Open discussion: Does frontal lobe oxygenation measured by near-infrared spectroscopy represent cerebral oxygenation ?

With accumulating evidence regarding an extracranial contamination of the near-infrared spectroscopy signal (here, here and here), it would be interesting to use this space to have a friendly debate around that issue…

So, does frontal lobe oxygenation measured by near-infrared spectroscopy represent cerebral oxygenation ?

What do you think ?

Update (14/03/2014 – 14h23): Initially, I wanted to have this debate with colleagues involved in studies related to vasopressors/exercise/whole body heating/etc. However, after a discussion on twitter with researchers involved in neurocognition, you guys are more than welcome to comment ! I am here to learn !

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10 thoughts on “Open discussion: Does frontal lobe oxygenation measured by near-infrared spectroscopy represent cerebral oxygenation ?

  1. In a scenario of unchanged skin oxygenation it’s a measure of changes in brain oxygenation. In a scenario of unchanged brain oxygenation it’s a measure of changes in skin oxygenation…

    1. And in situations of unknown changes in brain oxygenation and changes in skin oxygenation (let’s say administration of vasopressors…) ? In that case, the NIRS signal will be “influenced” or “explained’ by changes in skin oxygenation ?

  2. Also, if administration of phenylephrine/noradrenaline(+ maintained PaCO2) leads to : no change in ICA blood flow+increased MCAVmean+reduced ScO2+small reduction in Skin O2+no change in SjvO2 or ScapO2…what is the interpretation ? The reduction in ScO2 is “explained” by changes in skin O2 because there is no change in global brain oxygenation or there is a redistribution of blood flow within the brain?

  3. Nirs can be used to assess changes in regional flow/O2 extraction. During surgery I use to NIRS as a quality monitor to check whether the level of circulation is sufficient for peripheral flow. Importantly individual CO2 reactivity is unknown and especially in elderly patients and patients with diabetes and Vascular disease. In anethesised patients ventilation is adjusted in accordance to capnographic determined CO2 that may be higher than arterial CO2 and therefore endtidal CO2 is maintained at 4-4.5 kPa. This level however may be too low. With NIRS it is easy to evaluate whether the selected CO2 is sufficient for the brain. Muscle usually do not react to changes in CO2 contrasting to the respons of the brain.

    1. And if you add vasopressors to your mix, are you still confident that the NIRS signal follows what’s going on in the frontal lobe of your patients 🙂 ?

  4. Nice Article above Patrice? I would second Peters response, and state that as long as the baseline conditions for which the relative NIRS signal was acquired remains the same then the NIRS does accurately reflect cerebral tissue oxygenation. If this is true, then we should be able to observe changes in the oxygenation kinetics of the cortex as long as the possible contaminations at baseline stay the same.
    I have one question pertaining to the relationship of weighted a-v ratio measured via arterial jugular lines. Can anyone think of a reason why the a-v ratio would change during iso-oxic hypercapnic increases in CBF, but not during iso-capnic hypoxic increases in CBF. We have some data that suggest this, but we are struggling to form clear conclusions from our findings, and how to utilize this data in comparing it to the NIRS derived tissue saturation.

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