Case Notes
History
79 year old female presenting with sudden onset symptoms including Rt. facial droop, Rt. side weakness; the patient was nonverbal and not following commands; there is known history of secondary diabetes with hyperlipidemia.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 (tumefactive stroke).
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 (tumefactive stroke).
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 entire CTA1. Proximal left M1/M2 thrombus with reasonable pial collateral (pial collateral reaches the proximal thrombus on the delayed head CT.
2. There remains evidence of persistent significant oligemia mainly in the lateral lenticulostriate perfusion zone (likely completed stroke, and in the anterior insular cortex (ischemic penumbra. Lesser oligemia (tissue at risk) is evident the remaining MCA and lateral orbitofrontal territories.
3. The persistently oligemic sites in the rostral M3-MCA perfusion zones likely affect the white matter deep to Broca’s area, the uncinate fasiculus, the premotor cortex, and the facial portion of the primary motor cortex.
4. The combination of a focal 50-60% stenosis of the proximal right cervical ICA combined with incomplete circle of Willis shifts the watershed zone to the anterior insular area (end of the line watershed pattern), which likely contributes to the anterior insular ischemia. This end of the line ischemic effect is further supported by evidence of pial collateral reaching the M3 arteries in this area on the initial post contrast head CT.
5. Suspicious nodule in the left thyroid.
Concurrent MR diffusion
1. There is positive diffusion in the same areas corresponding to sites of reduced CBV and CT perfusion and reduced venocapillary pool on the delayed CTA consistent with post ischemic parenchymal injury in the left lateral basal ganglia/caudate body/centrum semiovle, in the lateral orbitofrontal, and in the anterior insula and much of the superior division of the left MCA to the operculum and lateral cortex. However, the degree of positivity is variable with the least prominent (lesser ischemia) involving in the posterior insula and all of the superior division MCA supplied lateral cortex. The most prominent (worst ischemia) is in the perfusion zone of the M1/2 lateral lenticulostriate perforators and the anterior insula.
2. There is reperfusion hemorrhage into the lateral lenticulostriate perfusion zone, which was positive on DWI but also had significantly reduced CT density within its’ venocapillary pool on delayed CTA.
3. There is minimal subfalcine brain shift secondary to post ischemic cytogenic swelling plus the hematoma in the lateral lenticulostriate perfusion zone.
Concurrent FLAIR sequence
FLAIR demonstrates post ischemic cytogenic edema consistent with ischemic injury in the left lateral lenticulostriate perfusion zone now with reperfusion hemorrhagic conversion. The hematoma produces local mass effect and early incisular herniation.
FLAIR demonstrates post ischemic cytogenic edema in the perfusion zones of the Lt. M3 (MCA) arteries to the anterior insula, Lt. lenticulostriate, and to the Lt. lateral orbitofrontal portions of the Lt. hemisphere. These areas did not develop hemorrhagic conversion.