Anesthesia induced burst suppression in humans - V1 is excluded

We've discussed anesthesia-induced burst suppression many times to do with NDE/OBE's, probably most notably with regards to Pam Reynolds NDE. But more generally with regards to general anesthesia in patients on the hospital operating table, who go into cardiac arrest, and sometimes later recall visual information apparently - quite bizarrely in my view - from the period of their resuscitation.

Up until now, the information I had was that anesthesia-induced burst-suppression was a cortex wide phenomena. But newer research opposes that view. Most interestingly is the finding that the visual areas of the human brain are completely disconnected from bursting... they don't burst at all! Could this interesting behavior of the visual cortex play some role with the typical hospital NDE/OBE during anesthesia?

Last year, Sirmpilatze's team published a paper where they mapped anesthesia-induced burst suppression in human brains (plus other primates, and rats) using fMRI. Their findings oppose the view that burst suppression is a global cortical event. Instead they find that the visual areas of the cortex in humans are completely disconnected from bursts. This confirms an earlier study from 2017 using both BOLD and EEG measurements.

There is an interesting discussion in the paper, with references to other papers, which report other interesting observations from other research teams.

Sirmpilatze et. al (2022) - "Spatial signatures of anesthesia-induced burst-suppression differ between primates and rodents"
https://doi.org/10.7554/eLife.74813

The main inter-species difference was the exclusion of visual areas (and parts of other unimodal
cortices) in primates, but not in rats. While bursts were traditionally viewed as synchronous cortex
wide events, recent work rather describes them as complex waves (Bojak et al., 2015) emerging
from a spatially shifting focus and rapidly spreading through the cortex (Ming et al., 2020).

Electrocortical recordings in propofol-anesthetized human patients revealed that some electrodes could
display continuous activity while others engaged in burst-suppression (Lewis et al., 2013). Together
with our results, this implies that brain areas may vary in their propensity for generating and/or
propagating bursts. Regional metabolic differences could underlie such variability, according to a proposed
neurophysiological-metabolic model of burst-suppression (Ching et al., 2012). This model posits that
suppressions occur when metabolic resources can no longer sustain neuronal firing, whereas bursts
constitute transient recoveries of activity—enabled by slow metabolic replenishment. The visual cortex
of primates could impose special metabolic demands and thus find itself at an extreme end of the
spectrum for burst propensity. Such special demands could arise from its many distinctive
characteristics—including cytoarchitecture, neurotransmitter receptor expression (Froudist-Walsh et al., 2021),
functional connectivity profile (Margulies et al., 2016), and cortical myelin density (Van Essen et al.,
2019).

We particularly suspect cortical myelin to play a role, considering that many areas excluded
from our primate burst-suppression maps—V1, MT, primary motor, and somatosensory cortices—are
among the richest in myelin (Van Essen et al., 2019). Conversely, rodents exhibit a more uniform
myelin distribution (Fulcher et al., 2019), which could translate in a likewise uniform propensity for
bursting

On the first row, you can see the BOLD Burst-Suppression pattern, and on the right, a heat-map showing that this pattern occurred across the majority of the cortex. On the second row, you can see the BOLD does not show the Burst-Suppression (BS) pattern, and the heat-map on the right shows that this is confined to the V1 Visual cortex area at the back of the head.


Click image to enlarge

It seem clear that V1 is acting differently from the majority of the cortex which is in burst-suppression. Why, or how, is unclear. They still don't have a good understanding of what is going on in burst-suppression, so it's also unclear what is going on in V1.

An earlier study Golkowski et. al. (2017) seemed to find the same disconnect between the majority of the cortex in burst-suppression, and the occipital parts of the brain (back of the head) https://doi.org/10.1002/brb3.679

This image Golkowski et. al. (2017) shows horizontal heat-map slices through the brain, with hot areas positively correlated with EEG, and cold areas anti-correlated with EEG. You can see the cold (blue) areas in the occipital regions, at the bottom of each slice.



It's unclear why the visual cortex is disconnected from the rest of the cortex under very high levels of anesthesia. It's clearly a very interesting phenomena. Sirmpilatze et. al (2022) at least replicates Golkowski's results, but further shows that this disconnect in visual cortex doesn't seem to occur in rodents.

When you read the discussion in both papers, it becomes clear just how puzzling and interesting this discovery is.

Lewis et al., 2013 investigated Burst-Suppression using invasive EEG (iEEG) recordings - as opposed to scalp EEG - in propofol-anesthetized human patients, and revealed that some electrodes could display continuous activity while others engaged in burst-suppression.

In this paper we have shown local cortical dynamics in the state of
burst suppression induced by propofol general anaesthesia.
Specifically, our results establish that (i) bursts and suppressions
can occur in a limited cortical region while continuous activity
persists in other areas;

https://doi.org/10.1093/brain/awt174

We've discussed anesthesia-induced burst suppression many times to do with NDE/OBE's, probably most notably with regards to Pam Reynolds NDE. But more generally with regards to general anesthesia in patients on the hospital operating table, who go into cardiac arrest, and sometimes later recall visual information apparently - quite bizarrely in my view - from the period of their resuscitation.

Up until now, the information I had was that anesthesia-induced burst-suppression was a cortex wide phenomena. But newer research opposes that view. Most interestingly is the finding that the visual areas of the human brain are completely disconnected from bursting... they don't burst at all! Could this interesting behavior of the visual cortex play some role with the typical hospital NDE/OBE during anesthesia?

