Correlation between anxiety disorders and PTSD The mega study on the genetic correlations of psychiatric (and neurological) disorders published in Science this summer has one interesting non-correlation: between anxiety disorders and PTSD.

Are the two (anxiety disorders and PTSD) correlated epidemiologically though? If so, is there a good explanation for the lack of genetic correlation?

TLDR

The DSM-5 recognises the epidemiology of anxiety within PTSD, and the reason for the lack of genetic correlation is the fact that in PTSD, the anxiety is exogenous (environmental) rather than endogenous (biological via genes or other means).

The debate

The DSM-5, is the current version of the Diagnostic and Statistical Manual of Mental Disorders written by the American Psychiatric Association (APA, 2013).

As highlighted by Fizz,

  surprisingly, it looks like [the classification of PTSD] is not just a naming issue. It looks like there was a big brouhaha about moving PTSD out of anxiety disorders in DSM-5 (Pai, Suris, & North 2017).

Changes to the diagnostic criteria from the DSM-IV to DSM-5 include:

the relocation of PTSD from the anxiety disorders category to a new diagnostic category named “Trauma and Stressor-related Disorders”,
the elimination of the subjective component to the definition of trauma,
the clarification and tightening of the definitions of trauma and exposure to it,
the increase and rearrangement of the symptoms criteria, and
changes in additional criteria and specifiers.

Some people even question the validity of such a diagnosis (Summerfield, 2001).

  Summary points

  A psychiatric diagnosis is not necessarily a disease
  Distress or suffering is not psychopathology
  Post-traumatic stress disorder is an entity constructed as much from sociopolitical ideas as from psychiatric ones
  The increase in the diagnosis of post-traumatic stress disorder in society is linked to changes in the relation between individual “personhood” and modern life

An editorial in the American Journal of Psychiatry commented that it was rare to find a psychiatric diagnosis that anyone liked to have but post-traumatic stress disorder was one (Andreasen, 1995).

The History

War Cowardice

In World War One, the executions of 306 British and Commonwealth soldiers took place (Trueman, 2015; Taylor-Whiffen, 2011). Such executions, for crimes such as desertion and cowardice, remain a source of controversy with some believing that many of those executed should be pardoned as they were suffering from what later called shell shock, even during World War 2.

  Between 1914 and 1918, the British Army identified 80,000 men with what would now be defined as the symptoms of shellshock. There were those who suffered from severe shell shock. They could not stand the thought of being on the front line any longer and deserted. Once caught, they received a court martial and, if sentenced to death, shot by a twelve man firing squad. (Trueman, 2015)

Shell Shock

  Shell shock - now called post-traumatic stress disorder - was first recognised in print by Dr Charles Myers of the British Psychological Society in 1915. By the end of the war the army had dealt with more than 80,000 cases. (Taylor-Whiffen, 2011)

Britain was not alone in executing its own soldiers. The French are thought to have killed about 600. The Germans, whose troops outnumbered the British by two to one, shot 48 of their own men, and the Belgians 13. In 2001, 23 executed Canadians were posthumously honoured by their government, and five troops killed by New Zealand's military command also recently won a pardon. Not one American or Australian soldier was executed, but the Americans often used humiliation as a punishment for desertion.

PTSD

The US National Center for PTSD covers the start of PTSD being a diagnosis within the DSM.

  The risk of exposure to trauma has been a part of the human condition since we evolved as a species. Attacks by saber tooth tigers or twenty-first century terrorists have probably produced similar psychological sequelae in the survivors of such violence. Shakespeare's Henry IV appears to meet many, if not all, of the diagnostic criteria for Posttraumatic Stress Disorder (PTSD), as have other heroes and heroines throughout the world's literature. The history of the development of the PTSD concept is described by Trimble (1985).

  In 1980, the American Psychiatric Association (APA) added PTSD to the third edition of its Diagnostic and Statistical Manual of Mental Disorders (DSM-III) nosologic classification scheme (APA, 1980). Although controversial when first introduced, the PTSD diagnosis has filled an important gap in psychiatric theory and practice. From an historical perspective, the significant change ushered in by the PTSD concept was the stipulation that the etiological agent was outside the individual (i.e., a traumatic event) rather than an inherent individual weakness (i.e., a traumatic neurosis). The key to understanding the scientific basis and clinical expression of PTSD is the concept of "trauma".

DSM-III

Page 236 states

  Post-traumatic Stress Disorder, Chronic or Delayed
  The essential feature is the development of characteristic symptoms following a psychologically traumatic event that is generally outside the range of usual human experience.

  The characteristic symptoms involve reexperiencing the traumatic event; numbing of responsiveness to, or reduced involvement with, the external world; and a variety of autonomic, dysphoric, or cognitive symptoms.
  The stressor producing this syndrome would evoke significant symptoms of distress in most people, and is generally outside the range of such common experiences as simple bereavement, chronic illness, business losses, or marital conflict. The trauma may be experienced alone (rape or assault) or in the company of groups of people (military combat). Stressors producing this disorder include natural disasters (floods, earthquakes), accidental man-made disasters (car accidents with serious physical injury, airplane crashes, large fires), or deliberate man-made disasters (bombing, torture, death camps). Some stressors frequently produce the disorder (e.g., torture) and others produce it only occasionally (e.g., car accidents). Frequently there is a concomitant physical component to the trauma which may even involve direct damage to the central nervous system (e.g., malnutrition, head trauma). The disorder is apparently more severe and longer lasting when the stressor is of human design. The severity of the stressor should be recorded and the specific stressor may be noted on Axis IV (p. 26).

The current (DSM-5) definition of PTSD (under Specific Phobia: Differential Diagnosis within the Anxiety section of DSM-5)

  If the phobia develops following a traumatic event, posttraumatic stress disorder (PTSD) should be considered as a diagnosis. However, traumatic events can precede the onset of PTSD and specific phobia. In this case, a diagnosis of specific phobia would be assigned only if all of the criteria for PTSD are not met (APA, 2013 p.202)

Trauma- and stressor-related disorders include

  disorders in which exposure to a traumatic or stressful event is listed explicitly as a diagnostic criterion. These include reactive attachment disorder, disinhibited social engagement disorder, posttraumatic stress disorder (PTSD), acute stress disorder, and adjustment disorders. Placement of this chapter reflects the close relationship between these diagnoses and disorders in the surrounding chapters on anxiety disorders, obsessive-compulsive and related disorders, and dissociative disorders. (APA, 2013 p.265)

Psychological distress following exposure to a traumatic or stressful event is quite variable.

  In some cases, symptoms can be well understood within an anxiety- or fear-based context. It is clear, however, that many individuals who have been exposed to a traumatic or stressful event exhibit a phenotype in which, rather than anxiety- or fear-based symptoms, the most prominent clinical characteristics are anhedonic and dysphoric symptoms, externalizing angry and aggressive symptoms, or dissociative symptoms. Because of these variable expressions of clinical distress following exposure to catastrophic or aversive events, the aforementioned disorders have been grouped under a separate category: trauma- and stressor-related disorders.

See also: DSM-5 info. sheet on PTSD (Free PDF)

So, to your question

Are the two (anxiety disorders and PTSD) correlated epidemiologically? If so, is there a good explanation for the lack of genetic correlation?

DSM-5 recognises the epidemiology of anxiety within PTSD, and the reason for the lack of genetic correlation is the fact that in PTSD, the anxiety is exogenous (environmental) rather than endogenous (biological via genes or other means).

References

Andreasen, N. C. (1995). Posttraumatic stress disorder: psychology, biology, and the manichaean warfare between false dichotomies. The American journal of psychiatry, 152(7), 963–965. https://doi.org/10.1176/ajp.152.7.963

APA (1980). Diagnostic and statistical manual of mental disorders, (3rd ed.). Washington, DC: American Psychiatric Publishing.

APA (2013). Diagnostic and Statistical Manual of Mental Disorders, (5th ed.). Washington, DC: American Psychiatric Publishing.

Pai, A., Suris, A. M., & North, C. S. (2017). Posttraumatic Stress Disorder in the DSM-5: Controversy, Change, and Conceptual Considerations. Behavioral Science, 7(1), 7. https://doi.org/10.3390/bs7010007

Summerfield, D. (2001). The invention of post-traumatic stress disorder and the social usefulness of a psychiatric category. BMJ : British Medical Journal, 322(7278), 95–98. https://doi.org/10.1136/bmj.322.7278.95

Taylor-Whiffen, P. (2011) Shot at Dawn: Cowards, Traitors or Victims? BBC History [Online] Retrieved from: http://www.bbc.co.uk/history/british/britain_wwone/shot_at_dawn_01.shtml

Trimble, M. D. (1985). Post-traumatic Stress Disorder: History of a concept. In C.R. Figley (Ed.), Trauma and its wake: The study and treatment of Post-Traumatic Stress Disorder. New York: Brunner/Mazel.

Trueman, C. N. (2015). World War One executions. The History Learning Site [Online] Retrieved from: https://www.historylearningsite.co.uk/world-war-one/the-western-front-in-world-war-one/world-war-one-executions/


Neural Processes of Inducing Flow Related to my previous question: Improved Typing as a result of slight movement

For context: slight movement (<1 inch in any direction) improves typing, piano-playing, and writing, among other things.  I believe this is because the continuous movement helps induce a flow state.  Additionally, any mistakes made during the activity (a misspelling, an inappropriate piano note, etc) are more easy to recover from.

