Is "Karmic Punishment" more effective? When I was young, my parents consistently used "Karmic Punishments", punishments that had a strong relationship to the misbehavior. They believed that this was more effective.

Examples:

Swearing or lying was punished by rinsing mouth out with soap
Physical violence was punished by spanking
Laziness was punished by physical labor.

Is there research to support the idea that relating punishment to behavior in this way is more effective than an unrelated but equally harsh punishment? Information about "Karmic rewards" is also valued.

Sidenote: My father also did this to train the household dog. Excessive barking meant being shouted at/gunshy training (loud noise) while biting was punished with a rap on the nose.

Its difficult to understand exactly which type of parenting style and discipline you experienced so please allow me to describe what I was able to find on parenting.

There are many different styles of parenting. Authoritarian which are strict and rule based. Authoritative which has rules which are followed more responsive to the child's needs and feelings. Permissive which are the "lets be friends" type. Uninvolved which providing basic physical care without communicating or in some cases becoming neglectful.

Each of these parenting styles tend to follow specific punishment outlines.

Authoritarian parents tend to spank and say things like "Because I'm your parent. Because it is my house." rather than caring for the emotional needs of the child. Modern psychology never endorses spanking as healthy. Spanking teaches children to be aggressive. Possibly even associating such traits with love if a parent showed affection in association with spanking as is frequently practiced.

Authoritative parents provide guidelines for children to live by which are punished by a logical system of positive and negative punishment. A logical system of punishment is one where it follows from your behaviour that such actions could be eliminated and or added. The punishment fits the crime. For instance sass off toward the authority figure with a cell phone can lead to the loss of the cell phone. This would be a negative punishment where privileges are removed. A positive consequence for not doing laundry might be a fee for the laundry done that day. It adds the burden of a payment to the child. Sometimes bad behaviour can cause you frustration and its never appropriate to discipline a child while angry. Time outs are also an important healthy way to punish children. This is punishment by boredom so its important that the pre-established place be safe and uninteresting. In my experience a chair in the corner is more effective than the bed in the bedroom. Token economy a clear and consistent reward for behavior also works well. I never have experienced a situation where allowing a child to learn from their mistake by allowing "natural consequences" has worked well. Its labor intensive. Most parents simply use "natural consequences" as an excuse to by proxy harm/abuse, disengage or nag rather than prop up.

Psychology also doesn't endorse the passive parent who never disciplines their child either or the extreme of the passive the uninvolved which abandons their child.

The follow up to discipline is just as important as the discipline itself.

Like I said earlier with the information you gave its not possible to tell how healthy your punishments were. Its really not my place to judge your “Karmic Punishment”. From the descriptions I gave I think you can make up your mind.


What is "perceptual competence"? I have no idea what perceptual competence is? Does anyone know about it? I found no information about it on the web.

Short answer
"Perceptual competence" is "the ability to perceive".

Background
I Googled "perceptual competence" and the first hit was an open source article (Lencz et al., 2003). They define perceptual competence as:

  [The] initial representation of to-be-remembered material [in the context of working memory]. Perceptual competency itself can include multiple subprocesses, including sensory representation, attention, executive processes, and possibly verbal memory processes, if the stimuli are easily recognized or verbalized.

Reading their use and interpretation, I think "perceptual competence" can be simply literally semantically translated, namely:

PERCEPTUAL - of, relating to, or involving perception especially in relation to immediate sensory experience and
COMPETENCE - the ability to do something well : the quality or state of being competent

Reference
- Lencz et al., Arch Gen Psychiatry (2003); 60(3):238-43


How to measure dominance and submissiveness? Introduction

Interpersonal dimensions of personality (Sullivan, 1953) have been described in a circular model, the interpersonal circumplex, since Leary (1957). The two dimensions that define this circumplex are warmheartedness(pleasantness) versus coldheartedness and dominance versus submissiveness. Two better known measures based on Leary's concept are Mehrabian's Trait Dominance-Submissiveness (Mehrabian & Hines, 1978) and Trait Pleasure-Displeasure Scales (Mehrabian, 1978) (which combine with a Trait Arousability Scale, Mehrabian, 1977, into the PAD; Mehrabian, 1996b), and the Interpersonal Adjective Scale (IAS-R; Wiggins, Trapnell & Philips, 1988).

If you analyse the dominance/submissiveness scales from these instruments, it becomes clear that dominance is here understood to be the ability to assert oneself, while submissiveness is the complementary inability:

  The 26 items of the Trait Dominance-Submissiveness Scale ... assessed the generalised feelings of control and influence over one's relationships and life circumstances (e.g. 'I control situations rather than let them control me' (+), 'I work best when someone has outlined a job for me' (-), or 'Domineering people don't intimidate me' (+)). (Mehrabian, 1996a)

The adjectives related to submissiveness in the IAS-R make this negative construct of submissiveness even more clear: timid, bashful, shy, forceless, are four of the eight self-descriptors from this scale.

Contrary to this perspective on submissiveness as incompetent and powerless, other conceptions are possible: some egalitarian individuals might not be unable to dominate others, but simply unwilling; some loving individuals might find fulfillment in selfless devotion; and with the ever expanding service economy, hopefully professional service providers enjoy serving their customers – it would be a dismal life for a majority of us, if we didn't.

Submissive pleasure is an important factor in certain forms of romantic relationships, from the wife choosing a traditional provider/facilitator-household in feminist times to the happy spanking BDSM couple.

Question

Are there measures, scales or instruments that measure a positive, joyful concept of submissiveness, as it is conceived by BDSM?

If not, is there a measure of the "service provider personality"?

References

Leary, T. (1957). Interpersonal diagnosis of personality. New York: Ronald Press.
Mehrabian, A. (1977). A questionnaire measure of individual differences in stimulus screening and associated differences in arousability. Environmental Psychology and Nonverbal Behavior, 1, 89-103.
Mehrabian, A. (1978). Measure of individual differences in temperament. Educational and Psychological Measurement, 38, 1105-1117.
Mehrabian, A. (1996a). Analysis of the big-five personality factors in terms of the PAD Temperament Model. Australian Journal of Psychology, 48, 86-92.
Mehrabian, A. (1996b). Pleasure-arousal-dominance: A general framework for describing and measuring individual differences in temperament. Current Psychology, 14, 261-292.
Mehrabian, A., & Hines, M. (1978). A questionnaire measure of individual differences in dominance-submissiveness. Educational and Psychological Measurement, 38, 479-484. doi:10.1177/001316447803800235
Sullivan, H. S. (1953). The interpersonal theory of psychiatry. New York: Norton.
Wiggins, J. S., Trapnell, P., & Philips, N. (1988). Psychometric and geometric characteristics of the Revised Interpersonal Adjective Scales (IAS-R). Multivariate Behavrioral Research, 23, 517-530.

I am using TRUE (http://www.salleurl.edu/tsenyal/true/features.html) and SAM (Self-Assessment Manikin) interface includes a scale for dominance, along with valence and activation. The scale allows you to rate dominance from 'controlled' to 'in control' on a scale from 1 to 9.

References

Planet, S., Iriondo, I., Martínez, E., & Montero, J. A. (2008). TRUE: an online testing platform for multimedia evaluation. In Proceedings of the Second International Workshop on EMOTION: Corpora for Research on Emotion and Affect at the 6th Conference on Language Resources & Evaluation (LREC 2008). Marrakech, Morocco.


What are the major structures of the medial temporal lobe? Basic question here from a behavioral researcher: What are the major structures of the medial temporal lobe (MTL)? Can anyone link to a good diagram of these structures?

The MTL consists of (note that some structures overlap):

cortical areas, which can be categorized in at least three ways:

portions of two gyri

entire parahippocampal gyrus
anterior medial side of fusiform gyrus

five named cortical areas:

perirhinal cortex
parahippocampal cortex (see parahippocampal gyrus)
entorhinal cortex
presubiculum*
parasubiculum*

five Brodmann areas: 27, 28, 34, 35, 36

hippocampus
amygdala*

* indicates that not all literature includes this component in the MTL

I didn't find a diagram of only the MTL. The best diagrams I found were (not shown here because I don't own the copyright):

Figure 1
Figure 2
Figure 3

References

  Brodmann, K. (1909) Vergleichende Lokalisationslehre der Grosshirnrinde in ihren Prinzipien dargestellt auf Grund des
  Zellenbaues. Leipzig : Johann Ambrosius Barth.
  Squire, L.R., Stark, C.E.L., & Clark, R.E. (2004) The Medial Temporal Lobe. Annu. Rev. Neurosci. 27:279–306
  [pdf]


Does James Holmes diagnosis of schizotypal personality disorder indicate a predisposition for mass murder? On May 27, Dr. William Reid, a court-appointed psychiatrist who
  interviewed Holmes for a total of about 22 hours, testified that
  Holmes was mentally ill but legally sane, diagnosing him as having
  schizotypal personality disorder, which is characterized by
  constricted behavior and difficulties relating to others.

From Wikipedia

In other interviews and articles I have read, Holmes told psychiatrists that he had always had homicidal thoughts, in childhood they were to do with killing everyone via nuclear weapons, but progressed to more realistic scenarios (serial killing or gun rampage) as he got older. (This was contained in the recently unsealed psychiatric evaluation released by the court).

My question: does schizotypal personality disorder explain lifelong homicidal ideation / obsession, or predisposition to same? If not, why does James Holmes' psychiatric evaluation (both court-appointed and otherwise) fail to address the source or origin of his self-confessed homicidal tendencies (even speculatively)?

Such attempted explanation would seem to have had high intrinsic value.

So the question is

does schizotypal personality disorder explain lifelong homicidal ideation / obsession, or predisposition to same?

Schizotypal personality disorder does include paranoid ideation among its symptoms. Paranoid ideation has been linked to homicidal behavior in some studies

Patients who reported homicide attempts could be distinguished from patients with no homicidal behaviors by the presence of other aggressive behavior such as suicidal ideation and suicide attempts by themselves and their family members and by elevated current measures of interpersonal sensitivity, hostility, and paranoid ideation.

