Male, 16 years old, with weakness. Assess for transverse myelitis. Patchy, discontiguous ventral spinal cord T2 hyperintensity is redemonstrated beginning at approximately C3 and continuing down to the T1 level. These lesions are limited to the superficial ventral aspect of the spinal cord involving no more than the anterior one third of cord transverse area. No significant interval change is seen in the transverse or craniocaudal extent of this abnormality. The affected region of the spinal cord demonstrates volume loss compatible with chronicity.No additional or new areas of spinal cord signal abnormal are seen. No evidence of pathologic spinal cord or leptomeningeal enhancement is seen. Diffusion-weighted imaging is degraded in portions of the cervical and thoracic spine, but no definite diffusion restriction is seen. No epidural abnormalities are suspected.The cervical lordosis is straightened, but spinal alignment is otherwise unremarkable. Vertebral body height and morphology are within normal limits. No areas of concerning marrow replacement or pathologic marrow enhancement are seen. The intervertebral discs are preserved with no significant bulging or herniation. The spinal canal and neural foramina remain patent.
Again seen is a region of specifically ventral spinal cord signal abnormality spanning from approximately C3 down to T1 showing no significant interval change from the prior examination. This abnormality demonstrates features of chronicity including spinal cord volume loss and lack of enhancement.The differential diagnosis for this finding is broad and would include sequelae of prior viral myelitis as well as a postinfectious autoimmune process. Similar features can also be seen in demyelinating disease such as neuromyelitis optic. The possibility of spinal cord ischemia should also be considered, though this would be a somewhat atypical imaging presentation. Neoplastic etiologies are felt to be unlikely.