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Thoracic Spinal Cord Injury: Diagnosis & Treatment

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  • #46
    Originally posted by FIREGUY
    dr. young

    A little of your insight might help my problem. I’ve had Harrington rods in since 1985 after an auto accident where I had a compression fx of t-10 and broke the transverse processes off of t-8 thru t-11. My rod ends at t-12 there is a notable lump in that area. is it possabile that the hook is coming in contact with the spinal cord causing a reaction. In the past few years I’ve been experiencing what I can only explain as drop falls. During one of these episodes my back will lock up and I will fall to the ground. I know exactly what is happening during the event but I can't move to brace myself. Have you ever come a crossed something like this? I’ve been to my local dr. - I’ve been to Jefferson and U of P. i've had CT scans and an MRI but because of the rods it was unreadable in that area. In your opinion would you recommend to a patient of yours to have the rods removed.
    Fireguy,

    I am not sure what is happening. Your spine should have fused completely and you do not need these rods any more. It is not trivial surgery to remove rods but it may be a good idea considering your symptoms. It would also allow imaging of your cord to find out what is going on.

    Wise.

    Comment


    • #47
      Originally posted by rfbdorf
      I've only now happened upon this thread - I learned a lot. Thank you, Dr. Wise.
      It's just recently that I'm beginning to understand what happened to my wife: attempted correction of a 90 degree deformity to about 45 degrees was probably too much, causing ischemia at T5. It is very hopeful to know that there's still a chance of some return, though we haven't seen much of anything in the 10 months since. Still don't know why they didn't give her methylprednisolone.
      - Richard
      Richard, you are welcome.

      Unfortunately, most orthopedic surgeons don't publish their experiences with spinal cord injury during scoliosis surgery and so there is not much published statistics concerning recovery from such situations. However, I tried to find all the studies on the subject that I can for you. Stocki, et al. (2005) reported two cases of anterior spinal artery syndrome after scoliosis surgery and both recovered. Tribus (2001) reported a case of transient paraparesis during surgery that reversed completely with removal of instrumentation. Mineiro & Weinstein (1997) reported a case report of delayed postoperative paraparesis in scoliosis surgery, with complete recovery. Nordeen, et al. (1997) described the spinal cord monitoring results for 99 patients operated on for neuromuscular scoliosis and reported only one case of "permanent" injury. All those with temporary paresis recovered completely. Nordeen, et al. (1994) also reported a case of a person with syringomyelia who got worse and then recovered when the distraction was reduced. Forbes, et al. (1991) reported 1168 cases of somatosensory evoked potential (SEP) monitoring and found that 119 cases of significant intraoperative SEP changes and only 32 had clinically detectable neurological changes. Savini, et al. (1990) reported two cases of late neurological complication associated with scoliosis correction and recovery. Van Dem, et al. (1987) described 91 cases of scoliosis and found only one case with neurological complications, a transient paraparesis that recovered.

      So, in the recent literature anyway, there is not much insight to be gained. Permanent neurological loss appears to be rare. On the other hand, it may be that doctors only publish cases that recover. I assume that your wife's doctor reduced or removed the distracting rods when they discovered the paralysis.

      Wise.


