Whether it's your first Bonnaroo or you’re a music festival veteran, we welcome you to Inforoo.
Here you'll find info about artists, rumors, camping tips, and the infamous Roo Clues. Have a look around then create an account and join in the fun. See you at Bonnaroo!!
Post by snowmanomura on Jan 14, 2022 12:33:09 GMT -5
Based on the discussion from the people of inforoo podcast, I am following up with the "Brain Thread"
I study the brain, I think it's interesting and other people might also think it's interesting. This is a place for discussions and questions about neuroscience. or monkeys.
Could you theoretically "survive" as just a brain?
so, any moral or ethical concerns aside - yes*
brains are really just a collection of specialized cell that are all interconnected. like other cells, they require energy, nutrients, oxygen, and to remove waste. the cells themselves need to exist in some sort of medium (your brain is floating around in fluid) in order to help maintain some structure. however, the question of conciousness is still unclear.
Some researchers at Yale actually built a system to keep pigs' brains alive for hours after their heads were severed (at a nearby slaughterhouse). They were able to keep the brains intact and alive for up to 36 hours (it's unclear if they stopped the experiment or if the cells/brain tissue actually died.)
I dunno if people will have access to the article in Nature from 2019, but here's the abstract:
The brains of humans and other mammals are highly vulnerable to interruptions in blood flow and decreases in oxygen levels. Here we describe the restoration and maintenance of microcirculation and molecular and cellular functions of the intact pig brain under ex vivo normothermic conditions up to four hours post-mortem. We have developed an extracorporeal pulsatile-perfusion system and a haemoglobin-based, acellular, non-coagulative, echogenic, and cytoprotective perfusate that promotes recovery from anoxia, reduces reperfusion injury, prevents oedema, and metabolically supports the energy requirements of the brain. With this system, we observed preservation of cytoarchitecture; attenuation of cell death; and restoration of vascular dilatory and glial inflammatory responses, spontaneous synaptic activity, and active cerebral metabolism in the absence of global electrocorticographic activity. These findings demonstrate that under appropriate conditions the isolated, intact large mammalian brain possesses an underappreciated capacity for restoration of microcirculation and molecular and cellular activity after a prolonged post-mortem interval.
Basically, they were able to keep the brain cells from dying, observed normal autonomous brain response from immune cells, blood vessels that serve the brain, and preservation of neuronal connections. So, anatomically and physiologically, the "brain" was maintained and kept alive.
However:
Brain cells communicate through two major mechanisms - electrical activity and neurotransmitters (e.g. serotonin, epinephrine, glutamate, GABA, etc). The researchers at Yale were able to put electrode on the surface of the brain (electrocorticography - like an EEG but directly on the cortex) and record electrical activity. They only observed spontaneous electrical activity, nothing that was behaviorally directed or coordinated (i.e., no indication of consciousness).
Their conclusion:
Overall, the ability to utilize this technology to investigate neurophysiological recovery of the brain following global anoxia or ischaemia provides the basis for a new class of tools. We have found encouraging evidence that brings into question the time-course and cessation of molecular and cellular brain functions following prolonged circulatory arrest. Future studies and considerations will spur further development and implementation of this technology to study broad scientific questions in the large, mammalian brain.
So, you could survive, but literally only as a collection of intertwined cells carrying out basic cellular function. We aren't there yet to preserve conciousness or memories, etc.
I had a theory that tied the stoned ape theory to alien panspermia together in an effort to hypothesize that yawns are how our brains, or, “products of aliens panspermia” are communicating with each other without our Consciousness realizing.
Post by jorgeandthekraken on Jan 14, 2022 17:09:40 GMT -5
For anyone looking for a couple of great books about music and neurology, I’d highly recommend Musicophilia by Oliver Sacks and This Is Your Brain on Music by Daniel Levitin.
Do you want to dance while also thinking about all the ways you've failed as a human?
UPCOMING SHOWS 5/14 - Neil Young & Crazy Horse @ Forest Hills 6/8 and maybe 6/9 - Governors Ball 8/17 - King Gizzard & the Lizard Wizard @ Forest Hills 9/4 - Pearl Jam @ MSG 9/7 - Pearl Jam @ Wells Fargo Center 9/11 - St. Vincent @ Brooklyn Paramount
Could you theoretically "survive" as just a brain?
so, any moral or ethical concerns aside - yes*
So, you could survive, but literally only as a collection of intertwined cells carrying out basic cellular function. We aren't there yet to preserve conciousness or memories, etc.
thankfully, we will not need to worry about this:
Could VR or something more advanced even come into play here?
pretty sure it's just a social evolution like empathy but my personal tin foil is that people just suck all the oxygen when they yawn that other people compete for the available supply
What are your thoughts on consciousness? Keeping the question intentionally vague and nonspecific; feel free to interpret as you wish and ramble on from there.
