How does one identify relevant variables when performing research on perception?

Researchers are trained to address this problem by using literature reviews to isolate the specific variables that should be of most interest. At the start of research you generally examine the knowns and unknowns in the particular area of interest, so as to determine the state of the art in that area. Once you know the state of the art you have a better idea of how to proceed with the research.

For example, if you found that something was known about your research area then you could use this literature to justify looking at a specific set of variables when examining the problem. This relevant prior literature need not have examined the exact same area as the problem you are looking at. For example, if you were looking at factors that influence preferences for coke and pepsi you could look at research that examined brand preferences, or even something more fundamental such as the factors that lead to positive beliefs and attitudes. This research would give you an idea as to which particular variables were most deserving of consideration.

Depending on the extent that you could argue that little was known about the particular problem,  you could also consider doing exploratory or descriptive research to attempt to identify or categorize the different variables involved. In this case you might use an interview to get some factors that set up your experiment and then use experiment to assess their relative impacts on the behaviour.


What are good examples of applying dynamical systems in cognitive science?

Given your background and interest in modeling, I would highly recommend The Cambridge Handbook of Computational Psychology. The book provides an overview for several of the prominent modeling paradigms in cogsci, including dynamical systems, as well as many concrete examples--albeit most using other computational paradigms.

Dynamical systems, to my knowledge, are most used in the field of motor control. Though to be honest, dyn systems is not 'my' paradigm, and most of my knowledge comes from the aforementioned book.

In particular, the chapter "Dynamical Systems Approaches to Cognition" by
G. Schoner gives this example that has always stuck in my mind:

  A highly illustrative example comes from the orientation behaviors of
  the common house ﬂy (Reichardt & Poggio, 1976; Poggio & Reichardt,
  1976). Flies orient toward moving objects, which they chase as part of
  their mating behavior. Detailed analysis revealed that the circuitry
  underlying this behavior forms a simple controller: a motion detection
  system fed by luminance changes on the ﬂy’s facet eye drives the ﬂight
  motor, generating an amount of torque that is a function of where on
  the sensory surface motion was detected. If the speck of motion is
  detected on the right, a torque to the right is generated. If the
  speck is detected on the left, a torque to the left is generated. The
  level of torque passes through zero when the speck is right ahead. The
  torque changes the ﬂight direction of the ﬂy, which in turn changes
  the location on the facet eye at which the moving stimulus is
  detected. Given the aerodynamics of ﬂies, the torque and its on-line
  updating generate an orientation behavior, in which the insect orients
  its ﬂight into the direction in which a moving stimulus is detected.


Is sub-vocalization when reading and writing merely a symptom of lack of fluency?

My understanding was that at least some sub-vocalisation is a normal part of reading and writing. The wikipedia article on subvocalisation cites several sources supporting that claim. The article also claims that there is no evidence to suggest that speed reading training that involves suppression of sub-vocalisation is effective. There is also evidence that suppressing subvocalisation can in some instances result in decrements in performance (see Baddeley et al, 1981).

There is some evidence to suggest that degree of subvocalisation is related to complexity of the reading passage. Baddeley et al 1981 summarise the use of

  the  electromyographic monitoring of  the muscles involved in
  vocalisation  in order to study the role  of  articulation in  reading
  (e.g. Sokolov,  1966).  Using  this technique,  Hardyk  and
  Petrinovitch  (1970) concluded  that subjects were  able  to read  and
  comprehend  simple prose  without  the  occurrence  of
  electromyographic activity,  but that such  activity  did  occur in
  the case of  more complex passages.

One explanation would be that degree, prominence or frequency of subvocalisation increases as the reading task gets more difficult, where experienced difficulty would vary both based on the individual's ability with the language and with the objective difficulty of the reading passage.

References

Baddeley, A.,  Marge Eldridge & Vivien Lewis (1981): The role of
subvocalisation in reading, The Quarterly Journal of Experimental Psychology Section A: Human Experimental Psychology, 33:4, 439-454
HARDYK, C.  D.  and PETRINOVITCH,  L.  R.  (1970).  Subvocal speech  and  comprehension  level as a function of the difficulty level of reading material.  Journal of  Verbal Learning  and Verbal Behavior, 9, 647-52.
SOKOLOV,  A. (1966).  La parole intbrieure dans la pensbe concrete. In Recherches Psychologiques en U.R.S.S.,  les Editions du Progrks, U.R.S.S.


What does it mean to say that mental illness is a modern-day leprosy?

This term depicts a wide spread problem in society that the term 'mental illness' carries with it stigmas and negative connotations.

Firstly, From a psychologist's perspective, we want people with mental illnesses to recognise them and seek help/treatment so that the problem can be solved. However, negative labels often cause people to ignore signs of mental illness. The effect is that fewer people with problems are seeking help from them, causing them and those around them to suffer for it.

Secondly, mental illnesses carry no moral significance or worth. An individual afflicted by a mental illness has done nothing to deserve it. It is unfair on them to be ostracized for something beyond their control, however this is often what happens with mental illnesses.

Leprosy has been greatly feared and shunned for thousands of years by humans everywhere. An individual with leprosy would be separated from the society and would be forced to survive on their own or find a leper colony if they were lucky. This is similar to how many people suffering mental illness suffer today. Often they cannot take care of themselves, and are shunned regardless of their suffering.


Any studies that assess effects of treatment to individual depression symptoms

To my mind, there are several reasons why this isn't the standard procedure. One reason is that Likert-type items are ordinal data, which means that standard statistical methods such as linear regression and t-tests shouldn't be used. Instead, non-parametric tests need to be used, and those generally confer lower statistical power. In contrast, a scale score (the sum of several Likert-type items) is per convention handled as interval data, which means that those standard methods can be used.
Another reason is that this might increase the probability of false positives. If a scale used to measure depression has 17 items and the significance level is set to p < 0.05, there is a 1 - 0.95^17 = 58 percent chance of at least one false "significant" association between the test group (treatment vs. no treatment) and an item from the scale.
Furthermore, the idea (which is questionable) is that there exists an underlying pathological "depression process" in the brain, which is expressed through different symptoms such as depressed mood, sleep disturbances, loss of interest etc. This is the medical model, and it is analogous to, for instance, pneumonia, in which there is a pathological infectious/inflammatory process in the body caused by bacteria, and giving rise to symptoms such as coughing, fever, etc. From this theoretical point of view, it makes more sense to assess the total score of the depression scales, which is thought to represent the "latent variable" that is the "depression process", rather than just one of the isolated symptoms.
However, there are examples in the literature of the approach you suggest. Below is one example of a meta-analysis of some trials of SSRI for depression. The study is not without flaws in my opinion, so the results should be interpreted with care, but it is an example of the idea you had.
Influence of baseline severity on the effects of SSRIs in depression: an item-based, patient-level post-hoc analysis


Are there benefits to learning to write with your non-dominant hand?

Yes, there are benefits, but I don't think it requires long-term switches.  Studies have used this as a manipulation to try and increase self control and have found that it decrease aggression.  Based on this, once one has mastered using the non-dominant hand, it seems like the benefit of continuing to use that hand might be over (as it no longer requires effort).

See: Denson, T. F., Capper, M. M., Oaten, M., Friese, M., & Schofield, T. P. (2011). Self-control training decreases aggression in response to provocation in aggressive individuals. Journal of Research in Personality, 45(2), 252–256. doi:10.1016/j.jrp.2011.02.001


Neurosurgically grown neural link between two brains?

Research exists on craniopagus twins, maybe most notably Tatiana and Krista, who seem to share sensory input somewhat. I doubt that connective mechanisms such as this abnormal case would suffice to permit "compound cognition" in ways that would enhance cognitive ability similarly to your point about hominid evolution. Your relatively simple proposal for a connective cord of neurons strikes me as roughly equivalent, though more complex connections may not be entirely unfeasible in the long run.

Before I move on to speculating about that, consider a few other points from cognitive neuroscience thus far. Plenty of split-brain research (on people and animals with dysfunctional corpus callosums) exists as well, little of which shows what I would call "radical effects on cognitive abilities". Results are somewhat more subtle than that: e.g., involving object recognition more than what laypeople would recognize as intelligence, especially social communication and basic reasoning, which remain relatively intact. You might also be surprised at the modest effects of losing an entire cerebral hemisphere: again, it's not what I would call a 50% reduction in cognitive ability, at least as we understand and use such abilities in modern social contexts.

Non-biological methods are already being experimented with for brain-to-computer and even human brain-to-brain interfacing (Armstrong & Ma, 2013), but we're some distance away from really augmenting cognitive abilities through such methods in the way evolution seems to have augmented them in hominids. Consider also that evolution seems to have proceeded in far more complex manners than those by which we're connecting brains now. Changes occurring organically throughout the brain over millions of years of natural selection may have developed our cognitive abilities well beyond those of smaller-brained animals, but these changes have probably been much more sophisticated than simply wiring disparate parts together, let alone only one part to only one other. Cognitive processes are functionally dispersed broadly across our incredibly complex neural structures; we definitely use more than 10% of our brains. There's really no particularly promising hub-of-all-cognitive-ability through which one could connect and expect to provide consciousness-wide augmentation (that I know of), nor would it be as simple as connecting one brain to another.

To throw in a halfhearted computer metaphor, consider how little processing ability is gained simply by connecting two computers by LAN cable. In very many ways, computer processing augmentation has had to proceed much more incrementally, component by component. Multi-core processors and several sticks of RAM per computer are commonplace now, but to truly augment computing performance with these, fundamental architectural changes in connective design have necessarily occurred. Far more than one wire connects these compound components.

