Skip to main content

Sensing the senseless: Dizziness in the brain



Getting dizzy used to be fun. Tire swings and merry-go-rounds offered endless entertainment for my young friends and me. We would spin and spin and spin until we could no longer walk and we just collapsed into a pile of giggling goons. Not so these days. It is rarer and rarer that I find myself getting dizzy on purpose and more and more common for me to get dizzy without doing any spinning at all. Dizziness is one of those weird phenomena that everyone experiences, whether you’re a hyper kid or plagued with bouts of vertigo. But how do we get dizzy anyways?



Imagine yourself in your car with a full mug of piping hot coffee in the cup holder next to you. You know that you have to drive really carefully to keep all the coffee in the cup, because the motion of the coffee is directly affected by changes in your car’s acceleration. If you brake too hard or take a curve too fast the coffee sloshes out of the cup.



Similar movements are happening in your vestibular organs all the time to help keep you oriented. Deep inside your inner ears there are three loop-like structures called the semicircular canals that are filled with fluid. Just as the coffee detects the motion of your car, the fluid in these canals detects the motion of your head. Each of these canals also has a set of cilia—cells with hair-like projections that sway and bend as the fluid sloshes over them. When the force of the fluid on the hairs exceeds a threshold a signal is sent to your brain that says “Oh, your head just swiveled 62 degrees counterclockwise” or “you just did a cartwheel”. The motion you perceive depends on the amount that the hairs were bent and in which direction the bending occurred. This process is called mechanoelectrical transduction because a mechanical signal (motion of fluid) is being transduced into an electrical signal (neuron firing). Researchers are still trying to figure out the precise mechanism behind mechanoelectrical transduction in the vestibular system but they have two main ideas.



The first is that channels in the cilia cell membranes get stretched open as the hair bends. When the channel is open, charged atoms can enter the cell and cause the neuron to fire. The second idea is that the channels on each cilia are plugged with molecular stoppers which are connected by spring-like proteins. When the cilia are bent or deformed, the springs stretch and the stoppers get pulled out of the channels allowing charged atoms to enter the cell and cause the neuron to fire.



But what about dizziness? If you’ve been spinning like a top for 30 seconds or so the fluid in your canals is going to be sloshing around quite a bit. And even when your body has stopped spinning, it takes a little while for the fluid in your ears to stop sloshing. Your brain continues to get some signals from your semicircular canals that says “whoa we’re spinning in circles” while your eyes are telling your brain that you are standing still. This discrepancy between what your visual and vestibular senses tell your brain is the source of the sensation of dizziness.



What I want to know now is why getting dizzy was so fun when I was younger but is so nausea-inducing now. Do all kinds of dizziness come from similar molecular mechanisms? How does spinning dizziness differ from vertigo dizziness or heat stroke dizziness? If you know the answers to any of these questions or have any hypotheses of your own comment below!



Sources and Further Reading
St George, R. J. and Fitzpatrick, R. C. (2011) The sense of self-motion, orientation and balance explored by vestibular stimulation. The Journal of Physiology, 589: 807-813. doi: 10.1113/jphysiol.2010.197665


Pierre-Paul Vidal and Matthieu P. Robert (2012) Ocular vestibular evoked myogenic potentials: the missing link. J Physiol, 590.13, p2953


Martin Chalfie (2009) Figure 4: Dual Tether Model from Neurosensory mechanotransduction. Nature Reviews Molecular Cell Biology, 10, 44-52.
Labels:

Comments

Post a Comment

Popular posts from this blog

Precision murder -- wait, no -- medicine

A non-zero amount of what we call ‘medicine’ could be described as just controlled cell murder.  This was my revelation after researching a new treatment for certain cardiac arrhythmias called Pulsed Electric Field Ablation, which I became interested in when my father-in-law asked me how it worked during our Christmas visit. “How can it kill the heart cells and leave the nerves and blood vessels intact?” I had no idea. I know next-to-nothing about medical treatments for cardiac patients, much less how this Pulsed Field Ablation technique could have fewer side effects than the standard-of-care ablation techniques. A quick Google search piqued my curiosity when I learned that PFA is also sometimes called “high frequency irreversible electroporation”. While less catchy, that name revealed a bit more about the mechanism of action behind PFA - electroporation - which happens to be something I actually do know something about. Electroporation refers to the formation of holes (pores) in c...
Post a Comment
Read more

AlphaFold2 Part 2: The ion channel challenge

Last month I wrote about the wonders and perils of the artificial intelligence program that predicts 3D protein structures, AlphaFold2. As an ion channel enthusiast , I naturally wanted to know how AlphaFold2 performs at predicting the structures of proteins embedded in cell membranes. When I search PubMed for articles that mention both "AlphaFold" and "ion channel" I only get 34 hits. This surprised me, given the hype and the general paranoia around AI replacing humanity. If we use these search results as a proxy for the state of the ion channel protein structure prediction field, I'd say the juice is still in the coconut. I wanted to know how well AF2 would do at predicting an ion channel protein structure, so I asked it to generate the structure of Kv2.1, a voltage-gated potassium ion channel that I studied during graduate school. Kv2.1 is a pretty important protein. It regulates neuron firing throughout the brain and body where it helps us learn new stuff, ...
Post a Comment
Read more

iPSCs, the new model organism?

Induced pluripotent stem cells. The name doesn't exactly roll off the tongue and it certainly doesn't conjure images of mice, fruit flies, monkeys, or any of the other classic model organisms used for basic biomedical research. These so called "model organisms" are just that; animals that help scientists model the way that the most promising human therapeutics in the collective pipeline will behave in humans. And now induced pluripotent stem cells, or iPSCs, are becoming an increasingly popular tool used for developing and testing novel drugs way before we expose any real human patients to them. The upside to using model organisms is pretty obvious -- we minimize exposure of humans to potentially unsafe molecules. The downsides are many, but one big one is that sometimes potential new drug molecules look really promising when they are given to a mouse with a human-like disease, but then that same molecule does nothing (or worse, is toxic!) when it goes into human clin...
Post a Comment
Read more