5.5/four tet, daphni b2b floating points, avalon emerson 5.12/neil young 5.19/mannequin pussy 5.21/serpentwithfeet 5.25/hozier 6.12-16/bonnaroo 6.28/goose 6.29/goose 9.17/the national + the war on drugs 9.23/sigur ros 9.27-29/making time 10.17/air
Vieux
Global Moderator Moderator Goddess Extraordinaire
I love all this discussion. I'm fascinated with neuroscience and if I didn't hate school as much as I do/did I could have seen myself in this field. I am always doing research and trying to learn more. Especially when it comes to memories and dreams. I am super excited about this thread and your knowledge in this field.
what is the likelihood that we will ever be able to detect CTE in living persons? i've always been interested in knowing if the increase in knowledge of the issue would aid in its detection but have also figured it's potentially a bit too invasive of a test to ever be able to use when still living
Oooh, I'll give the podcast a listen so I know more about your work! Are you familiar with light sheet microscopy? My boo is a neuroscientist/microscopist. Hollar if you're ever in Nashville (I was excited to hear St. Jude/Memphis) and are interested in checking out his lab/core facility. The following papers were big for them last year:
Oooh, I'll give the podcast a listen so I know more about your work! Are you familiar with light sheet microscopy? My boo is a neuroscientist/microscopist. Hollar if you're ever in Nashville (I was excited to hear St. Jude/Memphis) and are interested in checking out his lab/core facility. The following papers were big for them last year:
haha, I actually interviewed a post-doc yesterday whose PhD work was all about light sheet microscopy in retinal vasculature. I had never heard of it before yesterday, seems like a really interesting imaging modality.
Post by BelgianCumCrabs on Jan 20, 2022 13:45:02 GMT -5
Not sure if helpful to anyone but I realized not too long ago that people who don't speak multiple languages, think it's strange I dream and think in English but still translate in my head at times as well. Especially idioms seems something that I don't auto translate. Which is a good thing because those aren't meant to be translated literally.
I'm guessing your brain auto adjusts to your environment. I wonder if I talk more Dutch to my son if he'll start to understand it more. For now he really only cares about English (he's 4yo).
Post by snowmanomura on Jan 20, 2022 13:46:33 GMT -5
Regarding yawns:
So, yawns are actually pretty fascinating and I sort of fell into a rabbit hole reading about them, because there has been research from a broad array of fields like neuroscience and evolutionary and social biology. the results of all this research are very mixed, and there isn't a whole lot of consensus or clear cut conclusions. If you want to read a bit of the literature, there is a great review that covers a lot of different aspects of yawning. Throughout the literature, I noticed that Robert Provine has stood out as a leading researcher into yawning (and other behaviors like laughing and hiccupping).
I'll try to summarize, and not get too into the weeds here.
First, a few things I found that were interesting about yawning. Pretty much all vertebrates yawn, and it has been observed in prenatal humans. Yawns are an example of a fixed action pattern - a highly stereotyped series of motor behaviors that occurs without sensory feedback (most of my PhD work was in multisensory integration/sensorimotor control, so this a bit parallel to my main expertise). However, yawning is not a reflex - reflexes are typically fast action responses that occur without conscious motor control in response to some external stimulus (like pulling your hand away from a hot pan). Many reflexes occur in neural pathways without involving the cortex at all - for the hot pan example, pain receptors in your hand send signals to spinal neurons that then innervate motor neurons. you "brain" isn't involved at all with the withdrawal reflex. Because they are fixed action patterns, yawns continue through completion once started (like say, a sneeze). there has been some research that has robustly correlated yawn duration with average brain weight (although the why here is unclear). The neural pathways involved in spontaneous yawning are believed to lie in the brainstem - from an evolutionary perspective this is why it is probably common among vertebrates. the brainstem is the "oldest" part of the brain. Neurons that control autonomous functions like breathing and circadian rhythms are located in the brain stem, and brain stem function is similar across all vertebrate animals - it is the sort of "base" level of our central nervous system. Locked-in patients who have lost all ability for voluntary motor control and anencephalics (people missing all/most of their cerebral cortex) can still yawn, and tetriplegics who cannot open their mouth are still able to gape their jaws when yawning, and jaw gaping is an essential part of the yawn motor pattern and may be why people report feeling "stuck" mid yawn when trying to stifle yawns by clenching their teeth.
Because of the brain stem circuits underlying yawning, and its preponderance among vertebrate animals, the yawning motor pattern is thought to be very old, from an evolutionary perspective, and involved involuntary motor circuits. However, why we yawn is still unclear. Yawning is most common after waking and before sleeping, and follows similar circadian rhythms in other animals, but there is no significant correlation with wake up time or amount of sleep and subjective ratings of sleepiness don't account for variance in spontaneous yawning frequency. Yawning is not a mechanism to resolved oxygen imbalance in the blood stream, and yawning and breathing are controlled by separate neural mechanisms. One hypothesis is that yawning may be a way to facilitate changes in cortical arousal during "state changes" or behavioral or envioronmental transitions, and has been expanded and/or adapted by some researchers to include modulation of attentional networks in the brain. Observational studies have found that people with higher levels of basal activity yawn less frequently, and yawns often follow stressful events (another change in arousal levels). In humans, yawning produces changes in heart rate, skin conductance and the sympathetic nervous system. Changes in blood oxygentation and blood flow subsequently lead to changes in arousal - your brain needs oxygen to work. The deep inhale of yawning, increase in heart rate, and mechanical forces induced by jaw muscle contraction increases cerebral blood flow. In an attempt to link the arousal/state change and enhanced circulation oberservations, a "cooling effect" hypothesis has been proposed; i.e., yawning cools the brain. Certain drugs that alter body temperature and experiments that manipulate ambient temperature have resulted in expected changes in yawn frequency that align with this hypothesis, though it isn't clear that isn't just a physiological side effect of yawning rather than a causal mechanism for yawning.
