Diagnosis: Unspecified convulsionsClinical question: Please evaluate for etiology (embolic etc) of seizuresSigns and Symptoms: Seizures MRI of the brainThere are small foci of diffusion restriction present along the right and left superior and middle frontal gyri bilaterally . Additional punctate foci of diffusion restriction are present in the parietal lobes and right periventricular white matter. The distribution is somewhat watershed. The ADC map abnormality is larger than the diffusion-weighted imaging abnormality for these lesions.Temporal horns of the lateral ventricles are large.There is a mild to moderate degree of periventricular and subcortical punctate hyperintense white matter lesions present identified on the FLAIR and T2 images. Compared to the prior exam there are a few more on the current exam than on the prior.A punctate foci of T2 hyperintensity scattered in the cerebellar hemispheres bilaterally which were also present on the prior exam and do not appear to have changed substantially. Similarly punctate T2 hyperintense foci in the basal ganglia are also stable.On susceptibility imaging there are multiple punctate foci of signal loss in the subcortical white matter.Normal vascular flow voids are present in the distal carotid and vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus.The visualized portions of the paranasal sinuses demonstrate mucosal thickening in the right maxillary sinus with near complete opacification as well as scattered opacities in the ethmoid air cells, mucosal thickening in the sphenoid sinus and an air-fluid level in the left sphenoid sinus. The visualized portions of the mastoid air cells are near completely opacified. The patient is status post endotracheal intubation.. The visualized portions of the orbits are intact. The eyeball lenses are thin.MRA brain:Antegrade flow is present in the distal internal carotid arteries, the distal vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries.There is no evidence for intracranial aneurysm or cerebrovascular occlusion.The anterior communicating artery is identified. There is fetal origin of the right posterior cerebral artery with a fairly large right P1 segment. The left posterior communicating artery is very small. Anterior communicating artery is also very small. The left vertebral artery is slightly larger than the right vertebral artery.
1.No evidence for cerebrovascular occlusive disease.2.No evidence for intracranial aneurysm.3.There are small foci of subacute infarction present bilaterally in the frontal and parietal lobes in a watershed type distribution.4.There are multiple microhemorrhages in the subcortical white matter. This pattern is suggestive more of amyloid angiopathy as a potential cause. Although some of these were present on the prior exam from 2009, there is no susceptibility weighted imaging on the prior exam just gradient T2. As a result a direct comparison cannot be made.5.Periventricular and subcortical white matter lesions are present which are likely vascular related at this age, however, they have only mildly progressed compared to the previous exam.