This shows a woman under anesthesia.
A key next question to answer is how propofol enforces that suppression. Credit: Neuroscience News

How Anesthesia Blocks Consciousness

Summary: A new study reveals insights into how general anesthesia affects consciousness and sensory perception.

Using animal models, researchers found that while propofol anesthesia allows sensory information to reach the brain, it disrupts the spread of signals across the cortex. This suggests that consciousness requires synchronized communication throughout the brain, and propofol’s effect of limiting this interconnectivity could explain its role in inducing unconsciousness.

Key Facts:

  1. Sounds and tactile sensations produce neural activity in the sensory reception areas of anesthetized animals’ brains, but fail to propagate to higher cognitive regions.
  2. The study suggests that synchronized activity across the cortex is necessary for consciousness, with propofol anesthesia preventing this synchronization.
  3. The findings could inform anesthesiology, potentially aiding in the monitoring and adjustment of anesthesia during surgeries to prevent intraoperative awareness.

Source: Picower Institute of Learning and Memory

Under propofol general anesthesia, sensory input still reaches the brain, but signals do not spread. Results suggest consciousness requires cortical regions to all be “on the same page.”

General anesthesia evokes a dual mystery: How does it disrupt consciousness, including sensory perception, and what might that say about the nature of consciousness?

Credit: Neuroscience News

A new study led by researchers at The Picower Institute for Learning and Memory at MIT provides evidence in animals that consciousness depends on properly synchronized communication across the brain’s cortex and that the anesthetic drug propofol cancels sensory processing by cutting it off.

In the Journal of Cognitive Neuroscience, researchers report clear evidence that in anesthetized animals, sounds and tactile sensations still produced neural activity in an area of the cortex that receives incoming sensory information.

But just as clearly, measurements of neural spiking and broader oscillatory activity showed that those signals failed to propagate to three other cortical regions with higher-level processing and cognitive responsibilities, as seen during normal wakefulness.

“What this study shows is that the cortex isn’t getting on the same page,” said study corresponding author Earl K. Miller, Picower Professor in the The Picower Institute and the Department of Brain and Cognitive Sciences at MIT.

“Information is making it to the cortex. It’s being registered in primary sensory areas. It’s just not reaching the rest of the cortex. Because of the anesthesia, it only makes it part of the way through.”

The significance of that, said co-senior author Emery N. Brown, Edward Hood Taplin Professor of Medical Engineering and Computational Neuroscience in The Picower Institute, is that “the study suggests that consciousness requires coordination of activities among cortical regions. Simply activating one or more of these regions is not sufficient.”

Study lead author John Tauber, who recently earned his PhD at MIT in Brown’s lab, said the study could aid efforts to improve anesthesiology care. Brown is an anesthesiologist at Massachusetts General Hospital as well as an MIT professor of Brain and Cognitive Sciences, a member of the Institute for Medical Engineering and Science, and a faculty member of Harvard Medical School.

“We hope our paper further highlights the importance of actively monitoring what is happening in the brain during anesthesia,” Tauber said.

“Future studies in this direction will help us develop clear indicators of whether a patient is still processing sensory information. This would allow anesthesiologists to adjust drug dosage and prevent intraoperative awareness from occurring.”

Stymied sensory processing

To conduct the study the team worked with two animal subjects to measure brain activity—both the electrical “spiking” of individual neurons and their collective rhythmic activity—via electrode arrays placed in four areas of the cortex both before and after they underwent propofol general anesthesia.

The researchers selected the areas of the cortex to represent its hierarchical continuum of functions from initial sensation (the superior temporal gyrus, or STG) to increasingly high levels of cognition (the posterior parietal cortex, or PPC; Region 8A; and the prefrontal cortex, or PFC).

During both states of consciousness, the animals experienced specific stimulations: two audio tones, including one on its own and another paired with a puff of air on the face. In the awake state, such stimulation produced an increase all cortical areas in alpha/beta frequency activity.

STG also showed a strong increase in higher frequency oscillations. The response changed dramatically under anesthesia. While the alpha and beta frequency response was diminished in STG, it virtually vanished in all the higher cortical regions.

“We expected to see a more gradual loss of responses and information,” Tauber said. “The drop-off in responses during anesthesia from auditory cortex (STG) to associative cortex (PPC) was striking.”

Along with the decrease in activity, the researchers measured a decrease in the sensory information detectable in the brain as they moved up the cortical hierarchy. “Decoder” software found sensory information in all areas of the cortex during the awake state but during unconsciousness, less and less information could be found the higher up the cortex the researchers looked.

An incoherent cortex

When the researchers next measured the synchronization of activity among brain regions, they found that it, too, broke down under anesthesia. When animals were awake, they exhibited a strong degree of synchronization in alpha/beta oscillation activity but when unconscious, “there was little or no stimulus-induced synchronization for any of the pairs of cortical areas,” the researchers reported.

A feature of the propofol-anesthetized brain is that neural oscillation activity takes on distinct “up” and “down” states of greater or lesser activity over time.

To test whether sensory information is cut off during both states or just the down states, the researchers developed a statistical analysis. They found that while all neuronal spiking was indeed low during the down states, even during up states when sensory signals were measurable in STG they still failed to go beyond that region.

“We expected responses in the higher cortical areas to at least be disrupted during up states, but it was a bit surprising to find the responses disappeared almost entirely,” Tauber said.

“The neural activity during up states is functionally quite different from the awake state, but we think we have just scratched the surface in understanding the differences between the two.”

In sum, the evidence in the new study shows that unconsciousness doesn’t arise from a wholesale shutting down of the cortex, as much as a suppression of communication within it, Miller said.

A key next question to answer is how propofol enforces that suppression.