      References
      1. Stockl B, Wimmer C, Innerhofer P, Kofler M and Behensky H (2005). Delayed anterior spinal artery syndrome following posterior scoliosis correction. Eur Spine J 14: 906-9. The authors report two cases of delayed post-operative anterior spinal artery syndrome (ASAS) following posterior correction with Cotrel Dubousset (CD) instrumentation for adolescent idiopathic scoliosis. Sensory pathways were continuously monitored from skin incision to awakening. In both cases intraoperative SEPs were normal and the wake-up test revealed no neurological deficit. Both patients were presented with incomplete paraplegia (no sensory impairment) three and ten hours after surgery. Without delay, both patients underwent revision surgery, and the CD instrumentation was removed. Immediately after surgery, both patients' motor power in their lower extremities improved rapidly. In cases with delayed ASAS after posterior scoliosis correction, the removal of the instrumentation system was shown to be sufficient to regain full motor recovery caudal to the level of impairment. Department of Orthopaedics, Innsbruck Medical University, Austria. bernd.stoeckl@uibk.ac.at http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15937672
      2. Tribus CB (2001). Transient paraparesis: a complication of the surgical management of Scheuermann's kyphosis secondary to thoracic stenosis. Spine 26: 1086-9. STUDY DESIGN: Transient paraparesis during the operative management of a 16-year-old patient with Scheuermann's kyphosis secondary to thoracic stenosis is reported. OBJECTIVE: To describe a treatable cause for paraparesis in a patient with Scheuermann's kyphosis undergoing surgical treatment. SUMMARY OF BACKGROUND DATA: Cord injury in the surgical treatment of Scheuermann's kyphosis is a rare event, yet it is felt to be more common in the surgical correction of kyphosis than in surgery for scoliosis. Suggested etiologies have included vascular insufficiency, hypotension, direct mechanical trauma, and neural element stretch. Concomitant thoracic spinal stenosis predisposing to neurologic injury during surgical manipulation has not been reported. METHODS: A 16-year-old boy with progressive Scheuermann's kyphosis measuring 80 degrees from T7 to T12 underwent an anteroposterior spinal fusion with somatosensory-evoked potential monitoring and wake-up tests. During the instrumentation posteriorly, somatosensory-evoked potential monitoring became markedly abnormal. This was followed by a wake-up test that demonstrated the patient's inability to move either of his lower extremities. All instrumentation was removed. The patient had recovered neurologic function by the time he reached the recovery room. A computed tomography myelogram was performed on the third postoperative day, which demonstrated severe thoracic stenosis from T8 to T10. The patient was returned to the operating room 1 week later to undergo a posterior laminectomy from T7 to T11 and instrumented fusion from T5 to L2. Somatosensory-evoked potential monitoring was stable throughout this procedure, and the wake-up test was normal. RESULTS: The patient's postoperative course and subsequent 2-year follow-up period were unremarkable. He progressed to clinical and radiographic union and maintained a normal lower extremity neurologic examination. CONCLUSIONS: A treatable cause for paraparesis secondary to the surgical treatment of Scheuermann's kyphosis is presented. The author currently obtains a thoracic magnetic resonance image (MRI) before the surgical correction of any patients with Scheuermann's kyphosis. University of Wisconsin Hospital and Clinics, Madison, Wisconsin, USA. tribus@surgery.wisc.edu http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11337630
      3. Mineiro J and Weinstein SL (1997). Delayed postoperative paraparesis in scoliosis surgery. A case report. Spine 22: 1668-72. STUDY DESIGN: A case report is presented of an unusual complication of scoliosis surgery that, to the authors' knowledge, has never been reported in the literature. OBJECTIVE: Neurologic complications can occur after an uneventful posterior spinal instrumentation and fusion for scoliosis. Careful observation during the post-operative period is crucial for early detection of impending neurologic deficit. SUMMARY OF BACKGROUND DATA: Nerve compression of the cauda equina has been reported as a complication of different types of surgery in the lumbar spine, but an ascending paraparesis has never been described as a complication of scoliosis surgery. METHODS: A 12-year-old boy with a right thoracic scoliosis measuring 68 degrees and a 72 degrees left lumbar curve underwent Cotrel-Dubousset instrumentation and fusion from T5 to L4. Spinal cord monitoring with somatosensory evoked potentials and motor action potential were recorded and stable through out the entire procedure. Thirty hours later, a rapidly progressive ascending para-paresis developed that required urgent decompression. RESULTS: This patient underwent urgent decompression and removal of the Cotrel-Dubousset instrumentation. After surgery, the clinical picture improved gradually, and at 2-month follow-up he had regained normal strength in his lower limbs except for a grade 4 left extensor hallucis longus. By 4 months postdecompression, he had made a total recovery. CONCLUSIONS: Although clinical examination may be difficult to perform in patients who are unconscious, on large doses of narcotic drugs, or mentally retarded, careful observation during the postoperative period and awareness of this complication can allow early detection of impending reversible neurologic deficit and provision of appropriate treatment. Department of Orthopaedic Surgery, Hospital Santa Maria, Lisbon, Portugal. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9253104
      4. Noordeen MH, Lee J, Gibbons CE, Taylor BA and Bentley G (1997). Spinal cord monitoring in operations for neuromuscular scoliosis. J Bone Joint Surg Br 79: 53-7. We reviewed retrospectively the role of monitoring of somatosensory spinal evoked potentials (SSEP) in 99 patients with neuromuscular scoliosis who had had operative correction with Luque-Galveston rods and sublaminar wiring. Our findings showed that SSEP monitoring was useful and that a 50% decrease in the amplitude of the trace optimised both sensitivity and specificity. The detection of true-positive results was higher than in cases of idiopathic scoliosis, but the method was less sensitive and specific and there were more false-negative results. In contrast with the findings in idiopathic scoliosis, recovery of the trace was associated with a 50% to 60% risk of neurological impairment. Only one permanent injury occurred during the use of this technique, and any temporary impairment resolved within two months. The Institute of Orthopaedics and the Royal National Orthopaedic Hospital Trust, Stanmore, London, UK. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9020445
