Do separate neural circuits express separate genes in the same type of brain matter? In other words, even though there may be two distinct neural circuits which process separate forms of information in the same type of brain matter (i.e. cerebral cortex processing language in one area and planning in another area) can gene expression differences be found between such distinct and separate neural circuits, despite being in the same type of brain matter?

So, I am revisiting your question as asked by community, and I discover I misunderstood it initially: you didn't say neurons process information, you said neural circuits do. And that distinct neural circuits process separate forms of information. Well, that is inexact. There are several types of neurons, adapted to create neural circuits able to process motor, sensory and a combination of the two. Here's a jolly picture of some of them from here   :

As for your question itself, it is quite confusing, at least at the level of knowledge of the brain we have at the moment: Do separate neural circuits express separate genes? We hardly know the surface of how the brain works, we consider a great improvement in science the fact that the psychotic spectrum gene pool has been somewhat mapped .

However, to somewhat answer your question, for example,  there is a gene  that is sometimes (not always) involved in Tourette syndrome and has been studied. The main idea is that "The SLITRK1 protein probably plays a role in the development of nerve cells, including the growth of specialized extensions (axons and dendrites) that allow each nerve cell to communicate with nearby cells. " Now, Tourette's  might be associated with Altered parvalbumin-positive neuron distribution in basal ganglia, which could be either the result of SLITRK1 gene mutation, or some other gene.

Let us put it this way: we do not have genes that suddenly create a third arm or a second heart, so we shouldn't have genes that suddenly create the wrong kind of neurons in the wrong region of the brain (I suppose that's what you mean by "type of brain matter", region of the brain, as neurons are generally all on the same level of the brain matter).

My best hunch, judging by the research I presented above, is that gene mutations might encourage or discourage the development of the type of neurons you'd expect in certain areas, which improves or disables the ability to process this or that type of information. Same as above, expressions of the genes involved in making this or that protein or physiological process that favors development of neurons in very specific areas of the brain - will also influence the way or intensity we process information with that specific region of the brain.

But - and it's a revelation I had myself while documenting this answer - genes do not express or suppress neuron development directly. The brain is what it is, and has the same format , if you will, no matter whose you dissect.

Genes influence metabolic and general physiologic process that are also part of the brain development. Your brain regions will process better or poorer due to the types of proteins that trigger development for the neurons, neurotransmitters that control the electric flow through the etc involved in the matter. Neural cells are hard-coded. Their development and functioning aren't.


Do men and women differ in their desire to have children? I was reading the comments of the following article on paternal health and birth defects. Someone made the following comment.

  The other thing is that mens interest in being a father is nowhere
  near a high priority as women's is to be a mother.

While this seemed like uninformed opinion, it seemed to raise an interesting question.

Is there any scientific empirical evidence to suggest that males and females differ in their desire to have children?

Caveats

Even when the degree of men's and women's desires to have children are forced by study parameters into yes/no pigeonholes, there are very few studies, and the results are arguably inconclusive. Also, men's and women's rates of desire to have children are continuously shifting, and thus the answer may change over time. Finally, the studies have been limited to the United States and/or the United Kingdom.

Findings

If you're wondering specifically about single men and women who don't yet have any children, this should help: In 2011, the website Match.com commissioned a study by SUNY Binghamton to answer your question and more. They found that 24% of the men and 15% of the women in the study want to have children, and "men in every age group are more eager than women to have children."
On the flip side, there has been at least one study of men and women who want NOT to have children, and the men in the study were more likely than the women to want to remain childless. This seems to contradict the aforementioned study in which more men than women want children... until you consider the third group -- ambivalent men and women.
According to McAllister, ambivalent women outnumber ambivalent men.

Conclusion?

A tentative conclusion could be that men are more decisive, outnumbering women in both categories -- wanting to have and wanting NOT to have children. But, more research is required to reliably answer your question, and by then the answer may have changed.

References

  Gore, D.L. (2002) I Don’t Want Any Children... Ever:
  Gender Differences in Voluntary Childlessness in the US, 2002 [pdf]
  McAllister, F. and Clarke, L. (1998) Choosing Childlessness. London: Family Policy StudiesCentre.


Is detection of angry faces more efficient in humans? Hansen and hansen proposed the anger superiority effect: threatening faces pop out of crowds, perhaps as a result of a preattentive, parallel search for signals of direct threat.

Pinkham (2010) demonstrated that we are faster when we have to spot an angry face than the happy one (below).

Can we really establish that we have an anger superiority effect?

Angry faces and non-angry faces differ for too many features...

How can we attribute this result (angry faces faster detected) to anger-related features, when so many other features (not necessarily related to anger) are different?

references

Hansen & Hansen, 1988

I'm not sure there's totally indisputable evidence on this, but I found a newer (2017) paper by Bayet et al. with infant subjects, but with fear rather than anger as the emotion tested (vs. happy), and (more importantly) using a different methodology (and IMHO better) because instead of different faces (in a crowd), they used the same face but mixed with noise, e.g. for fear [but for illustrative purposes only, see blow why]

They actually tried to determine which facial features enabled easier detection, eyes or mouth by mixing noise preferentially in that region (the resutling images were validated with SSIM, so there were four series of stimuli prestented (whith varying level of noise in each series).

Each of the face stimuli were presented in differents tests to the infant subjects; each test consisted of a noise-mixed face vs pure noise (two images on screen) and a camera was used to record the infant's reactions. The film was then analyzed to determine several measures of reaction, which were in turn used to calculate measures of face detection.

Two different measures of face detection were ultimately derived: A simple one based on percentages of total looking time [PTLT] and a more complex psychometric measure, the methodology of which is pretty involved (and thus perhaps a weak point of this paper):

  A multivariate measure of face detection was derived by classifying
  trials as ‘face is on the left’ or ‘face is on the right’. The
  rationale for this metric is similar to the idea of ‘double psychophysics’
  [48]: if one can reliably guess on which side of the screen
  the face was presented by looking at the infant’s behaviour, then
  it can be inferred that the infant is discriminating between the
  presence of a face or noise. We implemented this idea computationally
  using MVPA [42] to locate the side of presentation of the
  face (left or right) on each trial based on (i) PTLT to the left,
  (ii) number of looks to the left, (iii) number of looks to the right,
  (iv) duration of first look to the left, (v) duration of first look to
  the right, (vi) median duration of looks to the left, (vii) median
  duration of looks to the right, and (viii) direction of first look
  (left or right). Durations were log-transformed [56]. Continuous
  measures were z-scored within-subject. Measures were chosen
  a priori given the visual preference of infants for faces [57].
  PTLT to the right is equal to 100% minus PTLT to the left, and
  thus did not need to be included. Trials from all participants
  were pooled to maximize the number of training examples, and
  a logistic regression algorithm (a common classifier for MVPA)
  was repeatedly trained on all trials except one and tested on the
  trial that was left-out (leave-one-out cross-validation). Forward
  sequential feature selection was implemented inside each crossvalidation
  loop (see electronic supplementary material, table S2
  for results on the full dataset). This procedure led to locating
  the face side for each trial in a way that reflects generalization.
  We used logistic regression because it provides log-odds, a
  direct, criterion-free, continuous measure of evidence for each
  response (‘face is on the left’ versus ‘face is on the right’)—as
  opposed to accuracy, a binary measure dependent on a decision
  criterion. Raw evidence (log-odds for the right versus left side)
  was pooled to derive correct evidence (log-odds for the correct
  versus incorrect side) as a multivariate measure of face versus
  noise discrimination.

The overall results of their analysis look like this (one row for each detection measure):

Their interpretation of results:

  Psychometric curves of the PTLT to the face side revealed
  a significantly lower threshold for the Fearful eye+ face condition
  (44.41  ± 1.98% face signal; [...]; figure 3a) than for the Happy eye- face
  condition (difference: 5.20 +/- 2.62% face signal, 95% CI
  [0.001 0.103]), but not the other conditions ([...] figure 3a), across all age
  groups. [...]
  A similar result was found when applying psychometric
  curve modelling to the correct multivariate face versus
  noise discrimination evidence; the face detection threshold
  for the Fearful eye+ condition (44.07 ± 2.14% face signal;
  [...] figure 3c) was
  significantly lower than the detection threshold for the
  Happy eye- condition (increase in threshold: 7.90  ± 2.52%
  face signal, 95% CI [0.030 0.128]) but not the other conditions
  (Wald confidence intervals, alpha = 5%; [...]; figure 3c)

  Similar models were used to estimate the difference in
  threshold between the Fearful eye- condition and other conditions,
  or between the Happy eye+ condition and other
  conditions (electronic supplementary material, tables S5–S8).
  Results are summarized in figure 4. Overall, psychometric
  curve modelling of infant looking data revealed face detection
  thresholds at about 44% signal, with an increase of
  about 5% signal in threshold for Happy eye- condition
  compared to the Fearful eye+ condition, and intermediate
  thresholds for Happy eye+ and Fearful eye- conditions
  depending on whether PTLT alone (figure 4a) or correct
  multivariate discrimination evidence (figure 4b) was used
  as a measure of face versus noise detection.

