Is attraction between two people just physical, not neurological/psychological?

All attraction involves the brain. The brain is responsible for consciousness, perception, and motivation.

Not all attraction is physical. In two structural theories of love with which I'm familiar, physical attraction corresponds to a minority of what constitutes love. Love isn't exactly the same as attraction, but much of these theories' content implies attraction that is more than sexual and sometimes not sexual at all. In Sternberg's triangular theory of love, passion often entails physical attraction, but the theory frames intimacy and commitment as somewhat independent and based on other aspects of interpersonal relationships such as trust, closeness, benevolence, role identification, and cooperation.

People have many reasons to desire these relationships besides sex. Lee's love styles considers physical passion a defining aspect of only one of six styles. Other motives drive the other styles: power, affiliation, teamwork, emotional fusion and obsession, and altruism. However, one might argue that some of these are not clearly approach motives (mania in particular may be more fear-driven), or that the other person is more a means to an end than the object of desire (particularly pragma and ludus). Regardless, storge and agape are clearly more platonic (though not necessarily nonsexual) forms of attraction with a person as the primary object.

Separating the mind from the body is not possible at present within the scope of mainstream empirical science. Hence all questions that depend on this premise are very likely to be speculative and controversial, and probably off-topic for this site, which discourages opinion solicitation. Even so, the logic of these theories seems to indicate clearly enough that while many aspects of attraction do not depend on sexuality, some do, and that much might change if the physical object of sexual attraction changes. Furthermore, many physiological elements that influence the brain during attraction would have to be emulated in the alternate host to have unchanged consequences, such as adrenalin, which is produced in glands atop the kidneys. Dopamine and serotonin also play important roles in love style variation (see the reference below); their influence would require emulation as well if the mind were somehow separated from the physical sources of these neurotransmitters.

Reference
Emanuele, E., Brondino, N., Pesenti, S., Re, S., & Geroldi, D. (2007). Genetic loading on human loving styles. Neuro Endocrinology Letters, 28(6), 815–21. PMID 18063936.


What is the proper term for the synchronization of eye movements?

binocular coordination

Linked below is a general overview of binocular coordination which also describes how, due to independent saccades events, mammalian eyes are generally not actually very well "synchronized".

Kirkby JA, Webster LA, Blythe HI, Liversedge SP. (2008) Binocular coordination during reading and non-reading tasks. Psychol Bull. 134(5):742-63

http://www.ncbi.nlm.nih.gov/pubmed/18729571


How to design psychology tests for concept formation?

There's no one good answer to this unfortunately, the question is too broad. Seems like you have made a decent start, here are two more quite different methods-focused references to add to your reading that might help:

Divjak, Dagmar, and Antti Arppe. "Extracting prototypes from exemplars What can corpus data tell us about concept representation?." (2013): 221-274.

Lee, Michael D., and Wolf Vanpaemel. "Exemplars, prototypes, similarities, and rules in category representation: An example of hierarchical Bayesian analysis." Cognitive Science 32.8 (2008): 1403-1424.


How to assign numbers to response options on a bipolar scale?

Yes, it matters, and you should probably go with scale B if you have to use numbers. See my answer here on Cross Validated in response to, "Is 0 a valid value in a Likert scale?" The zero in the middle of A is confusing (this isn't to say I don't understand it, but do you really trust that every respondent you ever come across will?), but even if you were to replace it with 4 and add 1 to the options currently labeled 4–6, you might get different answers than if you go with (-3)–(+3). Either way, there's some connotation of "less" applied to the options on the left, which may bias responses. Option C even confuses me, so I'd say you should throw that out completely...

IMO, the safest bet would be to label your rating options with words, not numbers. To make responding easy, let people check boxes or provide abbreviated codes for their preferences such as "Strongly prefer left option" = SL or "Right option is a mildly better fit" = Rm. Here's how I presented these suggestions in my other answer, and the supporting reference (Schwarz, Knäuper, Hippler, Noelle-Neumann, & Clark, 1991):

  Allow respondents to check cells in a table corresponding to their answer preference: each row can be a different item, and each column can be labeled with your rating anchor, or vice versa – no numbers involved. Here's how that might look (if one were to answer wisely):

  $\begin{array}{|c|c|c|c|c|c|c|}\hline&\tiny\text{Strongly Disagree}&\tiny\text{Disagree}&\tiny\text{Mildly Disagree}&\tiny\text{Mildly Agree}&\tiny\text{Agree}&\tiny\text{Strongly Agree}\\\hline\tiny\text{Tumblers: better than pumpers!}^*&&&&&&\checkmark\\\hline\tiny\text{I look fat in this dress.}&\checkmark\\\hline\end{array}$*

  Wikipedia gives another style using marked options (by Nicholas Smith):

  Letter codes can also be substituted for numeric options if blanks are to be filled for a list of very many items; e.g., {SD,D,MD,MA,A,SA}. Just don't forget to include the legend!

  Reference
  Schwarz, N., Knäuper, B., Hippler, H. J., Noelle-Neumann, E., & Clark, L. (1991). Rating scales numeric values may change the meaning of scale labels. Public Opinion Quarterly, 55(4), 570–582.


Modelling the Human Brain as a directed graph

Axo-axonic synapses and dendrodendritic synapses exist, and are not errors. They are particularly common in invertebrate nervous systems but are also found between particular cells in mammalian brains. I would say they are relatively understudied but not ignored.

True errors of the type you describe seem extremely unlikely to me. Synapses do not simply impinge on other fibers, there is extensive pre- and post-synaptic machinery, and bidirectional communication is necessary for proper synaptogenesis. Synapses are held together by connective proteins that are anchored in each membrane.

However, in terms of thinking of the brain as a "directed graph" one need not consider these uncommon synapses to have bidirectional connectivity: it is entirely possible, if not common, for cells to make traditional axon-dendrite synapses on another neuron that makes a reciprocal axon-dendrite synapse.

Graph theoretical approaches to understanding the brain are quite common, however, and certainly did not arise on StackExchange in 2016, as your own references make clear. There is no need for a directed graph to only have connections in a single direction, either. Any connectivity matrix can be interpreted in terms of graph theory.

Haydon, P. G., & Drapeau, P. (1995). From contact to connection: early events during synaptogenesis. Trends in neurosciences, 18(4), 196-201.

Kawaguchi, Y., & Kubota, Y. (1997). GABAergic cell subtypes and their synaptic connections in rat frontal cortex. Cerebral cortex (New York, NY: 1991), 7(6), 476-486.

Pinault, D., Smith, Y., & Deschênes, M. (1997). Dendrodendritic and axoaxonic synapses in the thalamic reticular nucleus of the adult rat. Journal of Neuroscience, 17(9), 3215-3233.

Somogyi, P. (1977). A specific ‘axo-axonal’interneuron in the visual cortex of the rat. Brain Res, 136(2), 345-350.


Is it possible to condition oneself to not be bothered by distressing sounds?

Short answer
Meditation may be key to block out distracting noise.

Background
One study has shown that during meditation, expert meditators with over 19,000 h of meditation experience show less brain activations in regions associated with discursive thoughts and emotions (prefrontal regions, basal ganglia, and subthalamic nuclei), and more activation in regions related to response inhibition and attention (ventral prefrontal cortex and intraparietal lobule).

The authors used neutral (restaurant background noise), positive (cooing baby) and negative sounds (a screaming lady).

However, meditation is probably not the conditioning training you are after for use in everyday life, but since the question has been silent I thought to start off with this lead.

Reference
- Brefczynski-Lewis et al., PNAS (2007); 104(27): 11483-8


A google search for neural network library will return many relevant pages, with neural network libraries written in several programming languages.

You could also look for tutorials on programming perceptrons which are among the most basic neural networks. This would teach you how to actually program the network from scratch, instead of using a pre-made library.

This walkthrough covers the development of a more complex neural network library if you are looking to jump right into building multilayer networks.


What does "veridicality" mean in terms of psychology?

Veridicality is a term used in cognitive science; it is the degree to which your internal representation of the world accurately reflects the external world.
Some background
Since the work on Humberto Maturana in color perception, it was considered very important to not always focus on the fact that there is some external stimuli to be cognized by the subject and then reacted on, but that instead there is an internal world or representation which is then cognized and responded to. In many cases the veridicality of the internal representation is very good, and the experimenter can focus on just the easy-to-observe external stimuli. However, in many settings (like color perception) the veridicality of the internal representation is low (easiest way to imagine this: think of a difference in internal representation between a color-blind and non-color-blind person). Hence the experimenter needs to explicitly measure the internal representation and try to understand how it acts. Once you have a measure of this (a 'criterion for veridicality') then you can start to think about how the subject cognizes the stimuli.
Specific to this paper
In the context of the first sentence, what the authors are saying is: even with the narrow focus, it appears that the accuracy of the internal representation does not improve. Thus, the experimental results depend not only on the external stimuli (psychophysical method used) but how good we are at estimating the accuracy of the internal representation (criterion of veridicality).
In the second sentence they propose a metric of veridicality: ask how far you think an object is (say in meters) if the results scale linearly with actual distance, then the internal representation of space is good, else it is not.


Is there any evolutionary theory for self-destructive behavior?

There are many different uses for the word "stress" that should not be confused with one another.  For example, Self-destructive behaviour may be used to cope with psychological stress.  Other examples are stress response, and biological stress, both of which have very different meanings.  An important driving force of natural selection - a key process in evolution - is called selection pressure, which is yet another entirely different kind of stress.

Evolution certainly has great explanatory power, but it doesn't explain all behaviour - especially not the kind that is learned rather than inherited.

I am not aware of any evidence that self-destructive behaviour is inherited, but there is some evidence that it may be learned.  As such, there is no impetus to explain this behaviour in an evolutionary context.  Having said that, self-harm is found in animals besides humans, suggesting that perhaps something may be inherited (eg, the basic "learning mechanism" in humans has many similarities to other animals) that has this side-effect.