      5. Noordeen MH, Taylor BA and Edgar MA (1994). Syringomyelia. A potential risk factor in scoliosis surgery. Spine 19: 1406-9. STUDY DESIGN. An 18-year-old patient with "idiopathic" adolescent scoliosis is presented. A thoracic syrinx was detected as an incidental finding during magnetic resonance imaging of the spine. OBJECTIVES. Syringomyelia may be a risk factor for neurologic injury during correction of scoliosis, and in these cases, spinal cord monitoring may be of particular value. BACKGROUND DATA. Spinal distraction and instrumentation carry a risk of neurologic damage in patients with scoliosis and associated syringomyelia. Syringomyelia is a cause of scoliosis, and although neurologic problems are the usual symptom, scoliosis may be the only sign at initial examination. A higher risk of neurologic injury has been reported in corrective surgical treatment of patients with syringomyelia. The mechanism of cord damage is unclear. Monitoring of spinal cord function is recommended to detect intraoperative neurological injury, which may be reversed on removing distraction and implants. RESULTS. Intraoperative somatosensory-evoked potential (SSEP) spinal cord monitoring detected possible cord damage during outrigger distraction. Reduction of distraction led to a recovery of SSEPs and a satisfactory operative outcome. CONCLUSION. Syringomyelia may be a risk factor for neurologic injury during correction of scoliosis, and SSEP spinal cord monitoring may identify and prevent intraoperative spinal cord injury. Middlesex Hospital, London, United Kingdom. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8066525
      6. Forbes HJ, Allen PW, Waller CS, Jones SJ, Edgar MA, Webb PJ and Ransford AO (1991). Spinal cord monitoring in scoliosis surgery. Experience with 1168 cases. J Bone Joint Surg Br 73: 487-91. Since 1981, during operations for spinal deformity, we have routinely used electrophysiological monitoring of the spinal cord by the epidural measurement of somatosensory evoked potentials (SEPs) in response to stimulation of the posterior tibial nerve. We present the results in 1168 consecutive cases. Decreases in SEP amplitude of more than 50% occurred in 119 patients, of whom 32 had clinically detectable neurological changes postoperatively. In 35 cases the SEP amplitude was rapidly restored, either spontaneously or by repositioning of the recording electrode; they had no postoperative neurological changes. One patient had delayed onset of postoperative symptoms referrable to nerve root lesions without evidence of spinal cord involvement, but there were no false negative cases of intra-operative spinal cord damage. In 52 patients persistent, significant, SEP changes were noted without clinically detectable neurological sequelae. None of the many cases which showed falls in SEP amplitude of less than 50% experienced neurological problems. Neuromuscular scoliosis, the use of sublaminar wires, the magnitude of SEP decrement, and a limited or absent intra-operative recovery of SEP amplitude were identified as factors which increased the risk of postoperative neurological deficit. Royal National Orthopaedic Hospital, London, England. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=1670455
      7. Savini R, Di Silvestre M and Gargiulo G (1990). Late paraparesis due to pseudarthrosis after posterior spinal fusion. J Spinal Disord 3: 427-32. The authors report three cases in which paraparesis related to a pseudarthrosis occurred several years after a posterior spinal fusion, but with a different mechanism (stretching of the spinal cord for progression of the deformity in kyphosis in two cases, and spinal cord compression for bone overgrowth within the canal in the site of pseudarthrosis in the third patient). Treatment was different. Partial correction of the deformity and stabilization of the spine by combined fusion (anterior and posterior) was sufficient in the first two cases for a complete neurological recovery. Posterior spinal cord decompression and stabilization of the spine by combined fusion was necessary for complete recovery in the third. Centro Scoliosi, Istituto Ortopedico Rizzoli, Bologna, Italy. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=2134461
      8. van Dam BE, Bradford DS, Lonstein JE, Moe JH, Ogilvie JW and Winter RB (1987). Adult idiopathic scoliosis treated by posterior spinal fusion and Harrington instrumentation. Spine 12: 32-6. Ninety-one patients with idiopathic scoliosis, who underwent posterior spinal fusion and instrumentation from January 1977 to December 1982, were reviewed. All patients were 20 years or older at the time of surgery and none had undergone a prior surgical procedure. Indications for surgery included pain, progressive deformity, and pulmonary symptoms. All patients had a posterior spinal fusion with Harrington instrumentation and autogenous iliac bone graft, with the addition of segmental wiring in only eight. No patient had an anterior fusion or fusion to the sacrum. Follow-up averaged 3.5 years (range: 2-7 years). The average correction at the time of surgery was 38%, and 32% at the time of last follow-up. Seventy-nine percent of the patients reported complete relief of the symptom(s) for which they had surgery. There were 34 complications in 30 (33%) patients. Pseudarthrosis occurred in 14 (15%), requiring 15 additional procedures to achieve a solid arthrodesis. Urinary tract infection occurred in 8 (9%) patients and Harrington hook dislodgement in 5 (5%). One patient sustained a partial paraparesis with recovery to a minimal deficit. No deaths occurred. Although largely successful, posterior fusion with Harrington instrumentation for adult scoliosis has a significant incidence of pseudarthrosis and instrumentation problems. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=3554557
      Last edited by Wise Young; 04-13-2006, 01:34 AM.