“What is it about these changing dynamics that blocks the flow of information through cortex?” Miller asks.

“What’s the headwind that’s blowing back that sensory information and keeping it in the sensory cortex?”

Tauber added that the team looked at sensory processing only when they were certain the animals were fully unconscious. It could be informative, he said, to study how sensory processing changes during the transition from wakefulness to that fully unconscious state.

In addition to Tauber, Miller and Brown, the paper’s other authors are Scott Brincat, Emily Stephen, Jacob Donoghue and Leo Kozachkov.

Funding: The National Institutes of Health, The Office of Naval Research, The JPB Foundation and The Picower Institute for Learning and Memory funded the research.

About this consciousness research news

Author: Press Office
Source: Picower Institute at MIT
Contact: Press Office – Picower Institute at MIT
Image: The image is credited to Neuroscience News

Original Research: Open access.
Propofol-mediated Unconsciousness Disrupts Progression of Sensory Signals through the Cortical Hierarchy” by Earl K. Miller, et al. Journal of Cognitive Neuroscience


Propofol-mediated Unconsciousness Disrupts Progression of Sensory Signals through the Cortical Hierarchy

A critical component of anesthesia is the loss of sensory perception. Propofol is the most widely used drug for general anesthesia, but the neural mechanisms of how and when it disrupts sensory processing are not fully understood.

We analyzed local field potential and spiking recorded from Utah arrays in auditory cortex, associative cortex, and cognitive cortex of nonhuman primates before and during propofol-mediated unconsciousness.

Sensory stimuli elicited robust and decodable stimulus responses and triggered periods of stimulus-related synchronization between brain areas in the local field potential of awake animals.

By contrast, propofol-mediated unconsciousness eliminated stimulus-related synchrony and drastically weakened stimulus responses and information in all brain areas except for auditory cortex, where responses and information persisted.

However, we found stimuli occurring during spiking up states triggered weaker spiking responses than in awake animals in auditory cortex, and little or no spiking responses in higher order areas.

These results suggest that propofol’s effect on sensory processing is not just because of asynchronous down states. Rather, both down states and up states reflect disrupted dynamics.

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  1. In my opinion there is a lifelong bond between the conscious me and the other me the unconscious side. Most operations are scheduled for the morning and if you are able to sleep the night before then waking up, going to the surgery location and then being sedated basically tears at the lifelong bond of the two states. The conscious was awakened, then shut down, the unconscious state awakened without any input during a normal day. There is a sense of loss of connection like two rail cars that drifted apart and can’t seem to figure a way to reconnect.
    Perhaps sedation should occur at a time in the afternoon when the conscious has had enough time to accumulate information, feelings etc.. In a way it’s no different than when we take an afternoon nap, which often is more satisfying than regular sleep. Each state of conscious sharing what it need to be a whole.

  2. A neural network is to consciousness as an airfoil is to flying. It is the basic mechanism of consciousness. It (a neural network) is sufficient to explain consciousness. All psychological phenomena (including subjective experience) are consistent with the neural network model. Consciousness is the collective firing of the particular neurons of the organism or machine. If an anesthesia is preventing the neural network from propagating the activity, then of course consciousness ceases.

  3. Metaphysically speaking, when a person goes under anethesia, the person’s spirit leaves the body. As the drug wears off, it re-enters, thus the space of unconsciousness experienced.

  4. It’s becoming clear that with all the brain and consciousness theories out there, the proof will be in the pudding. By this I mean, can any particular theory be used to create a human adult level conscious machine. My bet is on the late Gerald Edelman’s Extended Theory of Neuronal Group Selection. The lead group in robotics based on this theory is the Neurorobotics Lab at UC at Irvine. Dr. Edelman distinguished between primary consciousness, which came first in evolution, and that humans share with other conscious animals, and higher order consciousness, which came to only humans with the acquisition of language. A machine with only primary consciousness will probably have to come first.

    What I find special about the TNGS is the Darwin series of automata created at the Neurosciences Institute by Dr. Edelman and his colleagues in the 1990’s and 2000’s. These machines perform in the real world, not in a restricted simulated world, and display convincing physical behavior indicative of higher psychological functions necessary for consciousness, such as perceptual categorization, memory, and learning. They are based on realistic models of the parts of the biological brain that the theory claims subserve these functions. The extended TNGS allows for the emergence of consciousness based only on further evolutionary development of the brain areas responsible for these functions, in a parsimonious way. No other research I’ve encountered is anywhere near as convincing.

    I post because on almost every video and article about the brain and consciousness that I encounter, the attitude seems to be that we still know next to nothing about how the brain and consciousness work; that there’s lots of data but no unifying theory. I believe the extended TNGS is that theory. My motivation is to keep that theory in front of the public. And obviously, I consider it the route to a truly conscious machine, primary and higher-order.

    My advice to people who want to create a conscious machine is to seriously ground themselves in the extended TNGS and the Darwin automata first, and proceed from there, by applying to Jeff Krichmar’s lab at UC Irvine, possibly. Dr. Edelman’s roadmap to a conscious machine is at

    1. I was thinking the same thing. This kind of thing makes me sick. You would think by now in all our superiority (lol) animals wouldn’t be considered for testing. Seems there are a lot of humans (especially those conducting medical research) are stuck in the barbaric state. Seems the human population isnt as evolved as we are lead to believe.

  5. If you’ve ever been under anesthesia even as an outpatient, I feel one can agree with the article’s contention that: “the evidence in the new study shows that unconsciousness doesn’t arise from a wholesale shutting down of the cortex, as much as a suppression of communication within it.” Stimulus from what a person sees upon waking from anesthesia still sends a basic form of communication to the simplest of motor functions that I feel induce “muscle memory” functionality to the body, yet without an analytical associated performance, IMHO.

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