What is the relative effectiveness of self initiated versus therapy approaches to repairing damaged body schema?

Background

Phantom Pain happens when a limb is lost over the course of one's life or missing since birth. Essentially the brain generates pain and sensations for the missing limb. It is thought to be a psychological problem brought on by inherit physiological traits of the human brain. As a psychological problem it is subject to conscious and unconscious retraining. No treatment has as yet proven completely effective against phantom pain.

Mirror Therapy is one scientific clinically useful treatment for phantom pain developed by Vilayanur S. Ramachandran. It normally involves the use of a mirror box in later stages of rehabilitation.

A mirror box was featured on the American Television show "House" as a treatment for a war veteran. This clip illustrating the fictional use of a mirror box from that episode is inaccurate as it shows the mirror box as a instant cure all however it does accurately describe the process by which the mirror box is used. The clip may be considered somewhat offensive because House is always somewhat offensive.

  In a mirror box the patient places the good limb into one side, and the stump into the other. The patient then looks into the mirror on the side with good limb and makes "mirror symmetric" movements, as a symphony conductor might, or as we do when we clap our hands. Because the subject is seeing the reflected image of the good hand moving, it appears as if the phantom limb is also moving. Through the use of this artificial visual feedback it becomes possible for the patient to "move" the phantom limb

-wikipedia

Mirror therapy has been proven by fMRI imaging to extort spatial attention.

  In this first study on the neuronal correlates of the mirror illusion in stroke patients we showed that during bimanual movement the mirror illusion increases activity in the precuneus and the posterior cingulate cortex, areas associated with awareness of the self and spatial attention. By increasing awareness of the affected limb the mirror illusion might reduce learned non-use. The fact that we did not observe mirror-related activity in areas of the motor or mirror neuron system questions popular theories that attribute the clinical effects of mirror therapy to these systems.

-The neuronal correlates of mirror therapy: an fMRI study on mirror induced visual illusions in stroke patients

Attention (which is in this case not the same word as "pay attention") is as William James deﬁned "withdrawal from some things in order to deal effectively with others.". Or as Shaun P. Vecera and Matthew Rizzo defined "The processes that permit an organism to choose some environmental inputs over others".

Spatial attention again defined by Shaun P. Vecera and Matthew Rizzo is "restricted to visuospatial attention—those attentional processes that select visual stimuli based on their spatial location".

Conclusion

Mirror therapy typically begins in a doctors office. A doctor trains a patient during in or out patient rehabilitation to look into the mirror and clench or move both the present and missing limb. After the technique has been proven useful to the individual it can be done at home without a doctor supervision and minimal training with the same overall results for both upper and lower body. Home based treatment results in nearly equal compliance.

It is my hypothesis that increased prevalence of virtual and augmented reality will allow for new kinds of spatial attention treatments for those with multiple amputations and chronic arthritis effecting both hands.


What was the experiment where you pour liquid from a tall container to a short one and ask a child which has more?

This effect is referred to as Piaget's Theory of Conservation.

Piaget constructed an experiement where children would be shown a tall, narrow glass of colored water (to make it clearly visible in a clear glass) and two shorter, wider glasses of the same exact size.

A single amount of water would be distributed in both small glasses. If a child is asked "which has more" they're likely to reply they have the same amout of water, as they look identical. However after pouring the water from one short glass into a tall glass, if you ask the child again they are likely to say the tall glass has more water because it looks bigger.

The interesting thing is not that the child assumes the taller glass holds more liquid but that they fail to understand conservation: the fact that the water from one glass is going to be the same amount after being poured into any other container. It's as if they did not realize the water came from the same glass.

Here is a video recreating Piaget's Conservation Experiment. It's common for developmental psychology courses to explain or show this experiment.


Why does autism sometimes only visibly appear later in life?

It is important to remember when reading this question and answer is that Autism Spectrum Disorder (ASD) does not develop in adulthood, but symptoms can change for individuals over time because learning occurs.

Symptoms of ASD come in all shapes and forms because this is a spectrum disorder and therefore people present somewhere on a spectrum, often referred to as from low functioning to high functioning.

To answer the question directly, people who present symptoms later in life, as you say, often do present those symptoms in childhood but they aren't noticed by the adults in the child's life until it becomes a real problem for the individual.

As an example, interpersonal skills are learned during childhood. It is perfectly acceptable for children to be at slightly different stages during development with regard to interpersonal skills. Some children will be more advanced then others. Interpersonal skills can be difficult for people with ASD to grasp and so someone with high functioning Autism can take longer to develop these skills, if they are developed at all. So that would potentially not show up until later when the other kids have developed these skills and the child with undiagnosed ASD has not.

Often, 30+ years ago, before we had more advanced treatments and assessments children would 'fall through the cracks' and be labeled as gifted, rather then as having high functioning ASD. This would explain why some people who are highly successful in adulthood are diagnosed in adulthood rather then childhood. People with high functioning ASD often have a savant type qualities, meaning they are very skilled in some specific area.
The diagnostic criteria (DSM) has been amended over the years which would account for some adults being diagnosed now, as they may not have qualified before the DSM changed the criteria.

This would be an interesting study to read to understand social interaction among children with high functioning ASD: Bauminger, N., Solomon, M., Aviezer, A. et al. J Abnorm Child Psychol (2008) 36: 135. https://doi.org/10.1007/s10802-007-9156-x

This article discusses changing symptoms (Behavioural) in youth and adults with ASD.

This might be a good book for you to read together a good understanding of ASD in development, which might give you a better understanding as to why people can go undiagnosed until adulthood. Handbook of autism and pervasive developmental disorders, 2nd ed.

In conclusion, There are many reasons that someone might not be diagnosed until later in life, and autism is a spectrum which means people have many different symptoms that range on a vast scale.

References

Bauminger, N., Solomon, M., Aviezer, A. et al. J Abnorm Child Psychol (2008) 36: 135. https://doi.org/10.1007/s10802-007-9156-x

Shattuck, P.T., Seltzer, M.M., Greenberg, J.S. et al. J Autism Dev Disord (2007) 37: 1735. https://doi.org/10.1007/s10803-006-0307-7


What is the effect of Binaural Beats on an Autistic brain?

The evidence in support of binaural beats as a therapeutic tool is sketchy: Is there scientific evidence on the benefits of binaural beats? Given our lack of understanding of if binaural beats can cause entrainment in the brain, never mind how they cause entrainment, it is not possibly to make conclusions about how the binaural beat would affect the autistic brain.


What is the role of non-synaptic plasticity in learning and memory?

The answer is yes. Non-synaptic plasticity exists as you can read in "Non-synaptic neuronal mechanisms of learning and memory in gastropod molluscs" by Benjamin et al. and "Compartmentalization of Non-Synaptic Plasticity
in Neurons at the Subcellular Level" by Nikitin and Balaban.

But the effect of hormones such as cortisol may also have an effect.

Non-synaptic mechanisms of regulation and plasticity play a very important role in the brain and its ability to learn in many aspects and at different scales.

A single cell can suffer internal modification that will modify eletrophysiological properties.

Variations of concentration of elements in the CSF also have an effect.

Glia also plays an important role.

So, the brain is a very complex system with a lot of interdependent mechanisms of adaptation, regulation and plasticity. Synapse is just one aspect of it.


Are there peer-reviewed psychology or neuroscience journal articles that include the raw data (data set)?

Check out Psychological Science articles with the "Open Data Badge".  There's also the Journal of Open Psychology Data.


What kind of data structuring is conducive to healthy debate?

I've been fascinated by this question for years, but unfortunately don't have a conclusive answer. So instead, I'll make an ad-hoc list of the things I've found/explored about this topic and hopefully this will give you a starting point until someone else can create a better answer with better references.

My current approach to this is MindMaps, which is similar to nodal network you propose. I've used Mindmaps in various scenarios, including trying to determine an appropriate scope for this site. However, I know of no formal study of this format of discussion and if it's better than linear forms of discussion as supported by forums.

Other models include Federated Wikis, which seems closer to your idea of an interconnected Wiki for discussion. However, these seems more targeted to spontaneous cross-fertilization of ideas, rather than debate. This is a new platform, so it's not surprising that there has been no formal study of the ideas that culminate from this form of digital interaction.

In terms of the content of documents, Bret Viktor has been investigating this and is trying to create a paradigm of Explorable Explorations. Explorable Explanations rely on manipulable data-driven proofs rather than rhetoric based argumentation to prove their point. See the link for further examples. There is a collection of Explorable Explanations available online, which address a variety of topics, including CBT. However, I know of no evidence that these forms of explanations are more effective than traditional narrative-driven explanations.

Finally, to unify all of these approaches philosophically, Joe Edelman is putting forth a philosophy which dictates that shared values are the root of empathy and understanding. I know of no system that implements this philosophy of finding common values between participants, but it does seem like a useful framework to guide design.

That's all I've found so far. I know lots of people doing research in Human Computer Interaction, but I've seen very little work in the domain of consensus building. I really hope further posters can provide superior references.


What is the neurological basis for the association between Bipolar type 2 and autism spectrum disorder (ASD)?

