Some Really Cool And Interesting Stuff On Dreams!

[jellyfish]

Hello, Im new to the forum and I'm really interested in everything about dreaming and the phychology behind it. Since I found this sub-section of the forum, I though i'd share this video I came across with you guys. It seems to answer some of the questions I see being asked here too. The video can be found here:

[VIDEO]

[/VIDEO]

 

The people who made the video don't really have a lot of viewers/subscribers which is unfortunate because they did a great job, lets give them the support they deserve?

 

-Jellyfish

[DrmDoc]

Hello Friend, I've studied dreams and dreaming for more that 30 years and have lectured and privately published on the topic.  I think that video provides an interesting introduction to a subject that too few consider as having any real value to the cognizant experience of life.  There is more than sufficient peer-reviewed evidence suggesting the very real importance of dreams and dreaming to our physical and mental health.  Although I enjoyed the video, it wasn't entirely accurate on some aspects of the dreaming process.  The aspect most prominently misunderstood, even by some researchers, is why we experience what some consider a paralytic state while dreaming.  The state of immobility that our gross body musculature enters prior to the dreaming state is called atonia​​. Contrary to what many assume, atonia did not evolve and do not arise to keep us immobile while dreaming.  Perhaps the best evidence of that is sleepwalking.  Atonia is that relaxed, inelastic state of muscle readiness which, by my investigation, our animal ancestors evolved to serve the metabolic processes of rest and sleep.  Before their primitive brains evolved the capacity to dream, our animal ancestors evolved this relaxed state of muscle readiness as a means to conserve energy amid prolonged periods of rest and food privation.  During those periods, atonia made more energy available to those physical systems more vital to the survival of these primitive animals, during rest periods, than muscle readiness.  Dreaming is a consequence of the physical systems receiving more energy amid this atonic state of sleep.  Amid atonia, our resting brain's activity increases (dreaming), which increases blood flow to the brain and other vital organs amid sleep. 

 

The video also mention our inability to remember most of our dreams' experiences and content.  Although the video didn't explore the reason for this deficiency, that reason involves how memory evolved. Succinctly, memory evolve through experiences that had a real physical/material impact on the survival of our animal ancestors.  Because our dreams do not involve real experiences in physical reality, we do not form memories of them easily.  Only those dream experiences perceive as having some real physical/material impact generally promote our memory of them consequently.  I welcome your thoughts and continued interest in this subject.

[CraigD]

Welcome to Hypography, Jellyfish and DrmDoc! Please feel free to start a topic in the introductions forum to tell us something about yourselves.

 

Although I enjoyed the video, it wasn't entirely accurate on some aspects of the dreaming process.

I agree. Though I found the video pretty and like the narrator’s voice and delivery, I was bothered that it presented many of its claims as if they were well-accepted mainstream hypotheses – that they play fast and loose with their science.

 

In particular, the 2nd of their 8 “things you didn’t know”, that the tryptamine DMT “causes a dream to take place”, is far from an accepted conclusion, though it was suggested at least as early as 1988 (eg: JC Callaways “A proposed mechanism for the visions of dream sleep”). Since then, I think there’s been a growing consensus that DMT is produced endogenously (naturally, by the body, most likely by the pineal gland), and that it plays a role in normal “hallucination-like” experiences, or which dreams are an example, but no evidence of which I’m aware that it is excreted more or plays an greater role when dreaming then when awake. I’m nearly certain it doesn’t “cause dreams to take place”, because the experience resulting from externally delivered doses of DMT feels little, to me, like that of dreaming, and the levels of DMT occurring naturally in the brain have not been found by any research to be nearly high enough to account for the vivid visual and other sensory experience of dreams.

 

I think that tryptamines and other endogenous and exogenous psychoactive chemicals have an underappreciated role in human consciousness, but that no single one is a “smoking gun” explaining dreaming or other distinct experiences.

 

The aspect most prominently misunderstood, even by some researchers, is why we experience what some consider a paralytic state while dreaming. The state of immobility that our gross body musculature enters prior to the dreaming state is called atonia. Contrary to what many assume, atonia did not evolve and do not arise to keep us immobile while dreaming. Perhaps the best evidence of that is sleepwalking. Atonia is that relaxed, inelastic state of muscle readiness which, by my investigation, our animal ancestors evolved to serve the metabolic processes of rest and sleep.

While you speculation about the evolution of sleep atonia makes sense, that I believe the description of REM atonia as paralysis-like is accurate, and that however it evolved, it does server now to keep us and other animals immobile while dreaming. Self-quoting from another thread,

Though not fully understood, we know from experiments going back more than 65 years that a well-defined brainstem structure, the pontine tegmentum, is responsible for inhibiting our muscles during sleep. If this structure is physically damaged or chemically suppressed, a dreaming animal physically acts out its dreams, walking, jumping, etc. This video is from one such experiment, I think by Michel Jouvet ca 1960. Malfunctions of this system are suspected to cause disorders such as sleepwalking and sleep paralysis.

So while we don’t understand REM atonia in complete detail, from observing what happens when the potine tegmentum’s normal function is suppressed, we know its cause and its effect.

 

I’ve had some interesting personal anecdotal experience with REM atonia. For as long as I can remember, I’ve had vivid and enjoyable dreams, usually but not always lucid, of which I’ve kept a journal of ones that especially impressed me since my early teens. Beginning in my mid-to-late 40s, my wife of then 15 years began to notice me “thrashing” in my sleep. We hypothesis that, whatever the mechanism for REM atonia, it’s working less well for me as I age. By waking me and asking what I’m dreaming at that moment, my wife has been able to identify several distinct body motions associated with my dreaming of running, flying, and fighting. When I dream of flying, I make a movement she describes as “flopping like a fish”.

