Case Notes
History
42 year old male presenting with acute right sided numbness and neck pain; history of seizures and hypertension.Exam
CT Perfusion
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.
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
Acute thrombus in the high cervical and vertical intrapetrous segments of the left cervical ICA without evidence of acute cerebral stroke. The history of acute upper neck pain makes dissection a likely possibility.Early post ischemic hypodensity in the left centrum semiovale.