Google Scholar identifies several learned articles that discuss the association/overlap between bipolar disorder type 2 and autism spectrum disorder (ASD), including:

Khanzada, N. S., Butler, M. G., & Manzardo, A. M. (2017). GeneAnalytics pathway analysis and genetic overlap among autism spectrum disorder, bipolar disorder and schizophrenia. International Journal of Molecular Sciences, 18(3), 527. https://doi.org/10.3390/ijms18030527

Stahlberg, O., Soderstrom, H., Rastam, M., & Gillberg, C. (2004). Bipolar disorder, schizophrenia, and other psychotic disorders in adults with childhood onset AD/HD and/or autism spectrum disorders. Journal of neural transmission, 111(7), 891-902. https://doi.org/10.1007/s00702-004-0115-1

Gandal, M. J., Zhang, P., Hadjimichael, E., Walker, R. L., Chen, C., Liu, S., ... & Shieh, A. W. (2018). Transcriptome-wide isoform-level dysregulation in ASD, schizophrenia, and bipolar disorder. Science, 362(6420). https://doi.org/10.1126/science.aat8127

Excerpts from the above include:

The conditions show similar neuropsychiatric behavioral disturbances, including impaired social interaction and communication.

Twenty-three genes were common to all three disorders.

Overlapping genes impacted dopamine and serotonin homeostasis and signal transduction pathways, impacting mood, behavior and physical activity level.

My non-expert interpretation of the above is that there are genetic processes at work that drive the similarities in behaviour associated with these conditions.


How to examine person's awareness of a certain topic?

I think what you may be after is the accessibility of people's attitudes. The idea is that people not only have different attitudes, but that they also differ whether these attitudes are on top of their minds (or how easy it is for them to retrieve them, when they are prompted to indicate an attitude). If an attitude is subjectively important or often thought about, it should be highly accessible. On the other hand, for other things, people may have a very negative or positive attitude, that is, nevertheless, relatively inaccessible to them. Accessible attitudes have been shown to guide behavior more strongly (there is a higher correspondence between attitudes and behavior). The classic paper is by Fazio and colleagues (1989).

Attitude accessibility can be measured by measuring the reaction time to attitudes questions. If people are faster in answering an attitude question, this is taken as an indicator of a highly accessible attitude. This would also be the kind of indirect measure that you might have in mind.

So in your example, you could ask participants to agree or disagree whether certain reasons for seeking asylum are important, and measure the reaction time of their answers. Quicker answers would indicate that these reasons are more accessible to them.

References

Fazio, R. H., Powell, M. C., & Williams, C. J. (1989). The role of attitude accessibility in the attitude-to-behavior process. Journal of consumer research, 280–288.


Based on my experience looking at factor analyses of personality facet structures like the NEO-PI and NEO-IPIP, I think that shyness is mostly captured by low levels of extraversion. Enjoying, getting energy from, and actively engaging in social interaction is a central component of extraversion.

That said, as with many general personality constructs, the Big 5 provides a general framework for understanding them. It is common for there to be a profile of meaningful correlations with the Big 5 where some are larger and some are smaller. Given the elements of anxiety and negative emotions that may be associated with shyness, especially extreme shyness, correlations with neuroticism are also likely.

From an empirical perspective, I've often found that the self-consciousness facet on the NEO-IPIP loads most strongly on a factor with other extraversion facets.

I also note that there are a range of ways of conceptualising introversion. Some  emphasise shyness and social anxiety. Others frame introversion more positively such as enjoying doing work and personal activities by yourself, or preferring one-on-one interactions as opposed to large group interactions.

Empirical example

As an empirical example, we did a study (Horwood et al, 2015) looking at factor and facet correlates of Type D personality. One of the subscales of Type D is called social inhibition, and it is related to shyness (e.g., items like "I often feel inhibited in social interactions", "I find it hard to start a conversation).

Table 1 shows how the largest correlation with the Big 5 (measured using the NEO-PI-R) for social inhibition was the negative correlation with extraversion (r = -.73), but that the correlation with neuroticism was still substantial (r = .59).

This next table shows the correlations (both zero-order and semi-partials controlling for the Big 5) with Social Inhibition. The largest correlations are for warmth and gregarisiousness (negative correlations), but the correlation with self-consciousness is almost as high.

References

Horwood, S., Anglim, J., & Tooley, G. (2015). Type D personality and the Five-Factor Model: A facet-level analysis. Personality and Individual Differences, 83, 50-54. full-text


What to expect from a seriously mentally ill individual when a poor prognosis is revealed through improper channels?

There is an answer to a similar question regarding narcistic behaviour and negative feedback reaction:

How can a narcissist be given negative feedback without triggering aggressive behavior?

It is a more general answer. The case you described has surely a lot more facets and details to consider.
I would have just commented it, but I don't have enough reputation.


Can anyone see what is wrong with this implementation of the Pinsky-Rinzel model in Brian2?

If anyone ever finds this and has the same problem: The original paper has a flaw in the paper:

alphac=(exp((Vd/mV-10)/11)-exp((Vd/mV-6.5)/27))/(18.975)* (Vd<=50*mV)/ms+2*exp((6.5-Vd/mV)/27)*(Vd>50*mV)/ms : Hz

An errata published later changes this to:

alphac=(exp((Vd/mV-10)/11-(Vd/mV-6.5)/27)/18.975)*(Vd<=50*mV)/ms+2*exp((6.5-Vd/mV)/27)*(Vd>50*mV)/ms : Hz

After making this change it acts exactly how it should.


Generate fMRI from neurotransmitter consumption

The simplest equation for getting a BOLD signal from neurotransmitter that I could find was in "Tracing Problem Solving in Real Time: fMRI Analysis
of the Subject-paced Tower of Hanoi", which itself references many other publications where it was used:

$$H(t)= m \times(t/s)^a\times e^{-(t/s)}$$

The parameters $s$, $a$ and $m$ don't have an explicit meaning. Heuristically, from the text:

  $m$ is the magnitude of the response and $s$ is a time scale. The function
  peaks at time $a \times s$. The parameter a determines the shape of the
  function such that the larger $a$ is the more narrowly the function will
  be distributed around its peak.

So it seems you have to fit it to some previous data in the area you're trying to generate data from before it can be used.


The electric field of an external electrode provokes the opening of sodium channels, which in turn has the effect that the positive charged sodium ions travel into the cell body and invoke the wanted change to the Membran potential…

reference: Simulation Neuronaler Netze [("Simulation of Neural Networks")] / Andreas Zell. - Bonn; Paris; Reading, Mass [u.a.]: Addison-Wesley, 1994, first edition


Since pycnodysostosis is caused by mutations that cause deficiency in Cathepsin K, it makes sense to look at animal models for the latter; there's a fairly recent study Dauth, 2011...

Cathepsin K deficiency in mice induces structural and metabolic changes in the central nervous system that are associated with learning and memory deficits. [...]
Cathepsin K is a mammalian cysteine peptidase that is sorted to endo-lysosomes and secreted into the extracellular space by certain cell types [1]. It is abundant in osteoclasts and has a prominent role in bone remodeling due to its collagenolytic activity [2]. Indeed, cathepsin K deficiency has been linked to bone disorders such as pycnodysostosis and osteopetrosis [3,4], while the excessive activity of this enzyme may lead to osteoporosis [5], making it a likely target for rational drug design [6-8].
[...]
Interestingly, pycnodysostosis patients suffering from lifelong absence of cathepsin K activity have been occasionally reported to exhibit, in addition to the abnormalities in bone development, alterations in the CNS such as hyperplasia of the pituitary, demyelination of the cerebrum, and imbalances between brain growth, vascular supply, and cerebrospinal fluid pressure, with complications including sensorineural deafness and frontal porencephalic cysts. [66]

Unfortunately the trail gets pretty difficult from there because the paper cited for the last para, while mentioning "mental retardation" as known symptom, block-cites some 5 papers for that; I checked out one of them (in JAMA) but that one doesn't mention anything mental, so... who knows which of the other case reports might have some cognitive details, if any.
I guess the incidence of cognitive issues might depend on the specific mutation, since GARD says that only 5-29% of PSYD actually have these cognitive abnormalities.
Research on animal models of some genetic diseases usually starts with a substantial mutation, i.e. something that's nearly sure to cause the desired disease effect. Later on milder variants are studies. (For example see how the animal models of Huntington's advanced) With pycnodysostosis, at least as far neuronal/behavioral effects go, it seems we're at the fist stage (i.e. they published the publishable "sure thing").
The highly cited paper of Gelb, 1996, which catalogued the (few) known mutations for pycnodysostosis alas does not correlate them with symptoms beyond the mere diagnosis of pycnodysostosis. In fact, this paper doesn't even mention any mental/cognitive effects in the patients studied... which were alas only two or three families.


What is the term for human beings' tendency to obey without thinking?

Obedience

The most famous paper dealing with this issue is Milgram's paper, called Behavioral study of obedience[1]. From the abstract:

  This article describes a procedure for the study of destructive obedience in the laboratory. It consists of ordering a naive subject to administer increasingly more severe punishment to a victim in the context of a learning experiment.