A lot of human behaviour does not "make sense" in the immediate context.  Much human behaviour relies on heuristic rules that work most of the time, but fail some of the time.  So for example, if self-harm results from learning, then well, most of the time our built-in learning mechanism serves us well, but sometimes it fails us.


How can reaction times be measured, and what affects it?

Reaction times can be measured by a variety of techniques in the lab. The simplest test is to present a stimulus to a test subject and instruct the subject to press a button as fast as possible after the stimulus is perceived. Responses can be measured by using a response box. Often-used stimuli are either visual (e.g., a colored dot that pops up at random times on a computer screen), auditory (e.g., an acoustic beep), or tactile (e.g., a vibratory buzz or tap on the finger). These tests measure the reaction time from stimulus presentation up to the moment the subject presses the button. Hence, obtained response latencies include peripheral sensory processes, central sensorimotor processing in the brain, and motor output.

Age increases reaction time, mainly due to a slowed motor output (Woods et al., 2015). The stimulus modality also affects response latency. Visual stimuli result in long reaction times, tactile stimuli in shorter latencies, and auditory stimuli induce the shortest reaction time (Ng & Chan, 2012). These differences reflect the slow sensory processing in the visual system and the fast response of the auditory system. Neuro-supressants, such as alcohol, tranquilizers, antiepileptics- and anesthetics all increase reaction times (e.g., Mitchell et al.,, 1993).

References
- Mitchell et al., Pediatrics (1993);91(1):101-5
- Ng & Chan, Proc IMECS II (2012)
- Woods et al., Frontiers Human Neurosci (2015); 9:131-12p


Within psychiatry, how is homosexuality discussed or classified?

In 1973, the American Psychiatric Association (APA) removed the diagnosis of “homosexuality” from the second edition of its Diagnostic and Statistical Manual (DSM) (Jack Drescher, 2015).

Theories of pathology which declared that some internal defect or external pathogenic agent causes homosexuality, have been rejected, such as the theories of immaturity which considered the homosexuality a "developmental arrest".

It is rare to find a theory of homosexuality that does not draw upon gender beliefs that contain implicit cultural ideas about the “essential” qualities of men and women.
Who is a real man? Who is a real woman?
Since there weren't scientific evidences to claim: "Homosexuality is a mental disorder", after a vote, Homosexuality has been depathologized.

Accordingly, the answer to your question is no. Homosexuality is not a mental disorder, it's just a normal sexual orientation.

For further informations i suggest: "Out of DSM: Depathologizing Homosexuality" (Jack Drescher) 2015 : LINK:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4695779/


What are the neurological differences between those who have a high tolerance to pain and those who do not?

Much of the "higher order" sensation of pain is processed in the anterior cingulate cortex.

From Wikimedia Commons

There is a movement towards performing anterior cingulotomies in patients with intractable pain.  These procedures are also used to help patients with severe depression or obsessive compulsive disorder, so we have some idea that this area of the brain is a point at which emotional salience is associated with our experience of the world around us.  In the case of pain, post-surgical patients still experience all of the "lower level" symptoms (prostaglandin synthesis, etc.), but do not attach any meaning to them.

So, it is likely that individual differences in this anatomical region could partially account for those who can "work through" the pain versus those for whom it becomes overwhelming.  It's certainly possible that those who can tolerate pain have a lower sensitivity to prostaglandins in their spinal circuitry, but I can't speak to whether that's a valid explanation.

  Yen CP, Kuan CY, Sheehan J, Kung SS, Wang CC, Liu CK, Kwan AL (2009) Impact of bilateral anterior cingulotomy on neurocognitive function in patients with intractable pain. J Clin Neurosci., 16(2), 214-9.


Is there actually a correlation between emotional trauma and homosexuality

The widely accepted answer to this question is that homosexuality is not a choice but science has no concrete answer as to exactly why people are homosexual, heterosexual, or bisexual (or any other sexual orientations that one may identify with).

The Wikipedia page, Homosexuality, offers many great references and indicates that science has not definitive answer for what the 'cause' of homosexuality, only that it may be an interplay between generics, hormones, and environment.


Attractiveness bias, based on political views

It is a negative/reverse halo effect, aka a horns (or devil) effect.


I've also observed this behaviour in friends, and was curious to see what research has been done on the topic. Here's what I found (summary at the end).

Sechrest and Flores (1971) study of leg-jiggling

Sechrest and Flores (1971) performed an observational study of the prevalence of leg-jiggling

  leg jiggling was defined as a vertical, rhythmic movement of one or
  both legs while the subject was in a seated position

Their findings, albeit based on varying-quality data were that:

leg jiggling is more common in the Philippines than in the United States
individual differences exist in prevalence of leg jiggling
people may jiggle their legs more when alone than in company
leg jiggling appears to be more prevalent in males than in females
leg jiggling is facilitated by type of sitting position. Specifically, legs uncrossed makes leg jiggling a lot easier and more likely.

They tentatively concluded that leg jiggling is a symptom of tension and classified it as a nervous mannerism. They also suggested, given cultural differences, that it may be acquired through imitation of others.

Leg jiggling as communication

Smith and Naryan (2008), in their conference abstract, discuss features of leg jiggling and conclude that:

  while so far we can only speculate about the causal and
  functional properties of jiggles, they are clearly substantially
  rule-governed, sensitive to both formal and semantic aspects of
  ongoing discourse, widespread - both patterns were observed in all
  discourse contexts, and both languages - and deserving of further
  attention.

Restless leg syndrome

There is a disorder called restless leg syndrome. From the description the leg movement is voluntary but the desire to move the leg sounds much stronger than what we are talking about with normal leg jiggling.

Fidgeting

Mehrabian and Friedman (1986) did a general study of fidgeting where leg jiggling was classified with a wide range of other fidgeting behaviours.
Fidgeting was defined as:

  engaging in manipulations of one's own body parts or other objects, such actions being
  peripheral or nonessential to central ongoing events or tasks

They developed a self-reported fidgeting scale and proceeded to correlate the scale with a range of other measures. Given the composite nature of the scale, it is difficult to say what correlates leg jiggling specifically has with other measures. And even if such correlations were known, it would only say something about what types of people jiggle their legs rather than the effect leg jiggling has for those that do jiggle.

Student concentration

Appleton (1969) in a study of student concentration suggests

  Individual styles and habits reveal personal means of coping with the
  profound isolation of the concentrating state. Leg jiggling, for
  example, may be an outlet for sexual tension or a method of exercise
  and movement. Many students find the physical inactivity demanded by
  heavy work loads to be extremely difficult to bear.

Summary of links between leg jiggling and focus

So, in relation to your specific question on leg jiggling facilitating focus, the research that I've found is fairly limited. Researchers have noticed that leg jiggling is used by students when studying in order to deal with the otherwise, long periods of no movement. This is consistent with my own thoughts that it might be related to a general desire to increase circulation. Several researchers have also posited that leg jiggling may be  a way of dealing with stress, which arguably might assist with concentration. But ultimately, it looks like more research is needed on this topic, particularly experimental evidence on the effects of leg jiggling.

References

Appleton, W. S. (1969). The struggle to concentrate. Amer. J. Psychiat, 126, 256. FREE PDF
Mehrabian, A. and Friedman, S. (1986). An analysis of fidgeting and
associated individual differences. Journal of Personality,
54(2):406-429.
Sechrest, L. and Flores, L. (1971). The occurrence of a nervous
mannerism in two cultures. Journal of Nervous and Mental Disease. Asian Studies, 1, 55-63. FREE PDF
Smith, N. J. & Narayan, S. (2008). Fidgeting is Not Random: Rhythmic Leg Motion, Speech, and Gesture.9th Conference on Conceptual Structure, Discourse, & Language (CSDL9) LINK


Devices that detect when someone is falling asleep

I've used the Zeo (http://www.myzeo.com/sleep/). It seems to work pretty well. It tracks which stage of sleep you are using a very basic EEG. There are some details on how it operates here: http://radar.oreilly.com/2009/10/how-the-zeo-sleep-device-works.html

As I said, I've used it in the past and from what I can tell, it seems to be pretty accurate, assuming you don't knock the sensor off while you're sleeping.


Does eye contact improve attention and learning?

This is a great question on a highly fascinating topic for which evidence seemingly abounds among many species. From the standpoint of an evolutionary approach, the fight or flight stress response would be informed based on eye contact and movement - gauging the level of activity present in a potential predator's facial attributes.

Here is a cool link on the evolutionary aspect: http://www.sciencedirect.com/science/article/pii/S0031938403001562

Here is one on social signal processing as per the specific structure in the brain: http://pss.sagepub.com/content/15/9/598.short


What article looked at the relationship between bedtime stories and national productivity?

I believe this is referring to David McClelland's 1961 book "The Achieving Society."* McClelland proposed that an achievement motivation (desire for achievement) could predict economic growth and success. He examined this from a range of social and individual psychological factors, including the achievement content of "cultural products" such as children's stories and folk tales. He developed a value coding system for children's stories that centered on the impact of different story characteristics on the ego (this is your passive vs active term). Examples include whether the protagonist was of high or low social standing (ego status), influences on the ego (fate or man), how the ego responds (brains vs brawn), and whether the ego (protagonist) engages in work in order to achieve a goal. These in turn were coded into achievement motivation.

Among his findings, McClelland noted that cultural products high in achievement motivation were associated with how many full-time entrepreneurs were found in pre-literature cultures, the economic success of different historical empires, and the rate of growth in national consumption of electric power (and presumably industry) in the early twentieth century.

McClelland continued to publish on the topic (1975), though the theory received criticism and some subsequent studies failed to replicate his results (Gilleard, 1989; Mazur & Rosa, 1977). However, a more recent study suggested that an expansion of the theory would more readily capture the impact of motivation on economics in Eastern cultures, and might strengthen the predictive power of this method (Doyle & Doyle, 2001). Additionally, a 2009 study (Engeser, Rheinberg, & Moller) comparing achievement imagery in school textbooks in different German states found that the more economically successful regions had books with more achievement images. The introduction to the Engeser & colleagues paper also provides some links to related studies, for your reference.