Thinking in this manner might pave the way to future innovations that may someday achieve the effects you have in mind. Transhuman cognitive augmentation research is rapidly advancing in very many directions, some of which may bear satisfying similarities to your idea. They're all well beyond the scope of my knowledge or of this answer though, so I'll just toss some Wikipedia links at you to get things started. Please feel welcome to ask separate questions to follow up on cyberpsychological topics; I find them all very exciting, and would be very eager to explore them further with you and our community!

Intelligence amplification
Cyborgs, cybernetics, and cyberware

Exocortex – artificial external augmentation system for high-level cognitive processes
Neuroprosthetics – devices to substitute motor, sensory, or cognitive modalities

Visual prosthetics

Artificial brains

The Blue Brain Project – a molecular reverse-engineering of the mammalian brain
Artificial intelligence – arguably more on-topic at the dedicated AI Stack Exchange

Hierarchical temporal memory – online machine learning structural neocortical model

Wetware computers – built from organic, living neurons!

Nootropics – cognition, memory, intelligence, motivation, attention, and concentration drugs

See a related question, Do smart drugs (nootropics) make you smarter?
Ampakines – compounds that enhance attention span, alertness, learning, and memory

Transcranial direct-current stimulation

See a related question, Can learning be facilitated by transcranial magnetic stimulation?

Mind uploading – copying mental content from a brain substrate to another computational device

Depends on brain reading / fingerprinting / thought identification

Augmented reality

Consumer brain-computer interface devices
Neurofeedback – illustration of brain activity to teach self-regulation
Augmented learning – adaptive learning environments
Electronic learning
Web-based simulation
Wearable computers

Head-up displays – transparent data displays that accommodate users' usual viewpoints

Bionic contact lenses and virtual retinal displays
Optical head-mounted displays
EyeTap
Google Glass

Reference

Armstrong, D., & Ma, M. (2013, August 27). Researcher controls colleague’s motions in 1st human brain-to-brain interface. Washington University: News and Information. Retrieved from http://www.washington.edu/news/2013/08/27/researcher-controls-colleagues-motions-in-1st-human-brain-to-brain-interface/.


Does wealth cause (or correlates with) narcissism?

I found a review in a relatively obscure journal, but it seems a reasonable summary of the existing research, except for the fact that income and wealth aren't necessarily the same:

  A review of literature regarding income and altruism revealed mixed evidence. Chen, Zhu, and
  Chen (2013) showed that, under a dictator game setting, pre-school children from higherincome
  families give fewer stickers (endowment of the game) to others compared to kids from
  lower-income families. Miller, Kahle, and Hastings (2015) altered the game so that the tokens
  (endowment of the game) had to be earned via work and the kids were told that the recipients of
  their donation would be other sick kids who were not able to make it to the venue on that day.
  They still found that kids from richer families are less likely to donate their tokens compared to
  kids from poorer families. Piff, Kraus, Côté, Cheng, and Keltner (2010) conducted experiments
  on adults using economic games and scenarios and found that individuals of lower socioeconomic
  status appeared to be more generous, more trusting, and more compassionate.

  On the other hand, Hoffman (2011) investigated historical data during the World War II
  on people’s decision to rescue the Jews. He found that the higher the income of the people, the
  more likely they were to rescue the Jews. Holland, Silva, and Mace (2012) used a lost-letter
  experiment. They dropped letters on pavements in different neighborhoods in the United
  Kingdom and found that letters dropped in the richer neighborhoods were more likely to be
  returned to the address listed on the letters. Looking into this issue more thoroughly,
  Andreoni, Nikiforakis, and Stoop (2017) designed a more complicated version of the lostletter
  experiment. Under their setting, the envelopes used were thin enough so that contents of
  items in the envelopes (cash, or bank transfer cards) could be seen from the outside. The
  letters were mis-delivered to rich and poor households in the Netherlands. Their initial results
  revealed that the rich were more likely to return the envelopes compared to the poor.
  However, with further investigations, the authors found that the rich were not more altruistic
  than the poor. The fact that the rich were more likely to return the envelopes was because they
  faced lower financial constraint and had lower marginal utility for the found money.

  The above evidence showed that the relationship between income and altruism may be
  ambiguous. Thus, it cannot yet be concluded whether the degree of altruism [...] should be higher for the rich or for the poor.

Unfortunately, that may not be as relevant as I had hoped because

  It is unfortunate that a false dialectic between narcissism and altruism is in common usage. The two entities regularly co-exist. Vaillant, in his longitudinal study of healthy males, found that altruism increases significantly in the second half of life – not simply because we become more selfless as we age, but rather because helping others becomes more rewarding to us. A neuroimaging study demonstrated that those who are altruistic directly benefit from their altruism. Participants had to choose to endorse or oppose societal causes by anonymous decisions to donate or refrain from donating to real charitable organizations. The mesolimbic reward system was engaged when one donated money in the same way as it was when one received monetary awards. In other words, altruism activates brain centers that are associated with selfish pleasures like sex or eating.

Unfortunately the narcissism-wealth link alone has received less attention, perhaps because most researchers were interested in outward behavior (like altruism). Or in more prosaic terms, most people don't care how long you look at yourself in the mirror as long as you give them money :P


What correlation is there between breath control and personal self confidence?

I am not aware of any neuroscience papers that link breathing and self-confidence. One review that touched on breathing in yoga was Jerath et al. (2006). They discuss how deep breathing increases parasympathetic autonomic activity. This can change the physiological state of the body, leading to changes in affective state.

One area of the brain that may be relevant is a patch of cortex called the insula. The posterior insula receives afferent information from the body and creates the initial sensory representation of body state (Craig, 2000). From there, the mid insula begins to integrate body state with other sensory modalities, such as visual and auditory information. This progression continues, until you have a highly integrated, abstract representation of interoceptive and emotional state in the anterior insula (Craig, 2009).

Activity in the anterior insula has been related to a wide array of higher cognitive functions, including self-recognition, emotional awareness, risk prediction, conscious awareness of sensory stimuli, temporal perception, attention, perceptual decision making, performance monitoring, and more. We know that relaxation techniques can influence activity in this area of the insula (Critchley et al., 2002).

It is well supported that controlled breathing changes the state of your body and activity in the brain, including the insula. These changes can also directly influence our cognitive state and cognitive ability.  Changes in self-confidence may be a part of that, depending on how you might define self-confidence.

Craig AD, Chen K, Bandy D, Reiman EM. (2000) Thermosensory activation of insular cortex. Nature Neuroscience. 3, 184-190. PMID: 10649575.
Craig AD. (2009). How do you feel-now? The anterior insula and human awareness. Nature Reviews Neuroscience. 10(1), 59-70.
Critchley HD, Melmed RN, Featherstone E, Mathias CJ, and Dolan RJ. (2002). Volitional control of autonomic arousal: a functional magnetic resonance study. NeuroImage. 16(4), 909-919. PMID: 12202079.
Jerath R, Edry JW, Barnes VA, and Jerath V. (2006). Physiology of long pranayamic breathing: Neural respiratory elements may provide a mechanism that explains how slow deep breathing shifts the autonomic nervous system. Medical Hypotheses. 67, 566-571. PMID: 16624497.


Is fear in response to the sight of predators innate or acquired?

Alright, so my familiarity with this area primarily comes from Vanessa LoBue's work.  And what I get from her research is that we don't really know if certain fears are innate or acquired.
LoBue seems to favor a prepared learning model, which is just as it sounds.  Infants are not born fearful of things like spiders, snakes, and heights (Adolph, Kretch, & LoBue, 2014; LoBue et al., 2012), but they are biased (prepared) to learn to fear them.  She has supported this theory by showing that children are more rapid at attending to snakes than other stimuli (e.g., flowers, frogs, caterpillars), independent of snake knowledge/exposure (LoBue & DeLoache, 2008).  Infants are also biased to associate undulating snakes, but not other stimuli, with negatively valenced sounds (DeLoache & LoBue, 2009).  However, this wasn't true for static images of snakes.
Importantly, these stimuli are (ostensibly) evolutionarily significant (snakes, spiders, but not lions, tigers).  However, the evidence for their threatening presence in human evolution, at least for spiders, is lacking (LoBue & Rakison, 2013).  This has been a major criticism of the prepared learning model: which stimuli are 'prepared'?
LoBue suggests that the bias toward snakes might be mediated by low-level perceptual characteristics that pop out (i.e., curvilinear features) (LoBue, 2014).  However, it's not clear if this visual saliency leads to actual fear learning of snakes (LoBue & Rakison, 2013).  Moreover, this suggests that any predominantly curvilinear stimulus might bias attention.
Aside from her work, there are loads of mixed findings in this area that don't point to a clear answer. For example, there are studies that report a general attention bias for animals in general, threatening or non-threatening (e.g., Lipp, 2006). Plus there are several outstanding methodological problems in much of the past research.
Frankly, there just needs to be a lot more research in order to figure this out. Although I would argue that the "non-associative model" (that infants don't need to learn, in some way, to fear snakes, spiders, etc.) is out of fashion and not well supported. But for the most recent reviews, see LoBue & Rakison (2013) and LoBue (2013).
References
Adolph, K. E., Kretch, K. S., & LoBue, V. (2014). Fear of heights in infants?. Current directions in psychological science, 23(1), 60-66. doi: 10.1177/0963721413498895 PMCID: PMC4175923 PDF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4175923/pdf/nihms574402.pdf
DeLoache, J. S., & LoBue, V. (2009). The narrow fellow in the grass: Human infants associate snakes and fear. Developmental science, 12(1), 201-207. doi: 10.1111/j.1467-7687.2008.00753.x
Lipp, O. V. (2006). Of snakes and flowers: Does preferential detection of pictures of fear-relevant animals in visual search reflect on fear-relevance? Emotion, 6(2), 296-308. doi: 10.1037/1528-3542.6.2.296
LoBue, V., & DeLoache, J. S. (2008). Detecting the snake in the grass: Attention to fear-relevant stimuli by adults and young children. Psychological science, 19(3), 284-289. doi: 10.1111/j.1467-9280.2008.02081.x
LoBue, V. (2013). What are we so afraid of? How early attention shapes our most common fears. Child Development Perspectives, 7(1), 38-42. doi: 10.1111/cdep.12012
LoBue, V., Bloom Pickard, M., Sherman, K., Axford, C., & DeLoache, J. S. (2013). Young children's interest in live animals. British Journal of Developmental Psychology, 31(1), 57-69. doi: 10.1111/j.2044-835X.2012.02078.x
LoBue, V., & Rakison, D. H. (2013). What we fear most: A developmental advantage for threat-relevant stimuli. Developmental Review, 33(4), 285-303. doi: 10.1016/j.dr.2013.07.005
LoBue, V. (2014). Deconstructing the snake: The relative roles of perception, cognition, and emotion on threat detection. Emotion, 14(4), 701. doi: 10.1037/a0035898


why are all human brains so similar in brain structure, specialization of their parts and functioning?

