Vitamin B12 deficiency: hyporeflexia or hyperreflexia

[hantah]

First Aid 2012 (page 451) said hyperreflexia but the newest errata says hyporeflexia. At least from my google search, it seems that hyporeflexia is true,,, but in the diagram for B12 deficiecny, corticospinal tract is damaged with gray matter of anterior horn spared... which makes me think that it's an UMN lesion...which should result in hyperreflexia.

Does anyone know the mechanism by which B12 deficiency results in hyporeflexia? Or is first aid errata wrong to say that B12 deficiency causes hyporeflexia?

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[lemonade90]

B12 is key to preventing abnormal mylein production. When odd chain fatty acids are not properly metabolized, you get the production of abnormal myelin. Since the arc of reflexes has myelinated neurons, I would imagine this would be why you become hyporeflexic as the nerves wouldn't be functioning properly.

 

[Go Ducks]

I would imagine that it would be either/or depending on chance--whether you personally happen to have more demyelination of your upper motor neurons or lower motor neurons.

 

[Valadi]

I would imagine that it would be either/or depending on chance--whether you personally happen to have more demyelination of your upper motor neurons or lower motor neurons.

That was bright logic. And correct.

B12 deficiency leads to combined system degeneration. If you a gradual onset, usually subacute, symmetric pattern of this, think b12 first. Also vibration/proprioception diminished is a big buzzword to differentiate it from the below diseases in the ddx.

MS also leads to combined system degeneration, but you know its intermitted, not gradual. I think the only crazy disease they might test that does this is adrenomyelosomethingorother.

Diabetes and alcoholism are also be in the ddx for CSD. So look for visual and other DM probs to differentiate, and alcohol usually gives corticospinal/cerebellar probs.

 

[JackShephard MD]

I think it would be wise to assume that the UMN signs predominate in subacute combined deficiency.

 

[lemonade90]

I would imagine that it would be either/or depending on chance--whether you personally happen to have more demyelination of your upper motor neurons or lower motor neurons.

I could be wrong but I didn't think you had demyelination in Vit B12 def but just abnormal replacement of myelin which ruined function. I could see this for a demyleinating disease or a virus where selective/random parts of the nervous system are affected...but B12 is something ALL neurons needs so in that sense they should all be affected; it shouldn't be that one set of neurons happens to get more or less B12 than their proportional share of myelin. If thats the case, then the LMN symptoms would dominate over/mask the UMN symptoms.

 

[JackShephard MD]

I could be wrong but I didn't think you had demyelination in Vit B12 def but just abnormal replacement of myelin which ruined function. I could see this for a demyleinating disease or a virus where selective/random parts of the nervous system are affected...but B12 is something ALL neurons needs so in that sense they should all be affected; it shouldn't be that one set of neurons happens to get more or less B12 than their proportional share of myelin. If thats the case, then the LMN symptoms would dominate over/mask the UMN symptoms.

The UMN neuron portion is much larger, and even in the case of systemic deficiencies you will see localization based upon areas of higher metabolism. You would not see an immediate equally distributed response. I would argue there is much more UMN to attack and therefore those signs will predominate.

Either way, the demyelination we are referring to in the lateral corticospinal tract (subacute combined degeneration) will occur and it likely isn't critical to differentiate between UMN/LMN signs.

 

[lemonade90]

The UMN neuron portion is much larger, and even in the case of systemic deficiencies you will see localization based upon areas of higher metabolism. You would not see an immediate equally distributed response. I would argue there is much more UMN to attack and therefore those signs will predominate.

I can buy the argument of relative metabolism instead of the theory of proportional myelin problems I was suggesting. I guess you would still ultimately end up with LMN signs after an intitial period (several years) of UMN signs. I was a bit confused by the fact FA mentions abnormal myelin incorporation in its Biochem chapter but demyelination in its Neuro Chapter as the mechanism for B12 problems.

So true. The other signs are probably more important.

 

[Phloston]

It would have to be hyper-reflexia bc if it were hypo-, then we'd also expect fasciculations, atrophy, etc., and those aren't classic SCD signs (as far as whether there's actually a Babinski's or hypertonia to support my argument though, I actually haven't heard of those as being associated with SCD either).

 

[TimBothwelly]

Vitamin B12 is known as a water-soluble vitamin that is seen in various meats, fish and also dairy foods as well as adds tremendously for the production of red blood cells when supporting to maintain a wholesome neurological system. Besides that, this is great for the changing the energy. In addition, it takes a significant task in the taking advantage of of the ingestion of folic acid. Various other B12 Vitamin advantages would be the protection with regards to myelin (the particular material which takes care of the nervous system and also lets them broadcast signals between your neurological tissues through the entire human body) plus the amelioration of the fat loss ability (rate of metabolism) of the body which assists in losing fats.



Vitamin B12 Insufficiency



Not enough B12 Vitamin can easily get sometimes from the limited eating consumption as a result of an unbalanced diet system or perhaps because of the intrinsic factor insufficiency, resulted in pernicious anemia, an ailment which, if it is not dealt with, may regretably cause loss of life. Deficiency of the particular intrinsic factor signifies that the gastrointestinal tract of the person that is suffering from it has trouble when it comes to soaking up B12 Vitamin adequately. The possible lack of this vitamin typically brings about anemia, it also might occur in serious neurological and also human brain harm. Consequently, take note of the pursuing signs or symptoms that can help everyone identify the actual Vitamin B12 insufficiency.

To read the full article, visit this link : myvitaminb12deficiency.com

 

[ijn]

Subacute combined degeneration is not the only neurological presentation of B12 deficiency, nor is it even the most common. The most common neurological presentation of B12 deficiency is peripheral neuropathy. That'd likely result in hyporeflexia given it's a LMN lesion. The answer depends on the presentation a person's of B12 deficiency.

So peripheral neuropathy: hyporeflexia; subacute combined degeneration: hypereflexia.

 

[gravitywave]

Subacute combined degeneration is not the only neurological presentation of B12 deficiency, nor is it even the most common. The most common neurological presentation of B12 deficiency is peripheral neuropathy. That'd likely result in hyporeflexia given it's a LMN lesion. The answer depends on the presentation a person's of B12 deficiency.

So peripheral neuropathy: hyporeflexia; subacute combined degeneration: hypereflexia.

all correct up until the last sentence. B12 deficiency is large fiber disease, because those are the neurones most susceptible to myelin defects. as you say, typically the PNS is effected first, followed by disease of the dorsal and lateral tracts. Most common presentation of subacute combined degeneration is therefore stocking-glove paresthesias, loss of vibration sense and proprioception, spasticity, ataxia, hyporeflexia, positive Babinskis, and of course a macrocytic anemia and elevated homocysteine/methylmalonate levels. I know the Babinskis don't fit - don't ask me why - but this is the clinical presentation.

 

[tco]

I would think that, in real life, it would be detected before either hypo- or hyperreflexia would occur. B12 deficiency would, theoretically, lead to eventual dysfunction of most neurons due to abnormal myelin production, but the paresthesias and problems with coordination would likely lead to it being detected and treated before problems with motor neurons would occur.

To guess at the question, though - hyporeflexia.

 

[ijn]

I would think that, in real life, it would be detected before either hypo- or hyperreflexia would occur. B12 deficiency would, theoretically, lead to eventual dysfunction of most neurons due to abnormal myelin production, but the paresthesias and problems with coordination would likely lead to it being detected and treated before problems with motor neurons would occur.

To guess at the question, though - hyporeflexia.

You obviously haven't met a Medicaid or self-pay patient yet.