  To clarify whether these differences in detection
  thresholds reflected a main effect of facial expression, a
  main effect of eye visibility, or an interaction between the
  two, and to test for an effect of age, we conducted further
  analyses focused on the linear portion of the psychometric
  curves corresponding to trials around the fitted detection
  thresholds (40–50% signal). [...; figure 3b,c,e,f I'm omitting all the chi-square stats]

  Results were mixed when considering PTLTs for the
  face side alone, as the effect of face emotion was restricted
  to 3.5-month-olds on this measure. However, correct discrimination
  evidence, a more comprehensive multivariate
  measure inclusive of PTLTs and other aspects of looking
  behaviour (e.g. first look) revealed a detection advantage for
  fearful faces compared to happy faces across all age groups
  (i.e. it did not significantly interact with age).

Of course this doesn't answer the question whether the effect holds in a crowd (or any non-laboratory setting, or if applies to anger etc.) The authors themselves say:

  Future research should determine
  whether the readiness to detect fearful faces (compared to
  happy faces) in infancy generalizes to naturalistic settings
  beyond the laboratory. Comparing detection of fearful
  versus angry versus sad faces will also clarify whether the
  effect applies just to threat-relevant stimuli (anger and fear)
  or more generally to negative novel expressions (fear,
  anger, and sadness).


Are there distinct visual perception themes that have been recognized in dreams? I'm not aware of a distinct term for what I'm trying to describe, so I will attempt to describe this in hopes that someone can help me find if there's a term or research done in this direction.

I remember thousands of dreams, and can recall them spontaneously. From such large subset of dreams, I've observed that there are some dreams that share a common feeling/ experience/ perceptual theme. A lot of this can be described visually, but the experience extends to other senses as well.

These dreams can be experienced years apart, and the exact content does not matter. What I'm interested in is the overall theme and how perception of the visuals within the dream is affected. For example:

Dreams with very dark environments, there are no ambient glowing light sources, and the lights that exist are more like LED specs than light bulbs. Objects are still perceived, but the contrast is very low
Hyper-realistic dreams, bright and colorful, where details are extremely vivid, sharp, as if everything has been "photoshopped" to look better than reality.
Dreams with landscape and characters affected by death, decay and rot, predominantly brownish, greenish, grayish hues.

Is there a term for these different kinds of perceptual experiences in dreams?

I guess what I'm describing can be compared to a photo filter applied to the entire environment:

I think this is the closest article to what I'm attempting to describe -An artists illustration of the effect of 20 different drugs on perception. He draws the same image "under the influence".

Here's an example of an image with the color palette and "decay" attributes I was describing


Does the meta-analytic literature overestimate the relationship between conscientiousness and job performance? There are quite a few meta-analyses of the relationship between personality and job performance (for a review, see Barrick & Mount, 2012; and specific meta-analyses: Barrick & Mount, 1991; Murray R Barrick, Michael K Mount, & Timothy A Judge, 2001; Hurtz & Donovan, 2000; J. Salgado, 1997; Tett, Jackson, & Rothstein, 1991).

These often come up with raw meta-analytic mean correlations between conscientiousness and job performance of around r = .15.

However, there is a lot of discussion in general at the moment about replicability  and publication bias. In particular, if papers that showed a correlation between personality and job performance, were more likely to be published, then this would inflate the meta-analytic estimate.

Alternatively, there have been quite a few studies of personality and performance with huge sample sizes (10,000+) and these would quite likely be published regardless of the exact results, and they also would have sufficient statistical power to detect even small effects. And for most meta-analyses, large sample size studies get a greater weighting in the estimation process.

I seem to remember reading a paper a few months back that examined this question. If I recall, the authors concluded that the meta-analytic estimate of relationship between conscientiousness and performance might be inflated slightly. However,  I can't remember what was the reference.

Questions

What research has been conducted on publication bias or other factors that might influence the accuracy of the meta-analytic estimate of the relationship between personality (and conscientiousness specifically) and job performance?
What is the evidence for and against this?

I'm posting a summary here (thanks to @DJ Sims for directing me to the paper of interest). Kepes and McDaniel (2015) re-analysed data from an existing meta-analysis. The existing meta-analysis had been examining various moderators of the relationship between big 5 personality and job performance. Kepes and McDaniel performed a range of sensitivity analyses.

They summarise their results as follows:

  Publication bias analyses
  demonstrated that the validity of conscientiousness is moderately
  overestimated (by around 30%; a correlation difference of about .06).
  The misestimation of the validity appears to be due primarily to
  suppression of small effects sizes in the journal literature.

As evidence for publication bias, they show that the average validity for conscientiousness is lower in unpublished samples:

  The results for the sub-group distributions of samples from journal
  articles (k = 67) and non-journal sources (k = 46) [indicate that] samples
  published in journal articles reported larger average
  effect size estimates (   $\bar{r}_{oRE}$   = .19) than samples from non-journal sources (
    $\bar{r}_{oRE}$ = .12.

A few critical comments:

When publishing results showing the relationship between big 5 personality and performance, there are five correlations presented. Assuming that publication bias sometimes led to a requirement to have at least one significant correlation, then the publication bias should be less.

The study does not cite or discuss other common meta-analyses on the Big 5 and job performance, which interestingly have often obtained meta-analytic estimates similar to what they say is the correct value. For example, the famous early meta-analysis by Barrick & Mount (1991) using 12,893 cases and 92 correlations obtained a mean raw correlation between conscientiousness and job proficiency of $\bar{r}$ = .13. In a meta-analysis by Hurtz and Donovan that exclusively used correlations for measures using the big 5, they obtained an overall validity for conscientiousness of $\bar{r}$ = .14. This also is very close to what might be expected.

These traditional estimates of validity from previous meta-analyses are sample weighted means. Thus, they naturally weight large samples more. So, for example, one study with 2000 participants would be weighted as much as 20 studies each with 100 participants.

There are good reasons to assume that publication bias would have less of an effect on large sample studies (e.g., n > 1000). First, when the sample size is sufficiently large, the results become intrinsically interesting. Reviewers can not argue that it was merely a lack of statistical power. Second, such studies generally have sufficient power to detect correlations in the r = .10 area. For example, assuming a population correlation .10, alpha of .05, and a two-tailed test, to have at least 90% power to detect a significant correlation you would need at least 1,046 participants.

My take away from the paper:

There is probably publication bias in the literature in relation to small sample studies. I imagine this publication bias is relative. If I were to guess, I'd say strong bias at n < 100; moderate bias n < 200, and progressively less as you move to 500+.

References

Kepes, S., & McDaniel, M. A. (2015). The Validity of Conscientiousness Is Overestimated in the Prediction of Job Performance. PloS one, 10(10), e0141468. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0141468


Does Wim Hof really consciously control his autonomic nervous system? While there is no question about the validity of Wim Hof's abilities, I question some of the claims made about his ability.

He is claimed to be able to consciously control certain aspects of his autonomic nervous system with his mind.

But while his feats are undoubtedly impressive, and his training program was proven effective, I find it hard to believe he's reached a point where all he needs is his mind.

As much as I'd like to believe one can do the things he did without the special breathing techniques he uses.

Is there any reason to believe there is something to it beyond conditioning the body and breathing in a specific manner (which, from what I understand, causes the body to react in a certain way leading to the desired effects)?

Disclaimer: just an opinion of someone on the web, it's not health advice. And I might be wrong.

With that said...

In my opinion it's wrong. He can't control his ANS just by using his mind. He uses: breathing techniques, exposure to cold and having the right mindset in order to withstand the cold. There's also a Dutch article on the site that says this. The way he handles the cold is also the same way he handles his ANS in general.

I think the wikipedia page is wrong about it. Also, the researchers that did studies on him at the Radboud University of Nijmegen are not specialized in understanding meditation. In most cases I'd disagree that what Wim does is meditation at all. While I respect the knowledge of the researchers, I think they were dead wrong in understanding what meditation is back then. It's really more of a behavioural thing with your breath. The meditation I know is more about mentally focusing on your breath or body, not physically altering it. Their expertise is in all sorts of: viruses, bacteria and the human body in general -- including combining the 3 for experiments.

Here is a better source about the science of Wim Hof: http://www.icemanwimhof.com/science

In my opinion that source is a lot better. Then again, it is a very wise to be sceptic (hint: also with my post). I think a lot of people made wrong claims about his method. I think almost everyone involved made at least a wrong claim about something of it. People are enthusiastic and lack expertise in some area and that's when claims might be overstated or misinterpreted by the one reading about them.

You don't have to be too sceptic though, it definitely works and improved my life. I love all weather now with regards to temperature. I sometimes use his method as a natural painkiller as it releases adrenaline, though I'm still on the experimental side with that.

The reason I believe to know all this is because:

I participated in one of the experiment and trained for 4 days with Wim and other participants
I asked a ton of questions to the researchers who were there from the Radboud University.
I have 400 hours of meditation experience and read about 100 articles on them from Science Daily, and about 30 real papers and 1 book about meditation that uses science as its way of justification (Search Inside Yourself by Chade Meng-Tan).


How does obedience correlate with the Big 5 factors of personality? I am looking for correlations for any Big 5 traits with obedience.
Are there any research reports on this, available for me to read?

Bègue et al. (2015) have recently investigated how the Big 5 traits predict obedience in a variant of the Milgram paradigm.

Participants believed they were participants in the pilot screening of a TV show. The talk show host (as the authority figure of the experiment) asked them to deliver electric shocks of increasing intensity to another participant (presumably a quiz contestant) whenever he or she gave an incorrect answer. As the intensity of the shocks increased, the contestant (in reality a confederate of the study) could be heard screaming and protesting, asking to stop the shocks. Nevertheless, the host insisted that the shocks should continue for the sake of the game show. The central measure of obedience was the highest intensity of the shock (when the participant refused to continue).

