60 yo M with h/o AML with relapsed disease now with lower worsening back pain x 1 month after recent BM bx on L posterior iliac. Five lumbar type vertebral bodies are presumed to be present which are appropriate in overall height. The conus medullaris on sagittal imaging is grossly intact. In general the marrow signal is low diffusely.At L5-S1 there is anterior subluxation of L5 on S1 associated with elongation of the AP dimension of the spinal canal, disc desiccation, uncovering of the disc and narrowing of the neural foramina bilaterally. L5 is subluxed approximately 16 mm anteriorly relative to S1.There is T2 signal hyperintensity present in the adjacent vertebral bodies and some mild enhancement of the tissue surrounding the S1 segment and of the L5-S1 disc space. There is ligamentum flavum hypertrophy present at this level There is encroachment of the exiting nerve roots bilaterally within the neural foramina at this level and narrowing of the width of the spinal canal resulting in an element of spinal stenosis from left to right. At L4-5 there is no significant compromise to neural foramina. There is a disc bulge present at this level as well as bilateral facet hypertrophy there is narrowing of the spinal canal and partial effacement of the fat at the lateral recesses at this level with associated mild-to-moderate spinal stenosis.At L3-4 there is no significant compromise to spinal canal or neural foramina. There is a disc bulge present at this level as well as bilateral facet hypertrophy which is worse on the right compared to the left.At L2-3 there is no significant compromise to spinal canal or neural foramina.At L1-2 there is no significant compromise to spinal canal or neural foramina.
1.There is a spondylolysis with spondylolisthesis present at L5-S1 associated bilateral neural foramen encroachment and spinal canal stenosis. L5 is subluxed approximately 16 mm anteriorly relative to S1. There are associated inflammatory type change at this level.2.There is mild to moderate spinal stenosis at L4-5 related to facet hypertrophy and to a lesser degree disc bulge.3.There is diffuse marrow replacement present which is a nonspecific finding. Given the patient's history of AML this is the most likely cause.