Case Notes
History
42 year old male with right sided numbness and neck pain; history of seizures and hypertension.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
CT HeadThere is evidence of a left high-cervical ICA dissection. There is very subtle edema in the left hippocampus.
MRA Head and Neck
There are changes consistent with left high-cervical and vertical intapetrous ICA dissection. There is a short segment with non-filling of the genu segment of the ICA likely representing occlusion. However, the left ICA becomes patent in the horizontal, intrapetrous segment and beyond reflecting patent EC-IC collateralization.
Focal areas of absent MRA signal (consistent with down-stream thromboemboli) were evident in the proximal right ACA, the proximal left PCA, and the left MCA at the M2 trunk division (affecting flow into both the superior and inferior MCA perfusion zones).
MR Diffusion
1. Positive diffusion in the left hippocampus consistent with post-ictal effects of a recent seizure. A grand mal seizure may have precipitated the left high-cervical ICA dissection.
MR FLAIR
1. Known Lt. high-cervical ICA dissection with high-grade stenosis with positive FLAIR signal.
2. Positive FLAIR signal is evident in the left hippocampus consistent with post-ictal hippocampal edema.