Up until the 70s and 80s, there were decades of hot debate about whether some phenotype such as brain structure or some behavior were caused by genes or by environment. Wikipedia has a decent summary of the history and content of that debate, and I've linked to the section on estimating the relative contribution of genes vs. environment: https://en.wikipedia.org/wiki/Nature_versus_nurture#Heritability_estimates

The current consensus is that the #1 question isn't very meaningful. Genes and environment are both 100% necessary conditions for a brain to develop. Yes, the similarity between brains (and between species) show that a lot of the structure is conserved, and much of that design depends on genes. But those genes wouldn't develop into a brain without very specific environmental conditions.

There are three quite distinct questions under #2. Cells and regions differentiate in the body; brain plasticity isn't 100%. Some structure is conserved. Consider that "modularity", one type of which is that different areas of the brain do distinct operations, is at least partially false. The brain is not at all like a computer with a motherboard with distinct components. It might help to consider how you would answer your question for why people's thumbs don't look like their other fingers. What prevents a thumb from developing into a finger? Are the functions of a thumb determined by genetics? This might help you to zero in on the specific processes of the brain that are the mechanisms that explain how genes and environments interact to produce phenotypes.


A nice psychology article (media article) that provides answers to your question can be found at here. I will try to summarize briefly based on this article.

  How close to uniformly randomness can we expect each person to act?

The short answer is no. As explained in the article, on the first round of Rock-Paper-Scissors it is less likely that a randomly selected person will choose paper over scissors or rock. Moreover, as two people play many rounds of Rock-Paper-Scissors together, they tend to not play randomly but adjust their selections based on whether they won or lost.

  Will this be a stationary distribution or it will change over the time if there will be a lot of trials?

There are many definitions of stationary, but a paper mentioned in the above article found cyclical behavior which would violate some of the definitions of stationary. However, this might still fit into some definitions of stationarity.

While I'm unaware of a particular article which addresses the question of wide-sense stationary in this game, I would be surprised if this were found in Rock-Paper-Scissors played between humans. There is an interplay of affective (emotional) and rational decision making that tends to be influenced by the actions of human opponents.

I would be less surprised if this were found when a human plays a computer, especially if they knew the computer was playing completely randomly. People play different strategies in games played Human vs. Human as opposed to Human vs. Computer (e.g. the Ultimatum Game)


Isolating stable EEG data across all channels in EEGLAB

In this conference paper they propose an algorithm that roughly goes as follows (if you can't access it, just add "sci-hub.bz" after ".org" in the url and it redirects you directly to the pdf) :

Divide channels into four groups: 1) frontal, 2) central, 3) temporal and 4) parietal+occipital.
For each group take three signals: 1) the raw signal, 2) the alpha band(8-12Hz, using a 3rd order butterworth band-pass filter) and 3) the beta band(13-35Hz).
For each group and each signal calculate the four metrics: 1) max amplitude, 2) standard deviation, 3) kurtosis and 4) skewness. For the frequency band signals they also take the mean power and the standard deviation of the power.

They then go on and find optimal thresholds for each metric, group, and signal by using a differential evolution algorithm on training data, so unfortunately it's not immediately applicable for you. As I see it, you have at least two options here:

Create 5 seconds long epochs of your data and label a lot of them. Use that data to learn optimal thresholds (unfortunately they don't give any details on how to do that, so you would have to figure that out yourself). This would obviously take a lot of effort but at the end you can be quite confident about your classification.
Just try some value ranges for the different metrics, you can orient yourself on the values they found in the paper (you have to read them from the plots though).  Check the resulting classifications. Pick the threshold values that give the "best" results by inspections. This is not as systematic as the first option but might fit your needs already. For example if you just want to avoid to have segments that were falsely classified as "clean" you might just go for very conservative/safe threshold values. There is a big danger here though, that you will get lost in an endless loop of "maybe if I adjust this threshold a bit more" and will never stop exploring. To help with that, you might also reduce the number of metrics, groups or signals.


Are Rorschach (inkblot) tests still used as a diagnostic tool?

Yes, they are still in use, and they provide rather bad information. My former advisor once worked with a clinician who told him that the main reason they're any better than using the weather report as a projective stimulus is that the Rorschach tests have been in use as-is for decades. Hence we have a better understanding of how people normally react to them, and some catalog of unusual reactions that have been associated with particular characteristics. Had we started with a set of weather reports and stuck with them though, maybe not much else would be different.

Anyway, here are some excerpts from Wikipedia about usage:

  United States

  The Rorschach test is used almost exclusively by psychologists. In a survey done in the year 2000, 20% of correctional psychologists used the Rorschach while 80% used the MMPI.[8] Forensic psychologists use the Rorschach 36% of the time.[79]
  In custody cases, 23% of psychologists use the Rorschach to examine a child.[80]
  Another survey found that 124 out of 161 (77%) of clinical psychologists engaging in assessment services utilize the Rorschach,[81] and 80% of psychology graduate programs teach its use.[9]
  Another study found that its use by clinical psychologists was only 43%, while it was used less than 24% of the time by school psychologists.[79]

  United Kingdom

  Many psychologists in the United Kingdom do not trust its efficacy and it is rarely used.[82] Although skeptical about its scientific validity, some psychologists use it in therapy and coaching "as a way of encouraging self-reflection and starting a conversation about the person's internal world."[25] It is still used, however, by such prestigious mental health organisations as the Tavistock Clinic.[83]

  Japan

  Shortly after publication of Rorschach's book, a copy found its way to Japan where it was discovered by one of the country's leading psychiatrists in a second-hand book store. He was so impressed that he started a craze for the test that has never diminished. The Japanese Rorschach Society is by far the largest in the world and the test is "routinely put to a wide range of purposes".[26] The test has recently been described as "more popular than ever" in Japan.[83]

And about the objects of (intended / purported) measurement:

  The general goal of the test is to provide data about cognition and personality variables such as motivations, response tendencies, cognitive operations, affectivity, and personal/interpersonal perceptions. The underlying assumption is that an individual will class external stimuli based on person-specific perceptual sets, and including needs, base motives, conflicts, and that this clustering process is representative of the process used in real-life situations.[33] Methods of interpretation differ. Rorschach scoring systems have been described as a system of pegs on which to hang one's knowledge of personality.[34] The most widely used method in the United States is based on the work of Exner.

References
8. Raynor, P., & McIvor, G. (2008). Developments in social work offenders (Research highlights in social work) (pp. 138). London: Jessica Kingsley Publishers. ISBN: 1-84310-538-1.
9. Weiner, I. B., & Greene, R. L. (2007). Handbook of personality assessment. John Wiley & Sons. ISBN: 0-471-22881-8.
25. BBC News. (2012, July 24). What's behind the Rorschach inkblot test? BBC News Magazine. Retrieved July 31, 2014 from http://www.bbc.com/news/magazine-18952667.
26. Fidgen, J. (2012, July 25). On A. Hall (Producer), Dr Inkblot. BBC Radio 4. Retrieved July 31, 2014 from http://www.bbc.co.uk/programmes/b01l0kch.
33. Groth-Marnat, G. (2003). Handbook of psychological assessment. John Wiley & Sons. ISBN: 978-0-471-41979-2.
34. Mons, W. (1950). Principles and practice of the Rorschach Personality Test (2nd ed., pp. 30–31). Faber.
79. Hughes, Gacono, C. B., & Owen, P. F. (2007). Current status of Rorschach assessment: Implications for the school psychologist. Psychology in the Schools, 44(3), 281. DOI: 10.1002/pits.20223.
80. Butcher, J. N. (2009). Oxford handbook of personality assessment (Oxford Library of Psychology) (pp. 290).  Oxford University Press. ISBN: 0-19-536687-5.
81. Camara, Nathan, J. S., & Puente, A. E. (2000). Psychological test usage: Implications in professional psychology. Professional Psychology: Research and Practice, 31(2), 131–154. DOI: 10.1037/0735-7028.31.2.141.
82. Guardian staff. (2013, November 8). Hermann Rorschach Google doodle asks users to interpret inkblot test. The Guardian. Retrieved July 31, 2014 from http://www.theguardian.com/technology/2013/nov/08/hermann-rorschach-google-doodle-inkblot-test.
83. Hall, A. (2012, July 25). Dr Inkblot. BBC Radio 4. Retrieved July 31, 2014 from http://www.bbc.co.uk/programmes/b01l0kch.


Are there known cases where people can write upside down?

Leonardo da Vinci wrote both upside down, and in a mirror image.  He did the latter partly to make it harder for others to read his journals and copy his ideas (he was doing his research in a time when it was forbidden by the church), but also to avoid smudging his writing.  He was also left-handed.

