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Impaired eye movements - quicker diagnosis of concussion

Discussion in 'Other Health News and Research' started by Marco, Jan 24, 2016.

  1. Marco

    Marco Grrrrrrr!

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    There was a short news report on this on the Beeb yesterday which reminded me of previous findings.

    Impairments in eye movements are found after concussion and may provide a quicker and more reliable diagnosis. Specifically this test measures impairments in something called 'smooth pursuit' - the ability to accurately track a moving target :

    Taking the guesswork out of diagnosing a concussion

    http://www.cnbc.com/2015/11/15/taking-the-guesswork-out-of-diagnosing-a-concussion.html

    Normally these and other symptoms resolve within a few weeks of the concussion. But in the case of Post-Concussion Syndrome, symptoms (which include fatigue, cognitive problems plus exacerbation of symptoms with exercise and alcohol intolerance to name a few) persist for months or years leading some to suspect that psychological factors intervence.

    These objective eye movement impairments also persist though leading researchers to conclude that "Poorer subconscious oculomotor function in the PCS group supports the notion that PCS is not merely a psychological entity, but also has a biological substrate." :

    Impaired eye movements in post-concussion syndrome indicate suboptimal brain function beyond the influence of depression, malingering or intellectual ability

    (bolding added)

    http://brain.oxfordjournals.org/content/132/10/2850

    Interesting that similar problems have been found in ME/CFS :

    Characterising eye movement dysfunction in myalgic encephalomyelitis/chronic fatigue syndrome.


    (bolding added)

    http://www.ncbi.nlm.nih.gov/pubmed/23918092

    Do these ME/CFS findings also 'indicate suboptimal brain function beyond the influence of depression, malingering or intellectual ability' ?


     
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  2. Woolie

    Woolie Senior Member

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    Marco, I have never heard of exacerbation with exercise or alcohol intolerance as being symptoms of post concussion syndrome (PCS). Its generally things like headaches, difficulties concentrating, irritability, dizziness, memory problems, sensitvity to noise/light, etc. Really neurological stuff. Although there appears to be some overlap, its a distinctly different profile to MECFS.

    I suppose some people might find alcohol makes them worse, that's reasonable, but there's something suspect about the way this article blurs the distinction between PCS and MECFS. I think this suggests a sympathy with a psychological view of the condition (that is, both are about depression, anxiety and convincing yourself you're ill when you're not, therefore, they probably look much the same).

    Like MECFS, PCS has been targetted heavily by psychobabblers.These poor patients are told they are imagining it, subjected to CBT etc. You see the usual warning signs in medical descriptions of PCS: "controversial". "complex" "physiological and psychological factors". I love the last one, its like "okay, we can't deny any more that there may be an actual biomedical basis to this disease, but we're still keeping the 'psychological' in it". Like they somehow interact by some mysterious mechanism, so that the biomedical factors only "activate" if the person has the wrong attitude. Instead of the way simpler and more elegant explanation, which is that the biomedical abnormalities are to blame.

    Why go for a simple biomedical explanation when a more complicated one can be made? Especially if that allows the psychobabblers to keep some dominion over the area!

    That's starting to sound pretty familiar, isn't it?
     
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  3. Marco

    Marco Grrrrrrr!

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    I'm pretty sure none of the links even mentioned ME/CFS. Any suggestions of a possible link are mine (and I'm not suggesting they are in any way the same thing - but similar processes may be at work).

    Re the symptoms :

    source : Exercise Intolerance in Individuals With Postconcussion Syndrome

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784364/

    To which you can add autonomic dysfunction (increased sympathetic/reduced parasympathetic function), dysregulated cerebral blood flow plus the fact that only a minority of concussion patients develop PCS.


    Indeed!
     
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  4. Woolie

    Woolie Senior Member

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    Sorry, @Marco I misunderstood.

    I had a look at the above article, though. It involved asking people to perform an intense exercise test for as long as they could, until they felt they had to stop due to exacerbation of PCS symptoms (or for controls, if they could no longer maintain the intensity).

    The PCS patients stopped sooner, and all stopped due to symptoms exacerbation. But tricky to assess this study because they never report what PCS symptoms were exacerbated by the exercise. And some were nonspecific things like fatigue (so could just mean patients stopped when they were tired - given that the PCS patients were a little less fit to start with than the controls, that might not be surprising). Another interesting difference from MECFS was that PCS patients reported lower perceived exertion than controls.

    I think its very suspect that they didn't report post-exercise PCS symptoms (only pre-exercise). Even though they claim to have collected the data. Such an important outcome for the paper - the most important one. This suggests to me that the data didn't look good for some reason.

    There's lots of evidence that people with even minor brain damage experience heightened fatigue. So there probably is a reduced exercise capacity in PCS, and it seems reasonable that exercise might further limit cognitive resources, leading to more PCS symptoms (e.g., poor concentration, irritability). I just wonder whether we're talking about the same thing as PEM in MECFS.

    I guess first we'd need to show that symptoms exacerbation exists. Then we'd need to measure its duration (PEM in MECFS may have a delayed onset and can be of long duration. I'd be surprised if exercise effects in PCS have similar properties).
     
    Last edited: Jan 25, 2016
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  5. Marco

    Marco Grrrrrrr!

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    I'm not sure it matters that much that they didn't report exactly which symptoms were exacerbated by exercise - do we know which specific symptoms are exacerbated in ME/CFS?

    But it might well be interesting to compare PWME v PCS v controls on the 2 day CPET with measurement of autonomic function and cerebral blood flow added to other physiological and subjective measures.
     
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  6. chipmunk1

    chipmunk1 Senior Member

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    Do they really believe that lack of intellectual ability could cause PCS?

