Case Notes
History
64 year old female presenting with acute onset Rt. hemiparesis, left gaze deviation and aphasia; no depressed level of consciousness; history of 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
Final CTA Impression1. There is a short segment proximal superior division MCA stenosis consistent with a recanalized artery rather than underlying fixed arterial stenosis. Since the stroke-zone includes the lenticulostriate and lateral orbitofrontal perfusion zone in addition to the superior division MCA, the initial thrombotic occlusion must have involved the M1/2 ICA segments.
2. Persistently reduced CT density in the venocapillary pool within the Lt. lateral orbitofrontal and anterior insular cortex with enough oligemia to fall within the ischemic penumbra. The oligemia in the posterior insula and the Lt. lateral lenticulostriate perforator regions appear less extensive. Correlate with stroke protocol MR.
3. There is no hemorrhagic conversion at this time.
4. There subtle loss of BBB in the distal Lt. MCA (M4) pial branches consistent with post-ischemic arteriopathy.
5. Stroke-age, based on the findings on the noncontrast CT would fit the hypeacute timeframe.
MR Diffusion
1. Acute post ischemic injury affecting most of the superior division of the MCA and the left orbitofrontal region, and the left lenticulostriate perforator region consistent with an original afferent block at the left M1/2 junction (secondary stem) site, although no thrombus remains.
2. The ischemic changes are worse (likely dense ischemic core) in the rostral lateral lenticulostriate perfusion zone (especially in the rostral basal ganglia and caudate head), plus the lateral orbitofrontal perfusion zone, plus the anterior insular M3 arterial perfusion zone. Less advanced ischemic changes are evident in the distal M4 MCA superior division perfusion zone. There is less involved interval brain interposed between the rostral larger stroke and the distal cortical ischemic cortex. This pattern is consistent with initial thrombus, subsequent rapid clot lysis, and secondary distal embolization.
3. There is no hemorrhagic conversion.
MR FLAIR
There is well delineated cytogenic edema in the Lt. M3 and M4 MCA cortex, the Lt. lateral lenticulostriate perforator zone, & the Lt. lateral orbitofrontal perfusions zones consistent with stroke age beyond 8-10 hours.
The edema is clearly more evident in the anterior insular (rostral M3 arteries) and in the Lt lateral orbitofrontal artery perfusion zones than in the M4 MCA cortical areas indicating a difference in depth and duration of the ischemic event.
There is no apparent hemorrhagic conversion including the punctate hyperdensity on the noncontrast head CT (thus, represents incidental asymmetric BG calcification).
There is an old MCA stroke is evident in the Rt. posterior insular area.