[1] Behavioral Study of obedience, Milgram, S. The Journal of Abnormal and Social Psychology, 1963. doi: 10.1037/h0040525 PDF link


The brain has a lot of a fatty substance called myelin. It wraps around nerve fibers and enhances the speed of electrical communication between neurons (source: Brain Facts), and increases transmission efficiency (Fig. 1). It is produced by supporting cells in the brain called oligodendrocytes. Myelin is really just many wraps of membrane, and since neurons have long axons and dendrites, too, they also have a lot more membrane than if they were just spherical cells - all of this membrane is "fat" called phospholipid.

Now on to your questions -

  Is this fatty tissue structural building material? Or does it just serve as an energy source for the mitochondria?

Myelin and cell membranes are the most abundant fatty substances in the brain - they are structural fatty substances found around cells and neuronal axons, respectively, and they are not fuel.

  [I]s there also a water in our brain?

Every cell contains water, as nearly all biochemical reactions take place in a watery solution. An early report found the water content of neurons to be 55% (Saubermann & Scheid, 1985)

  [W]hat percentage of the brain is actually a neuron?

Scientific American performed a review on this and settles on a ratio of neurons : glia cells of 1:1 (although numbers of 10:1 have been reported). Glia are the brain's supportive cells and include the oligodendrocytes as mentioned above that produce the myelin (Jabr, 2012).

Fig. 1. Schematic showing a myelin sheath around an axon. source: WebMD

References
 - Jabr, Sci Am (2012), June 2012
 - Saubermann & Scheid, J Neurochem (1985); 44(3): 825-34


Is there a formal name for the compulsive and recurrent urges to pick one's nose in order to remove perceived imperfections?

Excoriation disorder (ED) formerly known as dermatillomania, and more popularly as Skin Picking Disorder (SPD):

  a mental disorder characterized by the repeated urge to pick at one's own skin, often to the extent that damage is caused.

The status as a separate disorder is somewhat controversial, because of high comorbidity:

  There has been controversy over the creation of a separate category in the DSM-5 for excoriation (skin picking) disorder. Two of the main reasons for objecting to the inclusion of excoriation disorder in the DSM-5 are: (1) that excoriation disorder may just be a symptom of a different underlying disorder, e.g. OCD or BDD, and (2) that excoriation disorder is merely a bad habit and that by allowing this disorder to obtain its own separate category it would force the DSM to include a wide array of bad habits as separate syndromes, e.g., nail biting and nose-picking.

Your case seems to be one of those overlapping ones.

There's also a 2017 neuroimaging study which concludes:

  data offer partial support for the view that sub-cortical structures contribute to the pathophysiology of SPD, both supporting its categorization as an OC-Related Disorder in DSM-5 and suggesting that there exists a pathophysiological difference between SPD and OCD.

Wikipedia has a lot to say about various treatments even though

  Knowledge about effective treatments for excoriation disorder is sparse despite the prevalence of the condition.

The usual suspects have been tried: SSRIs, anti-psychotics, anticonvulsants, glutamatergic agents (used to treat drug addictions) etc. As well cognitive-behavioral psychotherapies. It's not clear from there what might be most effective.

Wikipedia aside, there's been a "preliminary meta-analysis" published in 2014, but its review at CRD notes:

  Authors' conclusions:
  Both pharmacological and psychological interventions appeared to be effective in reducing the severity of pathological skin picking; psychological interventions could have a larger effect.

  CRD commentary:
  The authors did not report a quality assessment, so it is difficult to know how reliable the results of the individual studies were. Many of the studies had designs prone to bias. Details about the comparator interventions, in the studies with control groups, were not reported. Given the heterogeneity across the studies, the limited reporting of study details and the unknown quality of the included studies, it seems inappropriate that the results were statistically synthesised, particularly for pharmacological and psychological interventions, for pathological skin-picking severity.

So I wouldn't put too much stock on it.

A more recent (2016) meta-analysis has basically the same conclusions; this one was not reviewed at CRD, but it relies basically on the same small number of studies. Its conclusions were similar to the "preliminary" one: psychotherapy seems to work better than medication based on the limited data available. It only looked at SSRIs and lamictal for medication though.

There's also a 2016 RCT on N-acetylcysteine, published in a high-impact journal, concluding:

  N-acetylcysteine [NAC] treatment resulted in significant reductions in skin-picking symptoms and was well tolerated.

The result was fairly unsurprising given that NAC was previously found effective for trichotillomania (TTM -- hair pulling) as well; both studies with NAC were conducted by the same research group. But there were a few more interesting comments on those papers:

  In striking contrast with what we know about OCD, SSRIs
  have not been proved to be superior to placebo in TTM
  treatment. As for ED, the evidence regarding the efficacy of
  SSRIs is still scarce. So far, there are no US Food and Drug
  Administration–approved treatments for ED and TTM. The
  divergent results of the trials testing either SSRIs or NAC for
  ED/TTM and OCD suggest that treatments may not be used interchangeably
  between OCD and related disorders.

  In addition, results from genetic studies also suggest
  that the neurobiology of pathological grooming may not be
  necessarily related to OCD. It had been demonstrated that
  Sapap3 knockout mice groomed themselves excessively.
  However, using family-based association analyses, Bienvenu
  et al found that variation within the human equivalent of
  the Sapap3 gene appeared associated with ED/TTM, but not
  with OCD.
  The conflicting results regarding the efficacy of NAC for
  ED/TTM and OCD, in addition to the findings of translational
  studies, suggest that the neural basis of repetitive behaviors
  observed in patients with these disorders might not be the
  same. So far, similarities between ED/TTM and OCD do not
  seem to go beyond the characterization by repetitive behaviors
  and some degree of familial aggregation.

(But note that this last statement appears somewhat incorrect in view of the 2017 neuroimaging study--some overlap with OCD seems to exist after all.)

NHS Choices also has consumer-oriented page on "Skin picking disorder
" which doesn't say much I haven't told you already except for some behavioral tips. YMMV.


List of experiments contradicting the expected utility model

I asked the same question in the private beta of the newly open Economics.SE and got some interesting answers. You can check them out at https://economics.stackexchange.com/questions/95/experiments-contradicting-the-expected-utility-model


Effect of Physical Exercise on Intelligence/IQ

My general sense from reading the intelligence literature is that I would not expect there to be much of a relationship between exercise and intelligence.
For example, if you read Neisser et al (1996) you can get an overview of the intelligence literature. From the review, you can get a sense of just how difficult it is to systematically increase intelligence, especially over longer periods of time. This includes many cognitive interventions. It seems likely to me that cognitive interventions are targeting intelligence more directly and thus if anything should be more effective than more indirect interventions, such as those targeting physical activity. That said, aerobic, strength, and general physical health is presumably related to energy levels and as studies suggest below may also be related to a range of cognitive and motivational processes relevant to effective life functioning.

Exercise for sedentary adults

Colcombe and Kramer (2003) performed a meta analysis on sedentary older adults and found that performance on cognitive tasks improved by .48 standard deviation relative to to .16 standard deviation improvement for control groups. The average improvement in cardiovascular only programs was 0.41 standard deviations, and the average improvement for combined programs (i.e., including resistance training) was .59 standard deviations. These studies used a variety of psychomotor and cognitive tasks. However, it did not appear that the studies used intelligence tests.

I take from these studies that exercise can have a beneficial effect on psychomotor functioning. However, I'm not persuaded yet that it exercise has a major effect on intelligence.

Exercise for children

For a review of research on exercise on children's cognitive function and academic achievement, see Tomporowski et al (2008). The authors conclude that "similar to adults, exercise facilitates children’s executive function (i.e., processes required to select, organize, and properly initiate goal-directed actions)."
They provide a narrative review of many existing studies on the topic.

References

Tomporowski, P. D., Davis, C. L., Miller, P. H., & Naglieri, J. A. (2008). Exercise and children’s intelligence, cognition, and academic achievement. Educational Psychology Review, 20(2), 111-131. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748863/
Neisser, U., Boodoo, G., Bouchard Jr, T. J., Boykin, A. W., Brody, N., Ceci, S. J., ... & Urbina, S. (1996). Intelligence: Knowns and unknowns. American psychologist, 51(2), 77.
PDF
Colcombe, S., & Kramer, A. F. (2003). Fitness Effects on the Cognitive Function of Older Adults A Meta-Analytic Study. Psychological science, 14(2), 125-130.


Simulating Hudgkin Huxley neural network

I am old and my experience with this area is 20 years out of date, but I would still go with https://neuron.yale.edu/neuron/


Hmm. It's possibly I'm misunderstanding, in which case I will happily retract my answer. But does gamification really apply to, well, games? I thought the idea behind gamification was to take user engagement elements present in games and add them into non-gaming situations to increase user retention/satisfaction etc.

So I would say that if you're making a game, you're not using gamification. You're making a game, which inherently has some of these characteristics. After all it's called gamification because the concepts were borrowed from games, right?

That said, to answer your question, I think points are still valuable in games when they're used as currency. When you can use the points to get stuff, that adds a whole new level of value.


When was it recognized that thinking occurs in the brain and not in the heart?

