# Question
Title: Why is chess considered special for educating a mindful person?
I can find countless quotes like this

> In many countries chess is incorporated into the scholastic curriculum. Countless researchers and studies have shown over the years that chess does indeed strengthen a child's mental clarity, fortitude, stability, and overall health. In this technologically driven world, chess helps aid in the synthesis and growth of certain areas in the brain and mind where many children can benefit as they grow older from the game. "It's all condensed in a playful manner in a game format and it's extremely fascinating because first of all I'm in control of my own destiny, I'm in charge. You have to be responsible for your actions, you make a move, you had better think ahead about what's going to happen, not after it happens, because then it's too late. Chess teaches discipline from a very early age. It teaches you to have a plan and to plan ahead. If you do that, you'll be rewarded

These beilefs are so strong that even got a recognition in Wikipedia.

Here is another quote to highlight the gist of my question

> Chess has a unique and strong brand attribute, in that it is generally perceived that playing chess and being smart are connected.

I do not ask if chess really improve the mental performance. I am asking `Why are they considered unique/unmatched` in this respect? Almost any game demands strengthening your intellect for careful planning of your moves. Why other games are less useful?

# Answer
Chess is considered "special" due to certain attributes of the game. From "Beyond the 64 Squares: Does Chess Instruction Enhance Children’s Academic and Cognitive Skills? A Meta-Analysis":

> Two main explanations have been adduced to support this hypothesis. First, chess requires decision-making skills and high-level processes (such as acquiring and selecting relevant information from a problem) similar to those used in mathematics and reading (Margulies, 1992). Second, since chess is a demanding task involving focused attention and problem solving, playing chess should strengthen these cognitive abilities and thus be beneficial for children's school performance (Bart, 2014).

However, this consideration is only marginally valid. In "Enhancing Creativity in Children by Imparting Chess Training" the increase in mathematical skills from Chess was compared to mathematical instruction and playing the game Go. Although Chess outperformed Go, thus cementing it's "specialness", it did not beat basic mathematical instruction.

In conclusion, Chess is a bit "special" among games in terms of cognitive improvement, however it doesn't beat actually doing a task and it seems unlikely for any other game would be superior.
> 3 votes

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

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

# Answer
> 10 votes
There is a fairly recently recognized medical condition called stress-induced cardiomyopathy, associated with chest pain and physical damage to the left ventricle:

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

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

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

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

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

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

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

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

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

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

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Tags: social-psychology, emotion, pain
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title: Cognitive models for transfer of skills

text:
# Question
Title: Cognitive models for transfer of skills
Recently a question was asked about the benefit of playing chess on cognitive abilities. More specifically, how chess would improve understanding technical texts. Many other questions are also focused on learning and skim the topic of transfer of learning (e.g. Does learning one discipline improve performance in another discipline?, Why is training better when following an easy-to-difficult schedule?, How does task difficulty schedule affect the rate and efficiency of perceptual learning? ). However, it is not entirely clear to me how transfer can be explained, independent of the type of tasks.

**What does recent scientific research say about transfer of skill, or are there cognitive models that help explain it?**

# Answer
## Short Answer

A cognitive model is made that decomposes any skill in smaller elements or production rules. These elements (or combinations thereof) are often context independent and can be used for multiple tasks. The requirement for transfer of skill is that the tasks need to have some sort of overlap in how it is performed.

## Long Answer

I found a cognitive model that tries to explain how transfer works (and thereby acknowledges its existence). The theory is called primitive elements theory of cognitive skills (PRIMs; Taatgen, 2013). The model is implemented based on the ideas of the cognitive architecture ACT-R. I will not go in to that too much, but in Figure 1 is the PRIMs representation of ACT-R:

According to PRIMs, each production rule represents part of a cognitive task. While initially each production rule is a separate cognitive step, with learning you can accumulate these production rules into one (See Figure 4 for an example).

The idea is that some of these elements (gray and white ones) are context independent. Steps like "check for empty working memory" and "check for visual input" are used in almost any task that requires visual input. Being context independent makes it not necessary to learn this over and over for every new skill you want to learn. The final figure (Figure 9) shows how counting, or to be more precise, an iterative component of counting, can be transferred to a Semantic task (answering questions like "is a canary a bird?"). **The essence of transfer is thus that the tasks need to have some overlap in how the task is performed** (in terms of basic cognitive elements).

Taatgen, N. A. (2013). The nature and transfer of cognitive skills. Psychological review, 120(3), 439. ISO 690
> 5 votes

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Tags: cognitive-psychology, learning, transfer
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# Question
Title: What are shortcomings of query bases tools for measuring Situation Awareness?
A review compared many different ways for assessing Situation Awareness (SA), such as query based tools, external observers and self-report tools.

The paper argues that query based tools, such as the SAGAT (Endsley, 1988) and the (SPAM; Durso et al., 2004), are the most reliable way of assessing SA, compared to the other methods. **What are the shortcomings of these query based methods, however?**

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## References

Durso, F. T., Dattel, A. R., Banbury, S., & Tremblay, S. (2004). SPAM: The real-time assessment of SA. A cognitive approach to situation awareness: Theory and application, 1, 137-154.

Endsley, M. R. (1988, May). Situation awareness global assessment technique (SAGAT). In Aerospace and Electronics Conference, 1988. NAECON 1988., Proceedings of the IEEE 1988 National (pp. 789-795). IEEE.

Endsley, M. R. (2013). Situation awareness-oriented design. The Oxford handbook of cognitive engineering. Oxford University Press, New York, 272-285.

# Answer
## Short Answer

The SAGAT is incredibly intrusive and relies on the subjects' memory, which is fallible. The SPAM is less intrusive and is less dependent on the subjects' memory. However, it is difficult to match the SPAM questions to the decision making process of an operator. More complete explanations of the methods can be found in papers of Pierce (2012) and the review of Endsley (2013).

## Long Answer

**SAGAT**
The most well known query based tools are the Situation Awareness Global Assessment Tool (SAGAT; Endsley, 1988). The SAGAT is used by periodically asking a set of questions about the situation at hand, thereby covering each of the three levels of SA (See Table 2 for examples in the Train Traffic Controller domain). The amount of correctly answered questions is the measure for the quality of SA.

* The main drawback of the SAGAT (or any query based method) is that situation specific questions need to be formulated. The researcher must thus know what will happen in the simulator and how the subjects will try to gain SA and tackle the problems.
* Secondly, the SAGAT requires that the task is frozen for a while. The task is thus incredibly intrusive and is not well suited for field studies, because you cannot pause the task in real life. In simulators, the freezes may greatly impact the flow of the task and, subsequently, how the task is performed.
* Beside the freeze, the screen is also made blank, to prevent the subject from looking up the answers. The subject is thus entirely reliable on his memory. Memory is fallible, however, and it may very well be possible that the subject was aware of a cue a couple of minutes ago, but at the moment the SAGAT questions are shown not anymore. On top of that, it isn't even necessary to remember every piece of information; the operator perceives the information, acts on it, and can then forget about it an focus on other parts.
* Finally, with the SAGAT you only get a general idea of one's SA, because of two reasons: (1) without asking hundreds of questions you cannot capture the entire SA of the operator and (2) you only get one score of SA (the sum of correct answers). In other words, you will never understand how SA varied throughout the task.

**SPAM**
In an attempt to simplify SA measures, Durso et al (2004) developed the Situation Present Assessment Method (SPAM; see also Pierce et al, 2012). The SPAM uses the same questions as the SAGAT but presents them while the task is ongoing. Instead of a large list of questions, only one or two questions are presented at a time. The questions are in general presented every two to three minutes. The correctness of the answers plus the response times (RTs) are measures of SA. The idea is that when RTs are short knows (where to find) the answer and is therefore aware. Conversely, when RTs are long, the operator did not know the answer or where to find them, and is therefore considered to be less aware.

* The first and foremost shortcoming of the SPAM is that it is extremely difficult to formulate the questions and plan them at the right moments. Decision processes may vary between subjects. Some questions may thus be shown too early for some subjects (they had not attended that information yet), whereas it would be too late for others (it may have been forgotten already).
* Moreover, some subjects may find the content of the question irrelevant; One's SA may thus differ from another, which is not necessarily better or worse. One or two question can also impossibly capture the entire SA. To minimize these issues, it is again extremely important to understand what happens in the scenario and how the subjects will tackle the issues.
* The temporal resolution is also still lacking. Only one or two questions can be asked every two-to-three minutes. Although this is much better than the SAGAT, it still leaves room for a lot of interpretation.
* Finally, because the questions are presented while the task is ongoing, it can greatly increase the amount of workload. Moreover, it may fundamentally change the dynamics of the task; the questions may probe the subjects to focus on particular aspects, thereby losing the natural way of performing the task.
> 1 votes

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Tags: measurement, methodology, human-factors, situation-awareness
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# Question
Title: Can people improve their memory by training themselves to recall previously forgotten memories?
Apparently, somebody has recalled previously forgotton memories and become able to speak fluent french after a coma. I'm wondering if people can also train themselves to be good at recalling previously forgotten memories by training themselves to recall information they've forgotten that there's a record of.

