Case Notes
History
76 year old male presenting with acute slurred speech, left sided weakness, and left facial droop.Exam
Head MR FLAIR Sequence
Arterial stroke is not a single entity, but rather starts as an ictal event generating symptoms and then evolves. However, the ischemic process may have occurred earlier, but was clinically silent, and only becomes symptomatic following clot lysis with downstream secondary embolization or reperfusion hemorrhage. Likewise, collateralization begins immediately. If sufficient the ischemic event ends up as a TIA; if insufficient it ends up a stroke. However, the depth and duration of this event(s) determines whether there is a temporary neurologic deficit, a completed stroke (adds glutamate cascade with vasogenic edema), or a lesser ischemic injury (no glutamate cascade leaving only cytogenic edema). Thus, acute clinical stroke is actually an unstable dynamic process. The CTA venocapillary pool CT density provides information about depth of the ischemic injury at the time of the exam (i.e. is the venocapillary pool normal, or less than normal, or absent), but does not reflect the stroke-age.
MR FLAIR can provide information about stroke-age and depth and duration of the oligemic insult, but cannot distinguish these two effects. FLAIR becomes positive 2-3 hours after the stroke ictus from cytogenic edema (with minimal conspicuity). If the stroke is completed it becomes more positive (obvious conspicuity after 4-6 hours) with the onset of the proinflammatory response producing vasogenic edema. In essence, the conspicuity of FLAIR can reflect either the time of onset and the amount of ischemic injury. If there is no positive FLAIR the onset is either very early or the ischemic injury is minimal. If minimally positive the onset is either in the hyperacute timeframe or the depth of the stroke is less severe. If clearly positive, the stroke is passed the stroke therapy window and is likely likely to have moderate or greater ischemic injury. FLAIR positivity proceeds over time peaking in the acute phase (3 hours to 3 days). Thus, FLAIR adds useful information about the stroke timeline and/or the stroke depth and duration only during the initial period of stroke stabilization or if there has been a new event with progression of clinical findings. Findings on FLAIR, as used in this discussion, is graded as if on a stroke-age timeline (not positive=very early, somewhat positive=early, clearly positive=outside the treatment window). However, the FLAIR conspicuity could just as well be based on the stroke depth and duration (minimal, moderate, or advanced). Nevertheless, the less obvious the FLAIR the earlier the ischemic event for determining stroke therapy or the lesser the stroke injury (which is always good). It is up to the imager to use FLAIR conspicuity language to best fit the clinical context usually determined by timing of the MR exam relative to the stroke ictus and the interval from the CTA.
Purpose
1. Use FLAIR sequence to confirm recognizable ischemic arterial zone or zones (similar to the DWI scenario).
2. Use FLAIR to estimate the most likely stroke-age and/or depth of the ischemic injury based on the conspicuity of the FLAIR compared to the DWI sequences.
3. Use FLAIR to detect thrombus or prior recanalized thrombus (hyperintensity) in the wall of proximal arteries.
4. Use FLAIR to detect focal mass effect and/or whether there is herniation or impending herniation of brain.
Arterial stroke is not a single entity, but rather starts as an ictal event generating symptoms and then evolves. However, the ischemic process may have occurred earlier, but was clinically silent, and only becomes symptomatic following clot lysis with downstream secondary embolization or reperfusion hemorrhage. Likewise, collateralization begins immediately. If sufficient the ischemic event ends up as a TIA; if insufficient it ends up a stroke. However, the depth and duration of this event(s) determines whether there is a temporary neurologic deficit, a completed stroke (adds glutamate cascade with vasogenic edema), or a lesser ischemic injury (no glutamate cascade leaving only cytogenic edema). Thus, acute clinical stroke is actually an unstable dynamic process. The CTA venocapillary pool CT density provides information about depth of the ischemic injury at the time of the exam (i.e. is the venocapillary pool normal, or less than normal, or absent), but does not reflect the stroke-age.
MR FLAIR can provide information about stroke-age and depth and duration of the oligemic insult, but cannot distinguish these two effects. FLAIR becomes positive 2-3 hours after the stroke ictus from cytogenic edema (with minimal conspicuity). If the stroke is completed it becomes more positive (obvious conspicuity after 4-6 hours) with the onset of the proinflammatory response producing vasogenic edema. In essence, the conspicuity of FLAIR can reflect either the time of onset and the amount of ischemic injury. If there is no positive FLAIR the onset is either very early or the ischemic injury is minimal. If minimally positive the onset is either in the hyperacute timeframe or the depth of the stroke is less severe. If clearly positive, the stroke is passed the stroke therapy window and is likely likely to have moderate or greater ischemic injury. FLAIR positivity proceeds over time peaking in the acute phase (3 hours to 3 days). Thus, FLAIR adds useful information about the stroke timeline and/or the stroke depth and duration only during the initial period of stroke stabilization or if there has been a new event with progression of clinical findings. Findings on FLAIR, as used in this discussion, is graded as if on a stroke-age timeline (not positive=very early, somewhat positive=early, clearly positive=outside the treatment window). However, the FLAIR conspicuity could just as well be based on the stroke depth and duration (minimal, moderate, or advanced). Nevertheless, the less obvious the FLAIR the earlier the ischemic event for determining stroke therapy or the lesser the stroke injury (which is always good). It is up to the imager to use FLAIR conspicuity language to best fit the clinical context usually determined by timing of the MR exam relative to the stroke ictus and the interval from the CTA.
Purpose
1. Use FLAIR sequence to confirm recognizable ischemic arterial zone or zones (similar to the DWI scenario).
2. Use FLAIR to estimate the most likely stroke-age and/or depth of the ischemic injury based on the conspicuity of the FLAIR compared to the DWI sequences.
3. Use FLAIR to detect thrombus or prior recanalized thrombus (hyperintensity) in the wall of proximal arteries.
4. Use FLAIR to detect focal mass effect and/or whether there is herniation or impending herniation of brain.
Prior Study
Final CTA ImpressionCT head demonstrates ischemic changes in the Rt. lateral orbitofrontal artery and superior division Rt. MCA. The apparent post ischemic edema is of mixed age, but most are consistent with stroke age outside the treatment window.
CT perfusion had 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.
The Lt. ICA has a single stenosis in its initial cavernous segment, which does not appear to be more than 50% narrowing.
The Rt. ICA has Q limiting stenosis at its’ origin and becomes nearly occluded at the C2 level. There is no appreciable EC-IC collateral, leaving collateral from the circle of Willis and pial sources. However, these means of collateral leaves no apparent deficit in tissue perfusion (on the delayed post contrast head CT). CT perfusion matches these CTA findings.
MR Diffusion
1. Diffusion sequence demonstrates positive restriction consistent with ischemia affecting mainly the Rt. lateral orbitofrontal cortex and the Rt. basal ganglia; ischemia is these sites are the likely result of primary thrombosis of their arterial supply producing a primary type of stroke.
2. Positive diffusion in other areas, as the anterior insula and distal M3 cortex are more consistent with an end-of the-line hypoperfusion, secondary type of stroke, which typically benefit from reperfusion.
3. Mulitple individual (punctate rather than confluent) strokes in the ACA-MCA watershed zones is evidence that these are terminal arterial type of ischemic injuries.