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

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    #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; 22 Mar 2006, 2:47 AM. Reason: left something out

    Comment


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

      Wise.

      Comment


        #78
        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.

        Comment


          #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




          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.

          Comment


            #80
            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!

            Comment


              #81
              Surf-Sister,

              Raisman and Carlstedt have proposed doing such studies in human brachial plexus avulsions. For example, see http://carecure.org/forum/showthread...hlight=raisman

              Wise.

              Originally posted by Surf_Sister
              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!

              Comment


                #82
                Where can I find evidence for the ASIA dermatome maps as opposed to the Netter dermatome maps? Thanks.

                Comment


                  #83
                  Cauda Equina Symptom???

                  I'm a 47 year old guy with a recent L4-L5 disc burst after years of herniation, causing cauda equina syndrome. I had an increase in back pain (worst ever), which led to some weakness and I fell on my ass, bursting the disc. My feet and groin went numb and I called 911. I was in surgery within 11 hours of falling and had a discectomy and laminectomy on 1/8/08.

                  I can walk (though I look like frankenstein's monster clopping around on my heals), even though I'm weak through the outside of my legs and my glutes. I am quite weak pushing down on my toes, better pulling them up against resistance. My left side is weaker and I can only barely wiggle the toes on my left foot. I had left sided sciatica for many years. I can wiggle the right toes much better.

                  My bladder and bowel have been weakened, but I can voluntarily control them. Sensation is reduced and altered, but I can tell when my bladder is full, especially if I press on my bladder. The bowel is more difficult to judge since it feels like I have a stick up my butt, and my sphincter tone is reduced.

                  Both feet have a great deal of neuropathy, not well controlled with neurontin. The strangest symptom is perineal pain, however. It feels like I have a golf ball jammed in my rectum when I sit down, making sitting for any length of time very difficult. This has prevented me from returning to work more than any other symptom.

                  Is this literal pain in the ass something you hear about? Is there any way to guess if this will fade, or how long this may last? I have so many questions, but I better stop here for now. I'm going to fill out the ASIA classification form asap, but know that I have more sensation than my neurosurgeon expected, and can tell pins from dull almost everywhere.
                  Jonathan
                  L4-5 cauda equina syndrome (1/8/08)

                  Comment


                    #84
                    Originally posted by tralain
                    I'm a 47 year old guy with a recent L4-L5 disc burst after years of herniation, causing cauda equina syndrome. I had an increase in back pain (worst ever), which led to some weakness and I fell on my ass, bursting the disc. My feet and groin went numb and I called 911. I was in surgery within 11 hours of falling and had a discectomy and laminectomy on 1/8/08.

                    I can walk (though I look like frankenstein's monster clopping around on my heals), even though I'm weak through the outside of my legs and my glutes. I am quite weak pushing down on my toes, better pulling them up against resistance. My left side is weaker and I can only barely wiggle the toes on my left foot. I had left sided sciatica for many years. I can wiggle the right toes much better.

                    My bladder and bowel have been weakened, but I can voluntarily control them. Sensation is reduced and altered, but I can tell when my bladder is full, especially if I press on my bladder. The bowel is more difficult to judge since it feels like I have a stick up my butt, and my sphincter tone is reduced.

                    Both feet have a great deal of neuropathy, not well controlled with neurontin. The strangest symptom is perineal pain, however. It feels like I have a golf ball jammed in my rectum when I sit down, making sitting for any length of time very difficult. This has prevented me from returning to work more than any other symptom.

                    Is this literal pain in the ass something you hear about? Is there any way to guess if this will fade, or how long this may last? I have so many questions, but I better stop here for now. I'm going to fill out the ASIA classification form asap, but know that I have more sensation than my neurosurgeon expected, and can tell pins from dull almost everywhere.
                    This pain that you are referring to is, in my experience, not common. Because it is positionally related (i.e. when you sit), it seems to be something to do with your sacral injury. If I were you, I would be carefully investigating your S4 and S5 roots.

                    Wise.

                    Comment


                      #85
                      Thanks for your timely response. I've been told that the recovery process moves from the top down, and it doesn't get any lower than S4-5, so I suppose this may take a long time to calm down. That pressure is there when I do many things, and I can almost always feel the perineal issue. Sitting is the most painful, however. How do I investigate S4-5? Is this doing the ASIA chart or do you mean something else. Thanks again.