Result: Conscientiousness and Agreeableness predicted obedience as expressed in the willingness to administer electric shocks of higher intensity as demanded by the authority figure.

Here are the detailed results:

References

Bègue, L., Beauvois, J.-L., Courbet, D., Oberlé, D., Lepage, J., & Duke, A. A. (2015). Personality predicts obedience in a milgram paradigm. Journal of Personality, 83, 299–306. doi:10.1111/jopy.12104 (pdf)


How does a language deprived person think? Question

Let us say a person is deprived of language (of any form, including verbal and non-verbal) since birth to an age where normal adult brain functioning would be expected. Then how would they think?

Additional information

I have read accounts of this happening to feral children, but I can't find any description of how they thought before they acquired language. I also know that deaf who know sign language usually think in sign. Any sources would be great.

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.


In C. elegans, which neuron has the largest span, and why is it this large? The model organism C. elegans is about 1 mm in length.  This is quite small.  In fact, some C. elegans neurons span >25% of the length of its body (ref.).

This observation leads me to the following question: Which neuron in C. elegans has the largest span, and why is it this large?

I am a member of OpenWorm.org, an open-source project that aims to simulate a C. elegans cell-by-cell. I didn't know the answer to this myself off the top of my head, but I have access to a number of folks who have been working hard on C. elegans anatomy for the last couple of years so I went ahead and asked them this question on our discuss mailing list. Thanks to Chris Grove and Tim Busbice for providing the answer that I am reporting below:

Chris Grove:

  Finding the neuron with the largest span partly depends on your
  definition of "length" in this context. In terms of largest amount of
  total axon/dendrite length, this would most probably be the PVDL/PVDR
  sensory neurons. They produce a large number of branches of dendrites
  that act to perceive mechano and thermo-sensation. See the WormAtlas
  page here.

Tim Busbice:

  If by "length" one means, absolute longest extension from head to
  tail, that's a tougher call, as there are several that extend from the
  head to the tail. An example of these are the AVDL/AVDR command
  interneurons, that function as touch modulators for backward
  locomotion induced by head-touch, and also drive backward movement of
  the animal along with driver cell AVA neuron, AVE and A-type motor
  neurons.

You can find a lot of info on C. elegans anatomy on WormAtlas and on an OpenWorm data spreadsheet in which we are consolidating detailed anatomy data from different sources.

Also I would advise checking out the OpenWorm Browser - a web-based 3D viewer that you can use to explore the C. elegans anatomy cell-by-cell (the 3D model was developed by Chris Grove, see VirtualWorm for details). For instance you can easily search for those "longest" neurons mentioned above! Screenshot of one of them selected (AVDL) below:

Hope this helped!


Problem with IQ tests in Murray's "The Bell Curve"? Murray's The Bell Curve came up in a discussion recently.  I have a very clear memory of reading a review of the book at the time it came out.  The reviewer claimed that one of the many problems with Murray's methodology was that he relied on IQ tests written in English but given to African students whose first language was French.  I cannot find a link to this anywhere. Anyone have any info on this?  Is the critique accurate?  Is it possible that I am remembering the review of some other work?

After some significant searching myself I don't believe that what you've stated was one of the many criticisms of "The Bell Curve".

It wouldn't be impossible for the review you read to go something like,

"Murray's, "The Bell Curve" is akin to other racially biased research like as XYZ's "IQ Research", in which XYZ claimed that African students had, on average, lower IQs, but when the research was reviewed showed that those students had received a test in English, while their primary language was French."

Memory can be a tricky thing and the way connections are formed around subjects we don't use often is haphazard at best.


Does the International Affective Picture System (IAPS) contain weapon stimuli? I'm looking to use the IAPS for my research, but I specifically need to use images of/or containing weapons. Does anyone know if IAPS has any such stimuli, and, if so, roughly how many?

Use the MAPS https://www.ncbi.nlm.nih.gov/pubmed/26255051

You can request from Auburn Univeristy


How many memory systems do we have? I read that humans have 2 memory systems.

One is fight or flight memory located in amygdala. Another is episodic memory located in hippocamus.

Then I've heard that there is another memory system. Semantic memory located on the temporal lobe.

So, how many memory systems do we have?

If I can derive most math formula on top of my head but keep forgetting where I put my glasses, is something wrong in my hippocampus?

Okay, how many memory do we have?

Like many things in neuroscience & cognitive science, it depends on how you categorize it, it is also an evolving field and you might be surprised to know that the number of memory systems is closer to 10-12, although the number might go up or down in the future.

In general there are 2 ways of dividing memory: by time range ( Long term and short term) and by intentional recollection, each one further subdivides and overlaps at some points.

  One is fight or flight memory located in amygdala.

The Amygdala is a complex mass of gray matter that plays an important role in emotions, it both integrates and has a role in associative learning in between stimuli and experiences/feelings among other functions, so in a way it is involved in memory, ( emotional memory).

The fight or flight response on the other hand is a whole other complex subsystem of our bodies mainly involving the visceral motor system (the sympathetic division)

  Another is episodic memory located in hippocamus

Episodic memory is one of the subdivisions of memory, mainly dealing with events as opposed to facts ( that would be semantic)

The hippocampus is a crucial component to memory, but is part of a bigger system mainly involved with transfering and facilitiating the creation of short term memories to long term memories.

  If I can derive most math formula on top of my head but keep forgetting where I put my glasses, is something wrong in my hippocampus?

Most likely not, as this very brief and incomplete review hopefully shows you, there are a number of different systems at play for what we normally bunch up into the word memory, there are also different types of memories.

Deriving a math formula on the top of you head involves another type of memory, working memory, along with the phonological loop if you think in words about your equations ( these 2 are sort of buffers) , and long term memories across your neocortex with a number of connections and interconnections, in other words your whole brain lights up.

Forgetting your glasses on the other hand is usually a problem of not encoding the initial percept in the first place ( i.e. to increase the odds of you finding your glasses again, you need to consciously aknowledge where you are leaving them in the first place rather than just dropping them).

Additionally, what you do in between leaving your glasses and trying to recover them also influences how much you remember them.

As mentioned memory is a complex and deep subject, as way of sources here are a few books I consulted:

- Cognitive Neuroscience (Third edition)
- Neuroscience (Third edition)
- In search of memory
- The seven sins of memory


Does computer usage (YouTube, Facebook, etc. ) influence social abilities? With computers, tablets and smartphones, people spend more and more time in front of a screen, and perhaps, less time with actual people.

In my experience, after spending a lot of time on my computer, I notice I am less able to hold a good conversation, sometimes lose a little bit of self confidence and care more about what others think.

Is there any scientific research that shows a relationship between social skills and computer usage (especially watching YouTube-Videos)?

Social media usage is still quite new and there have been no major longitudinal study that I know of, that has looked into how usage influences social abilities in the long run.  If you limit it to youtube only, then I don't know of any study at all that looked at youtube usage only and social skills.

One of the reasons it's difficult to study this, is that people who are drawn to these online activities are not the same as others, and not everyone who uses them becomes "addicted" to them.  In other words, we don't start with people having the exact same social or cognitive skills.  In addition, people don't actually use them the exact same way (length of time, content, etc).  Not to mention that people often don't just use one particular thing like youtube but many different sites and so that's another reason it's difficult to make comparisons.

Of course, there are ways to use them that can be of benefit.  For instance, concerning younger people who use social media including youtube, The American Academic of Pediatrics mentions potential benefits, such as communicating and socializing, better learning opportunities, and access to health info, while warning of dangers such as cyberbullying, sexting, violation of privacy, powerful influence of advertisement, and last but not least, "facebook depression."

An interesting area of study is "internet addiction".  The final decision was made not to include it in the latest psychiatric diagnostic manual (DSM-V), partly because as one article asks "Problematic Internet use: a distinct disorder, a manifestation of an underlying psychopathology, or a troublesome behaviour?  Other authors however have a specific definition in mind, such as this editorial that states the four defining criteria of internet addiction:

  1) excessive use, often associated with a loss of sense of time or a
  neglect of basic drives, 2) withdrawal, including feelings of anger,
  tension, and/or depression when the computer is inaccessible, 3)
  tolerance, including the need for better computer equipment, more
  software, or more hours of use, and 4) negative repercussions,
  including arguments, lying, poor achievement, social isolation, and
  fatigue.

In summary: There is a lack of good longitudinal research in this very important area.  There is also problem with defining what is appropriate usage and what is not.  But it is speculated that proper usage (e.g. access to useful info, or socializing) can be beneficial while inappropriate usage (e.g. online bullying) can be detrimental to mental health.  Regardless of purpose of usage, excessive usage to the point of ignoring more important daily functions may also be a sign of mental illness, be it caused by the computer usage itself or as manifestation of another already present illness.

Hope this has been useful to you.

References:

Block J. J. (2008). Issues for DSM-V: Internet Addiction. American Journal of Psychiatry; 165, 306–307.

O’Keeffe, G., & Clarke-Pearson, K. (2011). Clinical report the impact of social media on children, adolescents, and families. Pediatrics, 127, 800–804.

Starcevic, V. (2010). Problematic internet use: A distinct disorder,
a manifestation of an underlying psychopathology, or a troublesome behaviour?
World Psychiatry, 9, 92.


