Male, 51 years old, with increased lower extremity reflexes, and fluctuating abnormality the brain of uncertain etiology, in the context of lung cancer. C-spine:Image quality is degraded by motion artifact but diagnostic information is still obtained.Alignment is anatomic. Vertebral body morphology is unremarkable. A focus of T2 hyperintensity within the C7 vertebral body is nonspecific.Given the limitations as above, no definite spinal cord abnormality is seen.C2-3: Minimal posterior disk osteophyte formation. No significant spinal canal stenosis or neuroforaminal narrowing.C3-4: Posterior disk osteophyte formation with a superimposed central extrusion and no significant cord impingement or generalized spinal canal stenosis. Mild/moderate left foraminal narrowing. C4-5: Unremarkable. C5-6: Minimal left paracentral protrusion. No significant spinal cord impingement or spinal canal stenosis. Mild left foraminal narrowing. C6-7: Unremarkable. C7-T1: Minimal posterior disk osteophyte formation. No significant spinal canal stenosis or neuroforaminal narrowing.T-spine:Alignment is anatomic. Vertebral body morphology is within normal limits. Small T2 hyperintense foci within the T4 and T7 vertebral bodies are nonspecific. Ill-defined T2 hyperintensity within the right anterior aspect of the T9 vertebral body is of uncertain significance.Visualized spinal cord shows normal morphology and signal characteristics allowing for motion artifact.A right upper lobe lung mass is seen.L-spine:Transitional morphology of the L5 vertebral body is seen. The lumbar vertebrae otherwise show normal morphology. A small T2 hyperintense focus within the L3 vertebral body is nonspecific.The visualized conus and cauda equina are unremarkable given the limitations of motion degradation.At L4-5, a disk bulge is present, asymmetric to the left, with resultant moderate narrowing of the spinal canal. Both neural foramina show mild to moderate narrowing.The remaining lumbar intervertebral disks are preserved with no additional areas of spinal canal or neuroforaminal stenosis.MRS:On limited anatomic images of the brain, T2 hyperintensity and edema has progressed within the left paramedian parietal lobe, affecting the cingulate gyrus as well as the splenium and part of the body of the corpus callosum.Single voxel spectroscopic assessment of this abnormal tissue was performed, along with contralateral normal appearing tissue, at multiple TEs. Cho, Cr and NAA peaks are proportionately decreased relative to normal, as is myoinositol, a glial cell marker. Notable lipid peaks are evident on short TE sequences, but no significant lactate is seen.
1. Relatively mild degenerative findings in the spine which would not adequately account for the patient's symptoms.2. Scattered areas of signal abnormality are seen within the spinal vertebrae as described above. These lesions are nonspecific and largely nonaggressive in appearance. Given the patient's history, and without the benefit of IV contrast, the possibility of metastatic disease cannot be entirely excluded, though it is not highly suspected at this point.3. Limited anatomic imaging of the brain shows progression of a lesion involving the paramedian left parietal lobe as well as the corpus callosum. Spectroscopic assessment of this lesion reveals a fairly proportionate reduction in the major brain metabolic peaks, indicating loss of both neural and glial elements. The presence of lipid is compatible with cellular degeneration. Absence of lactate would argue against a primary ischemic etiology. Overall, the spectroscopic pattern is most suggestive of a non-neoplastic inflammatory, metabolic or autoimmune phenomenon. An infectious or post infectious process may be considered, as well as a paraneoplastic encephalitis.