Difference btw Anterior Motor Neuron and Lateral corticospinal tact?

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phd89

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This may be dump question but I just got an NBME question wrong where they asked about the lesion of an UMN in the spinal cord and where it is seen. I choose the Anterior Motor horn the answer was the Lateral corticospinal tract.

I'm confused I thought the UMN for the corticospinal tract was in the Gray area (anterior horn) and but it is actually in the white lateral matter. So what is present in the Anterior Horn? does a UMN ever damage the Anterior Horn or only affects the Lateral White matter?

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This may be dump question but I just got an NBME question wrong where they asked about the lesion of an UMN in the spinal cord and where it is seen. I choose the Anterior Motor horn the answer was the Lateral corticospinal tract.

I'm confused I thought the UMN for the corticospinal tract was in the Gray area (anterior horn) and but it is actually in the white lateral matter. So what is present in the Anterior Horn? does a UMN ever damage the Anterior Horn or only affects the Lateral White matter?

The lower motor neuron nuclei are in the anterior horn. The UMN loss affects the anterior horn, but injury to UMN in the spinal cord only occurs in the white matter.
 
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Just so you can see how this applies to the real USMLE, there are a few other high-yield scenarios I can think of off the top of my head that require you know this difference:

1) in ALS, you need to know that the UMN signs are lesions of the lateral corticospinal tract and the LMN signs are lesions of the anterior horn.

2) In Brown-Sequard syndrome, concomitant to the hemi-section, the ipsilateral spastic paralysis (UMN sign) below the lesion is due to a damaged lateral corticospinal tract; the flaccid paralysis (LMN sign) at the level of the lesion is secondary to anterior horn trauma (you also get contralateral loss of pain/temp below the lesion, loss of sensation at the level of the lesion and loss of vibration/propioception ipsilateral and below the lesion with this syndrome).

3) Subacute combined-degeneration (B12-deficiency) causes spasticity (UMN due to corticospinal tracts being affected [spinocerebellar and dorsal columns also are in this syndrome]). Vitamin E deficiency causes similar symptoms, but the ataxia, high methylmalonyl-CoA, and classic haematological signs won't be seen (instead you'd get haemolysis). Friedreich's ataxia also falls into the UMN category.

4) Werdnig-Hoffman syndrome and Polio --> anterior horns --> LMN.

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That being said, FA covers all of that stuff.

Always remember that a corticospinal tract lesion is UMN and one of the anterior horn is LMN.
 
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The lower motor neuron nuclei are in the anterior horn. The UMN loss affects the anterior horn, but injury to UMN in the spinal cord only occurs in the white matter.

By affect I mean that it causes a loss of inhibition to the LMNs. Thus, you become spastic. You can think of it as since the UMN aren't there to stop reflex arcs, you are more prone to full force and continuous reflex arcs when reflexes are tested. You also lose muscle bulk slower since the direct connection to the muscles, the LMN, is still intact and thus muscle cells will still receive the "survive" signal from them even though the LMNs will no longer function appropriately without the information sent by UMNs. The area of injury that you will see in the pathology slice will only be in the corticospinal tracts, even though there are consequences to the funciton of LMNs.
 
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