Can working memory actually be improved? I'm skeptical of the claim that brain training (dual-n back) can improve working memory; the improvement seems to be task-specific rather than generalize.

The average human being can only keep 7 things in his or her mind at one time. Brain training claims to be able to increase this capacity, but as said above, I am skeptical. Are there any studies that have have shown that the 7-limit short term memory capacity can be increased? Of course, we can abstract and have an mnemonic stand for seven things, but we are still only holding one thing (the mnemonic) in our minds..

No program has been definitively proven to increase working memory in any generalizable way.

  The authors conclude that memory training programs appear to produce short-term, specific training effects that do not generalize. Possible limitations of the review (including age differences in the samples and the variety of different clinical conditions included) are noted.However, current findings cast doubt on both the clinical relevance of working memory training programs and their utility as methods of enhancing cognitive functioning in typically developing children and healthy adults.

-Is working memory training effective? A meta-analytic review.


What was the experiment where you pour liquid from a tall container to a short one and ask a child which has more? From Developmental psychology 101 I remember an experiment where the person conducting the experiment would pour liquid from a tall, narrow container into a short, narrow container and ask a child if the volume of the liquid had changed... or something similar to that. I can't remember if it actually involved pouring the liquid or just showing two containers. I remember it was used to determine if the child had reached some critical threshold and learned a specific skill, but my memory is very hazy on the details.

Who invented this experiment?
How did it work? is my description accurate?
What is the name of the skill it's testing for?

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

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

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

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

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


Are any kinds of behavior proved to correlate with testosterone levels? Are any kinds of behavior proved to correlate with testosterone levels?
Any studies done on this? Any indications of such correlations?

"There was a significantly higher level of plasma testosterone in the
  aggressive group as compared with the nonaggressive group or with the
  other two groups combined. The socially dominant group also had a
  significantly higher level of testosterone than the nonaggressive
  group."
  http://journals.lww.com/psychosomaticmedicine/Abstract/1974/11000/Plasma_Testosterone__Correlation_with_Aggressive.2.aspx

-

  "Analysis of archival data from 4,462 U.S. military veterans supported
  the first hypothesis: Testosterone was correlated with a variety of
  antisocial behaviors among all individuals."
  http://pss.sagepub.com/content/1/3/209.short

-

  "Plasma testosterone levels did not differ in fighting and nonfighting
  individuals. Although there were significant correlations between
  psychologic tests, the test scales did not correlate either with
  plasma testosterone or with fighting behavior. The 10 prisoners with
  histories of more violent and aggressive crimes in adolescence had a
  significantly higher level of testosterone than the 11 prisoners
  without such a history. An hypothesis is presented that within a
  population that is predisposed by virtue of social factors to develop
  antisocial behaviors, levels of testosterone may be an important
  additional factor in placing individuals at risk to commit more
  aggressive crimes in adolescence."
  http://journals.lww.com/psychosomaticmedicine/Abstract/1972/07000/Assessment_of_Aggressive_Behavior_and_Plasma.6.aspx

-

  "Statistically significant changes in MMPI–2 scale scores were found
  at 3-month follow-up after initiating testosterone treatment relative
  to baseline for transgender men compared with female controls (female
  template): reductions in Hypochondria (p < .05), Depression (p < .05),
  Hysteria (p < .05), and Paranoia (p < .01); and increases in
  Masculinity–Femininity scores (p < .01)."
  http://psycnet.apa.org/psycinfo/2014-32641-001/

-

  Baron-Cohen and his colleagues recently found that giving testosterone
  to women decreases their ability to empathize, particularly among
  women whose bodies show evidence that they were exposed to higher
  levels of testosterone in utero. And previous research has linked high
  levels of testosterone in the womb to autistic traits. (Interestingly,
  in-utero exposure to testosterone can be estimated by looking at the
  ratio between the length of the ring finger and index finger.)
  http://healthland.time.com/2011/05/18/study-why-some-transgendered-people-have-higher-levels-of-autistic-traits/

-

Contrary to what many believe:

  No direct associations were found between testosterone and solitary or
  dyadic sexual desire.
  http://www.eje-online.org/content/165/2/331.full.pdf

Some transgender people say they have changes parts of their personality, but I've found no studies to prove this.

  "Chris Edwards, a trans advertising executive, says that
  post-transition, he was given greater levels of responsibility—but he
  thinks it’s because the testosterone he took changed his behavior. He
  became less timid and more outspoken—and was seen, at work, as more of
  a leader. Indeed, some suggest that transmen might experience these
  workplace benefits partly because, post-transition, they are happier
  and more comfortable, and that this confidence leads to greater
  workplace success. But if that’s the case, one would expect that
  transwomen, armed with this same newfound confidence, would see
  benefits. The opposite seems to be true. "
  http://www.newrepublic.com/article/119239/transgender-people-can-explain-why-women-dont-advance-work

-

  "Now that we’re roughly two years into the process there has been a
  dramatic change in personality. This was expected, I knew there would
  be highs and lows because the process takes a huge toll. However now
  she just treats everyone like garbage. The whole world absolutely has
  to revolve around her. No one can be right unless it happens to be
  from her prospective. She exemplifies all of the negative stereotypes
  of both transgender people and women. The personality change went from
  laid back punk rocker to being what I can only sum up as a stuck up
  diva."
  https://answers.yahoo.com/question/index?qid=20100430043917AAYcyD8

Note that stories like the one above may have several possible causes, including identity changes (suddenly seeing oneself as a different gender), depression (generally bad mood) or placebo.


How to obtain adult norms for Raven's progressive matrices? Raven's Progressive Matrices:

  is a nonverbal group test typically used in educational settings. It is usually a 60-item test used in measuring abstract reasoning and regarded as a non-verbal estimate of fluid intelligence. source

Where can one find adult norms for Raven's progressive matrices?

For instance, how can I find the percentile for a raw score of 56 out of 60 for a 36 year old caucasian male?

You would need to obtain a copy of the test manual. It includes norm tables for different groups.

If you Google it you might be able to find out where to purchase a copy

Equally, many psychology departments have test libraries and they are likely to have a copy.

It's also possible that some journal articles that have used Raven's could provide a rougher approximation to actual test norms.


Abstract idealized mental visualization improves motor task performance I practice martial arts (Aikido), which involves a lot of rotation.

When practicing, I find that holding an abstract image in my head, instead of thinking about the actual technique, improves my performance of the technique.

For example, when rotation is required, my mental image is essentially a vertical spiral pulled tight in the middle (as if constrained by a belt), in that one comes in to the axis of rotation and must stay on it before moving off into the rest of the technique.

The question, then is:
What explains why an abstract mental image can improve adherence to an ideal set of movements?

And, can this be explained neuro-biologically and, if yes, how?

(I suspect that the two questions have similar, if not the same, answers - hence why I've included both instead of separating them)

If you prefer to not answer those questions, believe that I should be answering these myself, or believe that this is not high-enough quality for CogSci (I apologize for any improper terminology), please offer a direction in which I can start my research into this phenomena, as at the moment I am at a loss for where to begin.

I would hazard a guess that some type of motor system interference is taking place when you visualize the movement versus visualizing an abstract shape.

For example, Kilner et al. (2003) found that actions that are observed can interfere with incongruous executed actions.  They had subjects make arm movements that were either similar or dissimilar to those of another human or a robot.  Movements that were not similar caused a greater amount of error in the arm movement of the subject. Since motor visualization can recruit many of the same areas of cortex as actual observation and execution (Kosslyn et al., 2001), this could cause similar interference.

Other papers, such as Rémy et al. (2010), have shown that there is reduced motor learning when two movements were acquired at the same time.  Their hypothesis was that the two movements both recruited similar areas of cortex, which caused a form of competitive interference. Visualizing a movement before execution could generate competition between similar, but not identical, movement representations.

Finally, there is evidence that varied practice, or learning a motor movement in several different ways, can cause a short-term degradation of motor learning, but can cause long term increases in retention and generalization of a motor movement.  Magill and Hall (1990) had a nice review of this effect, called contextual interference.  Visualizing the movement could be causing reduced performance now, but it could be argued that it may be beneficial in the long-term.

Wikipedia has some surprisingly good articles on motor learning and task interference if you are interested in learning more:
Motor learning: http://en.wikipedia.org/wiki/Motor_learning
Interference theory: http://en.wikipedia.org/wiki/Interference_theory

 Kilner JM, Paulignan Y, Blakemore SJ. (2003) An interference effect of observed biological movement on action. Current biology, 13(6), 522–525.
Kosslyn SM, Ganis G, and Thomson WL. (2001) Neural foundations of imagery. Nature Reviews Neuroscience, 2, 635-642.
Magill RA and Hall KG (1990) A review of the contextual interference effect in motor skill acquisition. Human Movement Science, 9, 241-289.


How can IQ below 40 be measured? Common intelligence tests such as the WAIS or RIAS don't differentiate well (or at all) in very low IQ ranges, making it impossible to diagnose the degree of mental retardation according to the criteria put forward in the ICD-10.

How can IQ below 40 be measured?

With great difficulty. I'm half-joking because I'm not totally sure, but the first observation is that DSM-IV also used these brackets, so the ICD-10 isn't alone.

  The DSM-IV definition utilizes four degrees of severity that reflect the level of intellectual impairment: IQ levels between 50–55 to approximately 70 characterize mild mental retardation, 35—40 to 50–55 characterize moderate mental retardation, 20–25 to 35–40 characterize severe mental retardation, and IQ levels below 20–25 characterize profound mental retardation.

