Amongst the questions that I get asked regularly, this one is probably part of the top 5. How did this tension happen in my horse, with the underlying question of “how do I prevent it happening again?”.

There’s 2 theories that I know of, that try to explain the neurological process of dysfunction. The first one, that I’m going to describe today, is the widely and commonly accepted one. It’s the one that I was taught, and as far as I know it’s the one that is still being taught today. But when I was writing my thesis, I came across a very interesting article that put another theory forward, a theory that would explain certain things that the current theory doesn’t. So I thought I would write a 2 part article on it, starting with the widely accepted one and working our way to the second theory 

So let’s get to it.

The intrafusal muscle spindle is a receptor that is located inside your horse’s muscles. It basically looks like a muscle fibre but isn’t one, and because it’s located inside the muscle, it reacts to stretch. So whenever a muscle in your horse’s body gets stretched during movement, the intrafusal spindle warns the spinal cord which then orders the muscle to contract in order to stop the stretch. The idea is to prevent the tear of muscle fibre during movement, so it’s a pretty good mechanism 😊

Now, the current theory starts from the idea that this spindle is meant to always be in touch with the spinal cord, always giving feedback as to what state of stretch we’re in. But let’s say that your horse hits a fence post, or falls, or gets hit by another horse. The quick and unexpected shortening of the intrafusal spindle will cause it to be silent for a brief moment, making the spinal cord ask for contraction of the muscle to get that feedback again. The problem is that after the moment of shock happens, the body doesn’t rebalance itself. It keeps the muscle in slight contraction to maintain the lost feedback, and therefore changes the amount of stretch you can now get from that muscle during movement, so in short, it reduces the range of motion of an area and therefore is a dysfunction. It’s basically a fault in the electrical system of the body 

So this is the current theory, I’ve shortened it massively here but hopefully you guys will get the idea. As I said earlier, the problem with that theory is that it doesn’t cover certain points.
– it doesn’t explain how visceral pathologies can bring vertebrae into dysfunction as it is based on a receptor that you can only find in a muscle.
– it is well known from practitioners that dysfunction in the body brings an activation of the orthosympasethic nervous system, the system of stress. The spindle isn’t linked with this system and has no connection to it, so it wouldn’t explain why or how this activation occured.
– and finally it has been shown in studies that the stimulation of the spindle wasn’t enough to stimulate the muscle contraction.

These few points bring me to question if this is really how dysfunction occurs, and I came across another theory that covers more points and makes a lot of sense. So get ready for part 2!!

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