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Thread: Lower Thoracic, Conus, and Cauda Equina Injuries: Diagnosis & Treatment

  1. #61
    Diane2, I am not sure there is a "post-polio" syndrome in spinal cord injury. A number of experienced clinicians have commented to me that they believe their patients lose function as they grow older. However, I am not sure that this is the same as the post-polio syndrome which refers to a loss of recovered motor function in patients who had polio.


  2. #62
    Wow. I was totally sick of the way SCI has negatively impacted my life lately but all these posts have really tweaked my interest into figuring out where exactly the damage to my chord is. Hopefully this will be challenging as well as fun.

    Wise, the bigger question I have is how come doctors aren't sending patients home with a copy of the Asia scale score, so that the patient knows exactly is wrong with them? It appears that no one here has any clue what exactly is wrong with their own body, and I think this is completely ridiculous. Using my own case as an example, I left the hospital with a sketchy idea on how to cath and how to digi stim. This was obviously insufficient as I needed to post and read other posts here to essentially survive and attain a "high quality of life" relative to my injury. For example, some of the advice and techniques given to me by the hospital staff, such as the digi stim technique, were completely ineffective. Further, I had a terrible and confusing time trying to explain my situation to new health care professionals i would encounter and I'm sure my health and quality of life, at least in the first 12 months post sci, suffered from it. Anyway, without this place (Carecure), I seriously could not see myself participating in society to the extent that I do (I work full time, participate in sports, etc.).

    Now I understand that some patients don't want or care to know about their own issues, but they can throw their report out. I really think it should be mandatory to empower each SCI patient with this critical info so that they at least have the opportunity to take better care of themselves; and this would obviously have a positive impact on the SCI patient as well as the health care system as a whole (by relieving burdens, lowering costs, doctor's wasted time, etc.). Sorry, just had to post how strongly I feel about this topic.

    Now on to to the pen pricking!

  3. #63
    Senior Member
    Join Date
    Apr 2002
    katonah , ny, usa
    dr. young- regarding my injury- on your diagram of the spinal cord below let's just say that my sacral ( yellow ) area was infarcted. avm was just above anterior conus, giving me a vertebrel level of T12. Does this sound about right? If so, what the hell can be done to regenerate the entire sacral spinal cord. That should be relatively easy to do, due to the tiny distance nerves need to re-grow to muscles. But if it's primarily my sacral cord affected, then why can't I stand, walk, or have any bowel, bladder, sexuality? I suppose some of the venous ingestion from the dilated veins, and some vascular steal could've affected part of the Lumbar as well. When my paralysis started, it crept up, first bladder dysfunction, then weakening legs, etc. If the entire sacral region is affected, then what kind of brige could be made since there would be no living tissue beneath the injured tissue, since the cord just ends.

    sherman brayton

  4. #64
    Wise, I am no expert but as I understand it "post polio syndrome" may not be the technical term, but I am referring to a possible phenomenon where second growth nerves or spared nerves may not be as strong as the uninjured nerves and so deteriorate with the extra load over time. (Exercise, physio, BWS treadmill training and FES.) Since some of these therapies are new we do not know the long term effects. Until we get the research, I guess we rely on the clinical judgement of our therapists to know how much and what kind of treatment is optimum for strong nerve regrowth, if it can be influenced at all. I wondered if you had an opinion about all this.

  5. #65
    brayton, if you had damage to just your sacral spinal cord, your L1 through L5 spinal cord should be intact. In other words, you should have hip flexors (L2), knee extensors (L3), ankle dorsiflexion (L4), and long toe extensor (L5). If your S1 segment is intact, you should have ankle plantar flexors. You should have sensation down to your midcalf in your lower leg in the front. That is what I don't understand. You say that you can't walk but can you move your legs and knees? That is what I mean about your neurological level. You should figure out what it is and where your damage is.

    karupt411, thank you. What you posted makes me feel very good about this site and what it is doing. To tell you the truth, many doctors do not know how to do the neurological examination of the lower legs. They still rely on inaccurate dermatome charts and they are usually quite cursory about their muscle exams. Often, based in incomplete and sometimes misinformed data, they are making pronouncements to patients concerning their prognoses. For example, the diagnoses of conus and cauda equina lesions are frequently based on surmisal of symptoms and complaints instead of a detailed neurological examination. In the end, it is your body and you should be the one to educate the doctor about your body and not the other way around.

    Diane2, there are three forms of secondary loss of function after spinal cord injury with aging.
    1. The first and most common is non-use. We know that there is significant muscle atrophy even with several weeks of bedrest in normal people. What most doctors probably did not think about is that non-use may be accompanied by shutting down of neural circuits in the spinal cord as well. What do I mean by shutting down? I don't mean physical disappearance of the neurons but rather loss of excitability of the neurons. The neurons may change their shapes and are no longer receiving as many connections. When signals to do arrive at the neuron, it does not respond as quickly or as much.
    2. The second form of functional loss is degeneration of spinal cord motoneurons (the neurons that innervate the muscles). This is associated with specific changes in the denervated muscle, i.e. the muscle initially becomes hyperexcitable and then starts to undergo atrophy. This may be due to a variety of causes associated with aging. For example, there is some neuronal dropout with age. There may be some form of age-related motoneuronal disease (by the way, all motoneuronal disease is more or less age-related). There may be stroke or ischemia of the spinal cord.
    3. Post-polio syndrome refers to a loss of motoneurons years after the initial damage of the motoneuron, particularly in muscles that have recovered from the initial attack. It seems that motoneurons that have been partly damaged by the polio virus may be susceptible to over-activity. The few surviving motoneurons have to do the work of many motoneurons. Perhaps as a result of over-use of activity, some of the motoneurons may undergo degeneration. The actual mechanisms of post-polio syndrome, however, are not well understood because there is no good animal model of the condition and we don't really take apart humans undergong post-polio syndromes to find out what is going on.

