Case Notes
History
50 year old female presenting with acute-on set, left sided, weakness.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
CTA Final Impression1. There is dense calcification in the Rt. high cervical ICA on the noncontrast CT, which is the likely nidus precipitating the thrombotic occlusion of the Rt. cervical ICA.
2. There are moderate, non flow-limiting stenosis of both EAC & IAC origins in the 50% range. These could contribute to reduced Rt. cerebral perfusion pressure given there is also an incomplete circle of Willis.
3. Rt. cervical IAC occlusion beginning just beyond carotid sinus with evidence of soft clot in the lumen. The thrombus continues up to the posterior genu of the intracranial-extradural ICA segment. Both the proximal or distal ends of the thrombus are potential sources for secondary embolization.
4. Minimal evidence of post ischemic arteriopathy with subtle intraluminal irregularities, minimal filling delay, and subtle loss of BBB. Findings are consistent with recanalization after recent thromboembolic event.
5. EC-IC collateral provided by ascending pharyngeal-cavernous sinus EC-IC connection; this delays arterial filling on the right but all distal arteries are patent.
6. The post ischemic arteriopathy in the second M3 branch could affect the right premotor area, which would account for the symptoms of left sided transient weakness.
7. There is no pial collateral gap nor evidence of reduced venocapillary CT density to confirm completed infarction in the areas of dysautoregulation.
MR Diffusion
1. Acute Rt. high cervical ICA thrombosis with known soft clot in the right ICA stump and in the cavernous ICA as sources for emboli.
2. There multicentric of MR diffusion positive sites consistent with small volume embolic strokes in the distal M4-MCA branches, including involvement of the arm & trunk primary motor cortex.
MR FLAIR
1. There is positive FLAIR signal in the Rt. high cervical ICA consistent with recent thrombosis in this arterial segment.
2. Evidence of hyperacute multicentric small volume embolic strokes in the distal MR branches including those to the arm & trunk area of the primary motor cortex. These could arise from either the proximal or distal end of the thrombus, since the cavernous and beyond ICA is patent and the there are EC-IC collaterals arising from the neck. Stroke-age is estimated at 3-4 hours by FLAIR.
3. Older, likely subacute, small P4 embolic strokes are present in the Rt. occipital pole.