Is it easy in languages other than English to read a paragraph where all but the first and last letters of every word have been rearranged?

The neologism used to describe this phenomenon is Typoglycemia.

It relates to the cognitive processes behind reading written text.

Randomising letters in the middle of words have little or no effect on the ability of skilled readers to understand the text.

Because the human mind does not read every letter by itself but as a whole, it would work for any given language where we can apply the same randomisation and keep the words separated in the same order.

Let's take the notorious German example Donaudampfschiffahrtsgesellschaftskapitän, meaning Danube steamship company captain:

Our noun Donau remains the same
It is possible for our noun dampfschiffahrts to be reformed into dampfschifffahrts
Our noun gesellschaft becomes the adjective gesellschafts
Then our noun kapitän remains the same

Let's see what happens when we scramble the compound lexeme:

Unscrambled German: Donaudampfschiffahrtsgesellschaftskapitän
Scrambled German: Dsnegapcfssamspfkaihdoftctflhreulasihatän
Unscrambled English: Danubesteamshipcompanycaptain
Scrambled English: Dbipiutpaccmmaapeansytoeshann

Virtually impossible! Now let's see when we scramble each lexeme, then compound it:

Original German per lexeme: Donau-dampfshiffahrts-gesellschafts-kapitän
Scrambled German per lexeme: Doanu-dhsffhmftpiacras-glhcselefasts-kipatän
Scrambled German composition: Daonudhiahscfmffatrpsglhcselefastskipatän
Original English per lexeme: Danube-steamship-company-captain
Scrambled English per lexeme: Dnbaue-stahmseip-camonpy-citapan
Scrambled English composition: Dnbauestahmseipcamonpycitapan

The composition being nearly just as readable as per lexeme!

Feel free to try another here.

Now let's take an example in Mandarin.

Script:

研究表明
漢字的順序並不一定能影響閱讀
比如當你看完這句話後
才發現這裡的字全都是亂的

Pinyin:

Yánjiū biǎomíng
Hànzì de shùnxù bìng bù yīdìng néng yǐngxiǎng yuèdú.
Bǐrú dāng nǐ kàn wán zhè jù huà hòu
cái fāxiàn zhèlǐ de zì quándōu shì luàn de.

Now let's invert 6 disyllabic characters.

Script:

研表究明
漢字的序順並不定一能影閱響讀
比如當你看完這句話後
才發這現裡的字全是都亂的

Pinyin:

Yán biǎo jiū míng
Hànzì de xù shùn bìng bù dìng yī néng yǐng yuè xiǎng dú.
Bǐrú dāng nǐ kàn wán zhè jù huà hòu
cái fā zhè xiàn lǐ de zì quán shì dōu luàn de.

This rather tame example now makes little sense, but does not quite appear completely disordered (with the exception of the preserved third line).

Further materials:

Psycholinguistic evidence on scrambled letters in reading - Matt Davis
Reibadailty - Graham Rawlinson
The Significance of Letter Position in Word Recognition - Graham Rawlinson
Jumbled Chinese - Victor Mair


How do psychologists ensure they are measuring innate intelligence and not just education?

Short answer
Any intelligence test will be designed for a certain target population. That target population's score is set at an index of 100 for the standard IQ test. The same test applied to people from a different cultural background, or other socioeconomic status may yield numbers that are unreliable, as they my not understand the question (albeit knowing the answer), or they may lack the vocabulary, or even interest altogether.

Background
IQ is highly dependent on education; For instance, an illiterate person cannot perform an IQ test at all. And indeed, education can generally affect IQ scores (e.g., Dear & Johnson, 2010). Further, IQ tests are Western constructs and do not apply in many other cultures. So IQ tests are anything but objective. They only apply validly to compare people with a certain educational background. Bush people in the outbacks of Africa may not use numbers at all, but instead may rely on 'one', 'two', perhaps' three' and 'many'. They may be highly intelligent, we simply cannot assign a number to it, simply because they don't care about numbers, geometry, classifications, logic, and other standard components of IQ tests. The APA says rightfully

  Researchers of cultural differences in intelligence face a major challenge, however: balancing the desire to compare people from various cultures according to a standard measure with the need to assess people in the light of their own values and concepts.

Reference
- Dear & Johnson, Int J Epidemiol (2010); 39(1): 1362–9


Is there a term to describe the tendency to attribute the cause of a bad outcome to a recent event?

I don't know of a single term for it, but what you're describing is, in essence, causal inference driven by "statistics", "co-variation", "co-occurrence", or "contiguity" (the terms are largely interchangeable).

If you're interested, there's a quite in-depth discussion review of theories of different theories of causal inference, including statistical models, here.

I think your example can be tied in quite nicely with "dual process" theories too, which propose two kinds of thinking: automatic, intuitive processes, which are sensitive to things like co-variation, and more effortful reflective processes, needed for more abstract relational reasoning. In your case, intuitive thinking easily makes a causal inference based on co-occurance:

  "Mark touched the tower, and then the tower fell, so the tower must have
  fallen because Mark touched it"

while more effortful reflection is needed to construct a causal model involving foundational work done months ago. I don't know of any specific application of this intuitive/reflective distinction to causal reasoning, but I'm sure it's been done somewhere.

EDIT: I've just remembered this paper, which discusses a similar idea, but in "multiple
cue probability learning", a specific kind of causal learning. I feel a little obliged to plug this, because one of the authors is my PhD supervisor.


Are cycles possible in circuits of neurons?

There are tons of cycles in the brain. The study of how the brain uses these cycles are used for computation is called Theoretical Neuroscience. Browsing the tag on this website is one way to become introduced to those ideas.

Alternatively, these loops are framed in different ways in "How to Build a Brain" by Chris Eliasmith. Loops involving a population node connecting to itself are considered to be memories. Longer loops, such as the basal-ganglia$\rightarrow$thalamus$\rightarrow$cortex loop could be considered analogous to the "main event loop" of a program, but with a few caveats.


Does psychology have a name for emotions that a person can feel but cannot name?

The term used for recognizing emotions is affect labeling (also know as emotions labelling). The act of labelling an emotion requires similar cognitive mechanisms used for labelling a cat or a dog (Concept). Like any other concept learning, affect labeling requires training and experience.

Labelling emotions is very importand beacuse it can help regulate emotions effectively.

  This impoverished emotional labeling is, in turn, associated with
  deficits regulating those emotions (see Vine & Aldao, 2014). In other
  words, the less aware we are of our emotions, the less likely we are
  to figure out how to best regulate them.

In this article you can find some practical advice how to better understand your emotions.


Classical conditioning paradigm for hippocampal learning

Read this paper

Storage of Spatial Information by the Maintenance Mechanism of LTP

Eva Pastalkova*, Peter Serrano*, Deana Pinkhasova, Emma Wallace, André Antonio Fenton†, Todd Charlton Sacktor†
http://www.sciencemag.org/content/313/5790/1141.short

It uses a conditioning task that is primarily hippocampal as it is a spatial navigation task.  They monitor the strength of CA3-CA1 connections during and after training using the fEPSP (field excitatory post-synaptic potential) slope.

Also, for a review of hippocampal dependent tasks, see

The role of hippocampal subregions in memory for stimulus associations

Rosamund F. Langston, Cassie H. Stevenson, Claire L. Wilson, Ian Saunder, Emma R. Wood

http://www.sciencedirect.com/science/article/pii/S0166432810004857


Where to obtain and how to score the Bukowski et al "Friendship Qualities Scale"?

Obtaining: Yes, the items are listed in Bukowski et al (1994). See Table 1.
You could always email the author explaining your research project and ask him whether he would allow you to use the measure.

Scoring:
A quick look suggests that each item is scored on a 1 to 5 scale.
Table 1 suggests that there is a scale-level, and subscale-level of scoring (i.e., 5 scales, and 10 subscales). Table 1 shows how items relates to scales and subscales.

Scoring scales and subscales seems to be just a matter of getting the mean of constituent items.

References

Bukowski, W. M., Hoza, B., & Boivin, M. (1994). Measuring friendship quality during pre-and early adolescence: The development and psychometric properties of the Friendship Qualities Scale. Journal of Social and Personal Relationships, 11(3), 471-484.


Any studies as to whether internet groups create even more groups, ideologues and "separation" than pre-internet?

The literature you are looking for is regarding group polarisation in the Internet era (with "polarisation" being the main research keyword here).

There are supporters of your idea as well, most notably  Eli Pariser (2011) and Cass Sunstein (2001, 2009, 2017) and studies that show polarisation on the Internet. That being said:

  However, when comparisons are made between offline and online sources, studies find similar levels of segregation. Figure 1, taken from Gentzkow and Shapiro (2011), shows that segregation across website visits is smaller than segregation across national newspapers, but larger than segregation across local newspapers. Halberstam and Knight (2016) examine political networks on Twitter and find similar levels of segregation in the Twitter political networks as in offline political networks. Furthermore, while suggestive, segregation across information sources on the internet is neither necessary nor sufficient for the internet to increase polarisation.

(Source: "The internet, social media, and political polarisation" - Levi Boxell, 2017

So you are on the right track, your question was thought of before and the keyword "polarisation" might lead your research about it in more depth than this quick answer.


What is the evidence that mathematicians are more likely to have autistic traits than the rest of the population?

No. I can't seem to find a specific study into professional mathematicians or graduate students so far, the studies always seem to group the occupations together.

However, Baron-Cohen's team has done an impressive national survey (Ruzich et al., 2015) and recruited nearly half a million people through a UK TV show. They managed to get over 450,394 survey respondents which allowed them to analyse occupations. They found that people working in STEM scored higher in an autism screening questionnaire or AQ (Autism-Spectrum Quotient) test.

  individuals working in a STEM career (m = 21.92, SD = 8.92) scored higher than individuals non-STEM careers (m = 18.92, SD = 8.48)

Unfortunately, there wasn't a specific category for mathematicians as probably it is too specific and too small a field to analyse. The three categories (figure 3) forming STEM was Comp & IT, Engineering and Sci & Tech. Mathematicians would fit into one of those occupational roles.