    Concerning motor regrowth after spinal root damage, I had commented earlier that some motor axonal regrowth is possible after spinal root damage. Damage to the spinal root means injury to the axons that are leaving and entering the spinal cord. The axons that leave are of course motoneuronal axons. The axons that enter are sensory axons from dorsal root ganglion neurons that are situated just outside the spinal column. As we know, axons usually can regenerate in the peripheral nerve. So, for example, if you crush a peripheral nerve, one gets both motor and sensory axonal regeneration. If you crush a spinal root, you can get motor axonal regeneration but sensory axonal regeneration is much more limited. That is because the sensory axon has to re-enter the spinal cord, make synapses with neurons in the gray matter that in turn send axons to the brain (i.e. spinothalamic tract) for pain sensation, or the axons have to grow in the dorsal (posterior) columns all the way up the spinal cord to the brain for touch and propioceptive sensations to return. Therefore motor recovery may occur but sensory recovery is usually very limited after cauda equina injuries.

    Please ask and ask again if you don't understand. I am not sure what people don't know and realize that I need to learn what people are thinking about their bodies.


  6. #66
    Senior Member
    Join Date
    Apr 2002
    katonah , ny, usa
    good point dr. young- but in your humble opinion how could the sacral cord be regenerated, and how could it be with no healthy tissue to connect to, since as you know, the spinal cord ends? What I mean is with a mid thoracic sci, theoretically a bridge could be made above and below the injury site to make a scaffold for stem cells to cross over. With the sacral cord, it's like niagara falls, the stem cells would drop off the conus into oblivion.

    sherman brayton

  7. #67

    This discussion must be based on what damage you have. I am not yet convinced, although you seem to be, that you have no sacral spinal cord left. Please, before you conclude that you have no sacral cord left, at the very least determine your touch and pin sensations you have for the L1-S5 dermatomes and your L2-S1 muscle function.

    Regarding therapies, I have already posted half a dozen or more therapeutic options for restoring function to people with lower thoracic, conus, and cauda equina injuries. It is not possible to talk about therapies without specific information on what needs regeneration, replacement, or repair.

    The vision of stem cells falling off the Niagra fall is intriguing but let me give you a better analogy. Think of your sacral spinal cord as a television set, your muscles as the screen, and the knobs of the television are what your brain are turning. Say you turn on the power. What happens? Are you getting a picture at all? If you don't have a picture, you look in the back to make sure that the antenna is connected. You turn on your VCR and see if the VCR plays; if it does, you know that it is the tuner section. You look at the controls and make sure that something is lighting up, so that you know that power is getting to it. Suppose you are getting some picture but it is all fuzzy.

    Finally, after checking out everything, you open up the chassis. I am not convinced yet from what you tell me (from this or previous posts) that you will find nothing inside. If you have damage to your S2 and S3 segments, it can be partly rectified with lumbar spinal roots to peripheral nerve or root-to-root bridging. If some of your motoneurons are still intact but you are missing interneurons, neural progenitor cell transplants might be helpful. If you need motoneuronal replacement, some animal studies suggest that embryonic stem cell transplants can replace the motoneurons and either db cAMP or rho kinase blockers will encourage the motoneurons to send their axons out the ventral roots. If you need sensation, you will need regenerative therapies. By the way, your sensory neurons (dorsal root ganglia) are situated outside out spinal cord and they should not be as affected by the ischemia.

    Look, I can go on and on but none of this is meaningful unless you stop saying that you have no sacral spinal cord and figure out what your damage is and what needs to be repaired.


  8. #68
    Senior Member Kaprikorn1's Avatar
    Join Date
    Sep 2002
    S.F. Bay Area, Calif.
    Sherman...maybe when they open up your TV set, all they find is the "V-chip"!


    accept no substitutes

  9. #69
    dr young , is the neuropathic pain consistent with the detmatones? my spinal cord stim is implanted in my dura, t8 to t12 i think,
    since the coverage is not getting to my big toe, where most of my neuro pain is now, my pain management doc said he can implant another lead to a spinal root such as s1 , problem is the SCS only can take 2 leads, so i am trying to figure out what is the big toe for neuro pain? he was saying it could be s1 or l5

  10. #70
    Senior Member
    Join Date
    Nov 2003
    middle of nowhere
    Wise, a really excellent post.

    I'm a T8 (T8-T10 lesion) 3 years post possibly from a spinal cord stroke.

    You mention injuries to the vertebrae and injuries to the spinal cord.

    It is possible to have injuries to just the cord and not the vertebrae? For instance with a spinal cord stroke survivor?

    Haven't been on here for awhile....I'm still waiting for something worth trying.


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