Alcmaeon of Croton, who lived in the late 6th and early 5th century B.C., is said to have been the first to discover the optical and other sensory nerves. He believed that the nerves were hollow and conducted the sensation to the brain. Alcmaion saw the brain as the organ of perception, memory, thought and the control of action.

The Wikipedia article on the History of Neuroscience gives some more information on the later developments of this view.

Source:

Lloyd, G. (1975). Alcmeon and the early history of dissection. Sudhoffs Archiv, 59, 113–47.


How, other than pharmacotherapy, can those diagnosed with thought disorders be treated?

Dialectical Behavior Therapy (DBT) is a unique skills training that consists of four modules: core mindfulness, distress tolerance, emotion regulation, and interpersonal effectiveness.  Originally, this set of therapeutic skills were developed as treatment for the extremely unmanageable Borderline Personality Disorder.  However, after immense success, the treatment group expanded vastly.

The modules were carefully and specifically designed to help individuals manage their behaviors, emotions, and thoughts. Each module includes a number of 'little things' intended to assist the afflicted in their area of need.

For example, the core mindfulness module teaches individuals to (with practice) slow their thoughts, bring themselves into the present moment, how to regain control of their thoughts by training the mind to focus on only one thing--on the one moment.  This particular training is typically introduced in the form of deep breathing exercises where the focus of the exercise is to think of only the breath entering and leaving the lungs/body.

The other modules offer similar skillful training techniques specific to both the individual as well as the given module.  I imagine that you will find the answers you seek by delving into the curriculum, techniques, and purposes that lay just beneath the surface of the DBT modules.


What is a validated single-item measure of mood?

Many single item measures of mood can be found in the literature. Those two are based on the idea that affect is bidimensional and that one's current state can be reported using a grid:

Russell, J.A., Weiss, A., & Mendelsohn, G.A. (1989). Affect Grid: A Single-Item Scale of Pleasure and Arousal. Journal of Personality and Social Psychology, 57 (3), 493-502.
Larsen, J.T., Norris, C.J., McGraw, A.P., Hawkley, L.C., & Cacioppo, J.T. (2009). The evaluative space grid: A single-item measure of positivity and negativity. Cognition and Emotion, 23 (3), 453-480.

You might also want to look at http://studiolab.ide.tudelft.nl/studiolab/pmri/ [Disclaimer: I know the people who developed it]. It is conceptually similar to Russell's AffectGrid but purely non-verbal.

Finally, it seems necessary to mention the Self-Assessment Manikin. Technically, it's not a single-item instrument (the original version has three, many people use only the first two) but it is very popular. Main publication is Bradley, M.M., & Lang, P.J. (1994). Measuring emotion: The self-assessment manikin and the semantic differential. Journal of Behavior Therapy and Experimental Psychiatry, 25 (1), 49-59.

Edited (a long time) after comment: Most authors in this field argue that mood or affect are fundamentally bi-dimensional, if not more, so it makes sense that measures would also be bi-dimensional. The closest you can come to a single Likert-type item would perhaps be the SAM valence scale.

Another issue is that traditional psychometrics is almost entirely focused on dealing with item-specific variance, i.e. how to select items to build a scale, how many items are needed to reach a given level of reliability, how to model latent constructs using different items, how to equate scales or build population norms, how to adapt scales to different populations, etc. There is not much you can do with single items.

Consequently, it's not very complicated to create a new “valence measure” by drawing some smiling faces, altering the response format or slightly changing the wording. If the new measure is not completely idiosyncratic, you will obtain some level of correlation with other valence measures but beyond that what could make it a “valid” or superior measure of mood?


Sex With Ghosts - Possible Clinical Diagnoses

Sleep paralysis can sometimes result in hallucinations corollary to the paralysis experience. Similarly, bipolar I and other psychotic disorders (viz. the schizophrenia spectrum) could produce vivid enough hallucinations and delusions, though in general, vivid visual hallucinations are quite rare.

It is highly unlikely that someone who is describing these experiences is not experiencing any other symptoms.

Standard treatment would depend primarily on what other issues the patient might be experiencing.

If the patient is experiencing dissociation and misinterpreting this as sex with ghosts for some reason, cognitive or dialectical behavior therapy would be the indicated treatment.

If the patient were agitated, or disoriented to time, place, or person, the psychiatrist would likely prescribe psychotherapy and an atypical antipsychotic (e.g. risperidone, brexipiprazole).

--

Sharpless, Brian A., et al., Journal of Clinical Psychology, 2010; vol 66: pp 1292-1306.

Bell, CC, et al., " American J Psychiatry, 1986; vol 143: p 1484.

Ranier Biobehavioral Institute: "Sleep Paralysis."

Mayo Clinic. "Dissociative Disorders."


How are people able to wake themselves up after a pre-specified amount of time?

There is quite a lot of research on self-awakening (see this search on Google Scholar for self awakening). Hopefully someone else more familiar with this literature can add a more authoritative answer about the mechanisms of self-awakening. In the interem I briefly extract some relevant points from  Ikeda and Hashi (2012). The study does not directly address biological mechanisms. However, understanding the reliability of self-awakening and the correlates of the ability to self-awaken is presumably relevant to forming such an understanding.

First they summarise some existing research:

  Both the accuracy and success rate of self-awakening have been
  experimentally examined. More than half of the people who have the
  ability to self-awaken suc- cessfully awakened within 30 minutes of
  the predetermined time. For example, seven participants succeeded on
  nine of 14 days (64%) in a sleep laboratory, and 15 participants
  succeeded on 35 of 44 nights (80%) at their homes. Survey studies
  indicate that many people habitually self-awaken in daily life; for
  example, 52% of 269 adults (aged 21−84 years) and 10.3% of 643
  university students6 reported habitu- ally self-awakening. People who
  have a habit of self-awakening in the morning have regular sleep/wake
  schedules, tended to have a morningness chronotypology, awakened
  comfortably in the morning, and had less daytime dozing.

In their own study they found:

  The present study investigated self-awakening, both habitual and
  inconsistent, compared to awakening by external means in relation to
  sleep/wake schedules for five consecutive years in 362 students
  (starting at mean age 15.1 ± 0.3 years). Students who self-awakened
  consistently for five consecutive years (5% of all students) went to
  bed earlier than those who inconsistently self-awakened (mixed group,
  40%) or consistently used forced awakening by external means (56%).
  Awakening during sleep was more frequent and sleep was lighter in the
  consistently self-awakened group than in the mixed and consistently
  forced-awakened groups. However, daytime dozing was less frequent and
  comfort immediately after awakening was greater for the consistently
  self-awakened group than for the mixed and consistently
  forced-awakened groups.

Reference

Ikeda, H., & Hayashi, M. (2012). Longitudinal study of self-awakening and sleep/wake habits in adolescents. Nature, 4, 103-109. PDF
Bell CR. Awakening from sleep at a pre-set time. Percept Mot Skills. 1980;50(2):503–508.
Lavie P, Oksenberg A, Zomer J. “It’s time, you must wake up now.” Percept Mot Skills. 1979;49(2):447–450.
MoorcroftWH,KayserKH,GriggsAJ.Subjectiveandobjectiveconfir- mation of the ability to self-awaken at a self-predetermined time without using external means. Sleep. 1997;20(1):40–45.
ZepelinH.REMsleepandthetimingofself-awakenings.BullPsychon Soc. 1986;24(4):254–256.
Zung WW, Wilson WP. Time estimation during sleep. Biol Psychiatry. 1971;3(2):159–164.
Matsuura N, Hayashi M, Hori T. Comparison of sleep/wake habits of university students with or without a habit of self-awakening. Psychiatry Clin Neurosci. 2002;56(3):223–224.


Where does Freud say, "The unconscious mind can only wish?"

Paco Mitchell at Depth Insights lists the following reference for “the unconscious can only wish”:

  For an informed critique of Freud’s comment and of psychoanalytic theory in general, see C. G. Jung, The Theory of Psychoanalysis (New York: Journal of Nervous and Mental Disease, 1915).

Full text is available at Archive.org.
You may also want to search for "can only wish" on Scribd's copy of Jung's Freud and Psychoanalysis, and Archive.org's full text of William White's Mechanisms of Character Formation: An Introduction to Psychoanalysis. These provide plenty more context, though I'm not seeing a direct reference to the original source of the quote...


Is hand-writing analysis used for analysis of a person's behaviour or anlayzing a person's character?

The professional term for hand-writing analysis seems to be "Graphology" and there is no clear evidence that it could be used to predict a person's behaviour or character. For a starting point see the wikipedia page, then there are this article in the New York Times from 1993 and this more recent article from BBC from 2005 for more casual explanations of the phenomenon.

For more scientific references there is this paper from 1983 and this one from 1987 that both fail to show significant results. Also this book chapter might give a good overview but I can only tell from the abstract and you would have to find it at a library or purchase it somehow.

References

Rafaeli, A., & Klimoski, R. J. (1983). Predicting sales success through handwriting analysis: An evaluation of the effects of training and handwriting sample content. Journal of Applied Psychology, 68(2), 212.
Beyerstein, B. L. (2007). Graphology—a total write-off. Tall Tales about the Mind & Brain: Separating Fact from Fiction, 233-70.
Furnham, A., & Gunter, B. (1987). Graphology and personality: Another failure to validate graphological analysis. Personality and Individual Differences, 8(3), 433-435.