References

Ruzich, E., Allison, C., Chakrabarti, B., Smith, P., Musto, H., Ring, H., & Baron-Cohen, S. (2015). Sex and STEM Occupation Predict Autism-Spectrum Quotient (AQ) Scores in Half a Million People. PLOS ONE, 10(10), e0141229.


Why do our senses evoke different subjective experiences

Don't know the answer (I think no one does), but you should have a look at this paper: A sensorimotor account of vision and visual consciousness. O'Regan JK, Noë A., BBS 2001 PUBMED

In short the proposed answer is that modalities are subject to different sensory-motor contingencies. For example, when you move forward the visual input undergoes very structured changes, but auditory input undergoes a different set of changes. So what makes seeing feel different than hearing is that the relationships between motor output and sensory input are different.

You might also be interested in sensory substitution experiments. The brain is to some extend able to acquire new 'senses', when specifically structured information is provided to an existing sense. For example, it appears to be possible to 'see' (whatever this means in this context) when brightness information is transduced to touch or electrical stimulation of the tongue Wikipedia


Is it good practice to try to recall things when we are tired?

You might not be looking for an answer about sleep deprivation per se—you might just be interested in normal daily fatigue immediately before normal sleep—but of course sleep deprivation results in tiredness, so the answer seems likely to be equivalent (though I'm not a sleep researcher by specialty). Here's an answer for sleep deprivation and memory (Alhola & Polo-Kantola, 2007):

  Total [sleep deprivation] impairs attention and working memory, but it also affects other functions, such as long-term memory and decision-making.

And another equivalent answer (Chee, Chuah, Venkatraman, Chan, Philip, & Dinges, 2006):

  Performance accuracy declined significantly during the performance of...working memory tasks following [sleep deprivation].

Reference

Alhola, P., & Polo-Kantola, P. (2007). Sleep deprivation: Impact on cognitive performance. Neuropsychiatric Disease and Treatment, 3(5), 553–567. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/pmc2656292/.

Chee, M. W., Chuah, L. Y., Venkatraman, V., Chan, W. Y., Philip, P., & Dinges, D. F. (2006). Functional imaging of working memory following normal sleep and after 24 and 35 h of sleep deprivation: Correlations of fronto-parietal activation with performance. Neuroimage, 31(1), 419–428. Retrieved from http://www.med.upenn.edu/uep/user_documents/Cheeetal--Functionalimagingofworkingmemory--NeuroImage2006.pdf.


What is the subjective wellbeing instrument that is used by Science of Happiness for check-ins?

The background of the measure can be found here.
The article implies that it is an ad-hoc measure of emotions created for this study:

Every week, we checked in with our students to see how they were feeling. We showed them a sequence of six cartoon faces created by Pixar artist Matt Jones to convey fear, enthusiasm, anger, affection, sadness, and amusement (below). Under each, we asked them to rate, on a scale of 1 to 10, how much each face matched how they’d been feeling lately.  Then we transformed their collective weekly ratings into a single score.

The result? For students who responded at least 8 out of 10 times—suggesting that they were fully participating in the course—positive feelings went up, and up, and up. They felt progressively less sadness, anger, and fear, while at the same time experiencing more and more amusement, enthusiasm, and affection.
We also invited students to fill out a brief battery of research-validated questionnaires that are regularly used to assess feelings like happiness, stress, flourishing, or satisfaction with life.

The last sentence suggests the ad-hoc nature of the measure (as compared to validated scales). Also, I couldn't track down any published research with this measure. The icons themselves stem from a collaboration of Dacher Keltner with Facebook, as described here, for example.


Is there an evolutionary psychology explanation why children have high pitched voices?

Children have high pitched voices relative to adults because their vocal folds are shorter and physics demands that short vocal folds result in higher pitches. The format frequencies of children are also higher than adults due to shorter vocal tract lengths.

I think your question is, is there a speech communication reason for the vocal folds and vocal tract of children to be shorter than adults to which I would argue that it is unlikely. While it is possible to be grown with adult sized features (e.g., the inner ear and the middle ear ossicles), generally babies are smaller than adults. There would need to be a strong evolutionary advantage to being born with a really long vocal tract. Second, from what I can piece together, (e.g., this article) a shorter vocal tract is desirable for suckling. Therefore I would conclude that evolutionary speaking babies have shorter vocal tracts because they are smaller than adults and if the vocal tract was longer it would make it harder to feed.


How is history of psychology taught around the world, and if it is not, why not?

The American Psychological Association requires graduate programs to cover a range of core competencies, including "the breadth of scientific psychology, it's history and development, it's research methods, and its applications. To achieve this end, the students shall be exposed to the current body of knowledge in at least the following areas:...history and systems of psychology..." (APA Guidelines and Principles for Accreditation of Programs in Professional Psychology, http://www.apa.org/ed/accreditation/about/policies/guiding-principles.pdf). This applies to all APA accredited doctoral programs in clinical, counseling, and school psychology. Many programs meet this requirement with a History and Systems course, which covers development of psychology as a field as well as different branches of psychological theory. However, some graduate programs may choose to meet the requirement by requiring students to complete an independent study on this topic.

The APA does not accredit master's or bachelor's programs, so there may be more diversity as to whether a history of psychology course is provided or required at that level. A 2010 APA Monitor article discusses this issue (Chamberlin, 2010). The reasons for teaching the history of psychology vary. At my undergraduate university a History and Systems course was a required course in your senior-year, as the program felt it not only provided a sound theoretical foundation but also served as an excellent review for the GRE Psychology subject test. A 2011 dissertation explored the content of history of psychology courses in APA accredited programs, and may provide additional information on the presence of the history of psychology in American education (Petzolt, 2011). The author noted that there are many reasons typically given for this APA requirement, including "the belief that the study of history is a way of unifying the different branches of the field, that it helps to ground current psychological research in tradition and theory, and that it establishes a framework from which all applications can be derived" (Petzolt, 2011).

Chamberlin, J. (2010). Don't know much about history. APA Monitor, 41(2), 44. http://www.apa.org/monitor/2010/02/history.aspx

Petzolt, N. M. (2011). Teaching the graduate course in the history of psychology in APA accredited programs. St. John's University (New York), 53 pages. UMI Proquest Publication number: 3445776.


Why would the brain flip the images perceived by your eyes?

It is not meaningful to talk about your brain processing something as 'right-side up"' or 'upside-down'. The 'images' in your brain are just collections of neural activations, and not actual pictures. Thus they cannot have an orientation. The only meaningful way to test your question is to try flipping the input the brain receives and seeing if it can cope.
Fortunately, the brain is capable of flipping your visual field if required as measured through perceptual adaptation experiments using inversion glasses. This has been demonstrated very drastically in studies, by for instance requiring a participant to wear inversion glasses for a long time. At first they are confused, and unable to orient themselves and do basic tasks, however after enough time the brain can adopt enough to even do activities like riding a bike. This suggests that from the only way you can measure things (i.e. behaviorally) the brain is capable of adapting to an upside down world (some participants even reported that after extended use the world even seemed "right side up"). This is functionally equivalent to the brain being able to process your visual information in either orientation. If it is capable of processing in either orientation, the question of "does my brain flip the image" becomes a pseudo-question and unanswerable.
References

Taylor, J. G. (1962). The behavioral basis of perception. New Haven: Yale University Pres

Harris, C.S. (1965) "Perceptual adaptation to inverted, reversed, and displaced vision." Psychological Review 72(6): 419-444. [pdf]]

Di Paolo, E.A. (2003) "Organismically-inspired robotics: homeostatic adaptation and teleology beyond the closed sensorimotor loop", {Dynamical systems approach to embodiment and sociality: 19-42 [pdf


Does night-sleep-deprivation have any effect on cognitive performance?

According to this article, yes it does have various symptoms including cognitive deficiencies that make us more prone to errors and less efficient :

  Circadian rhythms biologically program us to stay awake during
  daylight hours and sleep at night. Shift work goes directly against
  what our bodies desire to do, and those that struggle with this may
  suffer from shift work sleep disorder (SWSD).

  ... symptoms may include headaches, weight gain, gastrointestinal
  issues, fatigue, attention and concentration issues, work absenteeism,
  irritability and depression. ... Worst of all, shift workers are at a
  significantly greater risk for vehicular accidents and mistakes at
  work.

  The ideal situation is to maintain a steady sleep-wake schedule seven
  days a week, allowing for 7-8 hours of sleep. Although difficult to
  follow, it can be extremely helpful to help reset circadian rhythms.
  It can be especially tough on days off, when desires to socialize in
  the daytime and maintain more “normal” sleep periods kick in.

Additonal reference


Paper discussing economic rationale of IQ-based hiring practices

I believe I know which paper you're referring to. My guess is the widely cited Schmidt & Hunter (1998) paper. The paper summarizes 85 years of practical and theoretical implications of research in personnel selection. To see that they address what you're asking for, here is a quote from the paper

  If a superior worker is defined as one whose performance (output) is at the 84th percentile (that is, 1 SD above the mean), then a superior
  worker in a lower level job produces 19% more output than an
  average worker, a superior skilled worker produces 32% more
  output than the average skilled worker, and a superior manager
  or professional produces output 48% above the average for those
  jobs. These differences are large and they indicate that the payoff
  from using valid hiring methods to predict later job performance
  is quite large.

Then later they state

  At one extreme, if an organization must hire all who
  apply for the job, no hiring procedure has any practical value.
  At the other extreme, if the organization has the luxury of hiring
  only the top scoring 1%, the practical value of gains from selection
  per person hired will be extremely large. But few organizations
  can afford to reject 99% of all job applicants.

However, a more recent paper on the subject has been published. That's the Schmidt, Oh & Shaffer (2016), which summarizes 100 years of practical and theoretical implications of research in personnel selection. This paper is an update on the former, so you may as well just look only at this latest one.


Are there any critiques on the Self-Determination Theory by Deci & Ryan?

The University of Zurich has a pdf file of an article which was directly from the University of Rochester School of Arts and Sciences.