What causes seizures to develop years after a childhood brain injury? A friend of mine told me that her daughter was in an accident prior to the age of 12 which resulted in head trauma and brain damage. The child went through an extensive recovery process (relearning how to walk, speak, etc) and made a nearly full recovery, the only symptoms which remained were frequent headaches.

The doctors said at the time of the accident that when the child reached her late teens / early 20s, she might develop seizures. Sure enough, shortly after she turned 18 the seizures began.

What causes seizures to develop years after a childhood brain injury? What is it about the developing brain which can cause years to pass before such seizures begin?

there is a lot of info confirming Post Traumatic Epilepsy (PTE), but little on the exact causation, due to the mysterious nature of the causation of epilepsy.

There is much research supporting the link between brain injury and subsequent seizures, Post-traumatic epilepsy , including the onset of delayed seizures:

  Traumatic brain injury (TBI) has been recognized as a cause of
  epilepsy since antiquity, and it remains one of the most common and
  important causes of acquired epilepsy today. Epidemiologic studies
  have demonstrated a clear relationship between the severity of injury
  and the likelihood of developing epilepsy, with the risk approaching
  50% in TBI cases associated with direct injury to brain parenchyma.
  Importantly, many TBI victims develop epilepsy months or years
  following the initial injury, ...

Epilepsy after head injury: an overview.
Lowenstein DH. doi: 10.1111/j.1528-1167.2008.02004.x.

  Posttraumatic seizures may not appear for as long as 20 years after an accident.

Stanford Epilepsy Center Robert S. Fisher, M.D., Ph.D.

Increased incidence and impact of nonconvulsive and convulsive seizures after traumatic brain injury as detected by continuous electroencephalographic monitoring
Paul M. Vespa, M.D., et al

The risks of epilepsy after traumatic brain injury ☆
John F Annegers2, Sharon Pasternak Coan
The University of Texas Health Science Center at Houston, School of Public Health, USA

A Population-Based Study of Seizures after Traumatic Brain Injuries
John F. Annegers, Ph.D., et al
N Engl J Med 1998; 338:20-24January 1, 1998DOI: 10.1056/NEJM199801013380104

As to the causal relationship:

The cause of epilepsy is largely unkown.

  What causes epilepsy?
  There are many causes of epilepsy, which vary with the age at which seizures begin and the nature of the seizures. However 50% of cases, the cause is unknown.  ...
  A brain injury, which results in scar tissue, predisposes individuals to developing epilepsy, although there can be a long period, often years, between the damage occurring and the seizures commencing. ...

  What is a seizure?
  A seizure occurs when the brains nerve cells misfire and generate sudden, uncontrolled burst of electrical activity in the brain. ...

It has been shown that the nature of the head injury influences the likelihood of developing seizures.

  Nature of trauma
   Intracranial hematomas, in which blood accumulates inside the skull, are one of the most important risk factors for PTE.[23] Subdural hematoma confers a higher risk of PTE than does epidural hematoma, possibly because it causes more damage to brain tissue.[7] Repeated intracranial surgery confers a high risk for late PTE, possibly because people who need more surgery are more likely to have factors associated with worse brain trauma such as large hematomas or cerebral swelling.[7] In addition, the chances of developing PTE differ by the location of the brain lesion: brain contusion that occurs on in one or the other of the frontal lobes has been found to carry a 20% PTE risk, while a contusion in one of the parietal lobes carries a 19% risk and one in a temporal lobe carries a 16% chance.[21] When contusions occur in both hemispheres, the risk is 26% for the frontal lobes, 66% for the parietal, and 31% for the temporal.[21]

It is not clearly understood how traumatic brain injury  causes seizures.

  Epilepsy is a common outcome of traumatic brain injury (TBI), but the mechanisms of posttraumatic epileptogenesis are poorly understood. One clue is the occurrence of selective hippocampal cell death after fluid-percussion TBI in rats, consistent with the reported reduction of hippocampal volume bilaterally in humans after TBI and resembling hippocampal sclerosis, a hallmark of temporal-lobe epilepsy. Other features of temporal-lobe epilepsy, such as long-term seizure susceptibility, persistent hyperexcitability in the dentate gyrus (DG), and mossy fiber synaptic reorganization, however, have not been examined after TBI. To determine whether TBI induces these changes, we used a well studied model of TBI by weight drop on somatosensory cortex in adult rats. First, we confirmed an early and selective cell loss in the hilus of the DG and area CA3 of hippocampus, ipsilateral to the impact. Second, we found persistently enhanced susceptibility to pentylenetetrazole-induced convulsions 15 weeks after TBI. Third, by applying GABAA antagonists during field-potential and optical recordings in hippocampal slices 3 and 15 weeks after TBI, we unmasked a persistent, abnormal APV-sensitive hyperexcitability that was bilateral and localized to the granule cell and molecular layers of the DG. Finally, using Timm histochemistry, we detected progressive sprouting of mossy fibers into the inner molecular layers of the DG bilaterally 2–27 weeks after TBI. These findings are consistent with the development of posttraumatic epilepsy in an animal model of impact head injury, showing a striking similarity to the enduring behavioral, functional, and structural alterations associated with temporal-lobe epilepsy.

Physiological and Structural Evidence for Hippocampal Involvement in Persistent Seizure Susceptibility after Traumatic Brain Injury
Golijeh Golarai1,2,

Increase in extracellular glutamate caused by reduced cerebral perfusion pressure and seizures after human traumatic brain injury: a microdialysis study
Paul Vespa, M.D., et al

Brain injury induces c-fos protein(s) in nerve and glial-like cells in adult mammalian brain
M. DragunowCorresponding author contact information, 1, H.A. Robertson2

It would seem that seizure at the time of the injury, increase the chance of having late onset epilepsy.

  TBI is a relatively rare cause of epilepsy in childhood, although immediate seizures are associated with an increased risk of developing post-traumatic epilepsy

doi: 10.1080/02699050902973913.
Occurrence of epilepsy during the first 10 years after traumatic brain injury acquired in childhood up to the age of 18 years in the south western Swedish population-based series.
Emanuelson I, Uvebrant P.

  Posttraumatic seizures may occur almost simultaneously with head injury or be delayed for several years.
    • Once posttraumatic epilepsy has developed, it remits less often than previously reported.
    • Patients with posttraumatic epilepsy appear to have a higher mortality rate than patients with traumatic brain injury without epilepsy.
    • Posttraumatic epilepsy appears in many cases as temporal lobe epilepsy that possibly originates from the hippocampus.

  ... 40% to 50% of new cases of posttraumatic seizures occur within 6 months, 70% within 1 year, and 80% within 2 years after head injury ...
  ... Seizures occurring within 5 minutes of traumatic injury to the head are called "immediate" posttraumatic seizures (Majkowski 1991). Such seizures do not represent epilepsy, per se, and should be viewed as an acute response to the head injury.

Posttraumatic epilepsy
Contributors
Ravindra Kumar Garg MD, author. Dr. Garg of King George's Medical University in Lucknow, India, has no relevant financial relationships to disclose.
C P Panayiotopoulos MD PhD, editor. Dr. Panayiotopoulos of St. Thomas' Hospital received a publication grant and salary from UCB Pharma S.A.

J Neurol Neurosurg Psychiatry 2002;73:i8-i16 doi:10.1136/jnnp.73.suppl_1.i8
HEAD INJURY FOR NEUROLOGISTS
Richard Greenwood

Given the swelling can expand over time, and there can be delayed hemorrhaging; this could account for some delayed onset seizures.

  • A contusion consists of blood intermixed with brain tissue.
    • Data have shown that traumatic intracerebral hemorrhages often expand over time.
    • Delayed posttraumatic hemorrhages may sometimes result from coalesced blood within contusions.

Traumatic intracerebral hemorrhage
 Contributors
Ravindra Kumar Garg MD, author. Steven R Levine MD, editor.

My own thoughts would be, that if a brain injury occurs during childhood; given the degree of growth and change from childhood through to adulthood; and given the the predictive likelihood (that if epilepsy will develop) that it will do so before the ages of 18-21; I suspect that the growth and disruption to scar tissue and possible delay in disruption of existing contusions could account for the delay in onset of PTE.


How exactly do we construct perceived IQ by facial features? There are claims that humans can recognize others' IQ.

What's the difference between the below images that shows men's IQ?

Personally, I can "feel" that the guy with high perceived intelligence (on the right) does indeed look the most intelligent.

However, what is the reason behind this gut feeling? The nose being wider? Is it  the slanting eyes? I found the associated grid drawings, but I still can't seem to figure it out.

The images you've linked are composites, and so probably don't contain the characteristics by which raters were able to judge IQ accurately. The original article (Kleisner, Chvátalová, & Flegr, 2014) is freely available and appears to answer your question in its abstract:

  Faces that are perceived as highly intelligent are rather prolonged with a broader distance between the eyes, a larger nose, a slight upturn to the corners of the mouth, and a sharper, pointing, less rounded chin. By contrast, the perception of lower intelligence is associated with broader, more rounded faces with eyes closer to each other, a shorter nose, declining corners of the mouth, and a rounded and massive chin.

These differences only relate to perceived intelligence, not measured intelligence.
From the conclusion:

  No specific traits that correlated with real intelligence were detected with standard geometric morphometric methods. Men and women with specific facial traits were perceived as highly intelligent. However, these faces of supposed high and low intelligence probably represent nothing more than a cultural stereotype because these morphological traits do not correlate with the real intelligence of the subjects.

