Leukodystrophy and epilepsy. Assess progression of brain involvement. Bilateral subdural effusions over the cerebral convexities have increased in size mildly. They have a maximum thickness of 13 mm on the right and 11 mm on left, compared to 6 mm and 8 mm previously. As before, the fluid is T2 bright, similar to CSF, and T1 hyperintense to CSF. The underlying prominent subarachnoid spaces as well as the ventricles are slightly smaller than previously though remain abnormally enlarged. There is no susceptibility effect in either the subdural or subarachnoid spaces. The confluent, T1-hypointense, T2/FLAIR-hyperintense signal involving the deep and periventricular cerebral white-matter is slightly less prominent. However, this apparent improvement may reflect evolution of the white-matter injury and white matter volume loss rather than an improvement in the disease process. There continues to be signal abnormality in the subinsular white-matter but relative sparing of the subcortical U fibers otherwise. T2-hyperintensity along the corticospinal tracts extending into the posterior aspect of the posterior limb of the internal capsules is unchanged. There is also abnormal T2-hyperintensity in the corpus callosum. Striated T2-hyperintensity in the pons is unchanged. Confluent T2-hyperintensity involving the deep cerebellar white-matter has slightly increased since the previous examination.Brain parenchymal volume loss continues to be symmetric other than being slightly more pronounced in the frontal and temporal lobes. The degree of volume loss has perhaps slightly increased from the prior examination.There is mild, smooth dural contrast enhancement and thickening, likely reactive to the effusions. There is no abnormal intracranial contrast enhancement otherwise. No acute infarct is seen. There is no mass or mass-effect. The major cerebral flow voids are intact. The posterior pituitary bright spot is absent. The orbits, skull, and scalp soft tissues are grossly unremarkable. Fluid signal is present posterior ethmoid and right maxillary sinuses as well as the mastoid air cells. There are also secretions in the posterior aspect of the pharynx along nasogastric and endotracheal tubes.
1.Since the previous examination of November 2015, there has been evolution of the brain parenchymal (predominantly white-matter) injury. Though the cerebral T2-hyperintense white-matter lesions appear less prominent and less discrete, associated volume loss is suspected to have mildly progressed since the previous examination. At the same time, the cerebellar white-matter T2-hyperintense abnormality has mildly increased. 2.The bilateral cerebral convexity subdural collections have slightly increased in size, which may reflect passive dilatation due to progressive underlying brain volume loss. The lack of susceptibility effect within the collections suggests that they may represent nonhemorrhagic effusions, though chronic subdural hematoma remains in the differential.