For example, if a cell phone gets invented where you can type in somebody's name and then type what their phone number was and when you want to phone them, you have to go to their name and then start typing digits from beginning to end from memory and as soon as you type a digit incorrectly, you get notified and then you have to type that digit followed by the next digit and will be notified when you do so correctly, I wonder if the people using it would train themselves to recall memories of what phone numbers were.

I wonder if people would become even smarter if some of the memories they trained themselves to recall were memories from before they started the training because that way, their brain has to form complex connections in order to recall memories that were lost in the brain than to just not forget stuff they learn from then on. That's probably because lost memories get scattered to unrecognizability in the brain but that doesn't mean there isn't a complex method of extracting the memory from the disorder. Maybe unlike the man in the previously linked video who thought he was somebody else, with sufficient training, they'll learn how to properly extract their past experience correctly from the disorder and have undistorted memories. Maybe getting an actual defect in the connection suppressing ability making you do something like only have suppress unimportant connections from an accident like in that video could make it so easy to recall previously forgotten memories cause of not suppressing the connections for extracting them that much and be superior to any possible training to recall previously forgotten memories because you'll be hyper-aware thinking about a large amount of your past all at once because it's just as easy as thinking about a single past experience because the memories of the individual experiences were already lost in the brain, and the you can recall memories that were even more badly lost with the defect in the connection suppressing ability than you would with training alone.

I wonder if in general, it's easier for autistic people to train themselves to recall previously forgotten memories.

# Answer
Memory is not fixed - it is very plastic. If you look at Amnesia, there are many different causes and many different ways it can manifest itself. It can also be anywhere between mild and severe. There are methods which can be used to try and prevent further memory loss - by abstaining from alcohol when it is caused by alcohol abuse such as with Korsakoff's syndrome, by using diaries, calendars, wall planners etc. But just like with Alzheimer's Disease there is no effective (and ethical treatment) for memory loss.

Which brings me onto the ethics of memory recall therapy or training. If you look at studies into memory and PTSD (Post Traumatic Stress Disorder) \- also found in category F43.1 in ICD-10 \- methods used to try and help sufferers to remember the traumatic events for this example, have been found through research to cause False Memory Syndrome. Although as with many pieces of research, there are opponents to the idea.

From what I know, and believe from looking at research, once memory is lost, it is lost for good. You may recall parts of the memory through various ways but to **try** and recall the whole memory can lead to a change in what actually happened as @Arnon pointed out in his comment.
> 4 votes

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Tags: cognitive-neuroscience
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# Question
Title: Whats the difference between BDD and hypochondriasis?
I'm a new psychiatry trainee. I've run through the literature available to me (plus google), and the descriptions of body dysmorphic disorder (BDD) and hypochondriasis seem too similar. Here's what I've understood so far:

Hypochondriasis represents a general anxiety of disease/symptoms whereas BDD happens to revolve around a single issue. The former is more about somatic symptoms whereas the latter is about physical appearances. But I wonder if this understanding is correct and whether there is a clearer differentiation.

# Answer
DSM-5 is the go to book for psychiatric dignoses and I would strongly recommend you pick up a copy if you are studying Psychiatry.

I am going to split my answer in 3 as you are talking about two different disgnoses and the 3rd part will be making a comparison between the two.

## Hypochondriasis

The more recently approved Diagnostic and Statistical Manual of Mental Disorders (DSM-5) contains many revisions, but few are as sweeping as those involving somatoform disorders. In the updated edition, hypochondriasis and several related conditions have been replaced by two new, empirically derived concepts: *Somatic Symptom Disorder* and *Illness Anxiety Disorder*. They differ markedly from the somatoform disorders in DSM-IV.

To meet the diagnostic criteria for Somatic Symptom Disorder under DSM-5 (Page 311), patients must have:

The Somatic Symptom Disorder is considered **persistant** if it is characterised by severe symptoms, marked impairment, and long duration (more than 6 months).

The DSM also goes on to say that there are 3 levels of severity, which are:

* **Mild** if only one of the symptoms specified in Criterion B is fulfilled.
* **Moderate** If two or more of the symptoms specified in Criterion B are fulfilled.
* **Severe** If two or more of the symptoms specified in Criterion B are fulfilled, plus there are multiple somatic complaints (or one very severe somatic symptom).

Patients with illness anxiety disorder may or may not have a medical condition but have heightened bodily sensations, are intensely anxious about the possibility of an undiagnosed illness, or devote excessive time and energy to health concerns, often obsessively researching them. Like people with somatic symptom disorder, they are not easily reassured. Illness anxiety disorder can cause considerable distress and life disruption, even at moderate levels.

In DSM-5 Page 315 it states that the diagnostic critera for Illness Anxiety Disorder is

> 1. Preoccupation with having or acquiring a serious illness.
> 2. Somatic symptoms are not present or, if present, are only mild in intensity. If another medical condition is present or there is a high risk for developing a medical condition (e.g., strong family history is present), the preoccupation is clearly excessive or disproportionate.
> 3. There is a high level of anxiety about health, and the individual is easily alarmed about personal health status.
> 4. The individual performs excessive health-related behaviours (e.g., repeatedly checks his or her body for signs of illness) or exhibits maladaptive avoidance (e.g., avoids doctor appointments and hospitals).
> 5. Illness preoccupation has been present for at least 6 months, but the specific illness that is feared may change over that period of time.
> 6. The illness-related preoccupation is not better explained by another mental disorder, such as somatic symptom disorder, panic disorder, generalised anxiety disorder, body dysmorphic disorder, obsessive-compulsive disorder, or delusional disorder, somatic type.

The DSM goes on to say that there are two types of Illness Anxiety Disorder

> * **Care-seeking type:** Medical care, including physician visits or undergoing tests and procedures, is frequently used.
> * **Care-avoidant type:** Medical care is rarely used.
>
> **Diagnostic Features**
>
> Most individuals with hypochondriasis are now classified as having somatic symptom disorder; however, in a minority of cases, the diagnosis of illness anxiety disorder applies instead...

## Body Dysmorphic Disorder (BDD)

In DSM-5, BDD is described under Obsessive Compulsive Disorders.

**BDD as described in DSM-5**

> 1. Preoccupation with one or more perceived defects or flaws in physical appearance that are not observable or appear slight to others.
> 2. At some point during the course of the disorder, the individual has performed repetitive behaviors (e.g., mirror checking, excessive grooming, skin picking, reassurance seeking) or mental acts (e.g., comparing his or her appearance with that of others) in response to the appearance concerns.
> 3. The preoccupation causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
> 4. The appearance preoccupation is not better explained by concerns with body fat or weight in an individual whose symptoms meet diagnostic criteria for an eating disorder.
>
> **Diagnostic Features**
>
> Individuals with body dysmorphic disorder (formerly known as dysmorphophobia) are preoccupied with one or more perceived defects or flaws in their physical appearance, which they believe look ugly, unattractive, abnormal, or deformed...

## Comparison between Hypochondriasis and BDD

When you compare the two within the DSM they do differ as you suggest where Hypochondriasis is more about somatic symptoms as it is about **perception of illness** whereas BDD is about physical appearances. However when you look at the International Statistical Classification of Diseases (ICD) produced by the World Health Organisation, which is linked to in the DSM with the ICD codes at the top of each Diagnostic Criteria (for example 300.82 (F45.1) for Somatic Symptom Disorder - *see image above*), the 10th revision ICD code - ICD-10 - which is in brackets, refers to Section F45 of the ICD and this adds to the definitions.

> **F45 - Somatoform disorders**
>
> The main feature is repeated presentation of physical symptoms together with persistent requests for medical investigations, in spite of repeated negative findings and reassurances by doctors that the symptoms have no physical basis. If any physical disorders are present, they do not explain the nature and extent of the symptoms or the distress and preoccupation of the patient.

...

> **F45.2 - Hypochondriacal disorder**
>
> The essential feature is a persistent preoccupation with the possibility of having one or more serious and progressive physical disorders. Patients manifest persistent somatic complaints or a persistent preoccupation with their physical appearance. Normal or commonplace sensations and appearances are often interpreted by patients as abnormal and distressing, and attention is usually focused upon only one or two organs or systems of the body. Marked depression and anxiety are often present, and may justify additional diagnoses.
>
> Body dysmorphic disorder
> Dysmorphophobia (nondelusional)
> Hypochondriacal neurosis
> Hypochondriasis
> Nosophobia
>
> **Excl.:**
> delusional dysmorphophobia (F22.8)
> fixed delusions about bodily functions or shape (F22.-)

When reading this it confuses things as F45.2 considers BDD to be a somatic disorder as it is about perception rather than fact, however in my view, as psychiatry uses the DSM to distinguish between the two, in a psychiatric sense you get a definitive answer which you already have.