Is the Raspberry Pi capable of operating as a stimulus presentation system for experiments?

So I've had a chance to try out the RPi for this purpose. Short answer: it works great (with some limitations).

The RPi does not support OpenGL. I approached this system with the idea of using a python environment to create and present experiments. There are two good options for this that I know of, opensesame and psychopy. Psychopy requires an OpenGL python backend (pyglet), so it won't run on the Rpi. Opensesame gives you the option of using the same backend as PsychoPy uses but has other options, one of which does not rely on openGL (based on pygames). This 'legacy' backend works just fine. But the absence of openGL means that graphics rely solely on the 700 mHz CPU, which quickly gets overloaded with any sort of rapidly changing visual stimuli (ie. flowing gabors, video, etc.).

The RPi does have a very good video card (for a $25 computer) that supports OpenGL ES. Riverbank software provides python bindings for OpenGL ES (pogles), so there is the possibility for hardware acceleration in python. This has not currently been implemented on PsychoPy or Opensesame. It probably won't happen anytime soon, because there is currently an additional limitation on this system: there's no way to use OpenGL ES in the linux windowing environment (xwindows). This will probably be developed in the medium-term. But currently even a lightweight version of xwindows on the RPi is noticeably clunky and slow (overclocking the CPU helps with this). OpenGL can be used on the Pi through CPU emulation (via Mesa)... but this so heavily overloads the CPU that it's effectively useless.

So the RPi is not well suited for displaying rapidly changing visual stimuli (ie. flowing gabors, video). And PsychoPy effectively doesn't run. But Opensesame runs fine with the non-openGL 'legacy' backend. For a manual RT experiment involving the presentation of static images, this setup running on the Pi will have much the same timing resolution as the same setup running on any other computer.

And it will get better, probably pretty quickly. OpenGL ES support in xwindows should come pretty quick, and once this is available it will be possible to use OpenGL ES python bindings currently under development to make backends for PsychoPy and OpenSesame. These will support fluid moving stimuli and video, and free up the CPU for other tasks. My personal hope is that this will free enough resources to allow the RPi to interface with other systems... like an eye-tracker computer or an eeg amp.

But for now it seems just fine for basic no-video psychophysics. And it's very, very cheap... even factoring in the cost of a small DVI monitor you should be able to get a data collection system up and running for less than 100 euro.


Is there a function between loss of memory and time?

There is substantial research on both the functional relationship relationship between practice and retention and between time away from task and forgetting (e.g., see forgetting curve).
In general, retention is a monotonically increasing and monotonically decelerating function of  practice. And retention is a monotonically decreasing function of time where the rate of deceleration is decreasing. This general finding is tremendously robust, but there is substantial debate about the best fitting functional form for these two relationships.

Averell and Heathcote (2011) provide a good review of forgetting curve functions. See equations 2, 3, and 4 in the article for instances of pareto, power, exponential functions. They concluded:

  Our analysis revealed that, although for individual participant data
  the exponential function with an above chance asymptote had the best
  fit among the models we considered, this advantage was due to its
  extra flexibility (complexity). When we adjusted for complexity using
  a range of model selection techniques that varied in the degree to
  which they adjusted for complexity, in every case a power function
  with an above chance asymptote provided the best description of
  forgetting. Interestingly, previous analyses of retention functions
  without an asymptote (Lee, 2004) found that the power model was more
  complex than the exponential. Our findings suggest that the addition
  of asymptote parameters adds more complexity to the exponential
  function than the power function.

References

Averell, L., & Heathcote, A. (2011). The form of the forgetting curve and the fate of memories. Journal of Mathematical Psychology, 55(1), 25-35. PDF


How long could Henry Molaison keep his memory of the present?

The original paper describing Patient HM is available online, and makes for fascinating reading: Scoville, W. B., Milner, B. 1957. Loss of
recent memory after bilateral hippocampal lesions. J Neurol Neurosurg Psychiatry. 1957 Feb; 20(1): 11–21. (Direct PDF)

From page 14:

  This patient has even eaten luncheon in front of one of us (B.M.)
  without being able to name, a mere half-hour later, a single item of
  food he had eaten; in fact, he could not remember having eaten
  luncheon at all. Yet to a casual observer this man seems like a
  relatively normal individual, since his understanding and reasoning
  are undiminished.

On page 15, the authors describe the group of subjects with "Severe Memory Defects", which included Patient HM:

  In this category are those patients who since operation appear to
  forget the incidents of their daily life as fast as they occur. It is
  interesting that all these patients were able to retain a three-figure
  number or a pair of unrelated words for several minutes, if care was
  taken not to distract them in the interval. However, they forgot the
  instant attention was diverted to a new topic.

There are plenty of other interesting aspects to this paper; I high recommend it.  But I don't see any reference to the "thirty seconds" which @BenCole found in Wikipedia.

A followup paper on Patient HM — also well worth reading! — actually specifies that his memory can last indefinitely, yes, as long as he wasn't distracted. See Squire, Larry R. "The legacy of patient HM for neuroscience." Neuron 61.1 (2009): 6-9.

  […] H.M. had a remarkable capacity for sustained attention, including
  the ability to retain information for a period of time after it was
  presented. Thus, he could carry on a conversation, and he exhibited an
  intact digit span (i.e., the ability to repeat back a string of six or
  seven digits). Indeed, information remained available so long as it
  could be actively maintained by rehearsal. For example, H.M. could
  retain a three-digit number for as long as 15 min by continuous
  rehearsal, organizing the digits according to an elaborate mnemonic
  scheme. Yet when his attention was diverted to a new topic, he forgot
  the whole event.

What I think we can infer is that there wasn't a theoretical limit for his attention, but the practical one was pretty severe. I don't recall specific details of how long the "period of time" was, or even how or whether it was explicitly tested, but since he undoubtedly couldn't remember that it was crucial for him to remain attentive, it would have been more of a test of the researchers' ability to keep him away from distraction, not of his own competence.

A more complete history of Patient HM is available at Dossani, et al. "The legacy of Henry Molaison (1926–2008) and the impact of his bilateral mesial temporal lobe surgery on the study of human memory." World Neurosurgery 84.4 (2015): 1127-1135., but I'm afraid it isn't open access, so you'll need institutional access to ScienceDirect Journals. I found this detail quite impressive:

  Gabrieli et al. tested Molaison on several aspects of semantic memory,
  including understanding of the meaning, perception, and pronunciation
  of words, and showed that semantic memory acquired before the
  operation was normal compared with that encountered postoperatively.
  Molaison's inability to collect new semantic information did not
  affect his ability to carry normal conversations using the words he
  knew preoperatively. Molaison continued to have a sense of humor and
  understood complex sentences with ambiguous syntax. Longitudinal
  studies conducted over a period of 48 years showed consistency in
  scores obtained on four Wechsler subtests (Information,
  Comprehension, Similarities, and Vocabulary).

But if you don't have access to that, here are links to three other public bios, found via an image search of Patient HM found in the above article:

Meet the man with no memory: Patient who became world-famous after
botched surgery wiped his ability to remember anything is finally
identified after his death from DailyMailUK, 2013.
Permanent Present Tense: The Unforgettable Life of the Amnesic
Patient, H. M., a 2012 book by neuroscientist Suzanne Corkin.
Who Was H.M.? Inside The Mind Of The Amnesiac Who Revolutionized
Neuroscience from Popular Science, 2003.


Do graphemes relate to communication and thought disorders?

We have this tendency to explore, in detail, language abilities and label them "disorders". Some are disorders, like those stemming from autism, but, in any traditional sense, none of the listed qualify. They are simply biases in what people are good and not good at or classifications of errors. There's a title of a talk by Raymond Klein I've always liked.

Klein, R. M. (2002, November) Dyslexia, dysdrivia and dystennisia: Is it reasonable to expect everyone to read well? Handbook of Cognitive Neuroscience chapter presentations. Lake Tahoe, Nevada.

Imagine if we considered weak tennis playing a social problem. We would carefully examine these poor souls and work out very carefully the defects in their minds that cause them to be outcasts of society. We'd label said defects and work diligently to rehabilitate who we could...etc...you can see where it's going. What we've done with dyslexia is similar.

Of course there will be people who are good and bad readers and writers, and there will be characteristics that some of those bad (and good) readers have in common. And we can categorize them. This does not, in itself, a disorder make.

In any field of endeavour, if you change the requirements of something that's an acquired skill, which reading and writing are, then you change the set of cognitive abilities that facilitate that skill. Different people have different cognitive aptitudes therefore their abilities in different kinds of writing systems, and the translation of those to phonemes, will differ. Furthermore, some systems will be easier than others and in different ways. There may be systematic variations in how those errors work out.

If you had asked whether clay tennis players have differences from grass players would it really be a question worth considering? It's only one because there's some belief that the common errors in reading are named and the people who aren't good at it are labelled.

But, in spite of the fact that some people do it, I think it's pretty difficult to call any of those differences disorders.

