Neurogenic bladder

[Reperfused]

Can someone please explain how the cord section leads to spastic or atonic bladder?
I know that cord section above the sacral segments leads to spastic/flaccid bladder in which there's detrusor overactivity and frequent urination. And cord section at the sacral segments leads to atonic bladder with constant dribbling of urine since detrusor lost its tone.

But exactly how did this happen? Which efferent/afferent fibers are involved?

Also when we say neurogenic bladder, do we mean spastic/flaccid bladder? Or are both spastic/flaccid bladder and atonic bladder sub-categories of neurogenic bladder?

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[Pholston]

It's simply UMN vs LMN lesion.
At the spinal cord it will be an UMN type of lesion (spastic or overactive bladder) and at the cauda equina it will be LMN (flaccid or overflow incontinence).
Neurogenic bladder is described as either spastic or flaccid.

 

[Kobebucsfan]

It's simply UMN vs LMN lesion.
At the spinal cord it will be an UMN type of lesion (spastic or overactive bladder) and at the cauda equina it will be LMN (flaccid or overflow incontinence).
Neurogenic bladder is described as either spastic or flaccid.

so for UMN lesion - the detrusor is always contracting ?
for LMN lesion - flaccid means u r not urinating and u have overflow in bladder ?

 

[Pholston]

so for UMN lesion - the detrusor is always contracting ?
for LMN lesion - flaccid means u r not urinating and u have overflow in bladder ?

UML lesion means that the detrusor is not relaxing (loss of inhibitory control from higher centers), therefore, there is urge to void. Think of it like diastolic dysfunction.
LMN lesion means that the detrusor is relaxed and till it gets completely full it will not void but only a little. Think of it like sysstolic dysfunction.

 

[Reperfused]

It's simply UMN vs LMN lesion.
At the spinal cord it will be an UMN type of lesion (spastic or overactive bladder) and at the cauda equina it will be LMN (flaccid or overflow incontinence).
Neurogenic bladder is described as either spastic or flaccid.

UML lesion means that the detrusor is not relaxing (loss of inhibitory control from higher centers), therefore, there is urge to void. Think of it like diastolic dysfunction.
LMN lesion means that the detrusor is relaxed and till it gets completely full it will not void but only a little. Think of it like sysstolic dysfunction.

Thanks, this totally makes sense!

I have a question one step further into this. You said with UMN lesion there's loss of inhibitory control from the higher centers?
As far as I undetstand, detrusor muscle in innervated by the parasympathetics. Activation of parasympathetic system makes detrusor contract. So if we are cutting off the nerve supply to it, this parasympathetic activity can no longer make detrusor contract, right? Then why is it being overactive instead?
I know I'm missing something out there, cuz that's not what happens in the UMN lesion. What is it?

 

[canary90]

Detrusor muscle contracts in response to parasympathetic stimulation that is carried by Pelvic splanchnic nerves (LMNs). These LMNs have their preganglionic cell bodies in gray matter of spinal cord at the level of S2, S3, S4.
UMNs running in spinal cord coming all the way up from higher centres, serve to innervate these LMNs to kind of "tone them down", i.e: prevent them from firing excessively.
If you knock out UMN, LMN becomes autonomous, it starts firing as much as it wants without any check by UMNs. Hence this excessive firing by pelvic splanchnic nerves (LMNs) cause Detrusor muscle to contract excessively leading to urge incontinence.

That's exactly why you see spasticity in muscles in UMN lesions. When there's an UMN lesion, they are no longer able to keep a check on LMNs to tone them down. As a result LMNs become autonomous and start firing excessively at the muscle causing muscle spasticity.

If you knock out LMNs, that will end all kind of innervation to the bladder or muscle, hence a flaccid bladder/flaccid muscle.

 

[Reperfused]

Thank you so much @canary90
I understand it perfectly well now!

 

[Transposony]

Micturition control center is in the frontal lobe of the brain which sends inhibitory signals to the detrusor muscle to prevent the bladder from contracting (emptying) till appropriate (socially acceptable time and place is available) for urination.

Pontine micturition center is the major relay center (a switch) between the brain and the bladder and coordinates the urethral sphincter relaxation and detrusor contraction to facilitate urination.

Sacral reflex center at the terminal portion of the spinal cord in the lumbar area is responsible for bladder contractions ( primitive voiding center as in a baby). As the children grows, they learn to control their bladder (toilet training) as micturition control center in the frontal lobe develop and takes over.

Sympathetic nervous system via hypogastric nerves (β3) controls the bladder and the internal urethral sphincter and causes the bladder to relax (increase its capacity) and keeps the internal urinary sphincter closed (continence).

Parasympathetic nervous system via pelvic nerves (M3,α1) stimulate the detrusor to contract, the internal sphincter relaxes due to decreased sympathetic activity.
Sympathetic & Parasympathetic nervous system inhibit each other depending on the bladder (empty/full) and input from higher centers depending on social situation.

