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Thread: Transverse myelitis - frightened

  1. #1

    Transverse myelitis - frightened

    tmman posted in Acute spinal cord injury experiences:
    I'm new here so i don't know if this is the right place to post. I'm a 53 year old man that came down with transverse myelitis in January of this year. My rehab experience was as good as can be expected but I was and still am very frightened. I hate the way I am and despise being in a wheelchair. I'm having a very difficult time coping with this disease that I had never even heard of before I got sick. Does anyone else here suffer from TM and what has your experience been. Thanks for your help in advance
    tmman, transverse myelitis is indeed a frightening condition because it strikes suddenly and the cause (in most cases) are still largely unknown. I can't pretend to be in your shoes (although others might be able to share their experiences... the reason why I have set up a different topic for this discussion) but I have found the following approach to be useful.

    To reduce fear of the condition, knowlege often helps. Because it is a relatively rare disease, most doctors don't know much about it. Therefore, you must become an expert in your own condition, not only to interpret what is said to you and whether it fits with available knowledge but also what needs to be done. Knowledge also helps you anticipate problems and devise solutions for them rather than be surprised and frightened. You need to know what is known and what is not known.

    You should prioritize what you can do and leave what you can't do or won't be able to do immediately until later. This way, you don't spend unnecessary energy agonizing about things that you can't or won't do anything about and focus on what would help.

    1. Causes. The first priority is to rule out known causes of the condition and to determine if there is any treatment that would be needed to prevent further episodes (Krishnan, et al., 2004). Known causes of transverse myelitis include autoimmune diseases (Kerr & Ayetey, 2002) such as systemic lupus erythematosus (SLE), rheumatoid arthritis, viral or parasitic infections, and other potential causes of inflammation of the vascular system. Sometimes transverse myelitis is mistakend for ischemia of the spinal cord (less of blood flow) due to arterioclerosis. Occasionally, it may be associated with cartilaginous embolization of the cord. I assume that you have had an MRI and tests for general and specific inflammatory conditions such as SLE and rheumatoid arthritis. If your MRI suggests vascular problems such as enlarged veings, a arteriogram should be considered (injection of dye into the arterial system and x-rays to determine whether you any arteriovenous malformations. A recent study suggestst aht recurrent transverse myelitis may be associated with anti-Ro (SSA) autoantibodies and this should be tested for. Any potential causes of transverse myelitis should be identified and treated. About a third of people who have transverse myeltis do not have an identifiable cause, i.e. idiopathic (Harzheim, et al, 2004). Idiopathic transverse myelitis that recur have certain features (Kim, 2003) and MRI presentation (Tartaglino, et al. 1996; Choi, et al., 1996).

    2. Recovery. Like spinal cord injury, transverse myelitis may result in complete or incomplete loss of neurological function below the given spinal cord level. If you have some preserved neurological function below the level, the likelihood of further recovery in the coming months and even years is high. Some recovery from transverse myelitis is the rule rather than the exception. However, transverse myelitis produce many of the symptoms and deficits that are associated with spinal cord injury, including loss of motor and sensory function, loss of autonomic functions (such as bowel, bladder, sweating, and temperature control). Some people get neuropathic pain after transverse myelitis. In rehabilitation, they should have taught you all the techniques for taking care of these systems.

    3. Solutions. Many of the solutions for transverse myelitis are the same as those for spinal cord injury. On this site, there are many postings concerning almost every complication of spinal cord injury and various solutions that people and therapists have developed. You should know how to avoid urinary tract infections, what the options are for neuropathic pain if you have it, and how to prevent decubiti (pressure sores) and other problems.

    4. Hope. Understand that there is much research going that will be useful for reversing the effects of transverse myelitis, including therapies that may be able to regenerate, remyelinate, and repair the spinal cord. These include stem and other cell transplants, drugs and factors that regenerate and remyelinate the spinal cord, as well as anti-inflammatory and anti-immune approaches.

    I hope that this is helpful. Please do not hesitate to ask. I know that there are other people on this site with transverse myelitis and perhaps they can describe their experiences.

    Wise.