Doyle, K. O., & Doyle, M. R. (2001). Meanings of wealth in European and Chinese fairy tales. American Behavioral Scientist, 45(2), 191-204.

Engeser, S., Rheinberg, F., & Moller, M. (2009). Achievement motive imagery in German schoolbooks: A pilot study testing McClelland's hypothesis. Journal of Research in Personality, 43, 110-113.

Gilleard, C. J. (1989). The achieving society revisited: A further analysis of the relation between national economic growth and need achievement. Journal of Economic Psychology, 10(1), 21-34.

Mazur, A. & Rosa, E. (1977). An empirical test of McClelland's "Achieving Society" Theory. Social Forces, 55(3), 769-774.

*McClelland's book was originally published by D. Van Nostrand Co., Princeton, NJ, but seems to have been republished in 2010 by Martino Fine Books (ISBN:  978-1891396397).


Double blindedness in a fully remote trial

Double blind basically consists when the patient does not know to which condition it belongs (control, treatment A, treatment B) and the professional does not know to which group he/she is administering the treatment (control, treatment A, treatment B).

The double-blind designation is not based on the fact that the initial level of depression is not assessed. (I guess you know it and it has been erroneously specified in the question).

In online studies this denomination is not usually used although of course it is not incompatible. (The issue is that this denomination is not usually used because the trial is not common either).

In short I do not see problem with the double blind designation.

On the other hand, it would be necessary to pay close attention to the clinical level and the characteristics of the intervention (you do not specify, is the intervention also remote?).

In any case sounds very interesting.


What is the most common age for developing psychosis?

There seems to be no correlation between age and onset of psychosis. The only difference between early onset and late onset psychosis, is the individual with late onset psychosis, generally, possesses better coping skills.

  The aims of this study were to calculate the incidence of non-affective, non-organic psychotic symptoms across the life span and to explore the contribution of different sets of risk factors in relation to age at onset.  ..//..

  Onset of psychotic symptoms in late life is no rare event. Compared to early onset psychosis, the late-onset counterpart less often arises in a context of emotional dysfunction and negative affectivity, suggesting qualitative differences in aetiology and more effective premorbid coping styles. 1.

The incidence of psychosis is increased with factors, such as familial mental health. The following article provides a comprehensive table of high risk factors, incidence and age onset.

  These risk markers are divided into two categories: (1) precursors related to early etiological factors (family psychiatric history, perinatal and obstetric complications, neurobehavior deficits, early parental separation, institutionalization, and poor family function) and (2) precursors signaling latent mental illness (personality measurements indicating proneness to psychosis, and teacher ratings indicating emotional lability, social anxiety, social withdrawal, passivity, poor peer relations, and disruptive and aggressive behavior). Because teacher ratings have been shown to be powerful predictors of adult mental breakdown, part of this article focuses on a specific study that assesses such ratings as predictors of psychosis in a high-risk population. 2.

 2.

There is some correlation with the course psychotic illness takes and the age of onset.

  A diagnosis of schizophrenia, higher antipsychotic dose, and more negative symptoms were associated with earlier onset of illness, while female sex and a more chronic course were associated with later illness onset. Furthermore, earlier onset was associated with worse performance on immediate recall and sustained attention. However, male sex, more negative symptoms, and higher antipsychotic dose mediated the effect of age at onset on memory, while negative symptoms explained its association with attention/vigilance. 3.

I cannot find studies answering your question regarding familial history of psychosis and late onset psychosis. I have drawn the following conclusions from the information provided.

Disclaimer: The following are my own ideas:

In view that the risk factors for psychosis, are also associated with the likelihood of earlier onset psychosis, one could suggest (loosely) that is psychosis was to develop from such risk factors, it would most likely be earlier rather than later. As late onset psychosis, does not seem to be correlated with such risk factors. This would be no guarantee that a late onset psychosis could not occur with individuals with familial history of psychosis; however my guess  would be the later one with this familial history goes psychosis free, the less likely it is for that individual to develop psychosis beyond an age (perhaps mid 30s).

1. Soc Psychiatry Psychiatr Epidemiol. 2007 April; 42(4): 288–294.
Published online 2007 March 12. doi:  10.1007/s00127-007-0171-6
PMCID: PMC1913178
Psychosis risk as a function of age at onset
A comparison between early- and late-onset psychosis in a general population sample
Sebastian Köhler, Jim van Os, Ron de Graaf,3 Wilma Vollebergh, Frans Verhey, and Lydia Krabbendamcorresponding author
Acta Psychiatr Scand. 2012 Oct;126(4):274-81. doi: 10.1111/j.1600-0447.2012.01873.x. Epub 2012 May 14.
2. Risk Factors of Psychosis: Identifying Vulnerable Populations Premorbidly
By Su-chin Serene Olin and Sarnoff A. Mednick
Schizophrenia Bulletin, Vol. 22, No. 2, 1996
National Institute of Mental Health
3. Cognitive functioning and age at onset in non-affective psychotic disorder.
van der Werf M, Köhler S, Verkaaik M, Verhey F, van Os J; GROUP Investigators.
Source
Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON Graduate School of Neuroscience, Maastricht University, The Netherlands.


Does the Hodgkin-Huxley Model take into account the action of the ion pumps (e.g., Na-K-ATPase)?

HH doesn't "count ions", it pretends the reservoirs are infinite.

Specifically, the "reversal potential" for each ion species is a constant.  This constant is calculated from the Goldman Hodgkins Katz equation which uses the concentrations on either side of the membrane to calculate the reversal potential given the concentration gradient.

We could hypothetically keep this a function of the individual species concentrations and add a current to the model to represent the pump, but you would gain little in predictive power and much in computational complexity.


What are the neurobiological factors related to depression?

You can look into the research being done with ketamine as an amazingly fast antidepressant, even for those with severe treatment resistant depression. Other than that, they now think decreased neurogenesis and synaptogenesis are the more direct and important links to depression. There is also some early research into the links between depression and the immune system, as well as people's microbiomes.


In which situation should structural dissociation theory be applied?

According to a presentation given by Van Der Hart "Structural Dissociation of the
Personality: The Key to Understanding
Chronic Traumatization and Its
Treatment", this theory relates to the response to trauma, described further in the paper "Trauma-related dissociation: conceptual
clarity lost and found" (Hart et al. 2004).  From the abstract:

  It postulates a common psychobiological pathway for all
  trauma-related disorders. Trauma-related dissociation is maintained by integrative deficits
  and phobic avoidance. This conceptualization advances diagnosis, classification, treatment
  and research of trauma-related disorders.


Categorization studies with a procedure similar to Shepard et al (1961) and Medin & Schaffer (1978)

You've described a very general type of study design which has probably been employed in hundreds of studies or more. Your question might profit from a more specific description of the type of study you're looking for.

A few examples that fit the bill just off the top of my head are:

Goldstone (1996) Isolated and interrelated concepts

Zaki and Homa (1999) Concepts and transformational knowledge

Kornell and Bjork (2008) Learning concepts and categories: is spacing the "enemy of induction"?


Why are people inclined to praise or fear the unknown?

In the book "Six Impossible Things Before Breakfast: The Evolutionary Origins of Belief", Wolpert (2007) discusses the evolutionary origins of belief.

Although I haven't read it yet, abc news reviewed the book.

  Wolpert argues that our wide range of beliefs, some of which are
  clearly false, grew out of a uniquely human trait. Alone in the animal
  world, humans understand cause and effect, and that, he says, led
  ultimately to the invention of tools, the rapid rise of sophisticated
  technology, and of course, beliefs. Even the earliest humans
  understood that many events that shaped their lives resulted from
  specific causes. Therefore, there must be a cause behind every event.

  ...

  We want to believe there is a reason for it all, and that leaves
  us predisposed to believe in some things for which there is little or
  no evidence. If a certain belief makes sense out of an otherwise
  senseless event, then it must be true, right?


Is there a region of the brain that mediates pain in a manner reminiscent of the mesolimbic pathway?

Based on the most recent (all post-2009) research, it seems to be the same general pathway, just with different gradients in the same areas of the brain. From Taylor et al. (2016):

Recent studies suggest that dopamine neurons in the VTA [ventral tegmental area] and SN [substantia nigra] form a heterogeneous population tuned to either (or both) aversive or rewarding stimuli.
The heterogeneity of dopamine neurons in response to aversive and rewarding stimuli suggests that they serve unique functional roles. Cells activated by reward and inhibited by punishment are well suited to code motivational valence, whereas neurons activated by both rewarding and punishing stimuli are likely to code motivational salience [stimulus awareness]. Neurons coding motivational valence [whether the stimulus is positive or negative in value] would provide a signal for reward seeking, evaluation, and value learning, in line with current theories on the role of dopamine in reward processing. In contrast, neurons coding motivational salience would provide a signal for detection and prediction of highly important events independent of valence, pursuant to dopamine's role in salience processing. These distinct aspects of dopamine neurotransmission might be neuroanatomically separate: dopaminergic neurons coding motivational valence have been found more commonly in the ventromedial SN and lateral VTA with projections to nucleus accumbens [NAc] shell, whereas neurons coding motivational salience are more often reported in the dorsolateral SN with projections to the nucleus accumbens core.

The primary evidence for this updated view seems mostly based (in order of the number of citations) on 3 papers:

Matsumoto and Hikosaka, "Two types of dopamine neuron distinctly convey positive and negative motivational signals", Nature 2009;
Brischoux et al., "Phasic excitation of dopamine neurons in ventral VTA by noxious stimuli", PNAS 2009
Lammel et al., "Projection-specific modulation of dopamine neuron synapses by aversive and rewarding stimuli", Neuron 2011

The part of your question that probably confused Alice and also confuses me a little is that you also ask (in your final paragraph) about somatosensory mapping. The latter doesn't generally involve tracing any pathways beyond the sensory areas of the brain, e.g. for macaques

Also such maps are not totally fixed as there is some use-dependent plasticity.