As far as actually testing the profound levels of retardation, it seem to me that alternative tests might be used in practice, e.g. a 2018 Texas HHS guideline says:

  In some situations, an individual’s limitations may be so extensive that a full scale IQ
  score cannot be obtained from a standardized intelligence test. In these situations, an
  estimate of the individual’s IQ score, or, IQ score equivalent should be stated with clinical
  justification. For example, if an individual’s ability to comprehend oral instruction or
  visual demonstration is not adequate for a formal appraisal of general intellectual
  functioning, the use of an Adaptive Behavior Composite (e.g., provided by the VABS)
  may serve as an estimate of the individual’s intellectual functioning when accompanied
  by a clinical justification explained in the DID report. However, not all measures of
  adaptive behavior (e.g., ABAS, ICAP, and SIB) are appropriate for establishing an IQ
  score equivalent.

VABS is the  Vineland Adaptive Behavior Scales; there's a reasonably cited paper by Bölte and Poustka (2002) correlating the ABC subscale of that with IQ < 70 (which is measured on the WISC-R/WAIS-R scale). But it also notes that the because of floor effects with WISC/WAIS we can't be certain that the substitute is really appropriate. It also cites some other papers some of which disagreed with this idea of substituting VABS for IQ.

The ICD-11 has moved away from merely using the IQ as discriminator, but has kept it. The DSM-5 was a little bolder:

  DSM-5 abandoned specific IQ scores as a diagnostic criterion, although it retained the general notion of functioning two or more standard deviations below the general population.

As the Texas guideline explains further:

  the DSM-5 (pages 33-36)
  is the first edition to classify level of severity based on adaptive functioning rather than IQ
  score. The DSM-5 explains that “the various levels of severity are defined on the basis of
  adaptive functioning, and not IQ scores, because it is adaptive functioning that determines
  the level of supports required.” In other words, the DSM-5 recognizes that adaptive functioning has greater practical significance because it is a better indicator of the
  individual’s ability to function in society.

And Texas has basically adopted the DSM-5 in this regard, classifying ability by an (approved) ABL test, of which there are several, but since that's not the main topic here... I won't detail that any further.


What is the threshold where actions are perceived as "instant"? In Human Computer Interaction and User Experience there's some oft repeated rules of performance:

0.1 second is about the limit for having the user feel that the system is reacting instantaneously, meaning that no special feedback is necessary except to display the result.
1.0 second is about the limit for the user's flow of thought to stay uninterrupted, even though the user will notice the delay....
10 seconds is about the limit for keeping the user's attention focused on the dialogue...

I'm most interested in this "instantaneous" response. Related is this User Experience Question. A related answer does bring up some sources:

Card, S. K., Robertson, G. G., and Mackinlay, J. D. (1991). The information visualizer: An information workspace. Proc. ACM CHI'91 Conf. (New Orleans, LA, 28 April-2 May), 181-188.
Miller, R. B. (1968). Response time in man-computer conversational transactions. Proc. AFIPS Fall Joint Computer Conference Vol. 33, 267-277.
Myers, B. A. (1985). The importance of percent-done progress indicators for computer-human interfaces. Proc. ACM CHI'85 Conf. (San Francisco, CA, 14-18 April), 11-17.

However I can't access any copies of those articles. Also, frankly, they're all conference papers. Big HCI research often debuts at conferences, but ideally I'd like something robust which has been tested rather than something written 20-40 years ago for a conference.
One thing I've noticed is the "instant response" threshold quoted tends to be around 100ms to 200ms. Typical human reaction time is about 200ms so I'm wondering if there is a relation there. It seems possible; if something happens so quickly you can't react to it, it is practically "instant" in a way.
Approximately what length of time between action and reaction is perceived as instant by humans?

Preface

This is a very interesting question, that is also somewhat related to my area of research. I know of several related results (which I might add later in an edit), and I thought that with a few minutes of scholar search I'll find a paper dealing with this question exactly. I was surprised to find no such papers. So I decided to conduct an experiment...

Answer (preliminary. hopefully, will be edited)

As with many cases in psychology, the threshold is completely non-existant: there is no delay up to which the reaction is perceived as instantaneous, and after which it is perceived as delayed. You can measure the probability of the subject perceiving a delay, as a function of the delay time. You can choose any probability you want, arbitrarily, and call it the 'threshold'. If we decide on 50% (the chance of responding there was a delay is identical to the chance of responding it was instantaneous) then for me it is about 110ms.

The results presented here are based on 100 trials, performed by myself. Hardly counts as good study, but if a few more people run the test, I promise to process the results and post them here (and who knows, maybe even publish it somewhere :))

To participate in the experiment yourself

Sign up to ofri.webfactional.com. (It is a site I developed for web-based experiments conducted in my lab. It's still in beta, which is why its under a domain with my name, and not under huji.ac.il.  I promise we do not use your email for anything except for identifying you. No spam ever).
In the Group Name field in the registration, enter instant.
Login, and follow the on-screen instructions. Its really simple.
After running more than 60 trials another button will appear with the text 'show results'. Clicking it will draw a graph similar to the one presented here, based on your personal results.


Is there a neurological difference between someone experiencing a "normal" trauma response, and someone with PTSD? Or are they on the same continuum? I've been reading Dr. Bessel van der Kolk's book The Body Keeps the Score. Dr. Van der Kolk describes how, in people with PTSD, the brain actually undergoes changes in response to trauma. Their perception and interpretation of their world shifts on a neurological level.
Say a person doesn't fit all the criteria for an official PTSD diagnosis, but still experiences some (perhaps less intense or long-lasting) symptoms of post-traumatic stress. Is it likely that the same neurological changes would be taking place, just to a lesser extent?
Or is it more analogous to depression, where (if I understand correctly!) research on how the brain responds to depression isn't necessarily analogous to how the brain responds to feeling "sad" (i.e. while sadness can turn into clinical depression, clinical depression itself is a specific condition that feels different from just extra severe sadness)?
Context: I'm writing an article about the cognitive effects of trauma on students, but most of the studies I find screen participants for PTSD specifically. I'm wondering if these studies would still apply to students who don't necessarily have PTSD, but still suffer from the aftermath of a trauma.

First, your question pertains to two possible populations:

"less long-lasting" PTSD is diagnosed as acute stress disorder (ASD); PTSD cannot be diagnosed until at least one month after exposure to the inciting trauma, and ASD sometimes resolves without progression to PTSD.
"less intense" PTSD is usually diagnosed as an adjustment disorder, meaning a maladaptive response to some psychosocial stressor that somehow doesn't meet the criteria for ASD/PTSD.

Is it likely that the same neurological changes would be taking place, just to a lesser extent?

We need to define those changes:

Sherin, J. E., & Nemeroff, C. B. (2011). Post-traumatic stress disorder: the neurobiological impact of psychological trauma. Dialogues Clin Neurosci, 13(3), 263-278.

Table I. Summary of neurobiological features with identified abnormalities and functional implications in patients with post-traumatic stress disorder. CRH, corticotropin-releasing hormone; 5HT, serotonin; GABA, γ-aminobutyric acid; NPY, neuropeptide Y; ACTH, adrenocorticotropin; NE, norepinephrine; CSF, cerebrospinal fluid

Additionally, other studies have demonstrated reduced amygdala volume in PTSD patients. It should come as no surprise that ASD features many of the same neurobiological changes (especially hypocortisolism) as PTSD, although quantitative differences may not correlate with symptom burden.

Marshall, R. D., & Garakani, A. (2002). Psychobiology of the acute stress response and its relationship to the psychobiology of post-traumatic stress disorder. Psychiatr Clin North Am, 25(2), 385-395.

Studies of the acutely traumatized have found that those individuals who are at increased risk for chronic PTSD are relatively more likely to experience a more severe acute emotional reaction. This includes not only the intensity of emotions such as fear, anxiety, and/or despair, but also dissociative experiences and cognitive disruption. This clinical picture, in turn, is associated with increased heart rate, increased skin conductance, and relatively lower levels of blood cortisol compared to those who will not develop PTSD (discussed later in this article). However, an interesting caveat to this generalization is that the presence of acute dissociative symptoms appears to mediate the intensity of the peripheral sympathetic nervous system response. Griffin et al. found that peritraumatic dissociation was associated with both greater severity of PTSD symptoms, and relatively greater suppression of autonomic physiologic responses.

Similarly, more recent research confirms the expectation that comparable neuroanatomic changes occur in ASD as with those seen in PTSD (particularly amygdala activation). In summary: ASD and PTSD share many neurobiological characteristics.
In contrast, adjustment disorder (sometimes referred to as "situational depression") is far more nebulous. It can be acute or chronic, and it can present in a variety of ways to the extent that its existence has been contested as ‘a progression threshold from normal human adaptation under conditions of stress, change, and loss, into the dark web of “mental illness.”’ In the linked article, John Daniels argues that adjustment disorder should be treated as a collection of behavioral responses to normal emotional states that can act as a precursor to better-characterized clinical pathologies like anxiety disorder, depression, and conduct disorder. This group of behaviors, Daniels contends, should be treated with counseling instead of pharmaceutical "brief therapies" that might be better served in combating the biochemical changes seen in ASD. There is an abundance of literature regarding the lack of rigorous study of adjustment disorder (a,b).

Or is it more analogous to depression, where (if I understand correctly!) research on how the brain responds to depression isn't necessarily analogous to how the brain responds to feeling "sad"...