Here is someone who also writes upside down and backwards.  And here is a case of a mother asking if she should be concerned because her 2 1/2 year old daughter writes upside down.


Is it possible that people perceive time differently than others do?

Short Answer

Yes. People estimate time differently, by focusing their attention on time in more or lesser degree. Also within a person, time estimation may vary due to stochastic variations.

Long answer

This is a really nice paper that tries to explain time-perception in a cognitive architecture called ACT-R. It is a model of human cognition that tries to explain human behavior with only basic functions (declarative and procedural memory, vision, working memory a.o.).

Very shortly, the model is as follows: There is a pacemaker. This pacemaker creates pulses that are counted and saved in memory, and this memory is coupled to a particular time-frame. Each time you start counting, you reset the pacemaker to zero. So, for instance, after some practice, you learn that five seconds consists of 23 pulses, and eight seconds is equivalent to 30 pulses.

The pacemaker has two properties however. First, the pacemaker is not perfect. There are minor variations in the duration of each interval between the pulses. Five seconds may thus sometimes be perceived as 22 pulses and sometimes as 24 pulses. This is the reason variability exists in time estimations.

Secondly, the duration of intervals between pulses increases over time. Where the time between a pulse may be 200 ms (+- random value) when you start to count, it may be 400 ms (+- random value) after ten seconds. On top of that, the effects of random noise also becomes larger. If you count the pulses, the precision of the counting will thus decrease. Therefore it is increasingly difficult to estimate longer periods of time as compared to shorter periods of time. In figure 2 in the paper, this is depicted with the increasing width of the normal distributions.

Attention
So far I have only explained how one person may perceive time differently due to stochastic differences in pulse productions. What I left out so far is the attentional component of the model. When you focus your attention on the pulses your estimates will be rather good, because you perceive these pulses more consciously. However, as anyone may know, "time may fly" (when you're having fun). This is believed to be caused by the lack of attention to the pulses, therefore being unaware of how time passes. It is however not entirely clear how this attentional component works, and the debate is still ongoing.

Neuro-biology:

The model was based on a paper written by Mattel and Meck (2004), which provide a neuro-biological explanation for the pacemaker. The model they propose is the "striatal beat frequency model", which states that there is neuronal activity oscillating at different rates in different networks of neurons. The oscillations are then detected by Striatal Spiny Neurons, which result in a sort of "barcode"(i.e. an array neurons being active and inactive; see Figure 1A). It is these barcodes that are memorized and associated with a particular duration (See Figure 1B).

Figure 1: Striatal beat frequency model. Picture taken from Researchgate

As mentioned earlier, the pacemaker needs to be reset when you start counting from zero. It is theorized that this is done by a burst of dopamine.

Here is a review about the neural pathways for time-estimation by Buhusi and Meck (2005). My neuro-biology is a little rusty though, so if there is anyone that could comment/elaborate on this, that would be highly appreciated.

References

Buhusi, C. V., & Meck, W. H. (2005). What makes us tick? Functional and neural mechanisms of interval timing. Nature reviews. Neuroscience, 6(10), 755.

Matell, M. S., & Meck, W. H. (2004). Cortico-striatal circuits and interval timing: coincidence detection of oscillatory processes. Cognitive brain research, 21(2), 139-170.

Taatgen, N. A., Van Rijn, H., & Anderson, J. (2007). An integrated theory of prospective time interval estimation: The role of cognition, attention, and learning. Psychological Review, 114(3), 577.


Phase locking value (PLV) between $x(t)$ and $x(t-T)$

PLV is good for correlating signals that seem out of phase to our measurement techniques due to the digital nature of our recordings but are in sync because of the electro chemical biological nature of the CNS. If you transform two signals into phase you can determine the relatedness of the two signals.

Phase Locking Value NeuroBytes
The schematic below illustrates how PLV is computed in this implementation. Explanation for each step follows.


What articles use structural equation modelling in a meta-analytic context to model mediation?

I'd like to address important issues that Jeromy Anglim raised in the "Personal thoughts" section of his answer, namely that correlation parameters (i.e., true, population, or infinite-sample correlations) often vary and covary among studies, and this between-studies\interstudy heterogeneity implies heterogeneity in studies' parameters for a structural equation model (SEM).  I'll describe a method I've proposed to account for this heterogeneity when estimating and making statistical inferences about a SEM, such as a univariate or multivariate regression model, factor model, path model, or model for structural relations among latent variables, or specific quantities based on such a model (e.g., $R^2$, indirect\mediation effect, fit index).  This approach's core idea is simple:

Use random-effects (RE) meta-analysis to estimate attributes of the between-studies distribution of correlation-matrix parameters (e.g., its mean and covariance matrix).
Transform those results to estimate attributes of the between-studies distribution of SEM parameters.

Many commonly used MASEM methods are based on fixed-effects (FE) models, and although meta-analyzing heterogeneous correlation matrices using certain FE methods performs reasonably well in some situations, it's probably not advisable for making unconditional inferences about a larger universe of studies (Hafdahl, 2008a).

Here I'll just give overviews of the problem and a three-step version of my proposed meta-analytic SEM (MASEM) method -- actually a collection of methods based on different choices for critical tasks at each step.  To keep the exposition relatively accessible I'll gloss over several important technical details.  Although this is an active area of my methodological research, the methods I'll sketch here are based largely on unpublished work (I'll cite references).  Because some aspects of this approach would be prohibitively difficult for many applied researchers to implement, one aim of my work in this area is to develop user-friendly software.  Until that's available, feel free to contact me for help with these techniques; such requests may motivate me to devote more time and other resources to this work.

Overview of Problem

In this section I'll describe my view of the problems for which MASEM is typically used.  Suppose we have from each of $k$ independent studies a sample Pearson-r or Fisher-z correlation matrix among $p$ variables of interest (e.g., $X_1, X_2, \ldots, X_p$), and suppose we're interested in a particular SEM for those variables or a related quantity that can be expressed as a function of the correlation matrix (e.g., 1 or more [standardized] path coefficients, indirect or total effect, squared multiple correlation, fit index).  It's useful to distinguish between each study's correlation-matrix parameter and that study's correlation-matrix estimate from a particular sample of subjects.  Meta-analysts are typically interested in using several studies' estimates to understand their corresponding parameters or distributions thereof.

In this overview I'll mostly ignore several interesting but vexing complications that arise in practice.  For instance, studies might use different versions of one or more variables (e.g., different measures similar to $X_1$), some studies might not contribute all $d = p( p - 1) / 2$ distinct correlation-matrix elements (e.g., due to missing variables or unreported elements), some of a study's correlations might be based on different subsets of its sample (e.g., if some subjects are missing some variables), a study might contribute two or more independent or dependent correlation matrices (e.g., from different groups or the same group in different conditions or at different times), studies' correlations might be influenced by so-called artifacts (e.g., [un]reliability, range restriction, dichotomization), and study-level covariates\moderators might partially account for between-studies heterogeneity.

Now, if we take the RE view that correlation-matrix parameters vary among studies -- that is, our studies are from a universe of studies whose correlation-matrix parameters follow some multivariate distribution -- then most functions of that correlation-matrix parameter will also vary among studies.  In particular, an SEM's path-coefficient parameters and other quantities (e.g., indirect effects) will have a distribution over studies.  To be clear, these distributions' between-studies (co)variation is not due to within-study sampling (co)variation caused by finite samples of subjects; instead, it may be viewed as due to studies' different constellations of features that produce different values for their correlation-matrix parameters and, consequently, most functions of those parameters.  (As a simpler example, consider 1 Pearson-r correlation parameter from each of several studies: If it varies among studies, then so will various functions of it -- its square, coefficient of alienation, Fisher z-transform, common language effect size, etc.)

By analogy with typical tasks in conventional RE meta-analyses, we might be interested in the following for our SEM: estimates of the between-studies mean and variance of each SEM path coefficient or other related quantity (e.g., indirect effect) and inferences about each such quantity (e.g., confidence interval [CI], prediction interval [PrI], hypothesis test).  When we're interested in two or more quantities from the SEM, we might wish to obtain bi- or multivariate generalizations of these estimates or inferences (e.g., confidence or prediction region\set); these might include quantities based on two or more distinct SEMs we'd like to compare, such as fit indices from two or more SEMs.  We might also be interested in the entire between-studies distribution of one or more SEM quantities (i.e., not only its mean and [co]variance [matrix]), which we could in some situations depict graphically (e.g., density plot).

Most commonly used MASEM approaches neglect between-studies heterogeneity in the SEM parameters, which seems especially difficult to justify in the presence of heterogeneous correlation(-matrix) parameters.  Certain aspects of the SEM parameters' between-studies (co)variance might be substantively important, such as if we're interested in how much particular path coefficients, indirect or total effects, squared multiple correlations, or fit indices (co)vary among studies.  For instance, if we use RMSEA as a fit index, we might wish to know how much RMSEA varies among studies, a plausible range of RMSEA values (e.g., prediction interval), or what proportion of studies have RMSEA values within some "acceptable" interval (e.g., below .05).

Moreover, there's reason to treat heterogeneity cautiously even if we're interested in only the mean of SEM parameters: Because SEM parameters are typically nonlinear functions of the correlation matrix, it's unclear what's estimated by applying the SEM directly to a mean correlation matrix, as in most MASEM approaches; that might estimate the mean SEM parameter poorly.  As a simpler example, suppose that for a heterogeneous effect-size parameter $Y$ we know its mean and variance over studies, $\mathrm{E}(Y)$ and $\mathrm{Var}(Y)$, but want to know the mean for $Y$'s square: Because for most distributions of $Y$ it's a fact that $\mathrm{E}(Y^2) = [\mathrm{E}(Y)]^2 + \mathrm{Var}(Y)$, simply squaring $\mathrm{E}(Y)$ gives a value lower than the desired $\mathrm{E}(Y^2)$, especially if $\mathrm{Var}(Y)$ is large.  This basic problem with applying a nonlinear transformation to a mean of heterogeneous effect sizes was addressed for the case of a univariate correlation -- focusing on the z-to-r transformation -- by Hafdahl (2009) and Hafdahl and Williams (2009); the analogous situation was addressed for correlation matrices by Hafdahl (2008b, 2009b), for generic univariate effect sizes by Hafdahl (2011), and for generic multivariate effect sizes by Hafdahl (2009c).