 

Dreaming is a consequence of the physical systems receiving more energy amid this atonic state of sleep.

What’re source do you have supporting this claim, DrmDoc :QuestionM

 

I skeptical of it, because if it were true, wouldn’t animals in which REM atonia were suppressed, such as the cat in the video of Jouvet’s experiment above, be unable to dream?

 

Hard data about dreaming in the form of PET scans of FDG metabolism show that, generally and in specific areas, the brain uses dramatically more energy during REM sleep than during either non-REM sleep or awake. (a source: “The Brain During Sleep – Energy Consumption”, sleepdex.org) However, this increase in metabolism occurs before, and even in the absence, of REM atonia. REM atonia appears to be caused by the increased metabolism – specifically, in the pontine tegmentum – rather than cause it.

 

... atonia did not evolve and do not arise to keep us immobile while dreaming. Perhaps the best evidence of that is sleepwalking

Sleepwalking results, from what I’ve read, when dreaming occurs outside of the REM state.

 

I don’t think sleepwaking is evidence that REM atonia doesn’t keep animals immobile when dreaming, but rather that if REM atonia is absent, dreaming animals fail to be kept immobile.

 

(source: Wikipedia article Non-rapid eye movement sleep)

[DrmDoc]

Hello CraigD,

Though not fully understood, we know from experiments going back more than 65 years that a well-defined brainstem structure, the pontine tegmentum, is responsible for inhibiting our muscles during sleep. If this structure is physically damaged or chemically suppressed, a dreaming animal physically acts out its dreams, walking, jumping, etc.

is from one such experiment, I think by Michel Jouvet ca 1960. Malfunctions of this system are suspected to cause disorders such as sleepwalking and sleep paralysis.

I'm familiar with Jouvet's work and the results of the pontine studies you've cited.  Although I agree that they provide convincing evidence of the role pontine function provides in sleep, I believe that evidence has been misinterpreted.  We know that muscle movement, generally, is an efferent response to afferent stimuli; i.e., we generally respond to stimuli we perceive as physically or materially real during our waking reality. Although we may experience dreams that seem more real than waking physical reality, we do not leap from our beds and respond to those experiences because our dreaming brain is unconsciously able to detect and distinguish those experiences as not involving true physical/material reality.  In my opinion, the neural structure that enables our dreaming brain's distinction of stimuli arising from true physical/material reality is the pons. During REM, the pontine's partial suspension of sensory stimuli from the body's musculature informs our dreaming brain that its experiences doesn't involve true physical/material experiences. Rather than tonic muscle mediation, pontine function mediates the flow of tactile sensory stimuli from the body to the brain, which enables the consciously directed tonic muscle responses of the body.  When pontine function is impeded or destroyed, our dreaming brain loses its ability to distinguish the reality of its mental experiences (dreaming) from true physical/material reality.  Pontine function doesn't interrupt the flow of efferent commands from the brain to our musculature or cause our muscles to seize during REM, its function afferently informs the brain of our physical status relative to our mental perceptions of experience.  We don't act-out our dreams amid REM because they do not arise concurrent with sensory afferent from the body suggesting that ours dreams require efferent gross motor responses.

 

 

I’ve had some interesting personal anecdotal experience with REM atonia. For as long as I can remember, I’ve had vivid and enjoyable dreams, usually but not always lucid, of which I’ve kept a journal of ones that especially impressed me since my early teens. Beginning in my mid-to-late 40s, my wife of then 15 years began to notice me “thrashing” in my sleep. We hypothesis that, whatever the mechanism for REM atonia, it’s working less well for me as I age. By waking me and asking what I’m dreaming at that moment, my wife has been able to identify several distinct body motions associated with my dreaming of running, flying, and fighting. When I dream of flying, I make a movement she describes as “flopping like a fish”

.

 

Doesn't this somewhat suggest the limited nature of the pons roll in atonia mediations. In my opinion, your experience suggests to me that your dreaming brain was still receiving some sensory stimuli suggesting a motor response was required.  As I recall, some recent sleep experiments have shown increases in brain activity amid dreaming through physical stimuli such as heat without causing arousal.  Interesting as well, eye movement is not subject to the condition of atonia as is other muscle mediated movements because the neural circuitry associate with eye movement is distinct from that associated with gross locomotion and likely evolved concurrent with the brain structures that produce dreaming. 

 

What’re source do you have supporting this claim, DrmDoc :QuestionM

I skeptical of it, because if it were true, wouldn’t animals in which REM atonia were suppressed, such as the cat in the video of Jouvet’s experiment above, be unable to dream?

Hard data about dreaming in the form of PET scans of FDG metabolism show that, generally and in specific areas, the brain uses dramatically more energy during REM sleep than during either non-REM sleep or awake. (a source: “The Brain During Sleep – Energy Consumption”, sleepdex.org) However, this increase in metabolism occurs before, and even in the absence, of REM atonia. REM atonia appears to be caused by the increased metabolism – specifically, in the pontine tegmentum – rather than cause it.

 

I will honor your citation request further on but for now, due to time constraints, I can only provide this limited response.  If we agree that functional brain studies (fMRI, PET, EEG, etc.) are measures of brain activity and activations, function studies that show increased glucose metabolism by the brain amid sleep suggest an active brain particularly when that metabolic increase equals or surpasses the brain's waking levels.  An active brain amid sleep is likely a dreaming brain whether or not rapid eye movement (REM) is observed--as NREM dream reports and studies suggest. I welcome our further thoughts.

[KuKu]

Ya, sleepwalking occurs normally during Non-REM sleep.