Page 8 of 12 FirstFirst 123456789101112 LastLast
Results 71 to 80 of 112

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

  1. #71
    Walk, yes, many people have spinal cord injury without bony damage. Ischemic damage to the spinal cord, transverse myelitis, hemorrhage, arachnoiditis (inflammation), degeneration of spinal tracts and motoneurons, and viral or bacterial infection of the spinal cord are but a few of the ways in which spinal cord injury can happen without trauma to the spinal column. Wise.

  2. #72
    Originally posted by Wise Young:

    Walk, yes, many people have spinal cord injury without bony damage. Ischemic damage to the spinal cord, transverse myelitis, hemorrhage, arachnoiditis (inflammation), degeneration of spinal tracts and motoneurons, and viral or bacterial infection of the spinal cord are but a few of the ways in which spinal cord injury can happen without trauma to the spinal column. Wise.
    Or from a doctor having a "oops" during spinal fusion surgery.

    Dr. Young, you havn't really addressed mid-thoratic injuries. Can you put something together like what you've done here?

    My daughter (14 yr old, T5, incl., 10 mo post) has a contusion on her cord. And I'm thinking that she has the 'Brown-Sequard syndrom'. Her right side has weaker motor skills, while her left side has weaker sensory outputs. But she continues to improve, walking with walker and starting to use crutches, she can move everything, just some things are very weak. No bowel or bladder yet though. But I've been reading that this type of injury can have a have a pretty good prognosis for recovery, what is you opinion? She is fused from T3 to L3.

    Thank you for your time and concern.

    Rick

  3. #73
    rick, I will try to post something soon. wise.

  4. #74
    Member
    Join Date
    Sep 2004
    Location
    Menlo Park, CA, USA
    Posts
    32
    Dr. Young,

    I just went to see my surgeon for one year post operation appointment. He told me that my injury level is at vertebral L2 and that it is cauda equina injury. However, he doesn't know for sure if there is conus injury involved. But it definitely is not SCI.
    My current situations are these:
    1. I regained all my motor function to various degrees on my right leg and right foot.
    2. Other than a small amount of calve muscle working on my left leg, I have no left leg motor functions. For example, I don't have any left quadricep function. I can move a little of my small toes but not the big toe on my left leg. I regained a small amount of my left butt muscle function.
    3. I regained a large amount of sensation on the back of both of my legs. More so on the right leg than the left leg. However, I have no sensation in the front of both of my legs.
    I regained most of the sensation on my right foot and some small amount of sensation on my left foot.
    4. I regained most of the sensation on both sides of my butt.
    5. I regained my bowel movement and urine functions.
    6. Very rarely do I get erection and even if I do get it, it lasts about 15 seconds.
    7. I have no muscle spasm other than occasional cramp on my right toes especially the big toe.
    8. I get neuropathic pain on both of my legs and feet that can last from half an hour to 24 hours. The pain is similar to static electric shock that lasts about a few seconds but then repeat every 15 seconds or so.

    Questions:
    1. How do I find out if I have conus injury as well? Would an MRI scan tell me that?
    2. How are L2 vertebral injury different than L2 spinal cord injury?
    3. Are there any treatment for cauda equina injury? For example, AP-4 drugs and/or OEG surgery in Beijing.
    4. Do you know any expert in cauda equina injury that you would recommend to me?
    5. Are there any drug for neuropathic pain such as neuronton?
    6. Are there any drug for my right toes cramps?
    7. Do you recommend any electrical stimulation of my atrophy muscles on left leg so I can exercise them?

    Thank you so much for your answers.

    Dennis Chan

  5. #75
    Dennis, I am sorry that I did not answer your questions earlier.