(As an aside, several of the listed "thought" disorders are pretty independent of orthography. Most would be considered thought errors.)


What is the computational role of the cortical column?

Cortical columns are groups of neurons in the brain that are oriented perpendicularly to the cortical surface. Cells within a column respond to the same stimulus property (Fig. 1). For example, primary visual cortex columns extract small bars with a specific orientation.

A single cortical column consists of six distinct layers of neurons. The upper three layers (I-III) are functionally distinct from the lower two layers (V-VI). The upper layers project out to other cortical columns, both sending and receiving signals, with layer III cells projecting to adjacent columns and layer II cells projecting to more distant parts of the cortex. Layers V-VI receive input from the upper layers of adjacent columns and send their signals to extracortical structures, such as the thalamus, and motor and sensory centers.

Layer IV, which divides the column into an upper and lower part, receives its inputs from the thalamus and transmits signals to the rest of the column. The thalamus receives information from all parts of the cortex and subcortical areas. It works together with the cerebral cortex to create a feedback circuit by passing information from the infragranular cells of the cortex to the thalamus and then back to the layer IV cells of the cortex, with integration occuring both on in the thalamic and cortical centers.

Information flow in the cortex is mediated by the action of the supragranular cells, while additional information from the external and internal environment is integrated by the thalamus and arrives in layer IV of the cortical columns.It contains thousands or even tens of thousands of neurons corresponding to a few tens of micrometers and up to 1-2 millimetres for larger aggregated columnar structures (sources: Rice University and Phys.org news).

The presence of cortical columns is quite firmly established. However, the histological definition, as well as the function of various types of columns are dramatically different. Columns can be defined by cellular histological feautures, pattern of connectivity, myelin content, staining property, magnitude of gene expression, or functional properties. For example, in the primary visual cortex alone, there are ocular dominance columns, orientation columns, hypercolumns, and color columns.

Further, there are columns as well as various minicolumns. The only connections between these diverse structures and concepts is that they refer to the vertical or radial columnar organization of its elements as opposed to the horizontal or laminar organization that is more explicit in histological preparations of the mature neocortex. Thus, the term cortical “column” is used in so many ways that it needs specific clarification of the specific context in which it is applied (Rakic, 2008).

Even stronger assertions have been made, up until

  ...the disappointing realization that the column may have no function...

(Horton & Adams, 2005).

Having said that, and to home in to the computational processes within a column - some sources claim that columns are capable of memorizing relations and performing more complex operations than individual neurons. If a neuron is analogous to a logic gate, a cortical column may be viewed as a small subroutine. Columnar information processing may involve the column to be fully or partially activated. A fully activated column corresponds to an action, e.g. in a column in the motor area, layers V and VI may project to a sequence of neurons that contracts muscle fibers. A partially activated column corresponds to anticipation or searching, and waits for the lower levels to become active.

In this view, a column can be looked at as an adaptive automaton. An automaton being a function that chooses an action based on its current state and its inputs. Cortical columns may thus represent a goal and the initial and intermediate states. When a goal is defined, activations spread from the goal column along the upper layers (I-III). The spreading activation from columnar goals and the subgoal process of problem solving is called a Call Tree, because of the way the subgoals are solved by a recursive search (source: Rice University).

Fig. 1. Barrel columns in rat vibrissal cortex. source: Kurzweil

References
- Horton & Adams, Phil Trans R Soc Lond B Biol Sci (2005); 360(1456): 837–62
- Rakic, PNAS (2008); 105(34): 12099–100


Why is Internet Addiction Disorder not listed in the DSM-5 manual?

There's debate over whether Internet addiction is it's own disorder or a symptom of an underlying psychosis. See this essay by the first man to publish the term: https://theconversation.com/is-internet-addiction-a-misnomer-55727


What research has been done on attachment types in other primates?

Jaak Panksepp, in Affective Neuroscience: The Foundations of Human and Animal Emotions, describes seven brain systems, "raw feels", that are shared among human and non-human primates. One of these systems is PANIC (he capitalizes the systems' name to differentiate them from the similar terms used in speaking about emotions). He says, "a separation distress PANIC system is important in the elaboration of social-emotional processes related to attachment".


Are there any circumstances where schizophrenia or bipolar disorder are not lifelong?

The current understanding, I believe, is that symptomatic psychiatric disorders may or may not be lifelong according to many factors, but that the susceptibility to them probably is lifelong. Some examples. . .

Substance-induced psychosis (which is pretty much what it sounds like) is often though not always temporary.
Certain types and locations of brain tumors may cause psychotic symptoms, which may or may not reverse on treatment.
Afr Health Sci. Dec 2004; 4(3): 190–194.
Major depressive disorder has a highly variable course, and may reoccur or may not.
N Engl J Med 2008; 358:55-68. DOI: 10.1056/NEJMra073096


According the the Yerkes–Dodson law, a moderate level of arousal gives energy to the task, improving performance.

  The Yerkes–Dodson law is an empirical relationship between arousal and
  performance, originally developed by psychologists Robert M. Yerkes
  and John Dillingham Dodson in 1908. The law dictates that
  performance increases with physiological or mental arousal, but only
  up to a point. When levels of arousal become too high, performance
  decreases.

Anger is an emotion that creates arousal, but it is also a negative emotion that makes other people more hostile and negative. Other emotions that create positive arousal are excitement, interest, curiosity etc.


Which Cognitive Sciences are the most affected by the Replication Crisis?

One finding from the Reproducibility Project was the following:

Van Bavel et al wrote that

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

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

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

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

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

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

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

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

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

Reference

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


It really depends on your theory.  If you can write measurement of morality in google scholar you would find many morality theories and attempts to measure it such as (Ziv, 1976). Most theories, as far as I know, use stories and evaluate children's responces to those theories. I'm not aware of any scale to measure moral development.

By the way, one of the most commonly used theory of moral development is Kohlberg's stage based moral development theory (Kohlberg, 1971). In that article, although I have not read fully, Kohlberg talks about some stories he used to measure moral development.

Of course there are many critiques to this stage based measurement of moral development. (Bandura 2014) can guide you on current theories. I haven't read any of those articles but they seem to be good starting point.

References:

Bandura, A. (2014). Social cognitive theory of moral thought and action. In Handbook of moral behavior and development (pp. 69-128). Psychology Press.

Kohlberg, L. (1971). Stages of moral development. Moral education, 1, 23-92.

Ziv, A. (1976). Measuring aspects of morality. Journal of Moral Education, 5(2), 189-201.


By which neuronal mechanisms does music make us happy or sad?

In a comprehensive review that included 140+ primary research papers, Juslin & Laukka (2003) explain that there is a close relationship between vocal expression of emotions and the musical expression of emotions. Indeed, music and speech have similar characteristics and therefore can illicit similar emotions (table 1).

Table 1. Commonalities of speech and music in emotional expression. source: KTH Sweden

Wikipedia states that emotion is indeed linked with tonality in both music and speech:

  The tones in music seem like a characterization of the tones in human
  speech, which indicate emotional content. The vowels in the phonemes
  of a song are elongated for a dramatic effect, and it seems as though
  musical tones are simply exaggerations of the normal verbal tonality.

References
- Gramfors & Johansson, thesis KTH Sweden
- Juslin & Laukka, Psych Bullet (2003); 129(5): 770–814


how to correctly determine false alarm rate (in a specific experimental setup)

Check out chapter 3 of Macmillan and Creelman on rating scales. You have 3 ratings: left arrow (very confident it is on the left), space bar (not sure), right arrow (very confident it is on the right). You also have non-responses which may be equivalent to a space bar "not sure" or might be something else. I would probably want to know more about why they did not respond (and how often) before deciding what to do.

You also have 3 stimulus types (LVF-word, RVF-word, and double non-word) which makes things harder and I don't think is covered in M & C. That said, you can extend their examples to 3 stimuli pretty easily. The index of sensitivity d' is a measure of distance between two distributions. It sounds like you want to know the distance between the LVF-word and double non-word distributions relative to the distance between the RVF-word and double non-word distributions, but maybe you only care about the LVF-word and RVF-word comparison.


Can you practice and improve physical activities only by thinking?

Yes. In one famous experiment,a college basketball team was divided into three groups.

Group 1 was supposed to show up to practice shooting baskets for a week on a daily basis.

Group 2 was asked to "think about" practicing shooting baskets during the alloted time, without showing up.

Group 3 was asked to "forget about" basketball for the week.

After the one week period, Group 3 showed no improvement in shooting baskets.

Group 1 improved meaningfully.

Group 2 improved almost as much as group 1, and way more than group 3.


Does adopting personal routines accelerate cognitive decline?

SHORT ANSWER:

There is no evidence that adopting personal routines leads to cognitive decline in the way that you have described in your post. There is some evidence that a propensity against personal routine can be representative of underlying creative potential. Given that creativity is highly linked to openness to experience on the Big 5 measure of personality, this could be representative of higher intelligence in certain contexts. However, this does not implicate that personal routines decrease one's existing cognitive capacity.

