Case Notes
History
36 year old male diabetic who was found down. Patient initially was unresponsive, and later exhibited a markedly depressed level of consciousness. Patient was uncooperative on presentation and aphasic.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 CTA1. There is Lt. primary-stem ICA thrombosis affecting both the intracranial/extradural and the entire intracranial portions of the Lt. ICA.
2. Only minimal peripheral pial collateralization is evident; the bulk of the Lt ICA perfusion zone is within the dense ischemic core. The addition of the virtually no venous egress to no afferent arterial input is consistent with sequestrated form of stroke, which if large enough in size typically has a very poor clinical outcome. This patient did not survive this stroke.
3. There is no current hemorrhagic conversion.
4. There is early, but definite, downward incisural herniation.
MR DWI & FLAIR Sequences
1. Acute thrombus is now evident in the high cervical Lt. ICA, as well as the intradural ICA.
2. Aypical MR diffusion appearance related to suppression of signal most likely caused by the susceptibility artifact associated with high levels of deoxyhemoglobin within areas of venous stasis. This is consistent with a sequestered infarction, which is the worst form of arterial stroke. This involve all but the outer periphery of the left ACA and left MCA perfusion zone. Strokes of this type will not likely respond favorably to interventional stroke therapy.
3. There is evidence of mesial parahippocampal gyrus displacement, which is indicative of the start of downward brain herniation. This patient may, therefore, require cranial decompression if malignant brain swelling occurs.
4. There is a small mesial lenticulostriate perforator stroke without features of sequestered infarct.