The article has an outline of many criticisms of SDT from behaviourists such as Eisenberger, Cameron and Pierce, which were later discounted as invalid.

References to all relevant articles are within the pdf file.


How does the timing work out for dopamine to affect the development of long-term potentiation?

The ability of dopamine to work on different time scales is discussed by Schultz. More generally, the basic idea of prediction error reinforcement based learning and DA is that the prediction error signal "propagates back in time". There is some doubt for how temporally precise this DA signal actually is, and if DA is fast enough to support RPE TD learning.

Does that answer the question?


Intuition behind loss quadrant of prospect theory

Prospect theory states that people make decisions based on the potential value of losses and gains rather than the final outcome, and that people evaluate these losses and gains using certain heuristics (risk potentials) - Source.

When you look at Prospect theory graphs, you need to remember that it is all about perceived potentials. (Perceived potential gains/losses against the perceived potential value).

Let's look at the logic to start with. If the potential value of the prospective task is negative, it is perceived that the outcome result has a higher potential to be negative (loss); and the opposite is true also.  If the potential value of the prospective task is positive, it is perceived the outcome result has a higher potential to be positive (win or gain).

Now with the logic in place, more potential loss perceived will result in a perceived potential of a more negative outcome and more potential gain perceived will result in a perceived potential of higher gains.

The line crosses the $0,0$ $x,y$ axes because it is perceieved that a zero potential value will result in zero loss or gain and the potential losses increase as you move nagatively away from the $0,0$ reference point, and the losses diminish as you move positively away from the $0,0$ reference point.

Now you also have to factor the probability of win or lose into the equation.  With low expactation of any gains (low perceived value) it doesn't matter if you win or lose, it is perceived that you are going to lose overall.  With high expectation of gains, (high perceived value), you need to have a win in order to achieve the gain perceived.

If you also rotate the graph, you get this


Will hearing but not listening to a video mentor help me learn?

From experience and some knowledge gathered from all over the place, yes and no. For example, if you want to do two things that are both mind-engaging, you'll probably end up doing both sloppily, or one much better than the other. But if one task is mundane and other mind engaging, like listening to music and doing math problem, or listening to a lecture and cleaning a room, you can probably do them both with no problem.

Also, "multitasking" does not actually exist. You can find many articles on this subject. What we think of as multitasking is actually task-switching. Your brain does not do two things at once, but switches from one thing to another. Task-switching is demanding a lot of energy, so some people may feel tired from it.

Some people are better than the other at task-switching, and can do it for some time without getting that much tired. I don't know how good you are at it, but you can try. If you haven't trained your mind to work efficiently like that, you might get better after some time, or just keep doing one thing at a time. (I know person who wasn't much of a "multitasker" but got better after some years of practically forcing it.) Hope this helps.


Is there a mental illness that almost completely stops you from thinking?

Thinking is mainly supported by the frontal lobes (although the ARAS – the Ascending Reticular Activating System – is essential for its arousal and other cortical areas are essential for its sensory inputs and other associative functions, such as language, spatial orientation, and emotion, which are closely associated with thinking). So, anything that affects the frontal lobes can affect the thinking.
But frontal lobes never stops function if one is still conscious – neurons in the frontal lobes will keep firing as long as  there’s a stimulation from the ARAS. So, to literally stop thinking (or all neurons in the frontal lobes stop firing) in still-conscious people is impossible.
However, frontal lobes can be interfered to the degree that the thinking is significantly impaired or retarded and the person seems to stop thinking. This can happen in a varieties of conditions, such as:
Psychological: severe emotional overload (e.g., by a sudden loss of something so precious, an unexpected devastating event, or an overwhelming rage), schizophrenia in some stages (e.g. catatonic stage), severe depression
Pharmacological: overdosage of antipsychotic, sedative, or other psychoactive drugs
Pathological:

all metalbolic derangements (hypoglycemia, hyponatremia, hypercalcemia, etc.)
some medical conditions (hypothyroidism, hypocorticolism, hypothermia, etc.)
frontal lobes disorders: frontal lobe tumor, infarction, hemorrhage, encephalits, dementing diseases
other causes: post- cerebral contusion, post-ictal stage

At some stages of the above conditions, either before the patients lapse into coma or after they emerge from coma, the patients will appear dazed, muted, unable to think, and unable to respond. That is, apparently, they seem to stop thinking in these conditions.
References:

Wikipedia. Frontal lobe

WebMD. What Is Encephalopathy?

Roger F Butterworth. Chapter 38. Metabolic Encephalopathies. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition.

Wikipedia. [Delirium](https://en.wikipedia.org/wiki/Delirium


Are closed eye movements related to the content of dreams or the imagination?

In regards to actively trying to control your eyes while they are closed, like attempting to do visualization like NLP, I believe that you choose what to focus on and where to focus at, exactly the same as my "pitch black" analogy whereby if you look into, say, a pitch black room, then although you know it's only 15 feet towards the wall, your vision does not.

Therefore, if you believe that it extends for millions of miles, then you can choose quite easily to focus into the darkness that way.

In regards to if you close your eyes and just kind of forget about them without going to sleep...like "resting your eyes", then I believe Chuck in another answer answered this best in his bottom two paragraphs.  Quick link: https://cogsci.stackexchange.com/a/4467/3433

Now in regards to during REM sleep, this gets tricky.

I did not think I'd find a study that answers your exact question about "how is focal point determined during REM sleep?".  I'll just start with that study first, then throw in a few others that are related to something called the "scanning hypothesis" which will help to unravel some of your other questions more specifically if they're about REM sleep specifically.

Let's start off with a definition of the "scanning hypothesis":

According to psychologydictionary.com,

  The scanning hypothesis is a concept hypothesizing that rapid eye
  movements identified in the course of the REM stage of sleep correlate
  to subjective gaze adjustments of the dreamer casting their gaze about
  in the dream with fixations in particular places.

At first I was worried that all the studies would just focus on this "scanning hypothesis," then I came across this gem:

  Exp Brain Res. 1997 Oct;117(1):153-60. Binocular eye movements not
  coordinated during REM sleep. Zhou W, King WM.

  Department of Neurology, University of Mississippi Medical Center,
  Jackson 39216, USA. wuz@vor.umsmed.edu

  Abstract

  Rapid eye movements (REMs) are a defining characteristic of REM sleep
  during which vivid dreams occur. It has been suggested that REMs may
  be binocularly coordinated and related to "watching" dream images. For
  the first time, binocular eye movements were recorded during natural
  REM sleep in monkeys to test the conjugate nature of the oculomotor
  system and the "scanning hypothesis" of REMs during sleep. During REM
  sleep, the lines of sight of the two eyes are frequently misaligned up
  to 30 degrees horizontally and/or vertically. Since the lines of sight
  usually don't intersect, there is no fixation point. Instead, each eye
  is aimed at a different part of the visual field during REM sleep.
  Furthermore, REMs are not usually conjugate, but are disjunctive or
  even monocular in horizontal or vertical directions. These data argue
  against the idea that REMs actually "track" dream images, unless each
  eye is watching its own dream! Binocular misalignment and disjunctive
  (even monocular) REMs during sleep suggest that separate left eye and
  right eye pathways generate saccades in each eye and control the
  position of each eye. Binocular coordination cannot be the passive
  result of anatomical connectivity as has been argued previously, but
  instead must result from a high-level process associated with the
  awake state that coordinates activity in left-eye and right-eye
  pathways. Hering's law of equal innervation is not consistent with
  these data. PMID: 9386014 [PubMed - indexed for MEDLINE]

Apparently also, part of the "scanning hypothesis" is that your eyes are trying to track down something...in other words fixate upon it...which would cause them to focus.  This results from this study say no to that.

So, as far as...

  "By this I mean are the muscles moving in accordance with focusing.
  How is the focal point determined?"

...during REM sleep, this study says that there is no fixation upon one thing and thus there is no focal point.  So, no, according to this study the muscles are not moving in accordance with focusing.

As a precursor to this study, a definition of "rapid eye movement disorder" is good to know.  So here is wikipedia's definition:

  Rapid eye movement disorder is a sleep disorder (more specifically a parasomnia) that
  involves abnormal behaviour during the sleep phase with rapid eye movement
  (REM) sleep. It was first described in 1986. The major and arguably
  only abnormal feature of RBD is loss of muscle atonia (paralysis)
  during otherwise intact REM sleep. This is the stage of sleep in which
  most vivid dreaming occurs. The loss of motor inhibition leads to a
  wide spectrum of behavioural release during sleep. This extends from
  simple limb twitches to more complex integrated movement, in which
  sufferers appear to be unconsciously acting out their dreams. These
  behaviours can be violent in nature and in some cases will result in
  injury to either the patient or their bed partner.

It's important to note the difference between the first study which was done in 1997 and this one done in 2010.  Perhaps the overall definition of the "scanning hypothesis" changed, or there is slight subjectivity to it.

For instance, in the first study the author says,

  "It has been suggested that REMs may
  be binocularly coordinated and related to "watching" dream images. For
  the first time, binocular eye movements were recorded during natural
  REM sleep in monkeys to test the conjugate nature of the oculomotor
  system and the "scanning hypothesis" of REMs during sleep."

So he's trying to test the "scanning hypothesis" by looking to see if the monkeys actually do focus on something by looking to see if the eyes are working together (ie. trying to triangulate distance and thus focus) are actually working together.

Now these French people (they always seem to have creative ideas actually) admit that the "scanning hypothesis" has been testing in this way...as in...by monitoring the muscles in the eyes.  So they're taking a different approach and (cleverly might I add) exploiting people who essentially have a disorder that is very similar to sleepwalking...but they lay in bed...THEN they are mixing in control patients who are normal so that they can compare the two and use that mixture to extrapolate it to the normal population as well & noone can criticize them for only using patients with that 1st specific disorder.

They're looking to see how their eyes align/what direction they move to when they are acting out certain motions.