As to whether it's enough to "explain" such behavior... that's a tricky question as it depends on what you mean by "explain". If you interpret "explain" as "makes it more likely", a psychiatrists would say yes. If you interpret "explain" as "excuses in the eyes of the law", a jurist would say no.
According to Wikipedia (which does not cite any ref for this)

Most courts accept a major mental illness such as psychosis but will not accept the diagnosis of a personality disorder for the purposes of an insanity defense

Note however that the distinction between personality disorders and the rest (formerly axis I) has been abolished in DSM 5. So this is an area of fairly recent changes in psychiatric thinking. I don't know how courts will react (or maybe some have done so already) in reaction to this change in the DSM. N.B. you'll probably want to read https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3811091/ for more on the criminal law and personality disorders; it's written in 2013 (so after the adoption of DSM-5), but doesn't mention any cases where the new categorizatoin has influenced criminal-law decisions. I guess it was still too early for that. See also http://jaapl.org/content/42/2/141.long which is more focused on the DSM-5 change. From the latter is worth quoting:

The DSM-5 contains an expanded Cautionary Statement of explicit relevance to forensic psychiatry. It states in part that, “In most situations, the clinical diagnosis of a DSM-5 mental disorder … does not imply that an individual meets legal criteria for the presence of a mental disorder or a specified legal standard… .” It goes on to state that, “a diagnosis does not carry any necessary implications regarding the … individual's degree of control over behaviors that may be associated with the disorder” (Ref. 3, p 25).

So again a psychiatrist's view and a the law's view are different. Note than in mostly non-US (but still English-law-based) jurisdictions, there's a notion of diminished responsibility, often applied in cases of mental illness contributing to a crime. The US law use of this notion of diminished responsibility appears very limited; it seems to be used mostly in California (but not in Colorado where Holmes was tried.)
And since we're talking serial killers with psychotic tendencies it's probably worth recalling the case of Breivik and Norwegian law. It's hard to summarize that case here since it's an entire saga with front-page disagreements on the diagnosis etc., as well as peculiarities of the Norwegian law with respect to mental illness definitions. But in the case of Breivik, just like in that of Holmes, there was no agreement among psychiatrist what his diagnosis should be. In Breivik's case the court ultimately accepted the personality disorder diagnosis rather than an axis I diagnosis proposed by some psychiatrists. In the case of Holmes the alternative diagnosis was schizoaffective disorder, offered by another court-appointed psychiatrist. Given the difference in law between Colorado and Norway, it's less relevant what Holmes' actual diagnosis was; in Norway a psychotic disorder automatically qualified as incompetence to stand trial, but not in Colorado, where the M'Naghten test (telling right from wrong) applies.
And coming back to the meaning of "explain", the latter psychiatrist who examined Holmes said:

Metzner, who diagnosed Holmes with schizoaffective disorder, said he did not think Holmes went on his rampage to get notoriety or because of his longstanding hatred of mankind, which he described in a spiral notebook. Instead, Metzner said, Holmes' actions were "directly related" to delusions that killing people would increase his self-worth.
"I can come up with no other explanation for what he did," Metzner said.
Holmes knew what he was doing was illegal and that others would think it was wrong, Metzner reiterated in response to questions from District Attorney George Brauchler. The prosecutor brought up Holmes' statement that he did not want to date someone because he did not want anyone to be featured in news coverage as the girlfriend of a mass killer.

And paralleling the Berivik case, the judge didn't dig this

[Judge] Samour ordered a second evaluation after he found Metzner’s report was “incomplete and inadequate.”

And regarding some of the subsequent questions

Is it likely that such ideation could be kept secret for one's whole life?

Schizotypal personality disorder also has among symptoms a "reduced capacity for close relationships" usually manifested as "lack of close friends". So that makes it more likely such individuals will not have many people they could talk to about their weird ideas, so they may not get noticed until it's too late.
From the unsealed notes of Dr. Fenton and Ms. Roath

Holmes had been referred to Dr Fenton by University of Colorado social worker Margaret Roath in March 2012, who noted it was “hard to interview him as he would just start and take a long time to answer”.
“When I asked him about other symptoms, he said he did not want to say as I would have to report him. He says he wants to kill other people, but no one in particular and has never done anything to harm others,” Roath noted.
A note of Obsessive-Compulsive Disorder was accompanied by the description that “(Holmes) has problems concentrating, eats OK, does not have crying spells and does not have thoughts of suicide.”
In an email to Dr Fenton to see him “soon if possible”, Ms Roath described Holmes was the “most anxious guy I have seen”.
“Most concerning is that he has thoughts of killing others people, though I do not think he is dangerous,” she said, adding Dr Fenton would see him as it “might be best to keep him in the system”. [...]
In her notes, Dr Fenton expressed concern over Holmes’s homicidal thoughts but his lack of a willingness to address specifics with her. He told her if she revealed more details she would “lock him up.”
Those in charge of his courses has told her of his “extremely awkward” social interactions and “odd comments”, but “neither had heard of him making threatening remarks”, she noted in a June client summary.
A background check had revealed no weapons permits, she said.
“At this point. James is … intermittently functioning at a psychotic level,” Dr Fenton wrote.
But she concluded he “does not currently meet criteria for a mental health hold”.
“He is not gravely disabled and has no evidence of suicidal ideation. Longstanding homicidal ideation but denies any specific targets and there is no current evidence he is angry at the grad school (or anyone else).”
She noted that while Holmes had made hostile remarks to her and another psychiatrist, he had not made threats.

Captioned: "Psychiatric notes released to public. This one, a mental status exam, by Dr Fenton"

So your (2nd) question becomes mostly hypothetical in view of this. Also, whatever obscure statement he may have made to a friend about "floodgates" pale in comparison to the more direct statements made to mental health professionals before the murders, although had a professional heard those, they might have seen it as a sign he was going to act. We can only speculate at this point what some professional might have done corroborating all the evidence.
As an aside, Fenton was sued in 2013 by some victims' relatives. Fenton did warn someone on the campus police:

The documents show Fenton went to University of Colorado police officer Lynn Whitten and informed her that Holmes confessed homicidal thoughts to her and that he was a danger to the public, "per her requirement," the documents say. Whitten responded "by deactivating Holmes' key-card access to secure areas of University of Colorado medical campus buildings," the Denver Post writes. Fenton also told Whitten that Holmes had "stopped seeing her and had begun threatening her via text message," the documents state.

There's a bit more of the campus-level story:

Holmes started seeing Fenton in 2012 to help with his social anxiety. He soon confided that he was having thoughts about killing people.
His last visit was June 11, 2012. By then he had already amassed an arsenal of weapons and body armor and was meticulously planning his attack on a packed showing of a new Batman movie. But all Holmes told Fenton and another psychiatrist, Robert Feinstein, was that he had failed a key exam and was dropping out of the neuroscience program.
Holmes "left in a huff," Fenton told Whitten, whom she called the same day. She was concerned because Homes had told her "I want to kill as many people as possible," and she wondered if he was nearing a psychotic break, according to the documents.
Though he had "constant homicidal thoughts," Fenton told Whitten, he had never revealed specific targets or plans. But Whitten wrote in her notes that "Holmes indicated to Fenton that he liked thinking about it."
Fenton was alarmed enough to violate Holmes' health privacy rights and call his mother, Arlene. But Fenton did not tell Arlene Holmes about her son's homicidal obsession, instead mentioning that he'd dropped out of school.
The documents show that Fenton found Holmes' mother's reaction reassuring.
She left a voicemail for Whitten: "It's pretty good news on our guy James. It sounds like he's always been like this. I've talked to his mom, she and the dad are kind of putting some quiet support in place. They've got my number in case they need anything."
She concluded: "So, anyway, I think we've got everything in place for now, so if something else comes up I'll let you know."
Arlene Holmes testified during the trial that Fenton didn't return her calls seeking more information. Fenton chose not to detain Holmes because she felt he was "on the borderline" and didn't think it would help, she told Whitten, according to the documents provided by the university.
About the same time, Fenton called University of Colorado professor Sukumar Vijayaraghavan, head of the neuroscience program, about Holmes, according to documents provided by prosecutors.
"James had told her (Fenton) he did not think he would make a mark on the world with science so he could blow up people and become famous," Vijayaraghavan told Aurora police after the shooting. Vijayaraghavan said he then called Whitten, who told him "action would be taken immediately." She said she had suspended his student ID and "police are aware of the situation and are keeping an eye on the whole thing."
After the shooting, Whitten told Aurora police she "discussed Holmes" with her sergeant and checked with others on the status of his withdrawal from the university.
[...]
The university said in a statement that its faculty and staff acted responsibly. Campus police officer Lynn Whitten, who was not named in the lawsuit, has since retired. Her attorney, Tom Rice, said she did all that she could with the limited information she had, none of which gave her reason to believe Holmes was an imminent danger.

From this one can guess that the civl lawsuit against Fenton didn't get far because:

Under Colorado law, mental health professionals cannot be held liable in civil suits for failing to predict a patient’s violent actions unless it involves a “serious threat of imminent physical violence against a specific person or persons.”

And I was right on the money, the lawsuit against Fenton was dismissed in 2016.


Body Language: Why do we act differently around someone we're attracted to? Many professionals have said that when you're attracted to someone, you tend to fidget, run your hands through your hair, sit with your legs facing them, and that our faces light up around them, which are all actions that happen involuntarily. Why does this happen?

