I was diagnosed with Transverse Myeitis about 7 weeks ago. I am a level T9. I have recovered from an original T8. I also have slight movement (inches) in my right hip flexor on an friction free surface. I am 42 y.o.
The Drs. dont know what caused the swelling in my spine, I am not an injury and no virus was confirmed. They also can not give me any guess on return. If anyone here ( Dr, Nurse, member) can shed some light on this it would be appreciated.
Can spinal cord swelling cause permanent damage? What about when the swelling goes away? I am getting another MRI in a week. If the cord is all black in the MRI does that mean it is dead and this is permanent?
I am still on high dose Prednisone 70mg reducing 10mg per week. Was on 1000mg/day at onset and the 4 days after. Had one dose of Chemo (Cytoxan SP) and may have one more each month for five months.
10-27-2002, 12:13 AM
JD37, as you know from perusing the internet and talking to doctors, the cause of transverse myelitis (TM) is not well understood. In some cases, it may be due to inflammation of the blood vessels and subsequent occlusion and ischemia (loss of blood flow). There is also a theory that TM may be due to auto-immune mechanisms. For example, TM is sometimes associated with lupus erythematosis and another condition called anti-phospholipide syndrome (see below). Your prednisolone treatment should address all these. In your case, you are getting cytoxan as well. As you know already, it is sometimes associated with viruses such as cytomegalovirus but you indicate that virus has been ruled out.
Recovery is difficult to predict. Some people recover substantially while others do not. Because TM is a relatively rare phenomenon, there have not been sufficient study of the condition to yield prognosticators of recovery. In any case, know that substantial recovery can occur but there are no guarantees.
Finally, regarding the MRI appearance of your spinal cord, there should not be all "black" on your MRI. You must be looking at a section of the MRI that did not show the spinal cord. You should review the MRI with your neurologist the next time. Get him/her to point out the spinal cord to you. If anything, there should be increased signal (brighter) in the area where the TM has occurred (Scotti, et al, 2001).
• Durrani OM, Gordon C and Murray PI (2002). Primary anti-phospholipid antibody syndrome (APS): current concepts. Surv Ophthalmol. 47 (3): 215-38. Summary: Primary anti-phospholipid syndrome (APS) is a thrombophilic state characterized by recurrent arterial and venous thrombosis, recurrent pregnancy loss, and the presence of circulating anti-phospholipid antibodies that may be responsible for thrombophilia and pregnancy morbidity. Ophthalmologic features are present in 15-88% of the patients with primary APS, thus ophthalmologists are one of the first physicians to whom the patient will present. An accurate diagnosis may save the patient from recurrent, potentially life-threatening thrombosis. In the U.S.A., an estimated 35,000 new cases of APS-related venous thrombosis occur each year in a population that is several decades younger than the patient population typically affected by thrombosis. Clinical features, such as chorea, transverse myelitis, cardiac valvular lesions, and accelerated atherosclerosis, are hypothesized to be due to a direct tissue-antibody interaction and cannot be explained purely by thrombosis. The use of recently proposed, well-defined diagnostic criteria, and better standardization of laboratory assays for the anti-phospholipid antibodies should help enable epidemiological surveys to establish the prevalence of these antibodies in patients with thrombosis and in the general population. Diagnosis of APS should be considered in all patients with recurrent systemic or ocular thrombosis in the absence of known risk factors. Several well-designed prospective studies show an increased risk of thrombosis in the presence of medium to high antibody level. With ocular involvement in as many as 88% of APS patients, an ophthalmic assessment should be an integral part of the clinical work-up of any patient with suspected or confirmed APS. The presence of isolated ocular thrombophilia with persistently elevated anti-phospholipid antibodies or lupus coagulant should confirm the diagnosis of APS. Management of these patients must be a multi-disciplinary effort with either a rheumatologist or a hematologist having the overall responsibility for coordinating treatment and monitoring the patient's immune status and anticoagulation. Treatment of isolated ocular thrombophilia in the presence of moderate to high titers of antiphospholipid antibodies should be on the same principles as patients with APS to prevent recurrent ocular or cerebral thrombosis. Academic Unit of Ophthalmology, University of Birmingham, Birmingham, United Kingdom.