I am now curious as to what neural processes could be taking place here - by what process does this slight movement ease the primary activity, remove or reduce errors, and induce a flow state?  What mechanism of the human body allows this 'cross-entrainment'?

For bonus points, what neural activity is taking place during a flow state itself?

Although I find the concept of flow quite interesting, I'm not so sure about needing to invoke the flow state to explain motor enhancement from unrelated continuous movements. For example, one possible explanation for why continuous motion would improve learned movements like typing is that the motor cortex is typically used to model periodic movements as a dynamical system, and that short-duration movements are actually abnormal in a motor sense.

Consider how many of the movements we make are naturally periodic. Walking in particular is highly cyclical, but many other types of movements that we typically make (e.g., swinging the arms to counterbalance the trunk during walking, counter-rotating the eyes, head, and spine during a turn-to-look movement, opening and closing the jaw while chewing, inflating and collapsing the ribcage during breathing) show significantly periodic activity. This periodicity suggests that one could model these movements as a rotation in an abstract "phase space" defined by the differential equations that capture the dynamics of the movement. Seen from this perspective, cyclical movements are the norm for almost any animal, whereas short-duration, "single-use" movements like typing or playing the piano are rather unusual. It could be the case that if the motor cortex (or even the basic movements encoded in the spinal cord) is inherently tuned to modeling cyclic movements, then adding some continuous motion could help the motor cortex capture the intended typing or playing movements as part of the larger, continuous movement.

These references don't address the specific topic at hand, but they do address the periodicity of the motor system at a relatively low level. I would argue that this periodicity should be considered "normal" for movement modeling. Whether or not this periodicity is useful for enhancing other movements is, as far as I know, not known.

M. Churchland et al., "Neural population dynamics during reaching," 2012 Nature http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3393826/

A. Ijspeert, "Central pattern generators for locomotion control in animals and robots: a review" 2008 Neural Networks.

Neural correlates of flow

It's quite difficult to map between levels of abstraction as widely separated as neural activity and a "meta-cognitive" state like flow. However, a quick search online did reveal a couple of papers that have attempted to relate flow to physiological measurements like EEG :

D. Kramer, "Predictions of Performance by EEG and Skin Conductance," 2007 Indiana Undergraduate Journal of Cognitive Science -- not sure where this journal is published, but it seemed like an interesting article

M. Klasen et al., "Neural contributions to flow experience during video game playing" 2011 Social Cognitive and Affective Neuroscience, http://scan.oxfordjournals.org/content/early/2011/05/19/scan.nsr021.full


Do animals that sleep during the day have a different sleep architecture than those who sleep at night? A typical hypnogram, delineating the sleep architecture for a (human) mammal looks like

A distinct distribution of non-REM and REM sleep can be observed.

Is this pattern of sleep cycles particular to that of diurnal mammals, and if so, how would the sleep architecture of a mammal that sleeps during the daytime be different?

One study (Zhao et. al., 2010), investigating the sleep architecture of two bat species (one nocturnal, and one mixed), notes the following:

  C. sphinx was found to sleep predominantly throughout the day (60% of total sleep quota) during which time it spent significantly longer
  time in NREM and REM sleep. Compared to E. spelaea, C. sphinx had
  significantly less REM and NREM sleep episodes but their duration was
  significantly longer. E. spelaea appears to distribute its time at
  wake and in REM and NREM sleep equally throughout the light and dark
  phases.

Top three rows are for the predominantly nocturnal bat C. sphinx. Note the "Wake" rows for the two species.

Source:

Zhao, X., Sun, H., Tang, Z., Flanders, J., Zhang, S., & Ma, Y. (2010). Characterization of the sleep architecture in two species of fruit bat. Behavioural brain research, 208(2), 497-501.


What is this method used in the "it's not your fault" segment of Good Will Hunting and why does it work? I mean the "it's not your fault" part at the end of this movie segment. Could anybody explain this method and why it works?

What happens if the psychologist didn't get any reaction (like crying) from the case (Will), doesn't he look like a jerk repeating the same words 9 times?

An addition to the other answers:

We must remember that we are watching a movie. Movies are often called "dramatizations", a term that makes very clear what this type of movie does: it creates drama. It was not made to educate the viewers about how a therapy works, but rather to evoke intense emotions in the viewers. We should even assume that this movie does not faithfully depict any actual therapy but rather takes up the ideas that most viewers have of what would be helpful and reflects them back at them, because reinforcing a belief that you already hold will create the strongest emotional echo.

What do most people do in a situation like that in the movie? They tell their friend that "it is not your fault". Most therapists don't do that. Telling a patient how he or she should feel often has adverse effects: the person begins to defend his or her emotions from the devaluing judgment that they perceive the therapist's suggestion to be. What happens is that the belief in their own guilt gets cemented and harder to overcome.

A good therapists helps a patient to arrive at the conclusion by themselves. The most powerful ideas, when it comes to changing yourself, are those insights that you have yourself. A therapist might use questions ("Why do you think ...?") or careful suggestions ("Do you think it is possible that ...?") to direct the thinking of the patient, or the example of himself or a group of other patients with similar experiences (in a group therapy). Another component is psychoeducation, i.e. explaining to the patient that feelings of guilt are common symptoms and why patients experience them.

I cannot view the video, so my examples probably don't fit the situation at hand. Please always provide a short summary.


Do you know any good tutorial on designing EEG experiments with PsychoPy? I'm trying to find good documentation on using PsychoPy to measure Event-Related Potentials. In particular, I want to measure and compare the amplitude of the N170, a face-sensitive ERP, when presenting neutral versus threatening faces.
I would be using the Emotiv Epoc EEG headset, whose validity for research on the N170 has been documented.

A collection of classic EEG experiments implemented in Python and Jupyter notebooks.
Currently, all experiments are implemented for the Muse EEG device and using psychopy lib for stimulus presentation.
Classification is made offline though. But I'll post very soon an online tutorial:
https://github.com/NeuroTechX/eeg-notebooks/tree/master/notebooks


Classical or Operant Conditioning? I'm working on a conditioning experiment for my psychology class in which I tap my finger three times on a table and then ask my friend to sharpen a pencil for me. If she finishes the task I give a reward (ex. part of a cookie). However, I'm not sure if this would be classified as classical or operant conditioning because although it's a voluntary behavior, it's prompted by a stimulus. I think it's operant conditioning, but I just wanted to be sure. Any advice for this?

This is homework. But it's still interesting.

However, I'm not sure if this would be classified as classical or operant conditioning because although it's a voluntary behavior, it's prompted by a stimulus. I think it's operant conditioning,

There are multiple learning processes involved. Some of them have already been established e.g. asking your friend for something is already a salient motivational cue.
Anyways, what you're describing is reminiscent of the learning phenomenon classical-to-instrumental transfer (CIT), which is also referred to in the literature as Pavlovian-instrumental transfer (PIT). Essentially, its the phenomenon by which a conditioned stimulus (CS) eventually acts as a signal or a predictor of a reward contingency (or vice-versa). Think of it as motivation/focus/salience modifier.
It has particular relevance to relapse in drug dependency after a period of abstinence. An individual who has quit smoking, for example, would be more likely to relapse after years of abstinence if they are exposed to any stimuli that were present when they typically smoked. In fact, there is nothing stopping an anti-smoking billboard acting as that stimulus.
CLIFF'S NOTES SUMMARY
This is how you would break down your homework problem. However, you should note that this is NOT the way you would want to structure the training of CIT.
Also, I'm going to assume that the end game here is to get your friend to sharpen your pencil through mere desk tapping.
1. INSTRUMENTAL LEARNING
Sharpening your pencil results in receiving a cookie.  By linking a desired behavioural repertoire with a positive outcome, you increase the likelihood of the behaviour being repeated:
[response-outcome]   pencil sharpening => cookie

Your friend will eventually learn that pencil sharpening is something that is rewarded.
2. CLASSICAL CONDITIONING
Now it's time to add additional stimuli to the learning condition.
There are two parts to this. First, your friend will learn that you asking her to sharpen your pencil will be rewarded, but in its absence, she won't. It would be done along the lines of:
CS+ (asking)   sharpening => cookie

CS- (no asking)   sharpening => [no reinforcement]

Then, through simple conditioning of the two stimuli, tapping and asking will also become paired:
[classical conditioning]   tapping => asking

                                      sharpening => cookie [operant conditioning]

CLASSICAL-TO-INSTRUMENTAL TRANSFER
I will spare you the intricacies of how the training is performed, but needless to say, eventually you could expect to observe the following:

Tapping alone should instantiate the sharpening behaviour.

Ditto asking.

As a motivational cue, sharpening should become more vigorous  in the presence of tapping.

I suspect, but am not certain, that asking while tapping would have some effect on the vigour of sharpening observed in #3.

Tapping should produce spontaneous recovery after extinction of the sharpening => cookie contingency.

Below is an outline of how classic-to-instrumental transfer is demonstrated experimentally. If you note, you have an additional stimulus pairing (tapping=>asking) but it does not make this any more different to the following:

References
Domjan, M. (2014). The principles of learning and behavior. Nelson Education.


