Traumatic Brain Injury and Post Concussion Syndrome For traumatic brain injury (TBI) and post concussion syndrome (PCS).


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Old 06-14-2010, 07:35 PM #1
t97tab t97tab is offline
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I posted here a few weeks ago regarding my 13 year old who had suffered a back injury and concurrent concussion.
I wondered if someone might be able to send me in the direction of any medical abstracts that might help me to better understand what is going on with my son. We have had several frustrating sessions with doctors.

I am particularly interested in medical abstracts related to:
1. Late onset of concussion symptoms. (We have been told that if the symptoms do not present within 72 hours, they are not concussion related.)
2. Concussion symptoms that may not be supported by neurological tests.

Thank you so much for any help you can give me
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Old 06-14-2010, 10:20 PM #2
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t97tab,

You have asked a very BIG question. The delay of symptoms from concussion is well known. I will have to do some research to find abstracts. The basic physiology is simple. The brain is mildly damaged by the concussion in a way that does not kill brain cells. Over time, the brain tries to let these cells heal as they continue to provide some function.

After a few days to even a few weeks of letting/waiting for these cells to heal, (six weeks is not unheard of) the damaged cells release a signal in tRNA (transmitting RNA) that shuts down the injured cells. This continues to happen until a clean margin is formed (clean margin means cells that have no damage). The healthy cells know how to ignore the shut down signal.

This is when the symptoms start showing up. In some cases, PCS symptoms are hidden by other causes. A head ache can cause cognitive problems. Insomnia can do the same.

The psychological community also knows that anxiety and depression can cause cognitive symptoms that are similar to concussion. These leads to many psychological professionals to claim anxiety or depression rather than concussion.

The MMPI-II (Minnesota Multiphasic Personality Inventory -2nd edition) has an over-lap. Scales 1,2,3,7 and 8 will elevate for both concussion and depression/anxiety. My own neuro-psych assessment showed this elevation but other tests showed no depression. The evaluating Ph.D. still tried to diagnose depression as the cause.

I would suggest you do some research on www.tbilaw.com Attorney Gordon Johnson addresses these problems.

A normal neurological exam is a very poor indicator of concussion for two reasons. First, the Mini Mental State Exam (MMSE) is rarely done adequately, if at all. Second, it is mainly a test of motor function. The nystagmus test is about the only indicator of concussion. Concussion may only be mildly indicated by a nystagmus test (horizontal gaze, follow the light from right to left). It takes a very precise observation to notice the nystagmus of some concussion subjects.

There is some research that says concussion will be indicated better in a standard neurological exam if the different tests were repeated enough times. The study showed that some subjects become very symptomatic after 6 to 12 repetitions of the individual tests. This is a result of mental fatigue that does not show up without repetition.

The best answer is that very few physician, even neurologists, understand the symptoms of a concussion, especially concussions that did not result in a loss of consciousness or post traumatic amnesia.

Of all the concussions I have had (13), only one caused prolonged symptoms from the start. Only one had mild confusion for a few minutes that cleared up. Then, various symptoms manifested a few days to weeks later. All of the others had delayed onset of symptoms.

The Howard Hughes Medical Institute has sponsored some lectures at University of Maryland and University of Washington School of Medicine has put on mini-medical school lectures that have been broadcast on the Research Channel. University of Wisconsin has also broadcast some mini-medical schools and CME (Continuing Medical Education) courses on their doit web site at http://www.doit.wisc.edu/streaming/researchchannel/

Here are some links for you to peruse:

http://www.ejbjs.org/cgi/content/citation/86/5/1047

http://uwmedicine.washington.edu/Sea...x?k=concussion

http://www.doaj.org/doaj?func=loadTempl&templ=about

http://cpancf.com
/NRE00151.pdf


http://www.givebackorlando.com/hepusef/hepindex.html

http://www.btflearning.org/go/ActivityFrontPage?id=58

This last one has some good information. It is worth the time to watch it, especially the diagnostic segment.

If you look back through my posts, I have probably posted about some of the other research I have found. I have so many links saved about concussion that it is hard to sort through.

Keep fighting for your daughter. As you read up on concussion, you will discover how much most neurologists do not know. Become an expert.

My best to you.
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Old 06-15-2010, 12:12 AM #3
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Quote:
Originally Posted by t97tab View Post
I am particularly interested in medical abstracts related to:
1. Late onset of concussion symptoms. (We have been told that if the symptoms do not present within 72 hours, they are not concussion related.)
2. Concussion symptoms that may not be supported by neurological tests.