LONG, DETAILED ANSWER:

In your first paragraph, you refer to these daily routine tasks as 'automated', in the sense that they 'spare... mental energies for [other] tasks'.

In your second paragraph, you wonder if said tasks could contribute to a decline in cognitive processing, given that you are (presumably) doing many of them over a long period of time.

For this reason, I think that a computer is not a perfect analogy. A computer may do things 'automatically' (as in, they are pre-programmed to do so). However, the computer still 'runs' this program as it would any higher-level algorithm. The automatic routine may take up less 'space', but I believe it still requires its own subroutine or threaded code (pardon me if my terminology is incorrect, I haven't quite learned how computer systems work yet), thus 'wearing down' the computer over time.

A human performing a daily routine is not the same as a computer performing a recursively-called subroutine. A human performing a routine is engaging in an unconscious and regularly-repeating habit. Because these habits are unconscious, they do not contribute to cognitive decline in the way that you are referring to. Certain routines may be harmful for other reasons (e.g. routine shopping trips without knowledge of money management, routines that aid procrastination, etc.), but in many ways, routines can actually reduce cognitive load, thus freeing up the mind to focus on other things.

The downside is that they take longer to implement, unlike an algorithm. Lally et. al (2009) found that habits take anywhere from 18-254 days to become asymptotically 'automatic', with an average of 66 days. They are also harder to eliminate if they turn out to be harmful. This is augmented by the fact that the basal ganglia remembers the 'triggers' that helped initialize the routine in the first place, and thus routines can be revived if the triggers reappear. (As this article from MIT points out, "Old habits don't die. They hibernate.").

From the third paragraph in your question:

  On the other hand, I can also see how personal routines and daily automation are an earmark of highly intelligent people who are capable of seeing patterns between two separate instances of a similar task. But can a side effect (automation) of that initial favorable cognitive state (IQ) lead to lowered cognition as a matter of lessened daily mental workout? In other words, can you become dull if you do things more routinely?

I don't think that daily automation and personal routines are necessarily the 'earmark of highly intelligent people...' in the way you are describing. Given that automatic routines are unconscious activities, they are marked by a lack of cognitive processing, no?

However, the ability to develop and stick to a pre-planned routine to the point that it becomes automatic does depend, to some extent, on specific areas of the brain that help regulate executive functioning. I already mentioned the basal ganglia, but the prefrontal cortex (and other areas of the frontal lobe) have been implicated in planning complex cognitive behavior, as well as decision making. These areas are further responsible for task switching, as well as cognitive inhibition of unnecessary impulses and short-term gratification.

IQ itself is not necessarily a matter of activity in the prefrontal cortical regions. You can have a high IQ and have decreased dopamenigernic activity in the mesolimbic reward pathway, thus making it more difficult to automate desired behaviors. You may also find yourself struggling with complex cognitive planning if you have decreased network connections in your prefrontal cortex. However, your intelligence quotient depends on a variety of other neuroanatomical factors besides chemical activity in these regions. The size and shape of the frontal lobes, the amount of blood in the frontal lobes, the total amount of gray matter in the brain, the overall thickness of the cortex, and the glucose metabolic rate all seem to affect IQ.

In terms of making oneself cognitively 'dull' by use of routine, I wouldn't necessarily go that far; however, it is worth mentioning a phenomenon called latent inhibition, which is a personality trait in humans (some more or less than others) in which routine or familiar events become hardly noticeable. Those with low latent inhibition may perceive stimuli as if it were brand new (like a child seeing the world for the first time). From the section on low latent inhibition (courtesy of Wikipedia):

  Most people are able to ignore the constant stream of incoming stimuli, but this capability is reduced in those with low latent inhibition. Low latent inhibition (that may resemble hyper-activity or ADHD in early decades of the individual life) seems to often not correlate with distracted behaviors. This distractedness can manifest itself as general inattentiveness, a tendency to switch subjects without warning in conversation, and other absentminded habits. This is not to say that all distractedness can be explained by low latent inhibition, nor does it necessarily follow that people with low LI will have a hard time paying attention. It does mean, however, that the higher quantity of incoming information requires a mind capable of handling it. Those of above average intelligence are thought to be capable of processing this stream effectively, enabling their creativity and increasing their awareness of their surroundings. Those with average and, less than average intelligence, on the other hand, are less able to cope and as a result are more likely to suffer from mental illness and sensory overload. It is hypothesized that a low level of latent inhibition can cause either psychosis or a high level of creative achievement or both, which is usually dependent on the individual's intelligence. When they cannot develop the creative ideas, they become frustrated and/or depressive.

So, in short, a natural propensity against personal routine may (or may not) be a sign of underlying creative potential, as low latent inhibition may make it naturally difficult to develop and stick with routines to the point of automaticity. However, like many things, this requires context and is not a blanket statement that can generalize people at large.


Is there a variance in acceptance of conspiracy theories by occupation?

I believe that a link to Google Scholar and an explanation of what it is should feature prominently on every page of this site. Many questions can be answered by a quick search there, and the rest will profit from the initial research that becomes easily possible with this tool. This explanation should include the fact that most academic institutions have access to many online journals, and that a trip to the next university library will make most of the articles readable for the general public through the computers in the library.

To answer your question: I have no knowledge of the subject matter, but a Google Scholar search yielded several articles on the topic of conspiracy theories, some of which deal with the phenomenon from an empirical perspective.

For example, one study found, that certain personal characteristics, such as fear of unemployment, correlated with belief in conspiracy theories, while occupational category did not correlate with belief in conspiracy theories.

If you did further into the Google Scholar search results, you might find further, possibliy contradictory, findings and opinions on the topic.

As to your observation that many medical professionals from your family believe in creationism, and the hypothesis you deduce from this observation that maybe medical professionals are more likely to accept such ideas, I would say that this is a classic case of not recognizing a confounding variable. All the medical professionals you know come from the same family. Since religious beliefs are mostly acquired through familial habits, it is most likely that it is your family, not medicine, that correlates with belief in creationism. What defines your family and could correlate with a similar belief in other people, you might be able to recognize if you take a step back an look at your family in relation to who else lives in your country: what is your family's social status, religious tradition, ethnicity, where do you live, how are your children educated etc. etc. From all the factor that you find, you could then build a working hypothesis and test it. Some factors have been tested in the linked article, others you might find discussed elsewhere.

Have fun!


What is the best way to turn EEG scans in to 3D images?

By 3D image, I assume that you want a projection of the topographic map onto a 3D model of the head. For an accurate resolution, you would need to have acquired the position of the EEG channels on the head as well as the shape of the participant's head. However, this kind of data is not often acquired.

The next best solution is to use an existing model of the channel position for your EEG system on a template head. The head plot function in EEGLAB can do that: http://sccn.ucsd.edu/eeglab/allfunctions/headplot.html

Transferring your files from SPM format to EEGLAB format should be quite straightforward. You can find solutions to this problem on both the EEGLAB and SPM mailing lists.


How many thalamocortical relay cells synapse onto each spiny stellate cell in neocortex?

From Shepherd's Synaptic Organization of the Brain (5th ed, pg 513):

  In the cat visual cortex, the terminal arbors of each individual
  thalamic afferent may extend over 1-5 mm of the cortical surface (Fig. 12.11)
  so that each point in layer 4 is covered by the arbors of at least 1000
  separate thalamic relay cells. Thus, the dendritic tree
  of an average layer 4 neuron, which extends for 200-300 micron, could
  receive input from many more thalamic afferents. However, the
  connections are not made randomly between the geniculate afferents
  and the cortical neurons. Selectivity is expressed in several ways.
  For example, there is a high degree of precision in the visuotopic map
  recorded in the first-order cortical neurons in the input layer, i.e.,
  those receiving mono-synaptic activation by the thalamic afferents.
  This clustering is made according to the eye preference of the arbors.
  The afferents of those thalamic relay neurons that are driven by the
  right eye cluster together in regions about 0.5 mm in diameter and are
  partially segregated from the afferents that are driven by the left
  eye. This segregation forms the basis of ocular dominance columns.

There are, of course, many other factors in the specificity of thalamocortical projections.
Point here being that thalamocortical projections are not necessarily limited to cortical neurons with a shared receptive field in visual space, but may be limited in other ways.

Interestingly, the corticothalamic feedback projection is also not limited to shared spatial receptive fields (Shepherd, p. 321ff.):

  Thus, for the lateral geniculate nucleus, this cortical pathway comes
  from visual cortex (mostly areas 17, 18, and 19), and likewise,
  somatosensory and auditory cortex project back, re- spectively, to the
  ventral posterior lateral and medial geniculate nuclei. One
  implication of this reciprocity is that the corticothalamic pathway
  faithfully ad- heres to the map established in the thalamic nucleus.
  For instance, the corticogenicu- late pathway conforms to the
  retinotopic map in the lateral geniculate nucleus. However, there is
  some question as to the extent to which the maps match at the cellular
  level. This is based on evidence that, in the cat (Murphy and Sillito,
  1996), the spread of an individual corticogeniculate axon arbor can be
  quite extensive, reaching well beyond the region within which
  receptive fields that match those of the cortical axon can be
  recorded. The corticogeniculate terminals have a maximal extent of 1.5
  mm compared with the spread of a typical retinogeniculate arbor of
  only about 0.2-0.4 mm (Bowling and Michael, 1984; Sur et al., 1987).
  The retinogeniculate arbor's expanse roughly corresponds to the size
  of a geniculate receptive field, implying that the corticogeniculate
  axonal arbor can contribute to subtle effects on relay responses
  beyond the "clas- sic" receptive field. However, the majority of the
  corticothalamic terminals lie in a central core that roughly
  corresponds to the classical receptive field.


