#there's a balance between inhibitions and disinhibitions

[shallowrambles]

I'm so bothered by the fetishization of twins and triplets, actually. If I could erase anything, it'd be the flippant references to this. :(

To be clear, I'm not pro-purity culture. I just- this one stings and I have to literally curate my experience so hard because of it

I can't stand when it's used as "code" for "queer experience" either because it's just positioning queer as "unnatural / evil," and that bothers the heck outta me when they're equated. Inappropriate boundary crossing, grooming, and abuse =/= insta-queer. It's like HMMM. The way ppl stan the crowley hookup when it's a shows canon incest kink interest squicks the fuck outta me and like...the whole Demon!Dean is a study in disinhibition! Disinhibition was shown as very evil / shameful / uncomfortable experience for Dean, like, the entirety of season 10...Sam even tries to comfort him about it. But because Crowley-Dean supports those sides of Dean ppl want in their ships, they overlook that aspect of it.

There's also the American-ness of howling at the moon and total "I do what I WANT" as being a good thing, when it's clearly shown as...not. There's gotta be balance, man.

Reduced inhibition is OFTEN used as circumvention of consent, as Dean recounts in his John-and-the-bar story. And disinhibitions are ofc not always a reflection of true self. I'm thinking of a neuro unit, where an injured TBI survivor hits on his granddaughter. Is that his "true personality?" Of course not! It's a loss of free will, judgment, and choice due to the injury and/or disinhibition.

And this is a show about free will, after all.

Drinking and drugging tend to ‘loosen you up’ by reducing inhibitions. But they remove your judgment and CHOICE about things, too. That's not necessarily free will. Reduced inhibitions can be enjoyable, but they can also create risks and dangers. Our inhibitions serve to keep us acting within an acceptable threshold; reducing these inhibitions can push you past the threshold.

Drug addiction is sometimes potrayed as "freeing" but ofc that isn't the complete story. Even so, the show doesn't agree that the punishment fits the crime. Like Crowley, Randy is complex, and he has real feelings and emotions for his relationships!

I feel like the Claire episode puts this in full display:

///

10x09

DEAN: All right, so I get there. I sneak in, and it is nuts. I mean, people are drinking and they’re smoking and they’re—they’re snorting whatever. There’s a five-hundred pound guy on stage with a Mohawk just screaming. And, uh, my mind is blown. I don’t even know what to do. Then this girls walks up and she says “Hey, why don’t you come over and sit down with me and my friends at our table?” All right!

SAM: Yeah, and they get him drunk. First time.

DEAN: But not fun drunk. I’m not quite sure what was in that stuff, but the room starts to spin, and I feel like I’m going to puke … forever. And right about that time, I hear him. “Dean Winchester!”

[Cas looks confused, but Sam just smiles.]

DEAN: My old man. I don’t know how, but he found me. And now I’m really freaking out, because he’s just standing there, not saying anything. I look around, and everybody else is freaking out, too. In fact, nobody’s even looking him in the eye. And finally, this one guy with, like, a safety pin through his nose and a—a “Kill Everything” tattoo looks up and he says, “Sorry, sir.”

---

[Claire is sitting on a bed by herself when she hears footsteps. The door opens, and Salinger is standing there. He motions for his men to leave, and he turns to Claire.]

SALINGER: Hi. [He finishes off his beer, then turns and locks the door.] It’s Claire, right?

[She won’t look at him, until he’s standing in front of her. He reaches down, taking hold of her chin, making her look up at him.]

You really are a pretty one, you know that?

[She lifts her leg, kneeing him in the groin. She runs to the door and tries to unlock it, but Salinger is right behind her, grabbing her as she screams.]

[One of Salinger’s men opens the front door to find Cas, Sam, and Dean standing there. Cas lifts a hand, and the man goes flying backwards.

--

CASTIEL:

Where’s the girl?

[They hear screaming come from upstairs. In the room, Claire is screaming, trying to fight Salinger off. He’s trying to hold her down, and the door flies open. Castiel is standing there, and Salinger turns to look at him, giving Claire enough of an opening to kick Salinger in the face and get up. She kicks him, over and over again.]

CASTIEL: Claire. Claire!

[Castiel grabs her arm, and she finally stops kicking. Cas leads her from the room. They walk downstairs, and Claire moves away from Cas.]

--

[Claire climbs into the back seat of the Impala, and Castiel sits beside her. Claire smiles.]

CASTIEL: Are you okay?

CLAIRE: Yeah.

[She moves over, laying her head on Castiel’s chest, wrapping her arms around him. Cas hugs her back. Sam climbs in the front seat and glances back. He turns his head back towards the house as he hears shouting, then leaves the car as fast as he can.]

///

10x10

(Scene changes to Castiel pacing in the bunker library.)

CASTIEL: She barely speaks to me.

(Sam comes into view, sitting.)

CASTIEL: She’s like a wounded animal, just watching me.

SAM: Look, Cas, you know what? You really tried to do the right thing that night. You did. This guy Claire was hanging out with, Randy, all he did was use her.

CASTIEL: Well, she thought he was kind. And for that, she loved him. Shows how little kindness there was in her life. You know, whatever Randy did, he didn’t deserve –

SAM: No, yeah, I know, I know. I hear you. Dean has had to kill before. We both have. But that was –

DEAN: That was what?

(Sam rises, surprised. Dean walks in from the war room.)

SAM: Dean.

DEAN: That was a massacre. That’s what it was. (Dean looks from Sam to Cas.)

DEAN: There was a time I was a hunter, not a stone-cold killer?

(Cas and Sam look troubled.)

DEAN: You can say it. You’re not wrong. I crossed the line. Guys, this thing’s gotta go.

(Dean looks down at the Mark of Cain on his arm.)

