Thank you so much for the invitation to be here. My name is Benjamin Baird, I’m a research scientist at the Wisconsin State for sleeping consciousness at the University of Wisconsin Madison. And today, I’m going to be talking about some recent findings from cognitive neuroscience on the interesting phenomenon of lucid dreaming.

Here’s what I have in mind for the outline for this brief talk. She’s going to give a little bit of background in terms of definitions. And I’m going to talk a little bit about some of the initial research that was done on lucid dreaming, which sets the foundation for some of the new studies I’ll talk about.

And in particular one, I’ll highlight that the research has really established that lucid dreaming is associated with markers of physiological activation and patterns of brain activation, the specifics of which we’re still working out. I want to conclude by telling you about some new research with a new promising method for the induction of lucid dreams using a pharmacological approach, which also has implications for how we think about the phenomenon of lucid dreaming, and also for charting future research and putting this all together.

So just briefly, I think most people are familiar with the term lucid dream. But just to make sure we’re all on the same page. The minimalist definition, which is the one that we adopt, is that you’re aware that you’re dreaming while you’re dreaming. So during a dream, while still running, you know, staying asleep and staying within a dream, you have the realization that what you’re experiencing is a dream, then you will be lucid. Some people have also argued that this term should include control over the dream and things like that.

But really, by our definition, and by the consensus, I think of most researchers in the field, if you’re aware that you’re dreaming while dreaming, that’s enough to say that you’re lucid, irrespective of any other dimension. So this is typically verbalized, although it need not be. But people do often say something like this is a dream, or I’m dreaming during the dream. And this has gained more attention in the public imagination with films like Inception and waking life, for example, becoming much more well known than it was 30-40 years ago, for example.

I want to give a brief example of what a lucid dream is. So those of you who aren’t familiar who have never had one, I think this does help illustrate kind of what the experience is like.

I was standing in a field in an open area, when my wife pointed in the direction of the sunrise, I looked at it and thought how odd I’ve never seen colors like that before. Then it dawned on me, I must be dreaming. Never had I experienced such clarity and perception. The colors are so beautiful, and the sense of freedom so exhilarating, that I started racing through this beautiful golden wheat field, waving my hands in the air and yelling at the top of my voice, I’m dreaming, I’m dreaming.

Suddenly, I started to lose the dream, it must have been the excitement. I instantly woke up. As it dawned on me what just happened, I woke my wife and said I did it. I did it. I was conscious within the dream state and I’ll never be the same. So this does illustrate a lot of the different features that we often see, particularly in novice lucid dreamers, there does tend to be this sense of kind of intrinsic exhilaration or excitement, of recognizing one state of being able to make that recognition that you’re actually dreaming. This of course does often lead to many people waking up very early on into a lucid dream. But with time with training in the practice, that is something that can learn to be controlled.

So it’s worth noting that we had anecdotes like this for a very long time, stretching back really 1000s of years and definitely within traditions within the Asian subcontinent for example. We know that there are practice schools of practice that have been practicing styles of meditation, Dream Yoga, for example, that involve lucid dreaming for a very, very long time. But there wasn’t scientific validation of the phenomenon until the last 40 years or so. This work really began in the late 1970s and early 80s. And before that time within the scientific community, there was a good deal of skepticism about the phenomenon simply because there wasn’t any objective evidence for it thus far.

But that sentiment really began to change in the late 70s and early 80s With the onset of the first physiological studies of loose Dreaming which proved that it was a true phenomenon of sleep with objective markers. And a little bit of the background for how that came about is that we know that the eye movements of REM sleep can track where the dreamer is looking within the dream, not always snap clear that many of those eye movements don’t have anything to do with the dream gaze. But some of them do.

This is one example, much of this work was done in Bill Dement's Lab at Stanford University. And so they had the subject in the sleep laboratory, the two top traces here show the ROC, right off to the gram measuring the electrical potential of the eye, the left ocular gram and the EEG. And they saw this interesting recording pop up when a subject was sleeping in the sleep lab. He looked left, right, left, right, left, right, left, right, right, left, right, about 12 times in a row. They woke the subject up and said just now what were you dreaming about. And he said, he was standing on the side of a ping pong table watching a long volley, the ball going back and forth from one side to the other.

