Is Hypnosis more effective than a placebo? Hypnosis has been proven effective as way to treat various illnesses. So have placebos. My question is, is Hypnosis more effective than a placebo?

In particular has there any experiments comparing the effects of real hypnosis v.s. fake hypnosis?

Answering your first question...

This paper does a handy job of describing the situation. Specifically, it describes how "more effective" may not be the correct way of looking at the comparison between hypnosis and placebo. Specifically, these methods may function differently, depending on the activity of the individual's prefrontal cortex:

  "In conclusion, whilst there are potentially informative similarities between hypnotic suggestion and placebos, their differences, particularly with regard to the differential contributions of regions of the prefrontal cortex, are also potentially informative as to the nature of suggestion more generally." (Parris, 2016).

I'd copy the whole 5th and 6th paragraph of this article if I could: I recommend giving it a glance!

Long story short: recent research seems to suggest that patients may be more or less susceptible to these different treatments depending on the level of activity in the PFC.

References

Parris, B. A. (2016). The Prefrontal Cortex and Suggestion: Hypnosis vs. Placebo Effects. Frontiers in Psychology, 7, 415. http://doi.org/10.3389/fpsyg.2016.00415


What coding scheme does NEF use? Rate or phase? There is a long-standing debate in theoretical neuroscience about what information of spikes is most important: rate or phase? What stance does the NEF take on this manner?

The NEF has no formal stance on whether rate information or phase information is of importance. All it cares about is spikes.

As proof, consider the derivation of the decoders, which is the core of the NEF.

The Decoders, $d$ are a vector of synaptic weights applied to the activities of neurons (one decoding weight per neuron) to approximate a given function $f(x(t))$. They can be thought of as the axons of a neuron.

Given the spiking neurons activities in the matrix $A$ (rows are neurons, columns are evaluation points), to an input $x$, this relation can be explained as:

$$A \cdot d = f(x(t))$$

Given an equation with one unknown, where a matrix $A$ is combined with a vector $d$ to get another vector $f(x(t))$, this can be solved using linear algebra to find $d$.

Note how there is no mention of rate or phase in this derivation. Admittedly, in the Nengo neural simulator, rate neurons can be used and functions that take phase into account can be calculated, but these design choices are up to the modeller and are not forced by the NEF itself.


Is it possible to calculate the probability of a child having an IQ in a certain range based on their parents' IQ? For instance, if two parents have IQs of 160, can one calculate the probability that their child has an IQ over 160?

This is precisely the question Galton had in mind when he invented regressions. He tested it with heights. Given parents heights, their children height is actually more likely to be closer to the population mean. So high parents tend to have smaller children, and short parents taller children (hence the term "regression"). To answer your question, a children of parents with high IQs (160 is very high), is likely to have a higher IQ than the average population, but lower than the parents. This is even more true than for height as IQ is a lot less heritable. The precise likelihood can be calculated given some assumption.

Galton, F. (1886). Regression towards mediocrity in hereditary stature. The Journal of the Anthropological Institute of Great Britain and Ireland, 15, 246-263.


Can you give an example of automatic appraisal process? I was reading this slide provided by my prof. of Affective Neuroscience.
I've read that appraisal is considered a constitutive component of emotion by most of the actual theories.
Appraisal is defined as the cognitive act to evaluate the potential impact that an external stimulus may have on me.

Can you provide an example of automatic appraisal?

We make automatic "appraisals" in more or less every waking moment.  We are constantly predicting the potential allostatic consequences of external input and behaving accordingly (e.g., here). Importantly, most appraisals are non-conscious and aren't at all specific to emotions.

Moreover, the automaticity of your appraisals relies on the extent and precision of your prior experience (see here).  If you are used to seeing snakes attack humans, then your appraisal about the danger of snakes will likely be quite fast.

Thus, there are virtually infinite examples of an automatic appraisal.  Automaticity depends on your prior experience and the precision of incoming sensory input.


How does chronic stress improve memory processes? There seems to be more information on the detrimental effects of stress on memory.

There is evidence to the contrary.

Stress effects on memory: an update and integration.
Schwabe L, et al  doi: 10.1016/j.neubiorev.2011.07.002

  It is well known that stressful experiences may affect learning and memory processes. Less clear is the exact nature of these stress effects on memory: both enhancing and impairing effects have been reported.

I am interested in the research available on stress positively effecting memory.

What are the biological reasons for stress enhancing memory processes?

There is a related question Can the brain work better in stressful conditions?; I am interested more in chronic stress. An examination of the effects of acute stress on memory, I believe, warrants a separate discussion.

Interesting question. Intuitively, I would have thought that chronic stress would uncompromisingly be a detriment to our memory and recall.

An article by Ohira et al (2011) makes note that it is accepted that chronic stress is seen to adversely affect memory, it may not be replicated in other studies:

  "However, results related to the effects of chronic job stress
  and cognitive functions remain controversial. Although
  chronic job stress is generally linked to reduced memory
  and learning (Holman and Wall, 2002; Taris and Feij,
  2004), a recent epidemiological study with a larger sample
  size failed to replicate these effects (Elovainio et al., 2009)."

Other studies may indicate that predictable chronic mild stress can improve hippocampal neurogenesis and memory (Parihar et al., 2011). Your question doesn't describe the level of stress experienced as a variable so broadly, this article might be very relevant:

  "Furthermore, enrichments in mood and memory after PCMS were
  associated with substantially increased hippocampal neurogenesis ...
  The overall stress reaction in an organism can be advantageous for
  cognitive functions when it induces moderate increases in
  corticosterone levels and leads to adaptation and resistance ... The
  PCMS regimen used in this study likely elicited moderate increases in
  corticosterone levels, which facilitated adaptive and beneficial
  responses in the brain."

It's implied that unpredictable chronic stress would have a detrimental effect on memory. Some of the biological reasons for enhancing memory processes are presented in that above study.

EDIT: Additional Information

Also see - McFadden, L.M., Paris, J.J., Mitzelfelt, M.S., McDonough, S., Frye, C.A. & Matuszewich, L. (2011). Sex-dependent effects of chronic unpredictable stress in the water maze. Physiology & Behavior, 102(3), 266-275. The research conversely highlights that unpredictable stress improves performance on a spatial memory task in female rats.

References

Ohira, H., Matsunga, M., Kumra, K., Murakami, H., Osumi., T., Isowa, T., Fukuyama, S., Shinoda, J. & Yamada, J. (2011). Chronic stress modulates neural and cardiovascular responses during reversal learning. Neuroscience, 193, 193-204
Parihar, VK., Hattiangady, B., Kuruba, R., Shuai, B. & Shetty, AK. (2011). Predictable chronic mild stress improves mood, hippocampal neurogenesis and memory. Molecular Psychiatry, 16, 171-183


Does stimulus-independent ERP make sense/ exist? Is anyone aware of any concept of stimulus independent ERP (an apparent oxymororn, an event related potential that is neither sensory, cognitive nor motor elicited) ...or a procedure that looks specifically at noise waveform during ERP trials.....

Basically I am trying to think of an analogue of resting-state fMRI for EEG. My logic is that we can find a stimulus-independent ERP signature by
a) either taking EEG values every say 1 sec without any repetitive stimulus and averaging them just like in traditional ERP to get a stimulus independent ERP waveform
b) we can have a repetitive sound stimulus say every 1 sec and average the square of the waveform over the trials and subtract the square of the ERP calculated in usual manner. the resulting waveform will be reflective of noise.

The idea is that a waveform that is stimulus-independent / noise driven may be equivalent in value to resting-state fMRI procedures and the components of such waveforms may be of some help in delineating one person from another based around neural speed etc.

I want to find out if the concept already exists or makes sense?

An ERP is an Event Related Potential, making it inherently connected to an event. Having stimulus/response independent ERPs is thus impossible. There do exist potentials that seem to be stimulus independent, or at least vary in timing, but these are often the result of cognitive processes. These potentials are the result of Event Related (De-)Synchronization (Pfurtscheller, 1999), for which you need to look into the time-frequency domain, instead of the time domain (in which the ERP is visible).