Generally speaking, romantic love can be considered an emotional process. From an embodied perspective, emotions are to a large extent interactions with sensorimotor processes (connected to the body). http://www.iep.utm.edu/emotion/ provides a good overview of the various emotional theories, of which the feedback theories are my favorite. The feedback theories essentially state that body states cause valenced (positive or negative) feelings in a bottom-up manner, and that cognitions (higher-order thought on a 'symbolic' level, such as appreciating someone's qualities) cause embodied reactions in a top-down manner (these are the quirky love-induced reactions you speak of). This goes on in a feedback loop. In this process, neurotransmitter systems are highly important. One of the most popular theorists out there in this area is neuroscientist Antonio Damasio - his somatic marker hypothesis is a really interesting theory: http://www.iee.unibe.ch/unibe/philnat/biology/zoologie/content/e7493/e7854/e8920/e8926/DamasioPhilTransRSocB96.pdf. (He applies it to decision making in the end, but the basic principles are all there) If you're interested, you could also read his book "The Feeling of What Happens".

I would say that these quirky little habits we have when we are nervous around someone we care about in that special way are mostly unintended side effects of a significant release of neurotransmitters (like dopamine, serotonin, etc.). These neurotransmitter systems are connected to several brain areas, but especially also to our action systems, causing us to fidget, smile, shiver, or otherwise display exceptional behavior. Of course, some of these behaviors are socially adaptive - smiling is useful to communicate that you appreciate the other person, for instance, whereas fidgeting is probably not socially useful. The reason there is such a strong release of these is that romantic attraction is a mixture of a emotions/desires which are very important to reproduction. For a light (not too academic) read about the biological basis of love, I recommend http://www.amazon.de/Why-We-Love-Chemistry-Romantic/dp/0805077960. For a condensed version in a TED talk, see http://www.ted.com/talks/helen_fisher_studies_the_brain_in_love.


What makes people easily subscribe to pseudoscientific theories? There are many theories/disciplines that have been categorized as pseudoscience in the scientific community.
The list includes many things that are regularly even quoted in media like graphology, astrology, psychoanalysis, personality types, etc.
Questions:

What attracts people to such theories? Do any cognitive biases make people believe them easily? Which part of pseudosciences acts as a stimulus that triggers this cognitive bias?

If there's a cognitive bias behind people believing in pseudoscience, knowing that a majority of the population does that – is there any term for such a phenomenon in social psychology?

A majority of the population believes in some kind of pseudoscience. Does this signify an evolutionary aspect of our minds – that people are still evolving into better species that might one day believe in proper science? Pseudoscience seems to be older than science; correct me if I am wrong here.

There are two great TED talks that together help shed some light on your question:

David Deutsch (2005) "A new way to explain explanation", and
Richard Dawkins (2009) "Why the universe seems so strange"

At a fundamental level, science is about explanation (and sometimes using that explanation to make predictions). Thus, to most people, science is useless unless they understand the story it tells. The problem with modern science is that to have a good grasp of its explanatory power, you need a lot of (often difficult) background. As you gain this background, you develop what Feynman would call the most fundamental skill in science: always questioning, being able to say "I don't know", and to hold contrasting ideas together. If you don't invest in acquiring this background, most of science seems like witchcraft passed down by ivory-tower academics in funny gowns and hats.

What pseudoscience (or even cargo-cult science) provide is explanations that require less background, purport to be more certain, have something for everyone (Forer effect), and reassure you that "there is an answer". If you look at much of pseudoscience (or ancient myths) more closely, you will notice that they tend to personify their subject matter much more than science (my favorite example is the homunculus fallacy). They use this personification to provide agency, intent, and meaning to their explanations.

The great advantage of these human stories is that our minds are optimized for them. If you subscribe to Dunbar's Social Brain Hypothesis, then one of the main things evolution produced is a mind built to understand social structure, and other people. When an agent does not adhere to its role and violates our theory-of-mind and behaves erratically, without discernible intent and meaning, this is dangerous to us and our society; it causes us great discomfort. When you hijack the social mind to try to explain further and further afield parts of nature, you try to build the same sort of characters.

When you have to say "I don't know" or "I don't understand" this character, it creates discomfort. Pseudoscience thrives on this by giving an arbitrary, simple, shallow and easy to change explanation. Since most lay-people never pursue this explanation far enough to notice its contradictions, and since it shapes their observations (in the Popper-sense and through confirmation bias) they never get a strong enough cognitive-dissonance to overcome to positive feeling of having an understandable 'explanation'.

Unfortunately, all I can do in this answer is provide a intuitively appealing, intent and agency based explanation. Reread my answer and make note of unnecessary personifications I made -- just like much of pseudoscience, science is a story and there is the biggest rub.


What is a principle that describes competitive advantage in this case I gave up long ago on formulating what seems like a new concept as I came to peace with the fact that billions of people alive and dead means there's very little room for new concepts. (just an anecdote, not the focus of my question)

So I want to know what theory or concept describes the idea in which constantly comparing two things (or more?) in a "yin and yang" like opposition would associate rivalry between the two things even if non existed before the intentional creation of this comparison.

This idea came to me through observation of how politics and media works, whether scientifically intended or just mere learned through experience, in instigating seemingly unrelated concepts in a comparison situation, and enforcing that comparison on the masses to create such rivalry between the two concepts; then have the ability to influence external factors to skew the mass opinion one way or the other. It works because they're using it then with the oldest trick in the books: divide and conquer. So they get those two things, put them in such a rivalry comparison where if one existed the other can not exist at the same time, creating division and "teams" of sort, then appealing to each team in some way or the other to win its loyalty.

So the question is:

What theory or concept describes the creation of rivalry between two ideas to instigate division?

One idea I had was really just describing it as "competition". But this doesn't work; In competition, there's variable degrees of existence of each competing idea. However in the case of my question, where one idea exists in some context, the other idea can't.

"Binary Opposition"

Systems are "binary" when they are composed of only two parts.  It's easy to imagine things "in opposition," like the Boston Red Sox and the New York Yankees, or the World War II alliances known as the "Axis Powers" and "the Allies."  For an opposition to be truly "binary," however, the opposing classes of thing/idea must be mutually exclusive.  That is, membership in one class must make impossible membership in the other. source

My observation is that this is being politicized and used in conjunction with other techniques to exert control. So they're creating "Binary Oppositions".


Can brain hemisphere activity/ dominance be inferred from the test subject's drawings? I'm aware that all tasks that a person undertakes involve both halves of the brain. At the same time, there are studies of people who have communication between brain halves severed or suppressed and they produce dramatically different drawings of the same object with different hands.

This makes me ask - is there some sort of a (non-FMRI) test that involves drawing or other activity and can:

Determine if one half of the brain is dominant at the given moment
Determine if communication between brain halves is fluctuating over multiple days
Determine if one half of the brain does not consistently function at the same level of activity?

I'm aware of this Ted talk: My stroke of insight, in which a neuroscientist describes the experience of having a stroke affect one half of her brain, dramatically altering her perception and ability to process real world information. For example she describes being unable to recognize digits in a phone number and "hunting" for the right digit by tracing its shape on the phone.

The images below were made using 100% input from one brain half and 0% from the other. I'm interested if different levels of activity in brain halves, like 100%/50% or 100%/80% or 60%/70% would also create noticeable differences in style.

You say you are "aware that all tasks that a person undertakes involve both halves of the brain". Then, On what kind of patients would this hypothetical test be suitable as healthy people use both hemisphere and split brain use just one hemisphere depending on the drawing hand ?

If you refer to healthy patients I don't think such a test is possible.
For the moment left-brain/right-brain dominance is usually considered as a neuromyth.For example:
- this blog article http://www.psychologytoday.com/blog/brain-myths/201206/why-the-left-brain-right-brain-myth-will-probably-never-die
- or this paper http://www.nature.com/nrn/journal/v7/n5/full/nrn1907.html .

Maybe some tests (drawing or whatever) would correlate a bit with partial and short term hemispheric activation with desirable inter-individual differences. But aiming for a test bringing more than that is in my humble opinion vain hopes, as hemispheric dominance on healthy subjects has weak (or no) scientific ground.


Can hocd change sexual orientation? Can sexual orientation change due to hocd (Homosexual OCD). And if it can change, is it possible to reverse the change and bring the person back to his/her original orientation.
[Change from heterosexual to homosexual]

First of all, it is important to note that the current version (5th Edition) of the DSM — Diagnostic and Statistical Manual of Mental Disorders, published by the American Psychological Association (APA, 2013) — does not recognise homosexual obsessive-compulsive disorder (HOCD) as a mental health condition (Smith, 2021).

Homosexual obsessive-compulsive disorder (HOCD) is a type of sexual orientation-obsessive-compulsive disorder (SO-OCD). A person with SO-OCD may have fears and anxieties relating to their sexual orientation.
[...]
A person with HOCD may have anxiety about experiencing same-sex attraction, even if they do not experience this.
Because HOCD is a type of SO-OCD, some people may use the term to refer to situations wherein people who are not heterosexual experience fears about their sexual orientation.

Reading this article will explain in more detail what HOCD is reportedly all about.
Can sexual orientation change due to HOCD?
The overarching point to put across regarding any sexual orientation is that nothing and nobody can make you homosexual, bisexual or heterosexual. There have been groups of therapists who tout that they can convert homosexuals into heterosexuals through conversion therapy, but:

conversion therapy in relation to gender identity and sexual orientation (including asexuality) is unethical, potentially harmful and is not supported by evidence (BACP, 2017).

For research on this, among many others there is:

Drescher, J., Schwartz, A., Casoy, F., McIntosh, C. A., Hurley, B., Ashley, K., ... & Tompkins, D. A. (2016). The growing regulation of conversion therapy. Journal of Medical Regulation, 102(2), 7-12. https://doi.org/10.30770/2572-1852-102.2.7

Assessments of the peer-reviewed literature from multiple professional organizations, including the American Psychiatric Association, the American Psychological Association, and the American Academy of Child and Adolescent Psychiatrists, have found no evidence that conversion therapy treatments result in changes in sexual orientation.