Yawning contagion: Spontaneous yawning is driven by uncncious, involuntary motor circuits. Contagious yawning occurs in response to social stimuli, and occurs in humans, non human primates (primarily chimps; investigations of contagion in bonobos, gorillas, orangtutans is sparse), some monkeys (macaques, mandrills, marmosets). contagious yawning is much less common, although observed, in some dogs, rats, and cats as well. Interestingly, dogs have been observed to yawn in response to human yawns. It is believed that contagious yawning, from an evolutionary perspective, is much newer than spontaneous yawning and deductively involves higher order cortical areas (complexity in brain structure increases with evolutionary "newness"), and probably evolved independently (i.e. no common ancestor for contagious yawning).
Contagious yawning is believed to be related to some sort of social trait. Humans don't exhibit contagious yawning until early childhood (~4 years), when they also begin to identify others' emotions. Contagious yawning in humans is also impaired in people who suffer from disorders that affect their perception of others' emotions, such as autism spectrum disorder and schizophrenia. This has led to a popular hypothesis that contagious yawning is involved in empathy. However, this is not straighforward. In an fMRI study of contagious yawning, subjects were shown pictures of people yawning (test condition), pictures of people making other mouth shapes (control), and blank screens. In this study the superior temporal sulcus (STS) was activated during test (but not control or blank). the STS has been implicated in a lot of different processes - theory of the mind, audiovisual integration, motion processing, speech processing, face processing, and encoding sensory information for subsequent motor output, and can be differentially activated within frontal and medial-temporal cortical networks depending on context. In regards to the fMRI study, activation of the STS agrees with previous work that the STS is involved in processing socially relevant information, particularly faces. However, this doesn't give us any really conclusive evidence on the "why" of contagious yawning, only that the STS is a neural correlate (this term can be fuzzy depending on the literature, but here I mean that it is an area of the brain whose activity is correlated with a specific stimulus) of contagious yawning. Interestingly, the STS is part of the mirror neuron system.
Briefly: the mirror neuron system is a network that is activated when we watch someone else do an action. Humans are rather unique in that we can learn through imitation, and we can actually start to develop the neural patterns required for executing a motor behavior just through observation. It's how we develop action understanding and imitation. Visual neurons respond when we see an object; other neurons respond when we recognize an object; mirror neurons respond when we observe goal directed action and is thought to play a funcitonal role in action understanding and imitation (importnat to note this isn't the only mechanism through we we can learn this). Mirror neuron system helps us (humans) develop motor representations in our premotor and motor cortices. Basically, we are able to observe someone do something and begin to formulate the motor patterns required to do that action. If anyone is interested, I can go into more detail in another post about how we develop motor patterns in premotor/motor cortex (and by extension, parietal cortex) but it's really outside the scope here. However, in that fMRI study, other nodes of the mirror neuron system, notably Broca's area (a region primarily involved in speed recognition) was not activated. Broca's region is important in imitation, and linking actions to specific goals. Thus the fMRI authors concluded that contagious yawning isn't a de facto imitative action; i.e., we aren't just yawning as an imiation of the inital yawner. And because yawning itself is a highly stereotyped action that we perform spontaneously, the involvement of the mirror neuron system as a whole isn't thought to contribute to the yawning contagion; we aren't just mimicking the yawner - there is some other mechanism triggering the beginning of the yawning motor sequence.
There is no evidence that yawning has a communicative function, and the subjective interpretation of yawning in social settings is widely disparate (misconceptions about why we yawn, e.g. boredom, sleepiness, etc. and not consistent among social groups). If we follow the line of thinking that yawning faciliates arousal/state changes, it could be that contagious yawning is a mechanism for heightening group vigilance or faciliate group adaptive responses to external stimuli (e.g., stanger danger) though this has not been explicitly tested. Which brings up empathy - our ability to to understand, share, and be affected by the state of others. Contagious yawning could therefore be a type of empathy processing known as state-matching (i.e., a sad person elicits sad feelings in others, etc). I found an interesting study where subjects were observed for hours, and researchers noted yawn frequency, duration, and social bonds within a group. The greater the bond (among strangers, acquaintances, friends, and kin/life partners) found that contagion, contagion frequency, and response latency increased as a function of social bond, supporting the idea that empathy may be an underlying mechanism of CY. There are other forms of automatic contagion social behaviors, such as contagious itch (humans, several macaques, mice), stretching (parakeets), "jump yips" (prarie dogs), scent marking (marmosets), laughter (humans), "play" (ravens, keas). All of these examples are non mimicry behavioral contagion.
Definitions of empathy are difficult though, and within the literature there has been a sort of cart-before-horse issue. An early model of empathy (Perception-Action-Model) actually uses contagious yawning as a prerequisite for empathy, leading to subsequent research to begin research with this as a prior. To quote one review on this conceptual problem:
The hierarchical structure of their proposed model (see also the “Russian Doll Model” in de Waal, 2008, and in de Waal and Preston, 2017) thus specifies CY as a prerequisite for empathy (Preston and de Waal, 2002, de Waal and Preston, 2017), which has led multiple researchers to infer that there is a direct link between CY and empathic processing. But, one could argue that a brain is also a necessary pre- requisite for empathy, and, as for CY, arguing that any animal with a basal ganglion of a particular size thus should be empathic is based on the fallacy of the converse, or affirming the consequent. Instead, one should also consider that there might be more primitive systems in which CY is included, which do not posses empathy. CY may be a primitive root of what evolved into empathy, or may involve a separate trend as a social coupling mechanism. Consequently, conceptually there is no reason to assume that the presence or degree of CY is re- presentative of empathic capacities.