Somatic pudendal nerve (Nicotinic)) is inhibited therby causing external sphincter to open leading to voluntary urination (Let it go, let it go, can't hold it back anymore..........)
.
Bottomline:

Bladder empty:
Sympathetics via hypogastric nerves causes the bladder to relax (increase its capacity-accomodation) and keeps the internal urinary sphincter closed (continence).

Bladder full:
Sacral cord receives the sensory information via pelvic sensory nerves from the bladder → signal travels up the spinal cord → pons → brain.
The brain interprets the signal and sends a reply (based on the social situation) via the pons → spinal cord sacral reflex center → bladder.

 

[Reperfused]

Micturition control center is in the frontal lobe of the brain which sends inhibitory signals to the detrusor muscle to prevent the bladder from contracting (emptying) till appropriate (socially acceptable time and place is available) for urination.

Pontine micturition center is the major relay center (a switch) between the brain and the bladder and coordinates the urethral sphincter relaxation and detrusor contraction to facilitate urination.

Sacral reflex center at the terminal portion of the spinal cord in the lumbar area is responsible for bladder contractions ( primitive voiding center as in a baby). As the children grows, they learn to control their bladder (toilet training) as micturition control center in the frontal lobe develop and takes over.

Sympathetic nervous system via hypogastric nerves (β3) controls the bladder and the internal urethral sphincter and causes the bladder to relax (increase its capacity) and keeps the internal urinary sphincter closed (continence).

Parasympathetic nervous system via pelvic nerves (M3,α1) stimulate the detrusor to contract, the internal sphincter relaxes due to decreased sympathetic activity.
Sympathetic & Parasympathetic nervous system inhibit each other depending on the bladder (empty/full) and input from higher centers depending on social situation.

Somatic pudendal nerve (Nicotinic)) is inhibited therby causing external sphincter to open leading to voluntary urination (Let it go, let it go, can't hold it back anymore..........)
.
Bottomline:

Bladder empty:
Sympathetics via hypogastric nerves causes the bladder to relax (increase its capacity-accomodation) and keeps the internal urinary sphincter closed (continence).

Bladder full:
Sacral cord receives the sensory information via pelvic sensory nerves from the bladder → signal travels up the spinal cord → pons → brain.
The brain interprets the signal and sends a reply (based on the social situation) via the pons → spinal cord sacral reflex center → bladder.

Perfect! Thanks for sharing

 

[DrIvanhoe]

Hi guys,

Jump an itsy bitsy bump to clarify something. Hope you don't mind.

Now uworld explanation mentions MS spinal cord lesion causing UMN damage which leads to spastic bladder that contracts fine, but doesn't fill.
Here's what they have to say:
Bladder does not distend/relax properly due to the loss of inhibitory control from the UMN.

Here's what I'm struggling to wrap my head around:
There's a triple pathway control of the urination:

1. sypmathetic - hypogastric nerve
2. parasympathic - pelvic
3. somatic - pudendal

How in the world the above happens if lack on inhibitory UMN action would make external sphincter hypertonic [unchecked LMN action] and that would lead to retention and maybe overflow incontinence [when i/v pressure too high] due to inability to relax the external sphincter, rather then spastic detrusor, that is controlled by parasympathetics.

What UMN has to do with autonomically controlled detrusor muscle?
What am I missing here? I feel dumb after reading through 5+ sources and not finding the answer, but cannot help digging further.

So thanks in advance!

 

[Reperfused]

It's the lack of UMN's inhibitory effect on the detrusor muscle that makes its contract normally (spastic) but not relax (hence, can't fill).

 

[DrIvanhoe]

Detrusor is a smooth muscle and is innervated by parasympathetics. There's no motor neurons there afaimc.
UMN and LMN parts of of various tracts e.g. corticospinal, corticobulbar and others, none of those are ANS tracts.

ANS does consist of preganglionic and postganglionic neurons, but I cannot find nor recall anything about preganglionic being inhibitory and postganglionic somehow excitatory and having it's own firing rate. Moreover never heard them being called UMN and LMN before, which at least in my understanding ultimately relates to MOTOR function aka skeletal muscle innervating.

Post a proof link, please, if available. I keep waking up at night without explicitly knowing how does my bladder works.

 

[Reperfused]

Detrusor muscle contracts in response to parasympathetic stimulation that is carried by Pelvic Splanchnic nerves (LMNs).

 

[Reperfused]

You just need to read all of the posts above in this thread, and it will clear the misunderstanding.

 

[DrIvanhoe]

You just need to read all of the posts above in this thread, and it will clear the misunderstanding.