In TD learning, is the weight function used as a linear filter? In the Temporal difference learning algorithm (TD-learning), an agent seeks to predict the total value of future rewards that will be received during the current trial. The agent updates the prediction as the trial progresses, based on conditioned stimuli (CS) that have been seen so far. Specifically, the prediction is calculated as a weighted sum of the intensities of past CS presentation. At time $t$, the prediction is calculated as

$$v(t) = \sum_{z=0}^t w(z)u(t-z)$$

where $v(t)$ is the prediction at time $t$, $u(t)$ is the CS intensity at time $t$, and $w$ is an array of weights.

My question is: why are we summing the terms $w(z)u(t-z)$, rather than $w(z)u(z)$, i.e. why isn't each weight associated with the CS strength at a particular time?

[Thanks to user honi's reply, I subsequently understood that each element of the weight array is associated with an elapsed time since seeing the CS. For example, $w(3)$ is the weight given to the CS strength experienced three units of time ago.]

[Original phrasing of the question: I am reading Theoretical Neuroscience by Dayan and Abbot, and I am confused by the use of $w(t)$ in equations (9.6) and (9.7). In the former, it is a window function (linear filter) and in the latter it is the weight function. Is this (a) an unfortunate use of the same name for two different things, or (b) is the weight function really used as a linear filter to calculate $v(t)$?]

They are the same in the two equations.  See equation 9.3:  v = w*u.  w and u are bolded in that equation to indicate that they are vectors.  In equation 9.3, they are vectors of simultaneously presented stimuli, but you can apply the same equation if u is a vector of a single stimulus over time and w are the weights of each time step of that stimulus.  Indeed, a linear filter is simply a way to weight different time steps of a time-varying input.  Note that v in equation 9.3 is a single value, whereas v in equation 9.6 is a function of t, i.e. it has a different value at each time point depending on what part of u is currently occurring.


Why do humans need emotions? If the emotions' only purpose is to stimulate certain behavior, why can't this task just as effectively, or even more effectively be done by the reasoning part of the brain?

Are emotions really necessary for survival?

This question becomes more complicated if we think in terms of "emotions" (e.g., angry, happy, sad, afraid, etc.) than in terms of "affect" (positive and negative feelings, high and low arousal).  I'll start with affect and move on to emotions.

An affective state tags an object with a certain value--and it does so very quickly (e.g., Pham, 2007). For example, if a snake makes you feel bad, then it must be undesirable. This motivates a plan of action that could involve elimination of the snake (fight) or withdrawal from it (flight). You do not have to spend time considering the value of the snake (i.e., that it's bad and dangerous) and developing a plan of action to deal with it. Instead, your negative affect facilitates automatic evaluation and action, which might increase your evolutionary fitness. Gerald Clore has suggested that negative affect serves a STOP function whereas positive affect serves a GO function.

Emotions are a bit more complicated, in part because we don't have a consensual definition of them.  If emotions are merely socially shared concepts (happy, sad, angry) that we use to describe and organize our situated affective experiences (e.g., Barrett, 2014), then we can say that emotion concepts serve self-regulatory and social-communicative functions.  For example, by labeling as anger my high arousal and negative affect in the context of having my autonomy violated, I've organized this multifaceted affective experience into a single concept (of anger). This enhances my capacity to develop ways to regulate my affective experience (Kashdan, Barrett, & McKnight, 2015) and it facilitates communication of it.  If I tell you that I am angry, then you'll have a general idea of what I'm feeling.  Self-regulation and social communication are certainly important for survival.

Emotions are involved in lots of other things, e.g., facilitating cooperation (e.g., DeSteno et al., 2010), motivating the pursuit of new goals (Bench & Lench, 2013), social bonding, deceptive behavior, cheating, and so on.  All of these can be adaptive in certain contexts.

It's also important to note that emotions are flexible. For example, we don't have a "fear module" in the brain that motivates a rigid pattern of action (e.g., Lindquist et al., 2012).  Instead, emotions (on one view) emerge from the interactions of more domain-general processes (including exteroceptive perception, language, interoception, conceptualization, executive attention, and core affect; Oosterwijk, Touroutoglou, & Lindquist, 2015).  These domain-general processes interact to produce emotional episodes with patterns of cognition, behavior, physiology, and experience that are flexible to the situation at hand (Barrett, 2015). The kind of flexibility and efficiency that you might expect from the "reasoning part of the brain" probably does not match up to the kind of flexibility that I just described.  Also, it's important to note that emotion and cognition are not separable constructs.

EDIT:  As far as reason vs. emotion is concerned, emotion is a much more potent motivator.  If you consider seizure patients with lesions to the majority of their amygdalae (from lobectomies), they don't show fear.  If you put them in a dangerous situation, they won't run away--despite having their prefrontal areas intact. (Although an alternative non-emotional interpretation is that these patients have lost the ability to discern what is salient, e.g., threatening, in their environment.)  If you have a hobby that you really enjoy, your motivation to continue doing it is largely emotional ("It makes me happy").  As onigame implied in his/her answer, emotions motivate these kinds of decisions.

Anyway, I think I've provided you a very incomplete view on the adaptiveness of emotions, but hopefully this clarifies some things.


Do distractors create false learning in multiple choice questions? I use quizzes in teaching, but have started to worry that they do more harm than good.

Here's why: We have all learned from "the testing effect" that the act of taking a test is part of the practice that leads to learning.

Say I give my students a multiple choice quiz, immediately after a lecture, to practice. And let's say question looks like this:

"Who wrote The Blank Slate?

[] Steven Pinker

[] Jessie Pinkman

[] Mr Pink"

A student that did not pay much attention at class, may vaguely recognise the second name, so he checks the middle box and moves on.

Has the student now reinforced the incorrect option, and thus created a net negative learning?

And then, as a part two of the same question:

Does it make a difference if the test is done on the same day as the lecture, when the new knowledge is still fluent, or after sleep, when the new knowledge is consolidated (and weak memories culled)?

Part three: Does it make a difference if the quiz is on paper, and thus gives no direct feedback, or online, and can indicate the correct answer?

I have searched Google Scholar extensively, but not found anything on this.

To answer your initial statement: no, I don't think they do more harm than good. The testing effect has been shown overall to improve scores compared to traditional studying (though only for long term memory, see (Roediger & Karpicke, 2006) for an interesting discussion), implying that it is doing more good than harm. This study assumes an overall positive effect without feedback to learners on whether they were right or wrong, and where students who incorrectly retrieved do not "learn" or maintain memory (Kornell, Bjork, & Garcia, 2011). Providing feedback to learners on correct and incorrect responses, however, will increase retention even for students who did not correctly retrieve, and may be one of the best ways for these students to learn (Kornell, Hays, & Bjork, 2009).

Part 1: So far as negative learning from selecting an answer, this directly relates to your third question (as mentioned above). Students who got answers correct (successful retrieval) are hypothesized to better maintain memory, while students who didn't will not better maintain (Kornell et al., 2011). Though this seems obvious, remember that retrieval rates naturally decrease over time (the goal is to maintain a high retrieval rate).

Part 2: In a word, yes. Given this, they each measure different things (and should be used for different purposes). Personally, I use a "post-lecture" quiz as an "exit-ticket" (sorry, background with high school freshman) to quickly check where misconceptions lie. These quizzes are reviewed prior to students leaving the class in order to identify and address misconceptions (formative assessment). I've found that waiting can allow more connections to be made (and thus, higher level responses), but if the material is not encoded correctly false connections can be made (reinforcing incorrect information).

Part 3: Not reviewing the quiz is hypothesized to create a "bifurcation" where those who got answers right better remember, and those who did not get the answers right steadily decrease (again, a natural pattern in retrieval over time). The "testing effect" exists because overall students are theorized to do better, but again, there will be a split in student growth between those who remembered and those who didn't (Kornell et al., 2011). Reviewing the quiz immediately (if paper, go over the answers right after the quiz!) is hypothesized to help all students, regardless of whether they initially got the correct answer or not, and thus would be the recommended method to improve students' knowledge retention (Kornell et al., 2009).

To summarize: review after taking quizzes acts much like a "studying" effect (where those who got right and wrong answers can learn), while quizzes without review are hypothesized to split learning (those who correctly recall retain, and those who fail to correctly recall don't retain). Both groups are able to be helped through quizzing and reviewing answers.

References

Kornell, N., Bjork, R. A., & Garcia, M. A. (2011). Why tests appear to prevent forgetting: A distribution-based bifurcation model. Journal of Memory and Language, 65(2), 85–97. doi:10.1016/j.jml.2011.04.002

Kornell, N., Hays, M. J., & Bjork, R. A. (2009). Unsuccessful retrieval attempts enhance subsequent learning. Journal of Experimental Psychology. Learning, Memory, and Cognition, 35(4), 989–998. doi:10.1037/a0015729

Roediger, H. L., & Karpicke, J. D. (2006). Test-enhanced learning: Taking memory tests improves long-term retention. Psychological Science, 17(3), 249–255. doi:10.1111/j.1467-9280.2006.01693.x


Why are the Big Five factors of personality correlated? One of main characteristics of Five Factor Model is that factors are not orthogonal as in some other personality models.