Why brain can't get used to low dopamine levels?

Look at it this way. When rain falls on a roof, the water runs into a gutter. Up to a point, that water can run down to the drainpipe. The gutter has caught all the water, and the system is in equilibrium.

In your first example, the problem is too much water. The gutter overflows. The drain is accepting the same amount of water, but the gutter can't hold all the incoming water.

In the other example, the problem is not enough water. The gutter is sending it all to the drain, and the drain is taking it all away. There's less water coming out of the system because there's less coming into the system. Even if you made the gutter larger, you'd have the same throughput.

To answer the actual question, those receptors can only process as much as they get. If there's not enough dopamine coming in, the receptors can't make more out of nothing. They can't multiply the effect, only dampen what's there.


Flow diagram of how information flows through the brain?

Most flow diagrams with the detail your require are for rudimentary sensory functions (such as seeing, eye tracking and other simple functions) can be found in any neuroanatomy textbook. The one I have experience with is "Neuroanatomy: Text and Atlas" by John H. Martin.

Alternatively, if you're looking for a more functional interpretation of how information flows through the brain in terms of behaviour, the most detailed model that I know is Spaun. A diagram of the brain model taken from the Science paper can be seen below:

Other models using the Neural Engineering Framework and the Semantic Pointer Architecture used in Spaun may also have the types of diagrams you are looking for. For example, consider this motor control diagram from Travis DeWolf's PhD thesis on Adaptive Control.


Is there any recent work on modeling how we rapidly acquire new knowledge?

Humans actually exhibit both slow and fast learning and they have somewhat different properties. One distinction is between "declarative" memory (for example, facts like "tigers have stripes" or "Paris is the capital of France") and "procedural" learning (such as perceptuo-motor skills like riding a bike or playing a musical instrument). Declarative memory lends itself to fast learning but procedural memory requires a lot of practice.

Perhaps even more relevant to your question is that neural network models are also capable of fast and slow learning, depending on the sparseness of the representations and tolerance for disruption. One of the foundational papers on this topic (McClelland, McNaughton, & O'Reilly, 1995) described a neural network model with two "complementary learning systems": (1) A fast-learning hippocampal memory system that relies on sparse representations and is not able to maintain previously-learned information when learning new information (sometimes called "catastrophic interference"). (2) A slow-learning neocortical system that relies on distributed representations and is able to integrate many different examples into an overall structure that can support generalization.

References:

McClelland, J. L., McNaughton, B. L., & O’Reilly, R. C. (1995). Why there are complementary learning systems in the hippocampus and neocortex: Insights from the successes and failures of connectionist models of learning and memory. Psychological Review, 102(3), 419–457.


What are the effects of visual deprivation on mental health and the other senses?

People that loose their eye sight do not go insane. They do tend to develop depression more often than sighted people (Koenes & Karshmer, 2000) and suicide rates are increased in the blind population (De Leo et al., 1999).

The reason why blind people tend to have enhanced functionality of the other senses (e.g., touch and hearing) is generally referred to as sensory compensation. In blind people, it has been shown that the brain undergoes a massive restructuring through the process of cortical plasticity (e.g., Cohen, 1997). The deafferented visual cortex is thought to loose its integrity due to a lack of synaptic input and therefore becomes prone to be taken over by other sensory modalities such as touch and hearing (Lee et al., 2014). Although it is tempting to speculate that this cross-modal plasticity is the neurophysiological correlate of compensation, much of the evidence to date points to the fact that blind people 'simply' train the other senses more intensively compared to their sighted peers. No solid evidence exists that cortical cross-modal changes in the blind improve their performance on, e.g., Braille reading or the use of other sensory substitution approaches like the BrainPort device. The BrainPort converts visual images to tactile sensations presented to the tongue. Studies using the BrainPort and comparing a blind group and sighted controls on their performance with this assistive technology consistently find that sighted people perform as well with the device and are not outperformed by the blind, as long as they receive equal amounts of training. This, despite the fact that gross cross-modal changes occur in the blind after device training, but not in sighted controls. These same findings generally hold for studies using other approaches like Braille reading or acoustic sensory substitution (reviewed in Stronks et al., 2015).

References
- Cohen, Nature (1997); 389: 180-3
- De Leo et al., Psychosomatics (1999); 40(4): 339–44
- Koenes & Karshmer, Issues Ment Health Nurs (2000); 21(3): 269-79
- Lee et al., Front Hum Neurosci (2014)
- Stronks et al., Brain Res (2015); 1624: 140–52


What's the percentage of people that are mental calculator prodigies?

There are two common ways someone can become a mental calculator via high iq or by savant ability. In exceptional cases someone may develop this ability while having only a average IQ but the level of dedication to such abilities is pathological interfering with normal development on the order of OCD.

Assuming the mental calculator abilities are the function of a savant ability. 62 out of every 10,000 are autistic and 10% of all autistic person have a savant ability finally half of all savants are autistic so multiply the number of autistic savants by two. Which gives you 12/10,000 as a maximum amount of mathematical savants.

About 1/1,000 people are geniuses with iq of 145 but i suspect it takes an Exceptionally Gifted person with an iq above 160 1/10,000 to have the capacity to become mental calculators.

So by my high estimations between 1 and 5 people out of 10,000 are capable of being mental calculators. Because savantism, autism and iq occur semi randomly (due as best we know to genetics) you should expect their to be an equal distribution among all populaces.


Is the visual cortex of a newborn baby immediately capable of object detection or is this skill learned over time, and if so, how?

A newborn baby has difficulty focusing its eyes or telling the difference between two objects presented to it.

A baby learns to recognise its mothers face within the first week after birth, long before it can recognise objects that are not faces. They already show a preference for face-like visual stimuli while in the womb.

  The Human Fetus Preferentially Engages with Face-like Visual Stimuli
  Reid et al. Current Biology, March 05, 2018
  https://doi.org/10.1016/j.cub.2017.05.044

Babies start to follow moving objects with their eyes at around three months. They are capable of depth perception and have good colour vision by five months (at birth many babies are incapable of detecting some colours).

The American optometric association has a page on infant vision:

https://www.aoa.org/patients-and-public/good-vision-throughout-life/childrens-vision/infant-vision-birth-to-24-months-of-age

In precocial animals object recognition abilities are apparent very early on. For instance, chicks which are presented with an object immediately after they have hatched will often follow that object as if it were their mother. They show a preference for moving objects over stationary objects. For more information on this check out http://www.scholarpedia.org/article/Imprinting.

The visual cortex already starts off with areas specialised for edge detection, colour detection, motion detection etc. However, much of visual perception is learned - if an animal has its eyes patched over at birth then it will have limited perceptual abilities when the patches are removed.

As for the question of how errors are propagated through the visual cortex, Seanny123's answer to this question might be relevant: Is back-prop biologically plausible?


Terminology for when a person starts to like something they previously didn't like due to exposure from a friend

I think the most obvious match to what you are talking about in terms of social psychology terminology is cognitive dissonance theory. This theory covers a lot of phenomena, but in relation to friendship an attitude formation, it suggests that we will tend to like what our friends like in order to achieve a state of belief consistency.

From a more sociological perspective, you could look into homophily. This is the idea that "birds of a feather flock together". But in addition to people being attracted to those similar to them, there is also a process by which such an effect emerges over time.

In general there many mechanisms that could describe the process of starting to like something because your friends like it.

mere-exposure effect: Merely experiencing something can help you to like something.
Persuasion, learning, etc: In general, a friend may help you to appreciate something. If its sport, they may explain the rules and communicate the finer points of strategy. If its music, the friend may explain the history of the style, the meaning of the lyrics, or the emotional importance of the music.
Positive associations: Spending time with a friend whose company you enjoy will help to create positive associations with other things you do with them.
Social norms: Spending time with your friend may create social norms that the things that they do are normal and appropriate.


Term for using hyperbole to make a softer argument seem more palatable?

There are several cognitive biases which describe why people are often more likely to accept a position after being presented with an unreasonable position.

Focalism

Focalism or anchoring is the cognitive bias in which humans rely heavily on the first piece of presented information (the anchor) to make subsequent judgments. From the wiki definition:

  For example, the initial price offered for a used car sets the standard for the rest of the negotiations, so that prices lower than the initial price seem more reasonable even if they are still higher than what the car is really worth.

Door-in-the-face technique

The DITF method is a compliance manipulation technique in which a persuader attempts to convince a respondent to agree or comply with an argument by initially making a substantial and unreasonable request, and then when it is turned down, making a second more reasonable request. See Cialdini (1975) for the founding investigation.


What's the technical name for this cognitive bias?

I am not entirely sure about the proper scientific names but I think your issue revolves around buying things because they are

cheap;
hard to find.

The first is a notorious reason to buy stuff; the impulsive purchase of goods, simply because they are advertised as 'buy two, pay for one!'. This bargain hunting can indeed become pathological and addictive (source: Psychology Today).

The buying simply because a product is hard to find is a bit harder to frame in behaviors, but it is indeed a common phenomenon that people tend to buy stuff because they are exclusive (#55 here). Also, perhaps you simply wish to buy it just because you can (#26 here).

Further, buying stuff in general makes you feel good as it activates the reward circutry in our brain. As a consequence buying stuff can become an addiction (shopaholics).

There is actually a disorder named compulsive buying disorder. It was included in DSM-III, but not in later DSMs. It's not strictly defined but it has been associated with addictive disorders, obsessive-compulsive disorder, or mood disorders (Black, 2007).

Reference
- Black, World Psychiatry (2007); 6(1): 14–18


Why are trans-women more common than trans-men?

Exactly like you, I would like to begin by saying that I have no animosity nor prejudice against anyone. What I am saying below is not meant to be offensive to anyone, it is just an honest account of what the data in my region says.

You wrote:

  "I can only think of 2 possible solutions ... either a difference in
  psychological predisposition between the sexes (but if so what), or
  some genetic component."