The authors speculate on (but did not analyze) other factors that might explain the perceptibility of actual intelligence apart from the factors visible in the composites, including:

  Particular configurations of eyes or gaze, colour of eyes, hair and skin, or skin texture.

All of these characteristics would be wiped out in facial composites, so you probably can't actually perceive intelligence accurately from the images you've embedded according to this study.

Reference
Kleisner, K., Chvátalová, V., & Flegr, J. (2014). Perceived intelligence is associated with measured intelligence in men but not women. PloS One, 9(3), e81237. Retrieved from http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0081237.


How do I determine whether my EEG signal needs denoising? I recently start to work on sleep study.
For my research i download sleep EEG data from physionet. The EEG data has 100 HZ sampling rate and was recorded from 2 bipolar EEG site.

When i start the preprocessing stage, i encounter a simple problem, how should i know if my signal has an artifact or noise?

It should be noted, based on nyquist theorem and my signal's sampling rate, the maximum frequency of my signal is 50 HZ, so i did not filter unnecessary EEG frequency.
In general i only used a simple notch filter at 50 HZ, and used simple threshold method in order to remove the epochs that were grossly contaminated by muscle and/or eye movement artifacts.

Back to the main question, how should i know if i need to uses more complicated method for removing EMG or EOG artifact from my signal?

Your recording necessarily has noise. That's a property of any physical apparatus, and you are recording the activity of noisy neurons. The other property of noise is that, by definition, it will average out. So don't do anything about that. 100Hz is quite a low frequency. Artifacts (e.g. blinks, but I doubt you would have that in sleeping subjects) would typically have a higher frequency than that so (1) it's unlikely it has been recorded by your system at all, (2) you can low-pass filter your signal to remove both the 50Hz artifact and possible other artifacts. Other artifacts such as sleeping position would have very low frequencies. So you can high-pass your signal to get rid of them. I'm not familiar with sleep EEGs but I would not worry too much about it. You can also check few papers and see how they filtered their signal.


Why are some people good at algebra and bad at geometry and vice versa? I've met people who say they did very well in algebra but were terrible at geometry in high school and some people who say they did very well in geometry but were terrible at algebra in high school.

I'm curious if people who do well in geometry are right-brained thinkers while people who do well in algebra are left-brained thinkers? Why is there a difference in ability, when algebra and geometry are just branches of the same subject, mathematics?

In short, algebra and geometry are different type of cognitive abilities. Geometry is more spatial and algebra more verbal-logic.

Kestenbaum, C., Williams, T. D., Handbook of Clinical Assessment of Children and Adolescents, NYU Press, 1988.


Is there a condition where a person doesn't feel emotional or non-physical pain? Congenital insensitivity to pain is a rare condition where a person cannot feel pain (physical). Is there any condition relates to emotional pain or any pain not related to physical that a person cannot feel?

Congenital insensitivity to pain (CIP) is a condition in which a person cannot feel physical pain.  There is no known analogue encompassing all emotional (psychological) pain.
There are certain conditions in which a person may not be able to feel certain types of emotions, such as in psychopathy and related anti-social personality disorder.  This may be related to abnormalities in the limbic system - an area of the brain associated with processing emotion.
However, it is not always clear whether or not individuals who appear to lack the ability to feel certain types of psychological pain (eg, PTSD) in fact cannot feel it, or they can feel it but are indifferent to it, as in emotional numbness or apathy.
Additionally, modern theories of emotion suggest that emotion is "subjective" (context-dependent) - that is, physiological aspects of emotion (such as pain) are only part of the picture, and many other cognitive factors come into play.  So for example, in the case of a broken heart, as with psychological pain in general, it appears to share some mechanisms with physical pain - ie, this type of pain is effectively the same as physical pain.  Nonetheless, CIP patients appear to be able to feel emotions such as heartache normally, suggesting that the mechanism is much more complex, and physical pain is neither necessary nor sufficient for feeling psychological pain.  The added complexity may be the reason why an emotional analogue to CIP is not known - the number of systems that would need to malfunction simultaneously is too unlikely.  It is also probable that given the importance of emotion to normal functioning, that a condition of not feeling it would be equivalent to death.
PS: Sorry that I don't have any book recommendations for you, but Wikipedia articles I linked to contain many references to literature you can check out.


Research on "probabilistic thinking" in non-human animals? We all seem to have a "probabilistic sense", which manifests itself in certain types of expectations (e.g. even if one has never used a bow to shoot an arrow, one expects that hitting a small target will be more difficult than hitting a large target, all other things being equal), and also in certain characteristic responses when events do not match those expectations (these responses consist primarily of surprise, but also include suspicion, and in extreme cases maybe even awe or fear).

For me at least, this probabilistic sense feels subjectively very fundamental, in the same way that physical pain, hunger, thirst, etc., "feel fundamental".  In other words, I could not describe them to someone in simpler terms.  (I may be able to explain to someone the mechanics of shooting an arrow with a bow, but I would not know how to explain to someone how to feel the immediate intuition that hitting a small target would be harder than hitting a large one.)

Motivated by the kind of questions that follow, I'm looking for a review of research on "probabilistic thinking" by non-human animals.

How analogous is this "probabilistic sense" to the more traditional
   ("classical") senses like vision and touch?
In particular, how much does it depends on human culture?

I've searched for these keywords online, but I have not come up with anything.  Maybe I'm not using the right keywords.  Also, since probabilistic methods as standard tools in research (and hence, the research literature is awash in terms like "probability", "expectation", "Bayesian", "statistical", etc.), it is very difficult to craft searches that are selective for the research I'm looking for.  Some specific pointers (i.e., to specific papers, or books, or at least specific researchers) would be appreciated.

FWIW, the clearest example I can come up with to illustrate what I mean by "probabilistic thinking" is this thought experiment.  Imagine presenting a human subject the opportunity to participate in a raffle for some prize that the subject finds desirable, and suppose the subject is just told that he/she has the choice of having (A) one, or (B) two tickets for the raffle (at no cost in either case).  We would expect, of course, that every "normal" subject would prefer (B) over (A).  (In fact we would question the sanity (or at least the seriousness and sincerity) of any subject who fully understood the situation, and still preferred (A) over (B).)

What makes the universal preference for (B) an example of "probabilistic thinking" is the simultaneous recognition on the subject's part that choice (B) is unequivocally better, and that still it could fail to lead to the prize, even if the raffle had only three tickets.

I'm not sure how one would go about setting such an experiment with non-human animals, but I've been impressed before by the ingenuity of the experiments that researchers devise to test animal cognition, so I remain hopeful that something like the "probabilistic thinking" I illustrate above has been investigated.

That said, I realize that it would be rather difficulty is to distinguish between pure "probabilistic thinking" (as a distinct, independent faculty) and conditioning.  In fact, it can be (and has been) argued that what I'm calling "probabilistic thinking" is nothing more than a special case of conditioning.  (After all, conditioning may be thought of as the nurturing of certain expectations, and preferring two tickets over one could be simply a manifestation of one such expectation.)  Ironically enough, when it comes to humans, I can't think of any ethical experiment that would be able to establish "probabilistic thinking" as a faculty that would be present even in the absence of any conditioning.  With animal subjects, however, it may be possible to set up experiments that minimize the possible confounding by conditioning.

Try an internet search on animal learning probability.  Although that might not be what you want because it sounds like you specifically want insight as opposed to learning in general.

Your particular example is problematic because you're inferring far too much on the subjects part. They might prefer B because they just want more of anything offered. The experiments need to be much more careful than that in order to attribute effects to probabilistic thinking. What kind of response will occur doesn't just depend on the probability of events but what kind of reward contingencies are associated.  Both people and animals do dumb things with simple probabilities and rewards.  But they do the same thing. Does that justify an argument that they have a probabilistic sense?

Deriving a distinction between insight and conditioning is sometimes problematic (for example food aversion in rats) and insight is usually only accepted when it can pass the interocular impact test.  While I can show you lots of papers on probability learning I'm unaware of any that tap insight about probabilities.

Consider the problem for the researcher. In order to establish insight into probabilities the subject has to experience the events repeatedly in a relevant way so that they become learnable. Given this takes a degree of exposure in the first place it would be very hard to dissociate conditioning from insight based learning.

Also consider that people sometimes can learn probabilities but don't always do intelligent things with them. For example, when there are two possible events and one happens 75% of the time people tend to select the frequent event 75% of the time. This is rather boneheaded because selecting the frequent event all of the time will give you the most accurate performance. Animals actually learn to do the latter. So maybe animals have a stronger probability sense? Regardless, they clearly they learn probabilities.


Can autism spectrum disorders be acquired or are they inherited traits only? Can autism spectrum disorders be acquired or are they inherited traits only, especially in the case of Asperger syndrome or pervasive developmental disorders where they lie on the lower end of the spectrum? If so, does there seem the be a cut-off age, like the onset of adolescence or adulthood? Or can it be acquired at any point in one's life? I understand it can be discovered later in life, but can it actually develop due to one's environmental factors?

Anybody with enough will and persistence can find support for almost any viewpoint they desire concerning autism, depending especially on (lower) quality of source material. However, if you read enough, consistent patterns will emerge in the literature.

This issue of Dialogues in Clinical Neuroscience is all about autism. Although all of it is valuable, I strongly encourage you to work through the wealth of information in Autism risk factors: genes, environment, and gene-environment interactions by
Pauline Chaste, MD, PhD. and Marion Leboyer, MD, PhD.