Why it is tolerated that those factors are not independent?
Is it possible to find biological basis if factors are not independent?

There are no personality models in which the factors are orthogonal in the strict sense of being at 90 degrees from one another, unless an orthogonal rotation method is used to extract them. I think you meant to say that the Big Five factors are less independent (or more strongly inter-correlated) relative to the factors in other models.

Whether or not one wants to obtain orthogonal factors depends on what one is trying to achieve. In most cases, you want an orthogonal solution if you want simple structure, i.e. you want to figure out which factor indicators unambiguously cluster together to form a relatively independent factor. But in general, factors are allowed to correlate because that just happens to be the "reality" and there is no theory suggesting that they should be completely independent. There are of course plenty of reasons why relatively independent factors might correlate and it doesn't mean that biological bases cannot be found; it could mean that there are biological bases that are shared among traits and there are those that are unique to each trait. For example, the relationship between Openness and Extraversion could in part be due to shared genes related to exploration (I forget the source for this).


Limitations of Neural Engineering Framework (NEF) All frameworks have limitations. Although I ask a lot of questions on this site in regards to the advantages of the Neural Engineering Framework (NEF), there must be significant limitations. What are they?

The limitations of the NEF fall into three main categories.

1. Simplistic Use of Neurotransmitters

The NEF uses neurotransmitters and their rate of propagation to set a time constant on an exponential low-pass filter for spikes, as well as for modulation of learning rules (dopamine). This is currently the only use of neurotransmitters in the NEF, despite their being many functions that they could serve in terms of signalling and modulation.

2. Limitations When Using Complex Neuron Models

Although different filters are being investigated by Aaron Voelker, the vast majority of filters used, as mentioned in the last point, still rely on the single time constant and on linear decoding. More complex neural models, although easily included in a feed-forward connection, usually have multiple time constants and non-linear synpatic effects, which make it very difficult to capture their dynamics. This is covered in chapter 4 of Bryan Tripp's PhD thesis.

3. Lack of Developmental Explanation

This last problem may be more of a reflection on the state of neuroscience, than an actual limitation of the NEF.

The NEF describes fully formed, adaptive, but non-developmental networks. Although the NEF can learn functions, it does not describe how certain structures such as the Basal Ganglia came to be formed. Neither does it give any description of how neurogenesis might occur within the framework, although it is easy to imagine how it might be leveraged to increase accuracy of certain populations.

Conclusion

Although the NEF is the only framework I know of that tries base behaviour on a biologically plausible substrate, it is not the silver bullet of theoretical neuroscience. It is very much a zeroth-order guess at the computations that the brain my perform.


Why are children afraid of the dark? Why are children afraid of the dark, in particular more afraid than adults? Is it an evolutionary mechanism? What causes this?

Human's fear of the dark comes from our evolutionary past. Scientists believe it is genetically encoded in our DNA to be afraid of the dark due to the attacks of predators on our ancestors mostly occurring at night. Our ancestors who were afraid of the dark survived predator attacks and thus lived, transferring that trait to us.

Fear is normal and usually occurs when we try something new, something unknown. Children, more than adults, are always experiencing new things so they have more fears which can get to them especially at night.

Fear of the dark is highest among children between 4 and 6 years old, and begins to decline at around 9 years old. Sigmund Freud believed that the fear of darkness is linked to separation anxiety from the absence of our mothers. But psychologists believe it comes from children's highly active imagination.

Fear of the dark forms at the age when children are able to use imagination but not distinguish fantasy from reality. Their heightened imagination allows young children to make a monster out of a shadow. Plus there are not many distractions in a child's mind compared to adults. Most of this fear in children comes from watching TV and reading books. The sounds and images on TV are too stimulating to their young brains and the images in a book might be misinterpreted and provoke an already active imagination.

So the general fear of the dark is natural and evolutionarily derived from our ancestors. But children are more afraid of the dark than adults because they have a more active imagination, they're at an age where they can't distinguish fantasy from reality, and they don't have as many distractions in their head to occupy themselves with so their imagination runs wild.

For more information, see the following links:
http://www.lifehack.org/articles/lifestyle/why-are-we-afraid-of-the-dark.html
http://www.webmd.com/parenting/features/fear-of-the-dark


Is speed up of arithmetic calculations as a result of memorisation? In elementary school, it is typical for a student to learn "times tables" to increase their speed of mental multiplication. What is the mechanism for the increased speed of calculation resulting from the repetition of "times tables"? Is it memory based? That is, the pattern is recognized and the result is retrieved from memory. Is it optimisation based? Does the brain actually just become faster at multiplication? The same question could apply to the progression of addition as a result of memorised counting.

This is assuming a naive, limited approach without mental imagery optimisation, such Chisanbop, where a mental abacus is used.

I asked this question back when I was building a neural model of progression through counting strategies [1]. The quotes in this answer are taken from that publication.
Psychologically, there is some evidence of addition speedup being a result of memorisation.

Typically, children progress through various strategies before finally
memorizing the results of addition, as shown in Table 1 (Siegler,
1987). The Counting strategy involves choosing the larger number and
incrementing it a number of times equal to the smaller number. The
Recall strategy is where the two numbers form an association with a
previously memorized answer, which is then recalled from long-term
memory. Other strategies have been identified, although we focus here
on recall and counting [...]
[The] recall strategy [...] improves reaction time and accuracy,
consistent with the data from Tables 2 and 3, respectively.

There is also some evidence from the Cognitive Neuroscience point of view which ends up being supported by the neural model I built:

First, when doing mental calculation, age is correlated with the use
of parietal brain areas. However, it is inversely correlated with the
use of prefrontal and hippocampal brain areas, as well as the use of
the dorsal basal ganglia area (Rivera, Reiss, Eckert, & Menon, 2005).
Within the model, this transition can be framed as older children
using fewer iterative processes (no use of working memory in
prefrontal, no iterative process control requiring the basal ganglia,
and no loading of instructions from the hippocampus) and more
memorization.
Second, those with dyscalculia show greater activation
of the prefrontal cortex compared to individuals with normal numeracy
(Kucian & von Aster, 2015). Although this model make no claims about
why dyscalculia occurs, given that it is a complicated disability
usually accompanied by various comorbidities and no direct cause
(Rubinsten & Henik, 2009), it does provide part of a possible
explanation as to why such compensation occurs. Specifically, those
with dyscalculia are unable to consolidate the functional role of the
prefrontal cortex during the counting task within the frontal-parietal
region and must instead rely on their working memory. Given an
excessively noisy input, inaccurate feedback, or inappropriate
modulation of the error signal, the Fast-Net could fail to learn the
mapping between addends and sum. Consequently, there would be limited
progression from counting to recall and a continued dependence on
working memory.

Improving With Practice: A Neural Model of
Mathematical Development


Would you classify confusion as an emotion? I'm writing a short essay on emotions and I stumbled upon a few references of confusion being an emotion but no solid exclusive research results focusing on confusion as an emotion. If it isn't, what classification would it fit?

Few references: https://www.pnas.org/content/pnas/114/38/E7900.full.pdf (page E7901) which simply explains about 27 types of emotions mostly deduced from physical observations rather than neurological

And this paper, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5620019/, also explains what happens neurologically when a person is confused though it's focused more on the advancement of Machine Learning: Neural Networks than pure neuroscience. This is from another unanswered question https://biology.stackexchange.com/questions/67440/neuroscience-of-confusion

Cambridge Dictionary defines confusion as "a situation in which people do not understand what is happening, what they should do or who someone or something is." This means that confusion occurs in one's thoughts, in the brain.

I define emotion as "an irritation of the heart" or simply "a heart feeling." By heart, I mean a physical heart. Emotion is a heart response to whatever irritates it: thoughts, memories, what someone sees or hears, etc.

So, if you say that confusion is about thoughts and emotions are about heart feelings, then confusion is not an emotion. Confusion may or may not be accompanied by emotions, for example, someone does not understand what is happening (confusion) and, as a result, feels fear in the heart (emotion).

I'm not sure if I want to classify confusion, but it is a "problem with understanding," not necessary as a "condition" but as a temporary or chronic state.


Can autistic savants beat computers in known computationally hard problems? I'm always amazed when the exceptional mathematical skills of some autistic-savant people hit the news. My question is: can they outperform a computer in problems which we believe too hard for even a computer to solve?

Of course I haven't heard that any of them could. But I'm not sure if that's because they fundamentally can't or just no one bothered to ask them right questions.

For example if I ask:

  Sir, can you tell me which two integer numbers I need to multiply to
  get this huge number?

  30885595542097078048530024995687899997024041750973847393477559897447391573878575270082706367139186728487020986897882643061865394945737579541836152606087611656762824124167456134969494253726435638776260179938318355412387553479545957502637298284851360234398784003069626709425392069487597686079260312041858526437519290451126677173785415389420329825181564012716675865830263098249948022195474980538298331998208615558178711421936619071576025836780179671597012185469978359221693046590783292027645460672357953215860301121762021294392026714148819989367905598842533973708083447918228276991009085148912935055442293643589623179239

Any chance they can ever come up with a correct answer?

It would be a world sensation if they could as the number above is the RSA 2048 bit SSL public key modulus of a website. Which is currently believed to be secure enough (no computers can break it in reasonable amount of time). And integer factorization is a know hard problem and the entire RSA cryptosystem depend on it.