With psychosomatic disorders your mind can make your body act like it actually has the medical problem or make an actual problem like pain worse, where as in BDD your mind cannot alter the physical shape of the body.
> 4 votes

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Tags: psychiatry
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# Question
Title: What is the role of stress in the process of behaviour change (lifestyle)?
Clarification: I am specifically looking at lifestyle behaviour change.

I suppose that stress can influence the process of behaviour change in many different ways. One would be just the changing of behaviour itself that will cause stress. However, stress may also cause behaviour change (say, one may initiate behaviour change because of the diagnosis of diabetes). In the end, the aim is to feel better with your new healthy lifestyle, which should result in lower stress levels. This is my thinking based on a (non-literature-supported book) that I read, and now I am looking for scientific evidence for any of the influence stress may have in the process of behaviour change. Also, any other theories as to how stress may play a role in the process of behaviour change?

# Answer
> 1 votes
If you suffer stress or anxiety, a chemical warfare gets underway within the body and if not dealt with effectively, everything starts to self-destruct.

Stress and anxiety will activate the Autonomic Nervous System and cause Cortisol levels to increase to get us ready for conflict and prevent wind-down, which in turn will lower Serotonin levels. The low levels of Serotonin will affect our ability to have a restful sleep and because Serotonin helps to relay messages from one area of the brain to another, the low levels will also affect the ability of your brain to act on information received as efficiently as it should. (WebMD 2015)

Noradrenalin is affected by stress and anxiety, and noradrenalin is another “feel good hormone”, which when imbalanced will affect many aspects of our system, one of which is energy levels causing us to feel lethargic and not wanting to bother with life. Dopamine and endorphins are other happiness hormones which are affected by stress and anxiety affecting our ability to enjoy things, therefore it is no surprise that it can lead to depression.

Endorphins trigger a positive feeling in the body, similar to that of morphine. For example, the feeling that follows a run or workout is often described as "euphoric", which indicates the endorphine boosting effects of exercise. That feeling, known as a "runner's high," can be accompanied by a positive and energizing outlook on life.

As high levels of Cortisol and high levels of the "feel good hormones" cannot coincide together, the increase in endorphines will in turn lower Cortisol levels and therefore increase the Noradrenaline, Dopamine and Seratonin levels boosting the positive outlook on life.

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Tags: stress, health-psychology, behavior
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title: Paper (s) on enhancing self-control

text:
# Question
Title: Paper (s) on enhancing self-control
I am interested in learning more about self-control and how and if people have increased or enchanted it. I looked on Google scholar, but I don't think I am using the correct key words. Do you know of any papers that are on this topic?

EDIT: Specifically about either increasing daily exercise or something tied to physical health.

# Answer
> 1 votes
Along with many others, Google Scholar came up with the following articles for me

# Answer
> 0 votes
As I said in the comments you're unlikely to find many, if any, papers on enhancing self-control. The two most prominent researchers, Walter Mischel and Roy Baumeister, focus on whether self-control can be learned and self-control as a resource, respectively.

Some articles, like this one from the APA or this blog post based on work from Kelly Mcgonigal, will mention ways with which to help your self-control "cheat" temptation through little hints, life hacks, or roundabout ways like physical health and self-esteem.

Those articles also makes mention of the resource or "muscle" model of self-control. Which states that the more self-control you use the more fatigued it will become. **And**, like a muscle, the more you use it the stronger it will be. The resource model has gone back and forth on being debunked, mainly around the need for glucose to "refuel".

But, that doesn't really get to the heart of your question. Mainly because boosting self-control, building healthy habits, and increasing willpower and diligence will come down largely to the individual and the task at hand. Something that makes generic research almost impossible.

What I'd suggest you do, if your goal is physical fitness, is to look up how to make a habit out of things like; going to the gym, eating healthier, or just being more active.

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Tags: self-control, self-discipline
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# Question
Title: How image orientation influences perception
Im a painter for many years. When I paint, I usually walk around and look at my painting for many hours. When painting session is long, it harder and harder to maintain a "fresh look".

By fresh look; I mean state of mind (perception) when I am as objective about my work as possible. The longer the session continues and painting is changed; its harder for me to be objective about it.

To be objective and fresh, artists would take many 5-min breaks in one painting session. I used to do that too, until I learned a "strange trick" from my friend.

Whole trick is to take your painting and just rotate it about 90 or 180 degrees for a moment and look at it. Surprisingly, this gives a fresh (somehow new) perspective at painting.

I would like to ask; why is that?

It seems to me, that somehow brain filters out many informations about images that it knows. When I rotate my image; it is recognized as different (not "known").

Any research on described phenomenon?

# Answer
No life can emerge in chaos - for life to emerge the environment has to be orderly. Organisms have to adapt to their environment, meaning optimise (or satisfice) output in light of input. In a **patternless** environment, there is no chance doing so.

Our brain evolved in light of this - we constantly learn and update what the "norm" is - let it be there's light if it's day or the hair colour of your partner. Equally, the brain constantly compares stimuli to the norm - if it's all good, no action needed, but a deviation from the norm shall raise an alarm bell.

Thus, we are 'programmed' to ignore what's normal, and be alert to the abnormal. Perhaps the most famous example of it is the sound of mechanical clock, which is simply not perceived once we spend enough time in the room it is in.

In your specific case, seeing the same image for a prolong time results in it becoming a norm in our brain, resulting in reduced brain activity.
> 2 votes

# Answer
It is difficult to examine this phenomenon because we would have to define what it means to have a "fresh look" and how we could measure it. It is an interesting observation though. Here are a few possibilities for how we might interpret what's going on here, with some references to related cognitive science research.

One obvious point is that we recognise things more slowly when they are upside down. This is particularly well known in face recognition, but there are also (smaller) inversion effects in other types of stimuli such as scenes. This is often taken as evidence that when we encode or recognise something, we are not just remembering the pieces separately but are doing some sort of "holistic" processing which fits them together. In this case, you could say that when you turn the picture you take longer to recognise it, or that you see it as novel, and that makes you view it in a "fresh" way. https://www.researchgate.net/profile/Jesse\_Husk/publication/5857415\_Inverting\_houses\_and\_textures\_Investigating\_the\_characteristics\_of\_learned\_inversion\_effects/links/55dcbc1b08ae83e420ee5038.pdf

A related point is that objects often have a "canonical orientation" which we are most used to seeing them from. This has been a point of interest for models of object recognition, which often assumed that our representation is "view independent". So if you are painting objects, it certainly would be harder to process if you rotate them from the canonical. http://s3.amazonaws.com/academia.edu.documents/30745263/pdf699.pdf?AWSAccessKeyId=AKIAJ56TQJRTWSMTNPEA&Expires=1472559612&Signature=yDh4VqjQ%2Bsg1ibIebSzKt4fMvmM%3D&response-content-disposition=inline%3B%20filename%3DOrientation\_dependence\_in\_the\_recognitio.pdf

As we might expect from the above, viewing something from a different orientation does actually change the things that we pay attention to and look at. For example, people make frequent horizontal eye movements when looking at landscapes, but if you rotate the image they seem to make a different pattern and may be drawn to different things. http://supersaturated.com/papers/pdfs/horizonSaccade.pdf

http://jov.arvojournals.org/article.aspx?articleid=2158151
> 2 votes

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Tags: perception, vision
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# Question
Title: Why do children tend to choose the last option in a two-alternative forced choice task?
If I ask my toddler if she wants bananas or apples, she will consistently choose apples. The same goes for colors, other related objects, or even seemingly unrelated items - She always chooses last.

Why is she biased to choose the last option? Is this bias specific to children, or is it a common phenomenon in adults too?

Is it related to Modality effect?

# Answer
In general, and not specifically related to children, choosing out of a set of options often depends on people’s **memory**. In an ideal world, people’s options would be presented simultaneously, but in reality, options are often presented serially over time. Both the **delay of time** as well as **interference from other cognitively demanding tasks** are likely to increase uncertainty in one’s evaluations of more distant options compared to more recent options, and therefore increases the amount of regression to an overall category mean. In other words, **imperfect recall introduces uncertainty** in earlier options and judgments of the earlier presented options regresses as memory decays over time. Relatively **desirable options will therefore tend to seem less desirable with time**, and relatively **undesirable options will tend to seem less undesirable** with time.

People therefore tend to select the first option in a set when choosing between generally undesirable options, and will tend to select the last when choosing between generally desirable options (Li & Apley, 2009).

In terms of kids I can add that their working memory span is relatively short, in the order of 10 seconds for a 1-year old (Garon *et al.*, 2008), probably adding to the imperfect recall hypothesis stated above. Further, the executive functioning of kids is limited; most kids between 3 and 6 years are able to recall 4 digits or less in a digit span test (Espy & Bull, 2005), further complicating a seemingly simple task for small children, namely recalling the options, let alone choosing a preferred option between them.