In it you will discover that autism is more and more thought to be a disorder caused by a combination of genetics and environment: genetic factors, epigenesis, maternal environment, drug exposure during pregnancy and a host of other factors, all occurring before of during birth.

There seem to be two types: the slow progressive and the loss of developmental skills type. For this reason the American Academy of Pediatrics recommends screening for autism at 18 and 24 months, though some Pediatricians start screening at 9 or 12 months.

The short answers to your questions:

  Can autism spectrum disorders be acquired or are they inherited traits only, especially in the case of Asperger syndrome or pervasive developmental disorders where they lie on the lower end of the spectrum?

Autism Spectrum Disorder appears to be genetic and environmental, but that environment is strongly in utero or at birth. So, no, it does not appear that one can acquire ASD as one might acquire, say, chicken pox if unvaccinated.

  If so, does there seem the be a cut-off age, like the onset of adolescence or adulthood?

Although people with autism may take a long time to be diagnosed, it is not 'acquired' later in childhood or adolescence.

Other degenerative neurological disorders can occur later in life, for example lead poisoning or other diseases, but they are not autism.


Is there a research field which holds close connections between computational neuroscience and classical robotics Is there a research field which holds close connections between computational neuroscience and classical robotics, particularly building corresponding robots to  implement and test the theories from computational neuroscience ?

Yes, it's often called Neurorobotics. There are several labs doing this kind of research. Here's a small sample:

Jeff Krichmar at UC Irvine.
The Neurorobotics Research Laboratory at Humboldt Unveristy
The Neurorobotics Lab at Drexel University
Jun Tani at the Korea Advanced Institute of Science and Technology
NxR at Northwestern


Do feelings have a purpose? A car has dashboard lights, like "check engine" to indicate malfunctions, etc. Do human feelings have some similar, meaningful function (x produces feeling y), or are feelings just random glitches of cognition?

I can think of feelings that are easy to define:

pain, localized to the injury site as serving a purpose: do not use
the injured limb until it feels healed.
Heartburn may be a feeling associated with eating incorrect types of
foods: stop chewing gum and the feeling goes away.
Feeling heat/cold has a purpose that may be connected to metabolism
and thermoregulation.
Feeling of hunger is relieved by eating

For example, the feeling of hunger can be explained by the balance of hormones of leptin and ghrelin, which control appetite and the feeling of satiety.

But what about those other feelings, defined by abstract words from dictionaries? Jealous, silly, disgusted,motivated,comfortable, etc, etc. Here's a list of human feelings. One can imagine what they are, but to catch oneself in one of them is a completely different thing. I'm interested if feeling in some way has a purpose. Can we say something about the hormone/neurotransmitter levels based on how a person is feeling?

To me the question is equivalent to what is the function of consciousness itself.

Let me elaborate. There is a difference between affects/emotional circuits and feelings. The level at which for eg. Jaak Panksepp works is emotional circuits or affects that are primarily unconscious and can be conceived of in terms of instincts.

If fear circuit is activated, the organism exhibits a flight-fight-freeze response. Conscious feeling of fear may or may not be involved, but physiological changes like activation of sympathetic system happens. If the unconscious fear circuit is OK to keep us out of harm's way (predators) why do we also need to feel fearful? A related meta question is, if a zombie behaving like me, but having no qualia, can and will succeed similar to me, why have consciousness?

I'll address the questions, but first let me solidify the claim that unconscious processes are sufficient for most adaptive regulations. Consider your example of heat/cold as thermo-regulation of body temperature...but do you really need to 'feel' heat/cold for that. Consider when you are sound asleep- you still unconsciously cover with blanket or throw away blanket depending on how sweaty/ cold you are- you dont need to consciously register that. So thermo-regulation, like other adaptive actions of affects, can happen in absence of accompanying felt feelings.

So what is the purpose of consciousness/feelings? They provide flexibility to behavior and  leave it to us whether we want to indulge in adaptive hardwired behavior or do differently. Taking our cold/heat analogy, instead of wiring our thermo-regulation behavior entirely, feelings provide us a way to keep remaining cold, despite feeling cold.

Similarly, consciousness/'free wont' gives the ability to suppress prepotent (adaptive in short term) response in favor of our long term view or values. By way of another example, if all we had was an unconscious fear circuit, we would always run when confronted with large challenges that are insurmountable; but when the conscious feeling of fear comes into play, although we may feel sacred as hell when confronted with larger opponents, we can still act bravely and with integrity- and that may be far adaptive in the longer run.

So the short answer is that conscious feelings like jealousy etc. exist so that we can act contra to that feeling if we wished to do so and are not doomed to always act as per what the feeling dictates!


Is there any good evidence that sadness causes chest pain ("heart ache")? It's commonly believed that sadness from romantic rejection causes chest pain ("heart ache").  This isn't that outlandish of a hypothesis, given that affect is just the mental representation of sensory input (e.g., chest pain) from our body to our brain.

But is there any good evidence for this link?  It's a widely held belief that I've never seen systematically substantiated, so it would be cool to see a study on it.

There is a fairly recently recognized medical condition called stress-induced cardiomyopathy, associated with chest pain and physical damage to the left ventricle:

  Because this weakening can be triggered by emotional stress, such as
  the death of a loved one, a break-up, or constant anxiety, it is also
  known as broken-heart syndrome.

Although most patients recover within a few weeks, in some extreme cases, this condition is known to be fatal.  As this diagnosis is still fairly new, prevalence is not accurately known, but it might be quite common in break ups - see Koulouris et al (2010) for a review.

Psychological distress can be a causal factor in other heart conditions as well (eg, Carey et al 2014; Graff et al, 2016; Buckley et al, 2012) that may be associated with chest pain.  However, other than these indirect effects, test subjects can generally distinguish psychological pain from physical pain, so although people may report psychosomatic symptoms such as chest pain associated with romantic rejection, it is not expected to be an indicator.

Nonetheless, across cultures and in many different languages, the same terminology is used to describe both physical and psychological pain, suggesting a similarity in experience.

"Social pain" is the mental stress resulting from rejection, bereavement, heartache, exclusion, etc.  There are quite a few studies supporting a link between social pain and physical pain - see Eisenberger (2012) for a fairly recent review.  In the typical experimental paradigm, subjects who have recently experienced social pain are reminded of their experience, eliciting the social pain response, while being monitored using physiological and/or neurological measurement tools such as fMRI.

Such studies have demonstrated that social pain experience uses many of the same neurological mechanisms as physical pain.  For example, from Kross et al (2011):

  Here we demonstrate that when rejection is powerfully elicited—by
  having people who recently experienced an unwanted break-up view a
  photograph of their ex-partner as they think about being
  rejected—areas that support the sensory components of physical pain
  (secondary somatosensory cortex; dorsal posterior insula) become
  active.

Combined with similar results from lesion studies, pain sensitivity, and changes in dopamine and cortisol, this has led to the hypothesis that humans evolved a mechanism for social pain that recycles the physical pain system (Macdonald & Leary, 2005; Eisenberger & Lieberman, 2004), eg:

  It has been suggested that, in mammalian species, the
  social-attachment system borrowed the computations of the pain system
  to prevent the potentially harmful consequences of social separation.

Overlap between the neural mechanisms for physical and non-physical pain is not complete however, presumably accounting for the differences in reported experience.


Neurotransmitters appearance in the evolutionary process Recently I disagreed with the assumption, that lots of neurotransmitters came within recent 10,000 years of Homo Sapiens evolution.
Judging from the available information sources, there is possibility of minor changes of brain reaction on neurotransmitters, but first assumption seems like nonsense for me.

So, are there any neurotransmitters, appeared only in human evolution history?

Then, are there reliable sources which will connect the appearance and development of biological species with appearance of neurotransmitters?

At last, are there significant acceleration of human brain evolution within last 10,000 years, connected with social processes or brain evolution for Humans occurring more gradually?

Neurobiology and Evolution are not exactly my field of expertise, but I'll try to answer anyway.

  Are there any neurotransmitters that appeared only in human evolution history?

Probably not. The common human neurotransmitters we know of, are also found in other animals. More surprisingly, most of them are also found in organisms with no nervous-system, such as microorganisms and plants. This has even led some to advocate the change of the name neurotransmitters to biomediaters (Roshchina, 2010).

It is believed that most of the changes in the nervous system occur at the circuitry level, and are not the introduction of new types of neurotransmitters. For example, Venter et al (1988) write:

  The presence of hormones, neurotransmitters, their receptors and biosynthetic and degradative enzymes is clearly not only associated with the present and the recent past but with the past several hundred million years. Evidence is mounting which indicates substantial conservation of protein structure and function of these receptors and enzymes over these tremendous periods of time. These findings indicate that the evolution and development of the nervous system was not dependent upon the formation of new or better transmitter substances, receptor proteins, transducers and effector proteins but involved better utilization of these highly developed elements in creating advanced and refined circuitry.

And Winer and Larue (1996) write:

  Many features in the mammalian sensory thalamus, such as the types of neurons, their connections, or their neurotransmitters, are conserved in evolution.

However, it is important to remember that there are changes related to the neurotransmitters and how they are used in the brain. For example, Burki and Kaessmann (2004) showed that one gene encoding the enzyme glutamate dehydrogenase, which is important in the neurotransmitter glutamate recycling process has appeared less than 23 million years ago in our evolution. Grailhe et al (2001) show that one type of Serotonin recceptor has disappeared somewhere in the evolution between rodents and humans.

