Case Notes
History
42 year old male with right sided numbness and neck pain; history of seizures and hypertension.Exam
MR susceptibility (SWI) sequence obtained 3 months after initial presentation
Purpose
1. To identify sites of arterial thrombosis based on SWI blooming artifact in the proximal afferent arteries.
2. To assess the presence of venous stasis based on SWI blooming artifact within the deep medullary veins
3. To assess for venous collapse based on SWI blooming artifact in both the deep medullary veins and the draining central & cortical veins.
3. To identify sites of hematoma (blood extravasated into the neuropil) representing actual hemorrhagic conversion.
4. To identify sites of sequestered infarction (stagnant blood within the capillary bed), which implies virtually no transcapillary blood flow. This can be in the cortex (i.e. laminar necrosis), or in the parenchyma.
5. Compare the FLAIR & DWI sequences with the SWI sequence in order to differentiate between hemorrhagic conversion (hematoma formation within the neuropil) versus acutely sequestered completed infarction (non extravasated blood stagnated within the capillary bed).
6. To identify areas of hyperemia with dilated deep medullary veins, which are part of the physiologic hyperemia in the collateral stroke zone, since this is an expected finding and not evidence of venous stasis.
Purpose
1. To identify sites of arterial thrombosis based on SWI blooming artifact in the proximal afferent arteries.
2. To assess the presence of venous stasis based on SWI blooming artifact within the deep medullary veins
3. To assess for venous collapse based on SWI blooming artifact in both the deep medullary veins and the draining central & cortical veins.
3. To identify sites of hematoma (blood extravasated into the neuropil) representing actual hemorrhagic conversion.
4. To identify sites of sequestered infarction (stagnant blood within the capillary bed), which implies virtually no transcapillary blood flow. This can be in the cortex (i.e. laminar necrosis), or in the parenchyma.
5. Compare the FLAIR & DWI sequences with the SWI sequence in order to differentiate between hemorrhagic conversion (hematoma formation within the neuropil) versus acutely sequestered completed infarction (non extravasated blood stagnated within the capillary bed).
6. To identify areas of hyperemia with dilated deep medullary veins, which are part of the physiologic hyperemia in the collateral stroke zone, since this is an expected finding and not evidence of venous stasis.
Prior Study
CTA Stroke Protocol1. The initial prior MRA demonstrated Lt. ICA thrombotic dissection in high-cervical and proximal intrapetrous regions. Additionally, there was a short segment intrapetrous thrombosis. There was good EC-IC collateral beyond the thrombus. There were multicentric thromboemboli in multiple intradural arteries.
2. The current CTA demonstrated resolution of the extradural thrombus. There is substantial recanalization of the thrombi in the right A1/2 clot, and the left M1/2 clot leaving only minimal to moderate residual luminal narrowing in the proximal inferior division MCA. The P1 was developmentally hypoplastic (fetal variant) and not thrombosed.
3. CT perfusion and CT venocapillary pool analysis demonstrate normal tissue perfusion.
MR Diffusion: DWI/ADC Maps
The initial prior MR diffusion at presentation was normal for stroke but positive for seizure (presented in Case 9). The 2 day follow up MR diffusion (presented here in Case 10) demonstrates multiple focal areas of acute ischemic changes (embolic shower) in the left splenium and body of the corpus callosum (distal ACA-pericallosal perfusion zone), one mesial and one lateral lenticulostriate perforators, and several distal Lt. anterior insular M3 branches. These thromboembolic ischemic sites are all positive on both the DWI & ADC maps confirming their hyperacute timeframe.
MR FLAIR
1. The initial FLAIR demonstrated Lt. high-cervical ICA dissection with short segment of intraluminal thrombus within the intrapetrous left ICA. The FLAIR obtained at 3 months on follow up demstrate very minimal signal in the stroke sites consistent with minimal post ischemic leukomalacia.
2. The initial FLAIR demonstrated left hippocampus and column of the fornix consistent with hyperacute post ictal edema. This 3 month MR FLAIR demonstrated very minimal leukomalacia in the left hippocampus.