 Brain MRI: Again seen is hemorrhagic lesion in the medial right parietal lobe with linear enhancement corresponding to the previously embolized arteriovenous malformation. There is decrease in size of the hemorrhagic cavity associated with the lesion. No new or enlarging flow-voids within this region are demonstrated to suggest enlargement or persistent arteriovenous shunting. No new surrounding edema.Irregular linear enhancement involving the left lateral central gyrus related to known AVM also remains unchanged. No associated hemorrhage or edema.Previously described subtle area of abnormal linear enhancement/vascularity in the left posterior frontal lobe is not appreciated as a discrete lesion, but the appearance is similar to prior. There are foci of nodular enhancement which are best appreciated on the high-resolution post gadolinium 3-D sequence series 1601 in the left occipital lobe (image 72), right occipital lobe (image 70), right cerebellar hemisphere (image 39), as well as a slightly larger focus in the left cerebellar hemisphere measuring 5 mm (image 57). These are all unchanged since 10/20/2014. No associated susceptibility is seen.There are foci of susceptibility, one in the left anterior temporal lobe image 91, as well as one just lateral to the left thalamus, image 104 of series 1101. These appear to be present on prior study from 10/20/2014 and unchanged.The brain parenchyma demonstrates no evidence of acute infarct, intracranial hemorrhage or new mass effect. Ventricles are normal in size without evidence of hydrocephalus. No extra-axial collections. No midline shift or herniation. Calvarium and extracranial soft tissues are grossly unremarkable. Brain MRA:No definite MRA abnormality is noted in the region of the previously embolized right medial parietal arteriovenous confirmation. Abnormal vasculature is noted corresponding to the small arteriovenous malformation in the left central sulcus similar to prior.Additional areas of enhancement described above demonstrate no clear MRA correlate. There is antegrade flow within the intracranial internal carotid arteries, the bilateral anterior, middle, and posterior cerebral arteries, as well as the distal vertebral and basilar arteries. No significant stenosis or evidence of aneurysm.
1.Previously seen embolized arteriovenous malformation in the right medial parietal lobe is not associated with new edema, new hemorrhage, or new flow-voids to suggest persistent arteriovenous shunting. Associated hemorrhagic cavity is decreased in size compared to 10/20/2014.2.No significant change in appearance of the abnormal tangle of vascularity demonstrated with both MRI and MRA sequences within the left central sulcus. There is no associated signal abnormality within the adjacent parenchyma.3.Previously described focus of linear enhancement in the left posterior frontal lobe, presumably corresponding to the additional arteriovenous malformation demonstrated on prior angiogram remains unchanged.4.Additional nodules of enhancement are seen in the bilateral occipital lobes and bilateral cerebellar hemispheres as detailed above. No associated susceptibility or abnormal associated flow-voids. These are suspected to represent additional vascular lesions associated with HHT without arteriovenous shunting, although tiny AVMs remain a possibility. These however appear unchanged by MRI.5.Foci of susceptibility in the left anterior temporal lobe and one just lateral to the left thalamus as described above. While nonspecific these may represent additional vascular lesions, possibly cavernous malformations versus unrelated chronic microhemorrhages. These are also unchanged since 10/20/2014. 