Non-traumatic intracranial hemorrhage. Seizures. Follow-up. There is symmetric, diffuse cortical diffusion restriction involving both cerebral hemispheres. This is associated with increased cortical T1 and T2 FLAIR signal. The increased cortical T1 signal may reflect early laminar necrosis. There is also diffusion restriction diffusely involving the corpus callosum and the corticospinal tracks, the later best seen at the level of the internal capsules and cerebral peduncles, which is probably either from acute Wallerian degeneration secondary to the cortical injury. The deep gray nuclei and the cerebellum are fairly preserved. There is no brain herniation.There are bilateral subdural effusions that are more FLAIR hyperintense to the intraventricular CSF overlying both cerebral convexities, with a maximum thickness of 6 mm. More T1-hyperintense subdural effusions are present in the posterior fossa. There is only mild apparent mass-effect on the underlying brain. There are foci of susceptibility artifact reflecting the presence of blood products within the subarachnoid and subdural spaces. This is most pronounced in the subarachnoid spaces near the vertex and the subdural collections in the posterior fossa. There is no definite intraparenchymal hemorrhage. There are thin multifocal subgaleal effusions. Major intracranial vascular flow voids are preserved. There are secretions along the posterior pharyngeal wall.
1.Diffuse cerebral cortical diffusion restriction is most compatible with severe, global anoxic injury. The deep gray nuclei and the cerebellum are spared.2.Diffusion restriction along the cortical spinal tracts and corpus callosum is most likely reflective of acute Wallerian degeneration secondary to the severe cortical injury.3.Small subdural collections are present over both cerebral and both cerebellar convexities. There are blood products within the subarachnoid space and the subdural collections as described above.