Case Notes
History
64yo male on aspirin and Plavix presenting with acute gait difficulty and left visual field problems.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 CTA:1. Acute hyperdense thrombus in the distal basilar artery (last 3mm’s), and of the basilar apex.
2. No focal reduced CT density within the venocapillary pool is evident to confirm completed stroke in the rostral cerebellum, rostral brain stem, nor occipital poles.
MR Diffusion
1. Multicentric embolic-type strokes are present including the PICA perfusion zones in the caudal cerebellar hemispheres, the distal basilar perforators to the Rt. cerebral peduncle, the basilar tip perforators to the mesial thalamus, the Rt. posterior mesial choroidal artery perforators to the dorsal Rt. thalamus, and the P4 branches to both occipital polar areas.
MR Flair
1. Multicentric hyperacute to early acute (6 hours to 1 day) thromboembolic infarctions are evident involving: the distal PICA branches in both cerebellar hemispheres, the distal basilar perforator to the Rt. cerebral peduncle, the basilar tip perforators to the mesial thalamus, the Rt. posterior lateral choroidal perforators to the dorsal Rt. thalamus, a mesial P4 larger infarction right mesial occipital lobe, and finally, multiple small very distal the P4 branches to both occipital poles.