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Case Notes
History
59 year old male with COPD who developed tachycardia requiring therapy. Two days later he developed Rt. sided weakness, pupillary dysfunction, and slurred speech. Shortly thereafter, he became somnolent and unresponsive.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
CTA Final Impression1. Markedly reduced CT density in the venocapillary pool within the left pons, and both cerebellar hemispheres, as above. These areas are all included in the dense ischemic core.
2. There is a very recent left deep cerebellar reperfusion hemorrhage, which when combined with the stroke-related brain swelling, has producing mass effect with early upward transtentorial herniation
3. Lack of venous egress in the left cerebellum is indicative of venous collapse, and is likely the basis for the reperfusion hemorrhage.
4. Old infarct in the left P3 PCA perfusion zone.
MR Diffusion
1. Multicentric cerebellar and left pontine infarctions are evident, as listed above. Stroke age is likely 6-8 hours or beyond. There is a chronic completed infarction with encephalomalaica in the left P3-PCA perfusion zone.
2. There is hemorrhagic conversion with hematoma in the left deep central cerebellar watershed zone.
3. There is apparent sequestered infarction in the right deep deep central cerebellar watershed zone.
4. There is early upward transtentorial herniation.
MR FLAIR
1. Multicentric infarctions are listed above; stroke age is likely 6-8 hours or beyond. There is an old left P3 infarction with encephalomalacia in the lateral ventral temporal lobe. There is wide spread age-related ischemic demyelination in the centrum semiovale bilaterally.
2. There is hemorrhagic conversion with hematoma in the left deep central cerebellar watershed zone.
3. There is sequestered infarction in the right deep deep central cerebellar watershed zone; this can be confirmed on MR-swi sequence.
4. There is early upward transtentorial herniation.
