Ischemic Penumbra visible on CT?

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Immutef

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Is the penumbra visible on a CT scan?

A brief internet search leads to the conclusion that whether the penumbra is there or not, can be ascertained by CT, though whether it is 'visualized' is not clear.

On CT, a penumbra is demonstrated as a mismatch between CBF and CBV maps. This may be difficult for a clinician to interpret and often requires the expertise of a trained diagnostic radiologist. On the other hand, a diffusion-perfusion mismatch on MRI can be easily appreciated by a clinician with little or no training in diagnostic radiology.

Is the presence of the penumbra, something that can be inferred, or visualized as a hypoxic event?

Thank you,
Immutef
 
This quote you have referenced is talking about CT-perfusion slabs. This series is performed separately from the standard non-con head CT, and is also different from CTA. Depending on the way specific hospitals manage the decision-making and workflow of acute strokes, the CT-P can be very useful.
 
Is the penumbra visible on a CT scan?

A brief internet search leads to the conclusion that whether the penumbra is there or not, can be ascertained by CT, though whether it is 'visualized' is not clear.



Is the presence of the penumbra, something that can be inferred, or visualized as a hypoxic event?

Thank you,
Immutef

I worked on a 320 detector row CT perfusion imaging research project, the main goal being the ability to identify the ischemic penumbra with CT perfusion, in hopes of altering tPA administration times to a case by case basis, instead of mandating it's administration within 4 1/2 hours. We were definitely able to identify the ischemic penumbra (after playing around with the Cerebral Perfusion and Mean transit times), but the project hasn't been accepted for publication yet. It's definitely possible with the right tools. I was really impressed by 320 detector row CT perfusion, it can be done more quickly than standard CT and yields so much more information. (you can also see the level of the cerebellum while imaging the entire cerebral hemispheres, allowing phenomena such as crossed cerebellar diaschisis to be evaluated).
Basically though, if we're able to identify the reversible ischemic penumbra, tPA could be given on a case by case basis based on how much tissue was recoverable.
 
At our place, decisions on stroke thrombolysis & IA therapy are often made on CTA/CTP. The caveat is that CTP is an indirect & semi-quantitative measure of cerebral perfusion. It basically involves comparing the MTT & CBV (CBF is just a ratio of the 2 & is not helful in identifying dead or living penumbra) in the "normal" hemisphere with the one that is affected by acute stroke. Several factors like proximal carotid occlusions, very low EFs, contrast timing, chronic small vessel disease & gliotic areas from old strokes or other brain pathology can seriously impair interpretation of these scans.

Hard & fast threshold "cut-offs" for CVB decrease or MTT increase have not always correlated well with dead brain or tissue at risk (penumbra) as reported in some radiology journals. Penumbra is usually identified as an area with increased MTT with preserved CBV (the initial hyperemic phase of cerebral ischemia). This is what is traditionally "mis-matched" tissue (penumbra at risk of stroking out if reperfusion is not established). Completed strokes show up as increase MTT with matched reduced CBV (an area of matched defect). Reperfusing this tissue is not going to be beneficial & may in fact be harmful, as the stroke is complete . One can precipitate either reperfusion hemorrhage or malignant cerebral edema by opening vessels in such patients, specially if the size of infarcted tissue is >70-80 mls (one-third of the MCA territory) and or the patient is relatively young. However, in clinical practice, this is not always seen to be true.

In our experience, ASPECTS scores have proven to be better predictors of post-interventional functional outcomes than a CTP. In fact, we tend to make decisions on IA/Mechanical interventions based on both ASPECTS & CTP (if it is a good quality scan) provided the patient has a pre-morbid mRS of <3. If the ASPECTS are bad, the outcome is usually bad regardless of what the CTP shows.
 
Bonran, that's seriously impressive! Where can I find more information on the ASPECTS scoring system? (please don't tell me to 'google it' lol)
 
bblue

The reason why ASPECTS works so well in predicting functional outcomes in stroke is quite simple. The ASPECTS score is substracting dead "grey matter" sites in an MCA distribution from healthy ones. It represents early ischemic change. All these grey matter sites have some motor role which, if the threshold of 7 or<7 is crossed, will result in a bad functional outcome. These grey matter sites are not "usually" affected by chronic small vessel disease. Hence, we have a more quantifiable & replicatable scoring system than a semi-quantitative system prone to multiple imperfections like CTA/P.

For the original article on ASPECTS scoring & functional outcomes read:

Barber PA, Demchuk AM, Zhang J, Buchan AM, for the


ASPECTS Study Group.
The validity and reliability of a novel quantitative CT score in predicting outcome in hyperacute stroke prior to thrombolytic therapy.

Lancet 2000;355:1670&#8211;1674


 
bblue

The reason why ASPECTS works so well in predicting functional outcomes in stroke is quite simple. The ASPECTS score is substracting dead "grey matter" sites in an MCA distribution from healthy ones. It represents early ischemic change. All these grey matter sites have some motor role which, if the threshold of 7 or<7 is crossed, will result in a bad functional outcome. These grey matter sites are not "usually" affected by chronic small vessel disease. Hence, we have a more quantifiable & replicatable scoring system than a semi-quantitative system prone to multiple imperfections like CTA/P.

For the original article on ASPECTS scoring & functional outcomes read:

Barber PA, Demchuk AM, Zhang J, Buchan AM, for the


ASPECTS Study Group.
The validity and reliability of a novel quantitative CT score in predicting outcome in hyperacute stroke prior to thrombolytic therapy.

Lancet 2000;355:1670–1674



Thanks Bonran, I'm going to check out the article right now!
Did you or anyone you know ever look at crossed cerebellar diaschisis with CT Perfusion? We were starting to see a slight correlation with migraines when I wrapped up my portion of the study..
 
Crossed cerebellar diaschisis is the hypometabolism noted on functional MRIs or FDG-PETs in the contralateral cerebellum & ipsilateral pons/thalamus/cortex in patients with ipsilateral supratentorial lesions like strokes/tumors/trauma. The phenomena occurs because of suppression of cortico-ponto-cerebellar connections. Since migraines are vascular phenomena, it is quite possible to see cerebellar hypometabolism in contralateral structures on functional imaging.

In clinical practice, 326 detector CT scanners are not commonly used yet. So, we dont get to see posterior fossa structures often. Besides, we dont often do CT perfusions in patients with common migraines.

In patients with complex (symptomatic) migraines, some may end up getting CT perfusions as, by default, migraine is a diagnosis of exclusion & strokes have to be ruled out in them. But again, we do not image the cerebellum with the 64 detector CTs where just 4 predetermined slices of the MCA territory are looked at in a CTP.

Once large vessel strokes are ruled out on CTA, it would not be ethical to study the cerebellum anyway because of the dose of radiation involved with a 326 detector CT scanner in migraineurs (most being young women who may end up developing thyroid ca. or leukemias by the time they are middle aged if they kept getting scanned with a 326 detector CT everytime they had a headache-something which happens often in EDs specially in peripheral hospitals where a neurologist is not always present to confidently diagnose complex migraines at the bedside).
 
It's interesting because I was looking for research on crossed cerebellar diaschisis a few months ago, and there were some studies done in approximately 1980, then there's basically nothing for about 20 years. To be honest, from what I could tell while researching, it just seemed like an insignificant phenomena with variable correlation to strokes. I wanted to get your take though because you obviously know what you're talking about.
I'm not positive about this, but I thought there was actually less (or equal) radiation using 320 detector row CT Perfusion vs. 'standard' 64 CT..?
 
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