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Case Notes
History
50 year old female presenting with acute onset left sided weakness.Exam
CT Perfusion
Note CT perfusion is obtained after the 1st bolus (i.e. 1st pass) of contrast and timed based on opacification of normal proximal artery opacification in the head; there is no recirculation effect. Therefore, CT perfusion does not reflect the effects of functional collateralization. Thus, evidence of low CBV and CBF may overestimate the depth of injury in the stroke-zones.
Purpose
1. Evidence of abnormal prolonged TTP/prolonged MTT/ with partially reduced CBQ (flow)/partially reduced CBV (volume) is consistent with oligemia (tissue at risk); this may be improved by collateral on the CTA venocapillary pool analysis, or not;
2. Evidence of abnormal prolonged TTP/prolonged MTT/ with moderately reduced CBF & CBV is consistent with more significant oligemia (ischemic penumbra); this may be partially improved by collateral, or not.
3. Evidence of abnormal prolonged TTP, plus signal dropout within the central part of the prolonged MTT (out of range effect caused by virtually no transcapillary flow), plus markedly reduced or absent CBF & CBV is consistent with advanced oligemia (dense ischemic core). If the MTT signal loss is severe (all black) then venous stasis/venous collapse has likely been added to the afferent arterial block. These cases can end up as sequestered infarctions.
4. Are there findings consistent with the physiologic based hyperemia in the collateral stroke zone with increased TTP/MTT/CBF/CBV; collateral zone changes will be adjacent to the positive diffusion area on MR and does not show contrast leak on CTA.
5. Are there findings more consistent with post ischemic dysautoregulation with increased TTP/MTT but reduced CBV/CBF); these areas may show leak of contrast on CTA and will be within the positive diffusion area on the MR.
6. Final three observations (characteristic of arterial stroke): a.do the areas of oligemia match specific, recognizable, arterial perfusion zones; b. do these zones affect eloquent sites or major white matter tracts; and finally, c. there must be a sharp delineation at the border between the ischemic tissue and the adjacent non ischemic tissue.
7. Note: CT perfusion is insensitive to brainstem infarctions mainly due to beam hardening artifact produced by the skull base.
Note CT perfusion is obtained after the 1st bolus (i.e. 1st pass) of contrast and timed based on opacification of normal proximal artery opacification in the head; there is no recirculation effect. Therefore, CT perfusion does not reflect the effects of functional collateralization. Thus, evidence of low CBV and CBF may overestimate the depth of injury in the stroke-zones.
Purpose
1. Evidence of abnormal prolonged TTP/prolonged MTT/ with partially reduced CBQ (flow)/partially reduced CBV (volume) is consistent with oligemia (tissue at risk); this may be improved by collateral on the CTA venocapillary pool analysis, or not;
2. Evidence of abnormal prolonged TTP/prolonged MTT/ with moderately reduced CBF & CBV is consistent with more significant oligemia (ischemic penumbra); this may be partially improved by collateral, or not.
3. Evidence of abnormal prolonged TTP, plus signal dropout within the central part of the prolonged MTT (out of range effect caused by virtually no transcapillary flow), plus markedly reduced or absent CBF & CBV is consistent with advanced oligemia (dense ischemic core). If the MTT signal loss is severe (all black) then venous stasis/venous collapse has likely been added to the afferent arterial block. These cases can end up as sequestered infarctions.
4. Are there findings consistent with the physiologic based hyperemia in the collateral stroke zone with increased TTP/MTT/CBF/CBV; collateral zone changes will be adjacent to the positive diffusion area on MR and does not show contrast leak on CTA.
5. Are there findings more consistent with post ischemic dysautoregulation with increased TTP/MTT but reduced CBV/CBF); these areas may show leak of contrast on CTA and will be within the positive diffusion area on the MR.
6. Final three observations (characteristic of arterial stroke): a.do the areas of oligemia match specific, recognizable, arterial perfusion zones; b. do these zones affect eloquent sites or major white matter tracts; and finally, c. there must be a sharp delineation at the border between the ischemic tissue and the adjacent non ischemic tissue.
7. Note: CT perfusion is insensitive to brainstem infarctions mainly due to beam hardening artifact produced by the skull base.
Prior Study
Noncontrast Head CTDense mural calcification in Rt. ICA which projects over the arterial lumen; this could represent a site of high cervical Rt. ICA flow-limiting stenosis. No apparent hyperacute stroke is evident