Thus the link between empathy and contagious yawning has persisted in the literature, and studies have found data consistent with that prior. Some of these studies explore the link between CY and empathy using subjective reports/questionaires. These are great for correlational results but do not directly point to a causal mechanism. And, again, this brings up the somewhat nebulous definition of "empathy" as interpreted by quistionaire respondents.
As with defining empathy, measuring it through questionnaires and cognitive tasks also takes a multifaceted approach. This approach is needed when dealing with such a complex phenomenon, but it does impair overall analyses and the reproducibility of results, and with regard to links to CY the picture becomes rather unclear. For example, CY is correlated with some scales and appears to be unrelated to others, and to date no two studies on CY have used the same measurements of empathy. Notably, of the 22 identified tests for this relationship, only six (27.3%) are significant in the predicted direction. The emerging literature on this topic is rather unbalanced, with the papers showing predicted results being most often cited when discussing this connection. This creates a problem for progress in the field, since one could just as well interpret the few positive results as false positives, or type I-errors.
Schizophrenia and autism spectrum disorder have been linked to reduced empathy, and studies of contagious yawning have used these populations for study and found diminished contagion. This could be due to a relationship between CY and empathy. However, some confounds, particularly in ASD, may be due to attentioanl biases (e.g., ASD individuals typically focus less on facial expressions) and controlling for this by telling children with ASD to fixate on yawning stimuli found similar levels of contagion as typically developing children. Another studied controlled for this using eye tracking and found similar results when eye postion/focus was accounted for.
Multiple studies have found strong sex differences in level of empathy (female>male), however there in no difference in susceptibility to CY between males and females across multiple studies. It has been robustly and repetedly shown there are no sex differences re: contagious yawning. There were sex differences found in apes (chimps and bonobos) but these were dependent on the sex of the yawner, and more likely represent attentional biases due to hierarchical structures of these species. This could also explain some of the observational reports of contagious yawning in relation to famliarty/social bonds in humans. Attention in humans and monkeys is biased by familiarity, and gaze avoidance between strangers in humans is more common than the opposite. Additionally, our brains are really good at recognizing things we are familiar with and detecting changes in facial expressions among familiar vs non familiar individuals. i.e., the contagiousness of yawning may be due more to our attentionto and ability detect in-group faces.
Back to some more neuroimaging studies - the mirror neuron system is inherently a motor function. We can mirror actions (such as changing facial expression) but the mirror neuron system doesn't interpret these actions - they aren't invovled in coding the emotion of sadness, only the facial expression one makes when sad. I mentioned the most highly-cited neuroimaging study earlier, but other studies have found activation in the posterior cingulate, ventromedial prefrontal cortex, and frontal gyrus regions, however, none of the studies were consistent in their activations (likely due to study design, a common issue with neuroimaging studies). These regions are all a part of the default mode network, and are involved in diverse functions, but primarily cognitive processes such as working memory, awareness/attention, decision making, and similar executive function. Most of these studies are also dervied from people observing pictures of yawns, and do not involved a behavioral component, making it difficult to draw causal relationships; i.e., they aren't showing activations in response to contagious yawning, but activations arising from sensing others yawning. One thing that makes it difficult to truly asses this via neuroimaging is that the head is often constrained (you can't take good pictures of the brain if the subject is moving around in the MR scanner) and thus yawning is suppressed as a matter of course. The supression of yawns (and being told to lie still) also increases subject self-awareness, which could decrement the contagion factor of yawning in the first place. Intense self-awareness has been shown to inhibit the yawn response.
In one study, male subjects were given intranasal oxytocin, which has been implicated in empathy processing, with no subsequent change in frequency of contagious yawning.
So, in summary, we really don't know why yawning is contagious. It is present primarily in social, gregarious animals with more developed cortical regions for processing social cues. We know that certain regions of the brain that underlie higher order cognitive functioning are activated when viewing (or hearing) a yawning stimulus, but it cannot be definitely linked to empathic processing.
As for the aliens and collective unconcious Boner, I didn't find anything in the literature that addressed this.
So, yawns are actually pretty fascinating and I sort of fell into a rabbit hole reading about them, because there has been research from a broad array of fields like neuroscience and evolutionary and social biology. the results of all this research are very mixed, and there isn't a whole lot of consensus or clear cut conclusions. If you want to read a bit of the literature, there is a great review that covers a lot of different aspects of yawning. Throughout the literature, I noticed that Robert Provine has stood out as a leading researcher into yawning (and other behaviors like laughing and hiccupping).
I'll try to summarize, and not get too into the weeds here.
