Wise Young
04-14-2004, 04:32 PM
tmman posted in Acute spinal cord injury experiences (http://carecure.org/forum/showpost.php?p=235121):
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.
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.