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Case Notes
History
59 year old male with COPD who developed tachycardia requiring therapy. Two days later he developed Rt. sided weakness, pupillary dysfunction, and slurred speech. Shortly thereafter, he became somnolent and unresponsive.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
CTA Final Impression1. Markedly reduced CT density in the venocapillary pool within the left pons, and both cerebellar hemispheres, as above. These areas are all included in the dense ischemic core.
2. There is a very recent left deep cerebellar reperfusion hemorrhage, which when combined with the stroke-related brain swelling, has producing mass effect with early upward transtentorial herniation
3. Lack of venous egress in the left cerebellum is indicative of venous collapse, and is likely the basis for the reperfusion hemorrhage.
4. Old infarct in the left P3 PCA perfusion zone.
MR Diffusion
1. Multicentric cerebellar and left pontine infarctions are evident, as listed above. Stroke age is likely 6-8 hours or beyond. There is a chronic completed infarction with encephalomalaica in the left P3-PCA perfusion zone.
2. There is hemorrhagic conversion with hematoma in the left deep central cerebellar watershed zone.
3. There is apparent sequestered infarction in the right deep deep central cerebellar watershed zone.
4. There is early upward transtentorial herniation.