///

And 10x22

MR. McKINLEY: By suggesting my daughter was a slut?

DEAN: I'll admit that thought crossed my mind. Then I came here, and I smelled the deceit and the beatings and the shame that pervade this home.

MR. McKINLEY: You shut your face right now.

DEAN: And you know what? I don't blame Rose anymore. No wonder she put on that skank outfit and went out there looking for validation, right into the arms of the monster that killed her. (Dean looks at Mr. McKinley and in a very calm voice says) Joe, who did this?

[perfectlytinyworkspace]

Wang and Yang: Disinhibitory circuit motifs

[Abstract]

pathway gating: "mechanisms needed to flexibly route information to the right place at the right time"

i.e., blocking out one form of information and letting in another in a brain area that contributes activity to both

key: evidence supports use of a disinhibition mechanism to enact flexible 'pathway gating' in both sensory and association brain areas

[Body]

influx of understanding and evidence on GABAergic interneurons, esp. PV, SST, and VIP cells

VIP neurons inhibit SST neurons, disinhibiting pyramidal cells via double-negative mechanism

Question: is this disinhibition actually utilized in pathway gating? Evidence and applications within review article

perisoma: close to the cell body, meaning a synapse there has overall control of the postsynaptic AP

peridendrite: close to the dendrite and away from the cell body, meaning a synapse there may act in a modulatory manner to contribute to or reduce the postsynaptic AP

factor affecting the ways in which disinhibition could apply to pathway gating: relative densities of GABAergic IN types in different areas of the brain

activation of VIP/SST neurons in frontal cortex affects working memory, providing some evidence that disinhibition plays a role in working memory processing

key: "In layer 2/3 of primary somatosensory cortex...onset of locomotion is correlated with an increase of activity in both pyramidal cells and VIP interneurons, concomitantly with a decrease of activity in SST cells"

counterargument: some aspect of movement directly affects SST neurons, or impacts other inputs to SST neurons from external sources

a buffer: in vitro testing of neuron pairs give support to the disinhibition mechanism specifically [I wish there was more focus in the paper on this]

"This apparent inconsistency can be explained computationally by synaptic interactions between multiple neural populations..." Given that counter evidence is explained via "other, in-vivo factors" – how can we be certain that disinhibition exists between VIP and SST neurons?

knowing that SSTs build up charge over time and are slow to disperse it, responding best to repetitive firing over a window of time, how effective would disinhibition involving SSTs really be in pathway gating that requires instantaneous action as different external stimuli or associations appear simultaneously?

four conditions for the disinhibitory motif to act as a pathway gating mechanism:

nonlinear pyramidal cell response to SST synapsing, so that disinhibition of the relevant pathway renders a strong response in PCs | met via NMDA/Ca2+ spiking in PCs

localization of synapses that impact different pathways to pathway-specific dendritic branches and synapse clusters | no evidence...the article tells us to "imagine"???

branch-specific interneuronal control of PC dendritic activity | SSTs do "provide branch-specific inhibition onto dendrites of pyramidal neurons"

alignment between synaptic pathway-specific clustering and branch-specific control, i.e., "each pathway cluster controls a branch and the balance between branch controls = pathway gating"

"Even random activity is sufficient to create branch-specific inhibition/disinhibition."

I'm not sure I quite understand what is happening here. Are the authors alluding to the flexibility of the disinhibition circuit, in that it can be applied to "random" synaptic activity and then create a learned behavior?

I think I'm following the general logic of the four clauses for disinhibitory gating, but I'm thrown off by the lack of evidence for {2}

heavy focus on how a disinhibitory gating mechanism would 'logically' be better than excitatory mechanisms, but not as much evidence that they actually EXIST in the sense that we think they do

SST INs do exist in much heavier densities in the "higher level" cortical areas that may require more fine-tuning and pathway gating/information integration in comparison to primary sensory areas

[cleverwordsandotherstuffilike]

Gerson: Making room for genius and non-conformity helps society […] The Imitation Game, however, asserts a strong connection between Turing’s eccentricity and his brilliance. The association of scientific or artistic genius with unconventional behaviour is hardly new. Aristotle suggested a connection between creativity and depression. Isaac Newton, who displayed a rich variety of mental disorders, once stuck a needle behind his eye socket just for the heck of it. The honour roll of creative genius — Beethoven, Byron, Tolstoy, Van Gogh, Schrodinger, Godel, Turing — is often a story of obsession, compulsion, melancholy and mania.  There are, no doubt, happy, well-adjusted geniuses, pottering around their gardens and playing bridge with their neighbours. And manic or depressive illness is less romantic outside the movies. It is often life-consuming and horrible. But the association of genius with some mental disorder does not seem to be a myth. “When a superior intellect and a psychopathic temperament coalesce,” argued William James, “in the same individual, we have the best possible condition for the kind of effective genius that gets into the biographical dictionaries.” A study by British psychologist Felix Post asserted a strong historical correlation between creative distinction and mental disorder, with the highest levels of psychopathology found among writers. Which may also explain the mental challenges faced by editors. This connection appears to have a basis in neuroscience. Psychologist Scott Barry Kaufman, blogging for Scientific American, summarizes the research that “the siblings of patients with autism and the first-degree relatives of patients with schizophrenia, bipolar disorder, and anorexia nervosa were significantly over-represented in creative professions.” This presents the prospect that a milder version of mental illness is conducive to creativity. And the mechanism may be a form of disinhibition — a failure of the brain to screen out extraneous information that is then combined in original ways. “A reduced latent inhibition,” says Kaufman, “allows us to treat something as novel, no matter how many times we’ve seen it before and tagged it as irrelevant.” The lightning strike of insight seems to come in a mental storm of stimuli. So there may be a thin line between delusion and creativity. And, as The Imitation Game argues, a society often benefits from allowing space for nonconformity. This presents something of a challenge for conservatives. A broad adherence to social convention is important for a just and stable society. But there is clearly some tie between human progress and the rejection of social and intellectual convention. The existence of norms is essential to social cohesion; the creative violation of norms is essential to social advancement. The West has often gotten this balance right over the centuries (as opposed to, say, an overwhelmingly traditional society such as imperial China). In our culture (as in any other), tradition and religion reinforce social order. But an integral part of this tradition and religion is the priority of conscience, which sometimes dramatically overturns that order. This is the power of putting the individual at the centre of the moral order and building everything, including community, on the foundation of individual dignity. The room for nonconformity, it turns out, is also the room for genius.