References

Roshchina, V. V. (2010). Evolutionary considerations of neurotransmitters in microbial, plant, and animal cells. In Microbial Endocrinology (pp. 17-52). Springer New York.
Venter, J. C., Di Porzio, U., Robinson, D. A., Shreeve, S. M., Lai, J., Kerlavage, A. R., ... & Fraser, C. M. (1988). Evolution of neurotransmitter receptor systems. Progress in neurobiology, 30(2-3), 105.
Winer, J. A., & Larue, D. T. (1996). Evolution of GABAergic circuitry in the mammalian medial geniculate body. Proceedings of the National Academy of Sciences, 93(7), 3083-3087.
Burki, F., & Kaessmann, H. (2004). Birth and adaptive evolution of a hominoid gene that supports high neurotransmitter flux. Nature genetics, 36(10), 1061-1063.
Grailhe, R., Grabtree, G. W., & Hen, R. (2001). Human 5-HT5 receptors: the 5-HT5A receptor is functional but the 5-HT 5B receptor was lost during mammalian evolution. European journal of pharmacology, 418(3), 157-167.


Who first used the term 'heuristic' in a cognitive science context? I seem to recall that Herbert Simon borrowed the term from computer science, but I cannot remember the initial paper in which he made use of this borrowing.

A google scholar search reveals some papers from 1957-1958, for instance this one, but I really felt there was something from earlier in the 1950s.

A nice summary about heuristics can be found in:

Gigerenzer, G., & Gaissmaier, W. (2011). Heuristic Decision Making. Annual Review of Psychology, 62, 451–482.

In this review "satisficing" (accepting a good enough option) is referred to an earlier reference than the 1958 you cite:
Simon, H.A. (1955). A behavioral model of rational choice. Q. J. Econ. 69:99–118.

In their (Gigerenzer & Gaissmaier) history part they also refer to Einstein using the term in his 1905 paper on quantum physics, stating that the view he presented was "incomplete but highly useful".


Do stimulants increase the IQ tests score for everyone? There is some meta-analytic evidence that stimulants increase the IQ test scores of ADHD children by 2 to 7 points (Jepsen et al., 2009).
Although giving stimulants to non-ADHD children may be unethical, I'm still wondering if there is improvement in IQ test score in children (or adults) who do not meet the criteria for an ADHD diagnosis. An additional motivation for asking this is that a study by Tsai et al. (2013) found that the IQ test score improvement from methylphenidate "had no correlation with the decrement of ADHD symptoms."

Jepsen, J. R. M., Fagerlund, B., & Mortensen, E. L. (2009). Do attention deficits influence IQ assessment in children and adolescents with ADHD?. Journal of Attention Disorders, 12(6), 551-562.
Tsai, C. S., Huang, Y. S., Wu, C. L., Hwang, F. M., Young, K. B., Tsai, M. H., & Chu, S. M. (2013). Long-term effects of stimulants on neurocognitive performance of Taiwanese children with attention-deficit/hyperactivity disorder. BMC psychiatry, 13(1), 330.

IQ in ADHD sufferers indeed increases with the treatment of stimulants, such as methylphenidate (Meyes et al., 1994). This is thought to rely on the attention-narrowing effect of stimulants, i.e., they cause the
 easily distracted ADHD child to focus better on the IQ task (Aman, 1996).

It is an interesting question indeed whether such an effect also plays a role in healthy controls. Indeed it does, at least according to one study, where a control population was subjected to amphetamine.

Amphetamine improves performance on spatial working memory, Stroop tasks and enhances language production (Barch & Carter, 2005). The authors did, however, not measure performance on full blown IQ tests.

References
- Aman, J Development Phys Disabil (1996); 8(4): 347-65
- Barch & Karter, Schizophrenia Res (2005); 77(1): 43-58
- Meyes et al., DMCN (1994); 36(12): 1099–107


Does the person's walking say anything about the person's cognition? This afternoon I've been observing people at a local park and came up with some observations that lead me to this question:

Can the person's gait (manner of walking) say something about the person's internal experience at that moment? I'm thinking of arousal and cognition.

For example:
Have you ever seen a businessman or an office worker walk? They walk with a purpose, quite energetically with the body slightly inclined forward. Is it feasible to say that when such walk is observed, the person is going somewhere, and may be tense?

A child may be running around with arms in the air, along an irregular path. Can it be said that such child is energetic and excited at that moment?

Two elderly people may walk very differently. One couple walks at a regular pace of 3-4mph, while another couple may push one foot in front of the other at 0.5 mph. Can this tell us anything about the differences in the mental activity that takes place within these people?

A person may be strolling slowly at <1mph, observing the environment. Can it be said that such person is calm?

It appears to me that in the examples above, the person's mood/demeanor and  motion are connected.

I'm interested if there's really any correlation between how a person appears outwardly and how the person feels? In other words, if one is tense and feels pressed for time, would one start to "walk with a purpose", as opposed to strolling casually?

Thank you for your input.

In terms of answering this question I will address the one final question;
I'm interested if there's really any correlation between how a person appears outwardly and how the person feels?

A commonsense  answer to this question without any scientific research is; Yes.  All animals have non-verbal communication. Much of human communication is based on non-verbal factors. We ca interpret if someone is hostile, and unapproachable, or if someone is happy; from facial expression and body movements. A person's health and vitality is reflected in posture and gait.

Now scientifically:
There is correlation between how a person appears outwardly and how the person feels.
This question overlaps with interpreting body language and mood.

In terms of gait:
There is extensive research on the effect of a person's mood on gait. The studies I have listed below cover aspects of normal gait, and how gait is analysed, to the effects of mood on gait.

I have quoted from the article mentioned by Jeff in the comments.

  The authors examined the relationship between cognition and gait
  velocity, performed with and without  interference, in elderly
  participants. Neuropsychological test scores from 186 cognitively
  normal elders  were submitted to factor analysis that yielded 3
  factors: Verbal IQ, Speed/Executive Attention, and  Memory. Regression
  analyses revealed that these factors were signiﬁcant predictors of
  variance in gait  velocity, but the relationship varied as a function
  of task condition. All 3 factors predicted gait velocity  without
  interference. However, the Speed/Executive Attention and Memory
  factors but not Verbal IQ  predicted gait velocity in the interference
  condition. These ﬁndings suggest that gait velocity and  cognitive
  function may have both shared and independent brain substrates. Future
  studies should explore  gait velocity and cognitive function as
  predictors of dementia and falls.

Gait
Mansfield, P.J., Newmann, D.A., (2009),
Essentials of Kinesiology for the Physical
Therapist Assistant, Mosby: St. Louis, MO.

Psychosom Med. 2009 Jun;71(5):580-7. doi: 10.1097/PSY.0b013e3181a2515c. Epub 2009 May 4.
Embodiment of sadness and depression--gait patterns associated with dysphoric mood.
Michalak J, Troje NF, Fischer J, Vollmar P, Heidenreich T, Schulte D.

Can J Psychiatry. 1987 Apr;32(3):190-3.
Mood, depressive illness and gait patterns.
Sloman L, Pierrynowski M, Berridge M, Tupling S, Flowers J.

Neuropsychology Copyright 2006 by the American Psychological Association
2006, Vol. 20, No. 2,  DOI: 10.1037/0894-4105.20.2.215
Cognitive Processes Related to Gait Velocity:
Results From the Einstein Aging Study
Roee Holtzer, Joe Verghese, Xiaonan Xue, and Richard B. Lipton
Yeshiva University


Is Neuro-Linguistic Programming (NLP) a science or pseudoscience? Are there some branches of NLP which are considered scientific?

  Bandler and Grinder also claim that NLP can treat problems such as
  phobias, depression, habit disorder, psychosomatic illnesses,
  myopia,[8] allergy, common cold[9] and learning disorders, often in a
  single session.[10][11][12][13] NLP has been adopted by some
  hypnotherapists and in seminars marketed to business and
  government.[14][15] Reviews of empirical research find that NLP's core
  tenets are poorly supported.[16] The balance of scientific evidence
  reveals NLP to be a largely discredited pseudoscience. Scientific
  reviews show it contains numerous factual errors,[14][17] and fails to
  produce the results asserted by proponents.[16][18] According to
  Devilly (2005),[19] NLP has had a consequent decline in prevalence
  since the 1970s. Criticisms go beyond lack of empirical evidence for
  effectiveness, saying NLP exhibits pseudoscientific
  characteristics,[19] title,[20] concepts and terminology as
  well.[21][22] NLP is cited as an example of pseudoscience when
  teaching scientific literacy at the professional and university
  level.[23][24][25][26][27][28][29][30][31][32] NLP also appears on
  peer reviewed expert-consensus based lists of discredited
  interventions.[16]

Source: Wikipedia. I've made a fast search on Wikipedia, but I cannot access the papers. Also, going deep into this topic would be really demanding.

We have quite a few questions on this site about Neuro-linguistic-programming. In general I think it is more productive to talk about a particular scientific claim or a particular treatment rather than an entire paradigm. Paradigms that are not grounded in the scientific method may incidentally reflect the truth when studied relative to scientific standards.

In general, this question on NLP and sales effectiveness has mostly been answered in a general sense. In particular, @what's answer makes reference to the scientific evaluation section on Wikipedia which basically states that NLP is not scientifically based or validated.


