Submitted by Hola3008 t3_1238mmm in askscience

When a body part is compressed for a short period of time, why are only sensory neurons affected (paresthesia/anesthesia) by compression but not motor neurons (paralysis)? Like, the body part gets numb/tingly, but voluntary movement continues to function. Why is this the case?

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EDIT:

Yes, I am aware that mild paralysis occurs with compression, but this tends to occur later. Also, by "compression", I meant like when your arm, thigh, etc., is squished, not like carpal-tunnel-like nerve compression.

Also, thanks for all your wonderful input, but I would really appreciate some sources.

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DocTreeMedicinal t1_jdtyfnj wrote

Motor commands come from the brain into the periphery.

If you were somehow able to press your primary motor cortex in your brain, you'd see a loss of muscle function (paralysis)

It is most likely that when pressing on a body part you are temporarily compressing a peripheral sensory nerve. Hope this helps

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Mord42 t1_jdtyoy1 wrote

But why does the sensory neurons go before motor neurons? The same is true for peripheral hypothermia, for example. When your hands are exposed to cold temperatures and go numb, you can still move the muscles but not feel anything, even with your proprioceptors.

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BeneficialWarrant t1_jdu0rmz wrote

While I don't know the full answer, I can assure you that motor deficit does occur with even mild mixed peripheral nerve compression. Weakness and muscle atrophy is a hallmark sign of nerve entrapment, although I agree that sensory effects often seem more immediately noticeable.

Perhaps unconscious proprioceptive feedback circuits modulate motor tone to compensate for mild weakness and ensure normal posture. Or perhaps somatosensory deficit is more bothersome and therefore more consciously noticeable. Or perhaps it has to do with a difference in fiber physiology or myelination. I'd guess it has more to do with the first 2, and its simply that the body is more consciously aware of sensory deficit while mild motor deficit is handled more unconsciously.

Edit: As another person pointed out, the correct answer is that sensory fibers are conveyed around the periphery and motor towards the center of the nerve. Appreciate the love though. I tried my best.

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itssallgoodman t1_jdu6k70 wrote

It’s my understanding it’s due to the anatomy of a peripheral nerve. To keep this simple, the anatomy of sensory v motor fibers are akin to a coaxial cable. The sensory fibers are the outside of the nerve(insulative portion of the cable) and the motor fibers are the inside(copper wire).

Thus when compressing the nerve the outer layers are effected first and the inner fibers require more compression and time to be effected compared to the outer. This leads to sensory deficits superseding motor deficits.

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keestie t1_jdu6sfo wrote

When I sleep on my arm for long enough, I lose the ability to move it until the blood flow is restored. It takes longer tho, and as the blood returns, movement comes back first, then the the sensation.

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Black_Moons t1_jdud0qa wrote

I always worry when that happens that its going to be permanent, or damage the nerves...

How important is it not to sleep on your arm like that? Like is it a minor annoyance or major health hazard?

Any tips for how to make your arm not fall asleep when sleeping on your side? Like a certain shoulder position or place to avoid pressure? Pillow position?

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TheEastStudentCenter t1_jdudvkj wrote

When a body part is compressed, the pressure on the sensory nerves that carry information about touch, temperature, and pain can cause temporary disruption of their function. This disruption can lead to paresthesia, which is an abnormal sensation like tingling, numbness, or burning. In more severe cases, the compression can cause anesthesia, which is a complete loss of sensation in the affected area.

On the other hand, motor neurons that control voluntary movement are less affected by compression because they are less sensitive to pressure. These neurons are located deeper in the body and are more protected by other tissues like muscle and bone. Additionally, motor neurons do not rely on sensory information to generate movement. Instead, they receive signals from the brain and spinal cord that instruct them to contract or relax muscles.

Therefore, even if the sensory neurons are temporarily affected by compression, the motor neurons can still receive signals from the brain and spinal cord and initiate voluntary movements. However, if the compression is severe or prolonged, it can eventually affect the motor neurons as well, leading to paralysis or weakness.

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SignificantYou3240 t1_jdugit2 wrote

This is not really the case with me. When I sleep on my arm, I can pick it up with my other arm and it’s hella heavy. I used to drop it onto my face because it was crazy how it would land so forking hard.

But motor function came back before the tingly feeling left. I suspect that the tingly feeling, while it feels crazy, it’s not all your neurons, if it were it would hurt a lot more, like having the limb shredded or something. So maybe your neurons are at 80% but it feels like zero

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RobleViejo t1_jdvas5s wrote

Evolution. The monkes who couldnt move their legs after sleeping on it got eaten.

Most likely this distinction between nerves happened first in Amphibians or Reptiles and goes way back to the first land vertebrates who actually had to deal with the weight of their own bodies.

If Fish dont have this distinction then my guess is right

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RobleViejo t1_jdvblxw wrote

On a soft surface is not a big deal.

However on a hard surface it can lead to necrosis on muscle tissue due to hypoxia, which then needs to be surgically removed, which causes permanent lose of functions. (This is common on people who pass out on concrete and sleep on their arm, due to alcohol or drugs)

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uh-okay-I-guess t1_jdvc1ps wrote

> The sensory fibers are the outside of the nerve(insulative portion of the cable) and the motor fibers are the inside(copper wire).