And so from this, and a lot of other evidence, it became clear that the eye movements, the physical rotations of the eyes, do match very closely the dream content in some cases. And this gave a young researcher working in Dement's lab an idea, namely Dr. Stephen LaBerge. He could once become lucid in the dream, he could move his eyes and a pre-agreed upon volitional pattern in order to signal that he was aware of his state. And so this is actually the very first signal that was ever sent from a lucid dream. And the second trace here you’re seeing the EOG, the electro ocular gram, which is showing the electrical potential of the eye. And here, it’s just showing a single up down eye movement. And that was actually the very first signal sent from a lucid dream to the waking world. He also Morse coded his initials, as you can see on the bottom here with the EMG, which is picking up the muscle twitching from the left and right arms. But the signal that came to be used really as the gold standard and has now been replicated and used in laboratories all over the world, including our own, here at UW Madison is a single pair of left, right, left right eye movements. And you can see that illustrated here.

This is a subject who slept in a sleep lab here at University of Wisconsin Madison. And the LR LR is MC marking the pre agreed upon volitional movement signal of left, right, left, right and back to center. And you can see here we have concurrent measurement with the EMG, measuring the muscle activity, as well as the EEG and so we can see that the subject is in physiologically verified REM sleep when they make the signal and that they’re not awake. And so this provides objective evidence for lucid dreaming and objective markers and a precise, precise timestamp for when it occurred in the record. And so this opens up really a whole new domain of research within dream science and sleep science and cognitive neuroscience more broadly.

One of the things that allows us to do this is to study what’s different about the brain and the ongoing physiology, just prior to and during the lucid dream as compared to baseline REM sleep, for example. And a lot of the earliest work in this area that was done in the 1980s and 90s, again, from Stanford University was focused on the different physiological effects of becoming lucid, or said differently, the state of the brain that tends to be conducive to lucid dreaming. And one of the most robust findings that came out of that work, which has now been replicated many times, is that lucid dreaming is associated with the most physiologically active stage of REM sleep. And again, REM sleep is the stage of sleep when our brains become slightly more active, we see these rapid eye movements on the polysomnogram. And it tends to be associated with the most vivid narrative like dreams.

And so this is showing the eye movements in the top left, the heart rate in the top right, the respiration rate in the bottom left, and a skin potential response in the bottom right. And the center white line is marking the onset of lucidity. You can see in all these cases, I movement density, heart rate, respiration rate, all measures of physiological activation, cortical activation, and autonomic arousal are all elevated during lucid dream and also just in the period prior to the lucid dream. So here each bar is marking 30 seconds of activity. So you can see that 30 seconds just before the onset of lucid dream, the activation is also increased.

And so what this shows us is that lucid dreams tend to occur again in the most activated state REM sleep with increased eye-movement density, increased heart rate and increased respiration rate. So it suggests that lucid dreams are associated with autonomic activation of the central nervous system, markers of physiological arousal while maintaining the REM sleep state. That’s critical. But it suggests that overall lucid dreams are associated with a global activation of the brain.

But of course, this leads to an interesting follow up question, which is, well, is that global activation truly global? Or is it associated with specific brain regions, specific areas of the cortex, for example, or specific patterns of connectivity, or specific frequencies of neural oscillatory activity? And that question spurred a number of EEG studies which have appeared somewhat sporadically in literature over the last 40 years, which unfortunately, are just a mixed bag. And so there’s four different studies approximately, and they all found something different with respect to the EEG correlate of lucid dreaming, one found increased central alpha one crease, one found increased parietal beta, one found increased frontolateral gamma, one found decreased frontocentral delta activity.