Haldeman, D. C. (1994). The practice and ethics of sexual orientation conversion therapy. Journal of Consulting and Clinical Psychology, 62(2), 221–227. https://doi.org/10.1037/0022-006X.62.2.221

The literature in psychotherapeutic and religious conversion therapies is reviewed, showing no evidence indicating that such treatments are effective in their intended purpose

Adelson, S. L., & of Child, T. A. A. (2012). Practice parameter on gay, lesbian, or bisexual sexual orientation, gender nonconformity, and gender discordance in children and adolescents. Journal of the American academy of child & adolescent psychiatry, 51(9), 957-974. https://doi.org/10.1016/j.jaac.2012.07.004

Principle 6
Clinicians should be aware that there is no evidence that sexual orientation can be altered through therapy, and that attempts to do so may be harmful.

This led to the Coalition Against Conversion Therapy (CACT), a coalition of leading psychological, psychotherapeutic, and counselling organisations committed to ending conversion therapy, who prepared a Memorandum of Understanding (MoU) on Conversion Therapy in the UK (UKCP, 2017), and signed by many UK professional governing bodies, including (see the corresponding links) the National Counselling Society (NCS), British Association for Counselling and Psychotherapy (BACP), National Health Service (NHS), The British Psychological Society (BPS), and the Royal College of General Practitioners (RCGP).
References
APA. (2013). Diagnostic and statistical manual of mental disorders (DSM-5®). American Psychiatric Pub. https://www.psychiatry.org/psychiatrists/practice/dsm
BACP. (2017). Memorandum of understanding on conversion therapy in the UK https://www.bacp.co.uk/events-and-resources/ethics-and-standards/mou/
Smith, A. (2021). What is homosexual obsessive-compulsive disorder (HOCD)? Medical News Today https://www.medicalnewstoday.com/articles/hocd
UKCP (2017) Conversion Therapy https://www.psychotherapy.org.uk/policy-and-research/public-policy/conversion-therapy/


Can two neurons in the brain be connected more than once? Can two given neurons in the human brain can be directly connected more than once, either mutually or in the same or direction? Also, can the same neuron have transitive connections to itself (in order to amplify itself for example)?

The commenter below alerted me to the existence of autapses, which apparently are chemical synapses between a neuron and itself. So those clearly exist. At the same time, it does seem that there is a mechanism that would suppress self-synapses: a protein called Dscam that acts during neuronal development. Dscam is a membrane protein that can form a high number of isoforms through alternative splicing and thereby provides an identity to the developing neuron to prevent forming connections to itself.

I suspect that what is more common is for a neuron to be connected to itself indirectly. That is, neuron 1 stimulates neuron 2, which stimulates neuron 3, which stimulates neuron 1.

EDIT: Just heard about this article, which shows that two neurons can be connected via two different synapses!


Does research support the notion of mimicry building trust? Mimicry is the behaviour in which one person subconsciously imitates the gesture, speech pattern, or attitude of another person.

Some people believe that mimicry has strong social effects. For example, according to NLP, mimicry can be used strategically to build rapport (here, the technique is called "mirroring").

Has there been any scientific research on the effects of mirroring?
If so, does research support the notion that mirroring builds trust?

A good primer on the psychological effects of mimicry is the review by Chartrand and Lakin (2013), who define mimicry as "the automatic imitation of gestures, postures, mannerisms, and other motor movements" (also see this earlier question).

They cite several findings suggesting that mimicry indeed contributes to positive relationships between people. For example, people being mimicked become more prosocial to the mimicker, as expressed in increased liking, empathy, helping behavior, and felt closeness. Chartrand and Lakin describe mimicry as a kind of "social glue" bringing people together.

More specifically with regard to your question, several studies are in line with the idea that mimicry increases trust.

For example, as per Chartrand and Lakin (2013):

  Van Swol (2003) had a confederate, while trying to change the participant’s opinion on a topic, imitate his or her behaviors (or
  not). Later, participants reported that they perceived the mimicking confederate as more knowledgeable and persuasive, even though
  they did not ultimately change their opinion on the topics. In a twist on this, Bailenson & Yee (2005) found that participants liked a computer avatar that mimicked their head movements more than one that didn’t, and
  were more persuaded by its arguments.

They also cite studies that measured trust specifically:

  Trusting behaviors tend to increase after a person has been mimicked. For example, mimicked participants seem more willing than those who were not mimicked to divulge personal information to strangers, even when that
  information could be embarrassing (Gueguen et al. 2012). According to Maddux et al. (2008), mimicry also smoothes the progress of negotiations. They instructed negotiators to either mimic or not mimic partners’ behavior and later assessed mimicry’s impact on negotiation outcomes. Mimickers experienced higher individual and dyadic gains and were more willing to come to an agreement with others regarding a difficult decision, and the
  relationship was mediated by interpersonal trust (see also Swaab et al. 2011)

Does mimicry always work?

NLP holds that Mirroring is a powerful technique. Note, however, that the cited findings only document modest mean differences, showing that mimicry can have an effect. Nevertheless, the size and importance of this effect may still be questioned.

Furthermore, under some circumstances mimicry may not work or even backfire.

Lakin and Chartrand (2013):

  It turns out that one does need to mimic the “right” people to enjoy the positive consequences of mimicry. Recent research has found that mimicking may backfire (in terms of public opinion about one’s social competence) if
  someone mimics an unfriendly person. After watching someone mimicking unfriendly behaviors, people thought the mimicker was less socially competent than someone who mimicked a friendly partner or someone who mimicked no one (Kavanagh et al. 2011).

In addition mimicry may work less well if people mimic outgroup members, if one has to mimic nonaffiliative expressions (e.g., anger), or when people have a proself mindset or have high levels of social anxiety (Chartrand & Lakin, 2013).

Finally, in some situations, complementary (doing the opposite) rather than imitative behavior may increase liking. For example, Tiedens and Fragale (2003) asked confederates to mimic or complement bodily postures of dominance or submission (using an expanded or constricted posture). Participants whose behavior was complemented (the confederate showed a submissive posture when the participant was behaving in a dominant way, or vice versa) liked the confederate more. Thus, in power or status relationships mimicry may have different effects.

References

Chartrand, T. L., & Lakin, J. L. (2013). The antecedents and consequences of human behavioral mimicry. Annual Review of Psychology, 64, 285–308. doi:10.1146/annurev-psych-113011-143754


Can speech dysarthria occur in schizophrenia without other neurological or medication-induced disruptions? As I understand it, acquired dysarthria of speech is caused due to problems with motor neurons or other neurological, cerebral and peripheral, conditions in the CNS affecting those. And schizophrenia is primarily a problem in mesolimbic and mesocortical dopaminergic pathways, amongst possibly other problems. Can a purely schizophrenic or psychiatric condition without neurological diagnoses cause dysarthria as a symptom by itself? Or is acquired dysarthria always a sign of a comorbid neurological diagnosis?

There's one somewhat obscure paper by Varambally et al. (2012) that (apparently) says that dysarthria can be a part of the "Neurological Soft Signs" (NSS) of schizophrenia itself. They examined "32 never-treated patients with schizophrenia" vs healthy controls and found that

  A stepwise multiple discriminant analysis identified two ICARS sub-scores to be significant (Kinetic sub-score and Dysarthria sub-score), which accounted for 78% classification.

The broader topic of NSS in schizophrenia (either in patients or even in their relatives) has received a fair bit of attention, but the above is the only paper that mentioned dysarthria in this context. One potential problem that I see is that there isn't a commonly agreed way to measure NSS. One meta-analysis found that three studies used NES, two used SNE, and two the Rossi scale. I looked at these scales briefly and they don't seem to address dysarthria; it's possible that I've missed something and they call it something else...

The question is a bit vague (and given its age and one-time involvement of the asker it seems unlikely it will see clarification). The title seem to ask if medication can also cause dysarthria. Apparently, yes, there is one study by Caroff et al. (2011) which does mention it as an extreme form of (antipshyctohic) drug-induced dystonia:

  Dystonia is an acute, alarming involuntary movement disorder that can be painful and distressing, and erodes patient trust and compliance. It is characterized by briefly sustained or intermittent spasms or contractions of antagonistic muscle groups resulting in twisting and repetitive movements or postures. Drug-induced dystonia can affect any muscle group, but most commonly involves the head, neck, jaw, eyes and mouth resulting in spasmodic torticollis, retro- or anterocollis, trismus and dental trauma, forced jaw-opening or dislocation, grimacing, blepharospasm, tongue biting, protrusion or twisting, and distortion of the lips. It is not action or sensory stimulus dependent. More subtle signs, including muscle cramps or tightness of the jaw and tongue with difficulty speaking or chewing, may precede dystonia or occur alone. At the other extreme, dystonia may present as an oculogyric crisis or with other forced eye movements, or with dysarthria, dysphagia and potentially lethal respiratory stridor if pharyngeal or laryngeal musculature is affected. Less frequently observed, dystonia may affect axial, truncal or limb movements occasionally leading to camptocormia, pleurothotonus (Pisa syndrome) or opisthotonus.

The same paper mentions that dysarthria may also occur in the more dangerous neuroleptic malignant syndrome, in which the more classic symptoms of hyperthermia and generalized rigidity also occur (and can be used for differential diagnosis.)

There's one other paper by Mathews et al. (2005) about antipsychotic-induced movement disorders that I've looked at, but it doesn't mention dysarthria. From this I guess that it's a rather rare occurrence as a side-effect of antipsychotic medication. I didn't find anything more detailed about prevalence etc.


Do we pick partner most similar to opposite-sex parent? Do we pick partner most similar to opposite-sex parent? Do men pick life partner who is similar to their mother? Does it apply to women too? By similar, I mean mostly character/mental features. I dont consider appearance, but It would be interesting to know if that matters.

If yes, is it possible that man (for example) would look for/pick a partner who has character opposite to his mother? What could be scientific reason for that?

Good question. Here is what I found.

