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Thread: Good News on the Horizon

  1. #91
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    Ian, Edit; sorry I wrote some here now. Edit due to thath, but like above, axons can be and are loooong if compared to things we know. I am also very pleased to here about the progress of your daughter. The best.
    Last edited by Leif; 09-13-2006 at 09:42 PM.

  2. #92
    Same here, Ian, congrats! In accordance with what I posted earlier, I think it would do the SCI world a deal of good if as far as clinical trials went, simpler therapies which show some promise were implemented first, ie: remyelination. Apply this to some incomplete injuries, which would hopefully bring some positive results in our favor. With some sort of progress on our side, the project as a whole (and I don't mean the Miami Project) would just seem so much more feasible and this would bring in so much more financial support. I hate to dumb this up, but I can't help but feel that our community sometimes is viewed as James "Buster" Douglas going in to fight Mike Tyson in Japan. Douglas was a 42:1 underdog going in to that fight. Our odds in the eyes of the rest of the world are just as gloomy. As soon as that famous upper-cut landed, all of those odds, all of the hype and persona of "Iron" Mike being untouchable went out the door, much in the same way that we now know the Spinal Cord has potential to heal given the right key to unlock the door. I just wish the rest of the world would be behind us so we can follow through with the rest of this "knockout combination". I hate to say this, but maybe the approach to a solid therapy should be in smaller pieces, ie, remyelination. If we can come up with something, some sort of result to show for all of this hype, I think we have a better chance of getting the world to hop into our corner.

    PS: No offense to any Tyson fans out there.
    PPS: I don't even know if we have any way of remyelinating the axons, so my post might not hold any water, this was just on my mind and I wanted to throw it out there.
    No one ever became unsuccessful by helping others out

  3. #93
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    Quote Originally Posted by Tufelhunden
    PPS: I don't even know if we have any way of remyelinating the axons, so my post might not hold any water, this was just on my mind and I wanted to throw it out there.
    For chronic injuries myelin in itselfe might not be a good thing to hope for other than for an important factor to restore damaged “insulation” on axons, but myelin is just some fatty stuff (fat) and as for chronics as I see it, it can also block pathways for looong axons (nerve fibre) growth. Good and bad.

    PS. and remyelinating of axons has been done and is the goal for the Geron trial for acutes. Good stuff. The trick is to control this in chronics among a bunch of other factors.

    And no offence to M Tyson from this corner either; he was one of the best.
    Last edited by Leif; 09-13-2006 at 11:19 PM.

  4. #94
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    I think Dr Young has posted before that a cure will be different for different people. Some will require remyelination only, some neuron regeneration and some a combination of both. The difficulty lies in working out for the individual what will give the greatest degree of success, IMO the complete/incomplete diagnosis is not an accurate indicator for the individual as it is based on an arbitrary indicator of whether or not rectal sensation is present.

  5. #95
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    But Ian, in chronic SCI which could be a big as a hinder as the famous scare tissue will be the long gone dead axon pathways for some axons. How to get them back? I guess this will be one thing in common for all chronics. This is also why the Johns Hopkins Douglas Kerr study is so promising although in rodents so far because it deals with this problem. Another thing which was also promising with the Kerr study was that it was done on rats I believe up to six months after and also on grown up animals. Also, a rat year is not the same as a human year, but still for an axon to grow in a human so far a distance is a challenge as I understand. Some researchers compare the nature of neurons in the cord linked to other neurons by axons like the distance between electrons and the core in a hydrogen atom. It is small in distance as such but in the details the distance is huge (and this is just betwen i.e neurons in the grey mater). Just as for the time being though… Basic research is paving the way.
    Last edited by Leif; 09-14-2006 at 12:02 AM.