People easily solve cognition, but number crunching isn't what the brain's optimized for. Current generation hardware easily beat any savant at numbers due to their optimization and clock speed.
Look at this and this on hashing. The brain simply can't beat these things (trivial?), let alone with harder problems?


What is a good textbook for an undergrad Cognitive Neuroscience course? I am slated to teach an undergrad Cognitive Neuroscience course next year and I am not sure which textbook to use. This would be an entry-level course (no pre-requisites) primarily intended for students in psychology and biology. There seem to be a lot of books on the market, so I'm hoping people will share their experiences (either as students or instructors) with whatever books they've used, especially why they liked or didn't like a particular book.  Advice about strategies for selecting a book would also be helpful.

I'm in an undergraduate course on Cognitive Neuroscience and have found the textbook we chose, Principles of Neural Science, to be helpful and illustrative.  Strictly speaking, cognitive neuroscience is the subject of but one of the book's sections, but if you are not requiring prerequisites I think it is appropriate to have the basics (and some possible extensions) included.


Difference between real time and old information processing in the brain Can we differentiate between the following two processes?

Brain receives information via senses, such as eye, ear, nose, skin and tongue. That is, vision, hearing, smell, touch and taste.
Brain stops receiving information via senses; but continuously keeps processing previously accumulated information from the mind: for instance, death of a loved one.

Is it possible?

Of course. You've differentiated the two already by describing two mutually exclusive processes. If you're looking for terminological differences that delineate theory along this distinction, it seems you're looking to distinguish perception from cognition as it exists and operates independently from the direct influence of sensation. Plenty of cognition does not involve sensation or perception directly. Metacognition is a sort of self-perceptive process that operates apart from sensation in the traditional "five senses" sense, but not all cognition even involves self-perception or conscious awareness of the cognitive processes in question. This may be debatable, but I would call perception a special case of cognition – i.e., cognition is the broader domain of mental processes that subsumes perception, but does not always involve it.

One might also argue that you've only described sensation in your first sentence, not perception. Perception refers more directly to the processing of sensory information that the brain has received, whereas sensation refers to all processes leading up to sensory information processing. Thus sensation may include the process of delivering sensory information to the brain, depending on whose definition you subscribe to. Cognitive processes only enter the equation once the information has arrived, because cognition refers to the processes carried out by the brain – mostly the higher processes, so (again, maybe this is debatable) not even what happens in the rest of the central nervous system. E.g., the optic nerves feed cognitive processes, but do not carry out cognitive processes themselves.

Summary: If your first sentence only refers to raw sensory information being conveyed to the brain before the brain does any work to process this information, then I don't think it describes cognition at all, whereas the second sentence describes cognition directly. If you mean to include the brain's interpretive process in the "receives information" step of the first sentence, then it describes perception, which is only one kind of cognition (or maybe also distinct from cognition by some definitions).


Methods to find patterns or correlations in MEA spike trains I am looking for methods currently used to analyze micro-electrode arrays spike trains and figure out patterns, as repeated sequences of activation or spacial correlations.

I know about ISI histograms, power spectrum, anda DNA-sequencing-like-algorithms, but I am looking for other methods, from statistics or machine learning.
Any recommendations of papers/books exploiting these methods?

This is a very broad question. There is a very large literature on studying MEA spike trains: some classic methods are probably already explained in books such as Dayan and Abbott's Theoretical Neuroscience.

If you're looking for "statistical modelling", i.e. describing properties of a network's activity without caring for its actual structure and dynamics, generalised linear models (GLM) are a common tool (see articles by Liam Paninski 2004, Jonathan Pillow 2008) and maximum entropy models too (Schneidman et al. 2006, Shlens et al 2006). This literature is still quite popular, although probably not as fruitful as a decade ago.

There are certainly other things that could be mentioned in this area, but I don't know them all, and it also fundamentally depends on what you're trying to do. Hope this helps.


Does perception have a "frame rate"? Are the objects of visual perception processes divisible into individual, still frames, like video is? If so:

Are the perceptions from different senses synced to the same frequency?
Are these "stills" instances of perceiving motionlessness?
Is the perception of motion based on pattern recognition between the stills?

There is no true frame rate of the eyes, but there are limitations.  The brain uses blurring to simulate continuity.  Films are shot at 24 frames per second; if you go too much lower than that, the film will seem choppy.  This is because the motion blurring process is too fast and it finishes "blurring" before the frame changes, so you just see choppy frames.  If it's a bit faster, suddenly the blurring occurs in a time frame on the order of the frame changing and it looks smooth.

Similarly, audio doesn't really have a frame rate, but there are limitations to what frequencies the sensory can transmit into neural code. ~(20 Hz - 20kHz).

So you do see some kind of frame rate for perception being plausible, and it turns out that higher-level perception rates are not fixed, but depends on the modality of the perceptions themselves:

  Recanzone has recently demonstrated that the perceived rate at which people judge a light to be flickering on and off can also be modulated by the rate at which a concurrent stream of auditory stimuli are presented

Even if there weren't a frame rate, due to differences in processing times between the two systems, there would still be a synchronization process required:

  Light travels through air far more rapidly than sound: 300,000,000 versus 330 metres per second. Differences in arrival time also occur for events that occur much closer to us, and yet we are rarely aware of them. Part of the reason for this is that the mechanical transduction of sound waves at the ear takes less time than that required for the chemical transduction of light at the retina. These physical and biophysical differences in the arrival time of light and sound cancel each other out when stimuli are approximately 10 metres from us, at the so-called ‘horizon of simultaneity’. Given most audiovisual events are not perceived at this ‘optimal’ distance, however, psychologists, neuroscientists and even philosophers have long puzzled over why the perception of multisensory synchrony should be such a pervasive aspect of our everyday phenomenology.

Spence, Charles, and Sarah Squire. Multisensory integration: maintaining the perception of synchrony. Current Biology 13.13 (2003): R519-R521.


Morita therapy - does it have a western counterpart? I have recently read interesting article about Morita therapy.
I have a hard time finding articles,books or research on this subject, and how it works in the West since this therapy was developed and mostly applied in Japan.

What is interesting about it : this therapy (or just Morita's philosophy) doesn't try to change person's feelings of fear/anxiety. It teaches person to understand his/her feelings and live with them. Doing things that need to be done despite fear/anxiety.

Does Morita's idea have western counterpart? Any free reading on it ? (something I don't have to buy) And is there any research paper on it that is reliable and accessible?

Any idea of something similar is welcome. :)

Reminds me a bit of existential therapy and humanistic psychology in general. Unconditional positive regard and motivational interviewing both insist on approaching undesirable feelings from the client's perspective without imposing fixes or changes on the person through pressure or blunt confrontationality. Existential theory even presumes major, inevitable negativity in life experience for which no individual could be blamed. There are plenty of terrible realities for every individual to face and accept in the process of adjustment and maturation. The individual must do this freely, idiosyncratically, and earnestly for oneself, or so the theory goes. Focus is not on eliminating negativity but on finding meaning amidst it. I hope these Wikipedia pages give you plenty to read for starters, but I can try to find more if you like.


Problem understanding the calculation of normative (Bayesian) base rates I am having trouble understanding Table 1 of Gigerenzer, Hell, and Blank (1988, PDF, table on page 516):

Focusing on the Jack row, it is stated that the mean probabilities of Jack being an engineer were 71.4% in a low base rate condition and 81.3% in a high base rate condition. Thus participants partially took base rates into account. If they were completely ignoring base rates these values would be the same, rather than being separated by 9.9%. So I believe I understand what is going on in the Base Rate Neglect column.

However, I don't understand what is going on in the Bayesian column. There is an explanatory footnote on p516 but to me it was not illuminating. The footnote provides the following equations:

$$p_{70}(E|D)/(1-p_{70}(E|D)) = L\frac{0.7}{0.3}$$
$$p_{30}(E|D)/(1-p_{30}(E|D)) = L \frac{0.3}{0.7}$$

So, since the mean guess for the 70% condition was 81.3% we get

$$
\begin{align}
81.3/18.7 & = L ~ 0.7/0.3 &  \\
      & = 81.3/18.7 & = L ~2.33 \\
      & = 4.35 &= L ~2.33 \\
      & = 1.86 &= L \\
\end{align}
$$

However, then when I plug this $L$ value into the $p_{30}$ equation I get a value for $p_{30}(E|D)$ that deviates wildly both from the 'Bayesian' value and from what was actually observed. According to the table the average deviation from the Bayesian should be 16.1%, but according to my calculations it is much higher. It would be greatly appreciated if someone could tell me what I am doing wrong.

References

Gigerenzer, G., Hell, W. & Blank, H. (1988). Presentation and content: The use of base rates as a continuous variable.. Journal of Experimental Psychology: Human Perception and Performance, 14, 513. PDF

I think you are doing the computation correctly, but Gigerenzer and Blank did not provide us with the full results of their experiment, preventing us from repeating their computations exactly: The data provided in columns 1 and 2 of the table are only the averages. The data in column 4 (Bayesian) is not a transformation of the average value using some formula (see below), but the original data transformed, and then averaged:

  For each subject in the 70% base rate group we predicted, by using Bayes's theorem, how this subject would have responded in the 30% base rate group

If you divide the first equation of the footnote by the second, and derive a formula for p30 as a function of p70, you get:

$$p_{30}(E|D) \approx \frac{p_{70}(E|D)}{5.44-4.44p_{70}(E|D)}$$

Notice that this function is strictly convex in the region [0,1], meaning that if you compute it on the average p70, you'll get a value that is lower than the value you would get by averaging the values for several data-points.