People may be attracted to the physical features that our opposite sex parent posses {1,2} However, the jury is out as to whether people are more likely to be attracted to people who share the mental traits of parents {3,4}. As an example of this {3} write

  "Much of the current research on parental identification and mate
  selection is contradictory and inconclusive. The studies that are
  available suggest a similarity between partner choice and parental
  similarity, although the results for similarity between partner choice
  and parent vary by gender. Various theories suggest that individuals
  choose mates based on some type of similarity with their partners.
  Such similarities include values, religion, physical attractiveness,
  or expressiveness (Bailey et al., 1994; Boyden, Carroll, & Maier,
  1984; Howard et al., 1987; Murstein, 1976). Parental identification
  research also is inconclusive, with some studies finding same-sex
  parent identification and others finding opposite-sex parent or both
  parent identification (Geher, 2000; von der Lippe, 1965)"

I am happy to go into more detail about any of this, if you want me to.

References:

{1} Little, A., et al. (2003). "Investigating an imprinting-like phenomenon in humans: partners and opposite-sex parents have similar hair and eye colour." Evolution and Human Behavior 24(1): 43-51.

{2} Perrett, D. I., et al. (2002). "Facial attractiveness judgements reflect learning of parental age characteristics." Proceedings of the Royal Society B: Biological Sciences 269(1494): 873-880.

{3}van Eeden-Moorefield, B. and E. W. Lindsey (2005). "Intergenerational Effects of Parental Personality and Relationship Traits on Mate Choice Among Gay Male and Lesbian Offspring." Journal of Homosexuality 49(1): 123-143.

{4} Strokoff, Johanna, "Parental influence on romantic attraction with simulated online dating profiles." (2015). Electronic Theses and Dissertations. Paper 2232.
Retrieved from


Facet versus scale prediction of Big 5 personality NEO facets and scales: The NEO model of personality has 5 scales (i.e., extraversion, neuroticism, agreeableness, openness, and conscientiousness). For each scale there are 6 facets (e.g., neuroticism has anxiety, hostility, depression, self-consciousness, impulsiveness, and vulnerability to stress). See here for a list of the 30 facets and how they relate to the 5 scales.

Incremental prediction: I am interested in the degree to which the 30 facets predict important real-world outcomes over and above the big 5 scales. Examples of important outcomes might include financial success, life satisfaction, health outcomes, longevity, job performance, career success, marital satisfaction, criminality, and so on. While each of these outcomes would be interesting in itself, I'm particularly interested in any general claims that can be put forward regarding the incremental predictive validity that is obtained from using facets rather than scales.

Statistical baseline: I take a few points as self-evident. There is a difference between in sample prediction and true population prediction. The true population regression equation can not be worse for the facets than the scales. The facet level prediction could mirror the scale prediction merely through an appropriate set of regression coefficients (i.e., some form where facets are in some sense equal within a scale, adding up to the scale effect).

I also take it as self-evident that the population prediction would be at least a little bit better with facets. It seems implausible that the pattern of regression coefficients required to replicate the scale prediction would necessarily be exactly match the best population prediction model. However, there is still the question of what the size of the increase is, and how big the increase in prediction is relative to the prediction achieved by the scales.

Methodological challenges: There are also several issues around estimating the size of the incremental prediction of facets relative to scales. Adding an additional predictor increases sample variance explained even when the predictor has know incremental prediction in the population. Thus, procedures that compare sample r-squared of scales versus facets prediction models would be biased. Models that use a data driven variable selection procedure like step-wise regression to select an optimal subset of predictors would also be biased. The size of this bias would be greatest in smaller samples.

Thus, I'm particularly interested in studies that have accounted for these methodological challenges. For example, a good study might have (a) a large sample of 1000+ participants in order to generate robust results, and (b) a statistically valid procedure for estimating population r-squared for facet and scale predictor models (one possibility would be to estimate the model in half the sample and evaluate in the other half, although many other cross-validation procedures are possible).

Thus, my questions:

What is the incremental prediction of the 30 facets over and above the big 5 scales on important psychological outcomes?
In particular, how and to what extent have studies dealt with the methodological issues related to performing this comparison?
In totality, is the incremental prediction at the facet level sufficient to justify the added complexity to thinking and theorising?

Several studies have been conducted comparing facets versus factor prediction (e.g., Paunonen and Ashton, 2001; Mershon and Gorsuch, 1988; Ashton et al, 1995; Dudley et al, 2006; Ekehammar & Akrami, 2007).

Many of these studies have found substantial incremental prediction of facets over factors. However, there are several potential methodical issues that may potentially arise: (a) overcoming biased estimates of R-square particularly when comparing analyses with facets versus factors where more predictors increases the bias; (b) overcoming issues of multiple comparisons when there are many facets that can be compared to factors; (c) some studies only have small sample sizes.

By statistical definition, the population r-square for a factor model is less than or equal to the population r-square for a facet model where factors are defined as a linear function of the facets. Nonetheless, I have not yet read any systematic studies that have provided an unbiased estimate of population r-square in factors versus facets. Having read all the above articles, my hypothesis would be that I would expect an increase in r-square of around 5 to 20 percent, but that's just a rough sense.

References

Ashton, M. C., Jackson, D. N., Paunonen, S. V., Helmes, E., & Rothstein, M. G. (1995). The criterion validity of broad factor scales versus specific facet scales. Journal of Research in Personality, 29(4), 432-442.
Dudley, N. M., Orvis, K. A., Lebiecki, J. E., & Cortina, J. M. (2006). A meta-analytic investigation of conscientiousness in the prediction of job performance: examining the intercorrelations and the incremental validity of narrow traits. Journal of Applied Psychology, 91(1), 40.
Ekehammar, B., & Akrami, N. (2007). Personality and prejudice: From Big Five personality factors to facets. Journal of Personality, 75(5), 899-926.
Mershon, B., & Gorsuch, R. L. (1988). Number of factors in the personality sphere: Does increase in factors increase predictability of real-life criteria?. Journal of Personality and Social Psychology, 55(4), 675.
Paunonen, S. V., & Ashton, M. C. (2001). Big Five factors and facets and the prediction of behavior. Journal of personality and social psychology, 81(3), 524-539.PDF


Unable to run AxoGraph v1.7.6 on macOS 10.15 Catalina After a recent MacOS update, I am no longer able to run the (latest) AxoGraph software for electrophysiology data analysis on my computer, as I get the following error message:

"AxoGraph.app" needs to be updated.

The developer of this app needs to update it to work
with this version of macOS. Contact the developer for
more information.

Screenshot:

I understand that this is because AxoGraph is a 32-bit application, which is not supported by macOS Catalina. I have already contacted the support of the application for advice. In the meantime, is there any good solution besides switching to a different software?

Response from AxoGraph Support

I received an answer from John of AxoGraph suggesting to follow the steps outlined in this tutorial to set up a virtual machine (VM) on my computer with an earlier version of macOS using the Parallels software ($79.99/year).

He also discouraged using VirtualBox, the free VM manager, as "there's more work involved, and it’s not so smoothly integrated with Catalina." In his reply, John also promised "to finish the new completely re-written 64-bit version of AxoGraph," which "is not far from completion," first releasing a new data-acquisition-only version, subsequently followed by an update with data analysis features. It sounded like all of this would take at least several months, though.

My Solution

After some digging, setting up a virtual machine (VM) with an earlier version of macOS indeed did seem to be the best option for me at this point. What I was after, however, was a free solution - and eventually, I managed to get a Mojave VM to work on my Catalina using VirtualBox. Getting through the whole process was a patchwork of several different sources (mostly following this tutorial and its comments), so I decided to re-write the detailed steps I took below (some steps may be adjustable but I used these specific settings with success):

1. Download macOS Mojave Installer:

Go to this link: https://support.apple.com/en-us/HT210190
Click on Get macOS Mojave in step 4, and open in App Store.
Click on GET - that will open the updater, which will download the installer (if you already have Catalina installed, the "update" will stall after the download automatically)
Find it in your Applications folder as Install macOS Mojave.app

2. Create an ISO installation media using Terminal:

Create a temporary disk image from the install file & make a bootable installer using Terminal:

hdiutil create -o /tmp/Mojave.cdr -size 7000m -layout SPUD -fs HFS+J

Attach that file, with Terminal command:

hdiutil attach /tmp/Mojave.cdr.dmg -noverify -mountpoint /Volumes/install_build

Build it, with command:

sudo /Applications/Install\ macOS\ Mojave.app/Contents/Resources/createinstallmedia --volume /Volumes/install_build

Move it to your mac’s Desktop:

mv /tmp/Mojave.cdr.dmg ~/Desktop/InstallSystem.dmg

Unmount the file:

hdiutil detach /Volumes/Install\ macOS\ Mojave

Convert it to ISO:

hdiutil convert ~/Desktop/InstallSystem.dmg -format UDTO -o ~/Desktop/Mojave.iso

Rename it to remove the CDR extension:

mv ~/Desktop/Mojave.iso.cdr ~/Desktop/Mojave.iso

Exit Terminal via Terminal command:

exit

3. Create a new virtual machine (VM) in VirtualBox:

Download Oracle's VM VirtualBox Manager (https://www.virtualbox.org) & install it on your Mac
Open VirtualBox
Click on New
Select Type: Mac OS X and Version: Mac OS X (64-bit)
Memory size: 8192 MB (at least 3 GB)
Hard disk: Create a virtual hard disk now
Hard disk file type: VDI
Storage on physical hard disk: Fixed size
File location and size: 32.00 GB

4. Tweak the VM before installation:

With your newly created VM selected in VirtualBox, go to Settings → Storage:

Click on Empty → Remove [square with a red cross at the bottom]
Click on Controller: SATA → Add optical drive [CD with a green plus sign] → Add → Find the .iso file you created and click Choose

Settings → Display: Video Memory - at least 128 MB
Settings → System: Processor(s) - at least 2

5. Install the macOS on your VM:

With your VM selected in VirtualBox, click Start
Wait until the Language selection appears; select your preferred language and continue
macOS Utilities: Disk Utility → Continue
Select VBOX HARDDISK Media → click on Erase in the toolbar
Name the drive as you wish and keep the default selections: Format: Mac OS Extended (Journaled) and Scheme: GUID Partition Map; click Erase
Quit Disk Utility when done
Select Install macOS, Continue, and Agree to the license
Select the hard drive you just erased and Install
MacOS starts installing; wait and be patient! (It took about half an hour for me. The VM may restart at least once in the process.)
Go through the MacOS setup (select your Country, keyboard, etc.)