<sub>**References**
**-** Espy & Bull, *Developmental Neuropsychology* (2005); **28**(2): 669–88
**-** Garon *et al.*, *Psychological Bulletin* (2008); **134**(1): 31–60
**-** Li & Apley, *J Behav Dec Making* (2009); **22**: 378–89</sub>
> 5 votes

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Tags: cognitive-psychology, bias
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# Question
Title: How can the effects of pain on cognitive functions be tested in an ethically accepted way?
I have devised a study that may provide an ethical way to invoke similar behaviours in participants, as those demonstrated by individuals in pain. Obviously it is extremely hard to correctly test people's cognitive abilites in a lab when looking at the effects of pain.

**My question is, would anyone be able to mention some citations I could look into where they have attempted to recreate in a lab an ethical way to demonstrate the same responses that pain creates in order to test memory, and other cognitive processes?**

My Idea is to utilize different diluted sample of capsaicin, and provide comparisons to the type of hot pepper for participants. I believe that if I could find a way to gain ethical approval that the feelings and then behaviors one experiences when eating an extremely hot pepper, are in fact similar to those of a person in the position of an aactual injury. If in fact correct it can provide a safe and controlled way to test cognitive functioning under these conditions. high fat dairy products would be on hand for the participants to assist, and in fact the distraction of participants for using on those to relieve symptoms during testing would add to the collective data. This can provide important information related to victim testimony, ability of individuals to make appropriate decisions, or give consent under pain.

I understand this is long, and that it is touchy within the ethics views, which is why I present to you my intent, thoughts, and ask for assistance in gathering other literature from those who have succeeded in attempting to study this in the lab as opposed to case studies.

# Answer
Pain is a form of stress. I would replace pain with another, ethically less problematic stressor. If you would want to do it elegantly, test a group of subjects with chronic pain (anything; *e.g.*, back pain) and use a control group where you submit a group of healthy subjects to a stress test (e.g. Stroop test - huge body of literature on this) and a third group without a stressor. See if the pain group matches the stressed group and whether they are both significantly different from the controls. If yes, you've found a way to prevent ethically kind of unacceptable tests, where the search for volunteers will likely be very difficult too.
> 1 votes

# Answer
There are definitely a few ways to ethically inflict pain, including electrical stimulation, pressure, and heat/cold. Lots of studies have used them, for example, Wager et al. (2004) and Wilson et al. (2014)

If you're looking for someone with lots of experience inflicting pain in a lab setting, Tor Wager is your guy.
> 1 votes

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Tags: cognitive-psychology, perception, experimental-psychology, test, pain
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# Question
Title: What are the effects of visual deprivation on mental health and the other senses?
How do blind people who haven't always been visually impaired deal with their day-to-day lives? I've heard rumors (very, very unreliable rumors) that once you stay in the dark for too long you'll start to go insane, but I haven't met one "insane" blind person yet, nor have I ever heard of one.

However, it's proven that low levels of dopamine result in depression, anxiety, etc. And low levels of dopamine just means a lack of production or intake by the dopaminergic receptors. If the lack of happiness results in disorders such as depression, what would a lack of light do?

Also, why do their other senses strengthen? I read a question earlier about how someone trained themselves to write and read upside down, but then had trouble writing b's, p's and q's, apparently this was due to a process called "negative transfer", does this have anything to do with it? Less energy used meaning more available to enlarge the other's capabilities?

# Answer
> 2 votes
People that loose their eye sight do not go insane. They do tend to develop depression more often than sighted people (Koenes & Karshmer, 2000) and suicide rates are increased in the blind population (De Leo *et al*., 1999).

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

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

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Tags: cognitive-psychology, neuroscience, cognitive-neuroscience, abnormal-psychology, vision
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# Question
Title: Is there a link between brain injuries (TBI) and PTSD?
Could (TBI) Traumatic brain injuries be linked to Post Traumatic stress syndrome (PTSD)? I know there is a lot of concern with veterans and PTSD, but I am more interested in all the other situations/civilian cases of PTSD. From what I have read, there are overlapping symptoms between PTSD and TBI? Is it possible for someone to have PTSD from damage to the brain and not from a specific event?

# Answer
> 1 votes
It is reported that mild traumatic brain injury does not produce Post-Traumatic Stress Disorder however, according to this report in the American Journal of Psychiatry, severe TBI **could possibly** lead to PTSD in approximately 27% of cases. In this study of 96 patients (77 men and 19 women), after 6 months following hospital discharge for severe traumatic brain injury, 27% of them suffered PTSD. Out of these patients:

* 19% reported having intrusive memories,
* 23% reported having nightmares,
* 31% reported having a sense of reliving the trauma,
* 65% reported avoidance of thoughts,
* 65% reported avoidance of places; and
* 73% had signs of hypervigilance.

However one point of note that the report detailed was that

> First, our patients were not selected consecutively, and their responses may not be representative of populations with severe traumatic brain injury. Second, we did not obtain neuropsychological information on each patient.

I must admit that when I was looking at the report, due to the high number reliving the trauma and avoiding certain places, I wondered whether the trauma leading to PTSD was actually the brain injury or if it was the traumatic effect of the event which led to the brain injury.

Another point of note is that it was also reported in a committee hearing in the U. S. House of Representatives, that people with TBI are more likely to develop PTSD than those who have not incurred a brain injury

Personally, from looking at these reports, I think the jury may be still out on this one.

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Tags: brain-injury, ptsd
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# Question
Title: Can split-brain patients sleep like whales?
Regular split-brain patients still have some remaining connection between the hemispheres, but would it be possible for their hemispheres to fall asleep independent of each other?

What about when not just the *corpus callosum*, but also the *anterior* and *posterior* commissures are not functioning for interhemispheric communication?

# Answer
**Short answer**
An animal study did not reveal any effects on the synchronization of the cerebral hemispheres after callosotomy, as based on EEG recordings. When one hemisphere showed sleep patterns on the EEG, the other half would show similar activity.

**Background**
If intact commissures are needed between the two hemispheres to synchronize the two halves of the brain, a callosotomy would be expected to result in different EEG patterns during sleep. The most extreme case being laid out in the question, namely one hemisphere being in a different arousal state than the other.

In a study in split-brain cats (Susic & Kovaevic, 1974) the authors performed a callosotomy or related surgeries, including the sectioning of the *anterior* and *posterior* commissures*, and recorded the EEG during various behavioral states, including wake and sleep states and their transitions. After separation of the hemispheres the authors **did not find any differences in EEG patterns across the two hemispheres** in cats. Specifically, during transition from the alert to the drowsy state, the onset of EEG slowing appeared **simultaneously** in both hemispheres in all cats regardless of the type of section made. The shift from the **synchronized to desynchronized pattern** occurring during arousal or at the beginning of the paradoxal sleep (REM sleep) was always **simultaneous** in both cerebral hemispheres. The transition from REM to short arousal or to slow-wave sleep patterns was also **bilaterally symmetrical**. These results demonstrate that shifts in behavioral states from vigilance to sleep and *vice versa* are characterized by a simultaneous bilateral symmetry of the EEG events.

* List of surgical groups (*n*= 14 per group)

1. Cats with sections of commissural systems between hemispheres and diencephalon (***corpus callosum***, *fornix*, *commissura hippocampi*, *septum*, ***commissura anterior***, *massa intermedia of thalami*, ***commissura posterior***, *commissura habenularum*, *commissura intercollicularis*).
2. Cats with interrupted left optic tract and sections of the commissural system between hemispheres and diencephalon.
3. Cats with an interrupted left optic tract and section of the left half of the midbrain tegmentum (the lesion passed intercollicularly in the dorsal part, and ventrally into the premesencephalic area).
4. Cats with an interrupted left optic tract section of the left half of the midbrain tegmentum and section of commissural systems, combined with the section of crossed fibers of the *commissura supraoptica*.

**Reference**
**-** Susic & Kovaevic, *Brain Res* (1974); **65**: 427-41
> 4 votes

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Tags: neuroscience, cognitive-neuroscience, sleep, lateralization
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# Question
Title: How is the focal point determined when looking into a clear sky?
When looking into a clear blue sky, no cloud, birds, trees or any object to give a frame of reference. When a person is actively looking, as opposed to day dreaming or gazing.

The sky goes for a long distance, and with uninterrupted view, and I guess the first question would be: \- At what point into the atmosphere can the human eye see *(which is not a topic for this site)*, following this,

**What I want to know; is at what point to the eyes come to rest and How is the focal point determined?**

Another consideration is:

**How can this be measured?
Would any attempt to measure this would involve putting a device between the eyes and focal point?**

# Answer
**Accommodation** is the process where the lens in the eye changes shape to focus on an object. The eyes have a default accommodation distance, called the **resting point of accommodation** (RPA). **The RPA is the distance at which the eyes focus when there is nothing to focus on**. The RPA is not identical to the acommodation state of the eye when focusing at infinity. Instead, the RPA can be measured in total darkness. There, the eyes' focal distance will equal the RPA after accommodation is complete. If the lights were then turned on, an object placed at that distance would be in clear focus. The RPA averages 30 inches (approximately 760 mm) for younger people and gets farther away with age (source: D. Ankrum).