Overview of Proposed Method

In the first paragraph above I mentioned the gist of my proposed two-stage MASEM method.  To facilitate explanation, it's useful to divide the second stage -- transformation of results -- into separate steps for estimation and inference.  For instance, if we start with $k$ studies' estimates of a Fisher-z correlation matrix, the first step might entail estimating the correlation-matrix parameters' between-studies mean and covariance matrix, and the second and third steps might entail transforming those results to obtain estimates of and inferences about the between-studies mean and covariance matrix of the SEM's path coefficients.  Below I elaborate a bit on these three steps.

For convenience, let's use the following notation for correlation matrices from Study $i, i = 1, 2, \ldots, k$:

$\theta_i$: vector of the $d$ distinct parameters in a correlation matrix for $p$ variables, in either the Pearson-r or Fisher-z metric
$y_i$: vector of the $d$ distinct estimates in sample correlation matrix (i.e., $y_i$ is an estimate of $\theta_i$)

For example, if we're interested in the correlation matrix for $p = 5$ variables, then both $\theta_i$ and $y_i$ contain $d = 5(5 - 1) / 2 = 10$ correlations.  In RE meta-analysis we typically assume that $y_i$ has a within-study (sampling\conditional) distribution whose mean is approximately $\theta_i$, and that $\theta_i$ (or just $\theta$) has the same between-studies distribution for all studies, with mean $\mu_\theta = \mathrm{E}(\theta)$ and covariance matrix $\Sigma_\theta = \mathrm{Cov}(\theta)$.  (For simplicity I'll slightly abuse notation for random correlation parameters and estimates -- instead of using $\Theta_i$ and $Y_i$ -- and I'll ignore other quantities used in certain meta-analytic procedures, such as each study's sample size and conditional covariance matrix, whose inverse [i.e., precision matrix] is essentially used as a weight matrix.)

In terms of SEM notation, let's similarly denote the SEM parameters of interest in Study $i$ by $\gamma_i = g(\theta_i)$, where the function $g$ transforms a correlation-matrix parameter into SEM parameters.  This $g$ might be a fairly complicated function, such as for the parameters of a SEM with respect to a particular objective\loss criterion (e.g., ML, WLS, ADF) or a fit index for that SEM.  Also, $\gamma_i$ might be just one number (e.g., 1 path coefficient, indirect effect, fit index) or a vector (e.g., 2 or more path coefficients).  At any rate, our MASEM goal might be to estimate $\gamma$'s between-studies mean or (co)variance (matrix), $\mu_\gamma = \mathrm{E}(\gamma)$ and $\Sigma_\gamma = \mathrm{Cov}(\gamma)$, and make inferences about either distributional attribute; we might also wish to estimate $\gamma$'s entire distribution.

Below are the three steps of my proposed method; Steps 2 and 3 presume we have in mind a specific SEM or related quantity that can be expressed as $\gamma_i = g(\theta_i)$.  This is similar to Hafdahl's (2009a, 2011) univariate methods and Hafdahl's (2008b, 2009b, 2009c) multivariate methods but specific to MASEM.

1. Meta-Analysis for $\theta$: Apply multivariate RE meta-analysis to $y_i$ to obtain estimates of at least $\mu_\theta$ and $\Sigma_\theta$, which I'll denote $\hat\mu_\theta$ and $\hat\Sigma_\theta$, and perhaps $\theta$'s full between-studies distribution; perhaps also obtain a covariance matrix for only $\hat\mu_\theta$ or both $\hat\mu_\theta$ and $\hat\Sigma_\theta$, depending on how inference is handled in Step 3.  Among several proposed methods for estimating $\mu_\theta$ and $\Sigma_\theta$, only a few handle incomplete correlation matrices -- nearly unavoidable in MASEM data sets -- in a principled way (e.g., Hafdahl & Wu, 2011; Kalaian, & Raudenbush, 1996; White, 2011).  In particular, Hafdahl and Wu's extension of Becker and Schram's (1994) EM algorithm permits any one or more of $y_i$'s correlations to be missing, doesn't require imputing values for missing correlations, and yields a posterior distribution for each study's entire $\theta_i$ (given its possibly incomplete $y_i$); it also yields an estimate of $\theta$'s full between-studies distribution as a mixture of the studies' posterior distributions.  Depending on the estimation method, a covariance matrix for $\hat\mu_\theta$ may be obtained by generalized least-squares (GLS) or other methods (e.g., based on Hessian matrix for maximum-likelihood estimators), some of which also provide a covariance matrix for $\hat\Sigma_\theta$.  Hafdahl (2004) demonstrated substantial differences in performance among different techniques for multivariate RE meta-analysis applied to correlation matrices.

2. Estimation for $\gamma$: Use an appropriate transformation method -- based on the function $g$ -- to obtain estimates of at least $\mu_\gamma$ and $\Sigma_\gamma$, which I'll denote $\hat\mu_\gamma$ and $\hat\Sigma_\gamma$, and perhaps $\gamma$'s full between-studies distribution.  One strategy is to use a first- or second-order Taylor series approximation, which essentially entails approximating $\gamma = g(\theta)$ by a simpler linear or quadratic function of $\theta$; estimates of this approximating function's mean and covariance can then be computed from Step 1's $\hat\mu_\theta$ and $\hat\Sigma_\theta$.  Another strategy entails simulation: Sample values of $\theta$ from its distribution estimated in Step 1, transform these to values of $\gamma$, and estimate $\mu_\gamma$ and $\Sigma_\gamma$ from this simulated distribution; we might treat $\theta$'s distribution as multivariate normal -- such as $\theta \sim \mathcal{N}_d(\hat\mu_\theta, \hat\Sigma_\theta)$ -- or permit it to take some other form estimated from the data (e.g., mixture of posteriors from EM algorithm).  Either strategy might also be used to estimate other attributes of $\gamma$'s distribution, such as tail or central areas (e.g., probability that 1 or more path coefficients or other quantities are near 0, positive, large, etc.) or $\gamma$ values bounding regions of interest (e.g., quartiles, middle 95%).  (We could in principle transform $\hat\mu_\theta$ and $\hat\Sigma_\theta$ to $\hat\mu_\gamma$ and $\hat\Sigma_\gamma$ via integration, using the definitions of $\mu_\gamma$ and $\Sigma_\gamma$, but that'll often be intractable analytically and infeasible computationally.)

3. Inference for $\gamma$: Make inferences about $\mu_\gamma$ and $\Sigma_\gamma$, such as CIs, PrIs, or hypothesis tests for single-valued parameters or their multivariate generalizations for vector-valued parameters (e.g., confidence or prediction regions).  One strategy is to use the (multivariate) delta method, which essentially entails using derivatives to transform the covariance matrix for $\hat\mu_\theta$ alone or both $\hat\mu_\theta$ and $\hat\Sigma_\theta$ to a covariance matrix for $\hat\mu_\gamma$ or $\hat\Sigma_\gamma$; the latter covariance matrix can be used to construct CIs or PrIs or test hypotheses.  Another strategy, at least for CIs or confidence regions, is to use a bootstrap technique to essentially construct an empirical sampling distribution of $\hat\mu_\gamma$ or $\hat\Sigma_\gamma$; numerous bootstrap options are available, depending largely on how the sample of bootstrap replicates -- $\hat\mu_\gamma$ or $\hat\Sigma_\gamma$ for each resample from the data -- is constructed (e.g., parametric vs. nonparametric) and how it's used to construct confidence intervals or regions (e.g., standard deviation\error vs. percentile, bias correction or not).

Because this is already a fairly long overview, I'll close with a few remarks.  First, despite its advantages over some other MASEM methods, my proposed method also has drawbacks and limitations; I won't elaborate here on these pros and cons, except to caution that my proposed method might perform unacceptably in certain circumstances.  Second, my proposed method would benefit from considerably more work, such as refining aspects of each step and studying its performance in realistic situations defined by characteristics of MASEM studies (e.g., number of primary studies, distribution of sample sizes, distribution of correlation-matrix parameters, pattern and mechanism of missing data, choice of function g).  To date there's been little evaluation of multivariate RE meta-analysis analytically or by simulation, for either correlation matrices (cf. Hafdahl, 2004, 2008b) or other multivariate effect sizes (cf. Riley, 2009; Riley, Abrams, Sutton, Lambert, & Thompson, 2007), and Hafdahl's (2009c) Monte Carlo studies of meta-analysis for functions of multivariate effect sizes did not include correlation matrices.  Third, Bayesian approaches to meta-analysis, such as Prevost, Mason, Griffin, Kinmonth, Sutton, and Spiegelhalter's (2007) proposed method for correlation matrices, might be especially well-suited to MASEM due to their natural -- though computationally challenging -- strategies for constructing posterior distributions for functions of a study's parameters.

References

Becker, B. J., & Schram, C. M. (1994). Examining explanatory models through research synthesis. In H. Cooper & L. V. Hedges (Eds.), The handbook of research synthesis (pp. 357-381). New York: Russell Sage Foundation.

Hafdahl, A. R. (2004, June). Refinements for random-effects meta-analysis of correlation matrices. Paper presented at the meeting of the Psychometric Society, Monterey, CA.