Michael Gerson, Washington Post

[ellymackay]

Quarendreaming: Why Your Pandemic Dreams and Nightmares are so Weird and Intense—and What to do About it

The following article Quarendreaming: Why Your Pandemic Dreams and Nightmares are so Weird and Intense—and What to do About it See more on: The Elly Mackay Blog

Are you dreaming more vividly these days, and remembering more of your dreams? Are you having nightmares that wake you from sleep, or leave you feeling anxious the next morning?

If you said yes to either of these questions, you’re not alone. These days, a lot of us are having darker, more upsetting dreams—and remembering them more often.

A recent poll of more than 2,000 people showed

53% of the audience has had an increase in vivid dreams since quarantine began 

21% of the audience have had an increase in nightmares, with at least 1 this past week 

45% of the audience has noticed a small difference in their sleep for the worse… and

29% have noticed a significant difference in their sleep for the worse 

What are the obvious offenders? Social isolation, massive upheaval to daily routines, fears about health, finances, and deep uncertainty about what lies ahead. As well as a shifting combination of boredom, overwork, stress and anxiety. That pretty much describes how most of us are living these days, since the onset of the coronavirus pandemic.

It’s challenging our diets. A lot of us are moving from one “comfort food” meal to the next (think of all the lasagnas and banana breads on Instagram).

It’s challenging our exercise. Stuck at home working and, in many cases, simultaneously taking care of children, many of us are struggling to get our regular exercise, mostly because we feel exhausted!

It’s challenging our sleep. I’m hearing from so many readers and patients about their insomnia symptoms, the restless awakenings, the racing thoughts they can’t quiet at night. I wrote recently about the deep connections between stress and sleep—connections we’re all experiencing strongly right now. And many of you are having nightmares and disturbing dreams. I wrote a couple weeks ago about the coronavirus and nightmares, and why our bad dreams aren’t an entirely bad thing.

Our dream content has changed (Normal vs Stress vs Nightmare)

I’ve had many people tell me their dreams are tackling the coronavirus directly, dreaming about hospitals and illness and trouble breathing (these dreams can also be signs of sleep apnea and snoring). Others are dreaming about the virus in different ways, such as nightmares about violence, loss, uncertainty, and threats.

One of my patients dreams of a friend who is an ER doc in a city hard hit by the virus, getting sick and dying on a gurney (This would be a nightmare. Thankfully that friend is healthy in real life.) Another told me she’s having a recurring dream about being lost inside an unfamiliar building she can’t find her way out of. (We consider this a stress dream.)

Dreams seem more REAL

People are having stranger dreams, with odd characters and vivid combinations of the ordinary and the bizarre. And these dreams often feel different—more striking, more charged with meaning, more vivid, more real—even if the circumstances of the dreams are fantastical. I’ve talked a lot about dreams and nightmares over the years, and the science behind how nightmares work, and how to help make your dreams more peaceful and positive.

The coronavirus pandemic is spurring a whole lot of bad dreams—and a lot of new science studying the phenomena of dreaming.

Here’s what’s being studied in the emerging science of the coronavirus dream world:

Scientists are racing to study every aspect of the coronavirus and Covid-19, the disease it causes. That includes the psychological impact of the global pandemic, its impact on sleep, and its effect on dreams. There is surely much more to come here, but these initial findings shine a light on the psychological upheaval that’s occurring, and how it is making its way into our dreams.

Anxiety is UP: There’s been a major spike in anxiety in the past several weeks—no surprise here. Scientists at Philadelphia’s Thomas Jefferson University conducted a survey in April and found that about 40% of respondents had symptoms of anxiety intense and frequent enough to warrant clinical intervention.

It’s almost like PTSD: People are having more nightmares and negatively-focused dreams during the pandemic. That’s according to research that’s been underway in several countries, including in Italy, one of the countries hardest hit so far by the coronavirus, as well as an ongoing study in France. The Italian study has found many of its subjects are experiencing nightmares with an intensity that corresponds to post-traumatic stress disorder.

Dream recall has increased, which increases stress: People are remembering more of their dreams, experiencing what’s known in sleep science as higher dream recall, according to research. That means more of us are taking upsetting dream and nightmare content into our waking days, for an even greater effect on mood and psychological balance, and another source of stress.

Why, exactly, are our dreams being so deeply affected by the pandemic? And how can we calm and quiet these upsetting, sleep disrupting dreams and nightmares so we can the sound sleep we need right now?

The answers to those questions touch on some of the most well-established, compelling theories of dreaming—and on the mechanics of sleep itself.

                      FYI, if you want to get straight to the recommendations, go to page 6 below!

Dream Theory

What do Dreams Do? Dreams are a way for our brains to process stress and emotionally-charged memories.

This is one of the most well studied, commonly held theories about dreaming—that our brains employ dreams to work through emotionally difficult and stressful experiences, to reduce their psychological load and make them less disruptive to daily functioning.