The RPA can be measured by using infrared optometry, which is a non-invasive technique to measure the refractive state of the eye and the accommodation (Roorda *et al*., 1998).

**Reference**
**-** Roorda *et al*., *Vis Res* (1998); **38**(13): 1913–24
> 3 votes

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Tags: vision
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# Question
Title: Standardised test to measure workplace stress
I'm trying to find a standardised test that is used to measure stress in the workplace. So far I've found Copenhagen Psychosocial Questionnaire - COPSOQ II, which looks good. But I want to see what other options there are, or if there are any known major problems with COPSOQ II. Equally even the short version of COPSOQ II is arguably too long for what I want to use it for, so shorter suggestions would be greatly appreciated too.

# Answer
> 4 votes
Although it is not exactly stress, there are many self-rating scales for workload. The most popular one is the NASA-Task Load Index (**NASA-TLX**; Hart & Staveland, 1988; see also here). The NASA-TLX consists of six dimensions, which a.o. describe temporal demands, mental effort and frustration. Although there is some weighting procedure accompanied with it, you can just sum the scores of each dimension to get a general workload score.

Another popular scale is the rating scale mental effort (**RSME**; Zijlstra, 1993). This scale is one-dimensional and is responded to by marking a cross on a line. The scale ranges from 0 to 150 and is marked with anchors points at uneven intervals.

Last one I know is the Integrated Workload Scale (**IWS**; Pickup et al. 2005). This scale consists of nine items which describe a particular degree of workload ranging from "not demanding" to "work too demanding". The scale acknowledges that workload is influenced by several dimension and, therefore, the items do describe several dimensions, such as mental effort and temporal demands. The scale has been developed for train traffic controllers but a validation study suggests that it can be used in different languages and in many other domains (Kramer, Johnson & Zeilstra, 2015).

The benefit of the RSME and the IWS is that they can easily be used during the task, since the rating procedure it rather simple and short. Of course, there are also several physiological (e.g. skin conductance, HRV) and performance measures (e.g. RT to a secondary task). For a comparison please refer to Brookhuis & De Waard (2001).

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Tags: test, io-psychology, stress
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# Question
Title: How common is it for twins conjoined at the head to share thoughts and visual stimuli?
I've always been interested in the possibility of a pair of conjoined twins, joined at the head, being able to read each other's thoughts, react to stimuli that one of them can't see/hear/feel, and being unable to keep secrets from one another. Until recently, every pair of conjoined twins I learned about said that they are very much two different people with different personalities and emotions.

Then I read a wikipedia article about Krista and Tatiana Hogan. It was a newspaper article, unfortunately, rather than a piece in a scientific journal, but the description of the girls is exactly what I had been thinking of:

If one girl is blindfolded, she can see what her sister sees. They share thoughts. They can't keep secrets from one another. If one of the girls hurts a limb that she controls, the other girl feels the pain as well as the girl who actually hurt herself.

I'm curious as to whether this phenomenon has been observed before. How common is it for conjoined twins to share thoughts, see through each other's eyes, hear through each other's ears, and be incapable of keeping secrets from one another? Has it ever been observed before this pair of twins?

# Answer
**Short answer**
Likely, the subject pool of *craniopagus* twins is too small to allow for scientific research.

**Background**
As far as I can see after a cursory search, there is no scientific data available on the shared thoughts and experiences of ***craniopagus* twins**. Note that the incidence is only 1 in 10–20 per million births in the US. The rare occurrence, together wit the fact that neurosurgical advances increase the odds of successful separation (Browd *et al*., 2008) make them a truly rare phenomenon. On top of that, parents with conjoined twins will practically be living in the hospital with frequent, stressful visits to a variety of caregivers. In those difficult living situations likely the last thing they are waiting for is another white coat asking questions. In other words, the subject pool for research is minimized further by low response-rates when invitations for research participation are distributed (educated guess, being a parent).

<sub>**Reference**
**-** Browd *et al*., *J Neurosurgery: Pediatrics* (2008); **1**(1): 1-20</sub>
> 2 votes

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Tags: cognitive-psychology, neuroscience, cognitive-neuroscience, abnormal-psychology, vision
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title: DSM and references to ICD

text:
# Question
Title: DSM and references to ICD
I am still studying and where I extensively use the DSM whilst writing essays etc. for my coursework, a question has arisen with regard to referencing the International Statistical Classification of Diseases and Related Health Problems (ICD) whilst researching, and whilst answering a question within Cognitive Sciences. Providing the answer raised this question when referencing the ICD codes used in the DSM.

Those familiar with 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) will know that with information on each mental health disgnostic criteria, there are ICD codes at the top, which are ICD-9 codes followed by the now compulsory ICD-10 codes in brackets. Whilst in my essays etc., just like in the DSM-5, I reference both ICD-9 and ICD-10 codes, however all HIPAA-covered entities had to transition from using ICD-9 codes to using ICD-10 codes back in late 2015.

The problem arises for me when looking in the ICD for the codes referenced in the DSM. I'll give some examples here.

In order for me to answer the question, I referenced DSM diagnostic criteria for Somatic Symptom Disorder, Illness Anxiety Disorder and Body Dysmorphic Disorder (BDD).

* For Somatic Symptom Disorder, in the DSM it references ICD-10 code F45.1 which in the ICD, that code is for Undifferentiated Somatoform Disorder, however as I highlighted in my answer, F45 which is the header of that section of codes refers to Somatoform Disorders.
* When looking at Illness Anxiety Disorder, the DSM references ICD-10 code F45.21 which doesn't exist.
* When looking at BDD, the DSM references ICD-10 code F45.22 and when you look in the ICD, again there is no such code, however there is F45.2 which refers to Hypochondriacal Disorder which in turn references BDD as a Hypochondriacal Disorder.

On page 23 of DSM-5 - under *Coding and Reporting Procedures*, which is within the **Use of the Manual** section - it indicates that the ICD codes are typically used by institutions and agencies for data collection and billing purposes and they were established by WHO, the U.S. Centers for Medicare and Medicaid Services (CMS), and the Centers for Disease Control and Prevention's National Center for Health Statistics to ensure consistent international recording of prevalence and mortality rates for identified health conditions.

Am I missing something when looking at the ICD publication to look the diagnoses up under the ICD-10 codes or am I looking at things in the wrong way?

# Answer
> 0 votes
There is this 2009 article on the APA website (The APA are the writers of the DSM)

It states that

> There is widespread sentiment that it is not helpful to the field to have two separate classification systems for mental disorders. \[However\], Many important distinctions between the two systems remain.

The article also mentioned that Geoffrey Reed (WHO psychologist) said:

> The American Psychiatric Association can really be credited with a revolution in psychiatric nosology with the publication of DSM-III by introducing a descriptive nosological system based on co-occurring clusters of symptoms,
> ...
> The ICD is produced by a global health agency with a constitutional public health mission, while the DSM is produced by a single national professional association.
> WHO's primary focus for the mental and behavioral disorders classification is to help countries to reduce the disease burden of mental disorders. ICD's development is global, multidisciplinary and multilingual; the primary constituency of the DSM is U.S. psychiatrists.
> The ICD is approved by the World Health Assembly, composed of the health ministers of all 193 WHO member countries; the DSM is approved by the assembly of the American Psychiatric Association, a group much like APA's Council of Representatives.
> The ICD is distributed as broadly as possible at a very low cost, with substantial discounts to low-income countries, and available free on the Internet; the DSM generates a very substantial portion of the American Psychiatric Association's revenue, not only from sales of the book itself, but also from related products and copyright permissions for books and scientific articles.

The article also says

> There was very little international participation in the DSM-III, but at the time it may have been impossible to make such a big shift at the international level, he explained. As a result, DSM-III and ICD-8 (the version in effect at the time) were quite different from one another but as the descriptive phenomenological approach to diagnose mental disorders became dominant, the DSM and ICD have become very similar, partly because of collaborative agreements between the two organizations.

The article asked if the DSM will be superseded by the ICD?

It said

> There is little justification for maintaining the DSM as a separate diagnostic system from the ICD in the long run, particularly given the U.S. government's substantial engagement with WHO in the area of classification systems. But, said Reed, "there would still be a role for the DSM, because it contains a lot of additional information that will never be part of the ICD. In the future, it may be viewed as an important textbook of psychiatric diagnosis rather than as the diagnostic 'Bible.'"

As there is more information in the DSM that will never be part of the ICD, plus, due to the fact that the DSM is the goto book for psychiatry, it is the DSM's criteria which needs to be followed when making psychiatric diagnoses. The ICD codes in the DSM should just be used for the purposes they have been designed for, which as mentioned in the DSM on page 23, they are for data collection and billing purposes and for health statistics to ensure consistent international recording of prevalence and mortality rates for identified health conditions.