But there is in fact a third factor, which is economics.

Where I live (Southeast Asia), there's quite a large number of many male -> female trans people that are prostitutes. I have lived in Indonesia, Philippines, and Thailand, which are all countries that appear lower than 80th in the list of countries by GDP per capita, and do have a large population of people living in poverty. If you go to the streets where most of the prostitutes advertise themselves (such as Jalan Jaksa in Jakarta, Indonesia) you will find these days that many of them (and in some areas, the majority of them!) are male -> female trans.

This may get quite controversial, so once again, I begin by saying that I have no animosity nor prejudice against anyone. I just want to point out, if I may, that for men, it is not as easy to make money as a prostitute as it is for women. Men statistically pay for sex more often than women do. I have not seen any homeless women in my city acting as "beggers" (I only see men doing this), but I see far more female prostitutes (in fact I have never in my life seen a male prostitute advertising themselves on a street!). Most of the trans-women I know in my city, started out as pre-operation trans people that made ends meet as escorts or prostitutes or "sugar babies" and many of them got the money for their operation by a "sugar daddy" or a wealthy client that developed a closer relationship with them.

I am not saying this is the only reason. I am just saying that there is at least one more reason in addition to the two that you have suggested as the only two you could think of. What I have written applies to my region of the world and may not apply to wealthier places such as Luxembourg where practically everyone (even the poorest people) are better off than the middle class here (and would less likely need to resort to prostitution).

It is also likely that the answer to the question depends heavily on the region in question, as is the case for sexual orientation demographics.

Let me start with the opening sentence to the Wikipedia article on "Demographics of Sexual Orientation":

  "The demographics of sexual orientation vary significantly, and
  estimates for the LGBT population are subject to controversy and
  ensuing debates."

For example, the same page has this:

It shows that males are more likely to be gay than females in every city in Brazil except for Manaus which is in the Amazon. We cannot rule out the possibility that in Manaus, there might be cultural or societal reasons why 10% of the women have become attracted to women more than the men. I am not saying that the men of Manaus are bad people, I am just saying that genetics and psychology are not the only factors and that culture and society can affect what type of people a population finds attractive (in a misogynistic society women might start to find men less appealing, for example, so it is not just genetics and psychology).

Interestingly, in USA the statistics are the opposite of in Brazil (women are more likely to be gay than men):

I suspect that just as the demographics of LGBT people "vary significantly, and estimates for the LGBT population are subject to controversy and ensuing debates", the same may be true for trans people (in fact trans is the T in LGBT, so already there's at least one other place that says that statistics will vary significantly and be hard to generalize).

I am  not saying that psychology and genetics don't play any role at all, but I do think we also have to consider other factors that would lead to more males becoming trans than females such as geography (are we in a place where it's acceptable for men to transform but not women? are we in a place where more women are in demand for certain jobs? are we in a place where more women are in demand for sex?) and in some cases even economy. Because of this added complication (which gets into "soft" sciences of sociology and economics which are harder describe in a more mathematical or clinical manner than "hard" sciences like neurology), it might be very difficult to get a straight answer regarding psychology and genetics, especially since all the data is also relatively new and people haven't been studying the topic for long enough yet!


What does it mean to "control for differences in factors" when looking at gun ownership and homicide rates?

There are various ways of controlling for other other factors.

Probably the most common is to include these control variable as additional variables in whatever statistical model you are running.

For example, you could run a multiple regression predicting homicide rate from gun ownership on a set of neighbourhoods.

You could then run another regression model that included all the control variables.

In both models you would get a coefficient for the effect of gun ownership on homicide rate. However, in the one with control variables, it would be statistically adjusted for the effect of these other variables.

There are lots of debates about how best to control for other factors and which factors to include. But that's the general idea.


What does it mean by "the resulting behavior doesn't produce the consequence"?

The slide is contrasting classical conditioning with operant conditioning.

In operant conditioning, you train that a behavior is paired with a reward or punishment. For example, a lever press dispensing a food pellet.

In classical conditioning, there is no relevant behavior. Some stimulus (rather than behavior) is paired with an outcome. For example, if there is a tone played before a shock, the tone will cause rodents to freeze in anticipation of the shock, but nothing about their freezing behavior is causing the shock.


The best "negative motivation" movies (or books, etc.)?

Goodfellas and the Wolf on Wall Street both leave the watcher contemplating the results of the actors bad behaviour. The two movies are highly related; one is about the mob and the other about the market place.

Learning from bad behaviour and seeing it fail is method used in moral storytelling called conditioning. Its an old idea that goes all the way back to ancient animal training but was first formally studied by Pavlov. Negative reinforcement causes people to lose an appetite for evil by seeing the devastating outcomes and punishment so that those behaviours are associated with pain and loss to cause avoidance.

Also worth noting are

The Great Gatsby (old and new)
Bruce Almighty
Click
Pay it Forward
Inception
Oedipus the King
Romeo and Juliet (West Side Story)
The Crucible
Dances with Wolves (Avatar)
The Necklace
The Tell-Tale Heart
Most episodes of Scandal
The Matrix Revolutions
Cloud Atlas
Star Wars: Episode III
Crouching Tiger, Hidden Dragon
House of Flying Daggers
A Beautiful Mind
Good Will Hunting
TRON: Legacy
How to Train Your Dragon 2
Harry Potter
The Butterfly Effect movies especially the last one


What is the definition of affective cueing?

There is no agreed-upon definition of affective cueing because it's not a proper name. If you google for "affective cueing" you only find a handful of hits and in them the term is used differently, mostly to indicate that some cue (a stimulus that carries information) is of positive versus negative valence.

In contrast, affective priming refers to a specific, experimental research paradigm:

  Affective priming investigates whether the evaluation of a first stimulus, the prime, that is to be ignored, affects the processing of subsequent stimuli.

(as described in the article you found)


Is 'your mom will be sad' actually a good argument to pose to someone thinking of committing suicide?

As with many mental health concerns, the situation for each individual is unique and therefore what we do and how we deal with the concern is also unique. Nothing said in this answer is a hard and fast rule, but are loose guidelines, for more information please check out these helpful links (thanks to @ChrisRogers):

ASIST Suicide Intervention, for Canadian
Suicide Prevention Training, for the UK
Suicide Prevention Programs, for the US

I often come across people pointing out that the close relatives of someone who is thinking about committing suicide will grieve, as an argument against doing it.

This is a true fact. Family and friends of people who have committed suicide do grieve for their lost loved one, and often will blame themselves for their death. Here is an interesting article briefly outlining what family can feel when a loved one dies from suicide.
There are many reasons someone might give if they are thinking of killing themselves, and you are correct in your assumption that something like family pressures are one of them, (Linehan, et al, 1983).

Life Over Limb
You asked:

Although accepting such an argument as a valid reason against committing suicide at present, couldn't it actually make it worse for them in trying to cope with the underlying problems in the long run?

The short answer to this is yes, you could talk someone off the ledge with 'people will miss you' and yes it may make the overall depression worse in the long run.
There are two distinct situations that we can discuss:

A person actively carrying out their suicide plan
A person who has suicidal thoughts but is not currently acting on them.

In the first case, your goal as the person who is witnessing the attempted suicide is to save a life. The most important thing is to make sure that the person attempting to commit suicide is not able to complete it. A good analogy is, in a medical situation we save life over limb. Which means that in the moment, if there is imminent risk of death, you do anything to save the life, even if it means cutting off a limb. We do the same thing with suicide intervention. In this case, the long run doesn't matter, because if you don't save the life, there is no way to heal that persons depression/suicidal thoughts. This is what the ASIST and other suicide interventions teach.
In the second case, the goal is different. In this case the goal is to reduce the cause of the suicidal thoughts, Major Depressive Disorder is often (but not always) a diagnosis that produces suicidal thoughts. It would be the role of a counsellor and the client to determine the root cause of suicidal thoughts (ideations) and determine what the client can do to reduce those thoughts.
You are right that if the root cause is family issues, mentioning those issues as a reason not to commit suicide during imminent threat of suicide could cause more long term issues. But I can not stress enough how important life over limb is, when it comes to imminent suicide.
You said:

couldn't it actually make it worse for them in trying to cope with the underlying problems in the long run?

In conclusion, yes it could make it more difficult for that person to deal with the underlying issues, but if that person is not alive they can't deal with the underlying issues. (Life over Limb).

Linehan, M. M., Goodstein, J. L., Nielsen, S. L., & Chiles, J. A. (1983). Reasons for staying alive when you are thinking of killing yourself: the Reasons for Living Inventory. Journal of consulting and clinical psychology, 51(2), 276. doi: 10.1037/0022-006X.51.2.276


Why is a cross-dominant/ambidextrous brain more susceptible to mental illness?

This question is still a little broad...

On the issue of corpus callosum (CC) and mental illness, it's not clear that this follows the same pattern as ambidexterity. Highley et al. (1999) found that there fewer fibers in CC of women with schizophrenia:

  A reduction in the total number of fibres in all regions of the corpus callosum except the rostrum was observed in female schizophrenic patients (P = 0.006; when controlling for brain weight, P = 0.053). [...]  With age, all subregions of the corpus callosum except the rostrum showed a significant reduction in cross-sectional area (P = 0.018) and total fibre number (P = 0.002).

They also found "little change in the males".

In fact the press release you linked does not mention corpus callosum.

So whatever common factor drives ambidexterity and mental illness, it doesn't seem a simple as the (higher) number of fibers in CC.

Also, cross-dominance is a broader concept when it comes to the brain; the press release doesn't mention this term either. Even though Wikipedia considers it synonymous with mixed-handedness, one can have a cross-dominant vision but not cross-dominant handedness, for example. And in fact some of the more recent research has pointed out to different correlations with mental illness of these various types dominance, e.g.:

  The rate of left or mixed-footedness, eye dominance, and any anomalous lateralization, but not handedness, discriminated between those who developed schizophrenia spectrum disorders and those who did not.