                      Tralain
                      Jonathan
                      L4-5 cauda equina syndrome (1/8/08)

                      Comment


                        #86
                        Originally posted by tralain
                        Thanks for your timely response. I've been told that the recovery process moves from the top down, and it doesn't get any lower than S4-5, so I suppose this may take a long time to calm down. That pressure is there when I do many things, and I can almost always feel the perineal issue. Sitting is the most painful, however. How do I investigate S4-5? Is this doing the ASIA chart or do you mean something else. Thanks again.

                        Tralain
                        The fact that your pain is positional, i.e. it is worse when you sit, suggests that sitting may cause the roots to be compressed. I guess that I would first look on MRI to see if there is anything unusual that may affect those roots, such as a disc or narrowing of the foramina for S4/5. Was this where the break occurred?

                        Wise.

                        Comment


                          #87
                          Originally posted by Wise Young
                          The fact that your pain is positional, i.e. it is worse when you sit, suggests that sitting may cause the roots to be compressed. I guess that I would first look on MRI to see if there is anything unusual that may affect those roots, such as a disc or narrowing of the foramina for S4/5. Was this where the break occurred?

                          Wise.
                          No, I had an L4-5 rupture hitting the cauda equina. There is always tightness and pressure at the perineum, but it is much worse when I sit. I have an MRI coming on Monday, since my neurosurgeon wants another peak. So we should pay attention to S4/5? OK.
                          Jonathan
                          L4-5 cauda equina syndrome (1/8/08)

                          Comment


                            #88
                            Originally posted by tralain
                            No, I had an L4-5 rupture hitting the cauda equina. There is always tightness and pressure at the perineum, but it is much worse when I sit. I have an MRI coming on Monday, since my neurosurgeon wants another peak. So we should pay attention to S4/5? OK.
                            Tralain,

                            As I tried to explain in this thread, the spinal cord ends just below the L1 vertebral segment. Below that point, the spinal roots from L2 through S5 are all present in the spinal canal. Thus, a herniated disc at L4/5 vertebral level can press on the S4 and S5 roots.

                            Wise.

                            Comment


                              #89
                              Hello,

                              I am a new member of this post. I have had a L5-S1 discectomy 50 days back for a large para-central disc herniation. I also have a disc bulge at L4-5 and it was left alone by my surgeon.

                              Till 45 days, everything proceeded nicely till I started the spinal toning and strengthening exercises. From the next day, I started losing a bit of feeling in my penis. Also, sometimes I cant feel when I am passing the urine. I can feel when the bladder is full, and also can hold it. I had a Post-void residue test done and it showed that the post void was 30cc, while pre-void was 440cc. I also have an erection problem. I also lost a bit of feeling when passing bowels.

                              I got scared and then got a repeat MRI done but it shows no nerve compression at L3, L4 and L5 vertebrae levels. L4 disc bulge is still present but it is small, the cut disc at L5 is still within the vertebrae bounds and no pressure is seen on any of the nerves. And he is not able to understand the reason for it ?

                              Will MRI confirm cauda equina symptoms ?

                              From the description, it seems I have CES but MRI shows no nerve decompressions. Then what could be the reasons for it ?

                              Would really appreciate if you could let me know what to do ?

                              Regards
                              Misbah

                              Comment


                                #90
                                Originally posted by misbahuddinka View Post
                                Hello,

                                I am a new member of this post. I have had a L5-S1 discectomy 50 days back for a large para-central disc herniation. I also have a disc bulge at L4-5 and it was left alone by my surgeon.

                                Till 45 days, everything proceeded nicely till I started the spinal toning and strengthening exercises. From the next day, I started losing a bit of feeling in my penis. Also, sometimes I cant feel when I am passing the urine. I can feel when the bladder is full, and also can hold it. I had a Post-void residue test done and it showed that the post void was 30cc, while pre-void was 440cc. I also have an erection problem. I also lost a bit of feeling when passing bowels.

                                I got scared and then got a repeat MRI done but it shows no nerve compression at L3, L4 and L5 vertebrae levels. L4 disc bulge is still present but it is small, the cut disc at L5 is still within the vertebrae bounds and no pressure is seen on any of the nerves. And he is not able to understand the reason for it ?

                                Will MRI confirm cauda equina symptoms ?

                                From the description, it seems I have CES but MRI shows no nerve decompressions. Then what could be the reasons for it ?

                                Would really appreciate if you could let me know what to do ?

                                Regards
                                Misbah
                                Misbah,

                                I am not sure what is happening. One possibility is that a disc is not herniating when you are lying down (the position that the MRI is taken) but only when you are sitting up. This can happen. Are you symptoms worse when you are sitting up or standing?

                                Wise.

                                Comment

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