Clearly most of us are coping with unusual levels of stress right now, and our brains are using dreams to process it. As unwelcome as nightmares and disturbing dreams feel, they may be a sign of the brain doing some essential, important work to ease the intensity and emotional charge of our currently heavy daily load of stress and worry. And our nightmares can also serve the purpose of alerting us to anxieties we haven’t yet become aware of, or given name to.  

Research into trauma and its relationship to dreaming and sleep has shown that the more closely and directly people are affected by traumatic events, the more likely it is for their sleep to be disrupted and for nightmares to be intense. Nightmares are highly common among people with post-traumatic stress disorder. Nightmares associated with PTSD also are more likely to be direct replays of the trauma triggering event. In 2009, researchers looked at the impact of an earthquake in Italy, and found the most disturbing dreams and disrupted sleep occurred in people who were nearest the epicenter of the quake.

The people in the “epicenter” of the coronavirus pandemic include health care workers and other first responders, people who are sick or who are close to someone who is sick. There are also millions of people who have been laid off from jobs, and people who are facing economic crises that place them in an economic “epicenter.”  

But it’s important to note: You don’t need to be at any of these “epicenters” of the crisis to experience trauma, sleeplessness, anxiety, and nightmares from the effects of the pandemic. Trauma and its fallout on sleep and dreams is in no way exclusive to first responders or the sick and their families. We’re living through unprecedented, frightening times, with a future outlook that is deeply uncertain. That’s a universal—and potentially traumatic—reality right now.

How does the brain process emotions during sleep and dreams?

We know something about these mechanisms, and it’s pretty interesting. During stages of sleep, areas of the brain enter a state of what’s known as “emotional disinhibition.”

This occurs particularly during REM sleep, which is when we do most of our vivid, complex, emotionally-laden dreaming. To achieve this state of emotional disinhibition, a region within the brain known as the dorsolateral prefrontal cortex shuts down. This part of the brain performs many complex executive functions involving memory, self-awareness, attention, and inhibition and control of emotional responses. The effect of this part of the brain shutting down creates an unselfconscious free flow of emotion within dreams. Basically, it’s “Party Time” for your brain, and it can now go outside the realm of reality (because you are in the unconscious) where the laws of physics simply do not apply.

Bottom Line: Dreams are where your brain processes information.

An important exception is lucid dreams. During these dreams, part of the dorsolateral prefrontal cortex appears to become more active, not less, which scientists think contributes to the self-awareness and ability to control and direct activity within lucid dreams. I’ve written about lucid dreams—what they are, how they work, and how to encourage your brain to dream more lucidly.  

Dreams are a ‘rehearsal’ for real-life threats and challenges

This well-established, long-held theory of dreams provides another explanation for why so many people’s dreams are so heightened, intense and disturbing right now.

So much of the study of dreams revolves around the question: why do we do it? Amazing as it may sound, we don’t yet know for sure the purpose of dreams. Here’s a primer I wrote a few years ago on the basics of dreaming, including the most popular and well-researched theories about the purpose of dreams.

One of the most interesting and compelling hypotheses of dreaming is this one, known as the threat-simulation dream theory.

According to this theory, and the scientific evidence that supports it, dreams are a rehearsal space for the mind to “game out” threats and obstacles it anticipates facing in waking life, and practice how to best respond to these challenges. In this theory, dreams are a kind of virtual reality, “training camp” simulation in the brain, with a focus on tackling the challenges the brain has identified as the most pressing and important to prepare for.

When you think about it in evolutionary terms, this theory makes a lot of sense. Imagine our ancient human ancestors living under constant and immediate threats–from animal predators, from human rivals, from forces of nature. Today’s predators and challenges are somewhat different, but the capacity for the brain to run simulations when faced with threats and danger remains intact. Keep in mind, the body does not distinguish between the stress and agitation caused by thinking about losing one’s job or a loved one becoming sick, and the stress and agitation caused by being chased across an open field by a wild animal. When we’re constantly anxious and worried, our bodies take up residence in “fight or flight” mode, and dreams may take up the work of helping us rehearse our way out of our problems.

Bottom Line: Dreams are a good place to “practice” or “train” for real life situations.

We draw heavily on daily life for dream material

Pieces of our daily experiences show up in dreams all the time, a well-studied phenomenon known as “dream incorporation.”  Dream research has shown that some memories from daily life show up in dreams immediately, that same night. This immediate transfer of memories into dreams is known as “day residue.”  Other memories from waking experience are subject to what scientists refer to as a “dream lag.” That’s a delay, typically of about 7 days, between a memory being created in the waking day and it showing up in a dream.

For so many of us, the world we occupy is small right now—much smaller than what we’re used to. Right now, much of our activity, movement, and social interaction is curtailed. And many of us are consuming a daily dose of a lot of troubling news.  Under such restrictive, repetitive daily living conditions, our brains are likely drawing more heavily on older memories for dream material. That explains why your childhood friend or college roommate might pop up in the middle of a pandemic dream.

Plus, snippets of the media we’re consuming every day, whether in text, audio, or visual form, will make their way into dreams. If you’re on a heavy diet of pandemic-related news, you can expect to see that information your brain is taking in make its way into your dreams. Research, including a recent study from 2018, show that more emotionally intense daily life experiences tend to show up in dreams more often. A lot of daily life right now, however restrictive, feels pretty emotionally intense. And we can expect to see that reflect in our dreams.

Bottom Line: The content we consume during the day, ends up in your dreaming world, as either “Day Residue” or later as “Dream Lag”

Isolation may be leading us to remember more of our dreams

Being isolated means that your contact with a variety of people, places and things, is limited or non-existent. Your brain encodes information better when its connected to an emotion. If you are removed from these positive stimuli in your life, your brain will go in search of that data, which has been a regular part of your environment. If this positively-charged information is not to be found in your current waking life, your brain will begin to scroll backward, going back further into your old memory bank, to pull up the thoughts, ideas, and people associated with that input which is now missing from your present-day life.  

