Case Notes
History
71 year old male presenting with acute onset slurred or muffled speech, no weakness, was able to understand speech, with no loss of consciousness.Exam
Head MR Susceptibility (SWI) Sequence
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
Final Impression for Stroke Protocol CTA1. Prior occlusion of the posterior M3 trunk off the superior division Lt MCA, which has good pial collateral preventing extension of the stroke to most of the posterior superior division perfusion zone.
2. There is acute thrombus in single artery (artery to the central sulcus). The affected perfusion zone for this artery is much smaller than its’ full (normal) perfusion territory, which indicates there has been substantial retrograde pial collateralization from the A4 (ACA) pial vessels. However, there remains a small pial collateral gap in the mid-insula and the adjacent frontoparietal opercular cortex. In this case, the affected area includes the tongue part of the primary facial motor area, which correlates with the patients presenting symptom of dysarthria.
3. The improved CT density in the venocapillary pool is a good indication that the extent of final stroke-zone will remain quite small.
MR DWI/Flair Sequences
Both the DWI & ADC maps are positive for a small stroke in the mid-insular and intrasylvian frontoparietal cortices.
Very subtle edema is evident with the affect cortex is consistent with a hyperacute stroke timeframe.