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Thread: Umn And Lmn ?

  1. #1

    Exclamation Umn And Lmn ?

    Actually this is my basic doubt..i am really confused about umn and lmn....?
    i have learnt that UMN or UPPER MOTOR NEURONS refer to the pathways that originate in the layer 5 of cerebral cortex with fibres for each cranial nerve functions....for example a motor representation for the muscle STYLOPHARYNGEUS is there in the cotex....
    these fibres as tracts or pathways end in the CRANIAL NERVE NUCLEI ..at the corresponding level...
    --I MEAN THE ABOVE MENTIONED FIBRES END IN GLOSSOPHARYGEAL NUCLEI(NUCLEUS AMBIGUUS)....from here starts the LOWER MOTOR NEURON....that ends in the muscle........

    DOUBT...if so umn why do umn lesion behave differently from lmn?as everything is in a continuous pathway..?

    2.why shd thr b xaggerated reflexes?
    3.wats implied by bilaterall innervation..which all cases are the terms contralateral innervations applicable?
    4.wHAT ARE THE UMN/LMN FEATURES WITH REASON FOR THAT?

    i beleive reply to this scrap will help many to have the basic neurology clear without which..it willb difficult..i beg ur help

  2. #2
    This is very simplistic....I am sure Dr. Young can provide a more detailed explaination:

    Here is a diagram that helps to show both upper motor neurons and lower motor neurons.



    Upper motor neurons have their nucleus in the brain, primarily in the motor strip of the cortex (gray matter). They send their axons down through the brain, where they may synapse with lower motor neurons that are part of cranial nerves in various nuclei that have the lower motor neuron nuclei. They also send axons down the spinal cord, where they synapse with lower motor neuron nuclei in the gray matter of the cord that then leave the cord via spinal nerves.

    Damage to lower motor neurons results in flaccid paralysis because it interrupts the reflex arc. Damage to upper motor neurons usually results in spastic paralysis (hypertonicity), because it also damages the descending inhibitory nerves that keep reflexes under control.

    People with stroke and TBI primarily have upper motor neuron injury except if their lesion effects the nuclei associated with cranial nerves. People with ALS and polio have primarily lower motor neuron damage (brain and spinal cord) and usually have flaccid paralysis. People with SCI usually have both (except for those with cauda equina and conus injuries), since the damage to the cord damages upper motor neurons passing through the area of damage as well as lower motor neurons leaving that specific area.

    (KLD)

  3. #3
    I have a question about the process of damage of the UMN say from a TBI. From what I can gather when there is a UMN damage, the symptoms would be first the spasticity and hypertonic muscles (those affected) and as the damage progresses, it turns into a LMN injury as well? So the initial muscle condition is spastic, tight and prone to hyperreflexes and spasms, and then moves into a flaccid paralysis as the injury to the UMN causes LMN axon death. Is this right? I've read where the LMN damage can mask an UMN injury. So you could have spasticity and paralysis at the same time. (Us poor laypersons need so much help in understanding. LOL!)

    Because this is kinda what I have experienced myself. Muscles from the head/neck to leg were at first painful, tight, spasms, and now slowly it is not as bad, although too much activity to stretch the muscles affected starts a new cycle.

  4. #4
    It all depends on where the damage is, and WHICH UMN and LMN you are talking about. With a SCI you can certainly damage both, but it is unusual to progress from a LMN to a UMN or reverse for any given nerve or tract. It is common to appear to have a LMN injury to a given tract below the level of injury during spinal shock though.

    (KLD)

  5. #5
    great..........i reffered MERITT's NEUROLOGY ..yesterday........

    some idea that i got..(pls tel me whether i am correct)
    1.the cranial nerve nuclei in itself being an aggregation of neurons has some firing potential..i mean to say..even if UMN connection is removed by a lesion..it itself can trigger a response..
    2.the UMN connection till the nuclei has several alpha motor inhibitory connections..when that is lost it cause exaggeration of reflexes.........

  6. #6
    Quote Originally Posted by dranoop
    great..........i reffered MERITT's NEUROLOGY ..yesterday........

    some idea that i got..(pls tel me whether i am correct)
    1.the cranial nerve nuclei in itself being an aggregation of neurons has some firing potential..i mean to say..even if UMN connection is removed by a lesion..it itself can trigger a response..
    2.the UMN connection till the nuclei has several alpha motor inhibitory connections..when that is lost it cause exaggeration of reflexes.........
    Dranoop, please do not post these questions on the Announcements and Feedback forum. This is not a place to post such questions. Post them in the Science, Medicine, and Technology forum if they are not directly related to cure. Post them in Cure if they are.

    Wise.

  7. #7
    Senior Member jb's Avatar
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    so is it safe to say that ppl w/atrophy from lack of nerve innervation means that one has a lmn injury and someone who is spastic has an umn?

  8. #8
    See above. For those with SCI, you most probably have BOTH UMN and LMN injuries unless your injury is cauda equina or conus. When talking about UMN and LMN injuries you MUST specify the target organ or muscle. It is incorrect to say "my injury is LMN (or UMN)" but you can say "I have a LMN bladder" (ie, a flaccid bladder) or "I have a UMN injury for my quads and gluts" (ie, spastic paralysis)", or "I have a UMN injury for my bowel" (meaning the anal sphincter is spastic).

    (KLD)

  9. #9
    Quote Originally Posted by jb
    so is it safe to say that ppl w/atrophy from lack of nerve innervation means that one has a lmn injury and someone who is spastic has an umn?
    JB, spasticity generally indicates the presence of upper motoneuronal (UMN) injury with preservation of LMN but flaccidity (and atrophy) only suggests lower motoneuronal (LMN) injury. The reason is that there may be non-use atrophy resulting from UMN injury. Atrophy and flaccidity can also result from combinations of UMN and LMN. Wise.

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