By use of a Fourier transform you can subdivide brain activity into sinussoids with different frequencies and amplitudes. These sinussoids are grouped based on their frequencies in the groups commonly referred to as the "frequency bands". These include the delta- (0-4 Hz), theta- (4-8 Hz) alpha- (8-12 Hz), beta- (12-±30 Hz) and gamma frequency band (30+ Hz). The exact frequencies and groupings tend to vary between researches however (wiki).

It is the time-frequency domain that you can study independent of stimuli. The power in the frequency bands can be computed in real time by use of a time-frequency analysis. The steady state potentials are often used to compare brain activity between doing (nearly) nothing, and performing a particular task. This allows you to investigate what frequency bands show more (or less) activity (i.e. a higher or lower power) in particular brain areas. See Method/Unit for measuring activity in specific frequency band for EEG and Are brain waves electromagnetic waves? for some more specific info on EEG and analyzing data in the (time-)frequency domain.

Pfurtscheller, G., & Da Silva, F. L. (1999). Event-related EEG/MEG synchronization and desynchronization: basic principles. Clinical neurophysiology, 110(11), 1842-1857.


Why do we come to like some songs after re-listening to them a few times? It happens in the case of some songs that they don't strike as extremely good the first time one listens to them but after listening to them a few more times, one suddenly starts loving them. What difference does the re-listening do?

The phenomenom you describe is called Mere-exposure effect :

The mere-exposure effect is a psychological phenomenon by which people
tend to develop a preference for things merely because they are
familiar with them. In social psychology, this effect is sometimes
called the familiarity principle. The effect has been demonstrated
with many kinds of things, including words, Chinese characters,
paintings, pictures of faces, geometric figures, and sounds.
The mere-exposure effect has been explained by a two-factor theory
that posits that repeated exposure of a stimulus increases perceptual
fluency which is the ease with which a stimulus can be processed.
Perceptual fluency, in turn, increases positive affect.

The perceptual fluency is explained in detail by the article in @mrt comment.


Are scintillating scotomas really caused by cortical spreading depression? If so, how is this known to be true? I have just read about a visual effect called a scintillating scotoma.

Many variations occur, but scintillating scotoma usually begins as a spot of flickering light near or in the center of the visual field, which prevents vision within the scotoma area. The affected area flickers but is not dark. It then gradually expands outward from the initial spot. Vision remains normal beyond the borders of the expanding scotoma(s), with objects melting into the scotoma area background similarly to the physiological blind spot, which means that objects may be seen better by not looking directly at them in the early stages when the spot is in or near the center.
[...]The visual anomaly results from abnormal functioning of portions of the occipital cortex at the back of the brain, not in the eyes nor any component thereof, such as the retinas.3 This is a different disease from retinal migraine, which is monocular (only one eye).

It is a phenomenon that is believed to occur in the brain.

Scintillating scotomas are most commonly caused by cortical spreading depression, a pattern of changes in the behavior of nerves in the brain during a migraine.

That article is short and includes an impressive looking GIF of an optical image of the brain showing a wave-like pattern of blood volume which seems to come from the YouTube video Spreading Depolarization viewed using IOS. Santos et al. Neuroimage 2014 which links to Santos, E. et al. Radial, spiral and reverberating waves of spreading depolarization occur in the gyrencephalic brain NeuroImage, 99, 1 Oct. 2014, pp244-255.
The first Wikipedia article also says:

Symptoms typically appear gradually over 5 to 20 minutes and generally last fewer than 60 minutes, leading to the headache in classic migraine with aura, or resolving without consequence in acephalgic migraine. Many migraine sufferers change from scintillating scotoma as a prodrome to migraine to scintillating scotoma without migraine. Typically the scotoma resolves spontaneously within the stated time frame, leaving no subsequent symptoms, though some report fatigue, nausea, and dizziness as sequelae.

I don't completely understand the language there; I am not sure if it means that scintillating scotoma is always associated with some kind of migraine, or if they also occur as isolated events.
QUESTION: Why is it believed, or how is it known (if it is) that scintillating scotomas are caused by cortical spreading depression? Are these always related to some kind of migraine?
 Source
 Source
   Sources: 1, 2

The primary visual cortex is topographic, which means that specific parts of that brain region correspond exactly to specific parts of your visual field. In order to prove that a scotoma (literally a blind spot in your vision) is due to dysfunctional neurons, all you need to do is show that the neurons responsible for that spot in your vision are not working but the rest of them are. We can do this with a variety of tools, the most common one these days being fMRI. In addition to showing that the area of neuronal dysfunction maps onto the area subserving vision in that area where the scotoma is located, a spreading depression does exactly that: it spreads, at a predictable rate, from the location of its onset to adjacent brain tissue. fMRI will show you not only the area of brain dysfunction, but will allow you to "follow" the neuronal dysfunction as it moves over time, and show that it corresponds to the location of the scotoma in your visual field, which will also move in correspondence. HTH. See: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC31895/ for first reference to this type of research (more in pubmed with keywords fMRI and migraine aura).


Does a true hallucination need to go away while plugging one's ears? Can an auditory hallucination be true hallucination even if the person clàims that it doesnot reduces in volume when he plugs his ears. Similarly can a visual hallucination still be a true hallucination even when it doesn't disappear when person closes his eyes??

A hallucination is a perception in the absence of external stimulus that has qualities of real perception and hallucinations can occur in different ways.

Visual hallucinations can occur with the eyes open or closed (see also).  Visual hallucinations can also occur with people who have lost their sight

Just like visual hallucinations, auditory hallucinations can also occur with the ears open or plugged.  To highlight the point, I suffer with tinnitus and I hear the noise with my ears plugged or open. Auditory hallucinations can also occur in people with hearing loss


Who are the main authors who studied meditation with scientific methods? I wold like to know who are the main authors (and texts) which studied meditation using a scientific method and reported their results in a text that I can use for reference when I'm talking about meditation. Is there a scientific text which has been used for reference on this topic in the last years or there are only spread articles? An historical prospective is however welcome if is a good reference in the topic for the historical part.

Searching for "meditation" on Google Scholar  sorts articles by relevance and provides counts of citations that each has received. From the first page of about 686,000 results, these are the references with over 1000 citations each (I've sorted them by citations, which Google Scholar does not do easily):

Kabat-Zinn, J. (1994). Wherever you go, there you are: Mindfulness meditation in everyday life. Hyperion.

1971 citations!

Davidson, R. J., Kabat-Zinn, J., Schumacher, J., Rosenkranz, M., Muller, D., Santorelli, S. F., ... & Sheridan, J. F. (2003). Alterations in brain and immune function produced by mindfulness meditation. Psychosomatic Medicine, 65(4), 564–570.

1811 citations!

Kabat-Zinn, J. (1982). An outpatient program in behavioral medicine for chronic pain patients based on the practice of mindfulness meditation: Theoretical considerations and preliminary results. General Hospital Psychiatry, 4(1), 33–47.

1315 citations.

Peterson, L. G., & Pbert, L. (1992). Effectiveness of a meditation-based stress reduction program in the treatment of anxiety disorders. Am J Psychiatry, 149, 936–943.

1295 citations.

Kabat-Zinn, J., Lipworth, L., & Burney, R. (1985). The clinical use of mindfulness meditation for the self-regulation of chronic pain. Journal of Behavioral Medicine, 8(2), 163–190.

1002 citations; same author as the top result – probably one to follow for buzzworthy work.

Of course, you can edit the search terms, or set a custom range of publication dates if you want to look for references of more historical relevance. I don't think you should prefer textbooks over articles unless you're really looking to refer your audience to a comprehensive introduction to the topic.


Specification of SuperMemo 2 I'm confused about the exact specification of the SuperMemo2 algorithm for spaced repetition learning, as explained here. After each repetition, the E-Factor has to be updated like so:
\begin{equation}
  \text{EF}_\text{new} := \max \{1.3, \text{EF}_\text{old}+(0.1-(5-q)(0.08+(5-q)0.02))\},
\end{equation}
where $q$ is the quality of response on a 0 to 5 scale. The interval $I_\text{new}$ until the next repetition is supposed to be
\begin{equation}
  I_\text{new} = I_\text{old} \cdot \text{EF},
\end{equation}
but the specification does not explain whether to use the old or the new value of $\text{EF}$. Which one is it?