      Comment


      • #48
        Again, thank you for all that information and for your time, Dr. Wise.

        Actually, the rods came later... Immediately after her first operation, in which he placed a cage between T4 and T6, the neurosurgeon told me she had a blockage at T5 and he thought perhaps he had overcorrected her kyphosis (from an amazingly sharp 90 degrees), so he went in again that day and reduced the correction somewhat, but that was unsuccessful in restoring the function of her cord. A week later, he went in again (as planned) and stabilized her spine by placing the 2 rods from T3 to T7. That had no effect on her paralysis, but did relieve the pain somewhat.
        The surgeon says he doesn't know for certain what caused the paralysis. At first he was thinking compression (and in fact he dug into her a fourth time, several days after placing the rods, because he thought just maybe the MRI showed an area of compression), but he now tends to think it is likely due to ischemia.
        - Richard

        Comment


        • #49
          Originally posted by rfbdorf
          Again, thank you for all that information and for your time, Dr. Wise.

          Actually, the rods came later... Immediately after her first operation, in which he placed a cage between T4 and T6, the neurosurgeon told me she had a blockage at T5 and he thought perhaps he had overcorrected her kyphosis (from an amazingly sharp 90 degrees), so he went in again that day and reduced the correction somewhat, but that was unsuccessful in restoring the function of her cord. A week later, he went in again (as planned) and stabilized her spine by placing the 2 rods from T3 to T7. That had no effect on her paralysis, but did relieve the pain somewhat.
          The surgeon says he doesn't know for certain what caused the paralysis. At first he was thinking compression (and in fact he dug into her a fourth time, several days after placing the rods, because he thought just maybe the MRI showed an area of compression), but he now tends to think it is likely due to ischemia.
          - Richard
          Richard,

          Oh, I understand now. She had a 90% kyphosis... that is very severe. How long was that kyphosis in place? In most kyphoscoliosis, the spinal cord is draped around the curvature and may have had significant loss of axons already and was probably close to the edge. The ischemia pushed it over the edge.

          He was a neurosurgeon and not an orthopedic surgeon?

          Wise.

          Comment


          • #50
            Originally posted by Wise Young
            Fireguy,

            I am not sure what is happening. Your spine should have fused completely and you do not need these rods any more. It is not trivial surgery to remove rods but it may be a good idea considering your symptoms. It would also allow imaging of your cord to find out what is going on.

            Wise.
            i thank you for your advice, i was wondering is it possable with the hooks at t-12 and with the bending and moving over the years there a chance the rods are pulling the vertebrae slightly out of alignment, but it won't show up during and exam because of being in the prone position there's no stress being put on the spine?? I haven't had a mylogram done yet is that something to due prior to any surgical procedure. i also have a slight to mod herniation of l-4 - l5 i don't know if that would be the cause of my back to seize up
            ddd t1-6, f/x t8 thru t-11, fusion at t-9/t-10, 1 1/2" bruse on cord, fusion at t-12/1-1, lamy at L-1/L-2, foraminotomy at L-3/L-4 , protrusion at L5/S-1. ain't much left to fail
            Well I guess I was wrong.

            Comment


            • #51
              Originally posted by Wise Young
              Richard,
              Oh, I understand now. She had a 90% kyphosis... that is very severe. How long was that kyphosis in place? In most kyphoscoliosis, the spinal cord is draped around the curvature and may have had significant loss of axons already and was probably close to the edge. The ischemia pushed it over the edge.
              He was a neurosurgeon and not an orthopedic surgeon?
              Wise.
              Wise -
              The kyophosis had a 2 year history...
              In very early 2003 (at age 61), she got a staph infection at the entry site of a PICC line - she was getting ATG (antithymocyte globulin) for aplastic anemia. Oral antibiotics took care of it, so it was thought at the time. She complained to her hematologist of back pain; the response was "don't worry, my dear, joint pain is a normal side effect of the ATG, some of my patients have it much worse than you." A week later, she began to have difficulty controlling her legs, so I took her in to see him again, when he realized something was wrong. Xrays showed 2 spinal abscesses, where apparently the bugs had gone to ground, so to speak. Two operations that day and the next to relieve the abscesses. She went to a nursing home to recover & was walking around, but then (as the inflammation from the surgery subsided) her head began to sag and she developed extremely severe back pain. We were referred to an orthopedic surgeon, who didn't want to do anything because of the aplastic anemia (her platelet count then was about 15K). They did not want to put her in an external brace because of the pain. Over many months, she was able to walk again. Still a lot of pain requiring lots of medication, but she could function reasonable well.

              In late 2004 she had another MRI, this one showing that T5 had collapsed to a triangular shape, causing an abrupt 90 degree bend forward. We were then referred to the neurosurgeon who said her spine should be stabilized because it was at a severe mechanical disadvantage that would cause more problems in time. So he installed the rods in June 2005. BTW, her platelets at the time were up to about 35K; dropped to maybe 15K after the last surgery, and are now up to about 75K.

              So what's happened has been a series of errors: Not recognizing the infection, not providing support for the portion of the spine that was damaged by the infection and the first surgery, and finally overcorrecting (or even trying to correct and not simply stabilize) the resulting kyphosis.

