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It was interesting to discover the cause of motion sickness.  Now, not only can I explain to people experiencing motion sickness what exactly is going on to produce these symptoms, but I can also offer helpful tips on how to alleviate the discomfort.  I also feel that I have a much better understanding of the phantom limb phenomenon, because prior to class I was one of those people who would just assume an amputee complaining of limb pain was crazy.   However, while I understand that the basic underlying cause of motion sickness is that there is a disagreement between the sensory input and the corollary input that the brain is receiving, a few questions remain. 

People generally experience motion sickness only when they take long trips in the car.   This makes sense because there is some sort of threshold amount of disagreement that the brain can handle before it freaks out and makes you vomit and go to sleep.  The medications that are typically prescribed to people complaining of motion sickness are drugs that inhibit the input of sensory information.  Valium is a drug that is occasionally prescribed for the treatment of motion sickness.  Taking valium before a long car trip causes one to fall asleep, thereby cutting off all visual input.  Essentially, taking medication just cuts out the middle step (vomiting) of the process ones body would naturally go through.  Yet, even when one is asleep the brain is receiving lots of sensory inputs.  When the car windows are down does ones skin feel the wind blowing past and interpret it as an affect of you moving?  If so, then even if ones eyes are closed, cutting out the visual input that says “you are moving”, the brain will still be getting the message “hey, you’re moving!” but it will be coming from sensory receptors in the skin instead of the eye.  This makes me wonder if there is some kind of hierarchy in the nervous systems.  That is, do sensory inputs originating in the eyes have greater influence on the brain than inputs coming from the skin?

This question also came up in the discussion about phantom limb pain.  If one receives a corollary signal from the neurons of the amputated limb warning the brain to expect pain, but all of the sensory receptors are reporting that there is no limb in which to feel pain, then why don’t the sensory signals correct the corollary signal?  Do the corollary signals hold more sway over the brain than the sensory signals?

            Something that completely stumped me was the condition known as "mal de debarquement."  This is when one feels perfectly fine on a boat at high sea but becomes nauseous and disoriented on steady, dry land.  Can anyone think of an explanation for this?