34 years, Male, Reason: s/p TBI in 2002. Now with behavior changes History: mood instability, anger out burst. Several sequences are motion degraded. There are multiple scattered foci of susceptibility related to hemosiderin in the brain at the gray-white junction as well as at the cortical surface consistent with traumatic brain injury. Chronic hemosiderin deposition is relatively more prominent along the surface of the left inferior frontal and left temporal lobes as well as the superior parietal lobules. There is extensive encephalomalacia involving the left anterior temporal lobe as well as the left temporal lobe laterally along the left middle and inferior temporal gyri. There is also encephalomalacia involving the left superior parietal lobule. There is also small area of gliosis evident involving the right superior parietal lobule also likely related to prior trauma. Linear T2 signal abnormality with surrounding gliosis involving the right superior frontal gyrus may be related to prior ventriculostomy or ICP monitoring device.There is no intracranial mass or mass effect. No acute infarct. No extra-axial collections. No midline shift or herniation. There are areas of ex vacuo dilatation of the lateral ventricles. There is also multifocal thinning of the corpus callosum which may be related to Wallerian degeneration and/or traumatic injury. No hydrocephalus. There is polypoid mucosal thickening involving the bilateral maxillary sinuses. Evidence of prior left frontotemporal craniotomy.
Multifocal encephalomalacia and chronic hemorrhage consistent with chronic traumatic brain injury. Findings are relatively more prominent in the left temporal and left parietal lobes as described above.