              - Richard

              Comment


              • #52
                Originally posted by rfbdorf
                Wise -
                The kyophosis had a 2 year history...
                In very early 2003 (at age 61), she got a staph infection at the entry site of a PICC line - she was getting ATG (antithymocyte globulin) for aplastic anemia. Oral antibiotics took care of it, so it was thought at the time. She complained to her hematologist of back pain; the response was "don't worry, my dear, joint pain is a normal side effect of the ATG, some of my patients have it much worse than you." A week later, she began to have difficulty controlling her legs, so I took her in to see him again, when he realized something was wrong. Xrays showed 2 spinal abscesses, where apparently the bugs had gone to ground, so to speak. Two operations that day and the next to relieve the abscesses. She went to a nursing home to recover & was walking around, but then (as the inflammation from the surgery subsided) her head began to sag and she developed extremely severe back pain. We were referred to an orthopedic surgeon, who didn't want to do anything because of the aplastic anemia (her platelet count then was about 15K). They did not want to put her in an external brace because of the pain. Over many months, she was able to walk again. Still a lot of pain requiring lots of medication, but she could function reasonable well.

                In late 2004 she had another MRI, this one showing that T5 had collapsed to a triangular shape, causing an abrupt 90 degree bend forward. We were then referred to the neurosurgeon who said her spine should be stabilized because it was at a severe mechanical disadvantage that would cause more problems in time. So he installed the rods in June 2005. BTW, her platelets at the time were up to about 35K; dropped to maybe 15K after the last surgery, and are now up to about 75K.

                So what's happened has been a series of errors: Not recognizing the infection, not providing support for the portion of the spine that was damaged by the infection and the first surgery, and finally overcorrecting (or even trying to correct and not simply stabilize) the resulting kyphosis.

                - Richard
                Richard,

                I am sorry that I didn't see your post in April. Another member had pointed me back to this thread and I just saw it.

                While I understand why they would not want to put in rods when the infection was still active, I am astonished that her surgeons did not correct the kyphosis shortly after its discovery in 2004 and did not do so until June 2005. I can undertand why surgeons are reluctant to operate when there is severe platelet deficiency but a 90% kyphosis is very serious problem. Correction of severe kyphoses is often associated with paraplegia The cord would have been draped around a sharp corner and adhesions may have developed over the 6 or more months. In the 1980's, I used to direct the spinal cord monitoring program at NYU and was involved in many orthopedic cases. This is the kind of case that our surgeons would have insisted on monitoring during the surgery. However, as I realized the complex details of what happened to your wife, several other thoughts come to mind.

                The fact that she had the kyphosis at T4-T6 may be significant for three reasons. First, the thoracic spine at that level has mostly white matter at that level and is relatively resistant to ischemia that develops over a period of time. Second, T6 is a common entry point for the artery of Adamkievicz, the main feeder artery from the aorta to the thoracic spinal cord. The artery may have been compromised during the surgery. Third, the fact that the surgeon placed a cage in first (to replace the collapsed vertebrae) meant that he probably did not have much choice regarding the degree of correction.

                Please give your wife a hug for me. She must be an absolutely amazing woman. What a horrendous three years she and you must have gone through, from the aplastic anemia, the severe back pain, the paraplegia, and the multiple thoracic surgeries! By the way, I have been spending a lot of time talking to hematologists recently (because I have been trying to set up facilities in China to process umbilical cord blood cells for transplantation in the ChinaSCINet trial) and aplastic anemia is a common problem in China.

                Wise.
                Last edited by Wise Young; 08-02-2006, 06:09 AM.

                Comment


                • #53
                  what about this conundrum?

                  dr. young-
                  try this on for size- I had a type 4 spinal av fistula on the anterior pial spinal cord, judt above the conus. Prolonged venous congestion caused T12 complete paraplegia. Today, I have gotten some minimal function back, like toe movement, thigh contraction, in bed I can weakly move my legs, can pedal without e-stim on a sit down bike ( it's more like a leg pusher, I push against one pedal, and the other comes forward ).
                  My spasticity is brutal, almost to the point of tearing my tendons on my right leg. So where does this leave me? I obviously have some existing connections, but if my injury was low on the spinal totem pole, then why do I have severe spasticity, with pockets of sensation?

                  Comment


                  • #54
                    Thanks for your reply and for the information, Wise.
                    I'll show her your post.
                    We had no idea that the op was so dangerous. Of course we realized there was some danger involved.
                    But anyway, it's water over the dam.
                    We're learning to live with it.
                    At least the ATG treatment seemed to do the job on the anemia - her platelets are now around 85K.
                    Best regards,
                    - Richard

                    Comment


                    • #55
                      Originally posted by rfbdorf
                      Thanks for your reply and for the information, Wise.
                      I'll show her your post.
                      We had no idea that the op was so dangerous. Of course we realized there was some danger involved.
                      But anyway, it's water over the dam.
                      We're learning to live with it.
                      At least the ATG treatment seemed to do the job on the anemia - her platelets are now around 85K.
                      Best regards,
                      - Richard
                      Richard, the 85K is good news. In the meantime, let us push forward with the spinal cord injury research to restore function. Wise.

