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how to tell a chronic occluded MCA or ICA based on CT perfusion scan?
please enlighten me
please enlighten me
how to differentiate chronic from acute occlusion
- Thread starter neuronwangyu
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Determining whether or not there is a restriction in blood flow through the MCA or ICA is easy: you can see and measure the blockage in these arteries on conventional, digital substraction, or MR angiography...Whether or not the obstruction is acute, subacute, or chronic is more difficult to ascertain. Acute obstructions will lead to acute tissue damage, evidenced by such things as edema. More chronic obstructions will lead to frank infarction and neuronal loss/atrophy. MRI allows for this determination.
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You can look for vessel collateralization, and/or movement of the borderzone up or down. MTT can be increased in both acute and chronic ICA occlusion, but CBV should be relatively normal if the territory is chronically compensated, although it might be slightly high chronically because of vessel dilation from autoregulation.
Sometimes.
Sometimes.
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CTP is not for evaluation of chronicity of the intracranial vessel occlusion. The CBV coild be theoritically normal in chronic occlusion, and Mean transiene time and Peak time could be decreased in Both acute and chronic occlusion.
That's why people look at the plain CT and CTA instead, for all signs of chronic occlusion, such as old strokes, increase in collaterals and thickening of certain vessels such as Acom or Pcom or any other blood vessels which is compensating for the occlusion.
However, the most important thing is pt's clinical history with sudden onset of symptoms usually tells you something acute happened either in the patent artery or a partially stenotic vessel.
TCD is also helpful, if you have previous studies on pt.
That's why people look at the plain CT and CTA instead, for all signs of chronic occlusion, such as old strokes, increase in collaterals and thickening of certain vessels such as Acom or Pcom or any other blood vessels which is compensating for the occlusion.
However, the most important thing is pt's clinical history with sudden onset of symptoms usually tells you something acute happened either in the patent artery or a partially stenotic vessel.
TCD is also helpful, if you have previous studies on pt.
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You could take a history.
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zing!
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Apart from those already mentioned, sometimes CT/MR perfusion may be absolutely normal in the presence of an ipsilateral ICA/MCA occlusion due to good collaterals (indication chronicity). In few pts with Moyamoya or prior MCA/ICA occlusions that were followed overtime at my institution, the parent artery (ICA) in the proximal segment gets diminished in calibre over several years due to low flow downstream. Some neurosurgeons theorize that with low flow the proximal ICA arterial walls kind of 'sag' and collaterals from ext carotid and posterior circ develop over several years.
Another paradox, pts with chronic occlusion can present with a recent/acute stroke either due to collateral compromise or stump embolism. In any case we know that ECA/MCA bypass is not an option now as COSS has shown. In rare instances we still consider ECA-MCA bypass in pts who continue to remain pressure dependent despite medical regimen.
Another paradox, pts with chronic occlusion can present with a recent/acute stroke either due to collateral compromise or stump embolism. In any case we know that ECA/MCA bypass is not an option now as COSS has shown. In rare instances we still consider ECA-MCA bypass in pts who continue to remain pressure dependent despite medical regimen.
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In a similar vein to this...
In my residency, when using CT modalities for the workup of AIS, we were taught to evaluate the MTT and CBV maps to determine potential mismatch. This was usually done in cases of potential IAtPA or neurointervention. We would use the CBV as "baseline" and superimpose the MTT over the CBV to check for match or mismatch of the defect.
I try and keep up on neuroradiology as a hobby, and note that the trend appears in fact to be to compare the CBV and CBF maps when attempting to ascertain mismatch in acute stroke.
Do any of you guys have comments about the propriety (or lack) of these two methods. I would also welcome a paper reference if that works better. My only neuroradiology texts are Osborn's "Diagnostic Neuroradiology" and the "Requisites" book by Grossman and Yousem.
TN? Strokeguy? Anybody?
In my residency, when using CT modalities for the workup of AIS, we were taught to evaluate the MTT and CBV maps to determine potential mismatch. This was usually done in cases of potential IAtPA or neurointervention. We would use the CBV as "baseline" and superimpose the MTT over the CBV to check for match or mismatch of the defect.