It is recommended that you do not log in with your Apple ID at this time and click Set up later instead
I also did not allow Location Services, nor data collection from Apple
Once installed, you can eject the installation disc from within the VM
It also might be a good idea to go to System Preferences... → Software Update → Advanced... → uncheck Check for updates

6. Install the latest version of AxoGraph on your VM:

Open Safari within your VM
Go to https://axograph.com/download
Click on Mac OS X 10.4 and up*
Install AxoGraph

  Voilà!

  Now you can run AxoGraph, as well as other 32-bit applications, on your MacOS Catalina!

You should be able to turn off the VM from within, as you usually would shut down your Mac
It is booted again by selecting your VM in VirtualBox and clicking Start


What is the scope of the study of Neuroanatomy? I am now trying to understand the scope of the study of neuroanatomy as the discussion in meta surrounding the question Dorsum sellae, tuberculum sellae and sella turcica which of the 3 is referred to by the adjective sellar? has raised the question on whether the Neurocranium would be studied by Neuroanatomy?
If you apply that logic, in my view 90% - 100% of human anatomy could be under the umbrella of neuroanatomy.
Dermatomes relate to the anatomy of the vertebral regions of the spine. The nerves travel throughout the body, the organs and within the skin.
In my view, neuroanatomy covers the structure and organization of the nervous system which in turn involves the brain, spinal cord and related neural networks throughout the body.
Am I wrong and the whole body (or close to it) is under the umbrella of neuroanatomy?

It is the traditional division of anatomy by systems. Neuroanatomy is simply another name for anatomy of the nervous system - both macroscopic and microscopic. As opposed to anatomy of skeleton and muscles, internal organs and topographical anatomy. And of course one remembers the division of macroscopic anatomy and microscopic (which further goes into cytology and histology). So in summary -- yes, the whole body - but just as far as the nerve cells and structures are involved. And please remember - an extremely precise definition here will defy the reason because a lot of these words and divisions are traditional - therefore to be viewed with their own history of use, which may change with time.
Source: Dorland’s Illustrated Medical Dictionary, Sobotta Atlas of Anatomy and Anatomy Textbook. It also helps if one has attended medical school.


Comparison between IO psychology, Arbeitspsychologie and Psychologie du travail et des organisations Reading the Wikipedia pages on IO Psychology, Arbeitspsychologie and Psychologie du travail et des organisations you can see many differences on the topics and authors of the fields.

At a first sight, this is strongly opinion-based, it looks like in France it is given more importance to suicides at work, while Germany studies a lot of workplace health promotion, while US is more focused on productivity. Is that correct?

What are the common and different things between theories in US, German and French, IO Psychologies?

Is there a textbook or an article that draws the comparison?

In this case, wikipedia is not such a good starting point, because at least the German and the French articles do not seem very well developed and are unlikely to be representative of the research in the respective countries. This is in part my subjective opinion, but can also be seen in their length, which is very short compared to the English article.
Nevertheless, there are differences between research traditions in these countries. A good introduction is Peter Warr's chapter “Some Historical Developments in I-O Psychology Outside USA" in Koppes (2007) which compares US and European approaches.
For example with regard to differences between research in the US and Germany, Warr observes that

In general, German psychologists have been more sympathetic to broad conceptual frameworks (...) This German preference is illustrated by the development of broad "action theories". Those (...)[view] the concept of action as integrating otherwise unrelated issues of job performance, stress, errors, skill development, and other processes.
Whereas American I-O psychology has focused more on abilities, motivation, and similar precursors, action theory examines knowledge, cognitive understanding, mental strategies, and processes of self-regulation. (...) This traditional focus on regulatory processes between an environmental input and behavior has been different in both style and content from most American theorizing. (p. 85).

References
Laura L. Koppes (Ed.). Historical Perspectives in Industrial and Organizational Psychology. Mahwah, NJ: Lawrence Erlbaum Associates, 2007.


Measurement of phase difference between two signals using cross correlation vs. fourier transform I am studying eeg signals with the aim of distinguishing between preictal and interictal epilepsy states based on the eeg signal. I have read some papers and one of the metrics used to distinguish between the states has to do with measuring the phase synchronization between eeg samples from multiple electrodes. In this regard, I thought the most straightforward way to measure phase difference between two signals would be to compute the cross correlation function, and find the time $\tau$ at which the cross correlation function reaches a maximum - call this Method 1. However, in practice what is usually done is to fourier transform the signals and measure phase difference of the complex fourier transform (and possibly average it over a frequency band of interest). Details are explained e.g., here - see the section on phase synchronization. Call this Method 2.

So my question is: what is wrong with Method 1? It seems more intuitive, direct and computationally easier to me. Could someone explain this to me?

EDIT: thinking about this even further, it seems the method employed in practice and described at http://www.scholarpedia.org/article/Measures_of_neuronal_signal_synchrony is actually Method 3 and distinct from Method 2 above. This link shows how it can be implemented in MATLAB. Consider two signals $x(t)$ and a time shifted version of it $x(t+T)$. The Fourier Transforms will be $X(\omega)$ and $X(\omega)e^{j\omega T}$ respectively. Using Method 1 one would get $T$ as measure of phase difference. Using Method 2:
$\Delta \phi$ = $\omega T$ and this averaged over $[\omega_1,\omega_2]$ will give phase difference as $T\frac{\omega_1+\omega_2}{2}$.

But what would Method 3 give? Is there a difference between phase difference and phase synchronization of two signals?

Methods 1 and 2 are matematically equivalent, but I have experienced that method 2 is computationally more efficient for high sampling rates and large ranges of delay (notice that method 2 does not require a loop).


Computational Neuroscience software What are the most common software tools you use in your day to day work in computational neuroscience?

I am referring to neuroscience tools like GENESIS and NOT to generic tools like Excel.

Here is a comprehensive list of Computational Neuroscience Software

My opinion below comes form the perspective of nonlinear dynamics (using differential equations to model ion currents in neurons).  So more the math/physics/electrical engineering approach to Computational Neuroscience (not so much the Computer Science or Psychology approach):

Personally, I don't use pre-packaged tools like NEURON or GENESIS.  I take mathematical models established in literature (i.e. The Hodgkin Huxley model) and use Matlab or Python to model them.  I essentially do what Neuron or Genesis does, but I do it my way so I can extract the information that's relevant to me.  This is how I have been trained through physics and applied mathematics departments.  To not rely on other people's implementations.

For nonlinear analysis of dynamical systems (because there's really a lot of extravagant mathematics that you don't want to just code yourself) a lot of people use XPP/AUTO, designed, in part, by Bard Ermentrout (a well-known computational neuroscientist).  This is a good way to go if you're not into writing code, but I prefer a more hackable tool.  I've been learning Matcont, a similar toolbox for Matlab but since it is made with m-files (matlab's data type) you can hack it and make it into code to integrate with your own Matlab software, avoiding the GUI clicking and dragging.


How can psychopaths with no sympathy for their victims, exploit empathy to ensnare or torture them? I understand the difference between empathy and sympathy, but not the emboldened sentence. Please expound?

Empathy vs. Sympathy | Psychology Today Canada

  Sympathy (‘fellow feeling’, ‘community of feeling’) is a feeling of care and concern for someone, often someone close, accompanied by a wish to see him better off or happier. Compared to pity, sympathy implies a greater sense of shared similarities together with a more profound personal engagement. However, sympathy, unlike empathy, does not involve a shared perspective or shared emotions, and while the facial expressions of sympathy do convey caring and concern, they do not convey shared distress. Sympathy and empathy often lead to each other, but not always. For instance, it is possible to sympathize with such things as hedgehogs and ladybirds, but not, strictly speaking, to empathize with them. Conversely, psychopaths with absolutely no sympathy for their victims can nonetheless make use of empathy to ensnare or torture them. Sympathy should also be distinguished from benevolence, which is a much more detached and impartial attitude.

The theory, apparently backed up by some experiments, is that psychopaths can make use of empathy at will, which is what allows them to employ emotional manipulation. As related in a popsci account:

For example, consider one particularly fascinating experiment by Dr. Christian Keysers, Professor of Social Neuroscience at the University of Amsterdam.
In one study, Keysers and his team analyzed the brain activity of 21 convicted violent psychopathic offenders, comparing the results with 26 men of similar age and IQ. The participants were shown movies of people hurting each other while brain activity was measured. Later, a doctoral student would slap the patients on their hands to localize brain regions connected with feeling touch and pain. The goal was to see if patients' brains activated a feeling of pain in their own brain when viewing the pain of others.
"The vicarious activation of motor, somatosensory and emotional brain regions was much lower in the patients with psychopathy than in the normal subjects," writes Keysers. "The theory seemed right: their empathy was reduced, and this could explain why they committed such terrible crimes without feeling guilt."
But one question still plagued Keysers.
How could these same individuals prove to be so charming at times?
"I remember chatting with one of the patients...a particularly severe psychopath (he had scored the full 40 points on the psychopathy checklist)," writes Keysers. "Surrounded by the guards, he seemed a most pleasant person. He was smiling, engaging, and seemed to feel exactly what we wanted from him."
So Keysers and his partner decided to let the patients watch the movies again, this time asking them to try and empathize with the victims in the movies.
"What we found was that this simple instruction sufficed to boost the empathic activation in their brain to a level that was hard to distinguish from that of the healthy controls," writes Keysers. "Suddenly, the psychopaths seemed as empathic as the next guy. Their empathy was switched on."
Keysers' conclusion:

"Psychopathic individuals do not simply lack empathy. Instead, it seems as though for most of us, empathy is the default mode. If we see a victim, we share her pain. For the psychopathic criminals of our study, empathy seemed to be a voluntary activity. If they want to, they can empathize, and that explains how they can be so charming, and maybe so manipulative. Once they have seduced you into doing what serves their purpose, the effortful empathy would probably disappear again."

