Clinical question: Evaluate for ischemia, etiology of LUE stiffening, shaking. Signs and symptoms: LUE stiffening and shaking. Nonenhanced brain MRI:Negative diffusion weighted series.Examination demonstrate multiple small foci of T2/FLAIR hyperintensity in the subcortical and periventricular white matter of cerebral hemispheres and pons and with normal signal intensity of brain parenchyma otherwise on all MRI sequences. One of the foci of FLAIR hyperintensity is in the left precentral gyrus (axial flair series 701 image 28). Although the findings are nonspecific this appearance is more suggestive of chronic small vessel ischemic strokes however possibility of other white matter lesions and including demyelinating disease cannot be entirely excluded.Unremarkable cerebral cortex, cortical sulci, ventricular system, CSF spaces and brain myelination otherwise.Unremarkable images through the orbits, paranasal sinuses and mastoid air cells.Nonenhanced cervical MRI:The alignment of vertebral column is anatomical however there is mild reversal of cervical lordosis secondary to advanced disc disease and loss of disc height at C5-C6 level.Foramen magnum is unremarkable.C2-C3 is unremarkable.C3-C4 demonstrate mild degenerative/hypertrophic changes of posterior elements with mild left neural foraminal compromise and unremarkable otherwise.C4-C5 demonstrate mild degenerative changes and unremarkable otherwise.C5-C6 demonstrate advanced disc disease with near complete loss of disc height, moderate bilateral ligamentum flavum and mild facet hypertrophic changes. There is a hypertrophic spur traversing the entire transverse axis of the spinal canal at this level which results in effacement of subarachnoid space, flattening and posterior displacement of the cord and moderate central spinal stenosis and moderate bilateral neural foraminal compromise. Examination is degraded due to motion artifact and several sagittal T2 and T2 STIR series were repeated. On repeat sequences there is evidence of a large focus of T2/T2 STIR hyperintensity within the cord and extending from approximately C4-C5 disc level inferiorly to C6-C7 disc level and consistent with myelitis secondary to degenerative disease.C6-C7 demonstrate mild degenerative changes without spinal stenosis or neural foraminal compromise.C7-T1 is unremarkable.Upper most visualized thoracic spine and thoracic cord to T4 level is unremarkable.
1.Nonenhanced brain MRI demonstrate no acute intracranial process. Several small foci of FLAIR hyperintensity primarily in the subcortical/periventricular white matter (and including the lesion in the left precentral gyrus) and pons are noted. Findings are nonspecific however considering patient's stated age chronic small vessel ischemic strokes of mild degree should be considered. Less likely possibility of other white matter diseases and including demyelinating disease cannot be entirely excluded. Please see above comments.2.Nonenhanced MRI of cervical spine demonstrate advanced disc disease, loss of disc height and hypertrophic changes of posterior elements at C5-C6 with resultant moderate central spinal stenosis and bilateral neural foraminal compromise. There is increased T2 signal intensity of the cord extending from C4-C5 disc level to approximately C6-C7 disc level concerning for myelitis secondary to degenerative disease. No spinal stenosis or significant neural foraminal compromise at other levels however please review detailed report per level above.