First, a few things I found that were interesting about yawning. Pretty much all vertebrates yawn, and it has been observed in prenatal humans. Yawns are an example of a fixed action pattern - a highly stereotyped series of motor behaviors that occurs without sensory feedback (most of my PhD work was in multisensory integration/sensorimotor control, so this a bit parallel to my main expertise). However, yawning is not a reflex - reflexes are typically fast action responses that occur without conscious motor control in response to some external stimulus (like pulling your hand away from a hot pan). Many reflexes occur in neural pathways without involving the cortex at all - for the hot pan example, pain receptors in your hand send signals to spinal neurons that then innervate motor neurons. you "brain" isn't involved at all with the withdrawal reflex. Because they are fixed action patterns, yawns continue through completion once started (like say, a sneeze). there has been some research that has robustly correlated yawn duration with average brain weight (although the why here is unclear). The neural pathways involved in spontaneous yawning are believed to lie in the brainstem - from an evolutionary perspective this is why it is probably common among vertebrates. the brainstem is the "oldest" part of the brain. Neurons that control autonomous functions like breathing and circadian rhythms are located in the brain stem, and brain stem function is similar across all vertebrate animals - it is the sort of "base" level of our central nervous system. Locked-in patients who have lost all ability for voluntary motor control and anencephalics (people missing all/most of their cerebral cortex) can still yawn, and tetriplegics who cannot open their mouth are still able to gape their jaws when yawning, and jaw gaping is an essential part of the yawn motor pattern and may be why people report feeling "stuck" mid yawn when trying to stifle yawns by clenching their teeth.
Because of the brain stem circuits underlying yawning, and its preponderance among vertebrate animals, the yawning motor pattern is thought to be very old, from an evolutionary perspective, and involved involuntary motor circuits. However, why we yawn is still unclear. Yawning is most common after waking and before sleeping, and follows similar circadian rhythms in other animals, but there is no significant correlation with wake up time or amount of sleep and subjective ratings of sleepiness don't account for variance in spontaneous yawning frequency. Yawning is not a mechanism to resolved oxygen imbalance in the blood stream, and yawning and breathing are controlled by separate neural mechanisms. One hypothesis is that yawning may be a way to facilitate changes in cortical arousal during "state changes" or behavioral or envioronmental transitions, and has been expanded and/or adapted by some researchers to include modulation of attentional networks in the brain. Observational studies have found that people with higher levels of basal activity yawn less frequently, and yawns often follow stressful events (another change in arousal levels). In humans, yawning produces changes in heart rate, skin conductance and the sympathetic nervous system. Changes in blood oxygentation and blood flow subsequently lead to changes in arousal - your brain needs oxygen to work. The deep inhale of yawning, increase in heart rate, and mechanical forces induced by jaw muscle contraction increases cerebral blood flow. In an attempt to link the arousal/state change and enhanced circulation oberservations, a "cooling effect" hypothesis has been proposed; i.e., yawning cools the brain. Certain drugs that alter body temperature and experiments that manipulate ambient temperature have resulted in expected changes in yawn frequency that align with this hypothesis, though it isn't clear that isn't just a physiological side effect of yawning rather than a causal mechanism for yawning.
Yawning contagion: Spontaneous yawning is driven by uncncious, involuntary motor circuits. Contagious yawning occurs in response to social stimuli, and occurs in humans, non human primates (primarily chimps; investigations of contagion in bonobos, gorillas, orangtutans is sparse), some monkeys (macaques, mandrills, marmosets). contagious yawning is much less common, although observed, in some dogs, rats, and cats as well. Interestingly, dogs have been observed to yawn in response to human yawns. It is believed that contagious yawning, from an evolutionary perspective, is much newer than spontaneous yawning and deductively involves higher order cortical areas (complexity in brain structure increases with evolutionary "newness"), and probably evolved independently (i.e. no common ancestor for contagious yawning).
Contagious yawning is believed to be related to some sort of social trait. Humans don't exhibit contagious yawning until early childhood (~4 years), when they also begin to identify others' emotions. Contagious yawning in humans is also impaired in people who suffer from disorders that affect their perception of others' emotions, such as autism spectrum disorder and schizophrenia. This has led to a popular hypothesis that contagious yawning is involved in empathy. However, this is not straighforward. In an fMRI study of contagious yawning, subjects were shown pictures of people yawning (test condition), pictures of people making other mouth shapes (control), and blank screens. In this study the superior temporal sulcus (STS) was activated during test (but not control or blank). the STS has been implicated in a lot of different processes - theory of the mind, audiovisual integration, motion processing, speech processing, face processing, and encoding sensory information for subsequent motor output, and can be differentially activated within frontal and medial-temporal cortical networks depending on context. In regards to the fMRI study, activation of the STS agrees with previous work that the STS is involved in processing socially relevant information, particularly faces. However, this doesn't give us any really conclusive evidence on the "why" of contagious yawning, only that the STS is a neural correlate (this term can be fuzzy depending on the literature, but here I mean that it is an area of the brain whose activity is correlated with a specific stimulus) of contagious yawning. Interestingly, the STS is part of the mirror neuron system.
Briefly: the mirror neuron system is a network that is activated when we watch someone else do an action. Humans are rather unique in that we can learn through imitation, and we can actually start to develop the neural patterns required for executing a motor behavior just through observation. It's how we develop action understanding and imitation. Visual neurons respond when we see an object; other neurons respond when we recognize an object; mirror neurons respond when we observe goal directed action and is thought to play a funcitonal role in action understanding and imitation (importnat to note this isn't the only mechanism through we we can learn this). Mirror neuron system helps us (humans) develop motor representations in our premotor and motor cortices. Basically, we are able to observe someone do something and begin to formulate the motor patterns required to do that action. If anyone is interested, I can go into more detail in another post about how we develop motor patterns in premotor/motor cortex (and by extension, parietal cortex) but it's really outside the scope here. However, in that fMRI study, other nodes of the mirror neuron system, notably Broca's area (a region primarily involved in speed recognition) was not activated. Broca's region is important in imitation, and linking actions to specific goals. Thus the fMRI authors concluded that contagious yawning isn't a de facto imitative action; i.e., we aren't just yawning as an imiation of the inital yawner. And because yawning itself is a highly stereotyped action that we perform spontaneously, the involvement of the mirror neuron system as a whole isn't thought to contribute to the yawning contagion; we aren't just mimicking the yawner - there is some other mechanism triggering the beginning of the yawning motor sequence.
