USMLE Forums banner
1 - 10 of 10 Posts

·
Registered
Joined
·
36 Posts
Discussion Starter · #1 ·
Hi
In Lesion of corticospinal tract ipsilateral spastic paresis occurs below the level of injury..............can you guys plz explain this point that why the paresis occurs below the level of injury Why not at the level of injury?
I am totally confused about it:(
 

·
Registered
Joined
·
36 Posts
Discussion Starter · #3 ·
Of course you have ipsilateral deficit at the level of the lesion and below it.
Who told you otherwise?
In Kaplan it is written about the lesions. eg in Brown sequard Syndrome it is written that lesion of the corticospinal tract results in an ipsilateral spastic parasis below the level of injury. At the level of lesion,there will be an ipsilateral loss of all sensation................my question is that what is the concept behind it? how it occurs below the level of injury and why?:confused:..
 

·
Registered
Joined
·
3,316 Posts
Lateral Corticospinal Tract Lesions

In Kaplan it is written about the lesions. eg in Brown sequard Syndrome it is written that lesion of the corticospinal tract results in an ipsilateral spastic parasis below the level of injury. At the level of lesion,there will be an ipsilateral loss of all sensation................my question is that what is the concept behind it? how it occurs below the level of injury and why?:confused:..
You have ipsilateral LMN lesion at the level of the lesion and ipsilateral UMN lesion below the level of the lesion. Let me explain;

The lateral corticospinal tract is composed of the axons of neurons that were there in the motor cerebral cortex and so it's considered upper motor neuron. Once it reaches the anterior horn cell then the nerve emerging from there is considered lower motor neuron.

So let's take an example.
A lesion at T8 that has severed the lateral corticospinal tract.
This lesion will cause IPSILATERAL flaccid paralysis at the level of the lesion to all the muscles innervated by T8. But at T9 the anterior horn cell is not affected and therefore you don't have lower motor neuron effects in the muscles innervated by T9. Instead you'll have upper motor neuron effects (spasticity, increased reflexes) because the signals in the lateral corticospinal tract is no longer reaching the anterior horn cells in T9. So the lesion will also cause IPSILATERAL spastic paralysis below the level of the lesion.

Does that make sense to you? if not please ask again and tell us what is it that you still find confusing.
 

·
Registered
Joined
·
68 Posts
heyy very nice explanation.

i have a confusion.. how does UMN lesion result in lower limb weakness and LMN lesion result in upper limb weakness? eg. ALS.. kaplan says both upper and lower motor affected.. so FLACCID paralysis of upper limbs (so means LML upper limbs) and similarly SPASTIC paralysis of lower limbs ( so UML lower limbs).. the same thing applies to ASA occlusion also.

i thought UMN in lower limb supply the flexors more than extensors.. but cant really understand the application.. very confused.
 

·
Registered
Joined
·
487 Posts
also check out this

http://www.usmle-forums.com/usmle-step-2-ck-forum/2051-cns-lesion-location.html

http://www.usmle-forums.com/usmle-s...-root-ganglion-injury-nerve-degeneration.html

In Spinal cord you will probably be tested in this 6 classic lesions:
a. Tabaes dorsalis: seen in tertiary syphilis. Pt with bilateral loss of touch, vibration and tactile sense from lower limbs do tue lesion of fasciculus gracilis

b. Amiotrophic lateral sclerosis: is a combined Upper and lower motor neuron lession fot he corticospinal tract.
Let's break what i said.
corticospinal tract means form up to down...that is descendent way
upper motor neuron lession means......you will have spastic pareasia an babinsky
lower motor neuron means...the same patient will have flacid paresia ( some times not seen because there is an overlaping symptoms with upper neuron) but you will se fascilculations that are very characteristic of lower motor neuron.

c. Brown Sequard..is the typical pt going night to the bar and stabbed in back....come to emergency and has a complete hemisection of medula.
This patiente can have ipsilateral loss of touch and vibration adn ipsilateral spastic paresia becouse the upper motor neurone fibers were cut. Also ipsilateral will be some sort of lower motor neuron damage sometimes no seen.
Contralateral will be just loss of pain and touch.
If the hemisection is very high, I mean pt stabbed in neck above T1 you will see Horner on the side of lesions. Horner are always ipsilateral.
 

·
Registered
Joined
·
390 Posts
heyy very nice explanation.

i have a confusion.. how does UMN lesion result in lower limb weakness and LMN lesion result in upper limb weakness? eg. ALS.. kaplan says both upper and lower motor affected.. so FLACCID paralysis of upper limbs (so means LML upper limbs) and similarly SPASTIC paralysis of lower limbs ( so UML lower limbs).. the same thing applies to ASA occlusion also.

i thought UMN in lower limb supply the flexors more than extensors.. but cant really understand the application.. very confused.
I think it depends on the level of lession. Lession at the spinal cord level of brachial plexus origin (C5-T1) will cause weakness in upper limb, while at the level of lumbosacral plexus origin (L2-S3) will cause weakness in lower limb. Whether it is spastic or flaccid paralysis will depend on type of lession (UMN or LMN).

In case of ALS, it usually affects the cervical spinal cord that's why you'll see LMN type of lession of upper limb and UMN type of lession in lower limb.
 
1 - 10 of 10 Posts
Top