    • Kerr DA and Ayetey H (2002). Immunopathogenesis of acute transverse myelitis. Curr Opin Neurol. 15: 339-47. Department of Neurology, School of Medicine, Johns Hopkins University, Pathology 627 C, 6000 N Wolfe Street, Baltimore, MD 21287-6965, USA. dkerr@jhmi.edu. Acute transverse myelitis is a group of disorders characterized by focal inflammation of the spinal cord and resultant neural injury. Acute transverse myelitis may be an isolated entity or may occur in the context of multifocal or even multisystemic disease. It is clear that the pathological substrate--injury and dysfunction of neural cells within the spinal cord--may be caused by a variety of immunological mechanisms. For example, in acute transverse myelitis associated with systemic disease (i.e. systemic lupus erythematosus or sarcoidosis), a vasculitic or granulomatous process can often be identified. In idiopathic acute transverse myelitis, there is an intraparenchymal or perivascular cellular influx into the spinal cord, resulting in the breakdown of the blood-brain barrier and variable demyelination and neuronal injury. There are several critical questions that must be answered before we truly understand acute transverse myelitis: (1) What are the various triggers for the inflammatory process that induces neural injury in the spinal cord? (2) What are the cellular and humoral factors that induce this neural injury? and (3) Is there a way to modulate the inflammatory response in order to improve patient outcome? Although much remains to be elucidated about the causes of acute transverse myelitis, tantalizing clues as to the potential immunopathogenic mechanisms in acute transverse myelitis and related inflammatory disorders of the spinal cord have recently emerged. It is the purpose of this review to illustrate recent discoveries that shed light on this topic, relying when necessary on data from related diseases such as acute disseminated encephalomyelitis, Guillain-Barre syndrome and neuromyelitis optica. Developing a further understanding of how the immune system induces neural injury will depend upon confirmation and extension of these findings and will require multicenter collaborative efforts.

    • Hummers LK, Krishnan C, Casciola-Rosen L, Rosen A, Morris S, Mahoney JA, Kerr DA and Wigley FM (2004). Recurrent transverse myelitis associates with anti-Ro (SSA) autoantibodies. Neurology. 62: 147-9. Department of Medicine, Johns Hopkins University, Baltimore, MD 21224, USA. lhummers@jhmi.edu. Transverse myelitis (TM) is an idiopathic inflammatory disorder of the spinal cord. The authors observed cases of recurrent TM in patients where anti-Ro (SSA) antibodies were present and therefore performed a case-control study to examine the frequency of anti-Ro autoantibodies in patients with recurrent TM and control subjects. Antibodies to 52-kd Ro were demonstrated in 77% of cases (10/13) compared with only 33% of control subjects (4/12).

    • Kim KK (2003). Idiopathic recurrent transverse myelitis. Arch Neurol. 60: 1290-4. Department of Neurology, University of Ulsan College of Medicine, Asan Medical Center, Songpa-gu, Seoul, South Korea. kkkim@amc.seoul.kr. OBJECTIVE: To determine whether idiopathic recurrent transverse myelitis (RTM) can be distinguished from multiple sclerosis-associated RTM (MSRTM) on the basis of clinical manifestations of myelopathy, or findings from magentic resonance imaging or cerebrospinal fluid examination. DESIGN: A retrospective analysis of 37 cases was conducted. Patients were classified as having idiopathic RTM on the basis of recurrent myelitis confirmed by clinical manifestations of myelopathy and magnetic resonance imaging findings. On review patients with idiopathic RTM had normal cranial magnetic resonance imagings and did not demonstrate paraclinical evidence of spatial dissemination beyond the spinal cord of the disease process. Patients were classified as having MSRTM on the basis of criteria of Poser et al for clinically definite multiple sclerosis involving the central nervous system. Fifteen patients met study criteria for idiopathic RTM. Twenty-two patients had MSRTM. SETTING: Asan Medical Center, Seoul, South Korea, from January 1, 1992, through December 31, 2001. MAIN OUTCOME MEASURES: Presenting symptoms and clinical manifestations, relapsing times, magnetic resonance imaging features (involved spinal cord segments in T2-weighted images and gadolinium 64-enhanced lesions on T1-weighted images), IgG index, and oligoclonal bands in cerebrospinal fluid were compared. RESULT: Idiopathic RTM occurred preponderantly in male patients and presented more often with acute transverse myelitis than did MSRTM. More than 2 relapses occurred in 6 cases (40%) of idiopathic RTM. The involved segments of spinal cord on T2-weighted images were not significantly different in idiopathic RTM and MSRTM, with enhancing lesions mostly in the posterior columns, and the spinothalamic and spinocerebellar tracts of white matter. Additionally, almost all patients with idiopathic RTM had normal cerebrospinal fluid indexes. CONCLUSION: Idiopathic RTM might be a disease entity distinct from MSRTM, differing in its male preponderance, absence of oligoclonal bands, frequent multiple relapses, and frequent presentation as acute transverse myelitis.