    Questions:
    1. How do I find out if I have conus injury as well? Would an MRI scan tell me that?
      • Conus injury can be diagnosed both neurologically and by MRI although the latter is often not definitive and former is definitive. The conus holds the sacral segments of the spinal cord. Serious conus injury would result in saddle anesthesia and a flaccid anal sphincter.
      • The fact that you have bladder function suggests that your conus in intact.
    2. How are L2 vertebral injury different than L2 spinal cord injury?
      • The fact that you are asking this question means that you have not understood what I have been trying so hard to explain in this entire thread. Spinal cord levels and vertebral levels are different. L1 to S5 spinal cord are located between T11 to L1 vertebral bodies. Below L1, there is no spinal cord, just cauda equina.
    3. Are there any treatment for cauda equina injury? For example, AP-4 drugs and/or OEG surgery in Beijing.
      • 4-AP is for improving function of demyelinated axons. I don’t know or think that that you have demyelination.
      • OEG might help regenerate sensory axons back into the spinal cord but I am concerned from the above questions that you don’t understand what a cauda equina injury and that you are going to misinterpret my statement. I need to understand what you don’t understand so that I can try to explain the situation better.
      • One thing that you should rule out is continued compression of your spinal roots and tethering of your roots. If either is present, decompression or untethering may restore some function.
    4. Do you know any expert in cauda equina injury that you would recommend to me?
      • There are few surgeons who specialize in cauda equina injuries. Jim Guest at Miami Project has a lot of experience.
    5. Are there any drug for neuropathic pain such as neuronton?
      • Do you have neuropathic pain. If you do, there are several treatments and you need to go to the Pain forum and learn about therapies or ask the questions.
    6. Are there any drug for my right toes cramps?
      • Anti-spasticity drugs might help.
    7. Do you recommend any electrical stimulation of my atrophy muscles on left leg so I can exercise them?
      • Electrical stimulation of flaccid muscles would require special stimulator.


    Wise.
    Last edited by Wise Young; 03-22-2006 at 02:25 AM.

  6. #76

    brad

    u know something sad guys!! brad and i was sitting here reading this post and he has no idea about what category he is..doctors apparently left brad in dark about alot of things...so guess what we are definetly moving ..thanks for this info mr.wise ...will keep u updated..bradandtracy..oh all they said was c3 incomplete T4 T5 never walk again..yeah right i will get his butt up watch and see..
    Last edited by bradsgirl; 03-22-2006 at 02:47 AM. Reason: left something out

  7. #77
    SuzyQ, I moved your question and my answer to a new topic
    http://carecure.org/forum/showthread.php?t=60664

    Wise.

  8. #78
    Senior Member
    Join Date
    Mar 2005
    Location
    North America
    Posts
    397
    Dear Wise, this thread has been extremely informative-thank you.

    I am two years post burst/compression fracture of what my Docs said was probably T12/L1 or possibly L2 (they remarked how it seemed I was missing a vertebrae prior to my fall. I am very short five feet total, perhaps my spine in proportion to me, but not the anatomical charts?).
    My neuro-physiotherapist, whom I trust, believes I am more of a clinical cauda equina presentation based on motor improvement. Today i walked around a runner's track in 14mins with fore-arm crutches and minimal cloth bracing to keep my toes up, and prevent foot-drop.
    I have saddle anesthesia, and numb feet, but normal or tingingly/normal sensation everywhere else. I have strong hip-flexors, adductors and quads (4/5), weak, but improving hamstrings, abductors, and flickers in dorsiflexors, and glutes. flickers in planter flextion and toe movement is inconclusive at this point-if i have them, they're far too weak to be noticed.
    Also, i have a spastic (tight/tone) anal and bladder, with sensation of needing to go, but no voiding. just for curiousity's sake, what do you think i am?

    My real interest, however, lies in OEG, can you tell me more about that? And other ways to encourage peripheral axon regrowth and sensory regrowth back into the spinal cord? I'm taking some diet supplements, such as folic acid and serrapeptase because my father (also a Dr.) suggested, but I am intrigued to do more.
    Take your time replying, it's certainly not urgent. and thanks again for all you do for us.

  9. #79
    Surf-Sister,

    Most people with cauda equina (spinal root injury) recover some motor function but generally get less sensory recovery. The reason is that the nerve cells that contribute sensory axons are located in the dorsal root ganglion that are just outside of the spinal column. The peripheral nerve can partially regenerate when the injury is to the part of the peripheral nerve that is away from the spinal cord. However, when the injury is to the spinal root, the sensory axons that go from the dorsal root sensory neurons into the spinal cord and up to the brain have been disrupted. These axons generally will not regenerate back into the spinal cord.

