Case Notes
History
81 year old female presenting with acute onset mental status change, dizziness, nausea, and gait imbalance.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. Distal segment basilar artery partially occlusive acute thrombosis is present with mainly circle of Willis collateral to distal basilar tip and PCA trunks. Thus, there is filling of all pial arteries although limited on the left.
2. There is significantly reduced CT density in the venocapillary pool in the subcortical mesial occipital white matter bilaterally (dense ischemic core). Findings are most consistent with ischemic injury associated with the initial thromboembolic event. Currently there has been significant recanalization of the distal P4 arteries (better on the right) and partial clot lysis in the distal basilar artery. The depth and duration of the initial ischemic insult resulted in deep white matter occipital stroke.
2. Limited filling the left PICA resulting in completed stroke involving the mesial (caudal) cerebellum (dense ischemic core) and lesser ischemic changes in the remaining left lateral cerebellum (likely in the ischemic penumbra).
Findings on diffusion: DWI/ADC maps
The diffusion maps (both DWI and ADC) are positive for hyperacute stroke in both mesial occipital areas (P4 PCA perfusion zones).
There are separated small DWI positive areas in the right occipital lobe, which again are consistent with recent secondary emboli.
The diffusion maps (both DWI and ADC) are positive for stroke in the mesial left cerebellum and left peritonsillar region corresponding to the peritonsillar and mesial hemispheric trunks of the Lt. PICA.
Finding on MR FLAIR
1. Recent ischemic events in multiple sites including the mesial occipital lobes (P4 segment PCA perfusion zones) and in the Lt PICA (affecting the mesial cerebellar and peritonsillar trunks only). Stroke-ages are variable, as above.
2. Embolic source is likely (originally) thrombus in the left intradural vertebral artery segment based on FLAIR findings. This original thrombus likely occluded the left PICA resulting in mesial left cerebellar infarction, which is why this stroke is older than the others.