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Thread: What is the physiology of my injury? Need to answer before a cure

  1. #1

    What is the physiology of my injury? Need to answer before a cure

    One thing I cannot find a consistent answer to is "What is the physiology of my injury (or spinal cord injuries)?"

    There are clearly multiple answers to this question that are based on what type of damage your cord sustained. If it was severed (unlikely), compressed, partially infiltrated by bone fragments, stretched, etc. I don't see this question even explored by any studies I read, and many use the same basic animal/rodent model and contusion without exploring other alternative injury mechanics.

    OK, lets leave that aside. Let's get specific for the sake of discussion.

    I dove into a lake and hit my head on the earth beneath the water, compressing my neck and ultimately breaking the front and back of c7 vertebrae. Lets assume that vertebrae's bone fragments and the resultant force of the impact compressed my spinal cord in 3 dimensions. From there, what happened? Why doesn't the machinery still work?

    Are my axons's cell walls broken?
    Are they de-mylenated and in contact like crossed speaker wires?
    Is there a scar that interrupts the long axons in the cord?
    What happened to the axons below the scar, are they still alive longing to be met by the ones above?
    Are the upper axons still alive and trying to sprout across the scar?

    How come no one is talking about what actually happened physiologically. What problem are we even solving for? Is one rodent model enough?

    Can anyone help point me to some clues? Thankful in advance - Rio

  2. #2
    Given the scenario you describe, it is possible that your cord was 1) crushed, 2) pinched, or that the blood supply to the cord was damaged. These are the most common mechanisms.

    I am sure you know that these mechanisms are still being studied, and the actual mechanism are still not fully understood. The following is a very simplistic explanation of what happens:

    Crushing or pinching can often rupture the cell membranes of neurons, which kills them. Lack of blood supply obviously can kill tissue which depends on oxygen to live. We all are familiar with the 3-5 minutes of oxygen deprivation that can cause brain damage. In the cord, we are talking about roughly 15-20 minutes. There is a very complex cascade of biochemical changes in the cord tissue that also occurs in the first few minutes to hours after the injury. Some of these changes can actually increase the swelling (more compression) and may actually further limit the blood supply and oxygen utilization properties of the cord tissue.

    Axons that are separated from their cell nucleus will die. The upper motor neurons that control most voluntary movement have their cell nuclei in your brain, so the axons below the lesion will die. This is called Wallerian degeneration. In order for those nerves to be replaced, the motor neuron from above needs to grow across the gap or through scar tissue, and then find its way into the myelin on the other side, if it is still exists, but the myelin does eventually get replaced with scar tissue.

    Lower motor neurons (primarily peripheral nerve) have their nuclei in the gray matter of the cord, and are often damaged or killed at the level of the cord lesion, which can also result in Wallerian degeneration of the peripheral nerve. Below the level of injury, if the circulation was not disrupted in the injury, LMN continue to work, which results in reflexes and spasticity and reflexive paralysis because they are no longer connected to the brain by synapses with the upper motor neuron axon.

    Sensory (afferent) nerves have their nuclei in the dorsal root of the spinal nerve, and have an axon that goes both from the sensory ending in your skin, organs, muscles, etc. into the spinal cord and then ascends to the brain. If the cord segment is damaged, then the nerve cannot transmit sensory information past the area of damage. efferent arm. The sensory nerve within the central nervous system similarly cannot grow past the level of the cord damage, so cannot hook up to nerves on the other side of the defect.

    (KLD)

  3. #3
    Wow - great response! Thank you!

    A few more questions:
    - "the motor neuron from above needs to grow across the gap or through scar tissue, and then find its way into the myelin on the other side," does this mean there remains a myelin tube that basically guides a path to the peripheral nerve connection?
    - When the myelin turns to scar tissue, does that mean pretty much all the matter below the injury is scar tissue?
    - If yes, how would new sprouts drill through that to get to their connection points
    - its clear for me that circulation was not disrupted since all my muscles below injury are spastic right?
    - The sensory nerve sounds like it needs to grow UP across the lesion, is that right? All the way to the brain? Where? Impossible i'd think

    Thank you so much, your response made my month!!!

  4. #4
    Using the image from the link above:

    [img]http://missinglink.ucsf.edu/lm/ids_1...llerDegCNS.jpg[/img]

    And this text for the three diagrams:


    [TABLE="width: 100%"]
    [TR]
    [TD]Image #1 above: Damage occurs to spinal cord axons. The astrocytes are indicated in orange and the oligodendrocytes are the smaller black cells. Astrocytes form the "connective" tissue of of the CNS and also scar (glia), and oligodendrocytes make and maintain myelin.[/TD]
    [/TR]
    [TR]
    [TD="width: 62%"]Image #2:
    Macrophages (purple) enter to clear the debris and astrocytes begin to enlarge and proliferate. Macrophages are a type of white blood cell.
    [/TD]
    [/TR]
    [TR]
    [TD="width: 62%"]Image #3:
    A glial scar is formed blocking axonal growth.
    [/TD]
    [/TR]
    [/TABLE]

    (KLD)
    Last edited by SCI-Nurse; 05-27-2014 at 07:54 PM.

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