As an example, lets examine the Jack row: If you transform the mean p70 of 0.813, you get p30 of 0.44, which has a deviation of 0.27 from the observed mean p30 (as you probably found). Let's assume that the data in the Jack row, in the p70 column was obtained from two subjects, that responded 0.968 and 0.658 (yielding the average 0.813 that is reported in the table). Transform both of these values, and you'll get 0.848 and 0.261, respectively, yielding an average p30 of 0.553, which would give a Bayesian deviation of 0.161 exactly as reported in column 4.


How to estimate eye-in-head rotation (degrees of visual angle) from a 2D video of the eye? I am tracking eye movements in mice passively viewing naturalistic stimuli or experimental stimuli meant to elicit reflexive eye movements. I would like to define a transformation function that translates displacement in pixels (x, y) to degrees of visual angle (azimuth, elevation). Here is an example image:

I have seen this paper referenced several times in other papers that track eye movements in mice, but it seems like the position of my cameras relative to the eye is different than what is shown in the paper and I worry this will affect the validity of the transformation.
I have the ability to track any feature of the eye that is useful. Right now I am tracking the center of the pupil, the corners of the eye, and the center of the top and bottom eyelid.
EDIT #1
Here is a description of the camera's position relative to the animal. The solid black object represents the animal (A=anterior, P=posterior, D=dorsal, V=ventral). The angle from each orientation represents the angle from the animal to the camera.

In theory you can use the geometry of your setup to transform your data to the orientation reffered in the paper you mentioned using Scheimpflug Principle and then use the methods provided in it.
Practically, you can only approximate the geometry of your setup. If you have some idea about angles in something like this

please let me know, I might be able to do the math for you.
EDIT: The lens plane is parallel to image plane in cameras so now it is just the question of orientation of subject plane and lens plane(camera plane).


Do cats exhibit the bouba/kiki effect? I was fascinated when I first read Ramachandran's article about kiki bouba effect, and I was wondering if cats experience the same thing... As Ramachandran proved, our angular gyrus is responsible for this phenomenon, and I found a part of cat's brain, named FAES, which has neurons that spike for auditory and visual stimuli. Does anyone know if they experience it?

The bouba/kiki effect is the phenomenon that about 95% of subjects assign the name bouba to a blobby form, and the name kiki to a pointy shape (Fig. 1).

Fig. 1. Kiki and bouba, at least in 95% of the people. source: Synesthesia Test

It is thought that the reason behind the strong preference is that the sharp changes in visual direction of the lines in the left-hand panel in Fig. 1 mimics the sharp phonemic inflections of the sound kiki, as well as the sharp inflection of the tongue on the palate. Ramachandran poses that the bouba/kiki effect provides a clue for understanding the origins of proto-language, for it suggests that there sounds are mapped on to objects. Ramachandran poses that the representation of certain lip and tongue movements in motor brain areas are mapped in non-arbitrary ways onto certain sound inflections and phonemic representations in auditory regions and the latter in turn may have links to an external object’s visual appearance. These factors may have co-evolved, forming
a possible origin of proto-language (Ramachandran & Hubbard, 2001).

To get to your question: cats can't talk. Their vocalizations are relatively restricted, adding up to 16 different sounds. They include the familiar meows, hissing when angry and purring when happy. The purring comes from deep within the body and isn't related to speech at all. The hissing sounds a bit like an /h/ and the meows include more varieties. However, the variability in 'meows' is largely due to intonations (source: The Independent), and not so much the phonemes. Phonemes are: '[...] sound[s], or set of similar speech sounds, which are perceived as a single distinctive sound by speakers of the language or dialect in question. For example, the "c/k" sounds in cat and kitten represent the English phoneme /k/.

Human speech is extremely diverse and is produced by the interplay of various organs, includes lip, tongue and glottal movements that change the way the vocal cords produce sounds. There are 36 phonemes (speech sounds) recognized in English.

The bouba/kiki effect hinges strongly on the phonemes /b/ and /k/ and, perhaps, /i/ and /ou/. Both in Ramachandran & Hubbard's experiment (bouba/kiki) (Ramachandran & Hubbard, 2001) and the original study by Kohler (baluba/takete) (reviewed shortly in Ozturk et al. (2013)).

Cats don't have that kind of repertoire of phonemes. So regardless the similarity in some brain areas, I dare to say a bouba/kiki or baluba/takete effect can never be found in cats. I realize this is a rather mechanistic approach to the question and I am indeed not saying that cats cannot experience synesthesia. But that's another question...

References
- Ozturk et al., J Exp Child Psychol (2013); 114: 173–86
- Ramachandran & Hubbard, J Consciousness Studies (2001); 8(12): 3–34


Why is it that some (yet not all) people may struggle to retain information unrelated to what they are interested in? It seems to me that some people find it difficult to retain information that is not naturally salient to them. This isn't the case for all people, however. There exist people that will put in the effort to retain and use information related to material that is inherently uninteresting to them, particularly in a school setting. Is it the case that the latter group has more of a conscious control over what is salient to them at the time? Is this phenomena 'traceable' in the brain?

Preface

Your question can be phrased as: what controls storage of information in Long-Term Memory? And more specifically, declarative memory? And one answer to this is one of my favourite stories in neuroscience.

In the following, I'm ignoring a lot of important aspects about memory - especially the difference between encoding, consolidation and retrieval. But I hope it still answers the question.

Psychology of memory

We generally distinguish between two forms of memory. Procedural memory is about sequential, a-then-b type of stuff - for example, movement patterns, like dancing, or calligraphy. There's basically only one way to get stuff into procedural memory: grind it in there. Do it a lot. Do it so much, it stops being under conscious control, and submerges into cerebellum and motor cortex. This is so for everyone; even the people who're absolutely the best at some sport or instrument will practice day after day after day to really get it down, to effortless perfection.

The other kind is declarative memory. This is a-is-b memory; the three branches of government are judiciary, legislative and executive, and the dorsal stream is where and the ventral stream is what, and your wedding anniversary is on 11.9. and so on. In contrast to procedural memory, declarative memory is conscious and controlled, it's largely subserved by different brain areas, and it is acquired in a much different way.
If you want to learn to rumba, you got to learn to rumba a lot. But when you're at the [book store/nightclub/sports venue] and the most attractive [boy/girl] you've ever seen walks by, and up to their friends, and is greeted with "Hi Alex!", you'll immediately store that name. You won't have to listen to the friends say "AlexAlexAlexAlexAlex" again and again. You'll hear it once, and remember it immediately, and possibly forever.
This is because you're aroused.
Roughly the same thing happens if you eat something and get extremely sick afterwards, or if you get a shock after pushing one lever, and a treat after pushing the other. Why? Your arousal - be it positive, or negative - is high. Metaphorically speaking, your brain thinks "whatever is going on right now seems to be important, I better store what's going on".

One cool experiment in that regard I can't find the citation for right now goes like this: students saw either a neutral video, or a disgusting surgery video after the lecture. A few weeks later, those students who had seen the surgery video did significantly better on those questions of the exam relating to the lecture after which they'd been shown the video. Another example is how so many people know what exactly they were doing on 9/11, when they heard the news. Do you remember what you did two days before? 7? But 9/11 was uniquely arousing.

The reverse is, of course, that we don't remember boring stuff. You remember Alex' name, but not their 7 homely friends' names. You remember every detail of Star Wars: Empire Strikes Back, but not your math classes - or a boring movie (what was the plot of Star Wars Episode 2?). And why would they? Evolutionary speaking, there is very little point to storing memory about low-arousal situations; if they had been important, they would have been arousing, right? Memory formation is costly, so we only do it when we (think we) have to.

Individual differences

And that's the gist of it, really: low-arousal situations are not conductive to declarative LTM formation. And the stuff we study is very often low arousal.
Now to get it right, there are two options. The first is: be aroused! If you truly care about math, you will remember this stuff. It will be much easier to memorize information you actually care about. And this is one way by which people differ: some are more, some less bored by abstract, complicated information.

The next one is that our ability to focus obviously differs. Some people have short attention spans, some longer attention spans. A bit simpler than your question about salience, simply paying attention vs. not paying attention makes a huge difference, and some people are much better at paying attention to boring stuff than others. These people are often much better at reading something boring again and again. Because the situation is low-arousal, chances of encoding are still bad, but better than when you don't look at it, and eventually, it'll get there via mere exposure.

That is, then, my answer: two main factors concerning inter-individual differences in declarative LTM formation are 1. different propensity to find abstract, complex information interesting/boring, 2. different ability to study even though something is boring.