Of course they might not have had enough statistical power to detect it (for handedness.) But also a mini-review of prior work on this in the same paper points to somewhat contradictory conclusions, even for handedness, but still says that

  The preponderance of evidence, however, supports the hypothesis that
  schizophrenia patients are more often left or mixedhanded compared to controls. Left or mixed-handedness in schizophrenia may indicate abnormalities in
  neurological structure or functioning.

Interestingly this issue of failing to detect the effects of dominance in handedness has been encountered before:

  Several cohort studies have measured childhood
  laterality as it relates to later risk for schizophrenia
  (e.g., Crow et al., 1996; Cannon et al., 1997). Crow
  et al. investigated handedness in the National Child
  Development Survey, a study assessing all individuals
  born in the United Kingdom during a single week
  in 1958. Mothers of children who later developed
  schizophrenia were more likely to rate their children
  as ambidextrous at age 7 as compared to mothers of
  children who did not develop schizophrenia. Additionally,
  children who eventually developed schizophrenia
  were less strongly right-handed than controls
  at age 11.

  Cannon et al. (1997) studied laterality in a total
  population of 5362 children born in England, Scotland,
  and Wales during one week in March 1946.
  Results indicated that at age 11, children who later
  developed schizophrenia showed a significant excess
  of mixed-eye dominance as compared to the remainder
  of the cohort. The authors failed, however, to
  detect a significant difference in hand preference
  between children who later developed schizophrenia
  and children who did not. Nevertheless, Cannon et al.
  interpreted their eye dominance findings as an indication
  that lateralization might play a role in the
  pathogenesis of schizophrenia.

And in the genomic age, some genetic candidates correlating with both lateralization and some mental illnesses have been identified...

  Common polymorphisms in the gene PCSK6, whose protein product mediates the development of brain and body asymmetry through the NODAL pathway, have recently been associated with handedness in three studies, making it a key candidate gene for understanding the developmental and expression of human lateralization. We tested the hypothesis that the PCSK6 VNTR polymorphism rs1053972 influences the expression of handedness and aspects of dimensional schizotypy and autism. For a sample of 709 healthy individuals, rs1053972 genotype was significantly associated with categorical measures of handedness, and with dimensional handedness in subsets of the population with high schizotypy and magical ideation or a lack of strong right-handedness. Both findings showed evidence of stronger or exclusive effects among females, compared to males. Genotypes of PCSK6 also showed significant sex-limited associations with magical ideation, a component of positive schizotypal cognition measured using the Schizotypal Personality Questionnaire, and total autism score, measured using the Autism Spectrum Quotient. These results partially replicate previous studies on effects of PCSK6 rs1053972 genetic variation on handedness phenotypes, link the PCSK6 gene with the dimensional expression of neurodevelopmental conditions in healthy individuals, and show that associations of this gene with handedness and psychological phenotypes exhibit evidence of sex-limited effects.

Although the mechanisms by which PCSK6 causes lateralization are somewhat understood, the paper says nothing about how it might cause any of the mental illnesses mentioned. So it looks like researchers don't have any clue beyond the observation that [lack of] lateralization is a risk factor for mental illness... except for...

One theory that's been advanced (prior to any genomic knowledge):

  T. J. Crow suggested that the genetic variance associated with the evolution in Homo sapiens of hemispheric dominance for language carries with it the hazard of the symptoms of schizophrenia. Individuals lacking the typical left hemisphere advantage for language, in particular for phonological components, would be at increased risk of the typical symptoms such as auditory hallucinations and delusions.

And a 2009 paper that has Crow among its authors claims to

  show for the first time how the deficit of lateralization in the schizophrenic brain is specific for the phonological component of language. This loss of hemispheric dominance would explain typical symptoms, e.g. when an individual's own thoughts are perceived as an external intruding voice. The change can be interpreted as a consequence of “hemispheric indecision”, a failure to segregate phonological engrams in one hemisphere.

This study wasn't cited much, so I'm not sure how conclusive its evidence was considered by others.

A year later, a paper (in a more prestigous journal) concluded:

  As language lateralization was not significantly reduced in the non-psychotic individuals with auditory verbal hallucinations, a direct relationship between auditory verbal hallucinations and decreased language lateralization can not be established at present.


Raven Progressive Matrix: why's my chosen square wrong?

As the text you provide explains, there is a flow of thinking involved:

diamond-diamond / square - ? (answer: square - you got that one right)
bottom half becomes filled (you got that one too)
one stripe removed above

All this added yields the picture at the bottom right. You didn't notice, interpret or actioned on the stripe removal, perhaps.


To what extent does AFQT correlate with IQ?

An answer is found in an official memo, albeit from 1980, where

the correlation of AFQT with WAIS (no version specified) was stated as 0.8 based on a Army "fact sheet" from 1965; the details of the comparative test could not be found
an Air Force comparison found (in 1974) that the correlation (again with WAIS, no version specified) for white enlistees was (again) 0.8 but 0.77 for black enlistees.

(This ~0.8 is actually about the same as the correlation of IQ tests with SAT.) I don't know if the AFQT is still the same as back then.

A official-looking 2006 concordance/translation table of AFQT score with SAT scores can also be found, although it's rather summary; it doesn't mention a correlation coefficient.


Do the brains of non-altruistic persons mirror the observed experience of suffering?

I'd go for the jugular in non-empathetics: sociopaths and psychopaths, people who clinically lack the ability to empathize. There is a difference in their brains.
You might be interested in the story of the neuroscientist Dr. James Fallon..
Fallon wanted to identify lack of empathy as a brain patern. He had PET scans of serial killers mixed with a host of other mental illnesses and disorders in an attempt to predict accurately psychopaths. He found a particular pattern again and again which was striking.

“I was looking at many scans, scans of murderers mixed in with schizophrenics, depressives and other, normal brains,” he says. “Out of serendipity, I was also doing a study on Alzheimer’s and as part of that, had brain scans from me and everyone in my family right on my desk.”
“I got to the bottom of the stack, and saw this scan that was obviously pathological,” he says, noting that it showed low activity in certain areas of the frontal and temporal lobes linked to empathy, morality and self-control. Knowing that it belonged to a member of his family, Fallon checked his lab’s PET machine for an error (it was working perfectly fine) and then decided he simply had to break the blinding that prevented him from knowing whose brain was pictured. When he looked up the code, he was greeted by an unsettling revelation: the psychopathic brain pictured in the scan was his own.

Perhaps because boldness and disinhibition are noted psychopathic tendencies, Fallon didn't hide that discovery; instead he started to study it. He found that his family line included seven alleged murderers, including Lizzie Borden*. A series of genetic tests revealed the presence of high-risk alleles for aggression, violence and low empathy.
You can see normal empathy vs. psychopath scan differences in the linked source.
*Maybe you remember this childhood rhyme (I do): Lizzie Borden took an axe/ gave her mother forty whacks./ When she saw what she had done,/ She gave her father forty-one.


If one is flexing a muscle, for any given motoneuron involved, how many action potentials occur per second to keep the muscle flexed?

Second question: won't happen in the healthy individual/inapplicable.
Anatomically speaking, muscles don't flex, they contract. Joints flex. And muscles never fully relax to the point of zero contraction/zero firing. (The flexion of a joint can be achieved passively, even when the animal is dead.)
Even at rest, muscle is kept in a constant state of at least slight tension, the basic tonus. Skeletal muscles are usually set up in antagonistic pairs, with one flexing and one extending a joint. A specific balance of agonist and antagonist tonus implements a stable position of the joint, and stable positions can be achieved near-permanently.

First question: depends on effort.
Muscle firing during increased, active contraction is a function of effort, as muscle contraction is increased via rate coding. The stronger a muscle is supposed to contract, the higher the motor unit's firing rate has to become. (I should probably mention the size principle here...)
Motor neurons are reported to reach firing rates of a few tens (up to 50) of hz during high effort.

A question you're possibly interested in: for how long can extremely high firing rates be sustained? Or: is muscle failure under sustained extreme effort, corresponding to high firing rates, sometimes a result of motor neuron drop-out rather rather than e.g. ATP depletion at the muscle itself?
Note first that muscle force is greater for eccentric and isometric activity (ie., release under control or static tension); voluntary contraction is a bit weaker. From another perspective, if a muscle is electrically stimulated externally, it is still able to exert force far beyond the point where the subject cannot voluntarily uphold the tension. This means short-term fatigue following high tension is primarily neural.
I do not know what precisely causes this fatigue (nor do I think the experts have uncovered it yet), but the limiting aspect does not seem to be neurotransmitter re-uptake, or even metabolic processes in general. As Gandevia writes:

  intrinsic moto neuronal properties, reflex inhibition and disfacilitation, Renshaw cell inhibition, and insufficient drive from supraspinal sites may all contribute to the decline in moto unit firing rate in fatigue

Also see this.


A doctor told me that cephalic index can be used to measure human intelligence, is it true?

No, the index and its correlation to intelligence is not strong.

See the medchrome.com description on cephalic index:

  The underlying assumption of craniometry is that skull size and shape
  determine brain size which determines such things as intelligence and
  capacity for moral behavior. Empirical evidence for this assumption is not very strong.
  Cephalic index consistently produced a very low or negative correlation with mental ability.

See also this article on Smithsonian.com: Why Brain Size Doesn’t Correlate With Intelligence

Healy and Rowe (2007) provide a critique of comparative studies of brain size.

Healy, S. D., & Rowe, C. (2007). A critique of comparative studies of brain size. Proceedings of the Royal Society of London B: Biological Sciences, 274(1609), 453-464.


Humans don't understand the accumulation of small numbers - what is this phenomena called?

Humans have loads of cognitive biases.

The one you have in mind could either be so called 'denomination effect', the tendency to care about large currency denominations and be less careful with smaller currency denominations. For example, not to care about the .99 part in a US 9.99 price tag.

It could also be the less-is-better effect. Small amounts of something are preferred than one big lump-sum. For example, buying something in 10 installments of US 110 is chosen instead of one scary US 1000 price tag.