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Tags: abnormal-psychology, psychiatry, training, publication
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# Question
Title: How to analyze event-related fMRI data with missing fMRI trigger in logfile?
I have the following problem: we conducted an event-related fMRI experiment using Presentation software to display the experiment. Usually each fMRI pulse/scan is logged in the presentation log file so the times for event-related analysis can be derived later on. Unfortunately, for about half of the subjects these triggers in the log files are missing, so I don't know when the experimental events occurred relative to the first scan.

Do you have any ideas how I might still try to analyze that part of the data? All suggestions are welcome.

# Answer
I can see one case in which you still might analyze the data.

This only works under three conditions:

1. your paradigm has **no** variable durations of either stimulus presentations or breaks or others (or you can determine all the times retrospectively) **AND**
2. all your fmri scans have timestamps in their header information (which I think is always the case, at least in the raw file) **AND**
3. the pulse sequences and the presentation were always started at the same time (or the logfile has at least a starting time and the difference between both starts was consistent).

I guess you can answer immediately whether the first condition is met. For the second one, any appropriate software for opening the raw files should be able to show you the timestamps if they exist. For dicom files there are timestamps for study time, series time and acquisition time where the acquisition time is different for every single file (according to this help site from the AFNI program). The third one you might also immediately know but if not you could look into the timestamps of the subjects where you do have the triggers in the logfile and compare it with the starting time of the logfile (if that exists). If you calculate that difference for all subjects and it's always the same you are lucky and can calculate the trigger times for the subjects where they are missing.
> 5 votes

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Tags: methodology, fmri, analysis
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title: Open fMRI data?

text:
# Question
Title: Open fMRI data?
Are there any open fMRI datasets available on the internet? Experimental design doesn't matter much, since I would be working towards a new data analysis method. If the distributed data has been preprocessed (in a standard manner), that would be a big plus.

# Answer
> 9 votes
The fMRI Data Center (www.fmridc.org) was one such repository. About ten years ago it was a requirement for publication in the Journal of Cognitive Neuroscience that you submit your full fMRI dataset to the fMRIDC. This requirement was only around for a few years, but they ended up having 120+ datasets before the grant funding ran out. The archive is currently being moved to UCLA, so at the moment you can't request any data.

An easy way to grab some data might be to get one of the SPM tutorial datasets. They have the advantage that they are either already preprocessed or there are instructions on how to preprocess the data online. They also tend to be fairly high quality, so you will have fewer issues with noise as you work on your new analysis. You can find the tutorial data here: http://www.fil.ion.ucl.ac.uk/spm/data/

Finally, I think that most imaging researchers would be open to collaboration and data sharing. I worked with a grad student in the stats department for a few years on a new autocorrelation analysis that he was interested in. Just drop the researcher an email with a short proposal and see if they are receptive to the idea.

Other potential data sources:

* nitrc.org: Data has been preprocessed, but there is no complete list of what has been done, and how the data has been collected. Maybe the information is hidden in the previous publications. Anyway, I would not use it for research in the current state.
* birncommunity.org: Datasets come in the DICOM format, i.e. straight out of the MR scanner.
* oasis-brain.org: Seems to host only structural MR images (not functional as was requested)?
* humanconnectome.org: Data is offered in multiple versions, but again one would need to do much preprocessing him/herself.
* openfmri.org: Like with the others, the given amount of information is very minimal.

# Answer
> 4 votes
This might be better suited as a comment, but I'm not allowed to post such.

I went through the nice list collected by Craig Bennett:

nitrc.org: Data has been preprocessed, but there is no complete list of what has been done, and how the data has been collected. Maybe the information is hidden in the previous publications. Anyway, I would not use it for research in the current state.

birncommunity.org: Datasets come in the DICOM format, i.e. straight out of the MR scanner.

oasis-brains.org: Seems to host only structural MR images (not functional as was requested)?

humanconnectome.org: Data is offered in multiple versions, but again one would need to do much preprocessing him/herself.

One more option to the list is www.openfmri.org, but like with the others, the given amount of information is very minimal.

Really, isn't there any public dataset that would be ready-to-use for single-subject and group analyses? Like the OP, I would be interested in such datasets. Such that would come with the necessary details....

# Answer
> 2 votes
There was recently an issue about repositories for neuroimaging data. I just copied the table listing all of them from this paper. (Feel free to add links, I will do so when I have more time.)

Title, Author

1. The NITRC image repository,Kennedy D.N. et al.
2. The Function Biomedical Informatics Research Network data repository,Keator D.B. et al.
3. The image and data archive at the Laboratory of Neuro Imaging,Crawford K. et al.
4. COINS Data Exchange: an open platform for compiling curating and disseminating neuroimaging data,Landis D. et al.
5. Neuroimaging data sharing on the neuroinformatics database platform,Book G.A. et al.
6. XNAT central: open sourcing imaging research data,Herrick R. et al.
7. Vanderbilt University Institute of Imaging Science Center for Computational Imaging XNAT: a multimodal data archive and processing environment,Harrigan L. et al.
8. ConnectomeDB—sharing human brain connectivity data,Hodge R. et al.
9. MGH—USC human connectome project datasets with ultra-high b-value diffusion MRI,Fan Q. et al.
10. The Philadelphia Neurodevelopmental Cohort: a publicly available resource for the study of normal and abnormal brain development in youth,Satterthwaite D. et al.
11. Parkinson's disease biomarkers program brain imaging repository,Vaillancourt D. et al.
12. The diffusion tensor imaging (DTI) component of the NIH MRI study of normal brain development (PedsDTI),Pierpaoli C. et al.
13. The Northwestern University Neuroimaging Data Archive (NUNDA),Alpert K. et al.
14. The Age-ility Project (Phase 1): structural and functional imaging and electrophysiological data repository,Karayanidis F. et al.
15. The Open Science CBS Neuroimaging Repository: sharing ultra-high-field magnetic resonance images of the brain,Tardif L. et al.
16. The Pediatric Imaging Neurocognition and Genetics (PING) data repository,Jernigan L. et al.
17. SchizConnect: mediating neuroimaging databases on schizophrenia and related disorders for large-scale integration,Wang L. et al.
18. Sharing data in the global Alzheimer's association interactive network,Neu S.C. et al.
19. Data integration: combined imaging and electrophysiology data in the cloud,Kini G. et al.
20. OMEGA: the open MEG archive,Baillet S. et al.
21. The MNI data-sharing and processing ecosystem,Das S. et al.
22. Northwestern University Schizophrenia Data Sharing for SchizConnect: a longitudinal dataset for large-scale integration,Kogan A. et al.
23. The Cerebral Blood Flow Biomedical Informatics Research Network (CBFBIRN) data repository,Shin D. et al.
24. The PLORAS Database: a data repository for predicting language outcome and recovery after stroke,Seghier M. et al.
25. The Center for Integrated Molecular Brain Imaging (Cimbi) database,Knudsen M. et al.
26. Database integration of protocol-specific neurological imaging datasets,Pacurar E. et al.
27. BIL&GIN: a neuroimaging cognitive behavioral and genetic database for the study of human brain lateralization,Mazoyer B. et al.
28. Pain and Interoception Imaging Network (PAIN): a multimodal multisite brain-imaging repository for chronic somatic and visceral pain disorders,Labus J. et al.
29. Connected brains and minds — the UMCD repository for brain connectivity matrices,Brown A. et al.
30. NeuroVault.org: a repository for sharing unthresholded statistical maps parcellations and atlases of the human brain,Gorgolewski J. et al.
31. ANIMA: a data-sharing initiative for neuroimaging meta-analyses,Reid T. et al.
32. A database of age-appropriate average MRI templates,Richards J.E. et al.
33. The Cambridge MRI database for animal models of Huntington disease,Sawiak J. et al.

# Answer
> 1 votes
I would go for data in OpenfMRI https://openfmri.org/. It has, as of 2016, a growing collection of data and attempts to present data in a standardized form, so it will be easy to work across datasets.

As @craig-bennett noted there are problems with the fMRI Data Center: I am afraid that the fMRI Data Center is still (as of 2016) no longer well-supported. When I now try http://www.fmridc.org I see nothing.