Last year, Sirmpilatze's team published a paper where they mapped anesthesia-induced burst suppression in human brains (plus other primates, and rats) using fMRI. Their findings oppose the view that burst suppression is a global cortical event. Instead they find that the visual areas of the cortex in humans are completely disconnected from bursts. This confirms an earlier study from 2017 using both BOLD and EEG measurements.

There is an interesting discussion in the paper, with references to other papers, which report other interesting observations from other research teams.

Sirmpilatze et. al (2022) - "Spatial signatures of anesthesia-induced burst-suppression differ between primates and rodents"
https://doi.org/10.7554/eLife.74813

At first thought I don't think so - it would seem that behavior of the visual cortex under propofol anesthesia can't have anything to do with the paranormal veridical out-of-body perceptions, or for that matter with the transcendental realer-than-real heightened states of consciousness, both reported by NDErs. And there is the good old "hard problem" of consciousness. And in any case many NDEs occur when not under anesthesia.

However, there might be some sort of indirect connection. The paranormal experiences reported by NDErs can be partially understood via the filter or transceiver model of consciousness. In this model, immaterial spirit manifests in the physical via intricately interpenetrating into the neurological structure of the brain, and during deep NDEs the spirit apparently disengages from the brain to separate from the body. Under those conditions mind is unencumbered by the physical brain microstructure. 

Propofol or other anesthesia during NDE may affect the degree of disengagement of spirit from the physical brain structures involved, and assuming these include the visual cortex this might affect the extent or intensity of the paranormal visual perceptions experienced, or maybe just what is consciously remembered.

At first thought I don't think so - it would seem that behavior of the visual cortex under propofol anesthesia can't have anything to do with the paranormal veridical out-of-body perceptions, or for that matter with the transcendental realer-than-real heightened states of consciousness, both reported by NDErs. And there is the good old "hard problem" of consciousness. And in any case many NDEs occur when not under anesthesia.

However, there might be some sort of indirect connection. The paranormal experiences reported by NDErs can be partially understood via the filter or transceiver model of consciousness. In this model, immaterial spirit manifests in the physical via intricately interpenetrating into the neurological structure of the brain, and during deep NDEs the spirit apparently disengages from the brain to separate from the body. Under those conditions mind is unencumbered by the physical brain microstructure. 

Propofol or other anesthesia during NDE may affect the degree of disengagement of spirit from the physical brain structures involved, and assuming these include the visual cortex this might affect the extent or intensity of the paranormal visual perceptions experienced, or maybe just what is consciously remembered.

Visual cortex activity definitely doesn't explain how she could hear the unhearable, or her own veridical observations.  And from these findings, while some of the visual system isn't under burst suppression, around half of it is. The medial temporal visual area appears to be under burst suppression on the graphs of the study, which is associated with neural correlates of perception of motion. So to have a consistent, clear, vision like that with such inconsistency of activation of regions would be strange under a materialist view.
And not to mention, there's a difference between her OBE and NDE. The OBE was probably a different level of disconnection from the brain as you said. Her NDE most likely occurred after the burst suppression, when she had zero brain activity at all, and her brain stem activity flattened. That's pretty consistent with NDE reports, where they have zero brain activity in the visual areas, or really any area of the brain during cardiac arrest. Frequently people report an OBE right before their actual NDE, and the OBE occurs as their brain is losing activity. 

and I think for the second study, it can be easy to misread because if you look more deeply it says

These findings demonstrated that one region of cortex can be in a state of burst suppression, while neighbouring cortical regions exhibit continuous activity characteristic of a lighter stage of anaesthesia. Burst suppression can therefore occur in limited cortical regions, and does not necessarily reflect a cortex-wide phenomenon.

So it's not necessarily saying there's some giant insane activity showing someone can produce vivid memories and visions under burst suppression. It's just saying that not all regions will be under as deep of an anesthetic effect.

Visual cortex activity definitely doesn't explain how she could hear the unhearable, or her own veridical observations. 

Although I didn't mention it (for clarity), the first paper I referenced, Sirmpilatze et. al (2022) mentions that they found other areas of the cortex which were not correlated with burst-suppression, in addition to V1. These included areas of the auditory complex. (Shown in Fig 2, Section C-D of the paper).

In addition to V1, several other cortical patches were non-correlated with burst-suppression. We visualized these on an inflated representation of the cortical surface (Figure 2C–D). Some of them overlapped with primary cortices: somatosensory and motor areas around the central sulcus, and auditory areas on the dorsal bank of superior temporal gyrus—including Heschl’s gyrus. Additional inactive patches included the subcallosal cortex (subgenual cingulate), the parahippocampal gyrus, and the border between the insula and the frontoparietal operculum.

The only claim here is that some sensory areas of the cortex are doing something different under very high levels of anesthesia, than the rest of the cortex does. What these areas are doing, and how they are doing it, is completely unknown.

Although I didn't mention it (for clarity), the first paper I referenced, Sirmpilatze et. al (2022) mentions that they found other areas of the cortex which were not correlated with burst-suppression, in addition to V1. These included areas of the auditory complex. (Shown in Fig 2, Section C-D of the paper).


The only claim here is that some sensory areas of the cortex are doing something different under very high levels of anesthesia, than the rest of the cortex does. What these areas are doing, and how they are doing it, is completely unknown.

Well used in the first paper, fMRI data is notorious for being unreliable
https://www.pnas.org/doi/10.1073/pnas.16...to%2070%25
https://www.wired.com/2009/09/fmrisalmon/

And not to mention, if Pam Reynolds had some vivid visual activity going on, it would've showed up on her EEG