Case Notes
History
76 year old male presenting with acute slurred speech, left sided weakness, and left facial droop.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 CTA ImpressionCT head demonstrates ischemic changes in the Rt. lateral orbitofrontal artery and superior division Rt MCA. The apparent post ischemic edema is of mixed age, but most are consistent with stroke age outside the treatment window.
CT perfusion had evidence of prolonged filling rate (prolonged TTP/MTT) affecting mainly the Rt. lateral orbitofrontal perfusion zone with lesser post ischemic changes in the Rt. lateral basal ganglia (lateral lenticulostriate perforator perfusion zone) and the anterior insular M3 perfusion zones. However, the CBV is only minimally reduced in most areas and is only partially reduced in the right orbitofrontal artery perfusion zone indicating at least reasonable retrograde pial collateralization in most of the area included in the prolonged TTP zone.
The Lt. ICA has a single stenosis in its initial cavernous segment which does not appear to be more than 50% narrowing.
The Rt. ICA has Q limiting stenosis at its’ origin and becomes nearly occluded at the C2 level. There is no appreciable EC-IC collateral, leaving collateral from the circle of Willis and pial sources. However, these means of collateral leaves no apparent deficit in tissue perfusion (on the delayed post contrast head CT). CT perfusion matches these CTA findings.
MR Diffusion & FLAIR
Rt ischemic event affecting the RT orbital frontal artery perfusion zone, the Rt lenticulostriate artery perforator perfusion zone, despite evidence of good pial collateralization.
FLAIR imaging demonstrates well delineated cytogenic edema through the entire stroke zone indicating the stroke-age is likely at the outside limit of the treatment window