p53
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Major neurotransmitter of the pyramidal tract is glutamate - an excitatory mediator. At the same time damage of this pathway results in spastic paresis with Babinski sign, i.e. with hyperexcitability of the lower motor neurons, located in the anterior horn of the spinal cord. How could you explain this?
Edited by p53 on 08/22/05 - 06:18 AM
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| ssrpk
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upper motor neurons are divided into two broad groups : flexor and extensor biased
Flexor Biased : 1) Cortico-spinal tract 2) Rubro-spinal tract 3) Lateral Medullary reticulo-spinal tract (basically has inhibitory influence on the other flexor biased UMN a/a gamma-efferents of the LMN)
Extensor Biased : 1) Vestibulo-spinal tract 2) Reticulo-spinal tracts
Hyper-reflexia that is experienced, due to the lesions involving UMN's is basically due to the loss of this lateral medullary reticulo-spinal tract which has inhibitory influence on the LMN's.
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| SDK
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UMN tract has inhibitory effect on deep reflexes.....so lesion of UMN effect leads to exacerbation of these reflexes while absent of superficial reflexes.....
abow explanation is very nice by ssrpk......
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| p53
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Nice, but how could you explain that damage of the pyramidal tract (not whole medulla / spinal cord, it would be fatal) at the level of pyramidal decussation results in permanent flaccid, not spastic quadriplegia?
Edited by p53 on 08/22/05 - 10:02 AM
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| ssrpk
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not sure, flaccid paralysis won't occur due to the involvelment of CS tracts specifically, must be some other tracts involved, i'll look into it!
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| ssrpk
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hi p53,
i checked snell's clinical neuroanatomy, i did'nt find any such info regading occurence of flaccid paralysis due to lesions involving CS tracts at the level of pyramidal decussation! where did u read tht?
however, cerebellar lesions can lead to hypotonia!
lesions involving pyramidal tracts: babinskty sign, loss of sup. abdominal reflexes a/a cremastric reflex and loss of fine motor skills
lesions involving extra-pyramidal tracts: spastic paralysis, exagerrated deep tendon reflexes, clasp-knife reaction!
In reality it's more or less mixture of the two!
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| p53
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ssrpk, this info was from Ganong's physiology and more from Duus' Neuroanatomy.
According to them, pure pyramidal tract synapses on LMN and provides only voluntary control of body muscles, i.e. it's damage doesn't lead to spastic paresis - NO exagerrated deep tendon reflexes and clonuses (not sure about Babinski reflex, but I think it also would be absent)! This is in accordance with the fact that this is an excitatory pathway with glutamate as a neurotransmitter. Everything what is inhibitory to LMN comes from extrapyramidal tract, but these tracts (pyramidal and extrapyramidal, or to be more correct, part of the extrapyramidal) always trevel together, so that damage to the pyramidal tract (no matter it's on the level of internal capsule or spinal cord) always is associated with spastic paresis, i.e. hyperexcitability of LMN due to the damage of extrapyramidal tract. Exception is only pyramidal decussation - here these tracts don't travel together - so it's possible to damage pyramidal tract without extrapyramidal tract and get flaccid paresis. or if you resect only pyramidal cortex (precentral gyrus - brodmann area 4 with Betz pyramidal neurons) result would be the same.
Edited by p53 on 08/27/05 - 04:49 AM
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| ssrpk
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that was damn kool, i got your point  , same thing written in snell's could'nt get it earlier though!
but for step1 purposes spastic paralysis due to lesions involving UMN's would be a good generalization!
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| p53
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I agree, it may be extra info for step 1, but it's good info about brain for your brain. It proves that in reality things may be exactly the opposite what most people think about them!
Edited by p53 on 08/28/05 - 03:31 PM
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