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Postural Neurocognitive and neuronal activated cerebral blood flow deficits in CFS

Discussion in 'Latest ME/CFS Research' started by ramakentesh, Jan 29, 2012.

  1. ramakentesh

    ramakentesh Senior Member

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    Another one from Dr Julian Stewart:

    http://www.ncbi.nlm.nih.gov/pubmed/22180650

    Postural Neurocognitive and Neuronal Activated Cerebral Blood Flow Deficits in Young Chronic Fatigue Syndrome Patients with Postural Tachycardia Syndrome.

    Neurocognition is impaired in Chronic Fatigue Syndrome (CFS). We propose that impairment relates to postural cerebral hemodynamics. 25 CFS and 20 control subjects underwent incremental upright tilt at 0, 15, 30, 45, 60, and 75 with continuous measurement of arterial blood pressure and cerebral blood flow velocity (CBFv). We used an N-back task with N ranging from 0 to 4 (increased N= increased task difficulty) to test working memory and information processing. We measured N-back outcomes by the number of correct answers and by reaction time. We measured CBFv, critical closing pressure (CCP), and CBFv altered by neuronal activity (activated CBFv) during each N and every tilt angle using transcranial Doppler ultrasound. N-Back outcome in controls decreased with N but was independent of tilt angle. N-Back outcome in CFS decreased with N but deteriorated as orthostasis progressed. Absolute mean CBFv was slightly less than control in CFS at each angle. Activated CBFv in controls was independent of tilt angle and increased with N. In contrast, activated CBFv averaged 0 in CFS, decreased with angle and was less than control. CCP was increased in CFS suggesting increased vasomotor tone and decreased metabolic control of CBFv. CCP did not change with orthostasis in CFS, but decreased monotonically in control subjects, consistent with vasodilation as compensation for the orthostatic reduction of cerebral perfusion pressure. Increasing orthostatic stress impairs neurocognition in CFS. CBFv activation, normally tightly linked to cognitive neuronal activity, is unrelated to cognitive performance in CFS; increased CCP and vasomotor tone may indicate uncoupling of the neurovascular unit during orthostasis
  2. Vitalic

    Vitalic Senior Member

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    Am I correct in interpreting this as they started at a horizontal position and were gradually tilted upright? I've not had a tilt-table test carried out before so not sure how it works.
  3. adreno

    adreno 3% neanderthal

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    Not really news to me, but the more studies on CFS/POTS, the better. Thanks for posting.
  4. ramakentesh

    ramakentesh Senior Member

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    This one is interesting because ratehr than looking at what is happenng peripherally to blood flow in POTS it is looking at the cerebral consequences.
  5. adreno

    adreno 3% neanderthal

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    It is well known already that POTS causes cerebral hypoperfusion. Here's an example:

  6. ramakentesh

    ramakentesh Senior Member

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    That wasnt my point my good sir or madam.

    And infact the study I printed above does NOT demonstrate that there is cerebral hypoperfusion, but rather that there is not a vasolidatory response to neuronal challenge as occurs in normal people. There is perhaps a loss of control of cerebral vasomotor or parasympathetic-mediated cerebral vasodilation.

    Secondly that study you have printed doesnt actually demonstrate cerebral hypoperfusion - it demonstrates impaired cerebral autoregulation and thus lack of buffer of beat by beat blood pressure changes. There is sychronicity between blood pressure fluctuations in the peripheral and cerebral vasculature. This is in direct contrast to previously published work by Novak, et al.

    Some more recent work by Stewart and Medows contradicts their earlier finding. In some patients there isnt dramatic blood pressure/cerebral synchronity and even very mild reductions in cerebral blood flow seem to cause dramatic alterations of consciousness in some POTS patients. Also postural hypocapnia is present in a subset, which is not hypoperfusion.

    But feel please free to explain why there is alterations in neuronal control of cerebral vasodilation if you'd like.

    Infact I wouldnt even suggest that cerebral hypoperfusion is an established fact in POTS. Studies on this are actually limited. Two groups found postural cerebral vasospasm, yet other groups suggest the opposite, and still others found normal cerebral vasulare responses. Most of this data has never been published or peer reviewed.
    ahimsa likes this.
  7. adreno

    adreno 3% neanderthal

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    It seems you are more on top of the finer intricacies of this phenomenon than I am. I stand corrected.
  8. DaiWelsh

    DaiWelsh

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    Maybe standing is the problem, try sitting ;)
    Nielk likes this.
  9. ahimsa

    ahimsa Senior Member

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    I'm no expert but I have had a diagnostic tilt table test so I'll put in my two cents. :innocent1:

    My test was nothing like this. My test had only two phases, one phase while lying flat (to get baseline measurements) and one phase while at 80 degree tilt (head up - some people get this part confused and think we're being turned upside down).

    It might have included more phases (e.g., an IV of isoproternol or some such drug while the patient is tilted) but I passed out after 20 minutes just from the tilt alone, no drug needed.

    This study lists a whole range of tilt angles. This is lot more complicated than the tilt table test used to diagnose orthostatic intolerance (NMH and/or POTS). Plus they were also measuring different things, not simply heart rate and blood pressure. Perhaps someone who knows more can provide more details.
  10. ramakentesh

    ramakentesh Senior Member

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    sorry that came across worse that it was supposed to - the danger of multitasking.

    When I had my tilt test done they found a 42% reduction in carotid blood flow so for me at laest there was definaetly reduced cerebral blood flow. However the studies above are talking about alternative findings that account for the symptoms of abnormal cerebral blood perfusion.

    I think the aim of the study was to see when or at what level of orthostatic stress the abnormal neuronal control of cerebral blood flow kicked in.
  11. oceanblue

    oceanblue Senior Member

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    Blimey, this is complicated.

    I'm trying to reconcile this study with an earlier study by the same authors, also on CFS/POTS patients.

    Both studies tested mental performance under tilt with the N-back test:
    Both studies found that while, unsurprisingly, test performance decreased as the test got more diffiuclt, the POTS/CFS patients performed worse than controls when tilted, but not when supine.

    Both studies also looked at Cerebral Blood Flow velocity, CBFv, and both studies found no difference between patients and controls on this measure, eg from the first study:
    However, the second study did find a difference between the groups when it looked at activated CBFv, defined as "CBFv altered by neuronal activity" (activated CBFv wasn't measured in the first study, AFAIK).
    So if I've understood this correctly, the problem in CFS/POTS patients is not absolute CBFv but lack of regulation of activated CBFv, and this leads to (or is associated with) the decline in mental performance.
    Maybe ramakantesh could check I have this right.:D
    Persimmon likes this.
  12. Dolphin

    Dolphin Senior Member

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    And just to be clear, the first study didn't investigate activated CBFv.

    If people have both full texts, I would read the other one first as I think it gives a better explanation of what is involved with regard to the cognitive testing. Also, there is much less "biology". Then move on to this which will allow one to concentrate more on the biological mechanisms. (I think I pretty much understood this paper by doing it that way (just about or close to it) while I might have skimmed over some of the biology if I hadn't read the other paper first).
  13. Dolphin

    Dolphin Senior Member

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    I thought this was an interesting observation

    It is certainly possible. Whether the results of tests neatly divide up like this, I'm not sure.

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