  Brain. 2010 Jun;133(Pt 6):1737-46. doi: 10.1093/brain/awq110. Epub
  2010 May 16.
  Do the eyes scan dream images during rapid eye movement sleep? Evidence from the rapid eye movement sleep behaviour disorder model.
  Leclair-Visonneau L, Oudiette D, Gaymard B, Leu-Semenescu S, Arnulf I.
  Source Sleep Disorder Unit, Pitié-Salpêtrière Hospital, Assistance
  Publique - Hôpitaux de Paris, 75013 Paris, France.

  Erratum in Brain. 2011 Jul;134(Pt 7):1286.

  Abstract

  Rapid eye movements and complex visual dreams are salient
  features of human rapid eye movement sleep. However, it remains to be
  elucidated whether the eyes scan dream images, despite studies that
  have retrospectively compared the direction of rapid eye movements to
  the dream recall recorded after having awakened the sleeper. We used
  the model of rapid eye movement sleep behaviour disorder (when
  patients enact their dreams by persistence of muscle tone) to
  determine directly whether the eyes move in the same directions as the
  head and limbs. In 56 patients with rapid eye movement sleep behaviour
  disorder and 17 healthy matched controls, the eye movements were
  monitored by electrooculography in four (right, left, up and down)
  directions, calibrated with a target and synchronized with video and
  sleep monitoring. The rapid eye movement sleep behaviour
  disorder-associated behaviours occurred 2.1 times more frequently
  during rapid eye movement sleep with than without rapid eye movements,
  and more often during or after rapid eye movements than before. Rapid
  eye movement density, index and complexity were similar in patients
  with rapid eye movement sleep behaviour disorder and controls. When
  rapid eye movements accompanied goal-oriented motor behaviour during
  rapid eye movement sleep behaviour disorder (e.g. grabbing a fictive
  object, hand greetings, climbing a ladder), which happened in 19
  sequences, 82% were directed towards the action of the patient (same
  plane and direction) (Taal Note: Note what they just said in parenthesis). When restricted to the determinant rapid eye
  movements, the concordance increased to 90%. Rapid eye movements were
  absent in 38-42% of behaviours. This directional coherence between
  limbs, head and eye movements during rapid eye movement sleep
  behaviour disorder suggests that, when present, rapid eye movements
  imitate the scanning of the dream scene. Since the rapid eye movements
  are similar in subjects with and without rapid eye movement sleep
  behaviour disorder, this concordance can be extended to normal rapid
  eye movement sleep.

So,
1) Although behavioral movements and what the eyes are doing do not always seem to correlate:

  "Rapid eye movements were absent in 38-42% of behaviours."

When they do correlate at least during goal-oriented motor behavior, they do "imitate the 'scanning' of the dream scene." And that seems to happen about 82-90% of the time when they do this sort of behavior.

The math confuses me there as well though in contrast to how 38-42% of movements were absent of eye moments as well, but I believe the discretion is due to using the control vs. disordered group and lumping different group(s) into different calculated percentages.

Now also note above that when the goal-oriented behavior occurred and the eyes reflected this, they did so in the "same plane and direction."  This was peculiar as the word "plane" could mean horizontal or vertical plane I believe...it could also mean focal plane.  I wish they distinguished that better - I'm going to hypothesize it was just either the vertical or horizontal plane so that

In essence, a large part of the time people are acting out their behaviors when asleep the eyes correspond highly to the direction, but only to one plane, which means there wasn't really focal point - as you'd need to correspond to both the horizontal and vertical planes then.


Terror management theory: Is this a valid conclusion based on the conducted experiment?

Interestingly, the authors appear to have been aware of your concern:

  Given that the only difference between these groups involved a subject
  variable for which there could be preexisting differences in DTA, we
  included a third group of creationists who read a nonthreatening
  essay.

Since the evolutionist/anti-creation and creationist/control groups had very similar scores, there was seemingly no reason to suspect different baselines.  However, I agree with you that adding this third group may not have been sufficient to eliminate the potential for preexisting differences in DTA.

Dispositional DTA:

The study of preexisting differences in DTA baselines is relatively recent, and is called dispositional DTA.  This line of research is indeed showing significant variation in DTA between different groups in control conditions, variation in reaction to primes, and even variation in reaction to delay - see Mikulincer & Florian (2000) for examples of all 3.  So in light of this, I would not take it for granted that evolutionists and creationists should necessarily have the same dispositions.

Curiously, a study by Friedman and Rholes (2009) found religious fundamentalism to be negatively correlated with dispositional DTA (ie, greater fundamentalism = reduced effects on DTA).  Although fundamentalism is not the same measure as creationism, it does suggest that evolutionists may even have higher dispositional DTAs.

Ultimately however, a (not independent) partial replication of Study 5 is reported in Hayes (2011) Study 4, in which pro-evolution participants are subjected to an anti-evolution prime or the same control material used in Study 5, and the same DTA measure is used immediately thereafter.  While not having the creationist contrast, this experiment measures the evolutionists/control baseline missing from Study 5, as well as the effect of anti-evolution material on evolutionists.  I do note that the criteria for selecting participants was slightly different than Study 5, but not substantially different (n=93).

  DTA was higher in the Threat condition (M = 2.26, SD = 0.98) than in
  the Control condition (M = 1.68, SD = 0.96).

The results seem to indicate that the authors' assumptions about evolutionists' preexisting DTA may be valid.

Implicit primes:

The alternative explanation that reading about evolution might raise DTA in all participants due to the nature of the topic does not fit well within the context of existing DTA research.  Explicit primes increase DTA only after a delay or distraction.  For the immediate effects on DTA found in Study 5, an implicit prime must be used - ie, one that does not directly elicit thoughts of death.  This is presumably what Studies 1-4 establish.  Also see Steinman & Updegraff (2015) for a comprehensive review on the effects of explicit vs implicit primes on the need for delay.

In that context, had Study 5 not included evolutionists at all, the data gathered would have still been sufficient to conclude that reading about evolution increases DTA in creationists, substantiating the statement cited in your question.  The study's novel inclusion of a group with an opposing worldview adds some valuable information from which to consider additional conclusions.  That said, it would not be prudent in any case to make strong conclusions from a single, small, poorly controlled, unreplicated experiment.  In my view, this study has many flaws that I won't rant about here.  All I will say is:

Good on you for checking references, that is rare and commendable.
Good on you for applying critical thinking and questioning conclusions.

Re further references, the DTA hypothesis Wikipedia article contains many references to literature both supporting the cited statement and questioning the evidence for it.  Lots more on Google of course.


Can anticholinergics like benztropine be used to treat Catatonia?

Anticholinergics by themselves commonly have sedative effects. The reason you read about benztropine being used is that it has dopaminergic activity as well (in addition to anticholinergic activity). Specifically, benztropine and its derivatives are also dopamine reuptake inhibitors.
So from the perspective that benztropine is a dopamine reuptake inhibitor, i.e. a stimulant in the traditional sense, it would probably be a bad idea to use as a treatment for catatonia. If I remember right, its particular binding affinity is significant at the dopamine transporter.


Structural descriptions of neuronal networks are important for understanding brain dysfunctions; which dysfunctions, in particular?

Stam et al. have carried out a functional connectivity study in patients with Alzheimer's Disease. I don't know if that answers your question at all. Connectomics is just starting to kick off. It's far from certain that they it will end up being a key player in functional neuropathology in the coming decades, but it's one out of many promising new avenues of research.


What is the appropriate action when using poorly worded scales from previous literature?

If you change the items in a questionnaire, you have a different questionnaire. All the psychometric properties such as reliability or validity and the normative data no longer apply. You need to be able to compare your measurement to a normative sample to receive a meaningful measurement. If you change a questionnaire, you have to test it against your construct, calculate its reliability etc., and normalize it over a large representative sample. Otherwise any conclusions you draw from your experiments will be at best tentative and potentially false.

The meaning of a questionnaire item is not the literal meaning you make of that "sentence", but the relation that the behavior of answering this item has with other behavior that you know represents your construct. For example, the item "Weeds should be eradicated because they inhibit the full development of useful and ornamental plants." is from a questionnaire on environmental attitudes (Milfont & Duckitt, 2004) and measures "necessity of development" (NoD). If a significant number of your sample answer "yes" to the question about weeds, and they also rate high in NoD in a valid NoD task, then this item can be used to measure NoD. If you change the words, this correlation might no longer hold.

Milfont, T. L., & Duckitt, J. (2004). The structure of environmental attitudes: A first- and second-order confirmatory factor analysis. Journal of Environmental Psychology, 24, 289–303. Available online at http://gip.uniovi.es/gdiyad/docume/arti_jep01.pdf.


What are the standard mental health tests that are available online?

There's no "standard" on-line test for mood disorders. The only standard one is [semi-]structured evaluation (e.g. SCID-5) by a mental health professional.

With that disclaimer aside, there are some screening tools designed to be self-rated, e.g.

mania

MDQ, e.g. free as PDF/paper form at SAMHSA
a patient version of YMRS is also available: e.g. on psychology-tools.com although Wikipeida says it has an high false positive rate in younger people.
Altman Self-Rating Mania Scale e.g. also on psychology-tools.com.

depression and anxiety

PHQ a suite of tests developed by Pfizer, officially avaialble at https://www.phqscreeners.com/ There are different tests actually for depression and generalized anxiety; PHQ-9 is for depression; GAD-7 for the latter). They can also be found elsewhere, e.g. GAD-7 on SAMHSA or PHQ-9 on USPSTF; psychology-tools.com has both of them: phq-9 there, gad-7
CES-D for depresion found on http://cesd-r.com/ but also elsewhere (older version).
Zung Self-Rating Depression Scale e.g. on psychology-tools.com and Zung Self-Rating Anxiety Scale in the same place.
for anxiety there exist more specialized tests/screeners, depending on the kind suspected, e.g. social anxiety or phobias, but I don't want to go into a full list. See resources at the end of the answer if you're looking for those.