So unfortunately, at the current time, all we can really say from this is that the results are mixed. And we need follow up research to really understand more, the EEG correlates of lucid dreaming. Many of these studies, while they’re important, have a lot of methodological problems, so it’s difficult to interpret and compare them. On the other side, research using neuroimaging with fMRI in particular, has only had a couple studies come out, but they’re I want to suggest that the research is pointing us to more of a preliminary convergence. And so, at the current time, there’s only been one lucid dream that’s published in literature that’s been recorded inside of an fMRI scanner. And this came from the study by Dresler et al. published in sleep in 2012.

And you can see here overlaid on the cortex, the areas of the brain which showed increased activation during the lucid REM segment, as compared with the baseline room segment. And these included areas of the anterior prefrontal cortex, the lateral parietal cortex, the middle and inferior temporal cortex, and the medial parietal cortex, including the precuneus as well as some areas of visual cortex.

We did a recent study approaching this from a slightly different angle, we wanted to look at this from an individual difference point of view. And so we know that there are individuals, for reasons we’re still trying to understand that have lucid dreams on the order of every night, whereas most people, the majority of people will only have a few in their entire lifetime. And so we wanted to ask, is there anything different about the brain structure or the brain connectivity in these very high frequency lucid dreamers?

And surprisingly, somewhat surprisingly, we found that there were no significant differences in whole brain gray matter density, or in other words, any differences in the thickness of the cortex or in the structure of the brain. But we did find a very interesting difference in that the high frequency lucid dreamers showed increased connectivity between a network of regions which shows striking overlap with that network I just showed you, which include the lateral inter prefrontal cortex, middle temporal gyrus, and lateral parietal cortex. And you can see here the overlap between these two studies, definitely a case study on top this is from the lucid dream inside the fMRI scanner. And from our recent study on the bottom, showing the regions which show increased connectivity in high frequency lucid dreamers, you can see that there is a very striking overlap between these two sets of regions.

Another reason this is very intriguing to us is from what we know about the neuroimaging of REM sleep more generally. And there were a number of studies which were very well done during the 90s using PET imaging, which images glucose metabolism, or original cerebral blood flow. And you can see here it says from a meta analysis, this figure on the left and the blue icon show regions of the cortex which show reduced metabolism or blood flow during REM sleep compared to wake and the orange icon show regions which show increased glucose metabolism or blood flow compared to wake. And overall you can see there are some regions of the cortex during REM which show increased activation, including the parahippocampal cortex, amygdala, anterior cingulate, and visual regions, as well as the pons. Um, but again, we see this network of inter prefrontal cortex, lateral parietal cortex and middle temporal gyrus and precuneus all tend to show reduced metabolism and blood flow. during REM sleep compared to wake.

And so again, we're imaging that same network if you like in reverse. And so kind of putting all that together. What we see from this is that this frontal parietal network of the anterior prefrontal cortex, the lateral parietal cortex, and especially the Angular Gyrus, or AG, as well as the middle temporal gyrus are all to typically, this whole frontal parietal network are all typically deactivated during REM sleep, show reduced activity, reduced metabolism or blood flow, compared to wakefulness. The same region showed increased fMRI signal during lucid REM sleep compared to baseline REM sleep. And individuals who have lucid dreams with very high frequency have increased connectivity within the same network. So this is a really interesting, preliminary convergence. We do need much more research in this area. In fact, and I think the largest and most interesting and most important extension of research is to do a group level fMRI study of lucid dreaming with a group of subjects, which allows us to make more inferences in terms of generalizability of the results.

Nevertheless, I think this is a really interesting preliminary convergence of findings. I’m gonna come back at the end to talk about how this all fits together. But I want to briefly tell you about a recent study we did looking at a method to induce lucid dreams with pharmacology, which also has an interesting connection with what I just presented. So we know that from the early phase of research and from replications that have been done recently, that lucid dreaming is again associated with physiological activation with markers of physiological arousal, while maintaining the REM sleep state. And the main neurotransmitter involved in REM sleep is acetylcholine. And so it prompted research to look into whether increasing acetylcholine could aid thereby increased brain activation, and may increase the frequency of lucid dreams. And indeed, pilot work found that drugs such as Aricept, that are acetylcholine, esterase inhibitor inhibitors, which overall have a net effect of increasing acetylcholine, did in fact, increase lucid dream frequency.

