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    Lower Motor Neuron Lesion Cures

    Dr. Young,
    I was injured on Dec 8th 2007 in a motocross accident. I suffered a Spinal Cord injury at the T10/T11 vertebrae. My cord was compressed and 50% compromised as stated by my surgeon. My surgery was just to repair my spine and not fix the cord. The surgeon stabilized my spine by fusing me from T-9 through L-3. During my rehab I did not show any spasms and the doctor classified me as having a lower motor neuron lesion (flaccid paralysis). I have looked for clinical trials for my level of injury but NO one is holding trials for anything below a T-10 vertebral break. I have been told that the anatomy of the cord differs greatly below the T-10 level causing cell implantation treatments to be more complex. From my understanding all the trials will be for central nervous system SCI injuries (above T-10) first and then they will try to tackle the multiple complexities of the lower motor neuron lesion. Could you please explain how the anatomy of a lower thoracic break differs from the normal cord (T-10 and above?) and the obstacles scientist have to face in order to provide a cure for a lower motor neuron lesion?
    THANK YOU
    Brent
    Last edited by Brent A; 3 Aug 2010, 11:36 PM.

    #2
    Hey, Brent. Let me start by describing the anatomy of the spinal cord. If I have time, I will create some illustrations.

    The vertebral column. As everybody knows, the spinal cord lives in the spinal canal of the spinal column. The spinal column has 7 cervical (neck) segments, 12 thoracic (chest where the ribs are located) segments, 5 lumbar (lower back) segments, and 5 sacral (tail segments). The bony segments are called vertebraes. The spinal cord itself is segmented, having spinal roots that come out of the spinal cord and exit the spinal canal between the vertebraes, through openings called vertebral foramina. Each vertebra has essential three areas that it rests on vertebra below it and provides for the vertebra above to sit on: the left and right facets in the back and the vertebral body. A disc sits between the vertebral bodies and provide a cushion.

    The spinal cord. The spinal cord is an extension of the brain into the spinal canal. Connecting to the brainstem at the top, the spinal cord is covered by three membranes. The first is the dura, a hard and tough membrane called dura mater (which means "tough mother"). The second is a thin filmy transparent arachnoid membrane, located just below the dura. The third is the pial membrane (pia mater) which is on the surface of the spinal cord. Cerebrospinal fluid (CSF) is located in the space between the arachnoid and the pia mater.

    The spinal roots. At intervals that partly correspond to the vertebral segments, the spinal cord has spinal roots that go to openings between the vertebral bodies and exit the spinal column and become peripheral nerves. Just before they enter the spinal cord, the spinal roots divide into the dorsal (posterior) and ventral (anterior) roots that respectively hold sensory and motor axons (nerve fibers). The C1 root comes out between the head and C1 vertebra, the C2 between C1 and C2, etc. The C8 roots come out between C7 vertebra and T1. There is no C8 vertebral body. Thereafter, the roots come out below the vertebral body they were named after. For example, the T1 roots comes out from between T1 and T2 vertebral bodies, T10 exits between T10 and T11, T12 exits between T12 and S1, L1 exits between L1 and L2, S1 exits between S1 and S2.

    The cauda equina. The spinal cord ends at L1. From L1 to S5, there are only spinal roots in the spinal canal. These roots look like a horse's tail and therefore they are called the cauda equina (tail of a horse). The tip of the spinal cord is called the conus and it is located right at top of L2. Note that the spinal cord of some people go into L2. Some people (about 5%) have a 13th thoracic rib (T13). So, when one has an injury of L2 or lower, the injury is not to the spinal cord but to the spinal roots. An injury to L1 damages the conus. The L1 through L5 cord are situated between T11 and T12.

    Cervical and lumbar enlargement. The cervical and lumbosacral spinal cord segments are wider than the rest of the spinal cord because they contain the neurons that control the upper limbs and the lower limbs plus pelvic organs. Sometimes called the cervical and lumbar enlargements, these parts of the spinal cord hold most of the neurons. Injuries to these parts of the spinal cord damage the neurons. Damage to the neurons, particularly the motoneurons that innervate the muscles, has long been considered to be irreversible because no new neurons are supposed to be made after birth in large mammals.

    Long spinal tracts. These are bundles of nerve fibers (axons) that connect the brain to the neurons in the spinal cord (motor) and that bring information from the peripheral and the spinal cord to the brain (sensory). Motor spinal tracts include corticospinal, rubrospinal, cerebellospinal, vestibulospinal, reticulospinal, and propriospinal tracts. Sensory spinal tracts include the dorsal (posterior) column which carries propioceptive information (position-specific information such as touch, muscle spindles, tendon stretch, etc) while the spinothalamic tract carries pain and other sensation. In addition, there are tracts that carry information to the vestibular, cerebellum,and other specialized motor systems.

