[MRI symptomatology of non-tumoral myelopathies]

We present a retrospective study in order to analyze the abnormalities noted on MRI in 27 cases of myelopathy excluding tumors, explored between 1994 and 1996. The different lesions were: Multiple Sclerosis (n = 11), Spondylotic myelopathy (n = 3), Neurosarcoidosis (n = 4), CMV Myelitis (n = 1), Radiation Myelopathy (n = 1), Spinal Dural Arteriovenous Fistula (n = 1), Intramedullary Cysticercosis (n = 1), Infarct (n = 5). The exams have been made on 1.5 Tesla Magnetom Vision Siemens or GE Signa machine. All patients have had axial and sagittal views with coronal complementary study in 4 cases. Sequences were Spin echo pT1 (TR: 560, TE: 12), Fast Spin echo pT2 (TR: 3 500, TE: 99 or 128), and gradient echo pT2 (TR: 700, TE: 22, Angle: 25 degrees). Intravenous injection of Gadolinium has been made in 16 cases (0.1 mmol/kg). We have studied the presence or not of a signal abnormality in pT1 and/or in pT2, of enhancement, and its topography (cervical, thoracic, lumbar). We classified lesions in central and/or peripheral and according, to their topography in anterior, posterior or lateral type. The form has been classified in four types (nodular, triangular, "pen like", plage). Extension in transversal (superior or inferior to half medullary surface) and cranio-caudal directions (inferior to one vertebrae, between one and two vertebrae, superior to two vertebrae) has been also classified. Others intra or perimedullar and encephalic abnormalities have been noted. We analyzed the results for each pathology and underline the essential diagnosis criteria noted (low cranio-caudal and transversal extension with frequent triangular form of Multiple Sclerosis lesions, frequent suggestive abnormalities of the encephale (82%) in Multiple Sclerosis, intra and perimedullar enhancement with deformations of the surface of the spinal cord in Sarcoidosis' lesions, extended dorsolumbar "pen like" lesions with inconstant enhancement of infarcts, focal plage lesions centered on degenerative changes of the spinal canal in spondylotic myelopathy, bony lipomatous involution in front of intramedullary radiation plage lesion...) and also review the literature and confront their results to it. We insist on the difficulties in classifying myelopathy (radio-clinical terminology discordances, identical signal abnormalities frequently caused by different illness, necessity to compare to pathologic results). We propose a MRI study protocol that should interest the whole spinal cord and comport T1 weighted without and after gadolinium sequences, T2 weighted sequences (with always a gradient echo type). 2 or better 3 different plans should be made. A complementary study of the brain by MRI is often useful. Clinical study, biology, evolution, MRI and when possible pathology all are necessary to better understand myelopathy's mechanisms.