Bottom Line: When you are isolated, you miss the people, places, and things there were in your life, and your brain will go back to your old memories for those happy feelings. BUT it also has to incorporate the new data (probably stressful data you hear on TV), and then you get a scary dream.

Sleep is more restless

You might be waking more often during the night these days as well—and if you are, you’re more likely to remember parts of your dreams, especially if it’s a vivid or strange one, or a nightmare. Nightmares themselves, because they are frightening and upsetting, make us more likely to wake up from a dreaming state, with fresh memories of our nightmares intact. In addition, nightmares have a tendency to keep us awake, the data shows that if you are awake for more than about 5 minutes, you will begin to encode your dreams into your memory.

Current research happening right now in France suggests there’s been a 35% uptick in remembered dreams during the coronavirus pandemic. This research has also shown a 15% increase in negative dreaming since the pandemic began.

It’s not for everybody, but many people are interested in learning how to remember more of what goes on in their dreaming lives. I’ve talked about techniques that help you to remember more of your dreams.

How to help ease your nightmares and sleep better during a pandemic!

Focus your mind with optimistic thoughts before bed

Your mind frame at the time you fall asleep will greatly affect your dreams. Research has shown that our levels of optimism and peace of mind, or pessimism and anxiety, have a direct effect on the subject matter and emotional content of our dreams.  Dreams reflect several levels of emotional consciousness—our daily life experiences, our short- and long-term emotionally resonant memories, and our affect (aka our mood/outlook) right before bed.

If your dreams are currently disruptive and disturbing right now, create a nightly Power Down Hour that focuses on bringing you to a positive frame of mind before bed.

Bottom Line: Get Happy before bed!

Watch a funny or inspiring TV program. Talk to a friend or loved one who lifts you up. Pray or engage in a spiritual practice that elevates you. Read something that makes you laugh and feel good about life. Plan your next vacation. Open up old photo albums and enjoy some positive memories before bed. We all get there a little bit differently, but it is important, especially right now, to enter sleep with a peaceful, optimistic mind. Your dreams will follow suit.

“Re-write” your nightmares Image Rehearsal Therapy

A technique called “image rehearsal therapy”  has been shown to help reduce nightmares and make sleep easier and less stressful. I use this technique with my patients quite often. As part of this therapy, people re-write the stories of their nightmares, turning their scary scripts into happier, more peaceful ones. Image-rehearsal therapy can be especially effective for people who experience nightmares that are chronic or recurring. This technique was developed by Dr. Barry Krakow at The University of New Mexico.

Here’s how it works:

You write down the all the details of your nightmare, telling its story from beginning to end.

Then, you create a new version of the dream, one that turns a frightening story into a positive one. Once it’s been re-scripted, you visualize the new dream, playing over and again in your mind. You can even re-read the “new” version several times before bed, and over time (5-7 days) the content of your dream will begin to change.

A nightmare that originates like this:

I’m running along a dark and twisty path, I can’t see in front of me. Someone is chasing me, and getting closer. I can’t run fast enough to get to a safe place.

Might become something like this:

I’m walking along a peaceful road in the woods. I’m alone, and I feel completely safe. I can take my time, feeling the breeze pass through the trees, smelling the scent of the forest, and enjoying presence of the birds and other small animals that are moving around their natural home. I hear someone walking behind me and I turn to look, seeing a friend who I’m happy to run into.

Or like this: I can sense someone behind me, so I reach into my pocket and pull out a grenade launcher . . . you get the rest.

Bottom Line: Flip the Script- change your negatives into positive, and “Change the Channel” on your nightmares.

Limit your media consumption

I talked about this recently in another article that tackles the relationship between nightmares and stress in the age of coronavirus. There’s so much media out there to consume, on social channels and news sites, on TV and radio and podcasts. We’ve all probably fallen down a rabbit hole of endless scrolling and reading about the virus, or watching on social media how everyone else is living out their pandemic isolation. This constant media consumption will increase your anxiety and stress, leading to more negatively-charged dreaming. And some the details of the news and information you consume will find their way into your dream content.  Limit your overall daily media intake, and avoid reading the news and social sites at night before bed.

Bottom Line: Plug your phone in another room. Watch a Seinfeld or Friends episode and chill out, starting 90 minutes before lights out.

DON’T Sleep IN! 

The basic science on this one is simple. If you sleep in, you will ultimately get more REM sleep (which happens more in the final third of the night) which leads to more dreams and nightmares. It also throws off your circadian rhythms and we all know why that’s not a great idea!

Bottom Line: Keep your scheduled wake-up times during lockdown, and NO NAPS!

Consume Less:

Alcohol, (which I have written about many times before) affects dream content. It’s that simple. Whatever emotion you are having in a dream is often increased by the presence of alcohol. Not good. In addition, we know that alcohol affects our ability to get good quality sleep, which will also increase bizarre dream content (and it’s not like we need any help in that department). And don’t forget alcohol limits immune function–is that really the best idea right now?

Caffeine, (which I have also written about previously) is simply a bad idea right now. Let’s be 100% honest, it’s a stimulant and it increases anxiety, period, end of story. I can’t think of a time in life were more people were more anxious than right now. Do ANY of us really need to ADD to our anxiety right now? I don’t think so.

Bottom Line: Slow your roll, limit to 2 drinks 2-3 hours before bed, and stop caffeine by 2 p.m.