    Regeneration of spinal tracts. Most therapies of spinal cord injury attempt to preserve or restore long spinal tracts. For most of human history, the spinal cord was thought to be incapable of regeneration and therefore people with spinal cord injury were usually left to die. However, in the last 20 years, many animal experiments have shown that spinal axons can regrow if a hospitable path is provided for their growth across the injury site, sustained growth factor support is provided, and growth inhibitors such as Nogo and CSPG are blocked. Because cells provide growth factors, cell transplantation is a frequent treatment that is tested in clinical trials. At ChinaSCINet, we are transplanting umbilical cord blood mononuclear cells (UCBMC) that fill and forms a bridge across the injury site. We give lithium to stimulate the cells to produce growth factors.

    Spasticity versus flaccidity. Injury to the cervical (C2-T1) or thoracic spinal cord (T2-T10) usually produce spasticity. This is a situation where the neurons of the lumbosacral spinal cord are intact but disconnected from the brain and spinal cord above the injury site. Because much of the descending axons are inhibitory and also because there is sprouting of local nerve fibers to re-innervate neurons that have lost their connections, a condition called spasticity results. This condition is associated with increased activity and excitability of the legs, exaggerated reflexes, and even rigidity of the legs. However, if there has been injury to the lumbosacral spinal cord located at T11 to L1 vertebral segments, flaccidity often results. The muscles have little tone or reflexes. Flaccidity indicates a loss of excitability of the lumbosacral cord.

    Flaccidity does not mean loss of neurons and motoneurons. The presence of flaccid muscles does not necessarily mean that all neurons or motoneurons are gone from the spinal cord innervating the flaccid muscles. Flaccidity may result from damage to the spinal roots, which would essentially disconnect the motoneurons from the muscles. Note that the spinal roots for L1 through L5 all course down the side of the spinal cord at T11 to L1. Damage to the spinal canal from T11 to L1 may damage the spinal roots. Flaccidity may also result from damage to sufficient neurons that the spinal cord is not as excitable. Finally, flaccidity may result from too much baclofen (anti-spasticity drug).

    Assessment of Flaccidity. The first step is to do careful neurological and neurophysiological examination of the person to find out what has been damaged. For example, a person may lack reflexes but still has muscle tone, which would indicate that that the motoneurons are still intact. Very few injuries damage the entire the spinal cord. The level of injury has to be ascertained, i.e. whether it is at T10, 11, 12, L1, 2, 3, 4, 5, and S1, 2, 3, 4, or 5. These can be partly assessed through the sensory dermatomes, which may persist even though therefore little or no motor activity. Neurophysiological tests can be done to differentiate between root and spinal cord damage.

    Treatment of flaccidity. The most common cause of flaccidity is damage to the spinal roots. While there is currently no therapy for regenerating spinal roots, many laboratories are beginning to studying therapies that may regenerate motor and sensory axons in the roots. The solution is not very different from regenerating the spinal cord and may be easier. If the cause of flaccidity is due to partial loss of neurons or loss of excitability of the lumbar cord, perhaps the addition of neurons with certain neurotransmitters (such as serotonin) can restore excitability. If the cause of the flaccidity is due to neuronal and particularly motoneuronal damage, neuronal replacement may be necessary.

    Neuronal replacement. Many investigators have successfully transplanted neurons into the spinal cord, including neurons that express a variety of neurotransmitters and even motoneurons. Doug Kerr, for example, was able to regrow motoneurons in the spinal cord of rats that had been infected with a motoneuronal virus. He did this by transplanted motoneuronal precursor cells derived from embryonic stem cells. Recent work by Marius Wernig at Stanford has shown that expressing four genes in skin cells can convert the cells into motoneurons. This will provide a source of motoneurons for transplantation. This is very exciting and I believe that it will soon lead to clinical trials of motoneuronal replacement.

    Please ask questions and I would be glad to try to answer.

    Wise.

    Comment


      #3
      "T12 exits between T12 and S1"
      Dr.Wise,excuse me,may be L1,not S1.

      Comment


        #4
        Originally posted by kivi66 View Post
        "T12 exits between T12 and S1"
        Dr.Wise,excuse me,may be L1,not S1.
        kivi66, yes. You are correct. I was typing rather quickly. My statement is true but L1 is more meaningful than S1. Wise.

        Comment


          #5
          "Treatment of flaccidity. The most common cause of flaccidity is damage to the spinal roots. While there is currently no therapy for regenerating spinal roots, many laboratories are beginning to studying therapies that may regenerate motor and sensory axons in the roots. The solution is not very different from regenerating the spinal cord and may be easier."