In principle, could a brain be rewired to experience more pleasure and/or pain? I'm not sure if these are two separate questions, but I'm curious: in theory, could an existing adult mind/brain be modified to perceive pleasure/pain signals more intensely than otherwise? Without drastically changing the rest of the brain (i.e. while making sure that the brain is the same person; although this question is understandably complicated and potentially philosophical)?
As to the latter part of the question, the SCN9A gene might play a part. Maybe there exists a similar gene for pleasure?
(I made a post focusing on the genetic side on the biology SE. I think the questions are different enough for this to be acceptable, but it might be worth looking there to avoid duplicated effort.)

This is a difficult question to answer and likely can generate a variety of equally valid (or invalid) answers.
I thought to tackle this from a pathological vista - namely that of sensory processing sensitivity (SPS), which seemingly resembles your area of interest.
SPS can be defined as (Acevedo et al., 2018)

[A] genetically based trait associated with greater sensitivity and responsivity to environmental and social stimuli. [It] is characterized by greater empathy, awareness, responsivity and depth of processing to salient stimuli.

In their article the authors review the structural underpinnings as observed by fMRI scanning of SPS, alongside the brains of Autism Spectrum Disorder, Schizophrenia and Post-Traumatic Stress Disorder who also exhibit SPS alongside their other symptoms.
Common activated regions in all disease types were shown in the precentral gyrus.
SPS was associated with activity in reward processing centers (ventral tegmental area (VTA) and substantia nigra (SN), centers for regulation of bodily physiology and pain (hypothalamus and periaqueductal gray (PAG); self versus non-self recognition and empathy (inferior frontal gyrus (IFG) and insula), awareness and self reflection (temporoparietal junction (TPJ)) and self-control (prefrontal cortex (PFC)).
In terms of Autism Spectrum Disorder, Schizophrenia and Post-Traumatic Stress Disorder the authors continue with multiple brain regions that are activated commonly and uniquely with respect to SPS proper. I refer to the review referenced below for details.
I reckon, but am unsure, that re-wiring of the pathways or altering the structures themselves with, e.g., transcranial stimulation or with ablation techniques can emulate SPS symptoms, including pain and emotion processing. The practical ways to do this are difficult, given the complexity of the brain.
References
- Acevedo et al., Philos Trans R Soc Lond B Biol Sci (2018); 373(1744): 20170161


Relationship between cognitive load and self-indulgent behavior in simple task completion Background

A subject in an office-building setting is asked to memorize a list of numbers and to write them down on a whiteboard in another room on the opposite side of the building.

The subject must navigate a series of hallways in order to get from the first room to the other room.

At a certain point midway through the hallways, the subject is approached by a confederate who asks the subject if she would like a treat. The subject is given two choices:

1) a high-nutrition, moderately-tempting snack with a low level of self-indulgence
2) a low-nutrition-value, highly-tempting snack with a high level of self-indulgence

Hypothesis

There exists a relationship between complexity of the memorization task and the choice to accept the high self-indulgence snack, such that:

The subjects are more likely to accept the high self-indulgence snack if the memorization task is more complex and imposes a higher cognitive load.
The greater the cognitive load of an in-process mental task means the greater deficiency the subject will have in being able to resist or "self-censor" behaviors.

Question

Can anyone provide links or references that relate to the above hypothesis and test?

Gailliot et al (2007), didn't do it with a memorization task, but with a variety of other tasks requiring self-control:

  The present work suggests that self-control relies on glucose as a limited energy source. Laboratory tests of self-control (i.e., the Stroop task, thought suppression, emotion regulation, attention control) and of social behaviors (i.e., helping behavior, coping with thoughts of death, stifling prejudice during an interracial interaction) showed that (a) acts of self-control reduced blood glucose levels, (b) low levels of blood glucose after an initial self-control task predicted poor performance on a subsequent self-control task, and (c) initial acts of self-control impaired performance on subsequent self-control tasks, but consuming a glucose drink eliminated these impairments. Self-control requires a certain amount of glucose to operate unimpaired. A single act of self-control causes glucose to drop below optimal levels, thereby impairing subsequent attempts at self-control.

Gailliot, Matthew T., et al. "Self-control relies on glucose as a limited energy source: Willpower is more than a metaphor." Journal of personality and social psychology 92.2 (2007): 325. PDF


Can adults adapt to less sleep? I am asking whether adults, especially in circumstances like a monastery or Zen center, can become able long-term to sleep only about 4 to 5 hours a night? So, that would mean: no children to care for, no heavy labor, lots of time spent meditating and doing other things that the body would find restful and undemanding...

Can the mind get along on much less hours of sleep than the usual adult? I am not asking about the absolute numbers, only if it can be reduced and sustained over years, or permanently?

A paper by Kaul et al. from 2010 suggest that meditation can indeed decrease the need for sleep. Meditation acutely improves psychomotor vigilance, and may decrease sleep need

Quote from conclusions:

  These results suggest that meditation provides at least a short-term performance improvement even in novice meditators. In long term meditators, multiple hours spent in meditation are associated with a significant decrease in total sleep time when compared with age and sex matched controls who did not meditate. Whether meditation can actually replace a portion of sleep or pay-off sleep debt is under further investigation.


Can signals from the prefrontal cortex alone trigger a readiness potential in the pre-supplementary motor area? Background

In Haggard, Patrick. "Human volition: towards a neuroscience of will." Nature Reviews Neuroscience 9.12 (2008): 934., the author states in the caption of Figure 1 (pg. 4):

  The primary motor cortex (M1) receives two broad classes of inputs.
  One key input (left-hand panel) reaches M1 from the supplementary
  motor area (SMA) and the pre-supplementary motor area (preSMA), which
  in turn receives inputs from the basal ganglia and the prefrontal
  cortex.

Question

I'm failing to disambiguate the ending phrase (emphasis mine)

  basal ganglia and the prefrontal cortex

Is the "and" meant to be interpreted as a logical AND or logical OR? In other words, does a readiness potential in the pre-supplementary motor area (preSMA) require an active input from both the basal ganglia AND the prefrontal cortex concurrently or is a sufficiently strong signal from either region alone sufficient?

Hunch

My guess is that the latter is the case. For example, on the very same caption of Figure 1 part b, the author indicates that the signal from the frontopolar cortex starts a chain that ends with voluntary action of the right hand. This indicates that executive control from the frontopolar cortex  alone can trigger an eventual movement. Since this is only a hunch, I still want to clarify the point of confusion.

Intent

I'm asking this question because I want to figure out a situation at the behavioral level, namely if people can trigger movements purely by executive function and independently of primal urges/apprehensions.

Standards

It may be difficult to give a direct and bulletproof answer to the question without a deliberate experiment (see comment). However, I find it acceptable to have a lower standard for potential answer post - for example, conjectures based on indirect evidence.

The original author is not making a claim one way or another for logical AND or logical OR within this context. The statement

  the pre-supplementary motor area (preSMA), which in turn receives inputs from the basal ganglia and the prefrontal cortex

is referring only to inputs to the preSMA; it is not making any strong statements about which inputs are causal for the readiness potential, only mentioning that those connections exist and therefore could be involved in communication of the readiness potential.

There are in fact cortico-cortical loops that route through the basal ganglia (see for example Lopez-Paniagua & Seger, 2011; there is probably a better canonical reference but not one I have in hand right now); if there is a signal from frontopolar cortex that reaches motor cortex that does not tell you the basal ganglia were not involved. A signal originating in cortex could communicate with another cortical area both via direct cortico-cortico and via basal ganglia open loops, not that a basal ganglia signal preceded both.

The only way to truly answer your title question would be to somehow inactivate either basal ganglia or PFC inputs to preSMA. I am not aware of such an experiment, it would be quite technically and ethically difficult both in humans and primates, and PFC is less developed in rodents so it's difficult to make direct analogy there.

More generally, the basal ganglia are definitely involved in voluntary movement. One can simply observe Parkinsonian patients, who have difficulties initiating voluntary movements due to basal ganglia pathology (DeLong 1990 discusses some of the motor impacts of lesions of the basal ganglia).

If you want to know whether movements can be triggered "purely by executive function and independently of primal urges/apprehensions" you will not find the answer simply by identifying whether the basal ganglia are involved or not. Although yes, the basal ganglia are often associate with more "primal" actions, that is only relevant in the absence of neocortex. In the presence of neocortex, that organization no longer applies because cortex influences the basal ganglia (and vice versa).

Furthermore, it does not seem possible to separate out the basal ganglia from neocortex in terms of cognitive control networks (Duncan 2010, Cole et al 2013), since coactivation of those areas is typically observed and not dissociable.

Cole, M. W., Laurent, P., & Stocco, A. (2013). Rapid instructed task learning: A new window into the human brain’s unique capacity for flexible cognitive control. Cognitive, Affective, & Behavioral Neuroscience, 13(1), 1-22.

DeLong, M. R. (1990). Primate models of movement disorders of basal ganglia origin. Trends in neurosciences, 13(7), 281-285.

Duncan, J. (2010). The multiple-demand (MD) system of the primate brain: mental programs for intelligent behaviour. Trends in cognitive sciences, 14(4), 172-179.

Lopez-Paniagua, D., & Seger, C. A. (2011). Interactions within and between corticostriatal loops during component processes of category learning. Journal of cognitive neuroscience, 23(10), 3068-3083.