And here's a more extended disclaimer from one of those, which applies to all:

  The BDI suffers from the same problems as other self-report inventories, in that scores can be easily exaggerated or minimized by the person completing them. Like all questionnaires, the way the instrument is administered can have an effect on the final score. If a patient is asked to fill out the form in front of other people in a clinical environment, for instance, social expectations have been shown to elicit a different response compared to administration via a postal survey.

and from another (PHQ page actually):

  The influence of these biases can mitigated by following up with a structured or semi-structured interview, the gold standard for diagnostic assessment.

There's a longer list of tests on Wikipedia, not all of which might be on-line presently. https://www.outcometracker.org/library/ is an alternative list of printed questionnaires; not sure how long it will be there.  Also these are not all designed to be self-rated; the instruction at top of which page will give clue in that respect. https://psychology-tools.com/ is the most on-line-oriented of these collections.


Short answer, which is one of many:

One interesting hypothesis about this is the "reward hijacking" model. Essentially, when somebody becomes addicted their reward circuits become hypersensitive to drug-related cues and lack sensitivity to other rewards. Specifically, areas like their orbitofrontal cortex, which has to do with representing reward, and their ventral striatum, which has to do with dopamine and motivation, start to function strangely. So even when they replace the drug with new habits they still display heightened sensitivity to the drug. See Wrase et al, 2007 for one of many imaging studies on this. There are many neurobiological theories that explain why the reward sensitization occurs in response to addictive drugs.

The way this translates to function is that drugs appeal more and more to somebody with an addiction, while alternative habits appeal less and less. This contributes to the very high relapse rate. Interestingly, deep brain stimulation of the ventral striatum has helped curb alcohol cravings for some alcoholics. (See Knapp 2009 for rats, and Muller 2016 for a pilot study in humans.)

I hope this helps! The question you're asking is a very broad one, so you have a wide range of answers to explore.

Wrase, J., Schlagenhauf, F., Kienast, T., Wüstenberg, T., Bermpohl, F., Kahnt, T., ... & Heinz, A. (2007). Dysfunction of reward processing correlates with alcohol craving in detoxified alcoholics. Neuroimage, 35(2), 787-794.

Knapp, C. M., Tozier, L., Pak, A., Ciraulo, D. A., & Kornetsky, C. (2009). Deep brain stimulation of the nucleus accumbens reduces ethanol consumption in rats. Pharmacology Biochemistry and Behavior, 92(3), 474-479.

Müller, U. J., Sturm, V., Voges, J., Heinze, H. J., Galazky, I., Büntjen, L., ... & Bogerts, B. (2016). Nucleus Accumbens Deep Brain Stimulation for Alcohol Addiction–Safety and Clinical Long-term Results of a Pilot Trial. Pharmacopsychiatry, 49(04), 170-173.


How likely is it that rate-of-test-taking impacts on WM tests?

According to "The neuroscience of working memory capacity and training" by Christos Constantinidis & Torkel Klingberg asserts that training can increase WM capacity, however this does not translate into better reasoning power:

  Ongoing research  aims to elucidate the extent to which the
  improvements  also translate to various other abilities, such as
  academic  abilities, that statistically correlate with WM capacity.
  Indeed, transfer to reasoning ability has been reported to  be small,
  with inconsistent findings.

However, transfers to attention seem more promising:

  More-encouraging  transfer results are seen for attention: several
  randomized,  controlled trials, some of them including children with
  ADHD, show decreases in inattentive behaviour in every-day life after
  WM training

They cite to support this:

  Klingberg, T. et al.  Computerized training of working  memory in
  children with ADHD — a randomized,  controlled trial.  J. Am. Acad.
  Child Adolesc. Psychiatry  44 , 177–186 (2005)

  Brehmer, Y., Westerberg, H. & Backman, L. Working- memory training in
  younger and older adults: training  gains, transfer, and maintenance.
  Front. Hum. Neurosci.  6 , 63 (2012).

  Green, C. T. et al.  Will working memory training  generalize to
  improve off-task behavior in children with
  attention-deficit/hyperactivity disorder?  Neurotherapeutics 9 ,
  639–648 (2012).

  Bigorra, A., Garolera, M., Guijarro, S. & Hervas, A.  Long-term
  far-transfer effects of working memory  training in children with
  ADHD: a randomized  controlled trial.  Eur. Child Adolesc. Psychiatry
  http:// dx.doi.org/
  10.1007/s00787-015-0804-3  (2015).

  Conklin, H. M. et al.  Computerized cognitive training  for
  amelioration of cognitive late effects among  childhood cancer
  survivors: a randomized controlled  trial.  J. Clin. Oncol.  33 ,
  3894–3902 (2015)


Does evidence support Maslow's Hierarchy of Needs?

Mahmoud A. Wahba, Lawrence G. Bridwell, Maslow reconsidered: A review of research on the need hierarchy theory (1976), or a free pdf scan here

Its abstract says:

  The uncritical acceptance of Maslow's need hierarchy theory despite the lack of empirical evidence is discussed and the need for a review of recent empirical evidence is emphasized. A review of ten factor-analytic and three ranking studies testing Maslow's theory showed only partial support for the concept of need hierarchy. A large number of cross-sectional studies showed no clear evidence for Maslow's deprivation/domination proposition except with regard to self-actualization. Longitudinal studies testing Maslow's gratification/activation proposition showed no support, and the limited support received from cross-sectional studies is questionable due to numerous measurement problems. The difficulties with testing the theory are discussed and the conceptual, methodological, and measurement problems of the studies reviewed are detailed. The implications of the findings and future directions for research are outlined.


How can a human carry out a mass shooting whilst remaining calm?

There may be less apparent contradiction if the shooter doesn't consider those behaviors as immoral, disgusting, etc. Consider a soldier in wartime: they might sometimes appear calm as well.

If you look at the stated justifications for mass shootings, they often have a specific purpose and apparently see moral reasons for their actions. Broadly speaking, people differ widely in what they consider ethical or moral. One person's virtue is another's sin. There are shared features between many ethical traditions, such as a prohibition against murder, but murder and war remain common. There is no need for a specific physiological fault like a brain injury or a particular genetic variant for humans to disagree wildly on what actions are appropriate. It's famously difficult to sympathize with the moral intuitions of other people; see for example https://en.wikipedia.org/wiki/Moral_foundations_theory. Instead of universal reasons, we generally have the strong feeling that something is right or wrong, and then we construct reasons.


How can neuronal networks with local learning rules predict their future inputs?

see Lisman, J. E. and Otmakhova, N. A. (2001), Storage, recall, and novelty detection of sequences by the hippocampus: Elaborating on the SOCRATIC model to account for normal and aberrant effects of dopamine. Hippocampus, 11: 551–568. doi: 10.1002/hipo.1071: http://wwww.bio.brandeis.edu/lismanlab/pdf/socratic.pdf for one proposed mechanism.

in short, local learning rules can develop connections between items that occur sequentially.  if you have one network that pattern completes (i.e. identifies) the input, you can pass that identification to a second network which learns temporal associations between items.


How to pursue a Psychology career in academia from non-Psychology background?

Psychology is a very broad field. While some subfields require a license  (e.g., clinical psychology), a huge number of undergraduate fields can prepare you for academic related work, teaching and research. I know individuals with Bachelors in Math, Physics, BME, EE, CS, MechE, Statistics, Neuroscience, Biology, Chemistry, Sociology, Speech and Hearing, Music, and Education who have either gone on to get a PhD in Psychology or a faculty position in a Psychology Department.

As a former faculty member in a Psychology department with an engineering background, I cannot think of any major I would turn away out of hand for a PhD position.


Does it take more cognitive effort to tell the time when reading a digital clock instead of analog?

The answer depends of course on the factors mentioned in the comments; however, one important factor to consider is the intended purpose of reading the clock.

An analog clock presents information in graphical form, in a similar way to how a pie chart might present information. This is opposed to a digital clock, which presents symbolic information, in a similar way to what might be found in a table of values.

Cognitive Fit Theory
According to research by Iris Vessey (cognitive fit theory,) the least cognitive effort will be required when the presentation format of the data matches the intended cognitive use. Vessey's research shows that symoblic information, such as that presented by a digital clock, is best when one needs to evaluate a single number (for example, to answer the question "What time is it now?").  On the other hand, graphical information, such as that presented by the analog clock, is best when one desires to make a comparison between different numbers (for example, to answer the question "How much time has elapsed?").

Therefore, your example in the question (how much time has elapsed past the hour) is best answered with an analog clock, whereas if I want to know what time my alarm is set for, the digital clock on my cell phone is a better format.

I might argue that the analog clock format does not do a good job presenting the graphical information, but that is best saved for another paper.


Which morals are universal across the species?

This is a partial answer to your question.

According to "Only Humans Have Morality, Not Animals", (Guldberg, 2011), claims that morality is something unique to humans.  Basically the author concludes with:

  Human beings are not perfect and never will be, but we are special and unique among the animal kingdom. We are capable of making judgements about our own and other people's behaviour, and have the capacity consciously to change the way we behave and society as whole.

A key argument made in the article is that there is a great difference between instinctual connections and actions and human empathy and morality.

Further, according to the article "Is Morality Innate?" (Prinz), proposes that:

  Morality is a byproduct—accidental or invented—of faculties that evolved for other
  purposes.

and proposes a somewhat negative, yet true conclusion:

  Nonhuman animals are often
  violent, but their potential for bad behavior may be lower than ours. Because we can
  reason, there is a great risk that human beings will recognize countless opportunities to
  take advantage of our fellows.

Essentially, it seems that perhaps morality is unique to humans owing to our abilities to reflect, reason as well as react.


How does a language deprived person think?

Probably in "visuospatial thinking".

Thinking modalities:

I assume here that you are asking about the modality of thinking.  This is not a well studied area in cognitive science.  I believe the question stems from an underlying assumption that most people think in their primary language (or possibly switch if they are fully bilingual).  This was certainly the view early on in the history of psychology.

In fact, the earliest theories about the development of "inner speech" suggested that it develops around age 8 when self-talk or "private speech" - basically young children talk to themselves a lot - is gradually replaced by inner speech (children are often encouraged to use their "inside voice").  This seems to imply that prior to this age, children don't have the "internal monologue" that adults are familiar with.

