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Impaired eye movements - quicker diagnosis of concussion

Marco

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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

The PCS group performed worse on anti-saccades, self-paced saccades, memory-guided sequences and smooth pursuit, suggesting problems in response inhibition, short-term spatial memory, motor-sequence programming, visuospatial processing and visual attention. This poorer oculomotor performance included several measures beyond conscious control, indicating that subcortical functionality in the PCS group was poorer than expected after mCHI. The PCS group had poorer neuropsychological function (memory, complex attention and executive function).

(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.

Patients showed relatively intact ability to accurately fixate the target (prosaccades), but were impaired when required to focus accurately in a specific position opposite the target (antisaccades). Patients were most markedly impaired when required to direct their gaze as closely as possible to a smoothly moving target (smooth pursuit).

(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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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.
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?
 

Marco

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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'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 :

All patients with postconcussion syndrome (PCS) reported increased symptoms or the appearance of additional symptoms from baseline that led to exercise cessation.

The definition of PCS given by the World Health Organization10 includes a history of traumatic brain injury and 3 or more symptoms (headache; dizziness; fatigue; irritability; insomnia; difficulty in concentration or memory; intolerance of stress, emotion, or alcohol).10 No cognitive testing, exclusion of other disorders, or symptom threshold exists for the diagnosis of PCS.

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.


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?

Indeed!
 
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source : Exercise Intolerance in Individuals With Postconcussion Syndrome
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784364/
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).
 
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Marco

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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).

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.
 

chipmunk1

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Impaired eye movements in post-concussion syndrome indicate suboptimal brain function beyond the influence of depression, malingering or intellectual ability
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.
 
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chipmunk1

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765
http://www.tara.tcd.ie/bitstream/handle/2262/51408/PEER_stage2_10.1136%2Fjnnp.2008.171298.pdf

Diathesis-stressor models have been proposed to combine both “organic”
and “psychogenic” factors for the development of PCS.45 46 26 They typically have at their
centre the idea proposed by Lishman 47 that early physiogenic mechanisms may be
responsible for early PCS symptoms, but “vicious cycles” that emphasise non-organic,
psychological factors may be responsible for their persistence over time. For example, King48
outlines a number of potential “windows of vulnerability”, from early worries about symptom
longevity and dissonance between injury severity and early symptoms.

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

Implications for Psychosocial Treatment

Whilst MTBI may set the conditions for PCS to occur, there does appear to be a role for psychological mechanisms in persistence of symptoms - which provides potential avenues for treatment. The majority of the current literature on treatment of persistent PCS primarily focuses on the benefits of early interventions (typically in the first week to month post-injury) that focus on prophylactic prevention of persistent symptoms.101 Such interventions typically provide individuals with information about PCS as a common but transient phenomenon after MTBI. A meta-analysis of five studies up to 1997 102 found a modest, positive effect size average of 0.32 in terms of reduction of persistent PCS, and similar results have been replicated subsequently.103 104

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..
 
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lansbergen

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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.

As always confuse cause with effect.
 

chipmunk1

Senior Member
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765
Psychological Reaction: It is well established that there are elevated rates of psychiatric co-morbidity in PCS groups.79 This may represent a response to persisting effects of brain injury on cognition and associated limitations in functioning. However, the role of Post-Traumatic Stress Disorder (PTSD) – in context of other mood issues, particularly depression - has emerged as a critical issue in explaining PCS. It had been thought that TBI and PTSD were incompatible: without a memory of the event, the survivor of trauma might not have source material for intrusive thoughts to drive avoidance behaviour (see 80). However, a number of potential mechanisms have been identified for PTSD post- TBI – such as islands of memory, confabulated memory, external causal attributions and fear conditioning (81 82

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."
 
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Marco

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@chipmunk1

Thankfully not everyone swallows that claptrap :

A new paradigm for understanding incapacitating post-concussion syndrome

The authors’ analysis of the peer-reviewed literature revealed strong evidence that one of the underlying mechanisms for post-concussion symptoms, as well as similar symptoms found in patients without a history of head injury – such as patients with infections or PTSD - is a systemic inflammatory and immune response producing neuroinflammation. The authors suggest that a better term to describe this pattern of symptoms is “post-inflammatory brain syndrome” or PIBS.

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

Marco

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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?
 

chipmunk1

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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

In the United States, the annual incidence of traumatic brain injury (TBI) is 1.5-2 million people.[18]Of that population, 70,000-90,000 persons sustain a chronic, significant disabling condition. A retrospective study demonstrated that 4% of patients with TBI sustained an associated neuroendocrine disorder of the hypothalamic-pituitary axis. This condition is underdiagnosed,[19, 20]as demonstrated by evidence that 40-63% of fatal cases of TBI reveal postmortem pathologic findings of the hypothalamus/anterior pituitary.
 
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Fair enough but I don't see why that would rule out neuroinflammation as neuroinflammation is the appropriate response to tissue damage?
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.

Marco said:
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?
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.
 

lansbergen

Senior Member
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2,512
Problem here is, neurons never heal. They have no regenerative capacity whatsoever. Once they're damaged, you're screwed, basically.

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

Marco

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Only thing is, neuroinflammation is generally an acute response, not ongoing. Ongoing would be unusual.

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

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
 
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nappropriate 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

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:
"Depressive symptoms also predicted PSF at follow up"
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.