I'm not sure how well accepted this is... The BBC also ran a story on this with some additional more sketpical comments

Essi Viding from University College London, who was not involved with the study, said it was an extremely interesting finding, but that it remained unclear whether the psychopathic criminals' experience of empathy felt the same as that of the controls.
"It's dangerous to look at brain activation and say that it means they're empathising. They are able to generate a typical neural response, but that doesn't mean they have the same empathetic experience," Prof Viding told BBC News.
"We know they can generate the same response but they do that in an active and effortful way. Under free-viewing conditions they don't seem to. [...]"

There's also a newer study that seems to confirm the "empathy switch" in a larger class of "dark triad" personalities. (Also posci story on that.)


Survey Questionnaire design - What are the alternatives to Likert scale in measuring attitudes? I work in Social Science Research (Management)

In my school, Likert Scale is extensively used to measure attitudes.(Strongly disagree to Strongly agree). So, I kind of assumed that it's an absolute standard.

But recently, while I was reading material on designing surveys, I came across the argument that highly criticized this format of response categories, owing to a tendency called "acquiescence response set".

I'm working on my questionnaire and have drafted several questions that measure the attitude of respondents related to an information system. Ex: The system provides accurate information. (strongly agree, Agree, Neither, Disagree, Strongly disagree)

My question is - what are the alternative scales I can use to measure the attitudes of the respondents? what is the more reliable way to measure attitudes?

In attitude psychology Likert response scales are still the norm. They do have their problems (and there are a good deal of problems), but many of them can be addressed satisfactorily.

The acquiescence bias you mention is a small issue. It can be balanced out by reverse coding roughly half of your test items. The acquiescence bias then becomes random noise rather than a systematic bias, which is annoying but not very damaging as long as your analysis has good power.

For example, if you have a 4-item scale that measures roughly the same thing, you could mix items like "The system provides accurate information" with items like "I would not recommend the system to others".

Does that make sense?


How can I create a set of comparable symbols of different shapes? I was thinking about doing a small experiment during university course where participants have to answer a personality quiz and then they have to compare different symbols (like triangles, rectangles of different ratios) on a split screen view, comparing two symbols at the same time, choose the preferred one and taking reaction time. Just to get information about common preferences for shapes! Obviously these symbols should have some basic information in common (pixel density, color) so shouldn't be completely different.

How can I create a set of symbols that have the same area even if they varied in geometrical form (ratio)? How should I decide which forms in which ratios should be presented?

Presumably to have symbols with the same area but different shapes, you could do a little geometry to work out relevant angles and sides. Then in any reasonable drawing package you could draw the shapes and check that they have appropriate angles. Programming drawing packages might also make life easier, but I don't have much experience with these (e.g., tikZ).

You raise an interesting question of what represents equivalence of size. Area of the shape could be a way of making size equivalent, but alternatively you could see two shapes as being visually of a similar size if they could be contained within an equivalent sized square.

One general strategy for designing the stimuli is to consider what dimensions might contaminate pairwise judgements of preferred shape: e.g., colour, size, features of the shape (e.g., angles on a triangle, the depth of cut-ins on star like shapes, etc.).
Once you've defined those features, either hold them constant or vary them in a consistent way. So you can either set up a factorial set of stimuli or randomise over features hold a feature constant. If you set up a factorial design (e.g., 3 levels of size, 2 colours, 5 shapes). You could examine how preferences vary across the confounding dimension and see whether inferences on the dimension of interest (i.e., shape) hold up levels of the confounding dimension.


What is the name of this common anti-pattern When you work on a project, for instance a program in the computer science field, many people pause or "bypass" work on it to work on a side project, often smaller and often a "helper" project, whether being a website, forums, marketing or else.

This is a common-anti pattern that leads to an infinite cycle of getting increasingly far from the main and most important top priority product.

Now my question is what was the name of this problem?
Surely there must be a scientific name and description for that.

You could be talking about a number of issues.  You could be talking about

Freudian defense mechanism repression
Distraction
Procrastination or
Deferring

Maybe you are talking about something else entirely.

The thing is not all observations necessarily need a "scientific" name for them in psychology or neuroscience and whatever the situation is, it would need a lot of background information to determine exactly what it is and how it manifests itself.

As it stands right now, the question could be deemed open to opinion, especially when Freudian and Neo-Freudian psychology is considered by some here to be pseudoscientific.


What is the current status of Paraphrenia? First mentioned by Kalbhaum in 1863, and better known by Kraepelin's descriptions in 1912, paraphrenia seems to be forgotten after the publication of DSM-III. It is always described by its nosology, late onset, with very systematized delirium and typical theme, without losing too much contact with reality.

In general, it seems to have been fused with schizophrenia, persistent delirium, affective paraphrenia, and paranoid affection. Commonly described among delirium and schizophrenia.

ICD-10 includes it in F22 as a type of persistent delusional ideas, in ICD-9 included in paranoid states. It is not included in DSM-IV or DSM-V.

There are plenty descriptive studies, but few reviews with a focus on paraphrenia.

Can anyone find a well-focused and detailed experimental review or trial?
Do psychology / psychiatry associations claim it?
Are there manuals that address it in diagnosis or didactically (not in general form but with detailed author)?
Are there any authors especially focused on this disorder?

 1. I am not interested in medication;
 2. I am not interested in comorbidities such as paranoid affection (described as very characterized by a characteristic affection and there is some confusion with directly paranoid affection, affective paraphrenia).
 3. I am not interested whether it appears to be closely related to paranoid schizophrenia (confusion due to systematized delirium).

Paraphrenia is a late-onset mental disorder similar to schizophrenia in that it features the positive symptoms of the disease, such as delusions and/or hallucinations, but lacks the negative symptoms, such as the deterioration of intellect or personality. It seems to be an outdated term (source: Psychology Central).

  Can anyone find a well-focused and detailed experimental review or trial?

I have found a few, albeit all somewhat dated: Ravindran et al. (1999); Lubman & Castle (2002) and Sato & Idha, (2002). I can recommend to see whether these articles are cited in papers published on a later date if you prefer more recent literature.

  Do psychology / psychiatry associations claim it?

Difficult question. The International Late-Onset Schizophrenia Group recognizes the disorder’s late-onset version as “very late-onset schizophrenia-like psychosis Howard et al. (2000). The CCI in Australia describes it. Smaller, more isolated institutions seem to recognize it, for instance, the Cardif & Vale Action for Mental Health at least acknowledges its existence. As you said, it appeared not in the DSM-IV and V manuals. Instead, more recently paraphrenia has been classified as

  very late-onset schizophrenia-like psychosis

Patients who present these particular symptoms are generally diagnosed with a variety of other illnesses, including atypical psychosis, schizoaffective disorder, delusional disorder or persistent persecutory state (source: Psychology Central). I am sure when you search under this term you will end up with substantial amounts of resources, including for example the DSM-V manual, where it is included, albeit quite vaguely defined according to Sachdev et al. (2015).

  Manuals that address it in diagnosis or didactically?

Under the more popular name late-onset psychosis, you can find its diagnostic characteristics in the DSM-V manual as stated above, in The Psychosis Manual from Smith et al., in this Master's thesis, among hosts of other sources.

References
- Howard et al., Am J Psychiatry (2000); 157(2): 172-8
- Lubman & Castle, Current Psychiatry (2002); 1(12): 35-44
- MacDougall, Master's thesis (2011), McMaster University
- Ravindran et al., Can J Psychiatry (1999); 44(2):133-7
- Sachdev et al., Harv Rev Psychiatry (2015); 23(5): 320–8
- Sato & Idha, Psychogeriatrics (2002); 2(1): 20–5


Interclick interval resolution of the ear Let's say I have an almost perfect metronome which ticks at 60 beats per minute, except for one beat that is slightly off from time to time.
What's the maximum error this metronome can have without a human being able to notice the rhythmic default?
Is there any study related to that?
Also, would it depend on the metronome speed?

There have been studies on this, both with paired clicks and long streams of clicks.  Normal listeners can detect changes of the sort you describe with essentially perfect reliability down to about 45 ms and with better chance performance below 30 ms.  I haven't been able to find a study measuring the minimal threshold for this change, but from the studies I have found it should probably be in the 10-20 ms range.

As for how the interval affects it, the answer depends on the direction of change and the direction of interval change, so it is hard to give a single answer.  The affect seems to be larger at larger interval changes.

Note that this is a very low-level task, with slightly higher modulation rates processed at the very lowest levels of the auditory pathway.  It is also a task that is highly "conserved" evolutionarily, that is it is very consistent across species.  Fish have similar performance to humans at this task.  And not that in the stream study, it used mismatch negativity, which is a change in electrical activity in your brain that occurs even if you are not paying attention to the stimulus and don't consciously notice the change.


Does anyone know of any clinical psychology journals that use a double-blind review process? Through this question:

What kind of cognitive psych journals are receptive to clinicians without any publications?

I found out that a colleague of mine should submit a paper she is writing to a clinical psychology journal that uses a double-blind review process. For those who don't know, that means the reviewers don't know who wrote the article and vice versa.

However, I failed to find any such journal through googling.

My Question:

Does anyone happen to know of such a journal? I am looking for one that might accept an article (of a colleague of mine) written on ADHD, a learning disability.

If no such journal exists, what is the closest substitute that still uses a double-blind review process?

Note:

As I mentioned in the previous question, my colleague has developed a process model of the disorder based on 25+ years of clinical practice. She has used her model for several years now and is looking to publish her it to help others better understand the disease.

My impression is that many (perhaps most) psychology journals do double-blind review (or at least give you the option).

