Hyperacute Arterial Stroke XII - Clinical Case Summary
Hyperacute Arterial Stroke XII - Clinical Case Summary
Hyperacute Arterial Stroke XII - Clinical Case Summary
SummaryHistory
36 year old male diabetic who was found down. Patient initially was unresponsive, and later exhibited a markedly depressed level of consciousness. Patient was uncooperative on presentation and aphasic.
Exams performed
CT head; CTA neck; CTA head;
Delayed post contrast head CT for analysis of the venocapillary pool; MR diffusion; MR flair; MR susceptibility
Prior available imaging reports
Noncontrast head CT
1. Acute thrombus in Lt. intracranial primary and probably secondary stem components of the Lt. ICA
2. Early cytogenic edema in both Lt. ACA & MCA territories, likely stroke age in the latter hyperacute timeframe (6 hours)
CT Perfusion was not obtained.
CTA of the neck
1. No flow limiting stenosis in the cervical arteries; high cervical ICA was not imaged.
2. Reduced lumen size of the Lt cervical ICA related to more distal (out of field) blockade.
CTA of the head (using initial post contrast exam)
1. Likely source of the left ICA arterial obstruction is a dissection of the very highest cervical and intrapetrous ICA segments
2. Complete thrombosis of both the intracranial/extradural and intradural Lt. ICA with no filling of the secondary stem A1, M1 branches nor any filling of the distal (A4, M4) arteries, which results in absence of any effective pial collateral to either the left ACA or MCA perfusion zones.
3. No filling of the left cerebral cortical or deep central veins. These same veins are all well seen on the normal right side. This raises the possibility of hemispheric dense ischemic core with venous collapse.
4. Cut-off of the opacified left P-com is indicative of incisural brain herniation on the left.
Post contrast CT for venocapillary pool analysis (estimate of tissue perfusion from comparison of the initial & delayed post contrast head CT)
1. Lt. primary stem thrombosis of the intracranial/extradural and intracranial portions of the Lt ICA
2. Only minimal peripheral pial collateralization is evident; the bulk of the Lt. ICA perfusion zone is within the dense ischemic core. This lack of pial collateral has reduced the transcapillary flow to nearly zero, which in turn results in venous stasis with the likely result being acutely sequestrated cerebrum. Needless to say, such venous collapse usually has a very poor clinical outcome.
3. There is no current hemorrhagic conversion.
4. There is early, but definite, downward transtentorial brain herniation.
MR Diffusion
1. There is a variation of diffusion MR imaging characteristic of completed arterial stroke, severely limited transcapillary flow and venous collapse. The DWI sequence is positive only on the periphery of the stroke-zone while the bulk of stroke is NOT hyperintense. Meanwhile the ADC is positive (hypointense) throughout the entire stroke-zone. This is the most advanced state for a dense ischemic core type of stroke. Presumably, the altered diffusion is the result of high tissue levels of deoxyhemoglobin causing phase shift signal loss. This is an ominous finding and will not likely respond favorably to interventional stroke therapy. It may however, cause malignant brain swelling, which may require emergent cranial decompression.
MR Flair
1. Acute thrombus is now evident in the high cervical Lt. ICA, as well as the intradural ICA.
2. Aypical MR diffusion appearance related to suppression of signal most likely caused by the susceptibility artifact associated with high levels of deoxyhemoglobin within areas of venous stasis. This is consistent with a sequestered infarction, which is the worst form of arterial stroke. This involve all but the outer periphery of the left ACA and left MCA perfusion zone. Strokes of this type will not likely respond favorably to interventional stroke therapy.
3. There is evidence of mesial parahippocampal gyrus displacement, which is indicative of the start of downward brain herniation. This patient may, therefore, require cranial decompression if malignant brain swelling occurs.
4. There is a small mesial lenticulostriate perforator stroke without features of sequestered infarct.
MR Susceptibility (SWI)
1.There is blooming artifact in the proximal intradural left ICA indicating acute thrombus.