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Tags: fmri, data
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# Question
Title: Is memory biased towards positive or negative memories?
I am trying to understand the relationship between positive/negative memories and the congruence of memory to existing beliefs. These quotes are from Wikipedia, presented in alphabetical order:

* Choice-supportive bias: "positive aspects tend to be remembered as part of the chosen option, whether or not they originally were part of that option, and negative aspects tend to be remembered as part of rejected options."
* Egocentric bias: "This bias suggests that people remember the past as they want it to be rather than the way it was"
* Fading affect bias: "a psychological phenomenon in which information regarding negative emotions tends to be forgotten more quickly than that associated with pleasant emotions."
* Mood congruent memory bias: "the improved recall of information congruent with one's current mood."
* Mnemic neglect: "a pattern of selective forgetting in which certain autobiographical memories tend to be recalled more easily if they are consistent with positive self-concept."
* Negativity bias: "the psychological phenomenon by which humans have a greater recall of unpleasant memories compared with positive memories."
* Placement bias: "tendency to remember ourselves to be better than others at tasks at which we rate ourselves above average and tendency to remember ourselves to be worse than others at tasks at which we rate ourselves below average."
* Pollyanna principle: "the tendency for people to remember pleasant items more accurately than unpleasant ones."
* Positivity effect: "older adults' memories are more likely to consist of positive than negative information and more likely to be distorted in a positive direction."
* Rosy retrospection: "refers to the finding that subjects later rate past events more positively than they had actually rated them when the event occurred"
* Self-verification: "self-views bias memory recall to favor self-confirming material over non-confirming elements."

Most of these suggest congruence with existing beliefs rather than a strict positive bias, but since "on the balance, most people tend to view themselves positively," and most people are happy, it makes sense that there would be a positivity bias overall.

The oddball in the above list is Negativity bias, that appears to contradict other findings. Another exception is Mnemic neglect: "mnemic neglect is based on self-protection rather than self-verification" - ie, there is a strict positive bias, rather than a congruence with existing beliefs, in direct contradiction with research in Self-verification and others.

I think the resolution of these apparent contradictions is in the details: Is the memory about personal experience or just memorizing items? Is the memory self-referent or otherwise? Is the bias referring to memory encoding or memory recall? Is it an issue of missing or distorted memories?

So my question is, is anyone aware of any studies that look at the circumstances under which memory bias is strictly positive, congruent with existing beliefs, strictly negative, or unaffected by mood or belief? Or failing that, a comprehensive review of memory bias that might clarify this?

# Answer
> 6 votes
The short answer is: it depends on age. For younger adults, negative memories last longer than positive memories. The opposite is true for older adults (above 60 years old).

This paper is a good review of some of the above effects: Choice-supportive bias, Mood congruent memory bias, Positivity effect, and Negativity bias. It suggests that negative bias only exists among younger adults, while positive memories last longer than negative memories among older adults. The paper also provided several explanations. One of them is that older adults tend to exhibit auto-activation of emotional regulation ability, thus cognitive control comes into play during the memory recall process.

Mather, M. (2006). Why memories may become more positive as people age. Memory and emotion: Interdisciplinary perspectives, 135-158.

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Tags: cognitive-psychology, memory, bias, mood, happiness
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title: Is the brain inherently social?

text:
# Question
Title: Is the brain inherently social?
The concept of the "social brain" is thrown around a lot, but it's not entirely clear to me what it means.

To me, it could mean a few different things:

1. **Modularity**: We have some sort of modular, hardwired network that supports social behavior and cognition
2. **Domain-General Processes**: The benefits of human sociality through evolution have promoted certain psychological processes that are useful for human interaction, but these processes are not specific to sociality (i.e., they're domain-general)
3. **Domain-General and Specific**: Somewhere in the middle of (1) and (2).
4. **Prepared Learning**: Akin to (2), we are not born "social," but we are born with a set of more basic tools that prepare us to learn to be social

I have superficial familiarity with the area of social cognition and the brain structures (TPJ, DMN, mirror neurons) and chemicals that support it (oxytocin). Based on these literatures, my assumption is that social cognition is supported by domain-general processes that have been co-opted for social use--but we don't have "social" modules or chemicals.

Any thoughts? :)

# Answer
> 6 votes
The "social brain" concept likely originated with Robin Dunbar's Social Brain Hypothesis, proposed in 1998. However, Dunbar was not suggesting that the brain has dedicated "social modules". Rather, the hypothesis was that the evolutionary driving force behind intelligence (increased brain size and capacity) was social - most prominently the need to track relationships in communities of up to 150 people (henceforth known as Dunbar's number). However, I'll focus my answer on the question as asked.

**Plasticity:**

If the criteria for "inherently" social requires some "module" of the brain that has no value outside of a social context, then it is difficult to argue that the brain is "inherently" *anything* because the brain is so plastic (contrast this view with nativism).

For example, say we argue that the brain is "inherently" visual as there is a fairly distinct visual cortex dedicated to this function. However, in blind people and others, this area can be co-opted for auditory, tactile, and spatial processing, so there is nothing "inherently" visual about it. Perhaps we should focus on a "lower level" part of the visual processing system, such as the LGN, that really is only ever used for visual processing.

**Language:**

It is difficult (though not impossible) to imagine evolutionary value for language and speech production outside a social context, and this function does appear to have domain-specific modularity in the brain.

For example, Broca's area is considered the "motor speech cortex", and appears to be dedicated to speech production. But like most areas of the brain, the boundaries of this region are not well defined, and on closer inspection, neither is its function \- although just about all functions attributed to Broca's area are social. While language processing has for a long time been associated with Broca's and Wernicke's areas on the left side of the brain, language processing can spread out as far as the right hemisphere, and some individuals with lesions in these regions can retain largely unaffected language capabilities.

**Relating:**

The FFA, in the fusiform gyrus, is another potentially social part of the brain, critical for face recognition - a lesion in this region leads to prosopagnosia (face blindness). This function is distinct from the system for recognizing inanimate objects, such that other visual agnosias may not affect facial recognition ability. This function is already developed in infancy, and is a strong candidate for domain-specificity. However, once again, this region of the brain may have other functions, and facial recognition can be subsumed (although less efficiently) by other regions.

Fusiform face area

Both autism and Asperger's provide another hint at the social nature of the human brain. Though their etiology is not well understood, it is considered biological, suggesting a disruption of some inherent social mechanism of the brain. However, since ASD affects other cognitive functions as well, it is again not clear that a distinctly social element of the brain is involved.

**Learning:**

Both social reward and social pain have been shown to largely recycle the non-social reward and punishment systems, suggesting that there may be nothing inherent in the brain to support learning by social motivation. However, as pointed out in the question, Theory-of-Mind capabilities may have some modular support in the brain, though no domain-specific mechanisms have been implicated.

Noam Chomsky famously argued that language acquisition in humans happens far too quickly to be accounted for by simple learning - that is, our brain must be somehow predisposed for language acquisition. How this happens is still not well understood, but the same logic is applicable to many other aspects of our social capabilities: We are simply too well honed at social functions such as language, relationships, modelling, and other social behaviours to be accounted for by learning / culture alone.

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Tags: social-psychology, cognitive-neuroscience, social-cognition
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# Question
Title: Why are people better at distinguishing people of their own racial group and why are animals better at recognising animals of their own species?
Why can certain people only recognize certain people. For example, if someone white sees a bunch of African or Asian people, how come it's hard for him to differentiate between them, while they can differentiate between themselves so easily. And the same thing with animals, for example: how come apes can differentiate between themselves, but when I go to the zoo they all look the same. Also since facial recognition is not a thing from the past anymore, does anyone know how much are faces really are different?

# Answer
The ability of people to better recognise and distinguish faces of their own race has been well studied.

For a general discussion, see Cross-race effect where a range of hypotheses have been proposed.
> 2 votes

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Tags: perception, recognition
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title: Physiology behind EEG measurements

text:
# Question
Title: Physiology behind EEG measurements
Many questions were asked about general procedures of Electroencephalography (EEG), which were phrased in a rather specific context. Not only were these questions hard to find, they might also be difficult to generalize for novices. This was discussed in this meta-post. Providing a more generalized context could make the information more accessible. Therefore:

**What is the physiology behind EEG measurements and how is this recorded?**

# Answer
> 8 votes
EEG research all started with Hans Berger, who in 1929 reported that brain activity could be recorded by measuring electrical activity on the scalp. Although the notion of ‘brain waves’ that were found by Berger was controversial, over the years many researchers replicated the results, which led to the acceptance of EEG as a real phenomenon.

**Neurons**
Before going into all the different ways of analyzing EEG data, let us first try to understand the brain and how brain activity is generated. Let us therefore look at one of the smallest units in the brain: the neuron. Each neuron has a resting potential of 75 millivolts, meaning that the there is a difference in electrical potential of 75 millivolts between the inside of the cell and the outside. This resting potential is maintained by the Sodium-Potassium pump, by ensuring that there is a high concentration of sodium (Na+) outside of the cell, and a high concentration of potassium (K+) inside the cell.

The neuron can be stimulated by an external electrical potential, which will cause the permeability of the cell wall to change. The Na+ and K+ ions are then temporarily free to move through the cell wall, such that the concentration of Na+ and K+ will be the same both inside and outside of the cell. Accompanied with this free flow is a huge increase in voltage, which is also referred to as an *action potential*. This action potential will be propagated through the axon to the synapses, which will release neurotransmitters outside of the cell. These neurotransmitters will, in turn, attach to a receptor site at the dendrites of a new neuron, thereby changing the permeability of that neuron. Again, charged ions will flow into that cell, which will result in *post-synaptic potential*. This potential can be either inhibitory or excitatory. Thousands of synapses can be related to one dendrite. When enough excitatory post-synaptic potentials (EPSPs) occur simultaneously from these synapses, a new action potential can occur in the new neuron.