Journal of Consulting and Clinical Psychology is one example.
http://www.apa.org/pubs/journals/ccp/?tab=4

  This journal uses a masked reviewing system for all submissions.

It sounds like that (a) you are not aware of what clinical psychology journals exist in your area; and (b) how to determine whether they require or allow for masked review. I'll discuss each of these points.

Finding a relevant clinical psychology journal: If you are writing a journal article, you will need to perform a review of the literature. Identify journals from those that you cite in your references. There are also various lists of journals organised by topic (e.g., Science Citation Index) that often give an indication of journal prestige. If you are interested in clinical psychology, then you may also want to check out "psychiatry" journals as well.

Determining review policy. Every journal has a website, and a section of the website will include instructions to authors. Here you will typically find information about the reviewing process.


Is spiritual enlightenment a valid way attempting to understand the universe and consciousness Are traditional methods of spiritual enlightenment such as Zen, Buddist, etc accepted by psychologists as valid ways of further understanding the workings of consciousness, Or is it considered too subjective, and different from the scientific method to be of use.

Many scientists have argued that ancient introspection like Zen is too unscientific to be used in psychology, while others argue it is important, as its the only way to further our understanding of consciousness.

Is spiritual enlightenment accepted by psychologists universally at this time(2015) to be a valid, scientific way of understanding consciousness

I do have a question though, once you have an awakening, and realize as others have said, that you are in the matrix, aren't you aware of this fact forever? So how can you be not enlightened anymore, but you once were.
Question by tristo in a comment to my previous answer

I'm not sure about the matrix analogy because in the movie they simply replace 'reality' with 'real reality'. This new reality differs in detail from the first but not in nature. It is just one level of illusion down. Illusion hasn't been stripped away altogether.

How can you be enlightened only for a short while? Here's an example:

I stub my toe on a rock. I know intense pain; it's real; it's right now.  A month later I can remember what happened but I am no longer experiencing pain, I'm just remembering it. It's precisely the same with a short-term enlightenment experience.

This highlights the impossibility of communicating the experience. There are some scientifically documented individuals who are born without a sense of pain. How could we tell such a person what pain is like? We couldn't. On the other hand two people who have experienced pain can communicate with each other about it because they have it in common. Two people who have experienced an awakening can similarly discuss it because they both know what they are talking about from their own experience.

I hope this goes some way towards providing an answer.
P.S.
I can accept that some people could be permanently in that state. As I mentioned, I chickened out of staying in it or going even deeper - it was both joyful and scary. Nevertheless what I experienced was immensely powerful.


Why do we scream in pain and fear? Why do humans (other living things too, but not sure) scream and make high pitched sounds when in pain*  or when in fear that something painful* will imminently be inflicted upon them?

*  both physical and emotional.

This question came up in our tri-monthly site evaluation queue (Let's get critical: Feb 2014 Site Self-Evaluation), and I marked it as "needs improvement," so here's an indication why, and my attempt to do so.

The next-highest Google hit for this question's title, "Science: why we scream" (Highfield, 2008) seems pretty useful. Telegraph's terms and conditions are a little scary though, so I'll paraphrase some ideas rather than quoting directly.

Darwin himself argued that emotional expressions may improve selective fitness. This could explain the relatively universal uniformity of fear expressions, which generally include widened eyes and nostrils, lifted eyebrows, and maybe some inclination to scream (Susskind et al., 2008). This may improve olfactory and visual sensory intake and motion tracking. Pragmatic benefits aside, William James, another prominent historical figure in psychology, was well ahead of his time in pointing out that expressions affect emotions; they also affect neural circulation!

However, there are limits to the universality of fear expressions, and even to the uniformity of facial muscular anatomy (Waller, Cray, & Burrows, 2008)! Basic expressions like "happiness, sadness, fear, anger, surprise, and disgust" are handled pretty well by five essentially ubiquitous facial muscles, but people differ in the number of additional, facially expressive muscles they have (19 may be the maximum). I've edited this summary of Waller and colleagues' results into the Wikipedia page on the risorius muscle just now:

  A study of 18 Caucasian cadavers found individual differences in the presence and bilateral symmetry of risorius muscles. Seven of these individuals (both men and women) clearly lacked the muscle; two were inconclusive; only four were conclusively symmetric.

Highfield (2008) associates the risorius muscle with "expressions of extreme fear," but Wikipedia only associates it with an "insincere-looking" smile; Waller and colleagues (2008) associate no expressions explicitly with the risorius muscle, which they don't really discuss in specific depth. However, Highfield quotes Waller directly (suggesting further unpublished discussion that may have supported his interpretation of risorius' function) as follows:

  Everyone communicates using a set of common signals...so we would expect to find that the muscles do not vary. The results are surprising. Some less common facial expressions may be unique to certain people.

Other quick Google Scholar results for "scream fear" ("scream pain" didn't produce anything promising at first glance) seem useful to mention here too. A study of rats and 160 undergrads found (in the human research) that a "yell, scream, or call for help...was frequent for females, rare for males" (Blanchard, Hynd, Minke, Minemoto, & Blanchard, 2001). A more general discussion of the function of fear screams in humans and other animals has also been published (Högstedt, 1983), so you may want to check that out too. It includes some literature review, so its references could probably lead much deeper into the question than you may wish to pursue it... ;)

References

Caroline Blanchard, D., Hynd, A. L., Minke, K. A., Minemoto, T., & Blanchard, R. J. (2001). Human defensive behaviors to threat scenarios show parallels to fear-and anxiety-related defense patterns of non-human mammals. Neuroscience & Biobehavioral Reviews, 25(7), 761–770. Available online, URL: http://www.researchgate.net/publication/11558273_Human_defensive_behaviors_to_threat_scenarios_show_parallels_to_fear-_and_anxiety-related_defense_patterns_of_non-human_mammals/file/9fcfd50c755e22230b.pdf. Retrieved February 8, 2014.

Highfield, R. (2008, June 17). Science: Why we scream. The Telegraph: Science News. Retrieved from http://www.telegraph.co.uk/science/science-news/3344701/Science-why-we-scream.html.

Högstedt, G. (1983). Adaptation unto death: Function of fear screams. American Naturalist, 121(4), 562–570. Available online, URL: http://www.jstor.org/stable/10.2307/2460982.

Susskind, J. M., Lee, D. H., Cusi, A., Feiman, R., Grabski, W., & Anderson, A. K. (2008). Expressing fear enhances sensory acquisition. Nature Neuroscience, 11(7), 843–850. Available online, URL: http://www.yorku.ca/khoffman/Psyc6253/Susskind%2708_Meotions4perception.pdf. Retrieved February 8, 2014.

Waller, B. M., Cray Jr, J. J., & Burrows, A. M. (2008). Selection for universal facial emotion. Emotion, 8(3), 435–439. Available online, URL: http://eprints.port.ac.uk/1629/1/WALLERetal2008b.pdf. Retrieved February 8, 2014.


Why do we sometimes(i often) go to trance while listening to music? What's the scientific reason behind it?

I can't quite figure out what's around me and it feels so soothing same as the effect of meditation. It feels like an enlightenment.(I feel like I'm connected to a higher deity)

If you take a look at this quick article: The Neuroscience Of Trance or the full published study the article refers to: Brain Network Reconfiguration and Perceptual Decoupling During an Absorptive State of Consciousness scientists used fMRI to view what was going on in the brains of shamans as they either entered into a trance or purposefully stopped themselves from doing so while listening to drumming.

One of the things they noted was a dampening of the sensory pathways - there theory being that while the drumming beat was the most prominent external stimulus, it's repetitive and predictable patterns allowed it to be gated out/ignored while its ongoing presence prevented reorienting to the usual random environmental distractions.

I would expect the music your listening to is doing more or less what the drumming does for the shamans.


Which Cognitive Sciences are the most affected by the Replication Crisis? As many here are probably aware, a replication crisis seems to have been occurring in many scientific fields for some time now. Allegedly, Psychology is at the center of this crisis, with many of its high-profile studies turning out to be impossible to replicate.

As someone who tries to regularly consume academic literature in order to educate oneself, this makes me wonder what areas within the broader umbrella of 'Cognitive Sciences' have had the most replication attempts fail and/or have the most information available about replication failures.

One finding from the Reproducibility Project was the following:

Van Bavel et al wrote that

  Inbar (2) notes that the reproducibility rate of social psychology (28%) is lower than cognitive psychology (53%).

In general, one might expect that subdisciplines with the following features to have greater reproducibility issues:

particularly interested in novel effects
many researcher degrees of freedom (e.g., analytic choices, many possible outcomes variables, many possible predictors, etc.)
between subjects designs rather than repeated measures designs
lower statistical power (typically because getting a sufficient sample size requires substantial resources)
those embracing fewer open science practices (e.g., pre-registrration, open data, etc.)

So, for example, cognitive psychology often uses repeated measures designs to examine fairly intuitive cognitive effects.

Personality and individual differences research is often concerned with quantifying the degree of relationships and often has very large sample sizes.

A lot of neuroscience research traditionally used techniques like fmri that often involves many researcher degrees of freedom (e.g., many brain sites), and the research is expensive per participant so sample sizes are often too small.

Social psychology has a tradition of being interested in novel experimental effects. Many of these studies have traditionally been underpowered (e.g., 20 or 30 participants per group, when perhaps 100 or 200 per group would be required for adequate power), and they have often had some degree of flexibility (e.g., choice of outcome variable; case exclusion rules; whether to transform; whether to covary for something; etc.).

These effects also combine with publication bias (preferences to publish significant effects) and file draw effects to reduce replication (although the same bias reduces the awareness of these issues).

That said, in general, a lot is happening in the open science area to try to both increase understanding of replication issues, as well as change research practices.

Reference

Van Bavel, J. J., Mende-Siedlecki, P., Brady, W. J., & Reinero, D. A. (2016). Contextual Sensitivity Helps Explain the Reproducibility Gap between Social and Cognitive Psychology.