2. There is blooming artifact in the deep medullary veins indicating both venous stasis and venous thrombosis in the draining cortical veins and superior sagittal sinus. These findings confirm the presence of venous egress obstruction.
3. The stroke-zone, for the most part, is considered a completed, acutely sequestered infarction without transcapillary blood flow, which is very unlikely to be improved by stroke intervention.
1. Acute thrombus in Lt. intracranial primary and probably secondary stem components of the Lt. ICA
2. Early cytogenic edema in both Lt. ACA & MCA territories, likely stroke age in the latter hyperacute timeframe (6 hours)
CT Perfusion was not obtained.
CTA of the neck
1. No flow limiting stenosis in the cervical arteries; high cervical ICA was not imaged.
2. Reduced lumen size of the Lt cervical ICA related to more distal (out of field) blockade.
CTA of the head (using initial post contrast exam)
1. Likely source of the left ICA arterial obstruction is a dissection of the very highest cervical and intrapetrous ICA segments
2. Complete thrombosis of both the intracranial/extradural and intradural Lt. ICA with no filling of the secondary stem A1, M1 branches nor any filling of the distal (A4, M4) arteries, which results in absence of any effective pial collateral to either the left ACA or MCA perfusion zones.
3. No filling of the left cerebral cortical or deep central veins. These same veins are all well seen on the normal right side. This raises the possibility of hemispheric dense ischemic core with venous collapse.
4. Cut-off of the opacified left P-com is indicative of incisural brain herniation on the left.
Post contrast CT for venocapillary pool analysis (estimate of tissue perfusion from comparison of the initial & delayed post contrast head CT)
1. Lt. primary stem thrombosis of the intracranial/extradural and intracranial portions of the Lt ICA
2. Only minimal peripheral pial collateralization is evident; the bulk of the Lt. ICA perfusion zone is within the dense ischemic core. This lack of pial collateral has reduced the transcapillary flow to nearly zero, which in turn results in venous stasis with the likely result being acutely sequestrated cerebrum. Needless to say, such venous collapse usually has a very poor clinical outcome.
3. There is no current hemorrhagic conversion.
4. There is early, but definite, downward transtentorial brain herniation.
MR Diffusion
1. There is a variation of diffusion MR imaging characteristic of completed arterial stroke, severely limited transcapillary flow and venous collapse. The DWI sequence is positive only on the periphery of the stroke-zone while the bulk of stroke is NOT hyperintense. Meanwhile the ADC is positive (hypointense) throughout the entire stroke-zone. This is the most advanced state for a dense ischemic core type of stroke. Presumably, the altered diffusion is the result of high tissue levels of deoxyhemoglobin causing phase shift signal loss. This is an ominous finding and will not likely respond favorably to interventional stroke therapy. It may however, cause malignant brain swelling, which may require emergent cranial decompression.
MR Flair
1. Acute thrombus is now evident in the high cervical Lt. ICA, as well as the intradural ICA.
2. Aypical MR diffusion appearance related to suppression of signal most likely caused by the susceptibility artifact associated with high levels of deoxyhemoglobin within areas of venous stasis. This is consistent with a sequestered infarction, which is the worst form of arterial stroke. This involve all but the outer periphery of the left ACA and left MCA perfusion zone. Strokes of this type will not likely respond favorably to interventional stroke therapy.
3. There is evidence of mesial parahippocampal gyrus displacement, which is indicative of the start of downward brain herniation. This patient may, therefore, require cranial decompression if malignant brain swelling occurs.
4. There is a small mesial lenticulostriate perforator stroke without features of sequestered infarct.
MR Susceptibility (SWI)
1.There is blooming artifact in the proximal intradural left ICA indicating acute thrombus.
2. There is blooming artifact in the deep medullary veins indicating both venous stasis and venous thrombosis in the draining cortical veins and superior sagittal sinus. These findings confirm the presence of venous egress obstruction.