I try and keep up on neuroradiology as a hobby, and note that the trend appears in fact to be to compare the CBV and CBF maps when attempting to ascertain mismatch in acute stroke.
Do any of you guys have comments about the propriety (or lack) of these two methods. I would also welcome a paper reference if that works better. My only neuroradiology texts are Osborn's "Diagnostic Neuroradiology" and the "Requisites" book by Grossman and Yousem.
TN? Strokeguy? Anybody?
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Hi danielmd06,
The mismatch principle with CT perfusion is still CBV and CBF, but some people use TTP (time to peak) instead of CBF. In any case this is still theoretrical as far as CT imaging is concerned since we have no randomized thrombolytic trial using CT criteria (published or presented so far). What further confuses the picture is that most people use 'visual' inspection to look for mismatch which is highly dependent on the manufacturer of the CT scanner. There is still no standardization of the values of CBF/V and TTP on the CT scanners (we tend to look at the colored images) among the manufacturers (ie GE, Siemens, Philips, Toshiba...). In other words we just visually inspect the colored images to look for so called mismatch, but there is no standardization of the color coding yet. MRIs are still better. We have some trials looking at MRI mismatch criteria with IV thrombolytics in extended time windows, but again the mismatch theory is promising as seen with results from DEDAS, DEFUSE, EPITHET and DIAS2, but doesn't necessarily translate into outcomes. So we still need to further fine tune the mismatch criteria before using it clinically as a definitive marker of tissue at risk. MRI is further along the authentication road than CT perfusion, but a lot of work is still needed. We need to differentiate 'benign oligemia' (tissue that may be slightly ischemic, but will not infarct) from actual tissue at risk. It looks like CT tends to overestimate the tissue at risk. Further trials (perhaps MRRESCUE, and DIAS3/4) could shed more light on this.
The mismatch principle with CT perfusion is still CBV and CBF, but some people use TTP (time to peak) instead of CBF. In any case this is still theoretrical as far as CT imaging is concerned since we have no randomized thrombolytic trial using CT criteria (published or presented so far). What further confuses the picture is that most people use 'visual' inspection to look for mismatch which is highly dependent on the manufacturer of the CT scanner. There is still no standardization of the values of CBF/V and TTP on the CT scanners (we tend to look at the colored images) among the manufacturers (ie GE, Siemens, Philips, Toshiba...). In other words we just visually inspect the colored images to look for so called mismatch, but there is no standardization of the color coding yet. MRIs are still better. We have some trials looking at MRI mismatch criteria with IV thrombolytics in extended time windows, but again the mismatch theory is promising as seen with results from DEDAS, DEFUSE, EPITHET and DIAS2, but doesn't necessarily translate into outcomes. So we still need to further fine tune the mismatch criteria before using it clinically as a definitive marker of tissue at risk. MRI is further along the authentication road than CT perfusion, but a lot of work is still needed. We need to differentiate 'benign oligemia' (tissue that may be slightly ischemic, but will not infarct) from actual tissue at risk. It looks like CT tends to overestimate the tissue at risk. Further trials (perhaps MRRESCUE, and DIAS3/4) could shed more light on this.
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I second this. Plus it is only a snapshot of a moving process.
I've also wondered precisely what this "risk" word means. We use that word without any understanding of the degree of risk, but also without really knowing if this is the right word - with it's emotional implication of danger and ability to save. I've seen IV tPA cases become candidates of IA procedures - but then fail to get them for whatever reason - and have a volume defect matched to 24 hour stroke.
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It is not as easy as you mentioned here, YOU can see a pt with acute symptoms on chronic occlusion.
Second, there is no such a thing as chronic symptoms in stroke clinical presentations, except rare cases.
The history is very important, ie. the series of events.
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By chronic symptoms I meant old stroke symptoms (i.e. spastic hemiparesis, aphasia, etc...). Around here, there are rehab units full of these patients so I don't think it's that rare.
My first post was a failed attempt at humor.
My first post was a failed attempt at humor.
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