Thank you so much for any help you can give me
I am so sorry that you are going through this. It makes me FURIOUS that you are having to go through this with doctors that don't get it. It brings back all of my issues with one clinic we used. I don't have articles that I can point you to, but will look (and Mark had a good list already), but I do have experience.

Yes, symptoms can present beyond the 72 hours. If one was to look at my daughter's SCAT2 forms we filled out at every appointment early on - her symptoms were significantly worse 2-3 weeks into her concussion than the day after. New symptoms also cropped up during this time. Light/Sound/balance issues were present initially - but developed. Memory issues didn't present until 4-5 weeks into the process. (Perhaps they were there, but we didn't see them because of other issues.) My daughter also developed a tremor and stutter at about 5 week.

My daughter could pass all the memory tests of the SCAT2 two (numbers, word, etc) - but then couldn't retain new things from day to day. She was not able to learn new information and couldn't remember what she did day to day. On detailed testing, issues where show. She could also pass the balance tests - but at times couldn't walk down the hall without crashing into the walls.
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Old 06-15-2010, 05:25 AM #4
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I had not seen the SCAT2 before. It is an interesting system. It has some egregious errors. It suggests return to play with contact sports as soon as 5 days after a concussion. It could be very helpful if adjusted for return to play.

The memory test is a limited version of the MMSE.

As Nancys said, remembering the words is different than many of the day to day memory needs. The delayed memory is most likely the best indicator.

Memory is a very complicated function to evaluate. The word tests only evaluate auditory memory. There is a need to include a visual memory test.

Adding some background noise and visual distractions can enhance the value of such a test. Distractability is a very common symptom of PCS.

t97tab,

Were you present during the neurological evaluation? Did the doctor do the memory tests? besides the words to repeat right away and after three minutes, there is also a test where the subject is to count backwards from 100 by 7's. 100, 93, 86, 79 ....

It is not uncommon for the memory test to not be done, even by neurologists.

You can observe your daughter to see if she has more difficulty with auditory memory or visual memory. My auditory memory is at the bottom 5% of the population and my visual memory is at the 12% level.

It is also common for neurologists to ask about the level of impact force that was endured. They mistakenly try to rule out a concussion or continuing concussion symptoms based on a belief that the impact force was not severe enough. Studies show that severity of impact does not directly relate to ongoing symptoms. If there was no Loss Of Consciousness, not post traumatic amnesia, and a low impact force, then there was not a concussion.

Dr Julian Bailes in Virginia has coined a term, sub-concussive force. This is a concussion with minor force and minor immediate symptoms but prolonged or delayed concussion symptoms. He believes many concussions go unreported due to setting high standards of immediate symptoms of a concussion.

Also, a common problem is diagnosing subjects with high intelligence. This allows them to appear to be high functioning even though they have serious cognitive dysfunctions. Studies show that a big differential between tested intelligence and memory functions indicates an organic problem (physical trauma). A psychological problem will usually effect both the memory and intelligence scores at a somewhat equal level.

Be patient. You need to look for a better doctor to help with diagnosis. A neuro-psychological assessment may be a good indicator if you can find a neuro-psychologist who has good skills with concussion.

My best to you as you struggle with her diagnosis.
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Old 06-15-2010, 07:51 AM #5
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Quote:
Originally Posted by Mark in Idaho View Post
t97tab,

After a few days to even a few weeks of letting/waiting for these cells to heal, (six weeks is not unheard of) the damaged cells release a signal in tRNA (transmitting RNA) that shuts down the injured cells. This continues to happen until a clean margin is formed (clean margin means cells that have no damage). The healthy cells know how to ignore the shut down signal.

This is when the symptoms start showing up.
Hi Mark! You provid great info to people in need, but you really have to explain this to me. Do you mean that damaged cells release tRNA (transport RNA, not "transmitting RNA") and that this makes injured cells nearby "deactivated"? Im just a medical student right now but I dont get what you mean.

Is it possible what you mean is that when a cell gets injured, it or its leaked content causes an inflammatory process (which can be activated by almost anything that shouldnt be in the extra cellular environment as tRNA, ATP and so forth) which causes the neuroglia to phagocytize and remove damaged neurons that still are functional and that this is the cause for the delayed onset of symtoms?
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Old 06-15-2010, 11:50 AM #6
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rydellen,

I think you have said it better than my damaged brain can remember it. Either way you say it, the same thing happens when the damaged cells self-destruct/deactivate.

Some researchers do not mention the tRNA system but do relate a similar self-destruct process.