    Several studies have suggested the olfactory ensheathing glia (OEG) may enable the entry of sensory axons into the spinal cord. Raisman's group (Li, et al., 2004) published a study showing the OEG cells provide a bridge for axons to regenerate across the dorsal root entry zone. Despite enthusiasm for this approach (Aldskogius, et al. 2002), Raisman's results have been controversial because several other groups were unable to show similar results. For example, Ramer, et al. (2004) did not have similar success in getting dorsal root regeneration. Likewise, Riddell, et al. (2004) were unable to find any beneficial effect of OEG cell transplants on dorsal root regeneration. Gomez, et al. (2003) were unable to find regeneration of cervical spinal roots after OEG transplantation. However, Jiang, et al. (2003) had reported that enteric glia will help stimulate regeneration of dorsal roots into the spinal cord of rats.

    Wise.

    • Li Y, Carlstedt T, Berthold CH and Raisman G (2004). Interaction of transplanted olfactory-ensheathing cells and host astrocytic processes provides a bridge for axons to regenerate across the dorsal root entry zone. Exp Neurol 188: 300-8. A single fourth lumbar dorsal rootlet was transected at the entry point into the spinal cord. The nerve fibres were labelled with biotin dextran injected into the rootlet. An endogenous matrix containing olfactory-ensheathing cells (OECs) labelled with green fluorescent protein was applied to the opposing cut surfaces of the rootlet and the spinal cord, which were then brought into apposition and held in place by fibrin glue. Two weeks later, a ladderlike bridging structure has been formed by astrocytic processes growing out for about 200-300 microm from the spinal cord. The transplanted cells remained largely confined to this area. They were elongated along the nerve axis but did not enter the spinal cord itself. Labelled dorsal root axons crossed the repaired dorsal root entry zone in alignment with the bridging astrocytic processes and the transplanted cells and then proceeded beyond the transplant to enter the grey matter of the dorsal horn and send axons both rostrally and caudally for at least 10 mm in the white matter of the ascending dorsal columns. Division of Neurobiology, Norman and Sadie Lee Research Centre, National Institute for Medical Research, MRC, London, UK. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15246830
    • Aldskogius H and Kozlova EN (2002). Strategies for repair of the deafferented spinal cord. Brain Res Brain Res Rev 40: 301-8. Deafferentation of the spinal cord by interruption of the sensory fibers in the dorsal roots highlights the problem of regeneration failure in the central nervous system. The injured dorsal root axons regenerate steadily, albeit slowly, in the peripheral compartment of the dorsal root, but abruptly cease to elongate when confronted with the interface between the peripheral and central nervous system, the dorsal root transitional zone (DRTZ). The glial cells of the CNS and their products together form this regeneration barrier. Recent years have witnessed several successful approaches to, at least in part, overcome this barrier. Particularly promising results have been obtained by (1). the replacement of adult non-regenerating dorsal root ganglion neurons with corresponding cells from embryonic or fetal donors, (2). the implantation of olfactory ensheathing cells at the DRTZ, and (3). immediate intrathecal infusion of growth factors to which dorsal root ganglion cells respond. In all these instances, growth of sensory axons into the adult spinal cord, as well as return of spinal cord connectivity, have been demonstrated. These findings suggest routes towards treatment strategies for plexus avulsion, and contribute to our understanding of possibilities to overcome regeneration failure in the spinal cord. Department of Neuroscience, Neuroanatomy, Biomedical Center, PO Box 587, Uppsala University, SE-751 23, Uppsala, Sweden. hakan.aldskogius@neuro.uu.se http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12589928
    • Ramer LM, Richter MW, Roskams AJ, Tetzlaff W and Ramer MS (2004). Peripherally-derived olfactory ensheathing cells do not promote primary afferent regeneration following dorsal root injury. Glia 47: 189-206. Olfactory ensheathing cells (OECs) may support axonal regrowth, and thus might be a viable treatment for spinal cord injury (SCI); however, peripherally-derived OECs remain untested in most animal models of SCI. We have transplanted OECs from the lamina propria (LP) of mice expressing green fluorescent protein (GFP) in all cell types into immunosuppressed rats with cervical or lumbar dorsal root injuries. LP-OECs were deposited into either the dorsal root ganglion (DRG), intact or injured dorsal roots, or the dorsal columns via the dorsal root entry zone (DREZ). LP-OECs injected into the DRG or dorsal root migrated centripetally, and migration was more extensive in the injured root than in the intact root. These peripherally deposited OECs migrated within the PNS but did not cross the DREZ; similarly, large- or small-caliber primary afferents were not seen to regenerate across the DREZ. LP-OEC deposition into the dorsal columns via the DREZ resulted in a laminin-rich injection track: due to the pipette trajectory, this track pierced the glia limitans at the DREZ. OECs migrated centrifugally through this track, but did not traverse the DREZ; axons entered the spinal cord via this track, but were not seen to reenter CNS tissue. We found a preferential association between CGRP-positive small- to medium-diameter afferents and OEC deposits in injured dorsal roots as well as within the spinal cord. In the cord, OEC deposition resulted in increased angiogenesis and altered astrocyte alignment. These data are the first to demonstrate interactions between sensory axons and peripherally-derived OECs following dorsal root injury. International Collaboration on Repair Discoveries (ICORD), Vancouver, British Columbia, Canada. leanne@icord.org http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15185397