The implementations I found readable seem to be wrong in other places, so I'm not very confident that they are a reliable source on this issue.

$EF$ is the "easiness factor". This means that the greater easiness you have, the longer will be the interval to next review ($I_\text{new}$).

So if you will use the old $EF$, the new interval value will not take into account your last review quality, which makes less sense IMO.

For the other hand, as I can see in the original implementation of algorithm, they calculate the interval first and then they calculate the easiness:

procedure Repetition(ElementNo,Grade:longint;var NextInterval:longint;commit:WordBool);
  var DataRecord:TDataRecord;
  begin
    DataRecord:=GetDataRecord(ElementNo);

    with DataRecord do
    begin
      if Grade>=3 then
      begin
        if Repetition=0 then
        begin
          Interval:=1;
          Repetition:=1;
        end
        else if Repetition=1 then
        begin
          Interval:=6;
          Repetition:=2;
        end
        else begin
          Interval:=round(Interval*EF);
          Repetition:=Repetition+1;
        end;
      end
      else begin
        Repetition:=0;
        Interval:=1;
      end;

      EF:=EF+(0.1-(5-Grade)*(0.08+(5-Grade)*0.02));

      if EF<1.3 then
        EF:=1.3;
        NextInterval:=Interval;
      end;

      if commit then
        SetDataRecord(ElementNo,DataRecord);
      end;

The same is in the specification: they calculate next interval at step 3 and $EF$ is calculated at step 5.

I'd like to understand what all these magic coefficients mean and how they were found, but unfortunately didn't find this information.


Is it dangerous to take an antipsychotic drug irregularly? I've read the case of Witty Ticcy Ray: a 24 years old man with disabling Tourette’s syndrome.
The first Dr. Sacks's treatment, with Haldol, provokes a strong change in Ray's behavior: from tics and excitement to a catatonic state. Ray didn't like this.

They had a period of three months of therapy in which Ray could express himself, he said that he couldn't live without his disease.

Finally they found a compromise: During the week, Ray took Haldol, on weekends, he stopped it and he was again ’witty ticcy Ray’. This therapy was accepted by the patient and was succesful.

Is it in any way dangerous to take an antipsychotic drug with that discontinuity?

Haldol (haloperidol) is mainly known for its antipsychotic properties to treat schizophrenia. It's an aged antipsychotic with a lot of side effects. Because of this, haloperidol is nowadays mostly replaced by the atypical antipsychotics, such as clozapine as first-line treatment.
Haloperidol's primary mechanism of action is believed to be related to its antagonistic effects on the dopamine D2 receptor (Seeman, 2002). However, it indeed also finds use in controlling tics and vocal utterances that are part of Tourette's syndrome (Messiha et al., 1971).
Given that it may take several weeks before haloperidol's effects become apparent, it should be taken continuously. But perhaps even more importantly,  sudden termination of taking haloperidol can lead to unpleasant withdrawal symptoms, including

Delusions, hallucinations and psychotic episodes;
Breathing problems
Tremors, tightening of the muscles;
Dry mouth, loss of control of your tongue;
Blurry vision;
Restlessness.

In all, haloperidol looks like a medicine that should be taken regularly.
However, I couldn't find evidence that it is in any way dangerous to take it on an irregular regimen.
References
- Messiha et al., Life Sciences (1971); 10(8-1): 449-57
- Seeman, Can J Psychiatry (2002); 47(1): 27-38


Will smoking marijuana lightly during teens cause developmental damage to the brain? If someone were to smoke marijuana lightly during his teens and stop abruptly in his adulthood. Would he suffer from Some type of damage to his short term memory/iq and if so can the damage be reversed?

It is impossible to say with any degree of certainty whether a given individual will or will not suffer from any consequences of any amount of marijuana consumption, so we'll have to use the scientific data which can only say something about group-level effects.
It is quite well known that cannabis impairs cognition in the short-term*, and that the effects may last for at least a while of abstinence in heavy users. What you're asking about is whether there are any lasting and irreversible effects of cannabis on cognition, and this remains a debated and unresolved question in the scientific literature on harmful effects of cannabis. For instance, a recent review find inconsistent evidence for long-term working memory deficits in current heavy users and limited evidence for recovery after abstinence. In the same study, similar results are reported for other areas of cognition.
When it comes to IQ, there are some long-term studies that assess whether there are lasting long-term effects of cannabis on IQ. I believe the first such study was the one published by Meier and colleagues in 2012, in which they reported that among heavy users who had begun using cannabis before the age of 18, there was a lasting decline of IQ from childhood to mid-life with about 8 points, that persisted even after cessation of cannabis use. A similar study was published in 2016 by Mokrysz and colleagues, finding no decline of IQ between ages 8 to 15 in adolescents and pre-teens who had used cannabis during those years. Both studies may be subject to methodological criticism, and to my knowledge, there are no other studies with similar design.
Another issue is whether cannabis impacts brain development and/or causes morphological brain changes. The literature on this topic is also on the whole inconclusive, as shown in a recent review by Kroon and colleagues. However, it should be noted that there is actually some evidence ("limited evidence") for reduction in the volume of prefrontal cortex and hippocampus, which is consistent with animal studies in which especially a reduction of hippocampus volume can be induced under experimental conditions.
In short, the scientific literature in this area is on the whole inconclusive, and while it cannot be ruled out that there might be irreversible negative effects of cannabis on cognition, especially in those who start to use cannabis early and develop a heavy use over long periods of time, there are no hard evidence to support this either.
*. Though there is also some reports indicating positive effects of cannabis on divergent thinking (i.e. "out of the box"-thinking), which might be considered a positive effect on cognition.


A type of long-term memory where I can remember full dialogues My female colleague cannot remember a discussion (dialogue) from a couple days ago or even yesterday, much less the full, exact sentences spoken. She jokes about having sclerosis. I can remember many dialogues from the last couple of years and even further, including the exact sentences – not all the dialogues from my life, but like 80% of those which were interesting, odd, or very funny, or made at least small impact in my life. Is this kind of long memory normal in people? Does it have a name?
Thanks.

the cognitive skills of a human population have a great variance. I am more like your friend, with episodic memory below average but semantic memory above average. You seem to have episodic memory above average (I envy you on that, because a large part of our feeling of self identity depends on episodic memory). There are extreme cases of people that remember almost everything they experience or read, or hear. A nice book on the topic is Luria's book "the mind of a mnemonist". It is a short book, and I'm sure you'll find it pretty interesting.


Why are religious people seemingly unable to hypothesise about a universe without God? I know many devoutly religious people despite being totally atheist myself. I have occasionally discussed their beliefs and their religion with them, always respectfully. I am able to hypothesise scenarios assuming their beliefs are correct. However, when I ask them to consider my point of view, they seem unable to do so, because to them it doesn't make sense that God doesn't exist, or whatever else is said in their religious texts.

I view it like visiting their home. I can visit them and enjoy their hospitality and they enjoy showing me around their home but I don't want to move in with them (convert to their religion). If I invite them to visit my home (hypothesise a universe without God), they always refuse. I'm not suggesting that they move in with me (become an atheist), and in fact, I don't care whether they do or not, and I don't even have any expectation that they would.

It seems as though atheism is so uncomfortable to them that they reject it without examining it except in a very general and distant way. The strange thing is, that they all view me as a good person despite me not sharing their beliefs.

Why is it so difficult for them to discuss atheist principles when I have no trouble discussing their religion with them? In fact, I find religions fascinating in the same way that I find people living in other countries fascinating.