Move more:

Your total activity level has dropped dramatically (I saw one celebrity tweet this: “I’ve taken 200 steps today, and its 3 p.m.!” Lack of exercise, including daily movement, is affecting sleep quality. Increase opportunities to move throughout your day, it will help with sleep at night.

Bottom Line: Don’t just watch the exercise video, actually do it, 2 times a day. Take out the trash every day, walk to the mailbox every day, walk your dog 2-3 times a day. 

Agreed-upon Treatments for Nightmare Disorder in Adults 

The American Academy of Sleep Medicine, has created a position statement on Nightmare Disorder in Adults and evaluated the following treatments. Their website is a great resource.

POSITION STATEMENTS:

The following therapy is recommended for the treatment of PTSD-associated nightmares and nightmare disorder: image rehearsal therapy (see above).

The following therapies may be used for the treatment of PTSD-associated nightmares: cognitive behavioral therapy; cognitive behavioral therapy for insomnia; eye movement desensitization and reprocessing; exposure, relaxation, and re-scripting therapy; the atypical antipsychotics olanzapine, risperidone and aripiprazole; clonidine; cyproheptadine; fluvoxamine; gabapentin; nabilone; phenelzine; prazosin; topiramate; trazodone; and tricyclic antidepressants.

The following therapies may be used for the treatment of nightmare disorder: cognitive behavioral therapy; exposure, relaxation, and re-scripting therapy; hypnosis; lucid dreaming therapy; progressive deep muscle relaxation; sleep dynamic therapy; self-exposure therapy; systematic desensitization; testimony method; nitrazepam; prazosin; and triazolam.

Reach out for help

Anxiety and nightmares are health issues that need attention and can benefit greatly from treatments, even amid physical distancing. If you’re experiencing debilitating dreams, or waking anxiety that is affecting your ability to function normally, don’t try to tough it out or go it alone. Contact your physician, ask for a referral to a sleep and mental health specialist (www.sleepcenters.org). We all must do what we can not to compound the suffering of the coronavirus by allowing other emerging health issues, including sleep and psychological health, to go unattended.

Bottom Line: Isolation makes it worse, everyone is freaking out, share your story with a trusted mental health professional, contact your religious leader, talk to a friend. We are actually all in this together.

Stay Safe and have Sweet Dreams,

Michael J. Breus, PhD, DABSM

The Sleep Doctor

www.thesleepdoctor.com

    The post Quarendreaming: Why Your Pandemic Dreams and Nightmares are so Weird and Intense—and What to do About it appeared first on Your Guide to Better Sleep.

from Your Guide to Better Sleep https://thesleepdoctor.com/2020/05/12/quarendreaming-why-your-pandemic-dreams-and-nightmares-are-so-weird-and-intense-and-what-to-do-about-it/

from Elly Mackay - Feed https://www.ellymackay.com/2020/05/12/quarendreaming-why-your-pandemic-dreams-and-nightmares-are-so-weird-and-intense-and-what-to-do-about-it/

[compneuropapers]

Interesting Papers for Week 45, 2017

Multidimensional receptive field processing by cat primary auditory cortical neurons. Atencio, C. A., & Sharpee, T. O. (2017). Neuroscience, 359, 130–141.

Noradrenergic activation of the basolateral amygdala maintains hippocampus-dependent accuracy of remote memory. Atucha, E., Vukojevic, V., Fornari, R. V, Ronzoni, G., Demougin, P., Peter, F., … Roozendaal, B. (2017). Proceedings of the National Academy of Sciences of the United States of America, 114(34), 9176–9181.

Spontaneous Activity in the Zebrafish Tectum Reorganizes over Development and Is Influenced by Visual Experience. Avitan, L., Pujic, Z., Mölter, J., Van De Poll, M., Sun, B., Teng, H., … Goodhill, G. J. (2017). Current Biology, 27(16), 2407–2419.e4.

Milliseconds of Sensory Input Abruptly Modulate the Dynamics of Cortical States for Seconds. Deneux, T., & Grinvald, A. (2017). Cerebral Cortex, 27(9), 4549–4563.

Precision Functional Mapping of Individual Human Brains. Gordon, E. M., Laumann, T. O., Gilmore, A. W., Newbold, D. J., Greene, D. J., Berg, J. J., … Dosenbach, N. U. F. (2017). Neuron, 95(4), 791–807.e7.

Altered Balance of Receptive Field Excitation and Suppression in Visual Cortex of Amblyopic Macaque Monkeys. Hallum, L. E., Shooner, C., Kumbhani, R. D., Kelly, J. G., García-Marín, V., Majaj, N. J., … Kiorpes, L. (2017). Journal of Neuroscience, 37(34), 8216–8226.

LTP at Hilar Mossy Cell-Dentate Granule Cell Synapses Modulates Dentate Gyrus Output by Increasing Excitation/Inhibition Balance. Hashimotodani, Y., Nasrallah, K., Jensen, K. R., Chávez, A. E., Carrera, D., & Castillo, P. E. (2017). Neuron, 95(4), 928–943.e3.

Gain Modulation as a Mechanism for Coding Depth from Motion Parallax in Macaque Area MT. Kim, H. R., Angelaki, D. E., & DeAngelis, G. C. (2017). Journal of Neuroscience, 37(34), 8180–8197.

Cross-compartmental Modulation of Dendritic Signals for Retinal Direction Selectivity. Koren, D., Grove, J. C. R., & Wei, W. (2017). Neuron, 95(4), 914–927.e4.

Nonlinear Bayesian filtering and learning: a neuronal dynamics for perception. Kutschireiter, A., Surace, S. C., Sprekeler, H., & Pfister, J.-P. (2017). Scientific Reports, 7, 8722.

Neuronal Encoding of Self and Others’ Head Rotation in the Macaque Dorsal Prefrontal Cortex. Lanzilotto, M., Gerbella, M., Perciavalle, V., & Lucchetti, C. (2017). Scientific Reports, 7, 8571.