And so in a recent study, we wanted to quantify that in a large sample, to quantify the size and reliability of the effect of acetylcholine esterase inhibitors on lucid dreaming. What as well as to see how well we could do at Induced Lucid dreams, putting together a number of the techniques that have been studied to date. And these include things like sleep interruption, which is waking up during a period during the night, typically about an hour or two before you normally would wake up after going back to sleep after a period of approximately 30 minutes. That’s been shown separately to have an increase to result in increased lucid dreaming frequency. Also very critical. It is the mental set. It’s really the foundation for everything.

And here we study the mild technique, the mnemonic induction of lucid dreams technique developed by Dr. Stephen LaBerge, which I won’t have time to go into the details, but it is, in essence, a prospective memory technique in which you’re remembering your intention to have lucid dreams, you’re setting an intention, and you’re remembering to do that at a future time. This was a double blind placebo controlled study with 121 subjects and then within subjects counterbalanced design. This gives you a brief schematic of the study. Participants slept for about three REM cycles, here shown with the darker gray bars that then woke up and gave her dream report.

They then ingested one of three counterbalanced doses of galantamine, which was the acetylcholine esterase inhibitor we studied here. They've stayed awake for that 30 minutes of sleep interruption. They then returned to sleep practicing the mnemonic condition induction at Lucid dreams technique. And then in that last section, they engaged in the what we’re calling experimental nap portion. And then they gave a final dream report. And some of us did this on three different nights. So again, it’s all within subjects and counterbalance. So on each night, they got the zero milligrams, the four milligrams, the half dose for the full eight milligrams. And what we found was a very striking dose related increase in the frequency of lucid dreams with Galantamine.

On the left you can see the baseline rate of lucid dreams that was expected from this group of participants without any intervention. G zero shows the effect of the full placebo procedure if you like, which included not only the placebo dose of Glenn’s name, but also the sleep interruption and training in the mnemonic induction lucid dreams technique. g4 shows the same integrated procedure with the half dose of four milligrams, and GH shows the full eight milligram dose of galantamine. You can see what the full dose is, approximately 43% of participants are able to have a lucid dream and that experimental nap section. So this is a massive, massive effect. And so from this, we see that Galantamine stimulates lucid dreaming in a dose related manner.

Again, approximately 48 43% of participants were able to successfully have a lucid dream with this combined procedure with the full dose of galantamine. And we don’t understand the mechanism by which this is working, we assume that it is due to increasing acetylcholine, but in fact, acetylcholinesterase inhibitors can have auxiliary effects on other neurotransmitter systems. So we really need more research to firmly pin down exactly why galantamine has such a strong influence on the frequency of lucid dreams.

Okay, and so just wrapping all this up. All of this work, the work on induction with Galantamine, the neuroimaging research and the research on the psychophysiology of lucid dreaming all point to a picture of lucid dreams being associated with physiological arousal and activation during the REM sleep stage. And so cholinergic stimulation with acetylcholinesterase inhibitors can increase physiological activation and thereby induce lucid dreams. Neuroimaging data points to this as we discussed frontopolar parietal, middle temporal cortical network or simply the frontal parietal network for lucid dreaming. And this leads to a very interesting question, I think for scientific research in this field, which is does pharmacological induction with Galantamine stimulate lucidity, specifically by increasing activation within this particular brain network. And we do know from other research that pro-cholinergic drugs can increase activity within the frontal parietal network.

In situations in particular workflow, productivity is low, and that would be the case with REM sleep. So I think this is a very interesting direction for follow up research. And it also suggests that it may be possible to bias these networks towards increased awareness of dreaming during REM sleep. If you’d like to learn more about the recent scientific research on lucid dreaming, I would like to point you to my review paper in neuroscience and biobehavioral reviews, which was published in 2019.

And with that, I’d like to thank my collaborators, Dr. Giulio Tononi, Dr. Melanie Boly, Dr. Stephen LaBerge, and others and thank you very much for your attention and for the invitation to present