Neurological substrate

Surprisingly, the neurophysiology of this is relatively well understood. "[E]ntry of information into long-term memory", as the title of Lisman & Grace's paper goes, is mostly controlled by two sets of brain structures: an interaction between the medial temporal structures, especially the hippocampus, that controls the encoding of memories, and the mostly subcortical systems signaling salience and valence of events. The neighboring amygdala as the coder of valence, and, most importantly, the subcortical VTA (dopamine source) and the Locus Coeruleus (norepinephrine source) tell the hippocampus to "open its gates" for declarative memory formation in arousing contexts, to arousing stimuli. These systems are of course also generally relevant for setting the "tone" of the brain - from aroused to lethargic; this is under the control of the Locus Coeruleus. So, what's out there - arousing, novel, salient stuff? Dopamine/Norepinephrine up, hippocampus "gate" open, declarative memory in. Boring situation? Dopamine/Norepinephrine down, hippocampus shut.

You can still learn to rumba though. Just do it a lot. You don't need the hippocampus for that (as HM's ability to acquire new motor patterns shows).

Some references

Neurophysiology

Lisman & Grace, Hippocampus-VTA Loop/Dopamine

One specific experiment showing Dopamine is crucial for LTM persistence

Sara & Bouret, Locus Coeruleus/Norepinephrine

Psychology

Arousal and memory

Single-exposure rich memory formation for arousing events

And another one, for 9/11


Is Maslow's hierarchy of needs really accurate at labeling sex as a physiological "need"? Is Maslow's hierarchy of needs really accurate at labeling sex as a physiological "need"? If so, would that mean that single/celibate people cannot live self-actualized lives unless they have some sort of sexual outlet (e.g. masturbation)?

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

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

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

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

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

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

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

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

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

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

Need-Status Notwithstanding, Is Sexual Desire Primarily Physiological?

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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


Are humans biologically wired to lie? Are humans biologically wired to lie? It seems that people create morals and decree that lying is bad. Yet everyone has lied before. Why is this?

Young children often learn how to lie before they have truly developed a sense for what it is, or why it may be unethical. This is demonstrated by the propensity for children to tell exaggerated and implausible lies, as young children may not yet have a sense of social cognition (or 'theory of mind'), and thus do not yet understand what others may find believable.

A child who examines another adult lying will understand that the adult is not telling the truth, but will see that the achieved effect is often in favor of the liar. Thus they will learn that disguising the truth can achieve a certain (often favorable) result. Like all negative behavior, if the child learns that lying has more negative consequences than positive ones, they will be less quick to demonstrate the behavior.

Despite recognizing it as an unethical behavior, people may still choose to lie out of fear, or to defend from the consequences of truth telling. Lying can also be a pro-social attitude to spare the feelings of another, thus avoiding conflict and preserving civility in human relationships.

From a neurobiological standpoint, there may be parts of the brain that influence the decision to lie. One study showed that pathological liars had increased white matter volumes in certain regions (namely the orbitofrontal, inferior frontal, and middle frontal cortices). [1]

Sources used:

[1] Yang, Y., Raine, A., Narr, K., Lencz, T., LaCasse, L. Colleti, P., Toga, A. (February 2007). "Localisation of increased prefrontal white matter in pathological liars." British Journal of Psychiatry, 190, 174–175.


Link between reading news and deteriorating mental health? Given the prevalence of negativity and sensationalism in the news, I suspect individuals are also varyingly susceptible to (worsening) mental health issues arising from prolonged exposure. Perhaps as reports of distant events accumulate as an overall negative impression of the person's environment.

Research clearly shows that both nature and nurture play important roles in the genesis of psychopathology. (Tsuang, et al. 2004).

Have there been any studies at all investigating the significance of news as part of that environment as a cause of mental disorders?
References
Tsuang, M. T., Bar, J. L., Stone, W. S., & Faraone, S. V. (2004). Gene-environment interactions in mental disorders. World Psychiatry, 3(2), 73.  pmcid: 1414673

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

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


What are the methods to reject ocular artifacts in the EEG? Is there any way to remove ocular artifacts from an EEG signal, other than applying independent component analysis, or manual rejection?

According to a review by Croft & Barry (2000), a number of possible methods exist to prevent, or reject ocular artifacts in the EEG;

Prevention/reduction of artifact instances

Recording with eyes closed -
A very effective method, but eye closure alters the EEG, e.g., it increases alpha band activity;
Let subjects fixate on a target -
Method reduces blinks, but does not eliminate them.

Rejection

Exclude trials with amplitudes larger than, e.g., 50 microV  -
Method works only with a trial-based approach; artifacts below criterion level will remain.

Reduction

Subtract a certain standard voltage when an artifact occurs  -
A crude method;
Online attenuation of the EEG signal when an artifact is detected  -
Works better as the former technique, but is still crude;
Regression techniques where different electrodes are used to estimate the artifact component in other electrodes  -
A more sophisticated method with apparently good results.

For details I refer to Croft & Barry (2000) and the primary literature cited therein.

Reference
- Croft & Barry Neurophysiol Clin (2000); 30: 5-19


Can I teach my brain to understand binary? The question is if I could teach my brain to understand binary codes (for example, ASCII) just like I teach it to understand English, French or any other language.

That includes:

not to translate it each time I read some binaries, like 01100001 01100010 automatically reads 'ab'.
understand both written, pronounced and somehow sound-coded form (like Morse)
write and say it naturally

The idea is not to teach computer speak to people, but to teach people speak to a computer in his language. In general, human brain can be taught anything. It is a programmable computer. However, you can only program it very slow. If you can teach your subconscious to multiply numbers, why can't you teach it to encode MD5? Or decoding HTTPS data given a key? Even bruteforce?

So the question is if there are any researches on the topic, or the people who tried such learning? Are there any techniques? Also, what if we teach a 2-year old child this language, will it be natural for him just like the English is natural for English-grown child?

P.S. Some upgrade of this idea is to place some radiowaves-to-soundwaves direct converters and "listen" to the radiosignals around you. Somehow "spy" on neighbours Wi-Fi.

P.P.S. I've asked this questions on datascience stackexchange, and the community suggested moving it here. However, it is also moved to lifehacks, where I received a few answers: https://lifehacks.stackexchange.com/questions/7575/can-i-teach-my-brain-to-undersrand-binary/

Quite a bit of foundational research on skill acquisition is on how people learn to send and receive morse code. I'm no expert at morse code but it seems like it shares quite a bit with binary.
For example, here is a graph of letters per minute that an operator could receive as a function of weeks of practice (Bryan & Harter, 1897).
A general principle is that gradually people move from identifying letters to seeing larger patterns like words and phrases.

Reading is a little different to receiving information aurally. But I imagine some similar principles would apply. If anything, I imagine that ability to recognise patterns visually would make the task of reading binary easier. That said, binary does seem far from optimal as a system for encoding letters in terms of efficient visual processing.
Bryan, W. L., & Harter, N. (1899). Studies on the telegraphic language: The acquisition of a hierarchy of habits. Psychological Review, 6(4), 345.


Importance of interactivity in learning Not sure if this is the right place for this question that I find hard to formulate in the first place...

In a paper, I'd like to argue that interactivity helps to develop an understanding of a thing. This is in context is astronomy, scientists learning about the universe basically. I'd like to argue in favour of interactive data exploration. This is not going to be a psychology paper. To put it bluntly, I'd like to better understand this to write the motivational section, use the proper terms, and have a nice citation I can put at the end of it :)

Let me try to explain what I'm after.

Google Maps analogy:

Interative maps give an overview of the world and then allow the user to zoom in, pan around and look at streetview pics. If this information would be presented in a non-interative way, say a box you can put coordinates in and you get the streetview picture out a minute later, the user would not just be slower, but would not be able to explore and understand the world in the same way that interactive maps allow.

Slider analogy:

Say you have two parameters and an result value that results from it due to some hidden math. If I give you two sliders, you can play around with them and develop a sense for the correlation easily, a child would get an intuition for it. But if I give you a form where you have to type in two numbers and press a button to see the result, it be almost impossible to develop the same level of understanding.

I think that the instantaneous feedback and the ability to 'play' with it, really make it far easier for us to learn.

edit:

Has there been some study of this kind of learning? Does it have a name? Where would I start to research this? How do I go about arguing that interactivity offers a great benefit to explore, say, a dataset? That interactivity offers more than just the efficency gained from less waiting for results.

You can attack it from many different angles.

Perhaps a good place to start is the distinction between the behaviourist and cognitive learning theories. Although both can be facilitated using interaction, behaviourist theories put the teacher as the focal point, whereas cognitive ones put the learner first. In that respect, a good interactive learning design will give learners more control over the learning experience. I also believe you can demonstrate that interactive learning has greater potential to be mapped to experiential learning (see Kolb Cycle for instance).

Another related topic is that interactive learning based on self-exploration is likely to result in higher intrinsic motivation compared to guided learning.

Another line of argument can many aspects of interaction that can aid cognition (or reduce cognitive load, if you wish) - A book (non interactive) is a get-it-or-leave-it type of delivery; interactive systems enable techniques such as progressive disclosure or contextual help which can markedly improve comprehension.

Perhaps important to assert that interactive learning, on its own, does not secure better comprehension - the experience design is what really matters; interactive learning can simply enable features that non-interactive learning cannot.

You should be able to find some research papers on the topic via Google Scholar.

These are just a few leads.