                      Comment


                      • #56
                        Originally posted by damagedgoods
                        dr. young-
                        try this on for size- I had a type 4 spinal av fistula on the anterior pial spinal cord, judt above the conus. Prolonged venous congestion caused T12 complete paraplegia. Today, I have gotten some minimal function back, like toe movement, thigh contraction, in bed I can weakly move my legs, can pedal without e-stim on a sit down bike ( it's more like a leg pusher, I push against one pedal, and the other comes forward ).
                        My spasticity is brutal, almost to the point of tearing my tendons on my right leg. So where does this leave me? I obviously have some existing connections, but if my injury was low on the spinal totem pole, then why do I have severe spasticity, with pockets of sensation?
                        DG,

                        I am struck by your description of your spasticity. What is tells me clearly is that the motoneurons that are driving your spastic muscles are very much alive and kicking. The fact that you can weakly move your legs is also good news because it indicates that you have some descending connections. Parts of your lower spinal cord are intact. However, the severity of your spasticity is intriguing because it suggests that there is something stimulating your reflexes more than usual. There are solutions of course to the spasticity of limited muscle groups, including tendon lengthening (which takes the tension off the muscle and reduces its spasticity) or botox. But you really need a careful evaluation by an experienced clinician, to figure out what is going on and recommend specific solutions to get your legs to be more functional.

                        Wise.

                        Comment


                        • #57
                          I moved the posts by mortifier to /forum/showthread.php?t=89949

                          Wise.

                          Comment


                          • #58
                            Wise,

                            Comment


                            • #59
                              wise,
                              thank you so much for this info. i was diagnosed t6-7 complete after a motorcycle accident,but have had returns of sensation to almost my waist on my right side,and am at t8 on my left. this post has given me more understanding,and hope, than i've had in a long time? being a chronic complete-with the knowledge of how much force was required to dislocate and fracture my spine at this level,and it not being decompressed until 7 days after the incident my hopes were very low.

                              this has definitely helped my mood! thanks again for taking the time to give the detailed information, James.

                              Comment


                              • #60
                                Good to know

                                Originally posted by Wise Young
                                Diagnosis and Treatment of Thoracic Spinal Cord Injury
                                By Wise Young, Ph.D., M.D.
                                W. M. Keck Center for Collaborative Neuroscience
                                Rutgers University, Piscataway, New Jersey
                                http:sciwire.com, last updated 23 July 2005

                                Many people have been asking for an article about diagnosis and treatment of thoracic spinal cord injury. The following is a short description of upper and mid-thoracic spinal cord injury, emphasizing the anatomy, the neurology, treatment, recovery, and long-term changes, and hope for recovery and therapies.

                                Anatomy

                                The thoracic spinal cord is situated in the T1-T9 thoracic spinal canal. The thoracic vertebral segments form the chest wall and have ribs. The thoracic segments are the best protected of all the vertebral segments because of the ribs. It takes enormous forces to fracture the thoracic spinal vertebral bodies. Traumatic injuries of the upper thoracic spinal cord are relatively rare, accounting for only 10-15% of spinal cord injuries (compared to 40% due to cervical, 35% due to thoracolumbar injuries, and 5% due to lumbosacral injuries). Thoracic spinal cord injuries occur as a result of high-speed motor vehicular accidents, tumors that have compressed the spinal cord, and ischemic injuries of the spinal cord. When traumatic injuries of the thoracic spinal cord occur, they generally are severe and often result in complete loss of neurological function below the injury site.

                                Details of the anatomy are worthwhile noting. The C1 roots exit the spinal column just above the C1 vertebral body, that there is a C8 spinal segment but no C8 vertebral segment. The C8 root therefore exits the vertebral column between C7 and T1. The T1 root exits the spinal column below T1. The thoracic spinal roots form the intercostal nerves (nerves that run on the underside of the ribs). Although many clinicians say and believe mistakenly that the thoracic segments do not have a significant motor component and that all they control are the intercostal muscles for breathing, this is not true. As it turns out, the thoracic segments control muscles that attach to the ribs (which include the abdominal muscles, as well as most of the back muscles).

                                Neurology

                                Injury to the thoracic spinal cord causes paraplegia, or loss of motor and sensory function in the lower half of the body. Because the thoracic cord is situated some distance from the brain and lumbar cord, sensory and motor axons have a long ways to regenerate before they can restore function. Nevertheless, substantial sensory and motor recovery occurs in a majority of people with mid-thoracic injuries, even those with initially "complete" spinal cord injury. For example, recovery of 4-6 dermatomes of sensory function and upper trunk/abdominal muscles is common. Diagnosis of spinal cord injury usually is based on sensory examination. The axillary (armpit) region is T2, the nipples T4, the bottom of the rib cage is T8, the umbilicus (belly button) is T10, and the suprapubic region is T12.