    • Riddell JS, Enriquez-Denton M, Toft A, Fairless R and Barnett SC (2004). Olfactory ensheathing cell grafts have minimal influence on regeneration at the dorsal root entry zone following rhizotomy. Glia 47: 150-67. The effectiveness of grafts of olfactory ensheathing cells (OECs) as a means of promoting functional reconnection of regenerating primary afferent fibers was investigated following dorsal root injury. Adult rats were subjected to dorsal root section and reanastomosis and at the same operation a suspension of purified OECs was injected at the dorsal root entry zone and/or into the sectioned dorsal root. Regeneration of dorsal root fibers was then assessed after a survival period ranging from 1 to 6 months. In 11 animals, electrophysiology was used to look for evidence of functional reconnection of regenerating dorsal root fibers. However, electrical stimulation of lesioned dorsal roots failed to evoke detectable cord dorsum or field potentials within the spinal cord of any of the animals examined, indicating that reconnection of regenerating fibers with spinal cord neurones had not occurred. In a further 11 rats, immunocytochemical labeling and biotin dextran tracing of afferent fibers in the lesioned roots was used to determine whether regenerating fibers were able to grow into the spinal cord in the presence of an OEC graft. Although a few afferent fibers could be seen to extend for a limited distance into the spinal cord, similar minimal in-growth was seen in control animals that had not been injected with OECs. We therefore conclude that OEC grafts are of little or no advantage in promoting the in-growth of regenerating afferent fibers at the dorsal root entry zone following rhizotomy. Division of Neuroscience and Biomedical Systems, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, UK. j.riddell@bio.gla.ac.uk http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15185394
    • Gomez VM, Averill S, King V, Yang Q, Perez ED, Chacon SC, Ward R, Nieto-Sampedro M, Priestley J and Taylor J (2003). Transplantation of olfactory ensheathing cells fails to promote significant axonal regeneration from dorsal roots into the rat cervical cord. J Neurocytol 32: 53-70. The olfactory ensheathing cell (OEC) is a class of glial cell that has been reported to support regeneration in the central nervous system after various types of lesions, including rhizotomy of spinal dorsal roots at thoracic, lumbar and sacral levels. We have therefore carried out a detailed anatomical analysis to assess the efficacy of dorsal horn OEC transplants at promoting regeneration of primary afferents across the dorsal root entry zone (DREZ) at the cervical level in the adult rat. OECs were cultured from adult rat olfactory bulb and immunopurified (90% purity). Regeneration by large diameter afferents and by both peptidergic and non-peptidergic small diameter afferents was assessed using respectively cholera toxin B (CTB) labelling and immunocytochemistry for calcitonin gene-related peptide (CGRP) and the purinoceptor P2X3. Following an extensive (C3-T3) rhizotomy, CGRP and P2X3 immunoreactive axons regenerated across the rhizotomy site as far as the DREZ but there was no evidence of regeneration across the DREZ, except through sites where the OEC transplant was directly grafted into the DREZ. No evidence of regeneration into the dorsal horn by CTB-labelled axons was obtained. In addition, there was little sign of sprouting by intact axons in the vicinity of OEC transplant sites. In contrast to these results in vivo, cocultures of OECs and adult dorsal root ganglion cells showed that OECs stimulate extensive neurite outgrowth. The failure of the OECs to promote regeneration in vivo following cervical rhizotomy is therefore most likely due to factors in the environment of the graft site and/or the method of transplantation. Instituto de Neurobiologia Ramon y Cajal, Avenida Doctor Arce 37, 28002 Madrid, Spain. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=14618101
    • Jiang S, Wang J, Khan MI, Middlemiss PJ, Salgado-Ceballos H, Werstiuk ES, Wickson R and Rathbone MP (2003). Enteric glia promote regeneration of transected dorsal root axons into spinal cord of adult rats. Exp Neurol 181: 79-83. After spinal cord injury axonal regeneration is poor, but may be enhanced by the implantation of olfactory ensheathing glia (OEG). Enteric glia (EG) share many properties of OEG. Transected dorsal root axons normally do not regenerate through the central nervous system myelin into the spinal cord. We tested whether EG, like OEG, could promote regeneration in this paradigm. Three weeks after EG implantation, numerous regenerating dorsal root axons reentered the spinal cord. Ingrowth of dorsal root axons was observed using 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate. Primary sensory afferents invaded laminae 1, 2, and 3, grew through laminae 4 and 5, and reached the dorsal gray commissure. No axonal ingrowth was observed in control animals, indicating that transplanted EG enabled regeneration of the injured dorsal root axons into the adult spinal cord. Thus, EG implantation may be beneficial in promoting axonal growth after central nervous system injury. Department of Medicine, McMaster University Health Sciences Centre 4N71, 1200 Main Street West, Hamilton, Ontario L8N 3Z5, Canada. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12710936