Theta-paced flickering between place-cell maps in the hippocampus: A model based on short-term synaptic plasticity. Mark, S., Romani, S., Jezek, K., & Tsodyks, M. (2017). Hippocampus, 27(9), 959–970.

Hippocampal Neural Disinhibition Causes Attentional and Memory Deficits. McGarrity, S., Mason, R., Fone, K. C., Pezze, M., & Bast, T. (2017). Cerebral Cortex, 27(9), 4447–4462.

Dopamine D2 Receptors Enhance Population Dynamics in Primate Prefrontal Working Memory Circuits. Ott, T., & Nieder, A. (2017). Cerebral Cortex, 27(9), 4423–4435.

Morphological Diversity Strongly Constrains Synaptic Connectivity and Plasticity. Reimann, M. W., Horlemann, A.-L., Ramaswamy, S., Muller, E. B., & Markram, H. (2017). Cerebral Cortex, 27(9), 4570–4585.

Place and Grid Cells in a Loop: Implications for Memory Function and Spatial Coding. Rennó-Costa, C., & Tort, A. B. L. (2017). Journal of Neuroscience, 37(34), 8062–8076.

Asymmetry of the temporal code for space by hippocampal place cells. Souza, B. C., & Tort, A. B. L. (2017). Scientific Reports, 7, 8507.

Dynamic reconfiguration of cortical functional connectivity across brain states. Stitt, I., Hollensteiner, K. J., Galindo-Leon, E., Pieper, F., Fiedler, E., Stieglitz, T., … Engel, A. K. (2017). Scientific Reports, 7, 8797.

A study of problems encountered in Granger causality analysis from a neuroscience perspective. Stokes, P. A., & Purdon, P. L. (2017). Proceedings of the National Academy of Sciences of the United States of America, 114(34), E7063–E7072.

A Role for the Left Angular Gyrus in Episodic Simulation and Memory. Thakral, P. P., Madore, K. P., & Schacter, D. L. (2017). Journal of Neuroscience, 37(34), 8142–8149.

[oofta-oofta]

Neurodegenerative disorders

Neurodegenerative disorders are characterised by loss of neurones, progressive worsening and irreversibility. 

Types discussed are: Alzheimer’s disease Multiple sclerosis Parkinson’s disease Huntington’s disease

Alzheimers Alzheimers is a disease of ageing, with memory loss increasing. It is like the brain slowly forgets, until the person feels like a child again. It involves dementia, loss of cognitive processes, steady knowledge loss and loss of emotive detection.

Early symptoms •Short term memory •Disorientation - time then place •Difficulty with words, names, numbers •Clumsiness - motor changes, dyspraxia. •Visuospatial orientation (gets lost)

middle symptoms  •Loss of social skills •psychosis + paranoia/hallucinations/delusions - can get irritable, aggressive, say hurtful things and be oblivious to it. Become someone else. Paranoia, hallucinations, delusions. •bradykinesia/rigidity - similar to parkinson.

late symptoms •Mutism - unable to speak •Incontinence •Bedridden - curled in foetal position. unable to eat and drink.

Usually die of infected bedsores, respiratory condition of respiratory system. Starvation/dehydration.

Alzheimers pathology Note the widened sulci and rrowed gyri with Alzheimer’s. Cortical atophy damage to short term memory due to hippocampal destruction. Widened sulci due to loss of gyrus tissue, and ventricles.

Mostly temporal damage. Some cortical (where language centres are).

First symptoms affect memory.

 Radio labelled glucose - more absorbed, more metabolically active. Reduction in activity shown in scan.

Picks disease: frontal dementia.

Brain staining. Look for amyloid beta protein. 

Tissue insoluble plaques - heavily stained. external. abnormal. made of polypeptide amyloid beta protein. spherical.

Mild Cognitive Impairment: not necessarily due to develop alzheimers. doesn’t always progress.

Dense core plaques on Alzheimers. Much greater number of plaques. neurofibrillary tangles are made of hyperphosphorylated tau proteins. Age of 23-24 tangles begin to develop in everyone.

Plaques and tangles diagnose alzheimers.

Less interconnection - loss of dendrites. Mainly the cholinergic that are lost.

Current treatment: Based on AChE inhibitors. ACh turns into choline and Acetic Acid is converted by Cholinesterase. Inhibiting this enzyme increases ACh levels, and may slow the progression of the disease and could improve cognition (not strong evidence - might see slowing of symptoms - 2-3 months better function) with a nootropic effect. Look up inhibitors!

Multiple sclerosis •Sensory changes - sense of touch •Muscle weakness •Coordination and balance •Speech - oral cavity impairment •Swallowing •Visual acuity •Fatigue, •Pain •Incontinence •Cognitive impairment •Depression (linked or caused?) •Mood swings

It involves loss of neuronal tissues

Causes Autoimmune Oligodendrocytes affected - degradation of the myelin sheath. Myelin sheath degrades Most common in women

It progresses in 4 different ways.



Parkinson’s disease - 2nd most common. •Incidence increases over 70 •Extrapyramidal disorder •Loss of movement •Increased muscle tone

difficulty initiating movement: a lot of thought.

Symptoms: •Tremor •Rigidity •Speech •Micrographia •Akinesia Postural changes  Stoop  Shuffling

treated with levadopa/carbidopa

Substantia viagra, synapse with interneurone in striatum, then striatum, then thalamus, then motor cortex, then skeletal muscle.