                                The cervical segments innervate superficial trunk muscles such as the scapula and the latissimus dorsi. Multiple overlapping thoracic segments innervate most deeper trunk muscles. Injury to the thoracic spinal cord will cause partial paralysis of deeper trunk muscles such as the cervicis (T1-5), splenius (T3-T6), erector spinae and iliocostalis (T6-12), spinalis (T1-9), semispinalis, transversospinal, and segmental (T1-12) muscles. The thoracic segments and upper lumbar segments innervate the abdominal muscles including the rectus abdominus (T4-L3), external oblique (T6-L3), transverse abdominis (T9-L3), and internal oblique (T12-L3). The posterior oblique (T6-10) and the anterior oblique (T4-8) muscles attach to the lower and upper thoracic ribs respectively. In general, muscles above the belly button are innervated by T5-T11 while muscles below the belly button are innervated by T12 and L1.

                                Causes of Injury

                                Decompression of the thoracic spinal cord often requires surgery because traction alone often cannot reposition the thoracic vertebral segments. Because surgery on the thoracic spinal column usually requires the opening of the thoracic cavity, decompression of thoracic spinal cord injury may be delayed by many hours, days, or even weeks after injury. Continued compression of the spinal cord contributes to the damage. In my opinion, delays in decompressing the spinal cord contribute to neurological loss in thoracic spinal cord injuries. Compression of the spinal cord causes ischemia or loss of blood flow to the spinal cord. Pressure on the spinal cord exceeding blood pressure will reduce or stop blood flow to the spinal cord. Continued compression for many hours, days, or even weeks is likely to cause further damage to the spinal cord.

                                The thoracic spinal cord is vulnerable to ischemic injuries. In humans, the artery of Adamkiewicz is a major source of blood to the thoracic spinal cord and usually enters the spinal cord at T6. Compromise of this artery by traumatic aortic aneurysms, for example, can cause an infarct of the thoracic spinal cord. Arteriovenous malformations (AVM) often occur in the thoracic spinal cord. AVM's cause ischemia by "stealing" blood from the capillaries and increasing venous pressure. Finally, tumors of the spinal cord often occur in the thoracic spinal cord and they compress the cord, reducing blood flow. Ischemic injuries to the spinal cord may outnumber traumatic spinal cord injuries.

                                Treatment

                                The first goal of treating thoracic spinal cord injury is protection of the spinal cord. This includes treatment with high-dose methylprednisolone if the treatment can be started within 8 hours after injury. If there is continuing compression of the spinal cord, the spinal cord should be decompressed. It may be necessary to open the thoracic cavity to approach the thoracic spinal column from the front. In the United States, such surgery usually involve a thoracic surgeon as well as a spinal surgeon, and the surgery may be delayed until the patient is stable and major surgery can be scheduled. In lower thoracic spinal cord injuries, it is often possible to straighten out and stabilize the spinal column from the back, using posterior rods and screws. Care must be taken to evaluate the screws and whether or not they impinge on the spinal cord and roots.

                                Thoracic spinal cord injury disconnects the lower thoracic and lumbosacral spinal cord from the brain. While paraplegia (paralysis of the lower limbs) is the most obvious outcome of spinal cord injury, loss of sacral functions including bowel and bladder function are the most troublesome and a major cause of death before the 1970's. With the advent of antibiotics and intermittent catheterization, as well as better emergency care, most people with thoracic spinal cord injuries today survive their injuries and can live close to normal lifespan. Because the injury does not involve the lumbar and sacral spinal cord, lumbosacral reflexes are usually preserved and spasticity is frequently present. Thus, people with thoracic spinal cord injuries are good candidates for regenerative therapies aimed regrowing descending motor axons from the injury site to the lumbosacral segments or ascending sensory axons from the injury site to the brain.

                                Recovery

                                Most clinicians tend to be quite pessimistic about recovery from thoracic spinal cord injury. Part of this may be because most people with thoracic spinal cord injury were involved in severe high-speed motor vehicular accidents and prolonged compressions of the spinal cord. In the past, many clinicians often did not even decompress thoracic spinal cords. This has changed in recent years as many studies, particularly the work of Bohlman, et al. at Case Western University, have reported that decompressing thoracic spinal cords even up to 3 years after injury may result in some functional improvement in patients. Up to 80% of the patients got better from such decompressive surgery and only 10% got worse. Most had reduction of pain after the surgery.

                                Part of the pessimism associated with thoracic spinal cord injury derives from inadequate neurological examination of patients with thoracic spinal cord injuries. Many clinicians examine only the legs and not the trunk or abdominal muscles or thoracic sensory levels. In my experience, most people with thoracic spinal cord injuries regain 4 or more dermatomes below the initial injury level. For example, a person with a T4 injury (sensory level at the nipples) often regains back the T8 (bottom of the rib cage) or even T10 (umbilicus) dermatomes. Likewise, they often get back upper abdominal muscles representing T5-11. Although many patients with T2-T5 injuries show improved trunk control over several years after injury and many can even stand with bilateral knee-ankle-foot orthoses and a walker, suggesting that they have regained some hip control, these are often not credited as recovery of function. Individuals with T6-T12 injuries often recover lower abdominal muscles and may be able to ambulate short distances. Some with T9-T12 injuries become household walkers (Source).