To quote the great Aldous Huxley :

How shall we define a god? Expressed in psychological terms (which are
primary-there is no getting behind them) a god is something that gives
us the peculiar kind of feeling which Professor Otto has called
“numinous”. Numinous feelings are the original god-stuff from which
the theory-making mind extracts the individualised gods of the
pantheon.
— Aldous Huxley

Even "the Hitch" acknowledged the Numinous :

I’m a materialist…yet there is something beyond the material, or not
entirely consistent with it, what you could call the Numinous, the
Transcendent, or at its best the Ecstatic. […] It’s in certain music,
landscape, certain creative work, without this we really would merely
be primates. It’s important to appreciate the finesse of that, and
religion has done a very good job of enshrining it in music and
architecture.
— Christopher Hitchens

However, he also pointed out this :

I think everybody has had the experience at some point when they feel
that there’s more to life than just matter. But I think it’s very
important to keep that under control and not to hand it over to be
exploited by […] those who think that God has given them instructions.
— Christopher Hitchens

This is the cause of the divide between Theists and Atheists. Both experience the Numinous more or less the same way, but Atheists look for explanations in science whereas Theists look for ancient texts they believe to be divine revelations.
So why do some look for explanations in science whereas others look for explanations in ancient texts? It's a matter of cognitive style. More in particular, in depends on your empathy and systemizing quotients.
Extreme systemizers are not very likely to follow "their gut" (they may even be incapable of experiencing intuition). Because of that, they're also less likely to follow any kind of external authority. Their systemizing nature requires a rigidly consistent logical framework to make sense of things, which they often find only in science.
In contrast, extreme empathizers are more likely to follow "their gut", and also more likely to follow any kind of authority (including ancient religious texts). They tend to feel a lot more comfortable with experiencing cognitive dissonance and logical frameworks lacking consistence, which is common for religion.
Still, I believe the gap between Theism and Atheism largely relies on purely semantic differences with respect to how both approach the Numinous. I address this in greater detail in my article The Atheistic approach to God… or how to bridge the gap between Atheists and Theists.

Edit :
With respect to extreme empathizers being more comfortable experiencing cognitive dissonance, I'm refering to cognitive dissonance at the level of belief. It's more important to them that their emotions correspond with their beliefs than that their set of beliefs as a whole is a consistent set.
In contrast, extreme systemizers care mostly about their set of beliefs forming a consistent framework.


Why being ignored is 'painful' for human beings? Ignoring someone is a manipulatory technique used at times. Ignoring the attacks of someone else through emotional detachment has a very strong effect on the attacker.

Is there a name for this kind of manipulative behavior?

Ignoring is a type of social rejection see extracts from wiki:

Social rejection occurs when an individual is deliberately excluded
from a social relationship or social interaction. ... rejection can be either active, by bullying, teasing, or ridiculing, or passive, by ignoring a person, or giving the "silent treatment."
...
Researchers have also investigated how the brain responds to social
rejection. One study found that the dorsal anterior cingulate cortex
is active when people are experiencing both physical pain and "social
pain," in response to social rejection.


Why is white on black considered higher contrast than black on white? While researching to answer Why are "Inverted Colors" considered an accessibility feature? I noticed the puzzling claim that "White text on a black background is a higher contrast to the opposite, so the letterforms need to be wider apart, lighter in weight and have more space between the lines." It's repeated a lot, particularly by design folks, but I couldn't find psychological research to support (or refute) it.

In terms of actual contrast ratio, inverting a black on white scheme won't change the contrast at all; the colors themselves are just as distant. Yet I see many claims that "inverted colors" is high contrast. The only real difference between the two I can think of is that the white background of black on white produces considerably more light than a black background. If this difference is enough to induce some level of ocular adaptation perhaps that could be a cause.

So is there a perceived difference in contrast between black on white vs white on black, assuming the same intensities for black/white? What causes it?

Your question is referring to display polarity. A positive polar display consists of dark letters on a light background, a negative polar display consists of light letters on a dark background. Polarity by itself is independent of text-to-background contrast, as you rightly state.

Generally, positive polarity facilitates performance (e.g. Buchner & Baumgartner, 2007). This effect is due to the higher overall display luminance (Buchner, Mayr & Brandt, 2009) possibly leading to a greater constriction of the pupil (Taptagaporn & Saito, 1990, 1993) and thus increasing the depth of field and decreasing spherical abberation.

However, this advantage of positive polar displays does not generalize to readers with visual impairment. People with low vision due to cataract (ocular clouding) perform better with negative polar displays (Legge et al., 1985, Sandberg & Gaudio, 2006). This effect has been discussed to be due to a scattering of light leading to a resulting veiling luminance and reduction in text-to-background contrast (Rubin & Legge, 1989).

In short: At the level of the display, a change of polarity has no effect on the text-to-background contrast. If the reader's eyes are cloudy, however, the contrasts at the retinal level is decreased for positive compared to negative polarity. This is why offering negative polarity is considered an accessibility feature.

As to why design folks claim negative polarity to be higher in contrast, I can only speculate on the basis of these findings. I suspect that it has to do with the adaptation of the eye to the lower overall luminance of the display. The intensity of the white letters may be perceived as more intense. Also the wider pupil dilatation would lead to a decreased depth of field. This in turn would require wider spacing and lighter weights of letters to achieve readability comparable to positive polarity. Unfortunately, I don't know any research to substantiate these speculations (which doesn't mean that it does not exist).


How can I make a speller with BCI? I am trying to make a speller with BCI using EEG (SSVEP or P300, whichever is easier). I would be really grateful if someone could give me a plan of action so as to where do I get started and what skills or tools I might require. As for now, I have access to a cognitive neuroscience lab and EEG.
Thanks.

Yeah this is a very common and effective approach. Try doing a google search for: P300 speller github for some implementations. One issue that you should pay attention to is the limited refresh rate of computer monitors. You are going to want very accurate synchronization between what is shown on a monitor and the EEG being recorded. You'll want to use some type of framework that allows for this synchronization such as PsychoPy (for Python) or Psychtoolbox (for Matlab).

Here is a great writeup of how to implement a P300 speller in Python. Looks like they use Pyff.

First step, in my opinion, is to look at some examples that have already been implemented:

Here is a Matlab framework for BCI with an example P300 speller that uses PsychToolbox for good event timing. Looks like the repository is actively maintained.

Also, look at OpenVibe. Another framework for BCI. There are a lot of examples available there.

Try one or a few of these out and see if you can get something that has already been made working. Then you'll be in a much better position to implement your own speller.


What is the relationship between sociology and cognitive sciences? I want to know what is the relationship between sociology and cognitive sciences.
Let me start by short consideration of both:

Sociology - well established discipline or a field of research
Sociology is a part of social sciences.
Cognitive sciences - a bit more recent field of research. Cognitive
science cannot be considered a discipline, it lacks core basics,
there is bigger and less connected variety of research methods and
objects. Cognitive sciences is also part of social sciences, but has
stronger ties with biomedicine (neurology, pharmacology).

Sociology considers that main causes of our behavior lie outside, in the social environment. At the same time cognitive sciences look for causation within psyche/brain.

I believe that there are three ways of looking into relations:

Connections between sociological and cognitive-science journals?
Semantic relations like use of similar concepts and definitions?
Interdisciplinary projects that include both sociology and cognitive sciences?

The primary difference is two-fold:

1) Methods : Social sciences use mostly qualitative methods and content analysis, psychology and cognitive sciences use quantitative methods and statistical analysis. The one basic standard tool in psychology and cognitive sciences is the laboratory experiment, while social sciences usually collect data in the field.

2) Object of study : Social sciences deal mostly with social entities. The smallest social entity is two people. Psychology and cognitive sciences deal with individuals or, if they deal with populations, the general characteristics of the individuals of that population. Psychology and cognitive sciences deal with social processes only from the perspective of the individual: how individual internal mental processes are affected by them.

As usual, this is a tendency, and the borders between the disciplines are blurred. There is no clear distinction and there is a huge overlap where research could fall in either discipline and is associated with one only because the researcher comes from it. Also, in academic institutions, certain parts of one discipline might have found their home in a neighboring discipline for historical reasons, e.g. pedagogical psychology is often placed in the faculty for pedagogy (a social science), but there it is just as often taught by psychologists.

I wrote "psychology and cognitive sciences", because cognitive sciences is strongly associated with psychology, but also with information sciences / computer science and neurosciences. At our university, the degree program "cognitive science" is part of both the psychological and the computer sciences department. But other universities place it elsewhere. Like neurosciences, cognitive sciences is an interdisciplinary field or, if you want, a new and evolving discipline whose realm is even less clearly defined than that of older and more traditional disciplines. Nevertheless, I understand cognitive sciences to be concerned with cognition, which is an aspect of the individual, and a traditional field of study that lies mostly within psychology and other natural sciences like medicine and biology.

In short: cognitive sciences is a natural science, while social sciences are part of the humanities, with all the methodological and theoretical implications that follow from that.


