito-inertial acceleration (GIA) experienced with the reduction in gravity. There is still gravity in space, but only at the 0.003g level typical at the ISS level of orbit which is several orders of magnitude less than Earth at 1g. There is still linear acceleration force experienced in spaceflight from translational motion so the net GIA experienced during spaceflight is vastly different from that experience on Earth and the vestibular inertial detection system is quickly changed upon reaching orbit. Again the brain has a multisensory informational change that elicits SMS. However, unlike motion sickness at sea, it is from a loss of signal from the inertial sensing part of the vestibular inner ear, not from a continual motion dynamic like boat motion.
A number of studies from the Navy and from labs (including our own) has shown that roll motion similar to that experienced on boats in the frequency range of 0.2 Hz or lower is a major effector for producing motion sickness. Pitch motion is not as provocative. This unusual roll motion is compounded by focal vision (near viewing) high demand tasks such as reading, writing, or cooking where eye coordination to close visual targets is not matched to the boat motion and is very different from the priors stored in your brain memory for types of motion responses one is used too on stable substrates. That is why people find relief from sea sickness by going on deck, looking at the horizon, or eliminating any form of close visual focal behavior. That is also why some people find relief in the severity of sea sickness if the boat changes direction (downwind or similar to flatten the boat and reduce the 0.2 Hz roll component).
In terms of steering, that is two-fold introduction of motion signal augmentation that can help offset the vestibular mismatch experienced during sea sickness. First, is the proprioceptive signal from the joints and muscles in your arms, hands, body torso (if seated) and all of those plus ankles/hips (if standing) that provide motion signals about position/movement to feed into the multisensory vestibular brain regions. These same signals are known to be enhanced when an individual has vestibular ear disease, or loss of vestibular inner ear signals due to trauma or nerve cuts such as occur with certain types of cancer. When these proprioceptive signals are enhanced with vestibular loss, this leads to an improvement in balance and a reduction in motion sickness in people with vestibular disease. The same process happens with sea sickness. That is believed to be the compensation component of the brain that results in many people getting used to sea motion after 48 – 72 hours after at initial sea sickness onset. The second component of why steering helps some people is a concentration of vision away from focal tasks (near viewing) to distance viewing (horizon, steering targets in the distance, etc).
For drugs to be used for propholaxis and sea sickness treatment, there are many studies on the subject. The modern science points to promethazine, cinnarizine, and hyoscine as the most effective choices. But all have pluses/minuses, all have different dosages that are effective for different people. Again, we are talking specifically for sea sickness, not SMS, which has a different defined cause than sea sickness, although the same medications may be efficacious for both. There is no one right answer here!
Most vestibular scientists that are also sailors prefer cinnarizine or hyoscine, because of the lower side effect of drowsiness which is high with promethazine. However, once you are already experiencing sea sickness to the level of emesis, suppository promethazine is preferred. In addition, one does not have to take an antidrowsiness amphetamine/ephedrine necessarily with cinnarizine or hyoscine.
Other than the papers I already sent you from scientific journals last week, here are a couple more abstract. Hope this is helpful!
Here is the abstract of a study for cinnarizine from 1994 as an example:
Cinnarizine in the prophylaxis of seasickness: laboratory vestibular evaluation and sea study
Cinnarizine was evaluated for the prevention of seasickness in a laboratory and sea study. The effects of 25 mg cinnarizine on the vestibulo-ocular reflex were investigated in 13 subjects. Significant reduction of the gain in response to sinusoidal oscillations at 0.02, 0.08, and 0.16 Hz (p < 0.05) and increased phase lead at 0.16 Hz (p < 0.01) were observed. The effect of 25 and 50 mg cinnarizine on seasickness severity was examined in 95 subjects during a voyage in rough seas. Seasickness symptoms were improved in 69% of the subjects by 50 mg cinnarizine versus 35% and 31% in the groups receiving 25 mg cinnarizine and placebo (p < 0.05 and p < 0.01, respectively). The percentage of vomiting protection provided by 50 mg cinnarizine was 63% (p < 0.05). We conclude that 50 mg cinnarizine is an effective drug for the prevention of seasickness. The reduction in vestibular sensitivity observed even after administration of 25 mg cinnarizine may explain the potency of cinnarizine in the prevention of seasickness.
Here is the abstract from the Royal Naval Medicine journal about cinnarizine use and sea sickness:
INM investigations into drugs for seasickness prophylaxis.
Journal of the Royal Naval Medical Service, 01 Jan 1994, 80(2):76-80
Share this article Share with emailShare with twitterShare with linkedinShare with facebook
A summary is presented of a programme of work investigating the comparative efficacy of the two drugs most commonly used for seasickness prophylaxis in the Royal Navy, hyoscine and cinnarizine. The programme had both laboratory and sea-trial components. It was shown that hyoscine was a more effective drug than cinnarizine, but cinnarizine had less marked side effects. This comparative superior tolerability of cinnarizine decreased as motion sickness increased. Guidance is given as to the optimum indications for each drug, together with prophylactic regimens.