It is the DA pathway between viagra and striatum that is damaged. nigirostriatal pathway.  Substantia viagra has pigment: something-melanin. Lose dark stain

Huntington’s Disease •Inherited disorder •Autosomal dominant •Polyglutamine repeat •Huntingtin - don’t know function. More than 36 polyglutamine repeats show you will develop hunting tons. more repeats: more aggressive.

Symptoms: Irritability Moodiness Antisocial behaviour —> dementia. aggressive demential

Fidgeting & restlessness indicates gross choreiform movements (continual movements of body. head, tongue, fingers. opposite of parkinsons.

Pathology Loss of neurones in the cerebral cortex and corpus striatum; GABAergic / Cholinergic.

 Fig. 3 Striatal metabolism in five patients with Huntington’s disease, before (T0) and after (T2) bilateral neural graft in the caudate and putamen. In each individual, the normalized metabolic images have been superimposed on the corresponding MRI. The right side of the brain is on the left in the images. In patients 1–3, the arrows indicate grafted tissue in which metabolism increased compared with the baseline striatal metabolism. In patients 4 and 5, none of the graft was associated with a noticeable increase of metabolism. Note that in patient 4, a cystic cavity appeared in the grafted left putamen (arrow).

Disinhibits motor movement.

[perfectlytinyworkspace]

Tremblay et al.: Figures and Boxes

Figure 1: Diversity, Classification, and Properties of Neocortical GABAergic INs

Neocortical GABAergic IN: GABA-releasing (likely inhibitory) interneuron (connecting between perception/motor output?) within the fetal brain

all of these express one of [PV parvalbumin (relation to general albumin carrier in the blood?), somatostatin (insulin/glucagon balance regulator), 5HT3a serotonin receptor] and can thus be categorized by those markers

further classification of different neocortical GABA-ergic INs can be obtained via morphology, targeting biases, other biomarkers, and electrophysiological/synaptic properties

tree classification: 1 of 3 markers » morphology » targeting bias » anatomy » biophysical properties of firing (firing patterns, spiking, refractory) » synaptic properties » addt'l markers

Figure 2: Laminar Distribution of IN Groups

L1, 2, 3, 4, 5a, 5b, and 6 are all layers in the neocortex

distribution of the three major GABA-ergic IN types as distinguished by PV, Sst, and 5HT3a marker expression (5HT3a separated into VIP and non-VIP expressing cells) varies with neocortical layer

significance: varying compositional make-up of L layers signifies likely variance in roles they play in fetal brain function + later development of cognition

Box 1: PV FS Basket Cells Are Specialized for Speed, Efficiency, and Temporal Precision

physical properties of PV FS cells suit them for rapid, precise firing

machinery for fast EPSPs: AMPA receptors w/ GluR1 subunits only, low membrane resistance, very active dendrites

machinery for brief and highly repetitive APs: sub-threshold Kv1 channels that allow for quick repolarization, "Na+ channels with slower inactivation and faster recovery"

these components are all concentrated at the appropriate areas of the neuron to reach high efficacy

Figure 3: Cell-Specific Connectivity and Subcellular Domains Targeted by IN Subtypes

Sst martinotti cells synapse near the soma of the L2/3 cell

nonVIP 5HT3aR NGFCs synapse near the branches of the L2/3 dendrite/axon

in L5/6 pyramidal cells, NGFC inputs are broken up by different layers (?)

Figure 4: Circuit Motifs Involving INs

different functions of interneurons in modulating synaptic signaling are dependent on placement of IN and source of excitatory input

feedforward inhibition: distal excitation » IN and pyramidal cell; IN then also inhibits pyramidal cell to modulate the effects of the distal excitation

feedback inhibition: PC excitation » IN inhibits the original PC source of excitation to gradually modulate its signal » IN also inhibits same-layer proximal PCs to unify regional signaling pattern

disinhibition: IN » IN » PC so that the end result is the reduction of inhibition on the pyramidal cell's excitatory activity

Figure 5: Thalamocortical FFI by PV Neurons Imposes Coincidence Detection

FFI via PV neurons allows for temporal summation window in certain spaces/moments of time

this is achieved by increasing inhibition at all other time periods; now "near-synchornous inputs are required for efficient summation of EPSPs and to drive AP firing on the PC"

[I think that] NGFCs weaken the PV inhibition of PCs, allowing for a wider window of temporal summation and lateral signaling recruitment of other PCs?

FFI prevents saturation via PV cell recruitment; NGFC signaling weakens this mechanism. Thus, depending on how much FFI is needed in certain regions, the NGFC vs. PV cell population concentration ratios will vary

Figure 6: FBI and Differential Effect of PV and Sst IN-Mediated Inhibition

difference between PV and Sst IN inhibition: PVs show decreased response to repeated external inputs due to anatomical and synaptic features from Box 1; Ssts show increased response due to "opposing" or somewhat "antithetical" physical properties to PVs

thus PVs function to synchronize activity laterally across two or more pyramidal cells, i.e., spatial summation; Ssts function to amplify all inputs to a single PC, i.e., temporal summation

PVs have high permeability (low resistance) which means that EPSPs generated diffuse and disperse easily, so highly repetitive inputs do not build up and the cell is unable to undergo temporal summation; on the other hand, insensitivity to temporal summation means that the cell can 'detect' synchronized spatial summation » it's not just a LACK of temporal summation, it's that a "large amount of input at one time" must be present, which means it's uniquely suited to spatial summation

Ssts have low permeability (high resistance) which means they can essentially STORE charge and thus undergo temporal summation with highly repetitive inputs from external sources

Figure 7: Vip IN-Mediated Disinhibition

Vip INs selectively inhibit Sst INs that are targeting a single pyramidal cell, so that when Vips fire, PCs are disinhibited

area-wide excitability is increased broadly as Vips are recruited; or, if a single Vip is activated, so too are just a few selected PCs disinhibited