Ultimately, your analogy here is good for differentiating between the two possibilities you identified in being "sub"-PTSD (duration [ASD] vs. intensity [adjustment disorder]). Generally speaking, ASD has a similar neurobiological profile to PTSD with respect to chemical, physiological, and anatomic changes. To use your words, adjustment disorder "isn't necessarily analogous" to PTSD and rather encompasses a broad spectrum of (possibly normal) emotional responses to both acute and chronic stressors. This tracks with our understanding of other diseases: matching symptoms of variable duration are more likely to have the same underlying etiology (e.g. a mild runny nose lasting one week might be correctly ascribed to a host of different viral causes) as compared to symptoms of varying intensity that bear a passing resemblance to each other (e.g. rhinorrhea caused by a cluster headache doesn't implicate a virus).
You may find additional pertinent information on (and in the citations of) the Wikipedia pages for PTSD, ASD, and adjustment disorder.


How is the term "affect" different from "emotion"? I have encountered a vast variety of definitions for affect, each of which contrasts it with the term "emotion" in a whole different way. Here are a few:

Affect denotes the visible/objective expression of an emotion.
Affect is the actual underlying subjective feeling an emotion.
Affect means the initial automatic reaction to a situation before cognitive appraisal helps build-up to the more complex emotions.

Also, given how practically (amongst professionals) both of these terms are often used interchangeably, I wonder if there's a clear non-controversial distinction between "affect" and "emotions".

There is a difference between affect and emotion, and the first two descriptions you quoted sum up the main way the two words are different

Affect denotes the visible/objective expression of an emotion.
Affect is the actual underlying subjective feeling [of] an emotion.

Wikipedia summarizes that in psychology, the word affect is used to describe the experience of feeling or emotion.  The word also refers sometimes to affect display, which is

a facial, vocal, or gestural behavior that serves as an indicator of affect (APA 2006).

Think of it in the sense that if you have an emotion in play, how do you describe how the emotion affects the person experiencing the emotion?
Emotions can interfere with how the person reacts to stimuli through valence (the "goodness" of the event , which is positive valence, or the "badness" of the event, which is negative valence — perceptional or actual), motivation or arousal (the state of being attentive, alert and awake). This is why affective disorders such as depression and anxiety disorders are not referred to as emotional disorders.
References
APA (2006). VandenBos, Gary R., ed. APA Dictionary of Psychology Washington, DC: American Psychological Association.


Are ACT-R and Spaun the state of the art in cognitive science computational models? I've been looking for a computational model in cognitive science, and perused Anderson's "How can the human mind occur in the physical universe?".

I've also seen this question comparing ACT-R with a empirical model called Spaun.

Are Anderson's ACT-R model and Spaun the state of the art in Cognitive Science, or are there other competing models currently being researched?

There are TONS of other Cognitive Models being researched. Specifically, see this giant comprehensive list of Cognitive Models [1]. Given such a wide array of models, it might be more helpful to focus on which framework are still under active use, in addition to Spaun and ACT-R. In "How to Build a Brain" by Chris Eliasmith, he compares Spaun with some other architectures in active use, including:

LISA
Neural Blackboard Architecture (NBA)
ICS
Dynamic Field Theory (DFT)
Leabra
Soar

However, in my personal experience as a researcher, the only one in that list that I've still seen active publications from is Leabra.

In conclusion, the cognitive modelling community is still very heterogenous. You never know when an old framework is going to be revived or a new one started, but hopefully the references I gave you are a good starting point.

[1] "40 Years of Cognitive Architectures: Focus on Perception, Attention, Learning and Applications" Iuliia Kotseruba, Oscar J. Avella Gonzalez, John K. Tsotsos


3D Glasses Aftereffect I am wearing a pair a 3D glasses. The left lens is red and the right lens is cyan. However, when I take them off, my left eye sees in cyan and my right eye sees in red, the complete opposite of the glasses. Why does this happen?

Opponent-process theory explains this.  Here's an excerpt from the opponent process page on Wikipedia (different page than the opponent-process theory for some reason):

  Besides the cones, which detect light entering the eye, the biological basis of the opponent theory involves two other types of cells: bipolar cells, and ganglion cells. Information from the cones is passed to the bipolar cells in the retina, which may be the cells in the opponent process that transform the information from cones. The information is then passed to ganglion cells, of which there are two major classes: magnocellular, or large-cell layers, and parvocellular[disambiguation needed], or small-cell layers. Parvocellular cells, or P cells, handle the majority of information about color, and fall into two groups: one that processes information about differences between firing of L and M cones, and one that processes differences between S cones and a combined signal from both L and M cones. The first subtype of cells are responsible for processing red–green differences, and the second process blue–yellow differences. P cells also transmit information about intensity of light (how much of it there is) due to their receptive fields.[citation needed]

This Wikipedia page needs a little work, but it already knows more than I do about the wiring. Basically, in effect, strong and prolonged stimulation of one kind of cone (e.g., the red cone) will gradually build a visual signal of the opposite color (blue in this example). When the (red) stimulus is removed, the opposing signal begins to fade, but remains long enough to produce an opposite-color (blue) illusion or afterimage. Lots of fun optical illusions are based on this principle. It works with all colors.

Here's my favorite example for intro psych classes...stare at the black dot in the center and enjoy!

Not sure what the original source for this is BTW. It comes up all over the place with a Google image search, but I haven't found a proper citation yet.


What prevents a neuron from activating an incoming synapse? As is known, a neuron can have incoming and outgoing synapses. When a neuron fires, what does prevent that only outgoing synapses are activated?

Basically there are two reasons. First, (most) synapses are asymmetrically designed in such a way that synaptic transmission only works in one direction. Second, action potentials usually run in one direction only, from the axon hillock down the axon.

Saying that a neuron fires means that an action potential (AP) is effected, a series of  depolarisations along the axon which constitute a signal that moves down the axon, since APs are usually initiated at the axon hillock. Neural signal flow thus generally is directed orthodromically, i.e. along the axon and away from the soma.

A synapse is constituted partially by the presynaptic neuron, partially by the postsynaptic neuron. It is the axon terminals, located at the distal end of the presynaptic neuron's axon, which can carry a neural signal further over the synaptic cleft to effect an AP in the postsynaptic neuron. This generally works in one direction only – e.g. the presynaptic part of the synapse can release neurotransmitters, and the postsynaptic part of the synapse has receptors for the neurotransmitters, not the other way round (mind that this does not imply that the postsynaptic part of the synapse cannot have any effect on its presynaptic counterpart).

Since the propagation of the AP along the axon basically works through causing neighbouring parts of the axon to depolarize, it would be possible that at some point a second AP is generated which runs back into the direction the original AP came from. However, this is prevented by afterhyperpolarization (also called refractory period): the membrane potential falls below the usual resting potential and thus prevents this running back up of a second, antidromic AP.

The mechanism of afterhyperpolarization is largely responsible for unidirectional propagation. However, it has to be emphasized that this only applies if the AP is initiated at the axon hillock in the first place. If an action potential forms at some point down the axon, it is indeed possible that two APs are generated, one moving down the axon, another one moving upwards towards the soma. This is called neural backpropagation, and while it constitutes an actual phenomenon in the nervous systems, there is not much clarity yet about its (possible) functions. However, the above mentioned unidirectional design of chemical synapses prevents this signal to effect synaptic transmission.

Another phenomenon that can be said to reverse the »normal«, unidirectional flow in neurons is that of electrotonic potentials (but they don't effect anything like antidromic APs), and finally an autapse is a synapse from a neuron's axon onto its own dendrite, so that in some sense it is correct to say that a neuron with an autapse activates an »incoming synapse« (however not in the sense the question seems to imply). Finally, it should also be mentioned that in contrast to chemical synapses, electrical synapses work in both directions (notwithstanding the above).


What is the "personality of a relationship" called? I'm struggling to find this missing word, that I imagine would be part of the psychological literature.
Personality is to an individual what ____________ is to a 1:1 relationship.
Any thoughts? I imagine "Culture" would be the personality equivalent for an organization, but I'm unfamiliar with similar concepts for a 1:1 relationship. Does "culture" apply equally to organizations of size 2?
Many thanks in advance

Perhaps this?

An individual's personality
A couple's relationship
A group's dynamics
An organisation's culture


Why do people commit suicide? I don't understand why people commit suicide.

If I imagine myself in a really bad situation and make a list of what kind of things I would do in that situation, I don't have suicide even in my top-100 things to do in my list! In the worst situation I would abandon everything and go on a trip!

So why do people not just throw away everything instead of committing suicide?

People who kill themselves usually believe that they are in an unbearable situation from which they cannot escape and that things won't ever get better.
The problem with research into the reasons for suicide is that those that successfuly killed themselves can no longer explain their motives, and those that survived might – consciously or unconsciously – have planned not to die, so their motivations might not be motivations to die but motivations to affect others or to relieve tension (similar to non-suicidal self-injury).
A close friend who only accidentally survived a suicide attempt (because, not being a physician or apothecary, she had unknowingly chosen sleeping pills that cannot kill you, no matter how many you take) had been abused as a child, consequently lost all self-worth, felt she would never experience love and happiness, and finally tried to end her misery when she was 21. Her survival was followed by another, successful, suicide, which to me shows that her first attempt was earnest.
This is the only person I know who wanted to die and told me her reasons, between the two attempts. More abstractly, her reason was the one stated at the beginning of my answer: not simple depression or hopelessness. We all go through such phases, but we know they pass, so we bear them and wait for better times. This person had been depressed and miserable for so long, that she could no longer imagine things changeing for the better. Unable to bear the idea of having to endure another eighty years of unhappiness, she ended it.
There is some research into reasons for suicide, which, as far as I know, does not emphasise this point and thus fails to explain why some people kill themselves in a moment of hopelessness, while others don't. For example, Brown, Comtois and Linehan (2002) interviewed women who attempted suicide and compared their motivations to women who performed non-suicidal self-injury. Their abstract summarizes (my emphasis):

Overall, reasons given for suicide attempts differed from reasons for nonsuicidal self-injury. Nonsuicidal acts were more often reported as intended to express anger, punish oneself, generate normal feelings, and distract oneself, whereas suicide attempts were more often reported as intended to make others better off. Almost all participants reported that both types of parasuicide were intended to relieve negative emotions. It is likely that suicidal and nonsuicidal parasuicide have multiple intents and functions.