    • Krishnan C, Kaplin AI, Deshpande DM, Pardo CA and Kerr DA (2004). Transverse Myelitis: pathogenesis, diagnosis and treatment. Front Biosci. 9: 1483-99. Department of Neurology, Johns Hopkins Transverse Myelitis Center, 600 N. Wolfe Street Pathology 627C, Baltimore MD 21287-6965, USA. ckrishn1@jhmi.edu. Transverse Myelitis (TM) is a clinical syndrome in which an immune-mediated process causes neural injury to the spinal cord, resulting in varying degrees of weakness, sensory alterations and autonomic dysfunction. TM may exist as part of a multi-focal CNS disease (e.g. MS), multi-systemic disease (e.g. systemic lupus erythematosus), or as an isolated, idiopathic entity. In this article, we will summarize recent classification and diagnostic schemes (1), which provide a framework for the acute management of patients with TM. Additionally, we will review current concepts on the natural history, immunopathogenesis and treatment strategies for patients with TM.

    • Choi KH, Lee KS, Chung SO, Park JM, Kim YJ, Kim HS and Shinn KS (1996). Idiopathic transverse myelitis: MR characteristics. AJNR Am J Neuroradiol. 17: 1151-60. Department of Radiology, Kangman St Mary's Hospital, Catholic University Medical College, Seocho-Ku, Seoul, Korea. PURPOSE: To describe the MR characteristics that can distinguish idiopathic transverse myelitis from other intramedullary lesions. METHODS: A total of 32 initial and follow-up MR studies in 17 patients with clinically proved transverse myelitis were reviewed retrospectively. The location, size, pattern, and segmental length of areas of hyperintensity were estimated on T2-weighted axial and sagittal images. In 15 of the patients, whose neurologic abnormalities were limited to the spinal cord, the location and pattern of intramedullary contrast enhancement were evaluated on sagittal and axial T1-weighted images. Follow-up MR studies were available for 10 patients. The statistical significance of cord enhancement between the groups with and without cord expansion was calculated. RESULTS: Common MR findings of idiopathic transverse myelitis included a centrally located hyperintensity occupying more than two thirds of the cross-sectional area of the cord (88%); a length of 3 to 4 vertebral segments (53%), with variable presence of cord expansion (47%); a small central area of intensity, isointense with normal cord, in the core of hyperintensity (47%); focal, peripheral cord enhancement (53%), particularly in patients with cord expansion; and a slow regression of T2 hyperintensity with an enhancing nodule. Although no linear correspondence was observed between MR findings and neurologic signs and symptoms, all but 4 patients improved clinically as MR findings improved or remained stable. CONCLUSIONS: MR findings are helpful in detecting transverse myelitis and in differentiating this entity from multiple sclerosis and cord tumors, but clinical assessment and observation of MR changes over time are essential in making the diagnosis.

    • Tartaglino LM, Croul SE, Flanders AE, Sweeney JD, Schwartzman RJ, Liem M and Amer A (1996). Idiopathic acute transverse myelitis: MR imaging findings. Radiology. 201: 661-9. Department of Radiology, Thomas Jefferson University Hospital, Philadelphia, PA 19107, USA. PURPOSE: To analyze the magnetic resonance (MR) imaging findings in idiopathic acute transverse myelitis (IATM) in relation to pathologic findings and MR findings in Guillain-Barre syndrome and ischemia. MATERIALS AND METHODS: The cases of 19 patients with IATM seen over a 4-year period were retrospectively reviewed. Clinical parameters and laboratory test findings were recorded for each patient independently of the MR findings. RESULTS: Ten (53%) patients experienced upper respiratory infection or vaccination within 4 weeks of symptom onset. The majority (82%) of cases occurred between December and May each year. In seven of 12 patients who underwent electromyography and nerve conduction examinations, evidence of peripheral nerve injury was seen. On T2-weighted axial images, 13 of 18 lesions were depicted with holocord abnormal signal intensity, seven (39%) had gray matter involvement similar to that seen in spinal cord ischemia, and three (16%) had isolated white matter involvement. Enhancement patterns varied. In three (17%) of the 18 lesions, enhancement in the cauda equina was similar to that seen in Guillain-Barre syndrome. CONCLUSION: IATM may be caused by a small vessel vasculopathy. MR findings in IATM also occasionally are similar to those described in Guillain-Barre syndrome and suggest a possible relationship.

