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Thread: What Can Be Done?

  1. #11
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    Quadvet

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  2. #12
    Super Moderator Sue Pendleton's Avatar
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    I have a slight tilt because the spinal infarct started on the right side and seems to have damaged the cord where the artery entered on that side most. So I have stronger left back muscles than right and every so often it's enough to pull out the oxycodone. It's just two vertabrae being twisted so not much seat adjusting would work. I know. When summer hits it is back to PT.
    Courage doesn't always roar. Sometimes courage is the quiet voice at the end of the day saying, "I will try again tomorrow."

    Disclaimer: Answers, suggestions, and/or comments do not constitute medical advice expressed or implied and are based solely on my experiences as a SCI patient. Please consult your attending physician for medical advise and treatment. In the event of a medical emergency please call 911.

  3. #13
    Quote Originally Posted by Wise Young
    Redneck,

    At the present, I don't think that there are any therapies directed restoring function after spinal cord ischemia being tested in clinical trials. Almost all the studies in animals have been from the perspective of preventing ischemic rather than restoring function. One of the difficulties of restoring function in ischemic cords is the variety, distribution, and type of tissue damage. There are a lot of therapeutic targets.

    Based on what I have seen in animal studies, ischemic lesions in rats produce damage to the gray matter (excitatory sensory neurons, inhibitory interneurons, and motoneurons), small unmyelinated axons, and oligodendroglia (the cells that myelinate axons). Each of these may require a different therapeutic approach.

    To restore gray matter which contain both neurons and astrocytes, one would probably need stem cells that could make new neurons. However, to make functional motoneurons, the stem cells not only have to make motoneurons but the motoneurons must be persuaded to grow their axons out of the spinal cord to connect to muscles and existing axons from neurons in the brain and spinal cord must be persuaded to connect to the new motoneuron. Amazingly, this was successfully done by Doug Kerr an dhis colleages at Johns Hopkins University, where they used human embryonic stem cells to treat mice with virus-induced motoneuronal loss. When they combined the stem cell therapies with regenerative drugs, they found that they could create neurons that send their axons out of the spinal cord to contact muscle.

    Loss of oligodendroglia will produce demyelination. There are many ways to remyelinate axons, including transplanting oligodendroglial precursor cells that can be obtained from human embryonic stem cells or fetal stem cells. Both Schwann cells and olfactory ensheathing glial also remyelinated axons in the spinal cord. You might think of trying 4-aminopyridine, which is available from compounding pharmacies and improve conduction in demyelinated axons. If you respond to 4-aminopyridine, you may respond to remyelinative therapies.

    Loss of small unmyelinated axons. These axons are more sensitve to ischemia. However, they are also the most likely to regrow on their own.

    Wise.
    Can 4-ap be used on incomplete spinal cord injuries?

  4. #14
    Super Moderator Sue Pendleton's Avatar
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    Quote Originally Posted by Z~LEI
    Can 4-ap be used on incomplete spinal cord injuries?
    It only appears to work on incomplete SCI and MS. You can search the forums using the Google space up above for dose ideas, etc.
    Courage doesn't always roar. Sometimes courage is the quiet voice at the end of the day saying, "I will try again tomorrow."

    Disclaimer: Answers, suggestions, and/or comments do not constitute medical advice expressed or implied and are based solely on my experiences as a SCI patient. Please consult your attending physician for medical advise and treatment. In the event of a medical emergency please call 911.

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