Is there a difference between visual short term memory and visual working memory? As far as I can tell the two terms are used interchangeably.  Do these two separate terms exist for historical reasons, or is there a distinction I'm missing?

The distinction between these terms is a matter of ongoing empirical research.  They form part of a set of potential taxonomical categorizations of visual memory (VM).  So far proposed sub-parts of VM include: Iconic (or sensory) memory, short-term (VSTM), fragile short-term (fVSTM), working memory (VWM), and long-term (VLTM) memory.  The distinction between short-term and long-term visual memory is generally accepted, as is iconic memory; the others are still actively debated.

As the neurological validity of these terms is still controversial, it is not unusual for them to be used interchangeably.  For example:

  We consider VSTM and visual working memory (VWM) as the same set of
  processes.

The additional sub-part distinctions are proposed by Sligte and Lamme (2011) (who refer to VSTM as an umbrella term for all the non-long-term memory sub-parts):

  Traditionally, VSTM is thought to operate on either a short time-scale
  with high capacity - iconic memory - or a long time scale with small
  capacity - visual working memory. Recent research suggests that in
  addition, an intermediate stage of memory in between iconic memory and
  visual working memory exists. This intermediate stage has a large
  capacity and a lifetime of several seconds, but is easily overwritten
  by new stimulation. We therefore termed it fragile VSTM.


Can information theory be applied to human interactions and communication? I am not sure if this question is better suited for the computational science SE.

I learned a bit of Shannon's information theory in a course I took last year. In the class it was defined as the quantitative relaying of information between a signal and a receiver across a medium that introduces noise. In all the examples we explored it was typically defined in terms bits of information that can be quantified and conveyed across the communication channel. Some examples we discussed were data compression, the transfer of DNA from parent cells to daughter cells, and aspects of speech/written words.

Let's say two individuals are in conversation. One speaks a phrase communicating his current state of mind. He then speaks the phrase out loud. The second individual hears this phrase. She then processes it based on her own brain and the way it functions and produces a response.

Here the signal would be the person speaking the phrase and the receiver would be the person interpreting the phrase. Could we argue that the "noise" in this communication is the subjectivity of the two people? The first person is attempting to convey information that is derived from his particular subjective state and whatever patterns were generated by his brain from his experiences. The second person would have to weight this information against her subjective state and past experiences with the first person. This might introduce "noise" that would affect the intended interpretation of the phrase.

Essentially, my question is with regards to social communication - sometimes you must know the appropriate way to phrase something so that the correct information is conveyed and is not subject to misinterpretation.

Question: Would this be a proper application of information theory?

Note here that I am not talking about the actual information content of the sentences themselves (which may be noisy if imprecise language is used) but the interpretation on the part of the two people in communication.

Information and signal detection theory are commonly applied to cognitive situations. Examples include TSA agents searching for weapons among carry-on bags and sonar operators attempting to discern ships from fish. In addition, information theory itself is highly general, and has been proven to apply across disciplines. So I do think the premise is valid.

However, the example does not list an application, per se- it simply describes a situation where one might think about coming up with an information-theoric approach. Such an approach would certainly involve a lot of research because there are many confounding factors in communication between humans (not the least of which is the cognitive framework of the receiving individual). You would need to carefully define what is signal, what is noise, and where the boundaries lie. I contend that this would be particularly difficult in the general case.


Does the functionalism view of sociology assume that institutions are intentionally designed to serve their functions? From my limited knowledge, the structural-functional view focuses on the functions of different institutions.
However, that doesn't state what created these institutions in the first place. Even if institutions were created randomly, they will still serve whatever "function" they happen to serve.
Does the functional view assume that the institutions are purposefully designed to serve their functions? If so, does this view focus on particular mechanisms? Institutions can be designed by the government, or come up "endogenously" by groups of people getting together, or can just happen by chance (and survive if it happens to address certain needs).

Since there have been no answers in five days, perhaps I can give a partial answer. I am by no means an expert, so I hope someone will point out my mistakes or if there is any bias (which I am sure there is). Also, my knowledge is limited to political science, but still I hope there is something that you can get from this.
In Britannica, structural functionalism, is defined as "a school of thought according to which each of the institutions, relationships, roles, and norms that together constitute a society serves a purpose, and each is indispensable for the continued existence of the others and of society as a whole." So for Britannica, the view seems to be about mutually interdependent structures in society. According to wikipedia, a common analogy likens these structures to "organs." The wikipedia article also lists a lot of criticism to this approach. To give an example of "real research" along these lines; many view the Varieties of Capitalism-framework (Soskice & Hall, 2001) as functionalistic (but you should make up your own mind about that, of course ;)).
A common critique of structural-functionalism is indeed that it explains the existence of institutional arrangements based on some notion of efficiency or optimality. This critique seems to be very common among historical-institutionalists in political science, who stress that institutions are the products of historical processes, and even in cases where they are the products of some group of actors to solve a particular problem, they can often "outlive" their creators and, with time, change to serve entirely new purposes.
An example of this can be found in Kathleen Thelen's critique of the structural-functionalist perspective. In her book How Institutions Evolve (2004), she describes (among other things) how the German system of vocational training evolved from being a system initially designed to weaken the position of the labor movement, to the diametrically opposite position of being a central pillar in the cooperation between the state, employer associations and labor. I recommend reading the introduction and following the references therein - she also references research using the functionalist perspective!
Pierson (Politics in Time, 2004) defines a "functional interpretation" as a view where "institutional arrangements are explained by their outcomes," or where "institutions take the form they do because powerful actors engaged in rational, strategic behavior are seeking to produce the outcomes observed." This he calls "actor-centered functionalism," which he distinguishes from "societal functionalism," in which institutions exists because they fulfill a certain function for society as a whole.
For Pierson, functional accounts are seen as inadequate for historical research, as they are unable to account for "lag" between the moves of actors and actual institutional outcomes (among other things). I recommend reading Piersons introduction and chapter 4 and 5 if you are interested in what he says about functionalism (I really recommend the entire book, actually :)).
As for my subjective view (for whatever its worth to you ...), I'm not really sure what functionalism really is. I have read many articles that analyze institutions or human behavior using game-theoretic models and so on, and in my (narrow) view, this literature represents the stereotype of functionalist accounts. Even so, there are works that utilize game-theory in historical research (see especially: Greif, Avner, 2006, Institutions and the Path to the Modern Economy) and that tries actively to overcome the sort of criticism that I have cited above, so there is certainly a blurry line of demarcation here.

I am sorry for the heavily biased reply to your post, and I am not entirely sure it was the answer you were looking for. Reading the critique of researchers in the "historical institutionalism" camp will certainly answer your question positively - functionalism is indeed about purposefully designed institutions (but, as Pierson points out, this does not mean that the perspective is without merit!).
Moreover, due to my own narrow perspective; what researchers subscribing to functionalist views themselves think, I do not know. Also, if there is any difference between sociology and political science I cannot tell. Hopefully someone will reply with a more informed view if they feel this reply is inadequate :)


What is the independent variable in this memory experiment? I am planning the following memory experiment:
Participants study a list of words, a random half of which are followed by an instruction to remember and the other half by an instruction to forget.  Afterwards, they are given a recognition memory test which includes words that they have previously studied, unstudied words that sound similar to studied words they had been instructed to remember, unstudied words that sound similar to studied words they had been instructed to forget, and unstudied words that are unrelated to studied words.  Participants have to respond "yes" to words they recognize as having studied regardless of the associated memory instruction (remember or forget) and "no" to the words they don't.
If participants falsely recognize (respond "yes") to more similar sounding unstudied words than unrelated unstudied words it is taken as evidence that they encoded the sound of the words they studied.  Comparing "yes" responses between unstudied words that sound similar to remember instructed study words and those that sound similar to forget instructed study words can reveal whether the process of remembering or forgetting is more likely to lead to the encoding of sound.
With the above analyses in mind it would make sense that the dependent variable is the "yes" response.  But is the independent variable the memory instruction? the type of unstudied word on the recognition test? or something else?

It seems this experiment is trying to test two different things:

If participants falsely recognize (respond "yes") to more similar
sounding unstudied words than unrelated unstudied words it is taken as
evidence that they encoded the sound of the words they studied.