Hafdahl, A. R. (2008a). Combining heterogeneous correlation matrices: Simulation analysis of fixed-effects methods. Journal of Educational and Behavioral Statistics, 33, 507-533. doi:10.3102/1076998607309472

Hafdahl, A. R. (2008b, July). Meta-analysis for functions of heterogeneous correlation matrices. Paper presented at the meeting of the Psychometric Society, Durham, NH.

Hafdahl, A. R. (2009a). Improved Fisher z estimators for univariate random-effects meta-analysis of correlations. British Journal of Mathematical and Statistical Psychology, 62, 233-261. doi:10.1348/000711008X281633

Hafdahl, A. R. (2009b, May). Meta-analysis for functions of dependent correlations. In A. R. Hafdahl (Chair), Advances in meta-analysis for multivariable linear models. Invited symposium presented at the meeting of the Association for Psychological Science, San Francisco, CA.

Hafdahl, A. R. (2009c). Meta-analysis for functions of heterogeneous multivariate effect sizes. Unpublished master's thesis, Washington University in St. Louis, St. Louis, Missouri. http://openscholarship.wustl.edu/etd/439/

Hafdahl, A. R. (2011). Translating meta-analytic results: Techniques to express random-effects estimates in other metrics. Manuscript in preparation, Washington University in St. Louis.

Hafdahl, A. R., & Williams, M. A. (2009). Meta-analysis of correlations revisited: Attempted replication and extension of Field’s (2001) simulation studies. Psychological Methods, 14, 24-42. doi:10.1037/a0014697

Hafdahl, A. R., & Wu, W. (2012, February). An EM algorithm for multivariate random-effects meta-analysis with incomplete effect estimates. Manuscript in preparation, ARCH Statistical Consulting, LLC.

Kalaian, H. A., & Raudenbush, S. W. (1996). A multivariate mixed linear model for meta-analysis. Psychological Methods, 1, 227-235. doi:10.1037/1082-989X.1.3.227

Prevost, A. T., Mason, D., Griffin, S., Kinmonth, A.-L., Sutton, S., & Spiegelhalter, D. (2007). Allowing for correlations between correlations in random-effects meta-analysis of correlation matrices. Psychological Methods, 12, 434-450. doi:10.1037/1082-989X.12.4.434

Riley, R. D. (2009). Multivariate meta-analysis: The effect of ignoring within-study correlation. Journal of the Royal Statistical Society—Series A, 172, 789–811. doi:10.1111/j.1467-985X.2008.00593.x

Riley, R. D., Abrams, K. R., Sutton, A. J., Lambert, P. C., & Thompson, J. R. (2007). Bivariate random-effects meta-analysis and the estimation of between-study correlation. BMC Medical Research Methodology, 7, 3. doi:10.1186/1471-2288-7-3

White, I. R. (2011). Multivariate random-effects meta-regression: Updates to mvmeta. Stata Journal, 11, 255-270.


Is pedophilia a sexual orientation or a mental disorder?

Before trying to give any sort of answer, it is important to address a common misconception. In popular culture, the terms child-molester and pedophile are often equated. Scientifically, they are not at all the same. The approximate scientific definition for a pedophile is:

  an individual that has an unwavering sexual attraction to prepubescent children similar to attraction heterosexual men have for women

This means that a pedophile might or might not molest children, and a child-molester might or might not be a pedophile. Further, implicit in this definition is a close resemblance to a sexual orientation, and if you want a through and careful discussion of this (much better than my answer) then read:

  Seto, M.C (2012) Is Pedophilia a Sexual Orientation? Archives of Sexual Behavior 41(1): 231-236.

Now, the actually relevant scientific discussion (as opposed to merely a semantic distinction) is threefold: (1) can pedophilia be considered a choice in the legal sense? (2) what causes it? (3) can it be treated?

Note that for what we typically consider sexual orientations, questions (1) and (3) have clear answers: no, and no. However, for mental disorders, all permutations of answers to (1) and (3) are possible. Thus, answering these questions does not let you clear up semantic ambiguity.

To start with question (2): in broad strokes Blanchard, et al. (1999) and Cantor, et al. (2004) suggest that pedophilia has a prenatal cause. For question (3) there has been no evidence to suggest that pedophilia can be treated or "cured", much like how you cannot "cure" homosexuality. This lead to Van Gijseghem expert testimony before the Canadian Parliment's Standing Committee on Justice and Human Rights that you quote from in your question. He concludes that pedophilia cannot be 'cured' through penal intervention. However, it is possible for a pedophile to abstain from becoming a child-molester.

This leaves us question (1), the legal part of this. In Canada, being a pedophile is not a crime, but molesting children is a crime. The status of pedophilia as a mental disorder or sexual orientation is irrelevant to this since both mental status and sexual orientation are protected by Canadian law as long as they do not infringe on other's rights.  To help pedophiles abstain from molesting children there is the Circles of Support and Accountability (CoSA) program (note: it deals with all kinds of sexual offenders, not just child-molesters). This program is aimed to manage and not 'cure'. Wilson et al. (2007, 2009) have shown that CoSA produces dramatic decrease in re-offence rates for sexual offenders.


Link between reading news and deteriorating mental health?

There was a talk on this topic at the 2019 Society for Personality and Social Psychology (SPSP) conference. I haven't been able to find a published paper based on the study they presented, but the authors generally concluded that political engagement can be associated with significant mental, emotional, and social health costs.

Reference
Smith, Kevin; Hibbing, John; Hibbing, Matthew (2019). Friends, Relatives, Sanity and Health: The Psychological Costs of Politics. Presented at the annual conference of the Society for Personality and Social Psychology (SPSP). Portland, OR.
Description
Using a nationally representative sample this study investigates the impact of political engagement on the psychological health of the American electorate. Results suggest that among large numbers of Americans politics is linked to stress, depression, various compulsive behaviors and even thoughts of suicide.


Is there a term for a person who moves from one field of expertise to a new field and has an inflated belief in their competence in the new field?

Déformation professionnelle is probably the closest match:

  Déformation professionnelle is a French phrase, meaning a tendency to look at things from the point of view of one's own profession rather than from a broader perspective. It is often translated as "professional deformation" or "job conditioning". The implication is that professional training, and its related socialization, often result in a distortion of the way one views the world.[1]

Followed by the law of the instrument / Maslow's hammer:

  The concept known as the law of the instrument, Maslow's hammer, Gavel or a golden hammer[a] is an over-reliance on a familiar tool; as Abraham Maslow said in 1966, "I suppose it is tempting, if the only tool you have is a hammer, to treat everything as if it were a nail."[1]

References
1 [déformation professionelle]. Bönisch, J. (2007, November 30). Déformation professionnelle: Beruflich bedingte Missbildung. Süddeutsche Zeitung. Retrieved from http://www.sueddeutsche.de/karriere/deformation-professionnelle-beruflich-bedingte-missbildung-1.786888.
1 [law of the instrument]. Maslow, A. H. (1966/2004). The psychology of science (pp. 15). Maurice Bassett.


Major theories of motivation distinguish between implicit and explicit motives - the first refering to (relatively) unconscious, automatically operating motives, the second refering to motives and goals which are accessible for self-reports (McClelland, Koestner, & Weinberger, 1989). Explicit motives are translated into conscious goals, whereas implicit motives influence spontaneous, uncontrolled, and long-term behavior (without goal-planning behavior).

Furthermore, 'Motivation' referes to a larger process (e.g., selective attention, comparison of set points with actual situations, the processing of situational incentives), where the translation into goals and actions only is the last part of a sequence of processing steps.

Concerning your question, I would say that 'goal oriented behavior' indeed is a subset of motivation, namely explicit motivation.

References

McClelland, D. C., Koestner, R., & Weinberger, J. (1989). How do self-attributed and implicit motives differ? Psychological Review, 96, 690-702.

Schultheiss, O. C. (2008). Implicit motives. In O. P. John, R. W. Robins, & L. A. Pervin (Eds.), Handbook of personality psychology: Theory and research (3rd ed.). (pp. 603-633). New York, NY US: Guilford Press.


Often, we learn about brain functions when parts of the brain become damaged. One famous example is that of Phineas Gage. He survived severe brain damage, and his character and abilities were noticeably different. From the article:-

Some months after the accident, probably in about the middle of 1849, Phineas felt strong enough to resume work.  But because his personality had changed so much, the contractors who had employed him would not give him his place again.  Before the accident he had been their most capable and efficient foreman, one with a well-balanced mind, and who was looked on as a shrewd smart business man.  He was now, Harlow said, fitful, irreverent, and grossly profane, showing little deference for his fellows.  He was also impatient and obstinate, yet capricious and vacillating, unable to settle on any of the plans he devised for future action.  His friends said he was "No longer Gage."


As for future mind control/reading technology, can humans fight it?

For the question of whether humans could fight neuro"mind-reading", I can only say that there is very little evidence that information we know but are not thinking about could be extracted using current methods.  This means that the old scifi mind-reading-fighting standby of thinking of something else might work--although then we have the "don't think of a pink elephant" problem of ironic processing.

For the question of whether we could fight externally induced neural activity, I'm going to assume that it would be similar to fighting intrusive thoughts in obsessive compulsive disorder.  Currently, our best bets there are exposure, cognitive behavioral therapy, and drugs.  Since exposure is primarily involved with reducing the strength of the association between the anxiety-creating obsession and the comforting compulsion, I'm not sure it applies here.  Similarly, since the drugs used for OCD are generally anxiolytic or antidepressant, I'm not sure they would help in this case.  It might be possible to create a variant of cognitive behavioral therapy that treats the imposed neural activity as a compulsion. . . but since the technology to impose neural activity on humans (or animals who are good analogs of human compulsion) doesn't exist, all this is speculative!


