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-Barré 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-Barré syndrome. CONCLUSION: IATM may be caused by a small vessel vasculopathy. MR findings in IATM also occasionally are similar to those described in Guillain-Barré syndrome and suggest a possible relationship.
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-Barré 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-Barré syndrome. CONCLUSION: IATM may be caused by a small vessel vasculopathy. MR findings in IATM also occasionally are similar to those described in Guillain-Barré syndrome and suggest a possible relationship.