**Electrical fields**
The influx of ions at the dendritic side of a neuron, as the result of an EPSP, will result in a negatively charged extra-cellular space, relative to the axon-side of the neuron. This is especially interesting for a pyramidal cell, where the axons and dendrites are clearly separated (See Figure 1; left). Because of this orientation, a *dipole* will come to exist. A dipole is when a positively charged area is close to a negatively charged area which creates an *electrical field*: a space surrounding an ion in which force is exerted on other ions (See Figure 1; right). “When a large number of small dipoles, such as those generated by activity in a pyramidal cell, are summed together, the resulting electrical potential can be described as a single, larger dipole referred to as an ‘equivalent current dipole’ (ECD). The ECD has an orientation equal to the average of the orientations of the smaller dipoles” (Dickter and Kieffaber, 2014).

**Measuring EEG**
The geometry of the pyramidal cells is not all that makes the electrical fields measurable. The orientation is incredibly important. As stated earlier, the electrical fields have the same orientation as the pyramidal neurons (See Figure 1). If the pyramidal cells are perpendicular to the scalp, the electrical fields will be so as well. The electrical fields will then point ‘outwards’ and thereby affect the potential at the scalp (See Figure 2, right). This is what is recorded with EEG. Conversely, when the pyramidal cells are in parallel with the scalp, the electrical fields will be so as well, and therefore will not reach the scalp (see Figure 2; left) and will not be measureable.

The extent to which the electrical fields are summed, depends on the spatial and temporal contiguity of the pyramidal cells. Neurons that are closer together will have a higher summation than two neurons that are far apart. Although the human body is full of fluids and electrical flow can be conducted throughout it, the effect will diminish when the distance increases.

So now we know where the signal comes from. But how is it recorded? Well, an EEG cap contains electrodes, which are “connected” to the scalp by use of a conductive gel. This gel contains free ions that are able to move freely which, therefore, allows the gel to conduct the biological signal. The signal is then conducted to the metallic electrode through “redox (oxidation-reduction) reactions”, which is the interchange of electrodes between the gel and the metal of the electrodes. When considering Silver-Chloride (AgCl) electrodes, Cl- ions can be removed from the silver and, conversely, Cl- can be bound to free Ag+ ions, thereby creating the compound AgCl. This changes in the metal will then be conducted through the cable to the systems.

**Analog Digital Conversion**
At this moment, the signal is still analog, that is, a natural occurring signal that can have any natural value. The computer however, is nog capable of measuring analog values. Instead, the analog signal must be converted to digital values, such that it can be represented in bits (ones and zeros). This is done by taking a range of voltages that you expect to be measured, and divide that by the amount of bits that the system can take (see Figure 3)

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**Extra Note**

EEG can only measure the activity of pyramidal cells that are perpendicular to the scalp and at the surface of the cortex. Are the other pyramidal cells then just lost? Not really. Another really neat property of electrical flow is that it creates a magnetic field that is perpendicular to the dipole (See Figure 4). For the magnetic field to “move out of the head”, making it measurable, the pyramidal cells must lie parallel to the scalp. Magnetic fields also do not need conductive tissue to be measured. This can be recorded with magneto-encephalography (MEG). MEG is thus a perfect complement to EEG, although deeper positioned structures can still not be recorded.

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## References

Luck, S. J. (2014). An introduction to the event-related potential technique. MIT press. ISO 690
Dickter, C. L., & Kieffaber, P. D. (2013). EEG methods for the psychological sciences. Sage.

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Tags: methodology, eeg, neurophysiology, meg
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title: Why was MPD changed to DID?

text:
# Question
Title: Why was MPD changed to DID?
Why was Multiple Personality Disorder (MPD) changed to Dissociative Identity Disorder (DID)?

I am currently researching DID and working on an essay relating to its treatment. This change was made from DSM III to DSM IV. I am referencing those two manuals for the treatments and so I was required to explain the terminology change.

# Answer
DID is one of the most controversial psychiatric disorders, with no clear consensus on diagnostic criteria or treatment. To answer your question on why MPD was renamed DID, for completeness, there is a bit of history to bear in mind and we will look at the versions of the DSM over the years and how things changed.

The **DSM-II** used the term Hysterical Neurosis, Dissociative Type. It described the possible occurrence of alterations in the patient's state of consciousness or identity, and included the symptoms of "amnesia, somnambulism, fugue, and multiple personality."

The **DSM-III** grouped the diagnosis with the other four major dissociative disorders using the term "multiple personality disorder".

The **DSM-IV** made more changes to DID than any other dissociative disorder, and renamed it DID.

The name was changed for two reasons.

1. The change emphasises the main problem is not a multitude of personalities, but rather a lack of a single, unified identity and an emphasis on "the identities as centers of information processing".
2. The term "personality" is used to refer to "characteristic patterns of thoughts, feelings, moods and behaviors of the whole individual", while for a patient with DID, the switches between identities and behavior patterns is the personality.

It is for this reason the **DSM-IV-TR** referred to "distinct identities or personality states" instead of personalities. The diagnostic criteria also changed to indicate that while the patient may name and personalise alters, they lack an independent, objective existence.

The **DSM-IV-TR** criteria for DID have been criticised for failing to capture the clinical complexity of DID, lacking usefulness in diagnosing individuals with DID (for instance, by focusing on the two least frequent and most subtle symptoms of DID) producing a high rate of false negatives and an excessive number of **Dissociative disorder not otherwise specified (DDNOS)** diagnoses, for excluding possession (seen as a cross-cultural form of DID), and for including only two "core" symptoms of DID (amnesia and self-alteration) while failing to discuss hallucinations, trance-like states, somatoform, depersonalisation, and derealisation symptoms. Arguments have been made for allowing diagnosis through the presence of some, but not all of the characteristics of DID rather than the current exclusive focus on the two least common and noticeable features.

The **DSM-5** updated the definition of DID in 2013, and the summary of changes listed the changes as:

> Several changes to the criteria for dissociative identity disorder have been made in DSM-5. First, Criterion A has been expanded to include certain possession-form phenomena and functional neurological symptoms to account for more diverse presentations of the disorder. Second, Criterion A now specifically states that transitions in identity may be observable by others or self-reported. Third, according to Criterion B, individuals with dissociative identity disorder may have recurrent gaps in recall for everyday events, not just for traumatic experiences. Other text modifications clarify the nature and course of identity disruptions.
> 6 votes

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Tags: cognitive-psychology, abnormal-psychology, personality, personality-disorder
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# Question
Title: At what impedances should one gold plate 12.5-µm diameter nichrome wire tetrodes for targeting different brain areas?
Extracellular electrophysiological recordings of rodent brains using tetrodes requires plating them with gold solution in order to achieve appropriate impedances.

How does the ideal plating impedance depends on the size, depth of the desired recording structure, and the packing density of the objective cells?

# Answer
> 2 votes
The ideal impedance of any electrode aimed at recording low-amplitude neural signals (barred suction glass-pipette electrodes for patch clamping) is simply: **as low as possible**.

In case of tetrodes, *i.e.*, electrodes consisting of a bundle of four microwires that can record from multiple neurons simultaneously in the brain of freely moving animal, they are usually electroplated to reduce their impedance from 2-3 MΩ to 200-500 kΩ (measured at 1 kHz). Low impedances increase the signal-to-noise ratio and allow for the recording of small-amplitude signals. Tetrodes with lower impedances could theoretically further improve SNR, but this is technically not possible with the standard electroplating methods, per an article from 2009 (Ferguson *et al*., 2009).

A straightforward way of reducing impedance is to increase the surface of the electrode. Increasing the absolute size may very well be detrimental to the purpose of collecting single unit recordings, as larger electrodes inherently pick up the activity more neurons. A more feasible way is to increase the surface by means of altering the microstructure of the electrode, *i.e.*, increase its *roughness* (Fig. 1).

Fig. 1. smooth (A) and rough electrode surface (B). source: Jeff-Du *et al* (2015)

A method where tetrodes were plated with a gold solution with added polyethylene glycol (PEG) or multi-walled carbon nanotube (MWCNT) solutions was reported to to lower the impedance further to 30-70 kΩ. MWCNTs and PEG reportedly act as inhibitors in the electroplating process and create a larger surface area, thereby lowering the impedance on the tetrode tips (Ferguson *et al*., 2009).

**References**
**-** Ferguson *et al*., *Sens Actuators A Phys* (2009); **156**(2): 388–93
**-** Jeff Du *et al*., *J Mater Chem C* (2015); **3**: 6515-24

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Tags: neuroscience, methodology, electrophysiology, experimental-neuroscience
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