The colorful art and science of perfusion imaging

Deconvolution
Deconvolution in action

Do you know what deconvolution is and how it works? Although I seriously doubt that any Neurologist is richer knowing that, it certainly is reassuring to understand why CT perfusion has so many variations, interpretations and limitations.

In my view, CT perfusion has many applications in Neurology (not to speak of Oncology):

  • Determine the penumbra of a stroke: this deserves some comments. As a quantitative method CT perfusion fails. You just cannot expect to quantify the proportion of the penumbra, because there are too many unknowns in the computation and interpretation. But you can determine the mere existence of a penumbra quite reliably (and it is still the best thing we have apart from CT+CTA).
  • Distinguish status epilepticus from postictal paralysis: the former shows hyper perfusion, while the latter looks like a stroke without core (total mismatch).
  • Recognize migraines that you would otherwise treat with tPA (again, this looks like a stroke without core, but the hypoperfusion does not respect the boundaries of the arteries and the arteries are open!).
  • Prove hyperperfusion in a hyperperfusion syndrome
  • Show the downstream effects of vasospasm in SAH
  • Determine the vascular reserve with acetazolamide – ok, this is easier done with duplex ultrasound…

Here is how I use CT-perfusion in acute stroke:

  • Indications: unknown time window, stroke mimics in tpa situations
  • Require the clinician to determine the exact region where to look
  • Use MTT or TTP to screen for ANY problems in the perfusion of the brain – wherever it is slowed, you have to do the CBF/CBV magic
  • Where CBF is quite low (don’t rely on absolute values!) and CBV is also down, there is some infarct core. Now go back to the NCCT – there should be some early ischemic signs here.
  • Where CBF is not so low as in the core and CBV is only slightly down or up there is penumbra
  • If in doubt, do exact ROI comparisons (left vs. right)
  • Now decide: is the clinical picture dominated by the infarct core or the penumbra? How much cortical structures are in the core, prone to bleed if you open up the artery? Does CTA vessel occlusion (sometimes you find the occluded vessel easier, if you know where the problem sits in perfusion CT) correspond to the perfusion deficit?

Now to the gory details:

  • Arterial input function: You should use a good arterial vessel to get the arterial input function, often the ACA is in the slice studied. But the problem is that the ACA might take part in the supply of your stroke via collateralization and it might also be disturbed by stenosis (say A1 or ICA). This can lead to very bad data.
  • Without arterial input function you cannot do deconvolution (which basically shows you how your tissue perfusion would look like if the fuzzy contrast bolus would look like a perfect rectangle-shaped push of contrast agent, not a wave) properly, so you have to use things like maximum-slope-methods and so forth.
  • Same for venous outflow.
  • The choice of algorithm is quite important – there seem to be optimal ones, if you believe this paper.
  • There are plenty of assumption underlying most of the algorithms, such as intact blood brain barrier, which usually hold in acute stroke, but are violated in things like post-CEA-hyperperfusion or SAH.
  • Sometimes, the cardiac output is so bad that the perfusion curve ends too early. You can often still use TTP in that case, but all deconvolution methods must fail.

For many more details see

Thunderclap headache

We encounter one of these at least every week, so the question of how much diagnostics to order after a painstakingly thorough history and a complete physical including fundoscopy is quite important. Obviously, CT and a spinal tap is always necessary, but then what? I think, the minimum in fact includes CT-angiography (using a delay of 8-10s) to image both arteries and veins, in order to rule out SVT and RCVS (both of which are highly relevant). In addition, I recommend a follow-up MRI after discharge from the ER.
We discuss the differential, consisting of at least:

  • SAH/sentinel headache
  • RCVS
  • Dissection
  • Stroke
  • SVT
  • ICH and other bleeds (retroclival hematoma)
  • PRES
  • Meningitis
  • SIH
  • Pituitary apoplexy
  • a lot of zebras, such as third ventricle colloid cyst, MI, Takotsubo, …

As a reference I recommend this article by Ducros of 2013 (he seems to be an authority on this topic as well as RCVS).