What is it about our brain that breaks when we hear ourselves with a delay?

This phenomenon is called delayed auditory feedback. Why is still an open question, but two theories are:

Servomotor hypothesis: delayed auditory feedback creates an error signal, which the motor systems uses to attempt to correct the motor output.
Distruptive rhythm hypothesis: Speech is too fast for error correcting feedback (i.e. speech is feedforward), delayed auditory feedback disrupts the rhythm of motor output.


How do I interpret an effect of electrode position in ERP research?

The question is quite vague, as it is unclear what the sample size is and whether OP is talking about an anecdotal experiment or the outcome of a well-powered statistical analysis. Moreover, there is mention of two conditions, but I fail to see what the difference is between the two.

Assuming a normal sample size, I can say that the measured amplitudes of electrophysiological signals are often unreliable. This is due to a variety of factors.

Impedances affect signal size, as high impedances reduce the measured potentials. Impedances can vary between subjects, but also between sessions within subjects, due to for example differences in the effectiveness of the scrubbing and whether enough conductive paste is used in case of EEG.
Impedance differences between active and reference electrode affect noise level. Noise may vary from day to day and even within a session due to interfering background electric fields.

In contrast to amplitude, peak latencies are often far more reliable.

So it all depends on the power of your analysis. If there is truly a difference in amplitude, then you should look at the physiology involved in your task and see whether brain mechanisms can be involved.


Can you get addicted from using topical or local anaesthetics to ease pain?

Short answer
Basing an answer strictly on the DSM-V criteria, local anesthetics may, purely hypothetically, be associated with a mild form of addiction. But realistically, I think it is unlikely that a person (ab)using a topical anesthetic will ever be medically diagnosed as having a substance abuse disorder.

Background
I think the question hinges on the definition of [drug] addiction. The APA addresses addiction in DSM-V by the following criteria (entered in shortened form for brevity):

  A minimum of 2-3 criteria is required for a mild substance use
  disorder diagnosis, while 4-5 is moderate, and 6-7 is severe [...]

  Taking the opioid in larger amounts and for longer than intended
  Wanting to cut down or quit but not being able to do it
  Spending a lot of time obtaining the opioid
  Craving or a strong desire to use opioids
  Repeatedly unable to carry out major obligations at work, school, or home [...]
  Continued use despite [...] social or interpersonal problems [...]
  Stopping or reducing important social, occupational, or recreational activities [...]
  Recurrent use of opioids in physically hazardous situations
  Consistent use of opioids despite [...] physical or psychological difficulties [...]
  [Development of t]olerance [...]
  [Development of w]ithdrawal [symptoms]

In contrast to opiates, lidocaine has no rewarding or addictive properties. As a result, lidocaine can be used systemically and on a long-term basis for the treatment of chronic pain (Yousefshahi et al., 2017). In fact, lidocaine, has equally effective anelgesic effects in people addicted to opioids as in normal controls (Hashemian et al., 2013). Because lidocaine is a local anesthetic without central effects, and taken together with above findings, we can safely rule out the occurrence all of the criteria except, perhaps, the first three. Those first three may be, at least hypothetically, possible when topical or systemic application relieves some sort of untolerable pain. Given that meeting 3 criteria meets the definition of a mild substance abuse disorder (mild addiction), I wouldn't rule addiction to topical anesthetics out completely. It does seem unlikely, though.

Cocaine has strong addicitve effects, because of it's pronounced effects in the central nervous system - it is associated with strong feelings of reward and euphoria. It rapidly induces tolerance as well as dependence; a school book example of a substance of abuse. Lidocaine is a cocaine derivative that still exhibits its anelgesic properties, without its psychoactive component (Small, 2009).

References
- Hashemian et al., J Emerg Trauma Shock (2014); 7(4): 301–4
- Small, Subst Use Misuse (2009); 44(13): 1888-98
- Yousefshahi et al., Anesth Pain Med (2017); 7(3): e44732


How distantly related are research in computational neuroscience and neural networks/machine learning?

Computational neuroscience and neural networks are both studied on this MSc at the University of Sussex.
When I took the course in 2004/5, the Neural Networks module was compulsory, and the Computational Neuroscience was optional in the 2nd semester, so that would suggest the course designers (world leaders in biologically inspired computing) thought that studying neural networks first might aid the study of computational neuroscience.
I think some of the other subjects taught on the course would be of interest to you, e.g. evolving genetic algorithms for robot control (see Rodney Brooks – and the iRobot corporation).

Lastly to answer the question(!), I think you probably need some understanding of (simple) neural networks (artificial or otherwise) to understand more in-depth concepts in computational neuroscience.


Does STDP make the Hebbian learning rule redundant?

Short answer
Just like Mendel's ideas have been proven by the existence of DNA, Hebbian learning can be explained by STDP. That doesn't make Mendel's or Hebb's teachings obsolete.

Background
STDP is the long-term synaptic potentiation or depression governed by the timing of pre- and post synaptic cell firing. STDP depends on certain “critical windows” for spike timing. This critical window is on the order of tens of milliseconds (Dan & Poo, 2004). STDP is known for quite some time, but is by far a more novel idea than the idea of Hebbian learning posed in the 1940's (Markram et al., 2012). Hebbian learning has been popularly described as:

  ["C]ells that fire together, wire together.” In other words, if things keep happening more or less simultaneously, you may assume that there is a common cause for the firing. More importantly, if one of the cell is active systematically just slightly before another, the firing of the first one might have a causal link to the firing of the second one and this causal link could be remembered by increasing the wiring of connections, a notion we call synaptic plasticity. In short, timing matters because it may indicate causality.

In other words, Hebbian learning is mediated by STDP. Thus STDP may explain how Hebbian learning may come to exist.

But Markram et al. caution:

  ...this is not to say that STDP has been a panacea for all problems
  neuroscientific. Clearly cells that fire together wire together, there
  is no doubt about that, so the coming of STDP has not rendered the
  classical literature obsolete by any means.

In other words, Hebbian learning is more of a theoretical construct whereas STDP provides a neurophysiological explanation. Just like Mendel's ideas have been proven by the existence of DNA, and Darwin's ideas by a since buildup of fossil records, Hebbian learning has been explained by STDP, but that doesn't make Darwin nor Mendel's teachings obsolete.

References
- Dan & Poo, Neuron (2004); 44(1): 23-30
- Markram et al., Front Synaptic Neurosci (2012); 4: 2


I will focus on question #1:

Analysis of MRI scans is typically done using voxels (Fig. 1). Voxels have a volume defined by three dimensions (length, width and depth).

Voxel analysis. Source: Philips

The slice thickness plus the 2D in-plane resolution (pixel size) yields the voxel size. The time to scan a slice can be regarded to be negligible. Making a scan consisting of multiple slices takes time. Hence, the time dimension is not directly relevant for voxel size. Practically, voxel size depends mostly on slice size, as well as the capacity of the scanner. More Tesla's makes smaller voxels possible.


Is there a name for the natural human guilt complex?

Short Answer: I'm not aware of a specific name for this, but I would describe it as guilt-proneness, and it is almost always associated with a high degree of conscientiousness.

Long Answer: Conscientiousness is one of the five major personality traits. People with high levels of conscientiousness feel strongly compelled to adhere to societal norms and rules, and will experience more guilt when they fear they've broken them. If extreme, in combination with other criteria, it could be classified as Obsessive-Compulsive Personality Disorder (OCPD). The DSM 5 lists eight diagnostic criteria for OCPD, one of which is "overconscientious, scrupulous, and inflexible about matters of morality, ethics, or values." However, in the absence of OCPD criteria, if I was writing a psychiatric impression of someone like you describe, I would probably say that person demonstrates and high degree of conscientiousness and is prone to guilt reactions in the face of perceived violations of his or her morals.


Does the retina encode visual information like a Bitmap or an SVG?

Short answer
The retinal image corresponds more to a bitmap, than a vector-based image

Background
The retina contains a layer of about 100 million photoreceptors that are topographically organized. In other words, each photoreceptor codes one specific pixel in the field of view. In turn, the nerve fibers running from the eye to the brain are also topographically organized in the same way the retina is (retinotopy is maintained up until the higher brain centers and is lost only in the inferotemporal cortex). Hence, yes, basically, but grossly oversimplified I agree with @Krysta that the retinal image more closely corresponds to a bitmap than a vector-based image. Nonetheless, colors, contrasts and edges are coded in the retina.

Here is a picture on retinotopy. Basically a 1:1 topographic representation of the retina can be found in the primary visual visual cortex:

source: University of Leeds and Sydney

Retinal implants are devices that replace the lost photoreceptors in the retina in patients with retinitis pigmentosa or other retinal degenerative diseases. Retinal implants typically consist of a grid of electrodes (60 - about 1500 in commercially available systems) that are placed on (Argus II) or below the retina (alpha-IMS).

Here's a fundus photo of an Argus II implant:

The electrodes directly stimulate the surviving neruonal cells in the retina. Retinal implants make use of the retinotopy. An electrode in the center of the retina will elicit a spot of light (a phosphene) in the central fielfd of view, whereas a more peripherally situated electrode will generate phosphenes more eccentrically. Hence, camera images (in the Argus II device) are simply downsampled and projected onto the electrode grid as intensity-coded stimuli. In the alpha-IMS system the intra-ocular part consists of a grid of photosensitive diodes coupled to small amplifiers. Hence, in this device it is, quite literally, a photosensitive chip thrown on the retina. In both approaches, brighter areas in the image receive higher electric currents and result in brighter and/or larger percepts.

Reference
Stronks et al. Exp Rev Med Dev;11:23-30


Can scary movies trigger fight or flight and why can a person enjoy this while another does not?

I imagine individual differences in enjoyment derived from horror films would be multifaceted as with most preferences regarding consumption of different media. Some of the research mentions how males, teenagers/young adults, sensation seekers, and those who have a history of exposure to horror films (although this may be both cause and effect) tend to like horror films more.