Some old people who ask physicians for assisted suicide report that they don't want to burden their families. I think it is a true reason for some people, while others would probably rather want to live, if they could stop being debilitated by old age. Again, the underlying reason is that these people feel they cannot change their situation to the better. Borderline women might feel the same, since their emotional instability, inability to have functioning relationships, fear and depression, are not momentary but have usually been there for all their adult lives, often as effects of some trauma such as childhood abuse.
Adolescents, who are often thought to be more self-centered and less socially concerned in their motives than old people, also report more self-centered reasons to kill themselves. In their study of adolescent suicide, Boergers, Spirito and Donaldson (1998, my emphasis) found that

Consistent with prior research, the most frequently endorsed motives for self-harm were to die, to escape, and to obtain relief. More manipulative reasons for overdose (such as making people sorry) were endorsed less frequently. Adolescents who cited death as a reason for their suicide attempt reported more hopelessness, socially prescribed perfectionism, depression, and anger expression.

With the restriction that we don't know who of the suicide attempters really wanted to die, nevertheless for most of them the primary reason was to end a life they had no hope of changing to the better.
Because what does it mean that you feel you are not perfect enough? For adolescents it usually means that you feel you are so ugly no one will ever love you, or that you are introverted and cannot make friends and have been outside the ingroup for so long that you no longer believe that anyone will ever love you. It does not matter if other, less pretty people, can be happy, or if other loners can make loner friends, the important aspect is that you feel you are not good enough to be loved by those that you want to love you and that nothing you ever do (makeup, bringing home good marks) can change that, because in truth, for example, it is not actually you who are unlovable but your parents who are unable to love you because of their own mental disorders (and that is how some of them are passed on through the generations).
Studying successful suicides, Cavanagh, Carson, Sharpe and Lawrie (2003) found that

mental disorder was the most strongly associated variable of those that have been studied. ... Suicide prevention strategies may be most effective if focused on the treatment of mental disorders.

This is of course a very global result, but it shows that people don't usually kill themselves because they experience dire circumstances or a bad phase in their lives, but only if their long term mental well-being is destroyed.
Linehan, Goodstein, Nielsen and Chiles (1983) have studied the reasons why people do not kill themselves. The primary reasons for living, if suicide was contemplated, were:

Survival and Coping Beliefs, Responsibility to Family, Child-Related Concerns, Fear of Suicide, Fear of Social Disapproval, and Moral Objections.

Besides fear (of dying and death and the judgment of God and men) and responsibility for family and children, the main reason to keep people alive was their belief that they could survive and cope! If we turn this around, the main reason to die (besides having no responsibility and not being afraid, or overcoming those concerns) is the belief of not being able to cope.
What makes you kill yourself, in sum, is that you can no longer take it and believe you cannot change it. Very simple – and horribly tragic.

Sources:

Boergers, J., Spirito, A., & Donaldson, D. (1998). Reasons for adolescent suicide attempts: Associations with psychological functioning. Journal of the American Academy of Child & Adolescent Psychiatry, 37(12), 1287-1293.
Brown, M. Z., Comtois, K. A., & Linehan, M. M. (2002). Reasons for suicide attempts and nonsuicidal self-injury in women with borderline personality disorder. Journal of abnormal psychology, 111(1), 198.
Cavanagh, J. T., Carson, A. J., Sharpe, M., & Lawrie, S. M. (2003). Psychological autopsy studies of suicide: a systematic review. Psychological medicine, 33(03), 395-405.
Linehan, M. M., Goodstein, J. L., Nielsen, S. L., & Chiles, J. A. (1983). Reasons for staying alive when you are thinking of killing yourself: the reasons for living inventory. Journal of consulting and clinical psychology, 51(2), 276.


Does motivation and interest correlate highly with IQ and can someone be smart but perform poorly in a particular field? Suppose a person is considered intelligent based on his IQ score. For example, suppose Bob has a high IQ score and is very interested in pure mathematics. He would most probably excel in this field. Now suppose Bob hated biology. He can't bring himself to learn anything about this field. Does this mean that Bob is "not intelligent" in the field of biology and only intelligent in the field of pure mathematics?

In other words, does motivation and interest correlate highly with IQ? Somebody can be "smart" but still perform poorly in various fields?

I have to disagree with Arnon a bit and want to expand on some of his points. The following is not meant as an answer to the question but just an extended comment to Arnon's answer.

General intelligence vs multiple intelligences

There are theories of intelligence that posit a general intelligence which determins performance in all areas. According to these theories performance in different areas must be correlated. And there are theories which assume different "intelligences" (verbal, spatial etc.) and a possibly different performance in different areas.

Intelligence vs talent

There are psychologists that use the term "intelligence" for an equally high performance in all areas, and the term "talent" for high performance in only one area and relatively lower performance in all other areas. Example:

IQ profile of a highly intelligent individual
---------------------------------------------

 IQ   verbal   mathematical   spatial      etc.

130     x           x            x          x      <- high intelligence

120

110

100

 90

versus:

IQ profile of a talented individual
-----------------------------------

 IQ   verbal   mathematical   spatial      etc.

130                 x                              <- mathematical talent

120

110

100     x                        x          x      <- average intelligence

 90

Fluid vs crystallized intelligence

Many theories assume two different aspects of intelligence: fluid intelligence, that is the potential or capacity for cognitive performance, and crystallized intelligence, that is the knowledge and learning an individual has acquired.

Depending on which theory you follow – general versus multiple intelligences, intelligence versus talent, fluid and/or crystallized intelligence –, your concept of what intelligence is will differ. Since the scholars creating IQ tests also have different opinions on this matter, their tests are (often extremely) differently constructed and test results from different tests often correlate only to a certain degree. That is, an individual scoring a high IQ in one test can have an average IQ according to another. Which is why, when reporting an IQ, you must also report the test with which it was measured, because otherwise the result is meaningless.

Measurement error and confidence interval

IQ tests don't measure very exactly. There is always a certain measurement error involved. Beacause of this, psychologists always calculate a range of values (a confidence interval) in which the true value of the individual probably lies. The exact true intelligence is always unknown and can in fact differ widely from a given test result. Therefore serious psychologists do not put much faith in the IQ score (that is considered unprofessional and ignorant) but rather report wether the individual's intelligence is average, above average or below average. No current IQ test allows for a more accurate assessment. Repeating measurements (with different tests to avoid learning and on different days) can increase exactness.


How is a young child able to learn language so easily? It's a well known fact that the earlier children are exposed to languages the better, as young children have a better ability to learn new languages than adults.

Why is this?
At what age does a human's mind start to lose this ability?
What causes the change?
Does this phenomenon have a name?

It's theorized that there is a Critical Period of language development in children below the age of five (roughly, as age ranges always are in Developmental Psychology).

Probably the most significant and readily verifiable finding is that a critical period exists for the learning of Phonemes. Research has suggested children readily differentiate phonemes from all human languages at very early ages; less than 5 years old. There is much debate in Linguistics on this matter and many articles covering the discussion .

After this Critical Period most children and adults can only accurately differentiate and produce phonemes present in their native languages and have difficulty producing and differentiating phonemes from other languages. This is why when learning a language late in life learners often struggle with pronunciation.

A classic example of this is the difficulty native Japanese speakers have with English L and R sounds. As L2, late-in-life second language learners they struggle differentiating the actual sounds and thus producing the different sounds.

There are some interesting theories in what can overcome this deficiency in learning "late" (L2) second languages, see Age and Ultimate Attainment in the Pronunciation of Foreign Languages and Teaching Second-Language Phonetics to Adults.

In addition Noam Chomsky has some interesting interviews and publications about language development in children, such as his interview with Lillian R. Putnam.

Note that Chomsky's opinions and theories are controversial, particularly his concept of a "Language Acquisition Device", which is Nativist to an extreme. There is much material on Chomsky's Theories of Language Acquisition but I would take his theories with a grain of salt.

The Critical Period has been found to apply even to children learning sign language. A good overview on this situation is The critical period for language acquisition and the deaf child's language comprehension : a psycholinguistic approach by Rachel I. Mayberry.

  The critical period hypothesis for language acquisition (CP) proposes that the outcome of
  language acquisition is not uniform over the lifespan but rather is best during early childhood.
  The CP hypothesis was originally proposed for spoken language but recent research has shown
  that it applies equally to sign language


What safeguards are in place to prevent abuse of power? In the U.S., what safeguards are in place to prevent a mentally ill, or just spiteful or incompetent, psychiatrist / psychologist from abusing their position of power?
Assuming the person is already practicing.

For example, are there any diagnoses that require an independent second opinion because of the serious consequences of acting on that diagnosis?