    Quote Originally Posted by Surf_Sister
    Dear Wise, this thread has been extremely informative-thank you.

    I am two years post burst/compression fracture of what my Docs said was probably T12/L1 or possibly L2 (they remarked how it seemed I was missing a vertebrae prior to my fall. I am very short five feet total, perhaps my spine in proportion to me, but not the anatomical charts?).
    My neuro-physiotherapist, whom I trust, believes I am more of a clinical cauda equina presentation based on motor improvement. Today i walked around a runner's track in 14mins with fore-arm crutches and minimal cloth bracing to keep my toes up, and prevent foot-drop.
    I have saddle anesthesia, and numb feet, but normal or tingingly/normal sensation everywhere else. I have strong hip-flexors, adductors and quads (4/5), weak, but improving hamstrings, abductors, and flickers in dorsiflexors, and glutes. flickers in planter flextion and toe movement is inconclusive at this point-if i have them, they're far too weak to be noticed.
    Also, i have a spastic (tight/tone) anal and bladder, with sensation of needing to go, but no voiding. just for curiousity's sake, what do you think i am?

    My real interest, however, lies in OEG, can you tell me more about that? And other ways to encourage peripheral axon regrowth and sensory regrowth back into the spinal cord? I'm taking some diet supplements, such as folic acid and serrapeptase because my father (also a Dr.) suggested, but I am intrigued to do more.
    Take your time replying, it's certainly not urgent. and thanks again for all you do for us.

  10. #80
    Senior Member
    Join Date
    Mar 2005
    Location
    North America
    Posts
    397
    Thanks, Wise, my father and I were amazed you wrote such a referenced reply so quickly.

    The abstracts were intriguing, but with such inconsistent results, I don't think I'll be trying olfactory ensheathing glia (OEG) procedures anytime soon.
    But I have more quesions if you have time,
    Do you have any ideas of when this might be done in humans? Is OEG an invasive operation or more like the needle being used in China? I'm assuming these animal studies are similar to Dr. Huang's work, but I'm not sure on what those similarities are exactly. Hypothetically, if I were to get the procedure done in china, how would cauda equina treatment(s) be different from a higher SCI?

    Thanks Again!

Similar Threads

  1. Cauda equina injury: Diagnosis and Treatment
    By Wise Young in forum Cure
    Replies: 11
    Last Post: 11-29-2011, 09:49 AM
  2. Replies: 22
    Last Post: 09-03-2009, 01:06 AM
  3. Cauda Equina Injuries
    By Wise Young in forum Cure
    Replies: 28
    Last Post: 08-28-2007, 09:49 AM
  4. Replies: 2
    Last Post: 07-19-2005, 04:08 AM

Tags for this Thread

Posting Permissions

  • You may not post new threads
  • You may not post replies
  • You may not post attachments
  • You may not edit your posts
  •