3. The stroke-zone, for the most part, is considered a completed, acutely sequestered infarction without transcapillary blood flow, which is very unlikely to be improved by stroke intervention.
Overall impression
1. The initial CT and CTA demonstrates a complete left ICA occlusion at the dural ring. There is virtually no parenchymal filling of the venocapillary bed on the first pass head CT. Venocapillary opacification improves on the 2nd pass head CT from pial collateral along the ventral cerebrum and the occipital region. The remaining left MCA perfusion zone fails to demonstrate collateralization at the venocapillary level.
2. The MR exam performed hours after the CTA demonstrate features of venous stasis in the larger egress veins on the MR SWI. The MR diffusion evidence of virtually absent venocapillary stasis. The accumulation of deoxyhemoglobin produces a variation of positive diffusion restriction. The DWI is only positive on the periphery of the stroke zone; the central ischemic core deoxyhemoglobin prevents the expected hyperintense signal, while the ADC is positive throughout the entire infarcted area. These are the SWI and MR diffusion features of a large volume sequestered infarction.
2. The MR exam performed hours after the CTA demonstrate features of venous stasis in the larger egress veins on the MR SWI. The MR diffusion evidence of virtually absent venocapillary stasis. The accumulation of deoxyhemoglobin produces a variation of positive diffusion restriction. The DWI is only positive on the periphery of the stroke zone; the central ischemic core deoxyhemoglobin prevents the expected hyperintense signal, while the ADC is positive throughout the entire infarcted area. These are the SWI and MR diffusion features of a large volume sequestered infarction.
Lessons to be learned
1. This case illustrates what happens when larger areas of brain tissue perfusion approaches zero or virtually no transcapillary blood flow. Features of acutely sequestered infarctions include: no apparent afferent arterial input and no apparent venous filling on head CTA, absent central stroke zone venocapillary pool CT density, atypical reversed diffusion and FLAIR, and venous stasis or venous collapse if the cortical veins show blooming artifact. We point out that while large sequestered infarcts are uncommon, small areas of sequestered infarctions are not uncommon at all. These are seen in numbers of case examples in this instructional clinical stroke example. Later, they will be seen in venous stroke as well. We also point out that sequestered infarctions in moderate size areas can, and do, present in chronic phase, as ring enhancing masses simulating brain tumors. When these are resected the pathology reveals fibrin filled vessels and extensive parenchymal hemosiderin; these are currently called chronic completed infarctions, but previously were in fact called sequestered infarctions (which is the term I use in order to not cause confusion. I use the term completed infarction to mean an acute infarction which includes the ischemic cascade AND the glutamate cascade. In my parlance a completed infarction can then proceed to either liquefactive necrosis or chronic sequestration based on whether the stroke-zone is reperfused in the subacute stroke phase.
2. The case illustrates the value of FLAIR in identifying thrombus in the extradural arteries, while the SWI demonstrates thrombus in intradural arteries and intradural egress veins. MR-swi is the only sequence that can reliable directly image the deep medullary venous system. It can distinguish between hyperemia, venous stasis and venous collapse. Imaging the deep venous system is very helpful in predicting stroke outcome.
3. This case also illustrates how venous egress obstruction produces rapid brain swelling (malignant brain swelling), mass effect without hemorrhagic conversion, and potential early subfalcine and transtentorial herniation.
2. The case illustrates the value of FLAIR in identifying thrombus in the extradural arteries, while the SWI demonstrates thrombus in intradural arteries and intradural egress veins. MR-swi is the only sequence that can reliable directly image the deep medullary venous system. It can distinguish between hyperemia, venous stasis and venous collapse. Imaging the deep venous system is very helpful in predicting stroke outcome.
3. This case also illustrates how venous egress obstruction produces rapid brain swelling (malignant brain swelling), mass effect without hemorrhagic conversion, and potential early subfalcine and transtentorial herniation.
Recommendations
Watch the included summary video for this instructional case.