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Focal signal abnormalities at the depth of the cerebellar fissures in children have been reported and hypothesized to represent a novel pattern of bottom-of-fissure dysplasia. The authors report a series of 23 patients with a similar distribution and appearance of cerebellar signal abnormality attributable to watershed injury. T2 prolongation was observed at the depths of the cerebellar fissures bilaterally in all 23 patients, centered at the expected location of the deep cerebellar vascular borderzone. Diffusion restriction was associated with MR imaging performed during acute injury in 13/16 patients. Five of 23 patients had prior imaging, all demonstrating a normal cerebellum. The etiology of injury was hypoxic-ischemic injury in 17/23 patients, posterior reversible encephalopathy syndrome in 3/23 patients, and indeterminate in 3/23 patients.

Initial MRIs from 50 subjects with diffuse intrinsic pontine gliomas recruited for a prospective clinical trial before treatment were analyzed. Retrospective imaging analyses included FLAIR/T2 tumor volume, tumor volume enhancing, the presence of cyst and/or necrosis, median, mean, mode, skewness, kurtosis of ADC tumor volume based on FLAIR, and enhancement at baseline. Molecular subgroups based on EGFR and MGMT mutations were established. Histone mutations were also determined (H3F3A, HIST1H3B, HIST1H3C). Enhancing tumor volume was near-significantly different across molecular subgroups, after accounting for the false discovery rate. Tumor volume enhancing, median, mode, skewness, and kurtosis ADC T2-FLAIR/T2 were significantly different between patients with H3F3A and HIST1H3B/C mutations.