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.

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?

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.

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.

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.

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!
Emil

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.

Emil,

I think this is a thoughtful theory, but I think my case disproves it. I only had one concussion, and I have an IQ in the 130-140 range, so according to your theory I should have had enough of a "buffer" to not notice a slight loss of some functionality.

But I had delayed onset PCS that became most pronounced about three months after my original injury! For me a complicating factor was that I also had a ruptured ear drum, and I didn't get that repaired until almost two months after my injury. My neurologist said that the brain doesn't start to heal until the physical injury has healed. Other complicating factors were that I don't think I rested enough -- I went back to teaching a week after my injury, and started training for roller derby again about two weeks after. Plus, looking back, both derby and the summer school teaching job were unusually stressful. But when I really noticed symptoms was when fall came and I went back to teaching full time. Maybe I was able to deal with part time work but then full time was too much of a cognitive load.