What is the neurophysiology of a thought? PURPOSE

1) To find out if there is evidence in favor of one of Hebb's claim. In is book "The Organization of Behavior" he claimed that cell assemblies are the physiological foundation of thought. According to Sebastian Seung, in his book "Connectome: How The Brain's Wiring Makes Us Who We Are", a  thought is an association of ideas.

  Is there evidence that support Hebb's claim?

2) In addition to (1) I want to know in which other ways Hebb has contributed to neuroscience. I have provided some examples below.

  So, please leave links to research papers that support any other claim he has made.

BACKGROUND

The Organization of Behavior

"The Organization of Behavior - A Neuropsychological Theory", by D.O. Hebb, is one of the classics in the field of neuroscience, as you may know.

Hebb wondered about the nature of thought, and how ideas might be represented in the brain.

He was puzzled as to why the intelligence of some individuals remained intact after brain surgeries, where  a large part of their brain was destroyed.

In his book, it is suggested, that these high IQ scores were

  "due to a conceptual development which brain damage does not easily reverse."

Given these observations, Hebb asked:

  "... what is a concept physiologically ...?"

Which then prompt Hebb to claim that cell assemblies were the physiological basis of a concept/thought.

Hence, my question:

  Is there any scientific evidence that support that the cell assembly is the basis of thought/a concept?

HEBB'S CONTRIBUTION TO NEUROSCIENCE

Some of his ideas have been confirmed; for example, in "Biological Psychology",Breedlove, Watson, Rosenzweig, teach that memory storage requires neuronal remodeling. This finding is grounded on Hebb's observation, which was confirmed by Kelso and Brown, 1986, that

  "Ensembles of neurons, or cell assemblies, linked via synchronized activity of these Hebbian synapses, could then act together to store memory traces."

The above observation is related to the maxim:

  "cells that fire together wire together."

Hebb's hypothesis about how synaptic connections grow stronger or weaker in response to experience gave rise to the idea of Hebbian synapses.

A Hebbian synapse is a synapse whose strength depends on its effectiveness in driving the postsynaptic cell; for example, cells during visual deprivation do not fire together; consequently, they do not drive the postsynaptic cells. In turn, the synapses get weaker, i.e., less sensitive.
In contrast, if cells are stimulated by the visual field, cells fire together, driving postsynaptic cells. This in turn strengths synapses.

REFERENCES

Biological Psychology: An Introduction to Behavioral, Cognitive, and Clinical Neuroscience, Sixth Edition, Breedlove

Organization of Behavior - A Neuropsychological Theory, Hebb

Connectome: How The Brain's Wiring Makes Us Who We Are, Sebastian Seung

Hence, my question: Is there any scientific evidence that support that the cell assembly is the basis of thought/a concept?

This paper Thinking in circuits reviews this matter in detail, and its references can provide more related scientific evidence.

Question: What is the neurophysiology of a thought?

I think the following papers can provide some current information about the neurophysiology of thought:

1.How neurons make meaning

2.Brain Networks and Cognitive Architectures

3.Language and thought are not the same thing


Does a short nap improve learning efficiency? When one attempts to learn a new skill (e.g., play a guitar), it is often heard that the first hour of practice is more effective than the second. I have heard some people say that even 10 minutes of practice may be effective when you do so everyday.

On many (non-scientific) websites I have read that taking a little nap of 15-30 minutes during prolonged practice is enough to maintain effective learning. Is this true, or is more sleep required? Or is sleep irrelevant altogether?

Naps may help if you are so sleepy that you can't focus in learning/training anymore. More importantly however, even a short sleep gives start for the memory consolidation process. So all the things you learned before the nap, get better shielded against the new conflicting or overlapping information in future. Especially in procedural learning (e.g. fingers on guitar chords), which is slow, gets important boost by a training -> consolidation -> training -> consolidation loop. Deep sleep (slow wave sleep at night) is more important, but already nap with light sleep phases (state II with k-complexes) will help.

You can search research papers for "memory consolidation" and "sleep".


What is a reliable physiological measure  (e.g., serotonin levels)  of positive affect? Is there a reliable physiological measure or correlate to positive affect?
What does research say on this?

I thought that serotonin levels are correlated with self-reported happiness levels, but, after a google scholar search I am not so sure.
I tried google scholar and couldn't find any papers reviewing/summarizing multiple experiments. I only found a whole lot of papers with vague sounding titles than what i am looking for.

EDIT 1: Replaced happiness by positive affect. As Geek on Acid pointed out happiness is too general.

First - you might want to redefine you search. Are you looking for happiness or rather  positive affect? Happiness is fairly ambigious term, and it's much more associated with positive psychology studies on well-being. If you are interested in more global definition of happiness, check the work of Mihaly Csikszentmihalyi.

On the other hand, there is a large number of studies on physiological measurements of positive affect.

One such physiological measurement is Electromyography (EMG) - recording the electrical activity produced by skeletal muscles. EMG will detect very brief smiles or higher activity in cheek muscles (zygomaticus major) which are correlated with positive affect. There is quite classic (but very quoted) paper on that:

  Cacioppo JT, Petty RE, Losch ME, Kim HS. (1986) Electromyographic
  Activity Over Facial Muscle Regions Can Differentiate the Valence and
  Intensity  of Affective Reactions. J Pers Soc Psychol., 50(2):260-8. download

Another simple physiological assesment is heart rate measured by the interbeat interval (IBI). For example, study by Brosschot & Thayer (2003) shows that heart rate response is longer after negative emotions than after positive emotions.

  Brosschot JF, Thayer JF. (2003) Heart rate response is longer after
  negative emotions than after positive emotions. Int J Psychophysiol.,
  50(3):181-7.

In fact, the full spectrum of somatic measurements have been used along heart rate including pulse transmission time to the finger, skin conductance level or pupil dilation (Partala, 2003). All those are a bit less reliable methods and usually they detect arousal rather then indicate physiological differences between positive and negative affect.

  Partala T.; Surakka V. (2003) Pupil size variation as an indication of
  affective processing. International Journal of Human-Computer Studies,
  59(1):185-198. download

Finally, I would advise browsing literature on measurements of negative affect. You are likely to find some interesting methods there, like in this paper on the psychophysiology of crying (Gross et al., 1994).

  Gross JJ, Frederickson BL, Levenson RW. (1994) The psychophysiology of
  crying. Psychophysiology, 31(5):460-8. download


Does "hearing" give off an electronic signal? I'm thinking in terms of the middle ear and the very intricate and tiny bones that process a "sound wave" into "what we hear." Is there an output to the middle ear ossicle chain bones such that a signal is being sent from the ears to outside of our body too? If so what is that frequency?

No there isn't any output for these bones other than mechanically pushing against the oval window.

In short:

Sound waves travel through the ear canal.
They hit the ear drum (Tympanic membrane).
The three bones (ossicles) in our middle ear are simply an impedance matching device (very much like gears on bicycles). They amplify the ear drum movement with the Stapes pushing against the oval window (part of the inner ear).
The mechanical movement of the stapes against the oval window causes liquid within the Cochlea to oscillate.
Within the Cochlea there are tiny hair cells that discharge (snap) in response to a specific frequency/amplitude (See this answer).
When discharge, a nerve pulse is sent to our brain.


Day and month of 1980 DSM-III publication I cannot for the life of me find the exact date -- day, month, year -- for the original DSM-III publication. The Google Citation, Amazon info, APA page, and others only list 1980. Does anyone know? Thanks.

At this present moment I cannot find full date information, but looking at a copy of the DSM-III I have found, on the bottom of the 3rd page of the PDF it points out:

  First Printing, February 1980
  Second Printing, May 1980


Studies on the appreciation of works of art I am interested to know if the concept of a decreasing appreciation of a work of art through increased exposure to it exists, specifically:

Does this idea exist and is there a term for it ?
Have any studies been performed around similar ideas ?

For example, if one hears a Beethoven symphony for the 1st time, the listeners reaction may be much more positive as opposed the 100th time.

Many thanks in advance

There was a target article published in Brain and Behavioral Sciences on a theory of art appreciation (Bullott & Reber, 2013) that I read for some reason…but it looks like it will finally be relevant!

According to this theory, one of the ways that you might come to appreciate art is through basic exposure, which involves perceptual exploration of the artwork independent of your knowledge about its art-historical context. Exposure alone is not responsible for art appreciation; rather, it triggers a set of cognitive processes, whose nature determines your experience of aesthetic pleasure or displeasure.  This includes the ease with which you can process the artwork (i.e., processing fluency; Reber, Schwarz, & Winkielman, 2004) and the artwork's (un)predictability (Hogan, 2013).

With more exposure to the artwork, processing fluency increases, and so does your appreciation of it. However, over time, you also become more habituated to the artwork, view it as less salient, and appreciate it less.  This is akin to liking a song at first, then hating it after it's blasted on the radio 1,000 times. Indeed, repeated auditory exposure is associated with reduced emotional reactivity and reduced activation in a network involving the amygdala and certain cortical areas, thought to represent affective habituation (Mutschler et al., 2010).

Hogan (2013) thus suggests that the longevity of your appreciation for artwork depends on a mixture of predictability (fluency) and unpredictability. There are other variables like art-historical knowledge that influence liking over time, as well (Bullott & Reber, 2013).