For this part of the experiment, the independent variable is the type of word on the recognition test, specifically whether the words on the recognition test sound similar to the studied words or not. In this case, the dependent variable is the likelihood of recognizing the words, with the hypothesis being that participants will be more likely to recognize words that sound similar to the studied words than words that are unrelated to the studied words.

Comparing "yes" responses between unstudied words that sound similar
to remember instructed study words and those that sound similar to
forget instructed study words can reveal whether the process of
remembering or forgetting is more likely to lead to the encoding of
sound.

For this part of the experiment, the independent variable is the memory-instruction (and whether words on the test sound like remember-instructed or forget-instructed words, since these variables go hand-in-hand). In this case, the dependent variable is still the likelihood of recognizing the words, with the hypothesis (probably) being that participants will be more likely to recognize words that sound similar to remember-instructed words than words that sound similar to forget-instructed words.
Edit: I just realized you designed the experiment. I would recommend choosing a single hypothesis because there seem to be two hypotheses and corresponding independent variables which makes things kind of confusing.


Are there any personality theories that use the scientific method? Background

I have come across a number of personality theories. There are even disciplines of personality theories, dividing these theories according to the assumptions they are based upon. The most accepted/used theories seem to be Big 5 and Myers–Briggs Type Indicator (MBTI). However, I assume these theories use traits to determine people's personality types too.

For example, the Big 5 traits seem to be of very limited scope. Also, measuring traits like introversion and extroversion using some random questions which have polar opposite choices seems to be a fitting into a box sort of thing. There seems to be no scientific method while testing to determine whether people fall into one region or other for all the defined traits.

By scientific determination, I mean one could use methods like the one laid out in "Cerebral Blood Flow and personality: A Positron Emission Tomography Study" to determine between, say, introversion and extroversion traits. I am not sure whether the other traits have such methods researched enough to distinguish between them.

Question

Are there any personality theories that are based purely on scientific grounds?
Are there any existing personality theories (that are being researched) that could one day be backed up by scientific research? I think the Big 5 might come under this category, but any evidence to the above regarding any theory will be appreciated. Thanks!

What you may be interested are personality traits caught by some statistical correlations, rather than 'manually' merged by an author's intuition.
One of such tools is 16 Personality Factors.

The 16 Personality Factors, measured by the 16PF Questionnaire, were derived using factor-analysis by psychologist Raymond Cattell. This article summarizes the analysis that resulted in the 16 factors and allowed the development of the questionnaire, as well as the relation between the 16 factor theory and the popular five-factor personality theory.
[...]
This statement has become known as the Lexical Hypothesis, which posits that if there is a word for a trait, it must be a real trait. Allport and Odbert utilized this hypothesis to identify personality traits by working through two of the most comprehensive dictionaries of the English language available at the time, and extracting 18,000 personality-describing words. From this gigantic list they extracted 4500 personality-describing adjectives which they considered to describe observable and relatively permanent traits.

(from Wikipedia: 16 Personality Factors and 16PF Questionnaire)


How do mammals estimate the speed of moving objects? Has there been any research on how mammals predict the speed of moving objects? In particular, how do they integrate top-down information? For instance, do they have greater difficulty estimating the speed of a fast-moving sloth more than a moving mouse?

@AliceD gave a great answer on the bottom up pathway. Let me add some top-down processing bits into the picture, since that's what you are asking.

First of all, at a perceptual level, motion perception is biased by prior expectations and strength of motion signal. E.g., see:

Stocker, A. A. and Simoncelli, E. P. (2006). Noise characteristics and prior expectations in human visual speed perception. Nature Neuroscience, 9(4):578-585. http://dx.doi.org/10.1038/nn1669

The neural activity of MT (and behavior) is known to be modulated by attention. E.g., see:

Monkey Area MT Latencies to Speed Changes Depend on Attention and Correlate with Behavioral Reaction Times. Neuron. 78(4):740–750. http://doi.org/10.1016/j.neuron.2013.03.014


Visual Cortex percentage Could somebody help please in providing some research papers or a resource book that states how much the visual cortex occupies of our cortex?

I am trying to find some reliable source but I couldn't find any other than one article mentioning it is 30%. But still I need to cite a reference.

As Bryan Krause indicates in the comments, the statement that 'One third of the cortical surface is dedicated to vision processing' is disputable. Especially given that fact that there's evidence that even the primary visual cortex is involved in multimodal processing (MacPherson, 2018). Nonetheless, it is a valuable statement as it makes clear that a lot of our cortex can process visual stimuli and that it is an important sense for us.

If you need a reference for the one third statement, you can use Kupers & Ptito (2014) or (MacPherson, 2018). Note that these references are secondary literature, i.e., they are not research papers where they actually calculated the cortical surface involved in visual processing.

Fig. 1. Functional areas of the cortex. Source: Boundless Physiology Textbook

References
- MacPherson, Sensory Substitution and Augmentation, Proceedings of the British Academy 2018
- Kupers & Ptito, Neurosci Biobehav Rev (2014); 41: 36–52


Aren't MBTI and Big 5 connected? I have seen repeated suggestions that the Big 5 model is the preferred model of personality in psychology, and Myers-Briggs is used in pop psychology and industry and not presently taken that seriously by proper psychologists.

It seems to me that there is a connection between the two. Extraversion is one axis with the same name and similar or unchanged content. Openness on at least one test sounds like a rough gauge of old-fashioned IQ, and as such is a candidate for correlation with the Sensate-Intuitive axis. In the popular Please Understand Me!, the SP-SJ distinction sounds a lot like Conscientiousness. These suggestions could be challenged, but it seems grounds to suggest that three of the four Jungian preferences survive largely intact in Big 5.

Am I overestimating the continuity between the two models? If I am not, why does Big 5 have scientific validity where the MBTI is a bit of fluffy pop psychology?

--UPDATE--

I have un-accepted the answer as I find it bare assertion plus a statement of author's credentials, and I really want a more thorough response.

To flesh out what I meant by the question, I'm going to go with Jungian preferences as simplified in Please Understand Me!, said to be one more assertion of temperament theory as Kevin Trudeau's Mega Memory can be said to be one more assertion of (neo?)-classical standard memory techniques, which may be seen as a move from fluff to fluffier. I acknowledge this as a liability, and I further acknowledge that I do not engage whether the NT-NF polarity is relevant to people deemed Sensate, nor whether the SJ-SP polarity is relevant to people deemed Intuitive.

One can be deemed Intuitive without being good at, relying, or identifying with intuition as the term is usually used. The Sensate-Intuitive axis is one I would on consideration suggest might be better named Concrete-Abstract: where Abstract is paired with Feeling, it matches more closely with what one might pick a one-word label of "intuitive" for (other candidates might be "influencer, "spiritual" or "self-actualizing"). Combine Abstract with Thinking and you get STEM practitioners, analytic philosophers, and so on, and possibly liable not to hold common intuition in very high regard.

I don't think I have anything quite as striking to offer for the SP-SJ axis, but I think that people evaluated by Myers-Briggs as SJ with at least a square J, you'll get people who are diligent, believe in order, and so on, high performers on high Conscientiousness. I'm a little less sure with SP, but I would think squarely SP people would commonly register as highly primative, and I would expect solid SP's to score low on questions about "I diligently keep my home, my room, my cubicle, and my desk meticulously clean" used to assess degree of Conscientiousness on Big 5 scoring.

I assume that Extraversion will be accepted as an obvious point of contact, and people may argue traits versus preferences (Quiet: The Power of Introverts in a World that Can't Stop Talking asserts that one can be deeply introverted and learn to function as a consummate extravert if one deeply desires it), but it still looks to me like, if I may count better, all three other Jungian preferences appear to reincarnate in Big 5 in slightly different form.

If industry's popular MBTI is largely reincarnate in proper psychology's Big 5, it might explain why industry is reaping apparent benefits from the deprecated tool.

If Openness, which is said to be a crystallization of what is otherwise represented in IQ, is largely similar to "Sensate-Intuitive" (or "Abstract-Concrete"), and so on, and a personality psychologist does not see a need to give much more than bare assertion in a response, could this be a little more worth digging into...

