Clearance of perivascular wastes in the brain may be critical to the pathogenesis of amyloidopathies. Enlarged perivascular spaces (ePVS) on MRI have also been associated with amyloidopathies, suggesting that there may be a mechanistic link between ePVS and impaired clearance. Sleep and traumatic brain injury (TBI) both modulate clearance of amyloid-beta through glymphatic function. Therefore, we sought to evaluate the relationship between sleep, TBI, and ePVS on brain MRI. A retrospective study was performed in individuals with overnight polysomnography and 3T brain MRI consented from a single site ( n = 38). Thirteen of these individuals had a medically confirmed history of TBI. ePVS were visually assessed by blinded experimenters and analyzed in conjunction with sleep metrics and TBI status. Overall, individuals with shorter total sleep time had significantly higher ePVS burden. Furthermore, individuals with TBI showed a stronger relationship between sleep and ePVS compared to the non-TBI group. These results support the hypothesis that ePVS may be modulated by sleep and TBI, and may have implications for the role of the glymphatic system in ePVS.

Immune checkpoint inhibitors are increasingly used in treatment of metastatic renal cell carcinoma, melanoma, and nonsmall cell lung cancer, as well as in clinical trials for novel targets. We present a pediatric patient with metastatic alveolar soft part sarcoma who was treated with MPDL3280 (Atezolizumab), a monoclonal anti-programmed death ligand-1 antibody. Imaging results for the patient suggested disease progression of multiple brain metastases with stable systemic disease. The patient met response evaluation criteria in solid tumors (RECIST) criteria of progression of disease and was removed from treatment with MPDL3280. Subsequent surgical resection of the brain lesions revealed nonviable tumor with extensive lymphocytic infiltrates consistent with pseudoprogression. This case report adds to a growing number of reports that question reliance on RECIST criteria and suggest need for further refinement of RECIST or irRECIST during immune checkpoint inhibitor treatment for central nervous system metastatic lesions.

Ectopy of the thymus is a rare anomaly arising during fetal development, where the thymus does not make a complete decent into the thoracic cavity where it should involute in adolescence. The most common complications of an ectopic thymus include tracheal or esophageal compression presenting in childhood. This is a report of a single case of ectopic cervical thymus identified in a 2-month-old infant presenting with Horner's syndrome. Thymic ectopy should be on the differential when performing a radiologic evaluation of a neck mass when imaging characteristics are similar to thymic tissue.

The purpose of this study was to characterize an observation that the most severe lumbar stenosis is often displaced from the disc. Methods: A retrospective magnetic resonance (MRI) review of displacement and causes of lumbar canal stenosis, was undertaken. Lumbar MRIs (n=3000) were reviewed for stenosis defined as a canal diameter of ≤8 mm. Displacement of maximal stenosis from the disc was measured; measurements inferior to the disc were assigned negative values. Defined causes were; ligamentous hypertrophy, facet hypertrophy, lipomatosis, spondylolisthesis, synovial cyst, or adjacent segment disease. Results: Lumbar stenosis levels (n=1,042) identified in 749 patients were; L1-2 (3.8%), L2-3 (20.1%), L3-4 (35.3%), L4-5 (37.7%), and L5-S1 (3.2%). Of these levels 20.8% were attributed to facet hypertrophy, 29.8% ligamentous hypertrophy, 31.1% epidural lipomatosis, 11.2% spondylolisthesis, 5.6% adjacent segment disease, and 1.5% synovial cyst. Mean displacement stenosis (mm) was; synovial cyst (-0.3; range 7 to -5), epidural lipomatosis, (-1.1; 5 to -13), ligamentous hypertrophy (-3.5; 5 to -13); facet hypertrophy (-3.9; 7 to -11), adjacent segment disease (-4.7; 7 to -11), and spondylolisthesis (-4.9; 11 to -12). Sub-group analysis revealed a predominantly negative displacement for spondylolisthesis, adjacent segment disease, facet hypertrophy, and ligamentous hypertrophy. Conclusion: The site of maximal lumbar stenosis is at or near the center of the disc with lipomatosis or synovial cyst, but significantly inferiorly displaced when ligamentous or facet hypertrophy, spondylolisthesis, or adjacent segment disease is the major cause. Lipomatosis as a cause of stenosis is more common than previously reported.