Female, 2 years old, with history of hydrocephalus and VP shunt presenting with new onset seizures. A right parietal approach ventricular shunt catheter is in place with its tip to the left of midline at the level of the lateral ventricular body with tenting of the septum pellucidum.Since the prior examinations, there has been a significant reduction in the caliber of the ventricular system. The transfrontal diameter in the coronal plane now measures 42 mm and previously measured 76 mm. The third and fourth ventricles are also substantially decreased in size. The lateral ventricular margins are wavy and distorted.FLAIR hyperintense and T1 isointense subdural fluid collections have developed along both cerebral hemispheres, particularly in the left frontal region, and to a lesser extent along the tentorium. There may also be some component of diffuse dural thickening. There is no susceptibility effect or T1 hyperintensity to be seen within these collections.The cerebral hemispheres are diffusely dysmorphic compatible with long-standing hydrocephalus. The genu of the corpus callosum and adjacent cingulate gyri are deformed and demonstrate abnormal T2 hyperintense signal. A focus of abnormal T2 hyperintense signal is also seen in the left periventricular white matter. No evidence of restricted diffusion is seen to suggest acute ischemia.The cerebral hemispheres demonstrate reduced volume and a generalized loss of white matter. Myelination has progressed compared to the prior exam. The corpus callosum is diffusely thinned. The pituitary region is unremarkable. The posterior fossa structures are within normal limits.
1.Significant interval decrease in caliber of the shunted ventricular system.2.Interval development of bilateral subdural collections which are favored to reflect nonhemorrhagic, proteinaceous effusions probably secondary to relief of hydrocephalus and subsequent brain retraction.3.Sequelae of long-standing hydrocephalus are seen including parenchymal deformity and loss of white matter volume. 4.Deformity and signal abnormality affecting the genu of the corpus callosum and the adjacent cingulate gyri may represent chronic injury related to traction or perhaps a remote ischemic insult.