  6. #96
    Quote Originally Posted by Leif
    But Ian, in chronic SCI which could be a big as a hinder as the famous scare tissue will be the long gone dead axon pathways for some axons. How to get them back? I guess this will be one thing in common for all chronics.
    Lief,

    I was actually thinking of our posts this morning and I have to say that I think I disagree with you for the first time, buddy. Correct me if I am wrong, but I am sure others can chime in and testify with regards to this. I think that some of us can be placed in a bed and rolled up to a door by the DEA to kick it down during a drug raid because of our spasticity. When I say some of us, I mean upper thoracics, and most quads, basically anyone who has their lower motor neurology intact. If we are highly spastic, this means that our lower appendage axons must still be intact (not atrophied; however the pathway is undoubtedly interrupted) even though for the time being are dysfunctional. So I believe someone who doesn't have flaccid leg muscles (such as a high thoracic lesion) can benefit from a therapy which doesn't include a complete reconstruction of the lower neurology. There just has to be an easier way. Some of us have lower cords which are just as alive today as the day we ate shit. A therapy should be implemented which can utilize this. I believe it would be easier to use what we still got intact. On the other hand, there might not be a way of connecting something so small and intricate and it just actually might be easier to sprout a whole new set of axons out and let them grow, but this would no doubt take a while. So maybe it depends on our ability to reconnect axons. If there is a way, I am sure it would be easier to cross the lesion. If there is no feasible way, then we will just have to regrow these new axons. If we do, then what happens to our dysfunctional lower spinal cords? Would it be removed? Will my anatomy change to where my spinal cord just goes from C1-T4 and then becomes some sort of cauda equina conglomerate in the rest of my canal? No doubt we would have to have our lower cords removed, because of the spasticity interruption of functional motor movements. This just leaves a bunch of unanswered questions in my head. Let me know what type of ideas you guys got...
    No one ever became unsuccessful by helping others out

  7. #97
    rebuttal?

    f
    ight

  8. #98
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    Tufelhunden,

    First, thanks for the discussion - Yes I know that the lower neurology can be intact as such but say for a T4 injury like mine it is not just the local problem to the injury site which is the problem as I understand it. Some Descending and ascending axons in pathways in the white mater will die back, and that can be quite a distance too. In the Douglas Kerr study one goal was to have axons to grow back in those tracts.

    I found this quote from Dr. Wise where he talks al little about the dying of axons.


    Wise Young
    02-14-2004, 04:50 AM
    lyena,

    Neurons situated in the brain send axons down to the spinal cord. Neurons situated in the spinal cord send axons up the spinal cord to the brain.

    The term that your doctor used, i.e. "dieback", is not strictly correct. The axons (nerve fibers) that have been separated from their neurons by the injury die. Since about half of the axons in the spinal cord are going up and half of them are going down, you would expect loss of those axons. This is not dieback per se.

    Dieback refers to the dying back of axons that are still connected to the neurons. There is indeed some dieback, generally for a couple of centimeters from the injury site, usually back to the first branch point of the axon. However, in general, over time, those axons will often sprout back to the injury edge.

    Let me give an example to make sure that you understand. A neuron in your brain sends an axon down through the T11 injury site. The part of the axon below T11 will die (because it has been separated from the neuron). The part of axon that is close to the injury site will dieback a few centimeters and then tend to grow back towards the injury edge.

    In the opposite direction, a sensory neuron in your spinal cord below the injury site or in the dorsal root sensory ganglion just outside of your spinal cord will send axons to the brain. Your injury damaged those axons. The part of the axon in the spinal cord above the injury and separated from the neurons below the injury site will die.

    The process of regeneration is to get the axons to grow back across the injury site and all the way back to their original connection points. This is of course the goal of many of the therapies.

    Please keep asking if the above is confusing.

    Wise.

    http://sci.rutgers.edu/forum/archive...p/t-37351.html

  9. #99

    nice!

    That's such great news! I haven't been on this site in months because I was getting discouraged, and now I have more of a reason to work hard at therapy.

    How do you know -big- things will happen? Was it an off-the-record tip by some researchers?

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