Case Images
Case Notes
History
56 yo female with chronic hypertension and recent cerebellar symptomsExam
Prior Study
Pre and post contrast CT and CTA1. The noncontrast CT demonstrates an apparent hemorrhage in an area of tissue volume loss in the caudal right cerebellar hemisphere. Age of the stroke and age of the apparent reperfusion hemorrhage are indeterminate. The apparent hemorrhage could also represent dystrophic nodular post ischemic tissue calcification.
2. There is ventriculomegaly and tissue atrophy out of proportion to age. Temporal horn size remains normal and there is no optic hydrops to confirm hydrocephalus.
3. The CTA confirmed non antegrade filling of distal arteries to the caudal right cerebellar and deep portions of the right cerebellum. Pial collateral was derived from the right superior cerebellar artery.
Non contrast T1-w sequence
1. The modest tissue loss in the caudal right cerebellar is again evident on the T1-w sequence
2. The site of the deep cerebellar (possibly recent) hemorrhage on head CT actually demonstrates no signal on T1 indicating chronic-phase hemorrhage with hemosiderin or dense tissue calcium deposition, or both. It is not acute or even subacute blood, and is likely >2 months of age.
T2-w MR spin echo sequence
1. The modest tissue loss in the caudal right cerebellar is again evident on the T2-w sequence
2. There is evidence of the volume loss sequelae of a prior right PICA stroke, but the cortical margins remain slightly T2-hyperintense possibly from intercurrent ischemic related edema. The regional tissue loss and the deep cerebellar hemorrhage (or calcification) both represent chronic-phase findings of 2 months or longer from inciting event. Current symptoms could represent transient hypotension combined with ineffective right cerebellar collateralization with cortical marginal edema, but in all probablility these changes are more likely chronic post ischemic myelomalacia.
MR flair sequence
1. The modest tissue loss in the caudal right cerebellar is again evident on the MR flair sequence with no evidence of residual tissue edema to suggest persistent ischemia.
2. There is no transependymal fluid migration to suggest elevated CSF pressure. There is extensive cerebral leukomalacia without lacunar defects to suggest extensive atherosclerotic vascular disease.
Dicom
Findings
| MR susceptibility (SWI) | Correct Answer | Your Answer |
|---|---|---|
|
There is evidence (positive susceptibility artifact) of acute or prior subarachnoid blood. |
No | NA |
|
There is evidence (positive susceptibility artifact) of acute or prior intraaxial hemorrhage. |
Yes | NA |
|
There is evidence (positive susceptibility artifact) of acute or prior intraventricular blood. |
No | NA |
|
There is evidence (positive susceptibility artifact) of acute subpial blood. |
No | NA |
|
There is evidence of multicentric sites of parenchymal hemosiderin consistent with: chronic hypertensive encephalopathy, cavernous angiomata, amyloid angiopathy, or prior radiotherapy. |
No | NA |
|
There is "blooming susceptibility artifact" over arteries consistent with recent thrombosis. |
No | NA |
|
There is "blooming susceptibility artifact" over cortical or deep veins consistent with recent thrombosis. |
No | NA |
|
There are multicentric sites of pial surface microhemorrhages (result of mainly diapedesis rather than overt hemorrhage); evident in herpes simplex encephalitis, microhemorrhage in hypo-coagulopathy states. |
No | NA |
|
Other significant imaging findings are present. |
No | NA |
Impression
Expert Answer
MR susceptibility (SWI) can detect parenchymal blood products in all phases of clot evolution. MR SWI can detect hemorrhagic transformation in tissue as well as distinct hematoma's. MR SWI can detect thrombus in arteries and veins as well as within parenchyma.
Your Answer
Recommendations & Acuity
Recommendations
Expert Answer
Proceed with additional MR imaging sequences.
Your Answer
Acuity
Expert Answer
Emergent (Action Necessary now)