Obviously, this is especially important since- given the near complete power someone in this field could have over another person's life trajectory- the field will attract abusive people.

As @ArnonWeinberg mentioned, clinical supervision, detailed in my answer to the previous question will prevent abuse of position.

Clinical supervisors have a duty of care, not only to the supervisee (the therapist), but also the supervisee's clients, and if the supervisor feels that abuse of power is occurring they must refer it to the governing bodies to remove their licence to practice.

If they feel there are any mental health issues preventing the supervisee from acting effectively, then the supervisor will refer the supervisee for therapy. If necessary, they may also take further action to prevent the therapist from causing harm to their clients whilst undergoing therapy. I have added this point to my previous answer mentioned here.


How are real life events translated into dream symbolism? I'm interested in how significant events from daily life get encoded or translated into dream content. A personal observation can help clarify my question:

  I've observed that for me, "significant, futile mental effort"
  translates into dreams of me being in a classroom in my old middle
  school. The kind of mental effort dictated which classroom I will see
  - history, language or math.

It took me years to make the connection, as the frequency of the dream was rather high while attending school and college. It is only after I started working that I noticed dreams of classrooms were gone and only reappeared following intense, but perceived as pointless mental effort to learn or grasp or produce something.

I'm familiar with the Freud's theories on how wish fulfillment and repressed sexual desires show up in dreams. On the other hand I'm aware of the much discredited concept of "dream interpretation" with dictionaries of dream symbols.

Have there been studies that lay in between the two extremes listed above and attempted to elicit connections between daily events and how they appear in dreams? Maybe attempts to create personal dream dictionaries, like the one I described in the example?

We do not know a lot about how dreams work yet. However, there are some theories out there. One theory of particular interest is that are dreams are a means of reverse learning.

  In 1983
  Francis Crick of the Salk Institute in La
  Jolla, Calif., and Graeme Mitchison of
  the University of Cambridge in England
  proposed the idea of reverse learning.
  Working from the Hobson-McCarley
  assumption of random neocortical bombardment
  by PGO waves and their own
  knowledge of the behavior of stimulated
  neural networks, they postulated that a
  complex associational neural network
  such as the neocortex might become
  overloaded by vast amounts of incoming
  information. The neocortex could then
  develop false, or “parasitic,” thoughts
  that would jeopardize the true and orderly
  storage of memory.
  According to Crick and Mitchison’s
  hypothesis, REM sleep served to erase
  these spurious associations on a regular
  basis. Random PGO waves impinged on
  the neocortex, resulting in erasure, or unlearning,
  of the false information. This
  process served an essential function: it
  allowed the orderly processing of memory.
  In humans, dreams were a running
  record of these parasitic thoughts—material
  to be purged from memory.

At any rate, it seems that dreams are less a representation of an event and more a byproduct of random impulses coming from the brain stem. These may be made less 'random' (seemingly) only because the things we think about most and spend most our energy on are probably more likely to be 'happened upon' in the dream state.

Any further tendency to recognize a certain dream pattern after a certain event may be an occurrence of this, as well as an instance of selective remembering, or remembering the instances that support your case and neglecting the instances that don't. Having dreams of a classroom in college is normal because you are in classrooms (and you are unconsciously forced to remember the topics you have picked up on in your own middle school classrooms, which may be later 'dream material'), and associating these dreams with futile mental effort is a broad case, considering that college is essentially a four-year cycle of seemingly-futile mental effort. ;)


Way to influence readers subconscious to memorize technical data? I'm writing a technical book. Is there any studies/books on how can I influence the readers subconscious to help them memorize the technical data easier? Preferably ways that do not involve images, styles, etc.. as such techniques are not suitable for technical books.

Priming involves the perception of similar elements between information. The similarity between information influences the memory as it has already been primed by previous memory traces.

I do know of a study that suggests that when simple contours of an image are primed before complex versions of those contours, those contours are rated more positively (Reber et al., 2004).

The study relates to the theory of processing fluency, which proposes that the visual information is more liked because the information is more compatible than it would be otherwise (if the complex contour was shown without the simple one) that's only one part of the theory. The article is called:

The most simple answer is to relate the information with previously memorized information as it may be more likely to be recalled because it is connected to other memories.

Reference
Reber et al., Processing fluency and aesthetic pleasure: Is beauty in the perceiver's processing experience? Personality and Social Psychology Review ( 2004); 8(4): 364–382


How can one find out if he/she is brainwashed? By brainwashed I mean indoctrinated with some political, religious or other type of propaganda.

I assume that you can't be aware of this, because the lack of that awareness is the point of propaganda - to make you believe that something is true/false etc. But there must be a logical way to determine if you are brainwashed. Like "your" arguments following certain patterns maybe?

As Schroedinger's Cat pointed out, there's no clear dividing line between "brainwashing" and the normal processes of growing up in or assimilating into a culture or social group. Even in the case of deliberate, forced procedures, it can be unclear -- for example, the US military has recruits do drills and engage in synchronized practices that we know to affect thoughts, feelings, and beliefs, but most people wouldn't call that brainwashing. However, you could look into military training practices, as well as techniques used by abusive cults, and see if you've been subjected to those at any point in your life. That might answer your question.

Another way would be to think about the criteria you would use to describe a thoroughly un-brainwashed person, and work from there. For example, do you believe that you should be able to cite a preponderance of evidence for all of your beliefs? That you should have a clear and volitional explanation for your life choices? You can then work toward those goals, questioning or changing your beliefs as necessary. Be aware that hardly anyone really meets these criteria! We all absorb cultural values and prejudices, use unconscious heuristics to make decisions, and make choices that we rationalize later. But you could certainly work on moving in a more rationalist direction if you want to.


Can the Go/No-Go Association Task be faked? Go/No-Go Association task:

  The GNAT (pronounced like the bug) is a flexible technique designed to
  measure implicit social cognition.  Conceptually similar to other
  implicit measures like the Implicit Association Test (IAT; Greenwald,
  McGhee, & Schwartz, JPSP, 1998), the GNAT assesses automatic
  associations between concept (e.g., gender) and attribute (e.g.,
  evaluation) categories.  The GNAT has two features that distinguish it
  from other measures of implicit social cognition.  First, the GNAT is
  designed to be use signal detection statistics in its calculation of
  automatic associations (d-prime), but can also be adapted to utilize
  response latency as its operational dependent variable.  Second, the
  GNAT is flexible in the establishing of contextual characteristics for
  the evaluative situation.  For example, the IAT requires an attitude
  toward one category (insects) be assessed relative to a second
  category (flowers). With the GNAT, experimenters can vary whether
  insects are evaluated in the context of a single category (flowers), a
  superordinate category (animals), a generic category (objects), or
  with no context at all.

The GNAT is often used with the intention of obtaining an implicit measure of self-esteem, sexism, racism, aggression, and so on. In some cases, test takers may be motivated to score in a particular way on the GNAT (e.g., not implicitly sexist or racist).

Question

To what extent can the GNAT be faked?
If an individual does fake the GNAT, can the faking be detected?

I've never looked at the GNAT before but, even though it's just about as transparent as IAT, the critical thing making it difficult to fake bias is the deadlining.  In order to fake one would would have to respond in no-go trials where one would not and that also misrepresented their association.  That calculation would be difficult to do in the time window and possibly result in overall very high error rates.  I'm not a fan that they just throw out RTs.  Furthermore, calculating d' values does not by itself make a task better.

There's a general problem with many of these tasks in that the requested response is directly along the tested dimension.  What's implicit about that?  Asking you if bad goes with bug does not make for an implicit tests.  However, with something like the ALPS (Lebrecht et al 2009) you select an orthogonal dimension for the response (lexical decision in that case).  That seems much more like an implicit task and since people tend to be very response focused it makes it much less likely that subjects will pick up on how the test works and attempt to manipulate it.  You could also deadline that to make it even less likely that it's cheated.


What would be the result if a color-sound synesthete were to go color blind due to diabetes? Color blindness may be caused by diabetes. Would a color-sound synesthete lose her/his ability to hear two different tones when he/she is watching, let's say, magnets:
?

To whatever extent colorblindness is a consequence of sensation loss, perceptual loss should necessarily follow. If colorblindness results from diabetes solely due to retinal damage, this means diabetes prevents these two colors from causing different sensory stimulation. If the sensory stimulation is truly the same, it should be perceived the same. A signal (red) that cannot be discriminated from another signal (green) in terms of the basic sensation information received at the retina (stimulation of the same sets of cones, for lack of a more specially sensitive alternative) cannot be better discriminated in perceptual processes that occur thereafter in the brain, unless there's some other source of discriminating information involved in that perceptual process (I doubt there is in this case).

To answer @ChuckSherrington's expansion of the question, common cases of genetic colorblindness involve abnormal function at the retina as well, so there is likely to be some similarity. I'm unaware of any inherited conditions resulting in colorblindness through abnormal perceptual function (in the brain). However, the Wikipedia page draks linked lists quite a variety of manifestations for genetic colorblindness, so there probably are some subtle differences between the consequences of some genetic abnormalities and the consequences of diabetes. For instance, it seems genetically-based loss of color vision can affect one or more colors, partially or completely. Maybe diabetes-based symptoms are similarly various at certain stages! It is a degenerative process that can result in complete blindness, but which aspects of visual sensation are the first to go may vary across individual cases.


What was the quantified brain volume of Albert Einstein? I have read articles stating that Albert Einstein had an average brain volume but couldn't find a specific measurement. I'm curious because the articles are all so ambiguous. He could have been on the upper or lower side of average.

