 Examination is again limited by lack of intravenous contrast. Redemonstrated is diffuse destruction and replacement of the L1-2 disc space, destruction of the adjacent endplates, and significant collapse of the L1 greater than L2 vertebral bodies. There is no significant change in residual abnormal T2/STIR hyperintensity involving the bone marrow and intervertebral disc. The degree of moderate retropulsion appears similar at the L1 level with unchanged moderate spinal canal stenosis and bilateral L1-L2 foraminal stenosis. No other worrisome marrow signal is appreciated. Again seen are areas of T1 and T2 hypointensity involving the right greater than left psoas musculature which are again seen and not significantly changed compared to 4/1/2015; these correspond to sites of previously seen abscesses and may represent areas of cavitation/necrosis. No discrete fluid collections to suggest abscess. More extensive diffuse STIR hyperintensity in the iliopsoas and paraspinous musculature similar to prior and compatible with combination of atrophy and edema. The lumbar spine is otherwise in stable alignment. The vertebral body and disc heights are otherwise unchanged. The distal spinal cord and conus are within normal limits with the conus terminating at the L1 level. The previously described degenerative changes appear similar. Again noted is prominence of the epidural fat including focal epidural fat along the right lateral aspect of the thecal sac at the L3-4 level. Partially imaged are bilateral renal atrophy with innumerable microcysts. There is clumped appearance of the cauda equina nerve roots suggestive of arachnoiditis and present previously.
1. Lack of contrast again limits evaluation. Compared to 6/3/2015 and 5/6/2015, there is no significant change in residual signal abnormalities related to L1-L2 discitis-osteomyelitis. Please note imaging findings often lag behind clinical response and do not necessarily imply residual discitis-osteomyelitis. No worsening marrow or disc signal abnormalities to suggest progression of infection. 2. No significant change in compression fractures of the L1 greater than L2 vertebral bodies. No significant change in osseous retropulsion at L1 with associated moderate spinal canal stenosis as well as moderate to severe bilateral L1-L2 neural foraminal stenosis. 3. Extensive signal abnormality involving the iliopsoas and paraspinous musculature as described above compatible with combination of atrophy and edema. No convincing evidence of residual abscess. No new fluid collections.