Later on, "visual thinking" was examined, primarily in the context of determining and catering to "learning styles".  In this context, several different kinds of visuospatial thinking styles have been considered, including picture thinking, shapes and transformation, and spatio-temporal thinking.  The possibility of kinesthetic or tactile learning was also identified. The concept of learning styles is largely discredited now, though it did call attention to the special needs of children with learning disabilities such as dyslexia and autism, where visual thinking may be more common.

The more modern view is that while people may have a dominant mode of thinking, they switch between modalities depending on context - such as the nature of a problem that they are trying to solve.  In general, we can only really learn about thinking modalities from self-reports of introspection, which is not considered to be very reliable.  To improve reliability and validity, a formalized scale should be developed - this has been attempted in the past, but is not in common use.

Empirical evidence:

To learn more about what pre-verbal thinking might be like, we could try asking children how they thought prior to developing inner speech, but this requires a skill called "metacognition" - the ability to think about thinking - that is not well developed in children.  It also seems that adults no longer remember what their pre-verbal thinking was like.

Feral children do seem like a possible opportunity to get around this.  However, in practice, feral children are (thankfully) extremely uncommon, and are either discovered and taught language early enough, or in the very rare cases (case?) where it may be too late, we don't have a way to communicate to even ask the question.

A possibly better opportunity is deaf children.  Most deaf children are not born to deaf parents, and hence are not exposed to language (sign language) as early as hearing children.  In a few rare cases, deaf children learn sign language as their first language as late as adolescence.  However, even in these cases, it is unlikely that these children did not have prior exposure to at least some language concepts, as they communicate with their family and friends, and may learn to read, lip-read, and gesture.

Deaf people often report thinking visually - in sign, print, or lip-reading for example.  Blind people to some degree, and deafblind people to a greater degree report some tactile thinking - presumably if they use braille or a tactile sign language.  Thinking modality appears to match sensory modality and perhaps have a preference for language modality, but may still switch modalities depending on context.  Apart from these indirect hints however, we don't have much insight into the thinking of adults without language.

Language and thought:

Confounding matters further, there are also a variety of different theories about the relationship between language and thought that may have some relevance to the question.  For example, one influential theory suggests that language is essential for thought, that language shapes thought, and that thought without language is limited in that certain cognitive faculties cannot exist.  Empirical evidence supports some interpretations of this theory and not others.

Another approach suggests that thought has its own "language" - ie, that people think in a private language that is independent of their language acquisition - variously called "mentalese", "i-language", or the "universal grammar".  Although this view has much support in linguistics, it has also met some criticism.

Yet another view (tied to the private speech theory mentioned above) suggests that thought is language - a form of intrapersonal communication that is used for deliberation, speech rehearsal, and possibly stress relief for example.  Other scholars emphasize the relationship between thought and perception, suggesting that thought modality should reflect sensory modality.

The bottom line is that even the definitions of language and thought are under question, so it's difficult to say whether people without language think in any way comparable to verbal thought, or whether they think the same way that we do without the accompanying narrative, or whether they think in a way that matches their (visuospatial) perceptual experience.


Is Maslow's hierarchy of needs really accurate at labeling sex as a physiological "need"?

This is a trickier multi-part question to adjudicate than you might think.

Is Sex A "Need" (Physiological or Otherwise)?

Definitions of "Needs", "Motives", etc., are dime-a-dozen. Though I don't necessarily agree with all the ingredients, I like how well explicated the criteria by Baumeister and Leary (1995) are, according to whom a fundamental need should:

produce effects readily under all but adverse conditions
have affective consequences
direct cognitive processing
lead to ill effects (such as on health or adjustment) when thwarted
elicit goal-oriented behavior designed to satisfy it (subject to motivational patterns such as object substitutability and satiation)
be universal in the sense of applying to all people
not be derivative of other motives
affect a broad variety of behaviors
have implications that go beyond immediate psychological functioning

To me, sex meets several of these criteria (e.g., it clearly directs affect and cognition, is universal-ish [asexuality notwithinstanding, a point a return to in a moment], but is questionable for a couple that, in my opinion, are crucial for bona fide "need"-status.

First, it is not clear that thwarting of sexual desire leads to ill effects. Here, Baumeister and Leary (1995) are referring to big-ticket consequences, not affective tiddlywinks. In their words:

  A motivation can be considered to be fundamental only if health, adjustment, or well-being requires that it be satisfied. Also, motivations can be sorted into wants and needs, the difference being in the scope of ill effects that follow from nonsatisfaction: Unsatisfied needs should lead to pathology (medical, psychological, or behavioral), unlike unsatisfied wants. (p. 498)

And while it is true that sexual frequency is positively associated with well-being, the benefits eventually "level out" (Muise et al., 2016), and there is not a clear link between a "lack" of sex and more serious medical or psychological pathology. And when one considers the occasional medical/mental health costs of engaging in sex (e.g., Meier, 2007), or the considerable efforts people go to to sometimes conceal their sexual activity (e.g., Olson & García-Moreno, 2007), it's not at all clear that engaging in sex is always a plus for mental or physical well-being.

It's also debatable whether the "need" for sex is it's own drive, or rather, derivative of other bona fide need-status motives. Take Meston and Buss's (2007) work on identifying reasons (over 250!) people give for engaging in sex. And when you look at their list of Top 50 endorsed reasons (many of which are similar for men and women), many of them seems to be about other drives/motives that may be more fundamental (e.g., social, relational, growth-oriented, etc.,). This issue spills over into the "ill effects" discussion as well; even in situations where a lack of sex co-occurs with more serious pathology, it's difficult to decisively isolate the pathology as a byproduct of the lack of sex, specifically, as opposed to deficits in other fundamental needs (e.g., belonging/security).

Tl;dr: sex is probably better thought of as a strong, widely-shared "want", rather than a bona fide "need"

Need-Status Notwithstanding, Is Sexual Desire Primarily Physiological?

Sexual desire is surely physiologically driven to some non-zero extent. The association between physiological indicators (e.g., hormones like testosterone) and sexuality, however, is often a lot more complicated than the neat linear stories we like to tell (e.g., "Men have stronger sexual desire because they have more testosterone!"). An exhaustive review of this complexity would be overwhelming, but the work by Sari van Anders (e.g., her 2012 review + study) would be a good place to start. There's also plenty of evidence for non-physiological contributors to feelings of desire, such as those that are relational (for reviews, see Mikulincer & Shaver, 2007,  Muise et al., 2018, to name a few).

Tl;dr: Sexual desire (need or not) is determined by both physiological and non-physiological factors alike

Need- and Physiological-Status Notwithstanding, Is Sex Needed for Self-Actualization?

Probably not, but the state of the world makes it very difficult to cleanly appraise this. Looking at self-actualization in asexually-idenfitying folks would initially seem the clearest route to testing this claim, and if you took note of some of the mental health challenged faced by that community (e.g., Yule et al., 2013), you might be tempted to conclude that there was evidence that sex is needed for self-actualization. The problem, however, is that there is pretty clear evidence that asexually-identifying individuals are targets of prejudice and discrimination (e.g., MacInnis & Hodson, 2002), and so just as--if not more--likely that their mental health challenges are the result of chronic stigmatization of their identities/sexual orientation (which is currently the way that experts like Yule and Brotto and their colleagues conceptualize asexuality vs. alternatives conceptualizations [e.g., a sexual dysfunction], based on their research, see Brotto et al., 2014; Brotto & Yule, 2017)

tl;dr: Evidence currently challenges the construal of asexuality as a disorder, and mental health problems in asexual communities cannot be divorced from the broader social context in which these communities are routinely stigmatized--all of which is indirect evidence that it is premature (if not entirely mistaken) to argue that sex is needed for self-actualization

References

Baumeister, R. F., & Leary, M. R. (1995). The need to belong: desire for interpersonal attachments as a fundamental human motivation. Psychological Bulletin, 117(3), 497-529.

Brotto, L. A., & Yule, M. (2017). Asexuality: Sexual orientation, paraphilia, sexual dysfunction, or none of the above?. Archives of Sexual Behavior, 46(3), 619-627.

Brotto, L. A., Yule, M. A., & Gorzalka, B. B. (2015). Asexuality: An extreme variant of sexual desire disorder?. The Journal of Sexual Medicine, 12(3), 646-660.

MacInnis, C. C., & Hodson, G. (2012). Intergroup bias toward “Group X”: Evidence of prejudice, dehumanization, avoidance, and discrimination against asexuals. Group Processes & Intergroup Relations, 15(6), 725-743.

Meier, A. M. (2007). Adolescent first sex and subsequent mental health. American Journal of Sociology, 112(6), 1811-1847.

Meston, C. M., & Buss, D. M. (2007). Why humans have sex. Archives of Sexual Behavior, 36(4), 477-507.

Mikulincer, M., & Shaver, P. R. (2007). Attachment in adulthood: Structure, dynamics, and change. New York, NY: Guilford Press.

Muise, A., Maxwell, J. A., & Impett, E. A. (2018). What theories and methods from relationship research can contribute to sex research. The Journal of Sex Research, 55(4-5), 540-562.

Muise, A., Schimmack, U., & Impett, E. A. (2016). Sexual frequency predicts greater well-being, but more is not always better. Social Psychological and Personality Science, 7(4), 295-302.

Olson, R. M., & García-Moreno, C. (2017). Virginity testing: a systematic review. Reproductive Health, 14(1), 61.

van Anders, S. M. (2012). Testosterone and sexual desire in healthy women and men. Archives of Sexual Behavior, 41(6), 1471-1484.

Yule, M. A., Brotto, L. A., & Gorzalka, B. B. (2013). Mental health and interpersonal functioning in self-identified asexual men and women. Psychology & Sexuality, 4(2), 136-151.


Why do brains oscillate within specific frequency ranges?

What are brain oscillations?

I think it is first important to recognize what brain oscillations refer to: they are small, somewhat localized fluctuations in voltage that are often measured by EEG (electroencephalogram), though they can also be measured inside the skull or inside the brain.