I was interested in the same question a while ago. Unfortunately, Witelson et al (1999) reported here (http://penthai.sc.mahidol.ac.th/html/articles/newsletter/paper3.pdf) that  volume measurements haven't been taken at the time. Weight data is available, but weight and volume aren't correlated perfectly.

Witelson, S. F., Kigar, D. L., & Harvey, T. (1999). The exceptional brain of Albert Einstein. The Lancet, 353(9170), 2149-2153.


How to get anatomical masks? I recently read a paper called "An automated labeling system for subdividing the human cerebral cortex on MRI scans into gyral based regions". I want to use the method of this paper to apply to my dataset in order to get anatomical masks. I already installed fsl on my Linux system. But I still cannot fully understand this paper. Specifically, I want to get Temporal Occipital Fusiform gyrus (TOFC) and the lateral occipital Cortex (LOC) region of interest. Anyone can help me?

I'm a TMS, but not an fMRI, researcher but I have experience using anatomical masks. I can guide you through the steps to make an anatomical mask, but unfortunately I don't have any code to offer you.

First of all you need a set of x, y and z co-ordinates that specify where TOFC or LOC are. One way to find these is to find a paper that reports the x,y,z values corresponding to a voxel that contains the peak BOLD signal change co-ordinates within the LOC or TOFC. An alternatively way, might be to find some anatomical studies that provide these co-ordinates for you. I cannot recommend one or the other to you; this is a decision for you to make based on the analyses you are doing.

Once you have found some LOC or TOFC co-ordinates you are happy with, you can create a mask based on them using FSLView (type in fslview in the Linux terminal to open it).

First of all, open FSLView and open one of the standardized brain images. You can enter your TOFC or LOC co-ordinates (in MNI or Talairach space - I'd recommend MNI) in FSL using the x, y and z boxes in the bottom left corner. This will move a crosshair on top of the peak voxel. Then click file - create mask. This will enable you to use the toolbar, on this toolbar you will see an icon shaped like a pencil. Use it to mark voxel the crosshair is pointing at, making it sure it corresponds to the voxels you entered earlier. Do this separately for both site

You can then save this you will have an image containing an anatomical mask indicating where LOC and TOFC are. If this is unclear, try this blog - an fMRI researcher in my lab found it really useful.

http://andysbrainblog.blogspot.co.uk/2012/11/creating-masks-in-fsl.html

Good luck!


Activity in a brain region and additional blood requirement: What is the causal relation? May I know causal dependence of the blood flow in the brain?

How it is determined by the brain that particular brain region requires additional blood?

The ion gradient that neurons use to transmit electrical signals is not free and costs energy to maintain, therefore needs oxygen and blood.

A brain region is considered "Active" if the neurons in said region are firing (or at least some subset of them). If a neuron fires then it releases chemicals known as neurotransmitters that stimulate (or suppress) activity in the down stream neuron it is connected to.

The cool thing is that the entire process of creating and sending neurotransmitters produces Nitric Oxide (NO) and in fact released as co-transmitters along with the main neurotransmitter.

Nitric Oxide is a small gas and as such diffuses through the brain relatively fast and causes the nearby blood vessels to relax( know as vasodilatation). This causes the blood cells to open and increase blood flow to the brain region.

However their are a few caveats as the relationship is not perfect one to one. What I mean by this is a group of neurons could be releasing a inhibitory neurotransmitter (and thus Nitric Oxide) onto a brain region and thus producing less activation, but still increases blood flow.

Here is a source on the internet if your interested in more. Sections 14.8 and 14.13 are of particular interest for NO and vasodilation in general.

Hope this helps. :)


"st" global variable in SPM8 I have some legacy preprocessing code that is designed to use SPM8. In the alignment function, it refers to a global variable st, which as far as I can tell is not described in the SPM8 manual. I'm updating the code to SPM12, which does not refer to st.

What exactly does st do in SPM8? Is there an equivalent in SPM12?

it seems that it is a struct variable that is central to how images are visualized in spm. I found a description in the spm source code in this github repository (I linked to the exact line where it is described, 158). You can check if it's the same in your spm8 installation by looking at the code of the file "spm_orthviews.m" which should be in the spm8 folder but I'm pretty sure it is the original version. They also use it in this how-to on wikibooks but I'm not entirely sure if it's exactly the same.

You can look at the same file in the spm12 folder (if it still exists) to find out if there is an equivalent.

Comment:

If you use this variable in your own script do your future self and others a favor and give it a meaningful name.


How can a human carry out a mass shooting whilst remaining calm? In the wake of the horrific terrorist attack in Christchurch New Zealand, it became known that the shooter had live streamed 17 minutes of his rampage to Facebook. In the video, of which I have only watched about 15 seconds from the point of the first shot being fired, the shooter can be seen extremely calmly carrying out his attack.

My question to the people here is, what is the root cause of a human being such as the shooter, being able to carry out such inhumane, disgusting, horrifying and downright evil acts whilst remaining so chillingly calm?

As someone with very little to no knowledge or experience with the relevant psychological literature, I have to ask, is this shooter a straight up psychopath? Surely the people who carry out such attacks have had some prior brain damage or genetic mental condition?

There may be less apparent contradiction if the shooter doesn't consider those behaviors as immoral, disgusting, etc. Consider a soldier in wartime: they might sometimes appear calm as well.

If you look at the stated justifications for mass shootings, they often have a specific purpose and apparently see moral reasons for their actions. Broadly speaking, people differ widely in what they consider ethical or moral. One person's virtue is another's sin. There are shared features between many ethical traditions, such as a prohibition against murder, but murder and war remain common. There is no need for a specific physiological fault like a brain injury or a particular genetic variant for humans to disagree wildly on what actions are appropriate. It's famously difficult to sympathize with the moral intuitions of other people; see for example https://en.wikipedia.org/wiki/Moral_foundations_theory. Instead of universal reasons, we generally have the strong feeling that something is right or wrong, and then we construct reasons.


What is receptor tonic activation? From Long-term administration of the dopamine D3/2 receptor agonist pramipexole increases dopamine and serotonin neurotransmission in the male rat forebrain:

  The sensitivity of postsynaptic D2 receptors in the prefrontal cortex (PFC) remained unaltered following pramipexole administration, as indicated by the unchanged responsiveness to the microiontophoretic application of DA. Their tonic activation was, however, significantly increased by 104% compared with the control level.

What does this mean? How does it enhance DA transmission?

Thanks.

In physiology, "tonic" refers to something roughly continuous or static.

In terms of receptor activation, tonic typically means there is some small quantity of agonist present such that the receptor is always activated a little bit. The receptors mediating tonic effects are typically "extrasynaptic": outside the synapse, and typically have higher affinity for their agonist. The opposite of tonic would be phasic - where a release of neurotransmitter causes an immediate and brief receptor activation.

In the passage you quote, they try puffing on some DA ("microiontophoretic application of DA") and they get the same response with and without pramipexole, so there is no effect on the phasic response.

However, the tonic activation, when they aren't puffing on DA, was increased. You normally measure this tonic activation by using a receptor antagonist (in this case they use haloperidol). The tonic activation is equal to (without antagonist) - (with haloperidol).

The drug they are using, pramipexole, is a D2 receptor agonist. How I would interpret their result is that, because pramipexole is around all the time during their experiments, there is constant low-level activity at the D2 receptor. They did not find evidence that this low-level activity decreased the response to phasic dopamine release, however; if it did, they would have seen a decreased response when they puffed on DA.

Chernoloz, O., El Mansari, M., & Blier, P. (2012). Long-term administration of the dopamine D3/2 receptor agonist pramipexole increases dopamine and serotonin neurotransmission in the male rat forebrain. Journal of psychiatry & neuroscience : JPN, 37(2), 113–121. doi:10.1503/jpn.110038

Grace, A. A. (2000). The tonic/phasic model of dopamine system regulation and its implications for understanding alcohol and psychostimulant craving. Addiction, 95(8s2), 119-128.


Different neural structures for quick vs. methodical decision making In the book "Thinking, Fast and Slow", the author claims that there are two systems of thinking. System 1 is quick, instinctive and emotionally driven while System 2 is more logical and deliberate.

Firstly, has there ever been any physiological proof, in terms of brain activation areas or other signs, that these two systems exist. If they do exist, have they ever been capture in a cognitive model, regardless of biological plausibility?

I would disagree with @Krysta: the distinction between system 1 and system 2 processes goes far beyond that of cognition with/without emotion: it's a complex debates that's been going on since the 70s (in it's current form, it's echoed in a wider debate going back centuries). For the sake of brevity, let me resort to bullet points.

For psychologists, Evans (2008) is the go to reference on this matter. Obviously, Kahneman is the grandfather of this topic, and his book is a great introduction for the layman, you'll find a much more rigorous discussion here.
There's a lot of variation in terminology here - while "dual process theory" is the commonly accepted generic term for this idea, you'll also see it as "type, or system 1/2 processes", "intuition/logic", "associative/controlled processes", etc. Again, see Evans (2008).
A nice simplification of the distinction would be to say there's two kinds of processes, System 2 processes, which requires Working Memory (i.e. maintaining, updating, and manipulating a representation of information over a period of time), and System 1 processes, which don't. System 1, when taken this way, isn't a single "subsystem", its a diverse set of processes (this idea is nicely laid out in Stanovich, 2009,
who uses the term "The Set of Autonomous Systems (TASS")),
amongst other sources) including evolved, domain specific modules for solving specific problems (i.e. recognising faces), the emotion subsystem, and rules and associations which have become automatic through experience, and implicit learning (stereotypes, for example).