Can you cite a source to support this? I can't find one, and I did find a paper where they attempted to image the fibers (https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-021-02871-w). Their images seem to me to show them all mixed together.

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Any_Respond_9011 t1_jdvlcef wrote

It could be that they are more important for survival, therefore it's "worth" making them more robust. It's unpleasant to wake up with tingly/numb legs, but it's much better than not being able to run/defend from danger because you can't control them.

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malefiz123 t1_jdvmoi7 wrote

Paresthesia due to compression is happening because nerves are compressed, not because of the sensory neurons in the skin. Thats the reason your feet are tingeling when you compress your upper legs by sitting on the toilet but you don't get paresthesia in your handy by carrying something heavy

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QuerulousPanda t1_jdvo9vl wrote

Sleeping on it is less likely to cause permanent damage because you're going to tend to move around enough that you probably won't cut off enough circulation or squeeze an individual nerve for long enough.

Where it can become an actual problem is for alcoholics and drug users who pass out to the point of total unconsciousness and don't move at all.

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Xeronami t1_jdvonma wrote

This isn’t accurate. Motor and sensory nerves share a similar pathway. For example, look at the ulnar nerve (your funny bone). It splits at various points to give rise to partial sensation to your hand and partial to intrinsic musculature of your hand as well as some muscles of your forearm. This is just one example, but most spinal nerves have both sensory and motor function.

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Xeronami t1_jdvpfed wrote

My best recollection is that sensory nerves are thinner and motor nerves are thicker. The short term paresthesia you get is actually from compression of arteries that give blood to the nerves. When the nerve has a loss of blood, it starts function poorly. The large motor nerves don’t get affected as quickly because there’s generally more blood flow to these and have more stores nutrients. Eventually though, a motor neuron will get affected, look up “Saturday night palsy” which is basically prolonged compression of the radial nerve I believe. Again, this is my recollection from PT school about 6 years ago, so it could be wrong🤷‍♂️

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lollroller t1_jdvpuyf wrote

It is a good question. It is also true regarding both spinal disc herniation on nerve roots, and disc herniation on the spinal cord itself, that sensory pathways are involved far, far, earlier than motor pathways. And in fact, motor involvement is considered much more severe and is often what leads to surgical repair

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TheBoundFenrir t1_jdvy1pj wrote

Stronger muscles != stronger nerve signals.

But X muscle fibers working at 85% efficiency > 3X muscle fibers working at 85% efficiency, so someone who works out may find they're less noticeably hampered by the loss in muscle strength, since they had more to spare to begin with.

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Hola3008 OP t1_jdw58id wrote

Really? According to most of the websites I have looked at, like https://www.webmd.com/brain/paresthesia-facts, parasthesia is caused by nerve compression, not arterial compression, most mention this as a common misconception. Ig that was the accepted consensus 6 years ago. Thanks for mentioning Saturday night palsy, I didn't know about that. I also wasn't aware of the difference in thickness, that explains a lot. +1.

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i81u812 t1_jdwjbx6 wrote

I can help (multiple spine issues).

I was big, now im just a little big, but can do the same weight for the longest. Now that it's been a few years of compression I am noticing fatigue doing 'common' things like holding arms and shoulders up too long - yet can still do the heavy weight. So - it's complicated! My first spine doc visit schedule this week. But more or less the size goes real fast, and the strength far slower.

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keestie t1_jdx8h2p wrote

Interesting. Is enough known about nerves that we can understand the actual physical and/or chemical processes at work? The gradual return makes me think it's some sort of displaced fluid that slowly flows back in, but is that really it?

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kompootor t1_jdxd3zl wrote

One clue might be that of course seeing as your sensory neurons are not going to be completely saturated or suppressed in temporary parasthesia -- and certainly not all of them in an area will be -- and the same goes for any motor neurons that you might snag in a similar manner. The difference is that the translation from motor neuron stimulation to motor movement involves integrating a lot more components that might mitigate the effect that pinching a couple disparate nerve endings would have.

Taking from Knudson's Biomechanics (ch. 4 pp. 95--96):

>If the muscle fibers of a motor unit twitch in unison, how does a whole muscle generate a smooth increase in tension? The precise regulation of muscle tension results from two processes: recruitment of different motor units and their firing rate.

>Recruitment is the activation of different motor units within a muscle. ... Firing rate or rate coding is the repeated stimulation of a particular motor unit over time. ...

>When muscle is artificially stimulated for research or training purposes to elicit maximal force, the frequency used is usually higher than 60 Hz to make sure that motor unit twitches fuse into a tetanus. A tetanus is the summation of individual twitches into a smooth increase in muscle tension.

>... at the whole muscle level[,] muscles are activated to in complex synergies to achieve movement or stabilization tasks. Muscles are activated in short bursts that coordinate with other forces (external and segmental interactions) to create human movement.

And there's a bunch of more details to recruitment and firing rate, and it goes on in complexity and unknowns pursuant to further research. One relevant point is that in many cases you use only one firing per motor neuron, over several different neurons, to create a long smooth complex movement (the example they use is bicycling). Since it's an integrating effect, a single missing signal may not actually cause much of a problem -- but I don't know. Anyway, it's a clue.

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