Importance of colors in learning process?

You asked for

  an article that discusses the latest discoveries about how visualization, specially colors and moving images are important in the process of learning....It would be nice to know about a good book about it, but for now I need to start the project and I need an article in first place.

There is one free open access article by Lindelani Mnguni (2014) which funnily enough has a book reference in the quote I am putting below.

"Chunking" is the name given to a technique used to remember things learnt, and Mnguni's article discusses how visualisation helps with chunking, along with the idea that:

  there are at least four main factors that determine how humans “chunk” information, namely, closure, proximity, similarity and simplicity. The closure principle suggests that the mind tends to complete figures even in cases where information is missing. The principle of proximity (also referred to as the principle of contiguity) suggests that when visual features are placed closer to each other, they are perceived as a unit (Mullet and Sano 1995). According to the similarity principle, items that have commonalities such as shape, size, colour, texture and orientation are often grouped as belonging together (Mullet and Sano 1995). Finally, according to the simplicity principle, items are grouped together according to symmetry, regularity and smoothness. All these principles reflect the behaviour of the cognitive system towards new visual information that has been perceived. (Mnguni, 2014).

With regard to moving images, Mnguni also points out that:

  McClean et al. (2005) present evidence showing that student retention of content material in biology education is improved when such content is presented via a lecture coupled with the animations and when an animation is used as an individual study activity.

McClean et al. (2005) is also available free.

References

McClean, P., Johnson, C., Rogers, R., Daniels, L., Reber, J., Slator, B. M., ... & White, A. (2005). Molecular and cellular biology animations: development and impact on student learning. Cell Biology Education, 4(2), 169-179.DOI: 10.1187/cbe.04-07-0047 PMCID: PMC1103718 PMID: 15917875

Mnguni, L. E. (2014). The theoretical cognitive process of visualization for science education. SpringerPlus, 3(1), 184DOI: 10.1186/2193-1801-3-184 PMCID: PMC4000355 PMID: 24790828

Mullet, K., & Sano, D. (1994). Designing visual interfaces: Communication oriented techniques. New Jersey: Prentice Hall


Why is my SPM batch job printing a warning repeatedly?

Below is a corrected version of the script.  SPM seems to be quite finicky about the structure of the data passed to matlabbatch{...}.spm.spatial.realign.estwrite.daat{...}.

%%job_realign.m  SPM batch module.
% SPM's spm_jobman function will eval this file, and automatically launch a
% batch job if the parameters are valid.  Cryptic errors out of spm_jobman
% are usually an indication of a runtime error in batch modules.

%% Get configuration

cfg = config();

%% Get data
include = cfg.subdir(find(cfg.submask));

for isub = 1:length(include)
    subdir = include{isub};
    fprintf('In directory %s:\n', fileparts(subdir));

    runs = regexpdir(subdir, cfg.regex.rundir, false)';
    runs = [runs regexpdir(subdir, cfg.regex.locdir, false)'];
    runs = [runs regexpdir(subdir, cfg.regex.retdir, false)'];

    for irun=1:length(runs)
        rundir = runs{irun};
        scans = regexpdir(rundir, cfg.regex.funcscan, false);
        fprintf('Scans:  %d\n', size(scans, 1));

        matlabbatch{isub}.spm.spatial.realign.estwrite.data{irun} = scans;
    end

    matlabbatch{isub}.spm.spatial.realign.estwrite.eoptions.quality = 0.9;
    matlabbatch{isub}.spm.spatial.realign.estwrite.eoptions.sep = 4;
    matlabbatch{isub}.spm.spatial.realign.estwrite.eoptions.fwhm = 5;
    matlabbatch{isub}.spm.spatial.realign.estwrite.eoptions.rtm = 1;
    matlabbatch{isub}.spm.spatial.realign.estwrite.eoptions.interp = 2;
    matlabbatch{isub}.spm.spatial.realign.estwrite.eoptions.wrap = [0 0 0];
    matlabbatch{isub}.spm.spatial.realign.estwrite.eoptions.weight = {''};
    matlabbatch{isub}.spm.spatial.realign.estwrite.roptions.which = [0 1];    % [0 1] creates mean image only; [1 1] creates all images + mean
    matlabbatch{isub}.spm.spatial.realign.estwrite.roptions.interp = 4;       % 4th degree B-Spline interpolation
    matlabbatch{isub}.spm.spatial.realign.estwrite.roptions.wrap = [0 0 0];
    matlabbatch{isub}.spm.spatial.realign.estwrite.roptions.mask = 1;
    matlabbatch{isub}.spm.spatial.realign.estwrite.roptions.prefix = 'r';
end


Which personality traits relate to prosocial values?

Check out Schwartz (1992) on universal values. His Figure 2 places wealth within the power value space, but near achievement, and opposite from benevolence and universalism. Benevolence, universalism, and to some extent tradition would probably subsume the values you've mentioned in the OP, whereas power and achievement would probably more than cover "trying to maximize your own profit" as a value.

I also developed my own measure of values (Stauner, Boudreaux, & Ozer, 2010) to manage the ceiling effect I've found in using the Schwartz Values Survey. I've found a similar opposition between valuation of "Helping people" and "Being or becoming financially secure". This corroborates your intuition about the strong difference between these values. I have data from the same surveys on the Big Five traits, but I haven't analyzed these relationships yet, so it's a little too early for me to weigh in on trait relationships myself. If I ever get around to publishing these analyses of my data, I'll try to remember to edit in a summary here.

In the meantime, check out Roccas, Sagiv, Schwartz, and Knafo (2002) and Vecchione, Alessandri, Barbaranelli, and Caprara (2009). Roccas and colleagues found that benevolence mostly relates to agreeableness, universalism to openness, and traditionalism to agreeableness and a few facets of other traits. Conversely, power relates negatively to agreeableness and openness, basically. Achievement relates to certain facets of extraversion, conscientiousness, and (negatively:) agreeableness. It's somewhat more complex than this, so I hope you can access the article through a library and take a closer look yourself. Vecchione and colleagues' article is even harder to sum up without sacrificing its nuances, but to put it very bluntly, their results seem roughly comparable, though the method is different.

References
- Roccas, S., Sagiv, L., Schwartz, S. H., & Knafo, A. (2002). The Big Five personality factors and personal values. Personality and Social Psychology Bulletin, 28(6), 789–801.
- Schwartz, S. H. (1992). Universals in the content and structure of values: Theoretical advances and empirical tests in 20 countries. Advances in Experimental Social Psychology, 25(1), 1–65. Retrieved from Google Books.
- Stauner, N., Boudreaux, M. J., & Ozer, D. J. (2010). Factor structure of the Values Q-Set. Poster presented at the 118th convention of the American Psychological Association, San Diego, CA. Available at http://www.slideshare.net/NickStauner/apa-2010-poster-draft-1.
- Vecchione, M., Alessandri, G., Barbaranelli, C., & Caprara, G. V. (2009). Personality determinants of political participation: The contribution of traits and self-efficacy beliefs. Personality and Individual Differences, 46(4), 487–492.


Is it counter-productive to study while tired?

Yes. When studying sleep is crucial in consolidating memories. Recently a wave of research and opinion has hit around optimizing learning, sleep is always mentioned as key. To prominent authors are Benedict Carey and Barbara Oakley. There work is much easier to process than the below research paper, but we like well researched answers!

So here we go, why studying while fatigued is counter-productive and the underlying mechanism of memory consolidation.

  Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories

Further

  Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory.

This work is available for free from the NCBI here


What causes seizures to develop years after a childhood brain injury?

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

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

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

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

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

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

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

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

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

As to the causal relationship:

The cause of epilepsy is largely unkown.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


What is the Mechanism of 5-HT2A-mediated psychedelia?

Broadband cortical desynchronization "begins at the cellular level with
excitation of layer 5 pyramidal neurons, and extends to the macroscopic
level with cortical desynchronization and decreased
brain network integrity."

"Stimulation of the 5-HT2A receptor has been shown to
enhance spontaneous EPSPs/EPSCs (excitatory postsynaptic potential /
excitatory postsynaptic current) in neocortical layer 5 pyramidal
cells by reducing outward potassium currents (Aghajanian and Marek, 1997; Lambe et al., 2000) and to cause increased glutamatergic recurrent activity in layer 5 of the cortex."

"Speculatively, if deep-layer pyramidal cells were to become hyperexcitable during the psychedelic state, information processing would be biased in the direction of inference—such that implicit models of the
world become spontaneously manifest—intruding into consciousness without prior invitation from sensory data. This could explain many of the subjective effects of psychedelics."

http://www.jneurosci.org/content/33/38/15171.short