Case Notes
History
76 year old male presenting with acute slurred speech, left sided weakness, and left facial droop.Exam
Head MR Diffusion Sequences (with DWI & ADC maps)
Purpose
1. To use the diffusion maps (DWI & ADC) to identify sites of hyperacute stroke matching an arterial zone.
2. To determine whether the positive diffusion zone matches a primary stem arterial region, a secondary stem arterial region, a trunk/division arterial region, a major branch region; or a distal arterial cortical zone, or any combination;
3. In cases where there are more than one ischemic sites to determine whether changes could be from an extra cranial embolic site, or whether they represent proximal clot lysis and subsequent distal embolization;
4. To determine whether the areas involved fit best with an embolic event or embolic shower (could be from proximal plaque or cardiac source, etc;
5. To determine whether the affected areas as recognizable as a watershed zone; usually in the context of currently patent major afferent arteries (ICA’ & vertebral arteries); there are often chronic extradural carotid or vertebral occlusions;
6. To determine whether the affected area(s) could represent stroke with an end of the line watershed pattern, based on the combination of occluded major afferent brain arteries plus incomplete circle of Willis plus any additional flow-limiting stenoses;
7. Evaluate the diffusion Bo sequence for hemorrhagic conversion.
Purpose
1. To use the diffusion maps (DWI & ADC) to identify sites of hyperacute stroke matching an arterial zone.
2. To determine whether the positive diffusion zone matches a primary stem arterial region, a secondary stem arterial region, a trunk/division arterial region, a major branch region; or a distal arterial cortical zone, or any combination;
3. In cases where there are more than one ischemic sites to determine whether changes could be from an extra cranial embolic site, or whether they represent proximal clot lysis and subsequent distal embolization;
4. To determine whether the areas involved fit best with an embolic event or embolic shower (could be from proximal plaque or cardiac source, etc;
5. To determine whether the affected areas as recognizable as a watershed zone; usually in the context of currently patent major afferent arteries (ICA’ & vertebral arteries); there are often chronic extradural carotid or vertebral occlusions;
6. To determine whether the affected area(s) could represent stroke with an end of the line watershed pattern, based on the combination of occluded major afferent brain arteries plus incomplete circle of Willis plus any additional flow-limiting stenoses;
7. Evaluate the diffusion Bo sequence for hemorrhagic conversion.
Prior Study
Head CT1. Hyperacute thrombus in M1 and M2 segments of the Rt. MCA
2. The post-ischemic stroke changes affect the Rt. orbitofrontal artery, the rostral lateral lenticulate perforators, and the anterior portion of the intrasylvian MCA superior-division branch perfusion zones, and are likely beyond the IV treatment window.
3. The posterior M3 sylvian arterial perfusions zone may have some post ischemic changes, but likely are at least partially-spared by pial collateral. The same is true for most of the lateral cortex.
CT perfusion
CT perfusion evidence of prolonged filling rate (prolonged TTP/MTT) affecting mainly the Rt. lateral orbitofrontal perfusion zone with lesser post ischemic changes in the Rt. lateral basal ganglia (lateral lenticulostriate perforator perfusion zone) and the anterior insular M3 perfusion zones. However, the CBV is only minimally reduced in most areas and is only partially reduced in the right orbitofrontal artery perfusion zone indicating at least reasonable retrograde pial collateralization in most of the area included in the prolonged TTP zone.
Delayed 2nd Pass Head CTA
1. The initial noncontrast CT head demonstrated obvious well-delineated post ischemic cytogenic edema in the Rt. lateral lenticulostriate, the lateral orbitofrontal artery and the anterior insular M3 perfusion zone. The stroke-age was likely beyond 8 hours. There was no hemorrhagic conversion.
2.Known tandem Rt. carotid circuit occlusions in both the extradural ICA segment and the M1/M2 intradural segments. Pial collateral is good on the delayed post contrast CTA with retrograde filling all distal pial arteries and even outlined the thrombus within the M1/2 ICA segments.
3. CT density within the venocapillary pool is within normal limits in most of the areas of post ischemic cytogenic edema clearly evident on the noncontast head CT. The CT density within the venocapillary pool does not quite reach normal limits in the distribution of the Rt. lateral lenticulostriate perfusion zone. This disparity between the noncontrast CT and the venocapillary pool density implies than there has been intercurrent clot lysis with spontaneous reperfusion occurring since the initial ictus event.
4. There is no venous egress restriction, which is a good indication of reasonable transcapillary blood flow at this time.
5. There is minimal evidence of post ischemic dysautoregulation in the Rt. lateral orbitofrontal artery perfusion zone. This is consistent with vascular changes following at least some reperfusion in the 8 hours post ictus.