TPMA or the wonderful world of imaging features of seizures and status

We have a patient on our ICU that suffered through 3 weeks of insufficiently effective therapy of epileptic status from a right occipital astrocytoma after finishing his radiation therapy. MRI showed extensive bilateral insular, thalamic and bitemporal T2 bright and DWI dark lesions that even expanded with developing cortical microbleeds.

Before I list some of the relevant publications on this fascinating topic, let me mention a few take home messages:

  • Focal status can show up as DWI bright, ADC dark, T2 bright lesions that are potentially reversible.
  • Generalized status shows a peculiar distribution of these lesions in the insula, temporoparietal cortex and pulvinar. If advanced and ongoing, the changes can spread from the cortex to the subcortical white matter and even further.
  • The changes can mimic tumor progression (as in our case) although the pattern is quite succinct.
  • While in status, many patients have hyperperfusion (e.g. in CT-perfusion or MRI perfusion) around their epileptic focus. Afterwards, there may be hypoperfusion and in fact perfusion studies might help in distinguishing the two entities (if EEG is not immediately available) in nonconvulsive or subtle status, but remember that epileptics tend to get too many CTs anyway.

Literature

 

 

Sonoencephalography

We concentrate on the non-classical neurocritical applications of transcranial b-picture sonography, i.e., everything apart from investigating the vessels for their own sake. Starting with a female patient with ICH due to sinus thrombosis, we discuss the neuroanatomy of the mesencephalic and diencephalic slices and consider

  • quantification of midline shift
  • screening for temporal or deep ICH
  • monitoring of ICP (using the pulsatility)

References

  • The Widder (in its recent new edition)
  • This article on using transcranial midline shift assessment in deep ICH

Radiation risk of CT

 

Today we saw a 40 yo patient with symptomatic epilepsy after traumatic brain injury, who – always after a seizure – suffered through 18 CTs of his brain during the last 2 years. One of the residents rightfully asked about the quality of his eyesight and what his risk of brain cancer was.

Reminded of an excellent article in The Journal 2010 (someone downloaded the full text here) I looked up this study by the same author in order to be able to present our group some data. In essence we don’t really know much about the risk of CT and other medical radiation (such as DSA), since all our data stems from Hiroshima and Nagasaki – there is no better data.

Left with this uncertainty, we discussed the way, how ionizing radiation leads to cancer and how, faced with an uncertain risk, we can reduce the number and intensity of our scans, especially for those epilepsy patients. Maybe it helps a bit…

Stroke MRI

When do you order an MRI in stroke? This is absolutely unclear – at least to me. We certainly know that MRI is way better than CT for practically everything, but in which situation does MRI add benefit to a patient that already has a CT? Does it help to time anticoagulation? When do you use it to identify the stroke pattern? How often does it surprise you with things like vasculitis?

Regardless of these questions, we do invoke MRI in about half of our patients. So we better know how to read them and this is what we did in today’s session: use our PACS viewer (in this case ImPaxx), review the standard sequences of stroke MRI, talk about DWI, ADC, FLAIR, SWI, blade and so on.

 

Flow diverters for intracranial aneurysms

Due to our wonderful investigative reporters at Frontal we have a small PR catastrophe here. Lamentably a patient died after a flow diverter was used to treat a giant aneurysm of the distal ICA. Now the TV show couldn’t possibly get the details right, but we covered the topic of flow diverters nevertheless, since they are often the only option to treat inoperable and potentially lethal aneurysms (which are rare). In fact, they might become a tool to treat aneurysms more effectively endovascularly since they could break through the pathophysiological cycle that leads to regrowth of the aneurysm – but this is still controversial.

As for references

When evaluating papers about these technical gadgets, consider

  • how many acutely bleeding patients were treated (this is problematic since the theory implies that the aneurysm is only slowly shrinking after FD deployment)?
  • how many potentially operable aneurysms were treated (there is an ethic controversy)?
  • the usual EBM facts (length and completeness of follow-up).