File:Cerebral amyloid angiopathy- multiple intracranial hemorrhages (Radiopaedia 40475-43048 Axial T2 6).png

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Cerebral_amyloid_angiopathy-_multiple_intracranial_hemorrhages_(Radiopaedia_40475-43048_Axial_T2_6).png ‎(512 × 512 pixels, file size: 197 KB, MIME type: image/png)

Summary:

Description
  • Radiopaedia case ID: 40475
  • Image ID: 16758261
  • Image stack position: 6/21
  • Plane projection: Axial
  • Aux modality: T2
  • Study description: MRI Brain (10 days later)
  • Study findings: Image quality on some sequences are degraded by motion artefact.There is been recent left frontal craniotomy with expected changes in the overlying subcutaneous soft tissues. Thin extra-axial collection overlying the left frontal convexity measuring up to 4 mm in depth. Altered signal and cavity in the subjacent frontal lobe in keeping with partially evacuated left frontal parenchymal hematoma. Very small volume residual intraventricular blood in the dependent portion of the right lateral ventricle. Compared to previous MRI, lateral and ventricles are enlarged. Confluent T2 and FLAIR hyperintensity in the periventricular white matter. Altered signal, encephalomalacia, and gliosis in the left cerebellar hemisphere, left temporal lobe, and left occipital pole in keeping with previous parenchymal hemorrhage in these locations. Multiple foci of blooming susceptibility sensitive sequence in both cerebral hemispheres, with predilection for the grey-white matter junction. Allowing for differences in comparison between GRE (current study) and SWI (previous) these appear more numerous. Sulcal hemosiderin staining, most notably at the vertex, in keeping with previous subarachnoid hemorrhage. Susceptibility related signal loss in the left parietal lobe indicates location of the previous ventricular catheter. Multiple foci of T2 and FLAIR hyperintensity in the subcortical white matter of both hemispheres have increased in size compared to previous MRI. No abnormal contrast enhancement. Altered signal on DWI most likely a result of extensive blood products. Time-of-flight MRA demonstrates a slightly bulky anterior communicating artery, but no intracranial aneurysm. No evidence of intracranial steno-occlusive disease other than the distal M3 left side branch narrowing which could represent mass effect or intrinsic disease - of doubtful relevance. Conclusion: Appearance of left frontal lobe in keeping with recent intraparenchymal hemorrhage and subsequent evacuation. Enlarged ventricles compared to previous MRI. Periventricular T2 and FLAIR hyperintensity suggestive of transependymal fluid shift. Small residual intraventricular blood is noted. Distribution of punctate foci of blooming suggestive of amyloid angiopathy. Marked progression of subcortical white matter disease compared to the previous study. Prior left cerebellar hematoma, remote left occipital lobe hematoma.
  • Modality: MRI
  • System: Central Nervous System
  • Findings: A relatively stable ill-defined 2 cm area of gliosis/encephalomalacia and hemosiderin staining, compatible with old hemorrhage, remains centered posteriorly in the left inferior and middle temporal gyri. There is no evidence of underlying tumor, vascular malformation or aneurysm. Of note, a linear focus of T2 hyperintensity and diffusion restriction, consistent with a recent small vessel infarct , is now noted to course obliquely through the posterior left parietal lobe subcortical white matter. A stable 2-3 cm area of partly liquefied encephalomalacia/gliosis remains centered inferiorly in the left occipital lobe, with moderately extensive chronic small vessel ischemic change elsewhere in the white matter of both cerebral hemispheres and brainstem considered excessive even for a 62 year old patient.The remainder of the study is unremarkable.
Date Published: 24th Oct 2015
Source https://radiopaedia.org/cases/cerebral-amyloid-angiopathy-multiple-intracranial-haemorrhages
Author RMH Neuropathology
Permission
(Permission-reusing-text)		 http://creativecommons.org/licenses/by-nc-sa/3.0/

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