There is no evidence that yawning has a communicative function, and the subjective interpretation of yawning in social settings is widely disparate (misconceptions about why we yawn, e.g. boredom, sleepiness, etc. and not consistent among social groups). If we follow the line of thinking that yawning faciliates arousal/state changes, it could be that contagious yawning is a mechanism for heightening group vigilance or faciliate group adaptive responses to external stimuli (e.g., stanger danger) though this has not been explicitly tested. Which brings up empathy - our ability to to understand, share, and be affected by the state of others. Contagious yawning could therefore be a type of empathy processing known as state-matching (i.e., a sad person elicits sad feelings in others, etc). I found an interesting study where subjects were observed for hours, and researchers noted yawn frequency, duration, and social bonds within a group. The greater the bond (among strangers, acquaintances, friends, and kin/life partners) found that contagion, contagion frequency, and response latency increased as a function of social bond, supporting the idea that empathy may be an underlying mechanism of CY. There are other forms of automatic contagion social behaviors, such as contagious itch (humans, several macaques, mice), stretching (parakeets), "jump yips" (prarie dogs), scent marking (marmosets), laughter (humans), "play" (ravens, keas). All of these examples are non mimicry behavioral contagion.
Definitions of empathy are difficult though, and within the literature there has been a sort of cart-before-horse issue. An early model of empathy (Perception-Action-Model) actually uses contagious yawning as a prerequisite for empathy, leading to subsequent research to begin research with this as a prior. To quote one review on this conceptual problem:
The hierarchical structure of their proposed model (see also the “Russian Doll Model” in de Waal, 2008, and in de Waal and Preston, 2017) thus specifies CY as a prerequisite for empathy (Preston and de Waal, 2002, de Waal and Preston, 2017), which has led multiple researchers to infer that there is a direct link between CY and empathic processing. But, one could argue that a brain is also a necessary pre- requisite for empathy, and, as for CY, arguing that any animal with a basal ganglion of a particular size thus should be empathic is based on the fallacy of the converse, or affirming the consequent. Instead, one should also consider that there might be more primitive systems in which CY is included, which do not posses empathy. CY may be a primitive root of what evolved into empathy, or may involve a separate trend as a social coupling mechanism. Consequently, conceptually there is no reason to assume that the presence or degree of CY is re- presentative of empathic capacities.
Thus the link between empathy and contagious yawning has persisted in the literature, and studies have found data consistent with that prior. Some of these studies explore the link between CY and empathy using subjective reports/questionaires. These are great for correlational results but do not directly point to a causal mechanism. And, again, this brings up the somewhat nebulous definition of "empathy" as interpreted by quistionaire respondents.
As with defining empathy, measuring it through questionnaires and cognitive tasks also takes a multifaceted approach. This approach is needed when dealing with such a complex phenomenon, but it does impair overall analyses and the reproducibility of results, and with regard to links to CY the picture becomes rather unclear. For example, CY is correlated with some scales and appears to be unrelated to others, and to date no two studies on CY have used the same measurements of empathy. Notably, of the 22 identified tests for this relationship, only six (27.3%) are significant in the predicted direction. The emerging literature on this topic is rather unbalanced, with the papers showing predicted results being most often cited when discussing this connection. This creates a problem for progress in the field, since one could just as well interpret the few positive results as false positives, or type I-errors.
Schizophrenia and autism spectrum disorder have been linked to reduced empathy, and studies of contagious yawning have used these populations for study and found diminished contagion. This could be due to a relationship between CY and empathy. However, some confounds, particularly in ASD, may be due to attentioanl biases (e.g., ASD individuals typically focus less on facial expressions) and controlling for this by telling children with ASD to fixate on yawning stimuli found similar levels of contagion as typically developing children. Another studied controlled for this using eye tracking and found similar results when eye postion/focus was accounted for.
Multiple studies have found strong sex differences in level of empathy (female>male), however there in no difference in susceptibility to CY between males and females across multiple studies. It has been robustly and repetedly shown there are no sex differences re: contagious yawning. There were sex differences found in apes (chimps and bonobos) but these were dependent on the sex of the yawner, and more likely represent attentional biases due to hierarchical structures of these species. This could also explain some of the observational reports of contagious yawning in relation to famliarty/social bonds in humans. Attention in humans and monkeys is biased by familiarity, and gaze avoidance between strangers in humans is more common than the opposite. Additionally, our brains are really good at recognizing things we are familiar with and detecting changes in facial expressions among familiar vs non familiar individuals. i.e., the contagiousness of yawning may be due more to our attentionto and ability detect in-group faces.