To finally get to your question, yes, this does translate into specific neural systems.

Working Memory (and thus system 2 processes) is pretty clearly localised to the prefrontal cortex (see Braver et al, 1997, for example).
System 1, not being a single "system", obviously can't be localized to a single brain region. However, many of it's component processes can be: emotion to the limbic system, face recognition to the fusiform face area, etc. (I don't know much about localization of implicit learning, but I would guess the hippocampus is involved).

  I've just realised I haven't answered your second question, about cognitive models. I'll come back to this at a later date.
  EDIT I've just noticed you're working with Chris Eliasmith. I can think of few people better qualified to answer your second question than he is.

Reading

Evans, J. S. B. (2008). Dual-processing accounts of reasoning, judgment, and social cognition. Annu. Rev. Psychol., 59, 255-278.

Stanovich, K. E. (2009). Distinguishing the reflective, algorithmic, and autonomous minds: Is it time for a tri-process theory. In two minds: Dual processes and beyond, 55-88.


Provable ROI for call center rest periods? Think you can help make life better for a nation of call center workers?

At a large insurance company, I used to work in the call center for both Auto Claims and then Homeowner Claims, before I was promoted on to other things.  It's a complicated and stressful position, where customers are already upset because they have just gotten in a car accident or their house just burned down.

Call volume varies, but tends to be constant during many busy periods. As soon as you're done with one call, sometimes there's a lull, but usually another call is waiting.

The problem is that this leads to people taking a breather during "After Call Work," purposefully inflating their call time in order to catch a break from the stressful calls.

A potential solution, I've always wondered, is to pre-program an automatic break of no calls for X minutes after Y calls. (e.g. a 1 minute break after every 3 calls.)

My question is, would there be any scientific basis that could help justify a Return On Investment? Is a rest period worth the drain on phone coverage?  Or is it more beneficial to leave it up to the workers, to sacrifice their Average Handling Time at will to decompress at their own pace?

This is the paper you would want to read on this topic. The paper empirically compares four modes of managing interruptions. It is a great (and long) read so I'll try to summarize the bit for you:

There are thus four modes of managing interruptions:

Immediate interruptions. There is no management whatsoever. As soon there is a distracting stimulus/task, it has to be attended to. In your case, you could think of being in a conversation with one costumer and immediately being switched to another. You can already imagine this is not a very good one.
Negotiated interruptions. You can decide all by yourself whether and when to attend to the interruptions. You could choose to finish a difficult part of one task and only attend to the interrupting task when that is done.
Mediated interruptions. Some other metric decides when an interruption is deemed appropriate. A well known metric is workload, as measured by pupil dilation. To bigger you pupil is, the higher workload is. Interrupting would be best in low workload situations (Salvucci and Bogunovic,2010)). What you suggested, the cooldown time, is also a mediated system.
Planned interruptions. Interruptions only come at moments you have planned. Though this may seem nice, in many situations, such as yours, this is not possible. Even if you could plan the moments, in dynamic environments you cannot predict the best moments. You could have an incredible high workload on one day, and have nothing to do on another.

So which is best?

The results show that the best interruption management systems are a combination of negotiated and mediated management (believe me on this one, I do not want to discuss 20 pages of results here haha). Mediated management systems will determine the best moments of interruptions which is incredibly useful. However, if workload is very high for a longer period of time, the callers may be on hold for too long.

The negotiated management of interruptions allows people to work as hard as they can/want. Some people perform better under pressure than others and may choose to wait for a shorter period of time. The downside, however, is the fact that people are bad at this. Some people stress themselves out and never wait (Asking for reference here) and some people wait to long and may get distracted by other things (Katidioti et al.,2014).

A combination would thus be best. Mediate the interruptions, but allow the employees to continue working when they want to. In you case, you could have a short mandatory pause duration and a suggested longer pause duration (or conversely, an maximum pause duration). You could then determine the duration of the pause based on the length of the last call(s) for instance.

I hope this answers your question and if you have any questions just let me know.

EDIT: The literature I described above mainly focuses on multitasking, while your question is about sequential tasking. Nevertheless I do believe the above can be generalized to your problem. The interruptions are now in fact the breaks.

A final note, if people purposefully inflate there call time, this may be an indicator that workload is indeed too high. Talk with the people and ask what they think of the situation and what they think may be a good solution. When changing an interface/task/process, people accept the changes much more quickly if they are involved in the process (Asking for reference).

References:

Daniel C. McFarlane (2002): Comparison of Four Primary Methods for Coordinating the Interruption of People in Human–Computer Interaction

Salvucci and Bogunovic (2012): Multitasking and Monotasking: The Effects of
Mental Workload on Deferred Task Interruptions

Katidioti and Taatgen (2014): CHOICE IN MULTITASKING: How delays in the primary task turn a rational into an irrational multitasker


Quantify degree to which non-diagnostic features bias category-present response I need a measure of the degree to which each of several features biases participants to respond "yes" in a category present / absent task for each of several categories.

I have stimuli defined along 3 binary feature dimensions, let's call them a, b, and c. Each feature is perfectly diagnostic for 1 of 3 categories, let's call them x, y, and z, and perfectly non-diagnostic for the other 2. In other words, for example, a stimulus belongs to category x if it has feature a and not if it doesn't, and it is equally likely to belong to category y or not, and to category z or not, both when feature a is present and when it is absent. Participants are shown stimuli and asked whether or not they belong to a given category. In a given block of the experiment, they are only asked about 1 of the 3 categories.

So going back to my question, if the feature is the one diagnostic for the category, then correct response would be "yes" 100% of the time the feature is present and "no" 100% of the time the feature is absent. If the feature is one of the two irrelevant ones, then "yes" will be the correct response 50% of the time regardless of feature presence. In fact it turns out that people respond "yes" more than 50% of the time when the irrelevant features are present, and less than 50% of the time when they are absent, indicating that the irrelevant features bias them to respond "yes".

What I need is a way to quantify that effect. Things I've considered. (1) Subtract the positive response rate for feature absent from the positive response rate for feature present. 0% would indicate no bias for irrelevant features. (2) Divide the positive response rate for feature present by the positive response rate for feature absent. 1.0 would indicate no bias for irrelevant features. (3) Combining feature present and absent, divide the positive response rate by the correct response rate (i.e. the response rate of the perfect responder). 1.0 would indicate no bias for irrelevant features.

I am wondering whether there is a good "standard" measure for this kind of situation or, failing that, whether anyone can think of a good reason to prefer any one of the options above, or another one I haven't thought of.

I'm not sure whether or not signal detection theory is relevant here. My sense is that it's not, because I'm not looking for general response bias but rather the bias induced by specific features, and also because I have binary rather than continuous features, but I'm willing to be persuaded otherwise - maybe I just don't understand SDT well enough.

Oh, one other thing in case it matters - the stimuli in question are graphs and tables of data from 2x2 experimental designs, while the features / categories are presence / absence of main effects of each variable and the interaction.

I've been going through your question a couple of times now and I find it quite tricky to get all the details. So please correct me, if I misunderstood you in some point.

Basically you have a test and your subjects have to determine if a stimulus belongs to a certain category or not. Of the three possible features, one is a perfect indicator for a specific category, while the other two are unrelated to it. So far, so good. But I think that there are a couple of problems with the way that you framed the problem.

Correct Response vs. Expected Value

You say that,

  if the feature is the one diagnostic for the category, then correct response would be "yes" 100% of the time the feature is present and "no" 100% of the time the feature is absent.

Now, I think that there are three things mixed together in this statement:

the correct response,
a certain response rate whith which the correct response might be given and
the expected value of category membership given the perfect indicator.

These may seem like a subtle differences, but I would argue they are not. While you can determine, what the correct response to a question is, there is not really a correct response rate. When a subject answers a question correctly in 95% of the cases, he gave the wrong answer a couple of times. But the response rate is not right or wrong, it's just what it is. And the response rate does not have to equal the expected value (which is 100% in this case). Jeromy Anglim already commented somehting along these lines as well. This becomes even clearer for the next statement:

  If the feature is one of the two irrelevant ones, then "yes" will be the correct response 50% of the time regardless of feature presence.

Again, the expected value of category membership given an unrelated indicator is 50%. And since we know about that, we can formulate the hypothesis, that the subjects will catch on to it. But it's just a hypothesis and it cannot be taken for granted.

Is it really a bias?

Now, administering the test, you have found that

  In fact it turns out that people respond "yes" more than 50% of the time when the irrelevant features are present, and less than 50% of the time when they are absent, indicating that the irrelevant features bias them to respond "yes".

I'm not so sure that this really is a bias, at least not one that is caused by the features. As Jeormy Anglim mentioned in the comments, the subjects might come up with all sorts of strategies. A tendency to answer with "yes" might also be some sort of aquiescence bias (Ray, 1983). To be sure, that would be a bias, too, but it would not be caused by the features. But since it is not clear, how the subjects should respond to the test, it does not make sense to speak of a bias.

Quantifying the results

Having said all that, you could still quantify the results. A good way to do that would be to look at the conditional probabilities of a correct response, given a certain feature (which is what you already did). E.g. $$P(Y_x=1|a)$$ would denote the probability of getting a "yes" for an item $Y$ that asks about category $x$ when feature $a$ is present in the stimulus. You could do this for all combinations of categories and features. This would also allow for testing hypothesis about certain response rates like: Is the response rate for a certain combination significantly different from some value $P_0$?