Have different mental strengths evolved in men and women?

There is little neurological evidence that finds a difference between men and women. However there are psychological studies that do find a small difference in mental strengths. This interesting TED talk debunking psychological myths by a lecturer from the University of Liverpool discusses the psychological differences between men and women.

Males and females are slightly different when it comes to spacial awareness (the top 1/3 of females perform as well as the top 1/2 of men) and language (the top 1/3 of men perform as well as the top 1/2 of women), but the difference is so slight that its not worth taking into consideration.

I moved this answer over from the biology question.


Why could too much BDNF be detrimental in terms of depression and memory?

This is a fairly open-ended question...  One example of the potentially negative consequences of overexpressed BDNF is its effect on the likelihood and frequency of epileptic seizures.

I guess the short version of this effect is that BDNF appears to promote neuronal growth, including neurogenesis, axonal and synaptic sprouting, and neuronal excitation, in exactly the areas of the brain that are associated with epilepsy.  Epileptic seizures are essentially hyper-excitations of neurons, so any factor that increases the excitability of neurons in brain areas associated with seizures can be a culprit.

A good, fairly recent, and open access review of the role of BDNF and its primary receptor TrkB in epilepsy is McNamara & Scharfman (2012):

  Intrahippocampal infusion of BDNF and transgenic overexpression of
  BDNF or TrkB increase seizure susceptibility or severity. Conditional
  knockout of TrkB eliminated epileptogenesis altogether in the kindling
  model.

That is, in epileptic mice, adding BDNF increased seizure frequency, and removing it eliminated seizures entirely.  The authors suggest several mechanisms by which this might happen:

  ... long-term potentiation (LTP) of excitatory synapses between
  principal cells may contribute to limbic epileptogenesis; that
  is, potentiation of these synapses may facilitate propagation of
  seizure activity through synaptically-coupled neuronal populations
  throughout the limbic system and beyond.

  One interesting possibility is that enhanced TrkB activation reduces
  expression of the K-Cl cotransporter, KCC2, ... an important molecular
  and cellular mechanism contributing to limbic epilepsy.

  The effect of estrogen on NPY levels could be mediated by BDNF,
  because BDNF induces NPY synthesis following TrkB activation

In other words, (1) BDNF-induced LTP - the mechanism that underlies memory and learning - increases the excitability of neurons, potentially causing seizures; (2) BDNF may inhibit KCC2, itself a synpatic inhibitor, again increasing the excitability of neurons; and (3) hormone-induced BDNF may moderate neuron hyperexcitability through its effect on yet another another protein, the neurotransmitter NPY.

Another recent review, though not open access, is Iughetti et al (2018).  Similar to the previous review:

  ... BDNF has excitatory effects in neuronal cultures and animal brain
  slices.  Furthermore, both BDNF and its conjugated receptor (... TrkB)
  are increased  in animal models and humans with epilepsy, particularly
  in the temporal and hippocampal areas. Acute injection of BDNF in
  brain of mice induces seizures, which are almost or totally abolished
  [by] blocking its transcription and pathway.

The authors also implicate the effects of BDNF on axonal sprouting and neuronal hyperexcitability, KCC2 and NKCC1 downregulation, and NPY synthesis on seizure likelihood and frequency.

Neurochemistry is complex and not well understood, and there is indication that BDNF can also have protective properties against epilepsy under certain conditions (eg, long-term in low doses).  Lots more detail is available in the reviews cited.


How to counteract the deterioration of speech in stutterers by targeting sympathetic arousal?

The first line treatment for stuttering (I'm a stutterer myself) is speech therapy. Such therapies generally focus on helping stutterers to learn ways to minimize stuttering when they speak, such as by speaking more slowly, regulating their breathing, or gradually progressing from single-syllable responses to longer words and more complex sentences. Most of these therapies also help address the anxiety a person who stutters may feel in certain speaking situations (source: NIH). Anxiety management has especially worked well for me.

No drug therapy is currently approved against stuttering. I also don't know of any drug that targets the sympathetic nervous system. Having said that, there are a few interesting drugs investigated in clinical trials so far:

Dopamine-blocking medications against bipolar disorder, Tourette’s Disorder and Schizophrenia have been found to be effective in reducing the symptoms of stuttering (source: NSA). Their side effects, however, don't seem to weigh up against their effectiveness.
Pagoclone, a GABA-agonist used as anxiolytic has shown some effectiveness, but not enough to warrant it to be marked as anti-stutter therapy (source: BSA)


How to analyse 3 by 3 design with Likert scale ratings?

A rating scale is not necessarily a Likert scale.  It sounds like you have a single rating for each picture across each dimension but I could be wrong.  More details would be needed for better advice and Ana's comment should be answered in your question.

You would be best off doing a multi-level cumulative link model (multi-level ordinal regression).  You can include subject and picture as random variables.  See the ordinal package in R.  The vignettes will be very helpful.

Keep in mind that with the pictures you also have item level variance and generalization issues that people doing research on words struggle with as well.  Even if you can get reasonably good looking data for your analysis that satisfies an ANOVA you'll have to consider random and fixed effects issues of both the people and the pictures.  The multi-level modelling can include both and avoid the sort of patchwork hoops required with ANOVA.  Therefore, regardless of whether you have a true likert scale and you satisfy requirements for treating the responses continuously or you should be treating it as ordinal data, multi-level modelling is your best bet.


What is the phenomenon that one can recognize a movie after seeing a scene for a fraction of second called?

The subliminal recollection is called involuntary memory retrieval.

This triggers an implicit memory.

Further reading:

http://en.wikipedia.org/wiki/Subliminal_stimuli#Images

http://en.wikipedia.org/wiki/Subliminal_stimuli#Auditory_stimuli
http://en.wikipedia.org/wiki/Spreading_activation


Your question is around retaining information when you are immersed in four major fields of study. Yes you want a solid foundations from which to build- but perhaps you simply are taking on too much information.

There seems to be a focus in many educational systems on producing knowledge which is to be memorized in a formal, didactic, manner of "direct-instruction". However, much is to be said as well for the accrual of knowledge via conversation which seeks to solve a problem alongside another person or within a group- that which stays with you because you have an emotional connection to the process of procuring that knowledge- you feel rewarded once you've "won" the answer- and you remember these answers because you were both teaching and evaluating the answers alongside another person- developing and testing hypotheses and validities. Here you are not only processing content to reach an end result but also perhaps taking more time than you would on your own to assess content itself in relation to, say, the importance of the answer (or lack thereof). In this way the learning experience may feel more satisfying - you may feel a decrease in the drive to accrue lots of information on your own (phew- pressure, eh?) While it makes sense for one to want to document evidence of further validation of knowledge in a way that is, it could be that your process is dragging the knowledge down given the amount of purpose you find personally in documenting vs. that which is required to further good workmanship within the program.

In looking at context/environment of your learning: within academia, where is there overlap between your expectations vs. those of your program of study (i.e. do you have the capacity to develop a niche given your current psychosocial/socioemotional inputs?)

I would be curious to see a copy of a meta-mind-map if you were to draw one- you'd probably fill pages in minutes with the content of the information...and I wonder how the flow of this content would compare to the flow of a meta-mind-map of the processing of that content.

I hope that this makes sense and isn't too high on the advice-giving end especially since I'm sure that all of this writing could be so easily summed up in a visual involving just those systems which you study like a melted cpu or .... something...which of course goes against my own claim of the value of finding good mental heuristics..... .....


Does the structure of consciousness mimic that of the visual process?

You are describing an observation as old as Freud, where he divided human's experience into three levels, roughly along the same lines as you. The conscious as that clear and ill-defined concept that gives you the feeling of attention, awareness, and self. The preconscious as the level just outside of your current awareness but that could easily spring to your consciousness. Finally, the unconscious, which is a level that doesn't have an analogy in vision: it corresponds to experiences that cannot come to your consciousness but that still affect your behavior.

Unfortunately, this correspondence does not extend beyond analogy, for several reasons. From the point of view of introspection -- the oldest and arguably still only reliable method for studying consciousness -- it is not clear how you would distinguish the visual sensation of attending stimuli from the conscious. In particular, it is not at all clear that the experience you describe as visual is an artefact of the visual system and not consciousness itself. The reason to believe that this is a feature of consciousness and not the visual system is because you experience the same things for hearing, touch, and to-a-lesser-extent smell.

Moving onto the scientific basis is much more difficult, in particular, you write:

  It makes sense to me that the conscious mind would be patterned on the functional model of the visual field which is much older and more fundamental.

This to me seems like an unjustified assertion. Although we have some neurological models of consciousness, none of them are at the level where where we can start to date them on an evolutionary scale.


Do you ever think self diagnosis is called for?

I think this is a borderline question. As a rule of thumb, we do not answer questions about individual health problems in favor of asking the author to see a professional, for both ethical and practical reasons. And let me be absolutely unequivocal here: you should see a professional. But this is fundamentally a general question about self-diagnosis, so I'm going to answer that.

It's always good to educate yourself. Accurate self diagnosis is necessarily impossible, however―what you can see depends on what you know, and what you know depends on what you have seen, etc. This is uncontroversial. Being educated is therefore very helpful when seeing a professional, which I again strongly encourage you to do, but it is never a substitute for seeing a professional when you have problems.


What is a good book for studying incentives?

I guess what you are looking for is readings on applied behavioral economics. Here is a popular favourite: Freakonomics


Cultural brain hypothesis and gene-culture co-evolution

"evidence of recent co-evolution between genes and large-scale culture

This 2018 PLOS Computation Biology simulation study - The Cultural Brain Hypothesis examined the data from animals and humans. It found a relationship between brain size, adaptive knowledge, social learning, group size, and lifespan across the animal kingdom.

  relationships between brain size, group size, innovation, social learning, mating structures, and the length of the juvenile period that are supported by the existing empirical literature.