Back to some more neuroimaging studies - the mirror neuron system is inherently a motor function. We can mirror actions (such as changing facial expression) but the mirror neuron system doesn't interpret these actions - they aren't invovled in coding the emotion of sadness, only the facial expression one makes when sad. I mentioned the most highly-cited neuroimaging study earlier, but other studies have found activation in the posterior cingulate, ventromedial prefrontal cortex, and frontal gyrus regions, however, none of the studies were consistent in their activations (likely due to study design, a common issue with neuroimaging studies). These regions are all a part of the default mode network, and are involved in diverse functions, but primarily cognitive processes such as working memory, awareness/attention, decision making, and similar executive function. Most of these studies are also dervied from people observing pictures of yawns, and do not involved a behavioral component, making it difficult to draw causal relationships; i.e., they aren't showing activations in response to contagious yawning, but activations arising from sensing others yawning. One thing that makes it difficult to truly asses this via neuroimaging is that the head is often constrained (you can't take good pictures of the brain if the subject is moving around in the MR scanner) and thus yawning is suppressed as a matter of course. The supression of yawns (and being told to lie still) also increases subject self-awareness, which could decrement the contagion factor of yawning in the first place. Intense self-awareness has been shown to inhibit the yawn response.
In one study, male subjects were given intranasal oxytocin, which has been implicated in empathy processing, with no subsequent change in frequency of contagious yawning.
So, in summary, we really don't know why yawning is contagious. It is present primarily in social, gregarious animals with more developed cortical regions for processing social cues. We know that certain regions of the brain that underlie higher order cognitive functioning are activated when viewing (or hearing) a yawning stimulus, but it cannot be definitely linked to empathic processing.
As for the aliens and collective unconcious Boner, I didn't find anything in the literature that addressed this.
TLDR: There’s no evidence to suggest I’m wrong = I’m right.
Thanks dude!
Edit: thank god for Siri speak, That shit right there was a podcast man. There’s so much we now know with modern science, but it seems to only reveals how much more we really don’t know
what is the likelihood that we will ever be able to detect CTE in living persons? i've always been interested in knowing if the increase in knowledge of the issue would aid in its detection but have also figured it's potentially a bit too invasive of a test to ever be able to use when still living
This is an interesting question. I'm not an expert on CTE specifically, but I spent two years doing a post-doc at an Alzheimer's research institute, so I have a pretty good grasp of progressive dementia, tools for evaluation/diagnosis (for me, MRI/PET biomarkers). One of the complications of CTE is that it has many similar morbidities and symptoms as other forms of dementias. Because CTE is likely caused by repeated brain traumas/injuries, there can also be confounding factors that influence the pathology of the disease.
For years, there was a disease known as dementia puglistica, i.e. boxer's dementia that has been in the medical literature since the 30's or 40's. This syndrome is basically what we know now as CTE - cognitive, motor, and behavioral changes in people who have had repeated blows to the head. However, not all cognitive/neurodegenerative issues can be directly attributed just to these repeated injuries. Brain function gradually decreases with age through a number of factors, of which CTE, alzheimer's, parkinsons/parkinsonian syndromes, genetics, and other lifestyle factors (substance abuse, sleep disorders) can contribute to the rate and degree of degeneration. I.e., it is hard to find a clear cause-effect relationship of head injury to specific outcomes. There is a huge amount of research on the aging brain, with Alzheimer's taking a huge bulk of that research funding. CTE research is still relatively young, despite getting alot of popular discussion (probably due to the popularity of football).
For most brain injuries, including TBI there is a rather complex series of mechanistic changes in neural function and structure. The brain itself sort of floats in water in your head, and cells known as glia - which aren't directly involved in neural processing* (for the most part) - support the nervous sytsem by providing structure for neurons (think scaffolding), providing nutrients/oxygen, removing dead cells, and immune response. Brain injuries damage the vasculature and blood vessels, which can lead to lesions and an immune response in the brain, which can trigger neuroinflammation. Often a side effect of neuroinflammtory mechanisms is the development of intracellular neurofibrillary tangles (NFTs) created by phosphorylated tau proteins (tau). - essentailly the microtubulues in your cells get all twisted and can't be fixed. NFTs/tau are biomarkers of AD, however they are thought to derived from the accumulation of beta-amyloid plaques -something typically absent in those with CTE (caveat: assuming CTE isn't comorbid with other neurodegeneration). The molecular response to brain injury (cytokine and glial activation) are thought to accelerate tau deposition. Grey matter (the higher-order processing areas - motor, parietal, frontal cortices, etc.) are divided up into six distinct depth-wise layers that can be seen in histology, and are typically measured as a distance (in mm) from cortical surface on neuroimaging. In CTE, NFTs typically appear in layers II and III, whereas in AD they typically originate in layers III and V.
However, there is a large overlap in the clinical, psychological, cognitive, and behavioral symptoms of AD, CTE, and other tauopathies, and because the diseases are progressive it makes it difficult to differentiate them. PET is a neuroimaging modality that makes it possible to view tau deposits in the brain. Basically, a radioactive tracer (usually some derivative of fluorine) is injected into a patient, and then gamma rays pick up where that tracer is. different tracers have been devleoped that bind to different things for imaging (FDG is used to view glucose metabolism; PiB is used to view amyloid plaques in AD). Using PET, it is possible to view tau deposits in the brains of people with CTE, and compare that to what we know about tau distribution in brains from post-mortem studies. We just aren't there yet to be able to make individualized diagnoses from PET scans in people with CTE. PET neuroimaing is looking at correlations (there isn't really a PET equivalent to functional MR) by comparing groups (you need enough data points to accurately detect statistically significant effects). A paper from Boston Univsersity (in collaboration with my post-doc lab) looked at PET scans from former NFL players and control groups with no history of brain injuries, and were able to draw some conclusions about tau protein deposition in the CTE-risk group.
tl;dr : yes, one day. We need to improve our ability to quantify tau, better correlate tau deposits seen on PET with post-mortem confirmed CTE deposits, and better differentiate CTE from other tauopathies. But I think it will happen within the next decade.
