Female, 77 years old, history of lower extremity weakness, pain, fecal incontinence. Brain:Patchy periventricular T2 hyperintensity is identified, a nonspecific finding which likely reflects chronic microvascular ischemic disease. No evidence of restricted diffusion is seen to suggest acute ischemia.No parenchymal edema or mass effect is detected. No pathologic parenchymal or extra-axial enhancement is seen.There is no evidence to indicate significant intracranial hemorrhage or any abnormal extra-axial fluid. The ventricular system is within normal limits for size.Lumbar:Fluid-filled defects are evident running through both sacral ala most compatible with fracturing. The soft tissues and marrow surrounding the defects demonstrate pronounced enhancement. On the left, there is a fluid component with rim enhancement which projects from the defect into the posterior paraspinal soft tissues.No abnormal marrow signal or pathologic enhancement is demonstrated within the midline aspects of the sacrum. The sacrum is truncated at the S3 level. There appears to be a small ventrally angulated bony fragment below the S3 level which is suggestive of a prior distal sacral fracture. The presacral soft tissues demonstrate marked edema with strandy enhancement, but no discrete or rim-enhancing collections are seen.Spinal alignment is otherwise unremarkable. The remaining vertebral bodies demonstrate normal signal intensity and morphology allowing for scattered intraosseous hemangiomas.The visualized spinal cord, conus and cauda equina are unremarkable.L1-2: Unremarkable. L2-3: Unremarkable. L3-4: Facet hypertrophy and ligamentum flavum thickening. Mild bulging disc. No significant generalized spinal canal stenosis. No significant neuroforaminal narrowing. L4-5: Severe facet hypertrophy and ligamentum flavum thickening. Mild bulging disc. Moderate generalized spinal canal stenosis, particularly in the transverse dimension. Severe bilateral foraminal narrowing. L5-S1: Severe facet hypertrophy. No significant spinal canal stenosis. No significant neuroforaminal narrowing.
1.Bilateral fluid-filled defects in the sacral ala likely represent insufficiency fractures. The presence of enhancement within and along the fracture margins could simply be the result of reparative granulation which would indicate a subacute time course. Likewise, the presence of fluid within the defects, and projecting into the posterior soft tissues on the left, could represent inflammatory reaction. The possibility of superinfection is not excluded, though, and correlation with clinical and laboratory parameters is suggested. If a better anatomic assessment of the bony deformity is desired, further imaging with CT can be considered.2.Presacral soft tissue edema is also seen without evidence of any discrete rim-enhancing collections. As above, this may reflect a reactive process, but the precise nature of this inflammation is uncertain.3.Evidence to suggest a prior chronic distal sacral fracture.4.Degenerative findings most pronounced at L4-5 where posterior element hypertrophy results in a moderate spinal canal stenosis and significant bilateral foraminal narrowing.5.Apart from chronic microvascular ischemic disease, no significant intracranial abnormalities are detected.