With all due respect, the only coherent post in this thread is by Transposony, but s/he doesn't mention the pathophys of the spastic bladder. Everything written earlier to that is very dubious [at best].
Don't get me wrong - i'd be happy if someone could convince me that there are UMN and LMN in ANS and cutting out the UMN would lead to LWN overfiring.
If you have links to support those claims then go ahead and post them here. Otherwise, your only making me feel sorry for the folks in medicine who are happy to base their knowledge on hearsay info without confirming it with a solid article or a book paragraph. You should really consider relying more on solid sources. No offence.

 

[Reperfused]

Even UWorld called it an UMN lesion, right?

@Phloston can you please shed some light on the above confusion?

 

[DrIvanhoe]

It does mention UMN lesion that leads to decreased inhibition on the micturition, spastic bladder that cannot relax/fill properly. What it might be saying is that proper functioning of micturition reflex as a whole is impaired due to the loss of the voluntary external sphincter contraction. What leads to detrusor-sphincter dyssynergia. This is also mentioned in the Merck Manual and confirmed by my neurology friend. Called thoracic myelopathy. Uworld doesn't specify this.

After googling I ended up here and read my exact question in your original post. Then later posts brought the whole confusion up. ANS fibers are not the location of lesion in the spastic bladder, rather corticospinal tracts are. I guess they also somehow must be involved bilaterally b/c with hemisection damage in Brown-Sequard doesn't cause spastic bladder at least it is not included in the syndrome description. But the whole UMN and LMN ANS stuff is complete bull, sorry. Think of Horner's - despite the level of lesion (central, pre or postganglionic) a patient ends up with the sympathetic deficit whatsoever (anhydrosis part aside).

On a side note, was wondering what would happen if demyelination involved descending parasympathetic fibers. Apparently, this hasn't been observed/described before.

 

[Reperfused]

I know the lesion is not in the ANS, its in the descending tracts.

Looking at the basic anatomy, the pelvic splanchnic nerves (preganglionic, parasympathetic fibers) originate from the S2, 3, 4 segments of the spinal cord.
But there's something from the higher centers in the CNS that's controlling these nerves, right? It's the lesion of that thing (which are basically UMNs) that cause the lack of inhibition on these pelvic splanchnic nerves (pre and post ganglionic both) and cause spastic bladder.

 

[Reperfused]

Detrusor is a smooth muscle and is innervated by parasympathetics. There's no motor neurons there afaimc.
UMN and LMN parts of of various tracts e.g. corticospinal, corticobulbar and others, none of those are ANS tracts.

ANS does consist of preganglionic and postganglionic neurons, but I cannot find nor recall anything about preganglionic being inhibitory and postganglionic somehow excitatory and having it's own firing rate. Moreover never heard them being called UMN and LMN before, which at least in my understanding ultimately relates to MOTOR function aka skeletal muscle innervating.

Post a proof link, please, if available. I keep waking up at night without explicitly knowing how does my bladder works.

No, it's not that ANS has its own UMN or LMN and I never said that. There's also no pre/post-ganglionic inhibitory/stimulatory thing.

The whole of pelvic splanchnic nerve (including pre- and post-ganglionic fibers) act as one and provide a parasympathetic effect on the detrusor muscle, which is to contract.

The UMNs are in the CNS and it's them that provide an inhibitory check on the pelvic splanchnic nerves.

 

[Reperfused]

It does mention UMN lesion that leads to decreased inhibition on the micturition, spastic bladder that cannot relax/fill properly. What it might be saying is that proper functioning of micturition reflex as a whole is impaired due to the loss of the voluntary external sphincter contraction. What leads to detrusor-sphincter dyssynergia. This is also mentioned in the Merck Manual and confirmed by my neurology friend. Called thoracic myelopathy. Uworld doesn't specify this.

After googling I ended up here and read my exact question in your original post. Then later posts brought the whole confusion up. ANS fibers are not the location of lesion in the spastic bladder, rather corticospinal tracts are. I guess they also somehow must be involved bilaterally b/c with hemisection damage in Brown-Sequard doesn't cause spastic bladder at least it is not included in the syndrome description. But the whole UMN and LMN ANS stuff is complete bull, sorry. Think of Horner's - despite the level of lesion (central, pre or postganglionic) a patient ends up with the sympathetic deficit whatsoever (anhydrosis part aside).

On a side note, was wondering what would happen if demyelination involved descending parasympathetic fibers. Apparently, this hasn't been observed/described before.

See this is the thing, there are no "descending parasympathetic fibers".
Parasympathetic outflow is either at the cranial nerves level (CN 3, 7, 9, 10) or at the sacral level (called pelvic splanchnic nerves) and these originate from the gray matter in the sacral segments S2, 3 and 4.

 

[DrIvanhoe]

Do you mean UMN of the path that innervates the external urinary sphincter? Or you think there's another path that connects to detrusor or a parasympathetic neuron?