All personality models are related in that they are carving up the same variance into different factors, and some of the factors will overlap. Extraversion is probably the most similar trait between the two models, but it's still quite different.

As a personality psychologist, I would say yes, this is potentially an overestimation of their convergence. A brief description of why the Big Five is preferred over MBTI is that the measures of the former are dimensional rather than categorical, have more test re-test stability, and have more stable relationships with other levels of analysis (e.g., genes predicting traits; traits predicting behaviors). Reliability and validity are the cornerstones of quality measurement.


Implementation Intentions and Mental Contrasting vs Meditation Everyday I see so many studies on meditation. These include all types (mindfulness, TM, etc..). The studies only report positive results. Meditation has been purported to increase self-control and willpower. But it seems that implementation intentions combined with mental contrasting would be better. Implementation intentions take the following form: "If I encounter situation X then I will do this." Mental contrasting sets the future goal with the current obstacles and creates an "energization." So it seems that this intervention (MCII) would be better than meditation by itself.

The reason I ask is I have been meditating for a month and have not noticed changes in my self-control. It seems that the so-called benefits of meditation could all be part of a placebo effect.

I cannot fit this into a comment, so I would post this answer, hoping it may be useful to someone.

The affirmation of the form

  "If I encounter situation X then I will do this."

Has been tried by amateurs in the field of lucid dream induction. Lucid dreaming is about realizing that one is dreaming from within a dream. Normally people have very limited self control during dreams, and the affirmation statement attempts to increase it.  Such statement usually includes a "dreamsign", followed by an intention to realize the fact that the person is dreaming:

  "If I will find myself in math class, I will realize that I'm
  dreaming, because I have graduated from high school and college, and
  don't have to take any more math classes for the rest of my life".

Normally, rational thought is very hazy in a dream. For example, a typical scenario is a person may find himself in a math(chemistry/other hard subject) class dream, taking an exam that the person is not prepared for. The rational mind does not question this.

The interesting thing happens (at least to me) when the above mentioned affirmation does get triggered - still without clear rational thought I get up from the desk and walk out of the class. There's no clear awareness of why, but the behavior is changed when the stimuli is experienced.


What exactly happens to brain during anesthesia While anesthesia is given to a patient what changes in the chemistry of brain happens. Which part of the brain is affected by the medicine which causes anesthetic effects.
Can anesthesia be considered as sleep+painless state of body? Or is it more than that.

General anesthesia is a reversible drug-induced neurophysiological state comprised of unconsciousness, amnesia, analgesia, and immobility with maintenance of physiological stability. How anesthetic drugs create the state of general anesthesia is still not completely understood, but general anesthesia is essential for the safe and humane conduct of surgical and invasive diagnostic procedures.[1]

The goals of general anesthesia include amnesia, analgesia, unconsciousness, and immobilization. The ability of general anesthetics to produce these distinct therapeutic endpoints is not equal. For example, explicit memory is the most sensitive target of inhaled general anesthetics; consciousness (assessed by appropriate response to spoken commands) is preserved in the absence of memory during exposure to low doses; and unconsciousness is produced by lower concentrations of most general anesthetics than those that ablate movement in response to noxious stimuli. [2]

General anesthetics consist of many different drugs. [2,3] These different drugs display distinct relative potencies in their ability to produce different components of general anesthesia. For example, the ratio of the drug concentration producing immobility during incision to that producing unconsciousness is 1.5 for nitrous oxide, about 3 for most of the inhaled halogenated ether, and over 4 for the intravenous anesthetic propofol. They also have different effects on EEG during anesthesia. Thus, clinically, general anesthetics can be classified into 3 groups based on their relative potencies for different clinical endpoints and their impact on EEG:

Group 1 consists of etomidate, propofol, methoxital, and barbiturates. These are intravenous drugs that are much more potent at producing unconsciousness than immobilization and shift cortical EEG toward lower frequencies. Their effects are mediated mainly by a subset of γ-aminobutyric acid type A (GABA-A) receptors, which, when activated, reduce neuronal excitation.

Group 2 includes the gaseous anesthetics nitrous oxide (N2O), xenon (Xe) and cyclopropane, along with an intravenous agent, ketamine. Clinically, these drugs produce significant analgesia, while their potency as hypnotics and immobilizers are relatively weak, and they may increase cortical EEG frequencies. Anesthetic agents in this group have little or no effect on GABA-A receptors, but they instead potently inhibit N-methyl-D-aspartate (NMDA) receptors, which are excitatory cation channels activated by the amino acid glutamate. In addition, agents in this group also inhibit α4β2 neuronal nicotinic acetylcholine receptors, which modulate synaptic release of neurotransmitters.

Group 3 consists of the volatile halogenated anesthetics: halothane, enflurane, isoflurane, sevoflurane, and desflurane. These drugs induce amnesia, hypnosis, and immobility in a predictable manner and reduce the spectral edge frequency of cortical EEG. General anesthetics in this group lack significant selectivity for general anesthetic target molecules. They enhance the function of inhibitory GABA-A and glycine receptors while also activating 2P potassium channels and inhibiting excitatory glutamate receptors and a variety of excitatory cation channels.

Group 1 and Group 3 drugs that act by enhancing GABA-A receptor activity in various neural circuits appear to impair both unconscious and conscious processing, including associative cortex and synchronous integration among multiple cortical areas. Cortical EEG activity shifts toward lower frequencies in the presence of these drugs, and large doses can lead to the total loss of coordinated neural activity (iso-electric EEG). On the other hand, Group 2 drugs such as ketamine and nitrous oxide appear to act by impairing signal filtration to the consciousness, perhaps altering the amounts or intensities of sensory inputs, or by allowing leakage of unconscious signals into conscious processing. This lack of filtering “jams” or overwhelms the consciousness with signals, leading to a “dissociative” state, frequently associated with reports of vivid dreamlike experiences.

Therefore, while being under general anesthesia, the brain is still functioning, but it is functioning differently from when it is awake or sleeping. [4] Neural circuits that are responsible for consciousness, sensation perception, memory, and motor are not functioning as they do when being awake or sleeping. For different general anesthetics, different effects on neruotransmitter receptors and neural circuits are different; thus, various neural circuits in the different areas of the brain are affected differently, and the whole brain will function in different unconscious states even though, outwardly, the anesthetic patients appear to be in similar unconscious states. Also, for different dosages of the same anesthetics, overall neural circuits are affected differently, and the brain in different anesthetic stages will function differently too.

N.B. The above is a simplified answer about the complex actions of general anesthetics. More details can be found in the following references.

References:

Akeju O, Brown EN. Neural oscillations demonstrate that general anesthesia and sedative states are neurophysiologically distinct from sleep. Curr Opin Neurobiol. 2017 Jun; 44: 178–185.
Forman SA, Chin VA. General Anesthetics and Molecular Mechanisms of Unconsciousness. Int Anesthesiol Clin. 2008 Summer; 46(3): 43–53.doi: 10.1097/AIA.0b013e3181755da5
Brown EN, Purdon PL, Van Dort CJ. General Anesthesia and Altered States of Arousal: A Systems Neuroscience Analysis. Annu Rev Neurosci. 2011; 34: 601–628.doi: 10.1146/annurev-neuro-060909-153200
Müller CP, Pum ME, Amato D, Schüttler J, Huston JP, Silva MA.The in vivo neurochemistry of the brain during general anesthesia. J. Neurochem. (2011) 119, 419–446. https://doi.org/10.1111/j.1471-4159.2011.07445.x


Differences in reaction time on visual tasks with and without binocular disparity ques? Have there been any studies done that test the reaction time to vision processing tasks with and without the benefit of binocular disparities? I have been wondering how much depth information (such as the jutting out of the nose on a face) contributes to visual processing and object encoding in the brain - or if the visual scene is treated like a diorama with 2D images placed at various depths.

My assumption is that if the 3D aspect of the scene components are important then the reaction times would vary.

According to these three published studies I found below - reaction time is slower when depth disparity information is withheld, as to whether or not that extra information is actually encoded in the brain is still an open question.

This first paper by Young Lim Lee; Jeffrey A. Saunders used left and right eye rendered images of novel 3D shapes with and without binocular cues to time test subjects in discriminating whether two images were rotational views of the same object.  With a set of three experiments they concluded in all cases that the stereo information improved reaction times.