The other suggestions that you make would work, as well. E.g. taking the difference between the conditional probabilities (like in your first suggestion. A result of zero indicates that there is no difference between the proportions.

If you are interested in pairwise comparisons you might take a look at the odds ratio (Agresti, 2007). The odds ratio considering features $a$ and $b$ for a given category would be defined as
$$OR = \frac{P(Y=1|a)/(1 - P(Y=1|a))}{P(Y=1|b/(1-P(Y=1|b)}$$
which is the same as
$$OR = \frac{odds(a)}{odds(b)}.$$

References:

 Agresti, A. (2007). An introduction to categorical data analysis (Vol. 423). Wiley-Interscience.
Ray, J. J. (1983). Reviving the problem of acquiescent response bias. The Journal of Social Psychology, 121(1), 81-96.


Term for when the more you invest yourself in something, the less you agree to drop it I have got a few examples::

For instance when someone buys something and it turns out that it wasn't worth it, and this person tries to convince himself that he made a good choice or that the product he bought is actually worth it (he cannot accept that he lost money in that process). That might be at the cinema when the movie is bad and you stay until the end because you've paid for it.
The other example is when someone made something which is likely to end badly, but the fact he began to follow this way lets him prefer to make an error later than go back on it immediately.

It seems to me that both are the same. I learnt the term for this phenomenon in a philo/psycho course at school a few years ago, I think the term is similar to "heuristic of loss", or maybe "bias of loss", but my search engine doesn't know that, so it is likely to be something else. It is possible that I mix up terms and concepts.

Not certain this is what you are thinking about, but this sounds a lot like the idea of "sunk costs", which is a form of loss aversion.

Sunk costs means that you tend to overvalue the effort you have already put in to something (time, money, etc), and often are willing to put in more effort to try to rescue what you already put in, even though the additional investment (again: time, money, etc) is not worth it. Often people make poor decisions (financial, relationship, etc) because they feel like they have "put too much in" to it.

A related concept is the Endowment effect (first mentioned in another answer by JoaoBotelho). Like sunk costs, some of the endowment effect can be explained by loss aversion, though some experiments have also shown a smaller mere ownership effect which is not also explained by loss aversion. These effects describe how people tend to put more value on things they own or have some relationship to (for example, an object held versus an object at a distance) versus things they do not.


Is there a benefit for humans to lose memory access when under elongated periods of stress? Long term anxiety causes memory loss. Sources: https://www.calmclinic.com/anxiety/signs/memory-loss and https://now.uiowa.edu/2014/06/stress-hormone-linked-short-term-memory-loss-we-age
Are there theories about the biological purpose of this connection? Is there a benefit for humans to lose memory access when under elongated periods of stress?

Disclaimer : this answer isn't backed by any source, aside from personal experience.
Edit : found a source https://health-clevelandclinic-org.cdn.ampproject.org/v/s/health.clevelandclinic.org/what-happens-to-your-body-during-the-fight-or-flight-response/amp/?amp_js_v=a6&amp_gsa=1&usqp=mq331AQHKAFQArABIA%3D%3D#aoh=16167791861704&referrer=https%3A%2F%2Fwww.google.com&amp_tf=Source%C2%A0%3A%20%251%24s&ampshare=https%3A%2F%2Fhealth.clevelandclinic.org%2Fwhat-happens-to-your-body-during-the-fight-or-flight-response%2F
My psychiatrist explained to me that people with anxiety are often in "survival mode". Not only when they are having a panick attack, but most of the time, because of the high stress levels. Imagine being constantly in danger. Thats' how we feel.
When in danger, our bodies prioritize all other important organs (heart, lungs...), and our cognitive capacities become impaired. When in danger, the last thing our body wants to do is to remember what's happening. All it wants to do is to flee that situation, or to fight the danger.
In addition, anxiety leads to exhaustion, which also impairs our cognitive capacities.
Again, I don't know if my psychiatrist made this up or if it's scientifically proven, but I thought it was an interesting insight.
I also have a little theory about it. I know it sounds stupid, but from my personal experience, a lot of events can be traumatic for someone with anxiety. An event (or even a simple thought) that is stressful for a normal person can completely destroy me.
I had a tendency as a child to block those memories so I won't remember them and trigger a panick attack. I remember whispering to myself "forget it" 3 times and move on with something else. It came to the point that I didn't even force myself to forget. I forgot the thing right after it happened.
The point is that we probably don't remember things because we trained ourselves to forget. But that's just my theory.
Feel free to respond and tell me what you think. And if you have some sources to back up or refute what I just wrote, please share them :)
Edit : found an article on training memory suppression https://www.healthline.com/health/how-to-forget-something#how-to-forget


Neuroplasticity and Treatment of Depression After reading 'The Brain That Changes Itself' by Norman Doidge, 'The Mind and The Brain' by Jeffrey Schwartz and a few other books, I've become curious about the science of neuroplasticity, which, as I understand, is a new paradigm in neurophysiology that replaced the older doctrine of brain immutability.

There's a wealth of empirical evidence in studies conducted by Bach-y-Rita, Taub, and Merzenich that confirms that brain remains plastic for pretty much the whole life, after a period of hyperplasticity in childhood.

This seems to be a powerful tool that can contribute to treatment of various disorders, such as depression and anxiety, especially in cases when the condition is resistant to medication. I'd like to know if this idea has been applied with some success, and if anyone developed a specific neuroplasticity-based approach.

It may interest you to know that depression and anxiety relate to emotional stability (essentially the opposite of neuroticism), a personality trait which tends to decrease over the lifespan, especially in young adulthood (Roberts & Mroczek, 2008). Here's a figure depicting this trend (bottom left):

This article points out that most of the personality changes depicted above occur during young adulthood. This supports the hypothesis that plasticity is an important enabling factor in these changes. Roberts and Mroczek also describe these changes as mostly positive, which supports the hypothesis that these changes are a partly intentional process of social adjustment. I'm not aware of any evidence that supports these hypotheses more directly, but any such evidence would also support the plausibility of interventions that target neuroticism during earlier life stages when plasticity is generally greater.

The language of plasticity appears sparsely in a similar article that describes change in adult personality (Srivastava, John, Gosling, & Potter, 2003), though no explicit references to neural plasticity appear. However, this article also presents a complication and a challenge through its own evidence of change in neuroticism over the lifespan, depicted in this figure (top left; neuroticism $\approx (-1)\cdot$ emotional stability):

The complication is the sex difference in change over time: only women's neuroticism seems to decrease in this study's evidence. The challenge is the apparent linearity of both trends; neither supports the importance of plasticity. Therefore it's not clear that any intervention focused on altering neuroticism would function equally well for both sexes, nor take advantage of neuroplasticity. Nonetheless, a very recent article recognized the malleability of neuroticism and recommended exploration of options that would intervene at this basic trait level of disorder development (Barlow, Sauer-Zavala, Carl, Bullis, & Ellard, 2013, in press). Thus it seems further evidence to support your idea may be forthcoming!

Neuroticism aside, other recent articles have promoted biofeedback, neural decoding, and neural interface technology as ways of "targeting", "promoting", and "exploiting" neuroplasticity in treating neurological dysfunction (Wang et al., 2010; Seitz, 2013; incidentally, Seitz works at my alma mater and published this shortly after I graduated...it's a small world). Biofeedback and neurofeedback have established applications in the treatment of depression and anxiety (see for review Yucha & Montgomery, 2008). Biofeedback methods seem to have been around just about as long as theories of neuroplasticity (discounting one particularly early study at the end of the 18th century), so I wouldn't say biofeedback was intended as a neuroplasticity-based approach, but evidently it has turned out to be a somewhat inadvertent application of neuroplasticity. Clearly, theorists and clinicians are actively capitalizing on this convenient convergence of neurology and clinical methodology – this trend seems likely to continue.

References

- Barlow, D. H., Sauer-Zavala, S., Carl, J. R., Bullis, J. R., & Ellard, K. K. (2013, October 14; in press). The nature, diagnosis, and treatment of neuroticism: Back to the future. Clinical Psychological Science, DOI: 10.1177/2167702613505532.
- Roberts, B. W., & Mroczek, D. (2008). Personality trait change in adulthood. Current Directions in Psychological Science, 17(1), 31–35. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2743415/.
- Seitz, A. R. (2013). Cognitive neuroscience: targeting neuroplasticity with neural decoding and biofeedback. Current Biology, 23(5), R210-R212.
- Srivastava, S., John, O. P., Gosling, S. D., & Potter, J. (2003). Development of personality in early and middle adulthood: set like plaster or persistent change? Journal of Personality and Social Psychology, 84(5), 1041–1053. Retrieved from http://j.b5z.net/i/u/2043019/i/PersonalityDevelopmentInAdults.pdf.
- Wang, W., Collinger, J. L., Perez, M. A., Tyler-Kabara, E. C., Cohen, L. G., Birbaumer, N., ... & Weber, D. J. (2010). Neural interface technology for rehabilitation: exploiting and promoting neuroplasticity. Physical Medicine and Rehabilitation Clinics of North America, 21(1), 157–178. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2788507/.
- Yucha, C., & Montgomery, D. (2008). Evidence-based practice in biofeedback and neurofeedback. Wheat Ridge, CO: AAPB. Retrieved from http://web.archive.org/web/20101009135554/http://isnr.org/uploads/EvidenceBasedYuchaMontgomeryW.pdf.