The brain absorbs the shut down brain cells so quickly that it is difficult to image them. They can observe this behavior en vitro as the cells try to re-establish axonal connections where the damaged brain cells leave gaps.
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Old 06-16-2010, 11:20 AM #7
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Yeah..hmmm...I'm certainly not a medical student. However, my daughter recently visited an eye doc and started vision therapy. He described this process as follows:

Some cells die when you are injured and create a "toxic waste dump" where other cells fear to tread. You end up with gaps, like gaps between malfunctioning spark plugs. Therapies and time will allow the working transmitters to find new ways around the toxic waste dumps. Until then you experience deficits in certain brain functions.
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Old 06-16-2010, 02:20 PM #8
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PCSLearner,

This toxic waste dump concept addresses the dead brain cells. The question here is about delayed onset of symptoms. That toxic waste dump releases the tRNA that causes damaged, not dead, brain cells to shut down. This shut down of damaged brain cells can take place weeks later, thus causing delayed symptoms that manifests when these damaged brain cells shut down.

What the eye doctor was addressing is the way the brain will attempt to rewire around the dead or shut down brain cells. The healthy brain cells have lost their connection to other cells because they are dead.

They send out axons and dendrites that sort of probe for new connections. Their attempts to connect must be accepted by the dendrite contacted. If not, the axon will shrink back and try a different direction. This happens thousands of time as the new connections around the dead cells are built.

Therapy pushes this rewiring effort by causing blood flow to the area to increase supporting more of this rewiring effort. The blood flow must be re-established first, then the new axonal connections.

Researchers have been able to observe this with high power microscopes and rat brain tissue en vitro.
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Old 06-16-2010, 04:45 PM #9
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I think the inflammation + changed cellsignalling, due to dead cells in the close proximity to functional (parhaps not 100% functional) ones can lead to celldeath (apoptos) in the latter. This might be an explanation for the delayed onset of symtoms, yes.
The "cleanup" takes some time and might even clean some functional cells away. Possibly. At the same time I think the outcome would be even worse without a full scale cleanup by the glial cells in the brain. My first thought that came to mind, of immunosupression after an injury might not be a good idea..but who knows...

You could speculate that more rest after the incident could have made symtoms and deficits less severe. But if there is celldeath after the incident normally, maybe it is something you have to see as a part of the injury.

What MIGHT be the case in the first noticable symtoms of the delayed character is this (my personal and collected experience) :

Normally you have a buffert in the brains capacity. Lets say you have 110% capacity.

You have a first concussion and notice NO noticable deficits after the acute phase. What might have happened behind the scenes is that you have lost some cells or/and function in the cells. Your buffert is now used up and you are at lets say 100% capacity.

The next injury you have (or delayed celldeath because of the immuno-response (?)) might set you to 90% capacity and since you´re now under 100% you start noticing deficits!

Since concussions and braininjury in general seem to be cumulative its not hard to understand that the second and later injuries on top of another seem to be more severe, even if they caused the equal amout of damage.


You could (like everyone here in some stage of their recovery) sit and think about what happened. In some cases you can draw some valuble information out of it, but mostly it just takes energy from what you should be doing. And that is looking forward. THink about what you can do for the injured person from now on and be smart. Avoid things that aggrevates the symtoms and think about how you can make the new situation as good as possible for you and the injured person.

Best wishes from Sweden!
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Old 06-16-2010, 05:03 PM #10
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rydellen has it right. My neurologist, after seeing my brain functions on a qEEG, AEP and VEP and understanding my past history of concussions and partial recovery, believes that I had finally hit that point of damaging the critical mass of brain cells needed to continue full function.

In the past, I would have symptoms of cognitive struggles that would recover except for times of stress. Now, my brain performs like it did just after the previous concussions or during previous times of stress

My brain is now 24/7 in a state of dysfunction with even worse dysfunction during times of stress/overload.

One of the things that may be a part of the delayed symptoms is the brains tendency to share work load. If function A has lost 50 % of its functional ability, can it draw from an area of the brain that supports function B? If function B was at 90 % functional capacity, it may drop to a 70% functional level to allow function A to utilize some of the functional capacity and recover to ... maybe 65% functional capacity.

This happens when a function is not longer needed. When someone goes blind or has their eyesight temporarily blocked, the brain cells that support eye sight can be used by other sensory systems. The might allow hearing to become very acute by using unused vision processing cells to increase the auditory processing function. The fMRI studies and such have shown this sharing of brain cells can take place rather quickly, within 12 to 24 hours or less.

It would appear to make sense that the brain would share good cells with areas that lost cells to concussion damage. This sorting out of brain cell function could easily be part of the delayed symptoms. It could explain why some concussion subjects appear to, over time, recover in some functions but degrade in other functions. An intense imaging study of this would be very interesting.
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