The study found evidence of cumulative cultural evolution explaining the brain human sizes.


What is the average amount of new vocabulary adults retain when learning a second language?

Try keywords like: "second language learning number of words per"

Some suggest 3-6 words per hour of reading, which is afterwards used for calculation of average per week, month, year. References of studies to support this claim are missing though:
http://ip-173-201-189-182.ip.secureserver.net/archives/sla/waring120304.pdf

Several times I found references on this study: Miltion and Meara (1995).

  A longitudinal study by Milton and Meara (1995) found that adult
  learners of English as a second language could learn 2650 base words
  per year. more at:
  http://iteslj.org/Articles/Cervatiuc-VocabularyAcquisition.html

I remember it should be 7 words a day. If it is not, it should be at least divided into blocks of this size. If you google this number, it is mentioned on several sites, I do not remember the book I got it from.

I would be careful using these numbers, it is likely that they depend on the techniques that students and teachers tend to use.


Why don't we get regular checkups for mental health, as in physical health?

The short version is that in Europe and North America, at least, the answer is predominantly yes: your GP is supposed to refer you to a relevant mental practitioner on a case by case basis. This can be prompted either by voluntary disclosure (i.e., the patient brings up mental health issues themselves) or suggested based on comments made by the patients. GPs do not generally have a responsibility to 'catch' mental health problems unless they are potentially life threatening (e.g., suicidal ideation).

This is the most that can be said without knowing which country or countries you are interested in. There are vastly different models of mental health care at work in various countries, and the practice of mental health care varies accordingly. For example, the United States' health care model is primarily based on private insurance, while Britain's is an integrated public-private model, which affects how real practice is conducted. Besides the different incentive structures, countries also have different philosophies of mental health service.

You can often find information about a particular country's mental health care model and philosophy on the website of their public health institution (e.g., department/ministry of health).


Cognitive bias of comparing numbers on a relative scale

It's been called “relative thinking” in a few places (eg
http://journal.sjdm.org/11/10921/jdm10921.html). The earliest I can find is in a 2004 article by Ofer Azar. A Google Scholar search turns up many other references to the term as well.


What is the effect of viewing pornography on children?

Pornography laws are a relic of the Victorian era, and not based on any science.
Research that can conclusively determine the effect of pornography on children is hard to come by due to the resultant ethical environment.  Most research depends on self-reports: Surveys ask adolescents how much pornography they have been exposed to, and attempt to correlate this with other variables such as personal attitudes about sex.  Such surveys are subject to a variety of memory and other biases affecting accuracy, but more importantly, correlations fail to establish cause and effect - that is, it is equally likely that pornography consumption affects attitudes as it is that pre-existing attitudes affect pornography consumption.
Nonetheless, a number of reviews of current literature on adolescents conclude that there is an association between consumption of pornography and certain negative attitudes about sex, and promiscuous and/or risky sexual behaviour.  The reviews acknowledge that the data contains much contradictory evidence however, as well as failing to establish cause and effect.
UK Children's Commissioner's report (2013): "Basically... Porn is everywhere"
Owens et al (2012): "The Impact of Internet Pornography on Adolescents"
In contrast, a paper by Kendall (2006) found a correlation between pornography accessibility and rape for 15-19 year old adolescents - but in the opposite direction, that could be interpreted to mean that access to pornography reduces rape crime in this demographic.
Research on pre-adolescents is even more scant.  A more conclusive effect is seen between exposure to depictions of violence and negative effects on attitudes and behaviour, though these may be short-lived.  A landmark study from the 1960's (no longer ethical to replicate) demonstrated that children do role model from violent media.  The reviews listed above extend this finding to attitudes and behaviours of adolescents exposed to pornography depicting violence.  Evidence linking this to criminal offences in adulthood is still controversial however.
In adults, studies across multiple countries (eg, Diamond, Jozifkova, & Weiss, 2010) have documented significant declines in physical sex offenses as accessibility of pornography increases, again suggesting the possibility that pornography provides a substitute for sex crimes.


Best way to capture effect of making people upset?

Without knowing exactly what the factor you are interested in is, it is hard to predict how feasible it would be to manipulate it. For example, is it possible to make two videos of the speaker, one with the factor, and one without, with nothing else changing? My guess is that you probably can't do this, so I'm going to focus on how you might be able to run the experiment without that kind of very specific control.

One option would be to make several videos, half of them with the critical factor, and half without. There will be lots of other things that vary between these videos, but as long as the only thing that varies systematically is the factor you are interested in, then you can run an informative experiment.

You asked: How do I make sure that every subjects experience is the same expect for that one factor? The answer is that you can't really do this. You can try to get close, but subjects will always have slightly different experiences. This is why we need to run many subjects to determine if an effect is reliable. Any given subject may just be tired/hungry/cranky when they come to the experiment and this will affect your results. But, if you run lots of subjects then it is likely that tired/hungry/cranky subjects will be in both conditions, and therefore on average won't impact your conclusions.

Depending on how long the videos are, you could potentially show multiple videos to a single subject, and measure their emotional responses to each one. This is a within-subject design, and the advantage of this is that it controls for some of the random variation (tired/hungry/crankiness) between different subjects in your experiment. If subject A tends to be crankier than subject B, it will introduce noise into your results if each subject only sees one kind of video. But if subjects see both kinds of videos, you can test whether videos with the factor tended to make subjects more aggravated, controlling for their 'baseline' level of aggravation. If the videos are longer, then you could just show one kind of video to each subject (a between-subjects design) but this will probably require collecting data from more subjects to wash out the noise of some subjects being more prone to aggravation than others.


What is the difference between having a crush on someone and loving someone?

You may find Sternberg's triangular theory of love as useful framework for distinguishing different types of love. Quoting wikipedia, the theory describes types of love in terms of three dimensions:

  Intimacy – Which encompasses feelings of attachment, closeness, connectedness, and bondedness.
  Passion – Which encompasses drives connected to both limerence and sexual attraction.
  Commitment – Which encompasses, in the short term, the decision to remain with another, and in the long term, plans made with that other.

Using this framework, "loving someone" is the general term, and "having a crush" would be a more specific variant. So perhaps a crush could be conceptualised more in terms of passion and less in terms of long term intimacy and commitment.

Alternatively, you could just look at definitional concepts of a crush. For example, the term "crush" is commonly used in contexts where feelings are not reciprocated. I associate it with younger people (or when seen in older adults, a youthful approach to love). A crush often implies a short term quality, such that the feelings may change from one month to the next.


What is the most accurate name for the effect where people find excuses for flaws by leaders?

Confirmation bias is certainly at play here, but I'd narrow that down a bit. It doesn't have a Wikipedia page (yet) but Dan Kahan has been focusing on a variation of motivated reason he calls "Identity-protective cognition". (See Misconceptions, Misinformation, and the Logic of Identity-protective Cognition for a full discussion.)

Confirmation bias can creep in under many circumstances, but we have an especially strong motivation (very often non-conscious) to promote arguments which align with our own self-identity. The person making the kind of claim you're pointing to probably either feels quite strongly about the issue (a economic libertarian discussing the primacy of market-oriented policies, for example) or the person making the claim (a "tribal" leader, perhaps).

An earlier and more limited aspect of this is the Asch effect. As the wikipedia page on argument from authority notes —

  In repeated and modified instances of the Asch conformity experiments, it was found that high-status individuals create a stronger likelihood of a subject agreeing with an obviously false conclusion, despite the subject normally being able to clearly see that the answer was incorrect.


What is the scientific term for information overload?

If what you are seeking is how to present material so that cognitive overload does not occur, you are in the realm of learning theory.[1]

Cognitive load theory and schema (learning) theory go hand in hand in. Schemas are frameworks of information (like a steel-framed skyscraper in your mind); they start as very basic ("This is a cell") and become more complex and facile ("NADH-Q oxidoreductase, Q-cytochrome c oxidoreductase, and cytochrome c oxidase are mitochondrial transmembranous enzyme complexes responsible for oxidative phosphorylation, etc.") They allow (and form) Long Term Memory (LTM). We need a framework ("cell") into which we can stick a fact before we can remember it for more than a very few minutes. The more we know about something (the better our schemas are), the more easily we learn. Working Memory (WM) allows us to process what we are exposed to and place it into a schema so that we can remember it. Like a computer, we have limited WM (processing ability) available to us at any given time. Efficient processing results in placing material into a schema which then facilitates Long Term Memory (LTM).

Inefficient Processing results in an inability to understand what one was just exposed to. Failed schema identification means leads to inability to use information.

Where does cognitive load come in? Cognitive Load takes up processing speed (reducing WM). If cognitive load is great enough, all WM is used up, and we will be unable to identify/form a schema. There are several types of Cognitive load: intrinsic (how complex the information is), extrinsic/ineffective (a bunch of things including distractions, emotionally demanding states [e.g. stress], and especially the way in which material is presented, e.g. inducing splitting of attention, etc.) and germane (what's left over to actually form schemas). They are (kind of) additive. Good schemas reduce cognitive load (increasing WM).

The linked site presents different models of presenting information that promotes schema formation, identification and processing in different situations, and links to further work.

1 Schema Theory and Cognitive Load Theory


Are there any agent based cognitive models that are inspired by complex systems studies of ant colonies and economies?

Partial answer:
Douglas Hofstadter has written quite a lot about this from a more philosophical approach.
His style isn't for everyone, I think it's introduced well in this chapter ('Ant Fugue').
For more applied work from the same, you might look at Mitchell and Hofstadter's CopyCat model of analogies (described briefly here, as well as on wikipedia).
All this aside, I don't know of any empirical work along the same lines, but I wouldn't rule it out.