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The Pots Brain Does Not Vasodilate In Response To Difficult Tasks


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Basically the cerebral blood flow was similar between both study groups (the control and the CFS + POTS patients) however, the control group's critical closing pressure decreased as they were made to "stand up" which allowed for their neuronal circuits to become activated. In contrast, the CFS + POTS patients' critical closing pressure remained the same when they were "standing up" versus lying down, suggesting a defect in their compensatory mechanism.

How their cerebral blood flow remained fairly consistent despite the critical closing pressure malfunctioning is a mystery to me. Perhaps there's another compensatory mechanism at play.

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Interesting. My son is DXed with NMH and CFS, not POTS- although his HR got to 140 during his TTT (an 80 BPM rise) it didn't happen until 34 min- prior to his faint. Regardless, Mack gets VERY sick when he has to intensely concentrate on his school work. For instance, following his SAT, we had to go straight to the ER. He was so faint and had an unimaginable headache. In a high school English Lit class. he had to memorize PAGES of Shakespeare to recite for a test grade. Every time he tried, he started to vomit- really. I felt like such a fool trying to explain to his school counselor that studying too hard made my child sick. You can imagine the eye rolls. :angry: This study might provide the science behind this phenomenon. It makes my heart break for all of us, but especially the kids as sooooo much is expected of them.

Julie

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There is this one too:

Clin Sci (Lond). 2012 Mar 1;122(5):227-38.

Increasing orthostatic stress impairs neurocognitive functioning in chronic fatigue syndrome with postural tachycardia syndrome.

Ocon AJ, Messer ZR, Medow MS, Stewart JM.

Source

Department of Physiology, New York Medical College, Valhalla, NY, USA. anthony_ocon@nymc.edu

Abstract

CFS (chronic fatigue syndrome) is commonly co-morbid with POTS (postural tachycardia syndrome). Individuals with CFS/POTS experience unrelenting fatigue, tachycardia during orthostatic stress and ill-defined neurocognitive impairment, often described as 'mental fog'. We hypothesized that orthostatic stress causes neurocognitive impairment in CFS/POTS related to decreased CBFV (cerebral blood flow velocity). A total of 16 CFS/POTS and 20 control subjects underwent graded tilt table testing (at 0, 15, 30, 45, 60 and 75°) with continuous cardiovascular, cerebrovascular, and respiratory monitoring and neurocognitive testing using an n-back task at each angle. The n-back task tests working memory, concentration, attention and information processing. The n-back task imposes increasing cognitive challenge with escalating (0-, 1-, 2-, 3- and 4-back) difficulty levels. Subject dropout due to orthostatic presyncope at each angle was similar between groups. There were no n-back accuracy or RT (reaction time) differences between groups while supine. CFS/POTS subjects responded less correctly during the n-back task test and had greater nRT (normalized RT) at 45, 60 and 75°. Furthermore, at 75° CFS/POTS subjects responded less correctly and had greater nRT than controls during the 2-, 3- and 4-back tests. Changes in CBFV were not different between the groups and were not associated with n-back task test scores. Thus we conclude that increasing orthostatic stress combined with a cognitive challenge impairs the neurocognitive abilities of working memory, accuracy and information processing in CFS/POTS, but that this is not related to changes in CBFV. Individuals with CFS/POTS should be aware that orthostatic stress may impair their neurocognitive abilities. PMID: 21919887 [PubMed - in process]

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Does this tell us anything we didn't already know ? Upright bad. Supine good. Lol .. This sounds like

it could be from any of the reasons listed for dysautonomia.

Out of curiosity, I wonder how long patients were allowed to be supine before this test. My values

would've been very different if I'd been allowed an hour of supine time just prior to testing.

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From what I understand there is an adaptive mechanism in normal people that changes the point where a vein or artery has so little blood flow in it that it collapses and the result is an increased cerebral vasodilatory response to mental tasks and is independent of posture. Where as in POTS/CFS this change did not occur so the vasodilatory response to mental tasks did not occur orthostatically.

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From what I understand there is an adaptive mechanism in normal people that changes the point where a vein or artery has so little blood flow in it that it collapses and the result is an increased cerebral vasodilatory response to mental tasks and is independent of posture. Where as in POTS/CFS this change did not occur so the vasodilatory response to mental tasks did not occur orthostatically.

Um, I may have just accidently reported this post. My tablet is too sensitive to touch. Sorry if I did.

So this sounds like normal blood vessel response to lack of blood. Whether it's from low blood volume, a faulty heart or an impengmant (sp?) Of our blood supply anywhere in our bodies.

My reaction to this test would be

different if I'd been well nourished, rested and supine at least an hour beforehand but I can hardly think when upright.

I can feel this too if I strain my brain on medical research or talking on the phone while supine but i'd been told it was because I'd used up my neurotransmitters.

In fact typing on my computer for too long prior to eating breakfast will make me feel horrible. If I

stop, eat, and rest for about an hour, I feel fine supine again. I know our brains need glucose, fats and aminos but what else ?

Btw, I understand that this could be from physical brain damage but I'm keeping that in the background and hoping it's not. Fwiw, I think it's possible that our neurons are blocked via toxins or antibodies which may be undoable. I still have gluten antibodies and my mercury was high the last time it

was checked. My ataxia was probably from gluten antibodies.

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no worries dizzy you didn't report!

i have very much trouble with cognitive functions and had a few neuro cognitive tests done over the years, which show that i'm getting worse but they haven't been able (here in the netherlands) to actually link this to my pots. they do think so but can't scientifically prove it (thus far). i have been on ritalin in the past which was of help but can't toleratie it anymore, i'm soon going to try modafinil and hope it will help with cognitive funtion.

when i started octreotide in october 2010 most of my symptoms got much better (or went) but the brain fog doesn't seem to want to leave me.

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Yes, jangle is right. I have apenea and if I have a night where I can't tolerate my cpap . . .my brain is awful the next day. We don't get enough O2 to the brain when we sleep and/or forget to breathe - depending on which type of apenea we have. Not enough O2 makes for very foggy brains. I think some of us that have central apenea - some of our issues are breathing properly even while awake and that can cause a hopoxia state too.

Issie

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i actually hadnt thought of that. my hubby has sleep apnea and can't do without his cpap. i can't imagine how it would look like when we both would need one :lol:

as a lot of us i have a lot of trouble sleeping, so maybe there is more to it. i'll talk to my doc about it. thanks a lot for asking jangle and issie, i just hadn't thought of it. or maybe i did and then forgot :lol:

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Thank you Rama and Jangle - I get it! Issie - I think you're onto something with the breathing. I've wondered about this before because I am so much worse after I sleep. Deep breathing on autonomic testing brought on POTS symptoms for me, so I'm thinking the type of deep breathing we do while we sleep could cause some problems.

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