  2. #2
    Senior Member lynnifer's Avatar
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    Originally posted by tmman:

    Thanks for your support. i felt like I had the flu for a couple of days then I went to bed one night with aches and pains in my legs and woke the next morning a paraplegic. It's awful. Have you gotten used to it?
    Depends on your definition of 'used to it.'

    Have I made the best of things? Yes.
    Do I still wake up every day and think this can't be happening to me? Yes!

    Find my TM story here: http://carecure.org/forum/showpost.php?p=178877

    In keeping informed, there is a symposium in Baltimore sometime this August (19th-22nd I think?) ... 1) I couldn't afford to go at $300 US and 2) I can't get the time off work anyway ... but I would suggest to you that going might arm you with some information. At least it's near the east coast - maybe make a vacation out of it? After 19yrs, I attended two seminars on current SCI therapies and found them very informative - I felt renewed hope.

    If I had any advice to give you, it would be to keep exercising. Keep moving your legs - even if it's passive - try aquatherapy - stay limber. This seems to be key and if I had it to do over again, that is what I would do.

  3. #3
    Guest
    Thanks Lynnifer and Doctor Wise.
    Lynnifer I will read your story and look foward to learning from it.

    Dr. Wise I am one of the ones where they can't figure out what caused it. i have no sensation or movement at this point from the t10 level down.

    again thank you both very much

  4. #4
    Guest
    The quick treatment for tranverse Myelitis is IVIg you can check
    more at www.cidpusa.org

    IVIG can be uses in nearly all types of Tranverse Myelitis.

    Ik

  5. #5
    Super Moderator Sue Pendleton's Avatar
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    I hate to say I prefer to be an ostrich when it comes to this forum. I prefer believing that our "club" is growing at a snail's pace instead of leaps and bounds.

    Lynn, I thought your injury was traumatic for some reason. Sorry you couldn't make the symposium. I live 30 miles away and missed it due to a flare up of, well, IBS. Such thrills. I think the next one is in 2006 and planned for Seattle. I won't swear to it but I think it was in a recent newsletter. Do you belong to the TMA? If so maybe a nearby support group can start raising funds now to make it a group thing? Might mention it to doctors in the field in your area too. That's half the battle. The symposiums are to teach docs how to diagnose and treat TM versus all the other things it could be.

    Tmman, sorry to hear you've joined the club. At least you found the right place for good information. Someone else has probably hooked you to www.myelitis.org/ by now. Definitely sign up. Great information in the newsletters, news of where the nearest support groups and chapters are and, hey, it's free!

    As Wise said, unless you live near Johns Hopkins or the Mayo Clinic in Minnesota, you better learn a lot about your particular form of TM. What you describe sounds classic. Feel fluish for a few days and then once well for a few days to a few weeks the rug gets pulled out from under you. This is what makes finding a cause for TM so difficult. By the time you can't move there is no virus in your spinal fluid to identify what made you sick. In most cases where someone has felt sick and remembers it the likely hood of recurrent TM drops dramatically.

    Were you treated with steroids or had your blood plasma run through a machine? The window for treating TM is much longer than the 8 hours normally outlined for treating SCI. After a few days if the steroids don't seem to work a new therapy is to do plasmaphresis (run your blood plasma through a filter). Did anyone tell you to buy a medical dictionary? You can normally find one on the web so save your money.

    I had a spinal stroke but it took the docs about 3 days to decide on that over TM. My husband mentioned hayfever symptoms I had had for several days. We have a lot in common though. As for CIDP, like Gilliam-Barre Syndrome I believe it mainly attacks peripheral nerves and begins at the feet and goes upward. TM and strokes tend to travel downward. TM does have one characteristic I do not envy. Those who seem to recover the most movement also suffer through long term daily pain. I know very few SCIs who are prescribed Marinol for pain while quite a few TM folks are either toking legal marajuana or taking the prescription artificial equivalent Marinol. In an unofficial poll during a TM symposium most Marinol users said that they were able to function better on pot. It seems Marinol makes many too high while dealing with the pain. Not that the rest of us get off painfree either. I just think with most of us it comes and goes. With some though it is everyday and nasty.

    There is a great deal of hope for those with TM as Dr Young said. Between research on SCI, non-traumatic injuries such as TM, stroke, tumors, etc and what The Myelin Project contributes by studying leukodystophies there are treatments in the pipeline. 4-aminopyridine works for some and can be prescribed by your doctor and made up by a compounding pharmacy. If you have any feeling or reflex at the lowest sacral level (anal area) look through clinicaltrials.gov to see if you can get in on the trial of HP-184.