Most of these oscillations are also seen in the membrane potentials of individual neurons. Fast oscillations, like gamma oscillations, can also be seen in membrane potentials but are best associated with spiking activity. The cause of the skull-measured oscillations is the coordinated activity of many many neurons acting in concert.

Why certain frequencies?

Many brain oscillations are created by coupling of excitation and inhibition. The gamma oscillation, for example, is most associated with interactions between excitatory neurons and particular inhibitory neurons called fast-spiking and/or parvalbumin-positive cells. The frequency of the gamma oscillation is due to the time constants and conduction times between the reciprocal circuitry between excitatory cells and fast-spiking cells. If you were to maintain the same activity, but change these time constants, the gamma frequency would change.

Other frequencies may be slower because they involve circuits over a longer distance, such as interactions between thalamus and cortex.

Some of the slowest oscillations, called delta oscillations, come about due to long periods of high and low activity, sometimes called "UP" and "DOWN" states or "ON" and "OFF" periods. Oscillations are often nested within each other, referred to as cross-frequency coupling, or more specifically often phase-amplitude coupling. During the "DOWN" phase of a slow delta oscillation, amplitude in higher frequencies is low because there is little spiking activity; during the "UP" phase the amplitude in higher frequencies increases.

What is the purpose of brain oscillations?

We don't know. There are many theories that certain oscillations are important for certain functions, but most of the evidence for these theories is either theoretical or correlational. In very general terms, slower oscillations tend to be associated with rest whereas higher frequency oscillations are associated with active processing.

For example, gamma oscillations are possibly involved in 'binding' different types of information across different cortical areas: synchronous gamma activity could be the way a brain region primarily processing sounds can associate that information with a brain region primarily processing the visual object producing that sound.

It is also possible that many oscillations are simply epiphenomena: they result from particular types of activity, rather than being the cause of certain functions. Gamma, for example, seems to increase simply whenever overall neuronal activity increases.

The problem is that there is really no way to study an oscillation independent of the rest of the brain activity: anything that would impact an oscillation is necessarily going to be influencing neural activity in other ways.

Probably the best evidence for an actual functional role of brain oscillations is in phase coding in the theta band (and associated gamma oscillations), best-studied in the navigational networks of the hippocampus in rodents. The timing of spikes relative to the phase of an ongoing oscillation can carry more information than the spikes in solitude: the oscillation provides a reference signal.

What happens if brain oscillations were to magically change?

It sort of depends on what the mechanism of the magic is: you could certainly change oscillations by doing extreme things like stopping all neuronal activity: that would go quite badly. Epileptic seizures are a more naturally-occurring but similarly damaging example of oscillations gone wrong. Absence epilepsy is of particular interest since the mechanisms are a bit more complex than grand mal seizures.

However, you can also "magically" change oscillations as simply as closing your eyes: increases in alpha power are well-known to occur when you just briefly close your eyes. Changes in brain oscillations are a normal part of brain function: oscillations are very different during sleep and wake, for example. The amplitude and frequency of certain oscillations can be modulated by how alert or attentive you are. Depending on the specific type, anesthetic agents tend to produce brain oscillations that are at least qualitatively similar to sleep.

There are also correlations between different oscillation patterns and psychological diseases or disorders. People with schizophrenia show different patterns of gamma activity than non-schizophrenics, for example. However, it is unclear if it makes sense to think about oscillation differences as causal versus as a symptom. Autism, for example, is associated with reduced synchrony over long distances in the brain. This reduced synchrony is thought to be due to differences in connectivity. Depending on your perspective, you could highlight the change in synchrony as an important feature, or you could treat it as a symptom of the underlying difference in connectivity.

Summary, Conclusions, and Caution

Brain oscillations are a key window to understanding nervous function, especially in humans where they can be recorded more easily than any other type of neuronal activity. However, we need to be careful about thinking about oscillations as specific entities.

Oscillations in one frequency band could come about by completely different mechanisms in different situations. Changes in oscillations measured outside the skull can reflect changes in synchrony over long distances rather than changes in local oscillatory activity in individual columns. As an analogy, consider ripples in a pond: the amplitude of the ripples might tell you a bit about the size of an object that disrupted the water's surface, but if that's all you have you can't know whether the object came initially from above or below the surface, whether it was a bird, fish, or rock, etc.

Many papers are published that tie oscillations to certain states, conditions, or diseases, and these can be pathways to understanding but they are unlikely to directly identify underlying mechanisms.

For the references below, I've tried to use review articles where possible that are fairly digestible without too much additional information. In particular, I bolded a couple that I think are great starting points.

References:

Bazhenov, M., Timofeev, I., Steriade, M., & Sejnowski, T. J. (2002). Model of thalamocortical slow-wave sleep oscillations and transitions to activated states. Journal of neuroscience, 22(19), 8691-8704.

Buzsáki, G., & Wang, X. J. (2012). Mechanisms of gamma oscillations. Annual review of neuroscience, 35, 203-225.

Cohen, M. X., Elger, C. E., & Fell, J. (2008). Oscillatory activity and phase–amplitude coupling in the human medial frontal cortex during decision making. Journal of cognitive neuroscience, 21(2), 390-402.

Goldman, R. I., Stern, J. M., Engel Jr, J., & Cohen, M. S. (2002). Simultaneous EEG and fMRI of the alpha rhythm. Neuroreport, 13(18), 2487.

Harris, K. D., Henze, D. A., Hirase, H., Leinekugel, X., Dragoi, G., Czurkó, A., & Buzsáki, G. (2002). Spike train dynamics predicts theta-related phase precession in hippocampal pyramidal cells. Nature, 417(6890), 738.

Hasselmo, M. E., Bodelón, C., & Wyble, B. P. (2002). A proposed function for hippocampal theta rhythm: separate phases of encoding and retrieval enhance reversal of prior learning. Neural computation, 14(4), 793-817.

Kwon, J. S., O'donnell, B. F., Wallenstein, G. V., Greene, R. W., Hirayasu, Y., Nestor, P. G., ... & McCarley, R. W. (1999). Gamma frequency–range abnormalities to auditory stimulation in schizophrenia. Archives of general psychiatry, 56(11), 1001-1005.

Lisman, J. E., & Jensen, O. (2013). The theta-gamma neural code. Neuron, 77(6), 1002-1016.

Steriade, M., McCormick, D. A., & Sejnowski, T. J. (1993). Thalamocortical oscillations in the sleeping and aroused brain. Science, 262(5134), 679-685.

Tallon-Baudry, C., & Bertrand, O. (1999). Oscillatory gamma activity in humans and its role in object representation. Trends in cognitive sciences, 3(4), 151-162.

Uhlhaas, P. J., & Singer, W. (2006). Neural synchrony in brain disorders: relevance for cognitive dysfunctions and pathophysiology. Neuron, 52(1), 155-168.


Post alcoholic depression and mental health

There have been several studies that show links between binge drinking and depressive symptoms.

However, it's hard to make any strong statement about a particular level of drinking, because drinking behaviors are so variable, and also to quantify the "level" of the effect on depression, because depression symptoms are also variable.

Finally, it's hard to make causal statements because alcohol use could be a coping mechanism for depressive symptoms rather than causal: many studies approach the relationship from the opposite direction, implying the depressive symptoms are causal for alcohol use.

I've pulled a few papers and can discuss them briefly, though this is not a comprehensive review.

Paljärvi, T., Koskenvuo, M., Poikolainen, K., Kauhanen, J., Sillanmäki, L., & Mäkelä, P. (2009). Binge drinking and depressive symptoms: a 5‐year population‐based cohort study. Addiction, 104(7), 1168-1178.

  "This study found a positive association between baseline binge drinking and depressive symptoms 5 years later." "Binge drinking was related to symptoms of depression independently of average intake."

I'd note that this study shows some truly massive relationships, odds ratios of 4-9 for some subcategories; it also seems to have some potential for demonstrating a causal role when they are comparing time 1 drinking to time 2 depression, though still not conclusive.

I think this study gets closest to testing what your question is asking, because it explicitly includes measures of hangovers/binging that are missing from some other studies. It also shows a dose-dependent relationship where more frequent binge drinking is associated with more depressive symptoms, but the relationship is still present even at lower levels of binge drinking compared to non-binge drinking.

Grant, B. F., & Harford, T. C. (1995). Comorbidity between DSM-IV alcohol use disorders and major depression: results of a national survey. Drug and alcohol dependence, 39(3), 197-206.

  "Virtually all odds ratios were significantly greater than 1.0, demonstrating that comorbidity of alcohol use disorders and major depression is pervasive in the general population. The magnitude of the association remained stable across the three time frames but diagnostic and subgroup variations in comorbidity were noted. The association between alcohol dependence and major depression was greater than the association between abuse and major depression and the association between alcohol abuse and major depression was consistently greater for females and blacks, compared to their male and non-black counterparts."

This studied focused on older adults, age 57+.

Hill, K. G., White, H. R., Chung, I. J., Hawkins, J. D., & Catalano, R. F. (2000). Early adult outcomes of adolescent binge drinking: person‐and variable‐centered analyses of binge drinking trajectories. Alcoholism: Clinical and Experimental Research, 24(6), 892-901.

  "Adolescent alcohol use did not predict educational attain-ment, crime, family roles, or depression."

This study patterned adolescent (<18yo) drinking behaviors into several categories and showed relationships between alcohol use and several other outcomes, but not depression, at age 21.

Okoro, C. A., Brewer, R. D., Naimi, T. S., Moriarty, D. G., Giles, W. H., & Mokdad, A. H. (2004). Binge drinking and health-related quality of life: do popular perceptions match reality?. American journal of preventive medicine, 26(3), 230-233.

  "After adjusting for confounding factors, frequent binge drinkers were more likely than non-binge drinkers to experience ≥14 unhealthy days (physical or mental) in the past month (adjusted odds ratio [AOR]=1.39, 95% confidence interval [CI]=1.24–1.56), primarily because they had more mentally unhealthy days than non-binge drinkers (AOR=1.52, 95% CI=1.32–1.75)."

