Traumatic brain injury - similarities with and differences to ME/CFS, including PEM

Has anyone ever had all their pituitary and hypothalamus hormones tested (there are quite a lot of them) after severe illness or injury affecting the brain?

According to this link : https://en.wikipedia.org/wiki/List_of_human_hormones

(I'm dubious about the following numbers because I wasn't sure which column I should be counting!)

Anterior pituitary produces 8 hormones
Posterior pituitary produces 2 hormones
Hypothalamus produces 8 hormones

I don't think its true that if one hormone from the pituitary or hypothalamus is low that they will all be low. Nor that if one hormone is absent they will all be absent - but they might be.
 
I used to eat a lot of fruit but have a lot less now, after learning about the issues with fructose. Try to stick to the recommended 1-2 pieces a day, and shift the balance towards more vegetables.

Not always easy with lots of delicious tropical fruits available here, and often quite cheap. Mangosteens, of course, being the possibly the nicest food I have ever tasted, are exempt from that rule. :woot: But they are one of the expensive ones, even here where they are actually grown, so are self-limiting anyway.
 
Arnie Pye said:
Has anyone ever had all their pituitary and hypothalamus hormones tested (there are quite a lot of them) after severe illness or injury affecting the brain?

According to this link : https://en.wikipedia.org/wiki/List_of_human_hormones

(I'm dubious about the following numbers because I wasn't sure which column I should be counting!)

Anterior pituitary produces 8 hormones
Posterior pituitary produces 2 hormones
Hypothalamus produces 8 hormones

I don't think its true that if one hormone from the pituitary or hypothalamus is low that they will all be low. Nor that if one hormone is absent they will all be absent - but they might be.
Click to expand...

I want to look into this as I have a few abnormalities indicating I could have some hormonal issues.
 
Could PEM be, when neuron action potential fires, use of atp, atp require mitochondria and defective mitochondria generates more ROS, and then ROS causes DAMPS release from within the cell itself that the mitochondria is in, and that DAMPS released then activate glial cells which causes Inflammation cause pain and fatigue via activating pain nerves?
Do ROS damage the cells that they are released from?

Here i am just learning the very basics of biology and wondering
 
New Zealand scientists studying the brains of rugby players have made a significant breakthrough that could allow Chronic traumatic encephalopathy (CTE) to be diagnosed in living players.
article

Until now, the disease linked to repeated head knocks could only be confirmed after someone had died.

But new patterns of inflammation in affected people have been identified by Auckland University researchers, opening the door for diagnostic testing while someone is alive.

The discovery, a world first, could have far-reaching consequences for the treatment and management of people with head injuries, including rugby players.

“Our American colleagues are very confident that, within five to 10 years, we will have a more robust set of diagnostic tools for CTE,” said Dr Helen Murray, a research fellow at the Centre for Brain Research.

“Maybe it’s something we can actually treat and deal with during someone’s life. And that can be done through pharmaceuticals, thinking about resting and letting that inflammation go away.”
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The breakthrough was discovered by the Auckland University research team after examining the brain tissue of dozens of donors, including Guyton’s. The presence of tau proteins in someone with CTE was well known but Murray and her team discovered other proteins linked to inflammation.

"What we found is there’s a pattern of inflammation around blood vessels in CTE that is quite different to what we see in people who don’t have CTE,” Murray said.
Click to expand...

@SNT Gatchaman

Given the similarities in some of the symptoms and the hints we have had about issues with blood vessels in ME/CFS, it would be very interesting to have these researchers look at the brains of people with ME/CFS.

I have no doubt that some people with CTE are being diagnosed with FND, so, hopefully this discovery will at least stop some of that.

I don't know what the proteins they are suggesting are linked to inflammation are.
 
I was pleased to watch this too.

Hutan said:
I have no doubt that some people with CTE are being diagnosed with FND, so, hopefully this discovery will at least stop some of that.
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At least for rugby playing men an FND misdiagnosis would be less likely due to Neurologists’ bias.
Has the former player poster boy for LP/The Switch been active lately? EDIT - He’s doing fine Life Coaching & NLP& TV presenting etc - so obviously it was not CTE for him.
 
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Here is an old NYT article that empathized with ME/CFS patients after the columnist suffered concussion fatigue for a month. She didn't mention anything about her PEM though, so I asked AI for fun. The answer was: "While fatigue is a common symptom of post-concussion syndrome (PCS), post-exertional malaise (PEM), characterized by a worsening of symptoms after physical or mental exertion, is not a core defining feature of PCS like it is for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)"

It makes sense to me though, that PCS and ME/CFS should share features. The brain's immune system must get activated to make repairs after concussion and that obviously causes debilitating fatigue in PCS. But I can't think of a reason why PCS should involve PEM. In microglial model of ME/CFS, there are cells that are primed to get activated and they presumably cause PEM. PCS on the other hand involves normal activation. But maybe it's possible for some concussion to cause cells to get primed as well as activated.
 
poetinsf said:
Here is an old NYT article that empathized with ME/CFS patients after the columnist suffered concussion fatigue for a month. She didn't mention anything about her PEM though, so I asked AI for fun. The answer was: "While fatigue is a common symptom of post-concussion syndrome (PCS), post-exertional malaise (PEM), characterized by a worsening of symptoms after physical or mental exertion, is not a core defining feature of PCS like it is for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)"

It makes sense to me though, that PCS and ME/CFS should share features. The brain's immune system must get activated to make repairs after concussion and that obviously causes debilitating fatigue in PCS. But I can't think of a reason why PCS should involve PEM. In microglial model of ME/CFS, there are cells that are primed to get activated and they presumably cause PEM. PCS on the other hand involves normal activation. But maybe it's possible for some concussion to cause cells to get primed as well as activated.
Click to expand...

PCS does involve something that could be described as PEM though (at least a vague definition of worsening of symptoms after physical or mental exertion is very common, edit: an example where an athlete describes developing brain fog following physical activity). A majority of people with PCS describes something somewhat akin to this and from what I've heard treatment often also used to be "lie in a dark room until you feel better" whilst now it is, more often than not, seems to be something more akin to GET. I'm however not sure whether there is a delayed form of PEM though or whether it always tends to be instant in PCS. As far as I understand the cause of fatigue in PCS is unknown, what is obvious about "immune system activation causing fatigue" what exactly is it supposed to mean when nobody knows what PCS entails?
 
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EndME said:
PCS does involve something that could be described as PEM though (at least a vague definition of worsening of symptoms after physical or mental exertion is very common, edit: an example where an athlete describes developing brain fog following physical activity). A majority of people with PCS describes something somewhat akin to this and from what I've heard treatment often also used to be "lie in a dark room until you feel better" whilst now it is, more often than not, seems to be something more akin to GET. I'm however not sure whether there is a delayed form of PEM though or whether it always tends to be instant in PCS. As far as I understand the cause of fatigue in PCS is unknown, what is obvious about "immune system activation causing fatigue" what exactly is it supposed to mean when nobody knows what PCS entails?
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The old evidence based medicine tricking people into short term measures bolstered by false hope (and the natural frustration all humans have at not wanting to lie in a dark room) vs science and logic combined with long term outcomes
 
EndME said:
what is obvious about "immune system activation causing fatigue" what exactly is it supposed to mean when nobody knows what PCS entails?
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That was a poor choice of word on my part. I should've said "probably", not "obviously". "Probably" because immune system activation usually entails fatigue. Microglial activation in concussion has been observed, so the activation part is probably more than "probably".
 
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