• Kerr DA and Ayetey H (2002). Immunopathogenesis of acute transverse myelitis. Curr Opin Neurol. 15 (3): 339-47. Summary: 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. Department of Neurology, School of Medicine, Johns Hopkins University, Pathology 627 C, 6000 N Wolfe Street, Baltimore, MD 21287-6965, USA. email@example.com.
• Maschke M, Kastrup O and Diener HC (2002). CNS manifestations of cytomegalovirus infections: diagnosis and treatment. CNS Drugs. 16 (5): 303-15. Summary: Cytomegalovirus (CMV) infection of the CNS occurs most commonly in patients with severe immunosuppression such as those with advanced HIV infection (i.e. AIDS) or those who have undergone bone marrow or solid organ transplantation. Immunocompetent patients are affected very rarely. The infection of the CNS may affect the brain (diffuse encephalitis, ventriculoencephalitis, cerebral mass lesions) or the spinal cord (transverse myelitis, polyradiculomyelitis). Diagnosis is very difficult and should be based on clinical presentation, results of imaging and virological markers. The most specific diagnostic tool is the detection of CMV DNA by polymerase chain reaction in the CSF. Treatment should be initiated promptly if CMV infection is suspected. Antiviral therapy consists of intravenous ganciclovir, intravenous foscarnet or a combination of both. Cidofovir is the treatment of second choice. Patients who experience clinical improvement or stabilisation during induction therapy should be given maintenance therapy. After immune reconstitution (in HIV-positive patients) or discontinuation of immunosuppressive therapy (in transplant recipients), maintenance therapy may be stopped. Despite therapy, the prognosis for long-term survival is very poor, especially in patients with AIDS. Department of Neurology, University Clinic of Essen, Germany. firstname.lastname@example.org.
• Scotti G and Gerevini S (2001). Diagnosis and differential diagnosis of acute transverse myelopathy. The role of neuroradiological investigations and review of the literature. Neurol Sci. 22 Suppl 2: S69-73. Summary: Acute transverse myelopathy (ATM) is a clinical definition of an acute neurologic condition that reflects impairment of spinal cord function. The term "myelopathy" has a different meaning from "myelitis", even if the words are often confused. Both terms indicate spinal cord involvement by some pathological event; but while myelopathy does not imply any etiological factor, myelitis refers to inflammatory diseases of the spinal cord. Acute spinal pathology can be associated with intra-axial or extra-axial lesions; extra-axial spinal pathology, however, has more often a chronic and progressive presentation. In this paper, we discuss primarily intra-axial lesions with attention on the role of neuroradiological investigations in diagnosis and differential diagnosis. Magnetic resonance imaging is the modality of choice for diagnosis; it shows signal abnormalities, usually T2 hyperintensity, focal or extensive, gadolinium enhancement and sometimes cord swelling. Despite its high sensitivity, about 40% of acute transverse myelopathies remain undemonstrated. Concerning etiology (multiple sclerosis (MS), vasculitis, infection, autoimmune disorders) no clearly different and specific patterns have been found; however small multiple enhancing lesions are more suggestive of MS (or lupus) while extensive, multilevel abnormalities reflect vasculitis as in antiphospholipid antibody syndrome. Department of Neuroradiology, Scientific Institute H.S. Raffaele, Milan, Italy.
10-27-2002, 11:19 AM
JD37, I got TM 10 years ago at age 37, I am a t-9,10 complete. I am still having small neurological changes. I know it is frustrating, but no one can predict your recovery with any great accuracy. Any questions e-mail me.
Jeff C Holtan
Thanks for the replys. I did not mean to imply that an MRI showed a black spinal cord. I am having a followup MRI within the next week and was concerend about it. I read somewhere that a black section indicates it is "dead".
Funny you should mention APS. I was diagnosed with anti-phospholipid syndrome in 1999 after a DVT incident. The Drs. could not attribute the TM to the APS. They said it looked like a Lupus incident but coulnn't confirm that either.
If the MRI shows that the spinal swelling has reduced but I have no notable returm what can I infer from that? Blood tests show a normal SED rate. I am told that this indicates no inflamation in my system and could mean the swelling is gone. If the swelling is gone does that mean I have nerve damage?
10-27-2002, 09:02 PM
JD, the above is an excellent site for more information on TM. I also suggest joining the TM Internet Club list (TMIC). Instructions are in the additional web sites at the above URL.
Courage doesn't always roar. Sometimes courage is the quiet voice at the end of the day saying, "I will try again tomorrow."