This study combines depressive symptoms with other categories of mental/physical health to assay general quality of life.

And finally I'll end with one meta-analysis:

Boden, J. M., & Fergusson, D. M. (2011). Alcohol and depression. Addiction, 106(5), 906-914.

  The current state of the literature suggests a causal linkage between alcohol use disorders and major depression, such that increasing involvement with alcohol increases risk of depression.

They seem to make some arguments for a causal alcohol use -> depression relationship, though I haven't read closely enough to decide whether I am convinced by those arguments.


Not a real explanation of why writing or cities appeared where they appeared but by that time humans had already spread to many parts of the world so I am not sure there is any particular need to explain why they did not appear in southern Africa, specifically.

Also, the “cradle of humankind” in Gauteng is a large source of hominin fossils (possibly for reasons that have more to do with their preservation than anything else), not of homo sapiens sapiens or anatomically modern humans. We are not talking about the same periods at all (millions of years before present vs. 200 000 years for homo sapiens sapiens and 6000 years for writing).


One of the publications on engaged learning that you provide (the "Engaged Learning: Are We All on the Same Page?" one) seems to answer your question (here is a fuller version of it). The quote that addresses your question is given below (bold added).

Many of these concepts of engagement cover ground similar to that covered by initiatives in higher education known by other names:

Engagement with the learning process is similar to active learning.
Engagement with the object of study is similar to experiential learning.
Engagement with contexts generally is similar to multidisciplinary learning.
Engagement with social and civic contexts is similar to service learning.

Thus, the engagement seems to encompass active learning in that active learning is the piece of engagement related to the learning process.


Why have historically most inventors been men?

A large part is cultural, because, until recently, the people with the best education and most of the money have been men.

Sexism kept women out of schools for a long time. It also kept pushing women into what were perceived to be more appropriate studies (nothing technical) when they were allowed into schools.

Have a look at the sexism page at Wikipedia.

There is some evidence, as discussed in this Wikipedia article, there are differences between male and female human brains. Especially in spacial temporal reasoning regions and the language areas. As well as Wikipedia, in the book Cognitive Neuroscience: The Biology of The Mind[1], the authors state that human females are less good at the maths people are taught at school, which is linked to spacial reasoning.

However, this disparity is across the species as a whole. It is an average. Inventors, by their very nature, are not average. Thus the neurological differences are not the main contributing factor to why you see more men in your list than women.

Also, have a look at confirmation bias.

[1] Cognitive Neuroscience: The Biology of The Mind, 2nd ed. M. S. Gazzaniga, R. B. Ivry, G. R. Mangun. Page 602


For a general discussion of neural correlates of music perception, check out the review by Koelsch et al (2005).

Menon et al (2002) provide a starting point for learning about neural correlates of timbre processing. I quote the abstract. But have a look at the article for more info

  Timbre is a major structuring force in music and one of the most
  important and ecologically relevant features of auditory events. We
  used sound stimuli selected on the basis of previous
  psychophysiological studies to investigate the neural correlates of
  timbre perception. Our results indicate that both the left and right
  hemispheres are involved in timbre processing, challenging the
  conventional notion that the elementary attributes of musical
  perception are predominantly lateralized to the right hemisphere.
  Signiﬁcant timbre-related brain activation was found in well-de- ﬁned
  regions of posterior Heschl’s gyrus and superior temporal sulcus,
  extending into the circular insular sulcus. Although the extent of
  activation was not signiﬁcantly different between left and right
  hemispheres, temporal lobe activations were signiﬁcantly posterior in
  the left, compared to the right, hemisphere, suggesting a functional
  asymmetry in their respective contributions to timbre processing. The
  implications of our ﬁndings for music processing in particular and
  auditory processing in general are discussed.

Halpern et al (2004) provide another relevant study:

  The generality of findings implicating secondary auditory areas in
  auditory imagery was tested by using a timbre imagery task with fMRI.
  Another aim was to test whether activity in supplementary motor area
  (SMA) seen in prior studies might have been related to
  subvocalization. Participants with moderate musical background were
  scanned while making similarity judgments about the timbre of heard or
  imagined musical instrument sounds. The critical control condition was
  a visual imagery task. The pattern of judgments in perceived and
  imagined conditions was similar, suggesting that perception and
  imagery access similar cognitive representations of timbre. As
  expected, judgments of heard timbres, relative to the visual imagery
  control, activated primary and secondary auditory areas with some
  right-sided asymmetry. Timbre imagery also activated secondary
  auditory areas relative to the visual imagery control, although less
  strongly, in accord with previous data. Significant overlap was
  observed in these regions between perceptual and imagery conditions.
  Because the visual control task resulted in deactivation of auditory
  areas relative to a silent baseline, we interpret the timbre imagery
  effect as a reversal of that deactivation. Despite the lack of an
  obvious subvocalization component to timbre imagery, some activity in
  SMA was observed, suggesting that SMA may have a more general role in
  imagery beyond any motor component.

References

Menon, V., Levitin, D. J., Smith, B. K., Lembke, A., Krasnow, B. D., Glazer, D., ... & McAdams, S. (2002). Neural correlates of timbre change in harmonic sounds. Neuroimage, 17(4), 1742-1754. PDF
Halpern, A. R., Zatorre, R. J., Bouffard, M., & Johnson, J. A. (2004). Behavioral and neural correlates of perceived and imagined musical timbre. Neuropsychologia, 42(9), 1281-1292. PDF
Koelsch, S., & Siebel, W. A. (2005). Towards a neural basis of music perception. Trends in cognitive sciences, 9(12), 578-584. Koelsch, S., & Siebel, W. A. (2005). Towards a neural basis of music perception. Trends in cognitive sciences, 9(12), 578-584. HTML


Is what psychologists define as subconsciousness proven in neuroscience and can the psychological subconsciousness be visualized by neuroscientists?

The vast majority of neural processes (and their associated mental processes) in the brain are subconscious (or unconscious), i.e. we are not consciously aware of them and cannot consciously control them. Yet, without these subconscious processes, we will not be able to live as we do now – we will have to spend an incredible amount of time and effort to consciously control all the processes that are naturally subconsciously controlled now. As a matter of fact, we will not be able to consciously do such tedious yet demanding tasks well, and we will die.

All neural processes except the final-stage sensory perception neural processes and the highest cognitive neural processes are subconscious. The subconscious neural processes are in all parts of the brain:

Brainstem and autonomic system. For example, neural processes that control breathing, heart contraction, pressure in the arterial and venous systems, body temperature, sleep-wake cycle, secretion of various body fluids (sweat, tear, saliva, gastric juice, etc.), secretion of various hormones, various reflexes (pupillary light and accommodation reflexes, optokinetic reflex, vestibulo-ocular reflex, etc .), homeostasis of various blood constituents, etc.
Cerebellum. For example, neural processes that control contraction & movement of hundreds of millions of muscle fibers of various agonist and antagonist muscles for balance and accuracy in walking, writing, speaking, playing various sports, playing various musical instruments, etc.
Deep cerebral nuclei. For example, neural processes that control the tone of your trunk muscles (when sitting, standing, walking, etc.), emotion (*1), formation, storing, and retrieval of memory (*2), etc.
Cerebral cortex. For example, neural processes that perform early-stage sensory perception (*3), early-stage language functions (*4), some stages of decision, some forms of thinking (*5), etc.

And, if you include spinal cord, the majority of their neural processes are subconscious too.

N.B.

*1. That's why we can't completely control our emotions at will: we can't get out of anger, sadness, depression, etc. or get into any emotion we want instantly at will, because they are partly controlled by subconscious neural processes. Also, we will not be able to have any emotion even if we try to if the subconscious neural processes (in the amygdala and other nuclei in the limbic system) for emotion are impaired (such as in various apathy disorders: Alzheimer’s disease, Parkinson’s disease, fronto-temporal dementia, etc.)

*2. That's why you can't memorize new events or recall past events, even if you try, if the subconscious neural processes (the hippocampus and other nuclei in the limbic system) that form, store, and retrieve memory are impaired.

*3. That's why we can't consciously see in colors (achromatopsia), can’t recognize familiar faces (prosopagnosia) (including one’s own face), or can't recognize what the object is (visual agnosia) if the subconscious processes that process color, object identification, or face identification are impaired.

*4.That's why we can't understand what people say even if we hear them clearly (sensory dysphasia) or can't understand what the text in the book means even if we see it clearly (alexia) if the subconscious neural processes that processes the meaning of the sound or of the image is impaired.

*5. See more details in the references below.

References.
General, basic information about unconscious processes in the brainstem, autonomic nervous system, cerebellum, and deep cerebral neuclei (basal ganglion, thalamus, amygdala, etc.) can be found easily by searching the internet.

Some of the more in-depth, interesting articles about this matter are as follows (and more references can be found inside these articles):

Bargh JA, Morsella E. The Unconscious Mind. Perspect Psychol Sci. 2008 Jan;3(1):73–79. DOI: 10.1111/j.1745-6916.2008.00064.x.
Dehanene S. Fathoming unconscious depths. In: Consciousness and the brain. Penguin Books. 2014. New York, New York, USA. ISBN 978-0-670-02543-5, 978-0-14-312626-3. p 47-88.
Dijksterhuis A. First neural evidence for the unconscious thought process. Soc Cogn Affect Neurosci. 2013 Dec; 8(8): 845–846. doi: 10.1093/scan/nst036.
Dijksterhuis A, Strick M. A Case for Thinking Without Consciousness. Perspect Psychol Sci. 2016 Jan;11(1):117-32. doi: 10.1177/1745691615615317.
Hallett M. Volitional control of movement: The physiology of free will. Clin Neurophysiol. 2007 Jun;118(6):1179–1192. DOI: 10.1016/j.clinph.2007.03.019 PMCID: PMC1950571 NIHMSID: NIHMS24077.
Horga G, Maia TV. Conscious and unconscious processes in cognitive control: A theoretical perspective and a novel empirical approach. Front Hum Neurosci. 2012; 6:199. doi: 10.3389/fnhum.2012.00199.