Case Notes
History
72 year old male with transient left sided weakness; history of diffuse vascular disease; evaluate for arterial stenosis.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
Non-Contrast Head CTAge related changes and chronic post-ischemic lacunar infarct in the mesial Lt. thalamus.
No hyperacute post ischemic changes are evident.
CTA Final Impression
Diffuse atherosclerotic arterial disease with segmental occlusion of the proximal Rt. vertebral, Lt. high cervical vertebral, and proximal Lt. ICA. Only minimal EC-IC collateral is present through the Lt. ophthalmic artery.
There are tandem extradural ICA stenoses on the Rt.
There is ulcerative plaque in the Lt. common carotid and basilar arteries.
Despite extensive atherosclerotic vascular disease in the cervical region causing a delay in cerebral and cerebellar filling rates. The delayed post contrast head CT, however, demonstrates functional pial collateral to all areas of the cerebrum and cerebellum. As a result, there is normal CT density in the venocapillary pool in all areas that appeared abnormal on the CT perfusion.
MR Diffusion and FLAIR Sequences
1. Negative head MR without evidence of an acute ischemic event.
2.FLAIR imaging demonstrates expected age-related changes and a chronic lacunar infarct in the mesial left thalamus, but no acute abnormalities; there is a prosthetic Rt. optic globe.