                                Long-term Changes

                                White matter (myelinated axons) normally occupies over 90% of the thoracic spinal cord. About half of the axons are ascending sensory fibers from dorsal root ganglia sensory neurons situated just outside the spinal cord and the remainder come from neurons in the lower spinal cord. The rest are descending motor axons that come from brain, brainstem, and cervical spinal cord. Thoracic spinal cord injury interrupts most of these axons. The parts of axons that have been separated from their cell bodies will die. The neurons from which the axons come do not die and the neurons that they contact usually survive. Nevertheless, there is often substantial atrophy of the spinal cord at and around the injury site. This is natural and not something to be worried about.

                                Routine MRI and x-rays of the spinal cord and spine are important for people with thoracic spinal cord injury. In children, thoracic spinal cord injuries frequently lead to scoliosis. In older patients, there are progressive changes in the vertebral bodies that may need to be surgically corrected to prevent deformities or compression of the cord. Particularly if the spinal cord is not decompressed, adhesive scars may form between the spinal cord and the surrounding arachnoid/dura mater at the injury site. Such adhesions may interrupt cerebrospinal fluid flow between the upper and lower spinal cord. In such cases, syringomyelic cysts may develop. These are enlargements of the central canal in the spinal cord, usually a thin and barely detectable canal in the middle of the cord. Due to shunting of cerebrospinal fluid into central canal, the canal enlarges and may compress the cord.

                                Reasons for Hope

                                As pointed out above, people with thoracic spinal cord injury are good candidates for regenerative therapies in clinical trials. A number of recent clinical trials have chosen to focus on people with upper and midthoracic spinal cord injuries. For example, the Proneuron trial that transplanted activated macrophages and the Purdue trial that applied alternating electrical currents chose to focus on patients with thoracic spinal cord injuries. Many clinical investigators focus on thoracic spinal cord injuries for the following reasons. First, because of the pessimism surrounding recovery from thoracic spinal cord injury, any recovery of the lower limbs would be generally perceived as being a positive effect of therapy. Second, because the thoracic spinal cord is considered to be less crucial to body functions, any complications that might cause ascent of lesion level would not be as devastating. Third, the lumbosacral spinal cord is intact and therefore should be available to receive connections from regenerating axons from above.

                                People with thoracic spinal cord injuries have much reason to be hopeful. They will probably be among the first to benefit from experimental regenerative therapies of the spinal cord. Because their lumbosacral spinal cords are intact, they should have some atrophy and should not have as much muscle atrophy. Regenerative therapies alone should be sufficient to restore substantial function in many people with thoracic spinal cord injury. The regeneration distances for descending axons to travel from the thoracic spinal cord to the lumbosacral cord are shorter than from the cervical spinal cord. Many will recover trunk function and even proximal hip function without experimental therapies and hence can more easily engage in weight-supported ambulation training, swimming, and other exercises that can maintain bone and muscle.

                                Summary

                                Thoracic spinal cord injuries represent only 10-15% of people with spinal cord injuries. Because the ribs protect the thoracic segments, most thoracic spinal cord injuries are a result of high-speed motor vehicular accidents, aggravated by continued compression of the spinal cord. Perhaps because most thoracic spinal cord injuries are severe and frequently are not decompressed until late, clinicians tend to be pessimistic about the outcome of thoracic spinal cord injuries. However, most people with upper thoracic spinal cord injury do recover at least 4 dermatomes, improved trunk control, and upper abdomen muscles after the injury. Some with mid-thoracic injuries may recover proximal muscles of the legs. Because the lumbosacral spinal cord remains intact, most people with thoracic spinal cord injuries retain reflexes and spasticity in the lower limbs. Clinical trials of regenerative and other cell transplant therapies often focus on patients with thoracic spinal cord injuries because an ascent of lesion level typically is not as devastating as for cervical levels. Thus, people with thoracic spinal cord injury are likely to be amongst the first to benefit from experimental regenerative therapies of the spinal cord.

                                Reply

                                Good to know
                                by Christopher Rodrigues


                                My brother had an motor vehicular accident as a result of which he suffered a major spinal cord injury. The doctors said that he was a case of Monoplaegia . We had arranged for a physio - Therapist who Helped him get control of his legs quite quickly, However the right leg does'nt seem to be all that strong. The ankle does'nt seem to lift that well resulting in poor movement. He does work out 6 days a week trying to strenghten his leg which has lost a lot of muscle mass. This article has made me aware of a lot of things and would like more information or infact your tips on further therapy.
                                Thanks

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