Spastic vs Flaccid (UMN vs LMN)

[MudPhud20XX]

I'm still having trouble with these two terms. Sorry language isn't really my stronghold.

So the way Kaplan neuroanatomy explains is that when you have a UMN lesion you get a spastic weakness (ipsilateral) and with LMN lesions, you get a flaccid weakness or paralysis.

So how exactly the term spastic different from flaccid? Clinically would you be able to tell?

Also, in micro, I noticed that C. botulinum is associated with flaccid paralysis, which I think it makes sense since the botulinum toxin blocks the ACh release, so it's as if you have a UMN lesion, correct?

However, C. tetani which blocks the release of inhibitory mediators such as glycine and GABA result in extreme muscle spasm so called rigid paralysis. So would this be similar to the spastic weakness we see from UNM lesion since UMN sort of acts as an inhibitory to LMN, right?

Many thanks in advance.

---

Members don't see this ad.

 

[sanj238]

I'm still having trouble with these two terms. Sorry language isn't really my stronghold.

So the way Kaplan neuroanatomy explains is that when you have a UMN lesion you get a spastic weakness (ipsilateral) and with LMN lesions, you get a flaccid weakness or paralysis.

So how exactly the term spastic different from flaccid? Clinically would you be able to tell?

Also, in micro, I noticed that C. botulinum is associated with flaccid paralysis, which I think it makes sense since the botulinum toxin blocks the ACh release, so it's as if you have a UMN lesion, correct?

However, C. tetani which blocks the release of inhibitory mediators such as glycine and GABA result in extreme muscle spasm so called rigid paralysis. So would this be similar to the spastic weakness we see from UNM lesion since UMN sort of acts as an inhibitory to LMN, right?

Many thanks in advance.

I thought kaplan explained the UMn/LMN pretty well? You should re-read it because in that passage it states that UMN spasticity is the result of loss of inhibitory neurons from the cns- this leads to the inability to stop the myotatic reflex- thus the reflexs- patellear, biceps etc will be spastic- nothing to slow them down- they will be hyper-reflexic. Clinically you will see this as 3 or 4/4 reflexes- normal is 2/4 and hyporeflexic would be 1/4 or 0/4.

Sometimes I feel like your questions are for me 🙂

c botulinum is Ach inhibiton at the NMJ junction. why? because they get taken up in the premotor neuron - inhibit synaptobrevin which is important for the vesicular cleavage and release - the vesicles have Ach in them.

C tetani is correct- they act on the interneurons of the spinal cord.

 

[MudPhud20XX]

Thanks again sanj238. That's pretty awesome those bugs work like that mimicking either UMN or LMN lesions.

I also just realized that "flaccid paralysis" is really the constellation of lower motoneuron lesion signs combining paresis with suppressed or absent reflexes, fasciculations, and atrophy according to Kaplan neuro.

So for the board exam, when they just say "paresis" it could be either UMN or LMN right?

But if the question says "spastic paresis," it indicates it's a UMN lesion, correct?

Clinically, how would you know if it is just paresis (muscle weakness) or "spastic" paresis?

 

[ChessMaster3000]

Thanks again sanj238. That's pretty awesome those bugs work like that mimicking either UMN or LMN lesions.

I also just realized that "flaccid paralysis" is really the constellation of lower motoneuron lesion signs combining paresis with suppressed or absent reflexes, fasciculations, and atrophy according to Kaplan neuro.

So for the board exam, when they just say "paresis" it could be either UMN or LMN right?

But if the question says "spastic paresis," it indicates it's a UMN lesion, correct?

Clinically, how would you know if it is just paresis (muscle weakness) or "spastic" paresis?

You could probably youtube a video of it--spastic is like a spasm. paresis there is no spasm.

 

[sanj238]

Thanks again sanj238. That's pretty awesome those bugs work like that mimicking either UMN or LMN lesions.

I also just realized that "flaccid paralysis" is really the constellation of lower motoneuron lesion signs combining paresis with suppressed or absent reflexes, fasciculations, and atrophy according to Kaplan neuro.

So for the board exam, when they just say "paresis" it could be either UMN or LMN right?

But if the question says "spastic paresis," it indicates it's a UMN lesion, correct?

Clinically, how would you know if it is just paresis (muscle weakness) or "spastic" paresis?

again the motor reflexes- if they're hyperreflexic or not

 

[targ489]

With an UMN lesion, you're getting hyperreflexia because your lower motor neuron lost the tonic firing that it normally provides. So with this loss, the reflex afferent fibers up regulate to compensate the loss of tonic firing on the LMN. Now when you check the patients reflexes they will be greatly increased.

On the other hand a lower motor neuron results in loss of a substance called agrin which normally allows the LMN to tell the NMJ that hey I'm still here and this is where you need to insert your nicotinic receptors on the end plate. So when you lose the LMN the muscle no longer knows where to put the receptors and rye vesicles randomly insert all over the membrane, this leads to fasciculations, because it's randomly being depolarized by the ecf all the time.

With most usmle questions they will state flaccid versus spastic. Flaccid because you have no motor output, spastic because the LMN is retained and still has the ability to shock the muscle.

 

[sanj238]

With an UMN lesion, you're getting hyperreflexia because your lower motor neuron lost the tonic firing that it normally provides. So with this loss, the reflex afferent fibers up regulate to compensate the loss of tonic firing on the LMN. Now when you check the patients reflexes they will be greatly increased.

On the other hand a lower motor neuron results in loss of a substance called agrin which normally allows the LMN to tell the NMJ that hey I'm still here and this is where you need to insert your nicotinic receptors on the end plate. So when you lose the LMN the muscle no longer knows where to put the receptors and rye vesicles randomly insert all over the membrane, this leads to fasciculations, because it's randomly being depolarized by the ecf all the time.

With most usmle questions they will state flaccid versus spastic. Flaccid because you have no motor output, spastic because the LMN is retained and still has the ability to shock the muscle.

I'm sorry but can you please source this information? this is the first time I am hearing any of this and I have a hard time following it.

The reason why you have fasciculations is because retained Ach has nowhere to act on- once the LMN degenerates its stored Ach is released into the synaptic cleft- these Ach lead to fasciculations by constantly depolarizing post synaptic membrane.

in UMN- hyperreflexia is not compensated by afferent fibers. hyperreflexia results because interneurons which offer inhibition via glycine and GABA are no longer stimulated by the UMN- so the lmn are not controlled.

Agrin is found in the embryogenesis of Ach, more importantly residual reorganization post injury takes weeks to months

 

[targ489]

I'm sorry but can you please source this information? this is the first time I am hearing any of this and I have a hard time following it.

The reason why you have fasciculations is because retained Ach has nowhere to act on- once the LMN degenerates its stored Ach is released into the synaptic cleft- these Ach lead to fasciculations by constantly depolarizing post synaptic membrane.

in UMN- hyperreflexia is not compensated by afferent fibers. hyperreflexia results because interneurons which offer inhibition via glycine and GABA are no longer stimulated by the UMN- so the lmn are not controlled.

Agrin is found in the embryogenesis of Ach, more importantly residual reorganization post injury takes weeks to months

I apologize, I must have learned the information incorrectly then. Just always how I understood it. I don't think the mechanism is well defined though.