Sensation seeking: You might want to look into the personality trait sensation seeking. To quote Wikipedia quoting the originator of the concept, Marvin Zuckerman.

  Sensation seeking is a personality trait defined by the search for
  experiences and feelings, that are "varied, novel, complex and
  intense", and by the readiness to "take physical, social, legal, and
  financial risks for the sake of such experiences." (Zuckerman, 2009). Risk is not an
  essential part of the trait, as many activities associated with it are
  not risky.

Zuckerman discusses the psychology of horror films in this video (see transcript here). He frames sensation seeking in terms of habituation. Thus, the more horror films that a person has seen, the more intense the horror would need to be in order to induce the same rewarding level of arousal.

Exploring the concept of sensation seeking may also move you more towards a more primary concept of why people seek such arousal inducing experiences. You could for instance read Roberti's (2004) literature review of the biological and behavioural correlates of sensation seeking. In particular, see section 4 on biological characteristics related to sensation seeking:

  Zuckerman (1994, 1996) has proposed a multi-level approach in which
  sensation is a product of interactions between neurotransmitter
  systems (Zuckerman, 1996). Agonistic and antagonistic interactions of
  biological correlates are related to sensation seeking. Biochemical
  mechanisms provide major support for the relation of sensation seeking
  and associated biological systems (Balada et al., 1993; Ballenger et
  al., 1983; Daitzman & Zuckerman, 1980; Dellu et al., 1996; Gerra et
  al., 1999; Netter et al., 1996; Piazza et al., 1993; Ruegg et al.,
  1997; Zuckerman, 1984, 1991a; Zuckerman et al., 1980).

Tamborini and Stiff (1987) studied the appeal of horror movies:

  A survey was conducted to determine the antecedents of the exposure to
  and appeal of horror films. Audience members leaving the theater after
  viewing Halloween II were interviewed using a questionnaire that
  contained measures of specific reasons for liking horror films as well
  as measures of several individual-difference variables. A model
  emerged from structural equation analysis indicating that three
  important factors in the appeal of horror films are (a) the audience's
  desire to experience the satisfying resolutions usually provided in
  these films, (b) the audience's desire to see the destruction often
  found in these films, and (c) the sensation-seeking personality traits
  of audience members for these films. In addition, age and gender were
  important predictors. Horror films were enjoyed more by males and by
  younger viewers.

Tamborini, Stiff and Zillman (2006) summarise existing research linking sensation seeking with horror film preference:

  Several studies  have  attempted to  investigate  the  relationship
  between the attraction to horror films and sensation seeking. The
  first  attempt to  look at  this  issue was reported by  Sparks
  (1984), who  correlated his own 20-item scale measuring Enjoyment of
  Frightening  Films (EFF) with the Sensation-Seeking Scale, and found
  an overall  positive correlation between the two for both males (r=
  .22,p= .01) and  females (r = .28, p = .01). A second study (Tamborini
  & Stiff, 1984) also  found an association between the liking of horror
  films and a measure of  sensation seeking computed from  the
  combination of  disinhibition,  experience seeking, and thrill and
  adventure seeking scores (r= .14,p=  .05).  Finally, Edwards (1984)
  found a strong correlation between the  entire Sensation-Seeking Scale
  and interest in horror movies (r = 51, p  < .001). Unfortunately, the
  articles by Sparks (1984) and Tamborini and  Stiff  (1984) do  not
  report the  correlations between  the  individual  subdimensions of
  the Sensation-Seeking Scale and their measures of  attraction to
  horror films. This information is of particular interest to us  if  we
  want  to understand the  appeal found  in  horror  since  these
  subdimensions are thought to be unique. The study by Edwards (1984)
  does  provide  information  in  this  regard,  however.  According  to
  Edwards, each of  the subdimensions is correlated to interest in
  horror  films with disinhibition having the strongest relationship (r
  = .54, p <  .001), followed by boredom susceptibility (r = .41,p < .001), experience  seeking (r= .39,p < .001), and thrill and adventure
  seeking (r= .24, P <   .01).

References

Balada, F., Torrubia, R., & Maria Arque, J. (1993). Gonadal hormone correlates of sensation seeking and
anxiety in healthy human females. Neuropsychobiology, 27, 91–96.
Ballenger, J. C., Post, R. M., Jimerson, D. C., Lake, C. R., Murphy, D., Zuckerman, M., & Cronin, C.
(1983). Biochemical correlates of personality traits in normals: An exploratory study. Personality and
Individual Diﬀerences, 4, 615–625.
Daitzman, R. J., & Zuckerman, M. (1980). Disinhibitory sensation seeking and gonadal hormones.
Dellu, F., Piazza, P. V., Mayo, W., Le Moal, M., & Simon, H. (1996). Novelty-seeking in rats:
Biobehavioral characteristics and possible relationship with the sensation seeking trait in man.
Neuropsychobiology, 34, 136–145.
Personality and Individual Diﬀerences, 1, 103–110.
Gerra, G., Avanzini, P., Zaimovic, A., Sartori, R., Bocchi, C., Timpano, M., Zambelli, U., Delsignore, R.,
Gardini, F., Talarico, E., & Brambilla, F. (1999). Neurotransmitters, neuroendocrine correlates of
sensation-seeking temperament in normal humans. Neuropsychobiology, 39, 207–213.
Netter, P., Hennig, J., & Roed, I. S. (1996). Serotonin and dopamine as mediators of sensation seeking
behavior. Neuropsychobiology, 34, 155–165.
Piazza, P. V., Deroche, V., Deminiere, J. M., Maccari, S., Le Moal, M., & Simon, H. (1993).
Corticosterone in the range of stress-induced levels possesses reinforcing properties: Implications for
sensation seeking behaviors. National Academy of Science, 90, 11738–11742.
Roberti, J.W. (2004). A review of behavioral and biological correlates of sensation seeking. Journal of research in personality, 38, 256-279. PDF
Ruegg, R. G., Gilmore, J., Ekstrom, R. D., Corrigan, M., Knight, B., Tancer, M., Leatherman, M. E.,
Carson, S. W., & Golden, R. N. (1997). Clomipramine challenge responses covary with tridimensional
personality questionnaire scores in healthy subjects. Biological Psychiatry, 42, 1123–1129.
Tamborini, R. & Stiff, J. (1987). Predictors of Horror Film Attendance and Appeal An Analysis of the Audience for Frightening Films. Communication Research, 14, 415-436.
Tamborini, R., Stiff, J. & ZILLMAN, D. (2006). Preference for graphic horror featuring male versus female victimization. Human Communication Research, 13, 529-552.
Zuckerman, M. (1984). Sensation seeking: A comparative approach to a human trait. Behavioral and Brain
Sciences, 7, 413–471.
Zuckerman (2009). "Chapter 31. Sensation seeking". In Leary, Mark R. & Hoyle, Rick H.. Handbook of Individual Differences in Social behavior. New York/London: The Guildford Press. pp. 455–465.
Zuckerman, M. (1991a). Psychobiology of personality. New York: Cambridge University Press.
Zuckerman, M. (1994). Behavioral expressions and biosocial bases of sensation seeking. New York:
Cambridge Press.
Zuckerman, M. (1996). The psychobiological model for impulsive unsocialized sensation seeking: A
comparative approach. Neuropsychobiology, 34, 125–129.
Zuckerman, M., & Neeb, M. (1980). Demographic inﬂuences in sensation seeking and expressions of
sensation seeking in religion, smoking and driving habits. Personality and Individual Diﬀerences, 1,
197–206.


What causes people to rapidly lose skill after becoming moderately good at something?

S-shaped learning curves

As per A Umar Mukthar's comment, the phenomenon is known as an S-shaped learning curve. They have been a known phenomenon in psychology for many decades, and were originally attributed to trial-and-error learning sets (Harlow, 1949). Harlow defined a learning set in the following manner:

  The monkeys learn how to learn individual problems with a minimum of errors. It is this learning how to learn a kind of problem that we designate by the term learning set.

Meta-cognition and intra-individual performance variability

Harlow's explanation has fundamentally not been changed too much, except perhaps that in modern cognitive research, we now call these meta-cognitive strategies rather than learning sets.

When first encountering a novel problem, participants will adopt one strategy and work to improve their performance on that, but eventually they will discover other strategies. When participants shift strategy thus to an unpracticed strategy, their performance declines, then improves again.

Because all strategies for the same problem tend to share at least some overlap, as participants explore an increasing proportion of the space of possible meta-cognitive strategies, shifting to a novel strategy requires decreasing amounts of new practice. The magnitude of the performance decline associated with strategy shifts is therefore gradually eliminated with prolonged practice (Murre, 2014).

References

Harlow, H. F. (1949). The formation of learning sets. Psychological review, 56(1), 51.
Murre, J. M. (2014). S-shaped learning curves. Psychonomic bulletin & review, 21(2), 344-356.


The literature generally provides strong support for the use of self-testing in cases like this, particularly via the use of flash cards (Karpicke and Roediger, 2008). The efficacy of self-testing for facilitating learning of arbitrary or complex sets of items has been suggested to be driven largely by the combination of two effects: the generation effect (Slamecka and Graf, 1978) captures the tendency for active retrieval of memory (e.g. fill-in-the-blank) information to increase the probability of successful future recall, as well as the spacing effect (Donovan and Radosevich, 1999), which captures the tendency for learning at a moderate intensity over time to outperform learning all at once.
References

Donovan, J. J., & Radosevich, D. J. (1999). A meta-analytic review of the distribution of practice effect: Now you see it, now you don't. Journal of Applied Psychology, 84, 795-805.
Karpicke, J. D., & Roediger, H. L. (2008). The critical importance of retrieval for learning. Science, 319(5865), 966–968. doi:10.1126/science.1152408
Slamecka, N. J., & Graf, P. (1978). The generation effect: Delineation of a phenomenon. Journal of experimental Psychology: Human learning and Memory, 4(6), 592-604.