    For now, try to move the different muscles each day and exercise the ones you do have. Keep your upper body strength or, better, improve it. File for SSDI if an American or the equivalent in other countries. You may not need it for long but if you do might as well get the paperwork over with now. Depending on circumstances and what your rehab doc says you might prefer a scooter to a chair. Just don't get one of those cheap things on your own. Proper seating and posture will definitely help maintain your independence and avoid pressure sores.

    Good luck!

    Courage doesn't always roar. Sometimes courage is the quiet voice at the end of the day saying, "I will try again tomorrow."

  6. #6
    Sue,

    Thank you so much for your kind note. Yes I did have the plasmaferesis and steroids with no improvement. I am functioning as a complete paraplegic and have begun to accept my situation and now realize I will most likely spend the rest of my life in a chair.

    Once again thanks for your kind response.

    TM

  7. #7
    Since you're only spinal cord injured 6 months, received steroids and plasmapheresis, please don't get complacent. Work hard hard hard at strengthening. I'm not sure if TM results in spinal shock like traumatic sci does but I know a TM victim on this forum that is still getting return over 2 years later. With traumatic sci it seems like the 6-month point is when return peaks but it keeps coming pretty good for another year and a half in my experience.

    So work work work. Good luck-
    Betheny

    "...I mean the wheelchair would be a thing in the past
    And us quads can talk about the past and laugh"-Professirx
    http://unite2fightparalysis.org/

  8. #8
    Thanks Beth. My illness was actually January 2004 not 2005. I haven't gotten any return yet but am still trying. I've read a lot about you on these boards and I just want to say you are quite a lady and an inspiration to all of us.

  9. #9
    Senior Member lynnifer's Avatar
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    Quote Originally Posted by Sue Pendleton
    As for CIDP, like Gilliam-Barre Syndrome I believe it mainly attacks peripheral nerves and begins at the feet and goes upward. TM and strokes tend to travel downward.

    Extremely odd! I specifically remember mine starting at the toes and coming up until it stopped at my waist.. clear as a bell I remember that.
    Roses are red. Tacos are enjoyable. Don't blame immigrants, because you're unemployable.

    T-11 Flaccid Paraplegic due to TM July 1985 @ age 12

  10. #10
    Super Moderator Sue Pendleton's Avatar
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    Quote Originally Posted by lynnifer
    Extremely odd! I specifically remember mine starting at the toes and coming up until it stopped at my waist.. clear as a bell I remember that.

    Lynn, I don't think anything is 100% with the non-traumatic types of paralysis. With me the last thing to go was breathing. I distinctly remember still being able to wiggle my left toes and foot a bit while everyone was freaking that I was turning blue around the lips. The MRI pegs me as a C4-5 and most of the damage was on my right side. Today I consider myself, functionally, a C5-7 incomplete because I have full triceps on the left but only two-thirds on the right arm. All I can think of was the first pain was in the elbow bends which is C5 if I remember right. So the ability to breath stuck around as most of the damage from lack of oxygen to the cord went downward. But as we all know now there is secondary damage and I think this is where I lost my ability to breath on my own for that first week. The methylprednisolone is what most likely stopped permenant damage to my C4 and above cord levels.

    I remember speaking also with Cody Unser's mom Shelley and she said Codey's problem began in her legs. The ER sent her home with a UTI diagnosis and in the morning she was paralyzed from the waist or so downward.

    This is why the symposiums are so important for ER docs and neurologists who may not have gotten a good idea of how to diagnose TM versus the other atraumatic causes of paralysis. At the Baltimore symposium in 2001 I met a doctor from India who woke to a full bladder and could not go. He went to his hospital, cathed himself and then hit the library to diagnosis himself. He got it right with ATM and I believe he used methylprednisolone on himself. If not it was IVIG. The more I think about it the more I think he used IVIG. But his lumbar puncture and MRI all said TM. He was walking well with a regular cane when he was in Baltimore. He was very surprised to know how many of us there are with atraumatic cord syndromes.
    Courage doesn't always roar. Sometimes courage is the quiet voice at the end of the day saying, "I will try again tomorrow."

    Disclaimer: Answers, suggestions, and/or comments do not constitute medical advice expressed or implied and are based solely on my experiences as a SCI patient. Please consult your attending physician for medical advise and treatment. In the event of a medical emergency please call 911.

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