          Dr.Wise, what do you mean saying "easier"?

          Comment


            #6
            Originally posted by kivi66 View Post
            "Treatment of flaccidity. The most common cause of flaccidity is damage to the spinal roots. While there is currently no therapy for regenerating spinal roots, many laboratories are beginning to studying therapies that may regenerate motor and sensory axons in the roots. The solution is not very different from regenerating the spinal cord and may be easier."

            Dr.Wise, what do you mean saying "easier"?
            Spinal roots are peripheral nerves and we know that peripheral nerves support axonal growth. The problem is at the interface between the peripheral and central nervous system (PNS/CNS) interface. One this barrier is overcome, regeneration to and from the CNS should be easier to encourage that in the central nervous system.

            Wise.

            Comment


              #7
              Dr. Wise,
              Please, what cen you tell me About what kind of damage GSW gives to the cord, but the bullet does not touch the cord, only the vertebral column at T4,T5. What kind of damage get the cord from this tremendous impact from the bullet to the vertebral column, I can imagine, but I like you to explaint to me please.
              Is it axons, motor neurons etc, and how difficult are these injuries to regenerate

              Thank you so much in advance
              Last edited by Johnnie Walked; 11 Aug 2010, 8:40 PM.
              keep (rolling) Walking

              Please join me and donate a dollar a day at http://justadollarplease.org and copy and paste this message to the bottom of your signature

              Comment


                #8
                Waiting ur reply Dr Young
                keep (rolling) Walking

                Please join me and donate a dollar a day at http://justadollarplease.org and copy and paste this message to the bottom of your signature

                Comment


                  #9
                  Originally posted by Johnnie Walker View Post
                  Dr. Wise,
                  Please, what cen you tell me About what kind of damage GSW gives to the cord, but the bullet does not touch the cord, only the vertebral column at T4,T5. What kind of damage get the cord from this tremendous impact from the bullet to the vertebral column, I can imagine, but I like you to explaint to me please.
                  Is it axons, motor neurons etc, and how difficult are these injuries to regenerate

                  Thank you so much in advance
                  Dr. Young

                  Will you please give me Answer to my question

                  thank you in advance
                  keep (rolling) Walking

                  Please join me and donate a dollar a day at http://justadollarplease.org and copy and paste this message to the bottom of your signature

                  Comment


                    #10
                    Anything going on at the moment when it comes to those with lower injuries? I'm coming up to my 5 year anniversary and it seems very little progress has been made in that time period.

                    Comment


                      #11
                      No hope yet for few years. Also not much successful research in progress regarding lumbosacral injuries.

                      Comment


                        #12
                        Originally posted by scisucks View Post
                        Anything going on at the moment when it comes to those with lower injuries? I'm coming up to my 5 year anniversary and it seems very little progress has been made in that time period.
                        We are working on it and will figure it out, hang in there.

                        Comment


                          #13
                          Originally posted by scisucks View Post
                          Anything going on at the moment when it comes to those with lower injuries? I'm coming up to my 5 year anniversary and it seems very little progress has been made in that time period.
                          For what it's worth, I'm watching the Chen lab at Penn State for LMN. So far, the vast majority has been in ALS and brain lab work, but I believe they are getting closer. Here is link to a page where they are working on SCI. Lab LINK. Here's an abstract from SfN 2016 that I planned to put up later on the report and this article was given to me a couple days ago. I hope this helps. I believe I had another abstract ready for the lineup but I'll have to dig a bit for that one. (That abstract still had an affiliate author to Penn State).
                          Last edited by GRAMMY; 12 Dec 2016, 5:15 PM.
                          http://spinalcordresearchandadvocacy.wordpress.com/

                          Comment


                            #14
                            Originally posted by Jim View Post
                            We are working on it and will figure it out, hang in there.
                            Do you have any details on this at all? There hasn't been a shred of information/evidence about this so-called LMN strategy from Rutgers or Wise at any point in time - EVER! So Jim, tell us where the lab is with this please seen as you feel ballsy enough to say you will "figure it out"!
                            Last edited by Fly_Pelican_Fly; 12 Dec 2016, 8:35 AM.

                            Comment


                              #15
                              Originally posted by Jim View Post
                              We are working on it and will figure it out, hang in there.
                              Thanks for the response Jim and I hope you are correct.

                              Up until a couple of years ago I used to get really frustrated and angry at long term paras and quads who would talk down a potential cure - I thought to myself "why are you guys so negative" but now I understand their POV and whilst I'm still hopeful of a cure in the next 10-20 years I won't be holding my breath.

                              Anyway, on a more positive note merry xmas everyone for when it arrives.

                              Comment

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