 There are are non-enhancing densely calcified globular and irregular extra-axial lesions along the planum sphenoidale and sella, as well as along the left petrous apex. There are also calcified globular lesions in the left temporal lobe and left basal ganglia, measuring up. In addition, there are patchy susceptibility effect and T1 hyperintensity diffusely within the bilateral lenticular nuclei. Furthermore, there are gyriform calcifications in the right temporal lobe. There are also scattered foci of susceptibility effect in the bilateral cerebral hemispheres. There are postoperative findings related to frontal craniotomy with encephalomalacia in the bilateral anterior frontal lobe with ex vacuo dilatation of the frontal horns of the bilateral lateral ventricles. There is also volume loss of the bilateral prechiasmatic optic nerves. There is diffuse cerebellar volume loss. There is a right frontal linear T2 high signal tracking to the right lateral ventricle related to a previous ventriculostomy tract. There is no evidence of acute infarction. There are no enhancing intracranial lesions.
1. Apparent postoperative findings related to remote frontal craniotomy with encephalomalacia and susceptibility effect corresponding to calcifications in the bilateral anterior frontal lobes, as well as atrophy of the bilateral optic nerves. 2. Densely calcified extra-axial lesions along the planum sphenoidale and sella, as well as along the left petrous apex, may represent dystrophic calcifications from prior hemorrhage or radiation therapy if this were indeed administered, versus calcifying pseudotumors of the neuraxis or related to treated neoplasm, perhaps originally a craniopharyngioma, for example. 3. Densely calcified globular lesions in the left temporal lobe and left basal ganglia, as well as multiple punctate scattered foci of susceptibility effect in the bilateral cerebral hemispheres may represent treated tumors, chronic hemorrhages, and/or cavernous malformations. 4. Patchy mineralization present diffusely within the bilateral lenticular nuclei may represent dystrophic calcifications related to treatment effects, such as mineralizing microangiopathy, or an underlying metabolic disorder.5. Gyriform calcifications in the right temporal lobe with underlying white matter hypoattenuation may represent sequela of prior trauma or infarction. 6. Diffuse cerebellar volume loss is likely related to anti-epileptic use.