Post by snowmanomura on Apr 13, 2023 10:19:43 GMT -5
to really stick the landing on the title of this thread, here is snowman's brain:
this is a high resolution 3D T1-weight MRI of my brain. We were testing some imaging sequences for an upcoming research study and I was the guinea pig. fMRI, which is a series of images taken over multiple minutes, has much lower resolution than the 3D T1 image (MRI imaging is slow - so fMRI is "blurry"). The 3D T1 is spatially matched to the fMRI images to provide a more precise and accurate anatomical parcellation of the "blurry" fMRI signal so we can better isolate the regions of the brain that are activated/inactivated. So, MRI is anatomical/structural image. fMRI is imaging of the actual neural activity that is going on.
We are working on a study that measures brain activations during a working memory task called the n-back. A series of images are presented to a person while they are in the scanner. We have two paradigms, one that presents letters, and one that presents abstract, unnamed shapes. an example of the task:
Each time the target is presented on the screen, the subject would press a button in the scanner. We have the two paradigms for a reason - the brain is really good at recognizing things, and so presenting letters (or namable shapes like "circle") presents a confound because semantic regions of the brain can be activated that are outside the working memory networks (though there may be some overlap!) so, we have two tasks to remove that confound.
fMRI measures the blood oxygen level dependent (BOLD) signal. fMRI is an indirect measure of neural activity - neurons require oxygen to function, so when area of the brain are active during a task (or at rest, under different paradigms) there is an increase in cerebral blood flow and oxygen perfusion in those regions. So, increase BOLD represents increased neural activity. Using the BOLD signal, we are hoping to characterize how working memory networks are impacted in children with sickle cell disease. SCD causes red blood cells to have a sickle/half moon shape, and they cannot carry as much oxygen as normal red blood cells. Children with SCD often experience a number of problems (in many organ systems), but I am most interested in cognitive deficits such as working memory. SCD affects regional oxygenation in the brain (thus the BOLD signal) - basically the brain has to work harder to provide enough oxygen for the neurons to function, and there is a ceiling effect - you can only pump so much blood so fast - that can lead to cogntive and other functional deficits. St. Jude currently has two protocols testing curative therapies for SCD - one that uses gene editing to alter the gene that produces sickle shaped red blood, and one that use transplanted donor-matched hematopoeitic stem cells that will produce healthy red blood cells instead of the sickle shaped ones. In my lab we are investigating how these new therapies will impact cerebral blood flow, improving regional oxygen perfusion during working memory. It is a huge collaborative study, but my role is looking at neuroimaging biomarkers of working memory, and correlating that with performance on the n-back task, as well as other measures of cognitive functioning. These patients undergo a large battery of cognitive testing with neuropsychologists that probe working memory, IQ, spatial reasoning, executive function, processing speed, and others cognitive domains, and we are interested in how the BOLD signal and funcitonal connectivity before and after therapy relates to cognitive outcomes.
When I have some more time, I can show you guys a cool gif of my brain activations while I perform the n-back task. Typical regions that are activated by working memory are frontal, parietal, cerebellum, and cingulate regions.
snowmanomura I’ve meant to ask you about him for a while and reading this reminded me to pick your brain on it. as someone in a similar field, what’re your general thoughts on him? curious about perspective about him personally and also the work/information he produces
I probably first saw him in 2021 or 2022 and thought he was kind of interesting but also had this pretty intense feeling of ick and uncertainty, as I typically feel when people promote these mechanisms of self-growth that seem to either directly or indirectly align with a desired progression towards being an “alpha male” or whatever else you wanna call it. I haven’t watched anything from him in a long time and really haven’t even seen or heard much about him both online and in person lately so idk where he’s headed or what his status looks like at this point
snowmanomura I’ve meant to ask you about him for a while and reading this reminded me to pick your brain on it. as someone in a similar field, what’re your general thoughts on him? curious about perspective about him personally and also the work/information he produces
I probably first saw him in 2021 or 2022 and thought he was kind of interesting but also had this pretty intense feeling of ick and uncertainty, as I typically feel when people promote these mechanisms of self-growth that seem to either directly or indirectly align with a desired progression towards being an “alpha male” or whatever else you wanna call it. I haven’t watched anything from him in a long time and really haven’t even seen or heard much about him both online and in person lately so idk where he’s headed or what his status looks like at this point
Initially, I thought he was a guy I really didn't want to ever be around, although he deserved the acknowledgement of being a legit researcher who conducted good science. Now I kind of think of him as an egomaniacal dick, who revels in his own fame and talks out of his ass on a variety of subjects. His various lines of bullshit have gained him quite a following, but the scrutiny he has received recently has been warranted.
Reminds a bit of Mehmet Oz, obviously, except possibly less money/greed-driven than motivated by the acceptance, which he might even admit. Or maybe he's like a poor man's Elon Musk - they both know some wild shit, are highly driven, and possess a certain charisma, but their extremist attitudes and abrasive personalities can be pretty off-putting. Or I'm probably the one out of his element and should STFU.
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My boo is a neuroscientist/microscopist. Hollar if you're ever in Nashville (I was excited to hear St. Jude/Memphis) and are interested in checking out his lab/core facility. The following papers were big for them last year:
incinnati Ohio babeyyyy