    How would that work? You have two groups of people and one is getting better and the other is not because they are too dumb to understand that they body can heal and believe they are still injured?

    What might have happened was that some psychobabblers noticed that some people with head injury seemed to be seriously intellectually impaired(from the injury) and concluded that the impairment was causing the symptoms.
     
    Last edited: Jan 26, 2016
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  7. chipmunk1

    chipmunk1 Senior Member

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    http://www.tara.tcd.ie/bitstream/handle/2262/51408/PEER_stage2_10.1136%2Fjnnp.2008.171298.pdf

    How was that? I believe it starts with a virus infection but later other factors are important as well?

    Read carefully what they are saying here. PCS is transient and you only have persisting symptoms if you BELIEVE it is not.

    This is circular reasoning:

    They decide that it is transient.
    If someone complains about persisting symptoms they deny they exist.
    If someone ask why they will respond that patients never have been shown to have legitimate persistent symptoms..
     
    Last edited: Jan 26, 2016
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  8. lansbergen

    lansbergen Senior Member

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    As always confuse cause with effect.
     
  9. chipmunk1

    chipmunk1 Senior Member

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    What are external causal attributions?

    Do they mean if i have a been hit on the head by a golfball i(incorrectly) attribute the pain to external causes and need CBT for that?

    Conversation of 2 ER docs:

    "What a day. I already had 3 somatizers, they just keep coming."

    The other replies:

    "Don't complain. I already had over 50 attributors."
     
    Last edited: Jan 26, 2016
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  10. Marco

    Marco Grrrrrrr!

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    @chipmunk1

    Thankfully not everyone swallows that claptrap :

    A new paradigm for understanding incapacitating post-concussion syndrome

    http://www.lexology.com/library/detail.aspx?g=db6b3d83-8b76-43b7-96b3-f6caae9d78d4
     
  11. Woolie

    Woolie Senior Member

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    @Marco, there are other explanations, too, not involving inflammation. Subtle changes in white matter connecvity due to twisting and shearing during the accident:

    Smits, M., Houston, G. C., Dippel, D. W., Wielopolski, P. A., Vernooij, M. W., Koudstaal, P. J., ... & van der Lugt, A. (2011). Microstructural brain injury in post-concussion syndrome after minor head injury. Neuroradiology, 53(8), 553-563.
    http://link.springer.com/article/10.1007/s00234-010-0774-6/fulltext.html
     
  12. Marco

    Marco Grrrrrrr!

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    Thanks. An interesting paper.

    Of course there is damage to the brain otherwise concussion wouldn't be classified as a mild traumatic brain injury. The question is why a chronic complex syndrome develops in a minority long after the damage is assumed to have healed?

    That paper suggests there is microstructural white matter damage that is missed by conventional scans and that this damage correlates with symptom severity. Fair enough but I don't see why that would rule out neuroinflammation as neuroinflammation is the appropriate response to tissue damage?
     
  13. chipmunk1

    chipmunk1 Senior Member

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    Some problems after head injury can be endocrine instead of neurological. I think this often gets missed.

    http://emedicine.medscape.com/article/326123-overview

     
  14. Woolie

    Woolie Senior Member

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    Only thing is, neuroinflammation is generally an acute response, not ongoing. Ongoing would be unusual. So yes, maybe in some unusual people this neuroinflammation is abnormally prolonged, and that contributes to the difficulties. But if we're able to detect microlesions involving white matter tracts longer time post concussion, then this is a simpler explanation for the PCS symptoms that requires no additional assumptions about abnormally prolonged neuroinflammation.

    It makes sense to me that not everyone will get PCS, it will depend upon the kinesthetics of the brain movement during the accident.

    Problem here is, neurons never heal. They have no regenerative capacity whatsoever. Once they're damaged, you're screwed, basically. I also don't think PCS develops a long time after the injury in most people. Its there pretty much all along.
     
  15. lansbergen

    lansbergen Senior Member

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    But the natural stemcells could fill the gap. Get rid of the damaged neurons and grow new ones. That will take a long time.
     
  16. Marco

    Marco Grrrrrrr!

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    Inappropriate prolonged 'neuroinflammation' is the problem increasingly identified in a whole range of conditions. Kinetically induced microstructural damage to white matter might explain symptoms in post-concussion syndrome. Likewise focal microstructural damage to white matter following stroke might explain post-stroke fatigue :

    http://bmcneurol.biomedcentral.com/articles/10.1186/s12883-014-0234-8

    but not similar microstructural damage to white matter found in MS and SLE patients and PWME (referred to in the same paper) or Sjogren's Syndrome http://rheumatology.oxfordjournals.org/content/49/8/1530.full and even schizophrenia (unlikely to have a history of mild traumatic brain injury) http://www.schres-journal.com/article/S0920-9964(14)00254-0/abstract
     
  17. Woolie

    Woolie Senior Member

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    Yea, I think that's pretty much my take on it. Most PCS probably due to structural damage to white matter from the accident. MS, SLE and ME more likely abnormal neuroinflammation.

    Your article about subcortical damage in stroke and fatigue is very interesting. Could turn out that those PCS cases where there's significant fatigue that subcortical damage is to blame (not all cases report fatigue). Probably not the same mechanism as for ME, but its always pleasing to see fatigue of any kind getting a proper biomedical explanation - its been so heavily psychologised in the past.

    I laughed when the article suggested psychological interventions. Yea right, that's really gonna fix it! This is pretty funny too:
    Hmm, or maybe its the other way around? Lots of subcortical disease associated with depression (e.g., Parkinson's)

    Just goes to show these cause-effect confusions are everywhere when it comes to psychological variables.
     
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