Stereo improves 3D shape discrimination even when rich monocular shape cues are available
The second paper by Darren Burke, Jessica Taubert, Talia Higman had test subjects view pairs of photographed human faces briefly through a stereoscope with and without stereoscopic information and were required to identify if it was the same or a different individual.  Results were that the subjects had faster reaction times and lower error rates when stereoscopic information was present.

Are face representations viewpoint dependent? A stereo advantage for generalising across different views of faces
And the third paper by Oliver ZJ, Cristino F, Roberts MV, Pegna AJ, Leek EC the test subjects were split into a mono and stereo groups before being required to memomrize a set of 3D objects and then determine amongst a series of test objects whether or not it was from the set. The test was conducted using a 3D stereo monitor and glasses with the images displayed either with complementary or identical images to either eye depending on the group while 128 channel ERP (event-related-potential) traces were recorded.  Results showed higher accuracy for the stereo group and while there was no statistics given for reaction times, the paper concludes with an analysis and discussion regarding the differences in ERP data collected from the two groups.

Stereo Viewing Modulates Three-Dimensional Shape Processing During Object Recognition: A High-Density ERP Study


Do ALL decisions arouse cognitive dissonance? I continue to see an oversimplification in the descriptions of the options available that arouse cognitive dissonance: some websites state that all decisions have positive and negative aspects that will lead to dissonance and some say that dissonance is aroused only when a decision is made between two equally desirable options.

In other words, do ALL decisions arouse cognitive dissonance? Or just the decisions made between options that are equally or near-equally desirable?

For example, if I were to choose between an Ivy league college or a SUNY school, I don't think I would very much regret going to the Ivy league school and not the other (or would I be reducing dissonance by telling myself that?). However, the website explaining cognitive dissonance simply labels these options as "colleges".

Also what if the decision making was something trivial (in my perceptions)? Do whimsical decisions arouse dissonance as well?

For example, if I had a very large sum of money and I was selecting between two equally desirable cars, and I could very easily afford both, would I still experience much dissonance?

Short answer: This is mostly a question about statistical significance.
Cognitive dissonance theory encompasses several different research paradigms.  I believe this question is about the "free-choice" paradigm - the only one that involves decision-making.  This paradigm is also sometimes referred to as "choice-induced dissonance", or "post-decisional attitude change" (though the latter may be a misnomer, as attitude change may happen during the decision-making process rather than after).
Traditional view:
In the original formulation of this paradigm by Brehm (1956):

A second prediction, that dissonance and consequent attempts to reduce
it would be greater, the more closely the alternatives approached
equality, also received support.

That is, it was suggested that dissonance occurs in all decisions, but decisions arouse more dissonance the more difficult (closer) they are, and presumably less dissonance the easier (more distanced) they are.  The problem with this formulation is that at some point, the dissonance induced by sufficiently easy decisions is so small as to fail to reach statistical significance (p-value), making it essentially impossible to test this aspect of the hypothesis.
In the first 50 years or so since the theory was proposed, much support has been found for dissonance aroused by difficult decisions (for reviews, see Cummings & Venkatesan, 1976; and Harmon-Jones & Mills, 1999).  Numerous variables other than "closeness of alternatives" have been proposed to moderate dissonance, such as importance of the decision, relevance to self, how public the decision is, personality traits, etc - see Kenworthy et al (2011) for a review.
Recent developments:
Then, Chen and Risen (2010) called the entire paradigm into question by pointing out that it is subject to a statistical artifact (first noted in 2008) that could be responsible for many false-positive results.  That is, statistically significant changes in preference may be even more difficult to induce in subjects than previously believed.
Researchers are currently in the process of replicating and reevaluating the body of work that this paradigm is based on, controlling for the statistical artifact.  Unfortunately, any assessments made prior to this of the level of cognitive dissonance produced by decisions are likely overestimated:

Using the free-choice paradigm, many social psychological studies have
investigated the effect of moderating factors on choice-induced
preference change ... (e.g., choice importance, choice reversibility,
etc. ...) ... However, without a proper control condition, any
argument about absolute preference change would not be warranted
(i.e., it is unclear whether or not significant dissonance reduction
occurred in each condition). ...
The same argument applies to past studies comparing preference change
between two groups of individuals with different personalities ... or
different cultural backgrounds ...
Data from Izuma et al. (2010) suggests that individual differences in
preference changes, which are measured in the typical free-choice
paradigm explain only about 28% of the total variance in true
preference changes.


How do reward signals strengthen synaptic connections in the human brain? In a vast simplification, the mid-brain sends reward signals (for example through dopaminergic neurons) that tell the rest of the brain whether it succeeded at fulfilling the needs of the organism. If there are certain activities in the brain that lead to a successful action, then these activities should have a higher probability of occurring again (since that is useful for achieving the organism's needs in future).

To increase the probability of the occurrence of an activation pattern as a response to a certain history of sensory input, the neurons that were involved to produce this pattern will need to adapt their synapses such that they become more sensitive to this input.

I'm wondering, how are the reward signals thought to affect the neurons that were involved in the previous actions of the organism at the synaptic level?

dopamine release changes the nature of synaptic long term potentiation (ltp) thought to underly long term memory. see http://www.sciencedirect.com/science/article/pii/S0896627305003971 for a paper i am familiar with, for an entry point to that field

for a review article:
http://www.nature.com/nrn/journal/v5/n6/abs/nrn1406.html
see section titled "Dopamine and memory at the cellular level"


Understanding the concept behind d-prime I know that sensitivity (d') is typically calculated as follows:

d' = z(Hit Rates) - z (False Alarm Rates)

I understand this as the idea is to standardize both distributions, and to then calculate the z-score, which allows to calculate a distance within the same scale so to say.

What is however very confusing to me is the visualization of the process.
I am using the following plots from these slides:

My questions are as follows:

(1) As in the plot above, d' is always depicted as the difference of the means of the two distributions (of signal and noise, for instance). Say however that I find in my data that the Hit rate (or Hit probability) is 0.8 - I would think that now, I would need to find z(Hit = 0.8), would this not be to the right of the mean:

Is this correct?

(2) In addition, I am am uncertain about the arrows associated with Z(CR) and Z(H) on panel A above.

For one, in my opinion, CR includes the entire area before the criterion. The arrow, however, associates Z(CR) with only the distance mean-criterion - why?

Then, if Z(X) refers to the cumulative probability density of variable X, Z(X) should be the entire density up to X.
In the case of Z(CR) in panel A,however, it seems that it is only the part from the mean of the noise distribution to criterion. So what does then the Z(..) notation mean in this context?

First lets write down some math for the above figures assuming Gaussian distributions with means $\mu_{n}$ and $\mu_{s}$ both with a standard deviation of unity. In this case the probability of a detection is
$$P_D=1/(\sqrt{2\pi})\int_{c}^{\infty}e^{-(x-\mu_{s})^2/2}dx$$
and the probability of a false alarm is
$$P_F=1/(\sqrt{2\pi})\int_{c}^{\infty}e^{-(x-\mu_{n})^2/2}dx$$
and the normal deviates are
$$Z_D=\Phi^\prime(P_D)$$
and
$$Z_F=\Phi^\prime(P_F)$$
where $\Phi^\prime(x)$ is the inverse of $\Phi(x)$
$$\Phi(a)=1/(\sqrt{2\pi})\int_{-\infty}^{a}e^{-x^2/2}dx.$$
We also need to note that
$$1/(\sqrt{2\pi})\int_{-\infty}^{c}e^{-(x)^2/2}dx+1/(\sqrt{2\pi})\int_{c}^{\infty}e^{-(x)^2/2}dx=1$$
and that
$$\Phi(-x) = 1-\Phi(x).$$
Now using integration by substitution on $P_D$ and the above equalities  gives us
$$P_D=1/(\sqrt{2\pi})\int_{c-\mu_{s}}^{\infty}e^{-(x)^2/2}dx=1-1/(\sqrt{2\pi})\int_{-\infty}^{c-\mu_{s}}e^{-(x)^2/2}dx=1-\Phi(c-\mu_{s})=\Phi(\mu_{s}-c).$$
You can play the same mathematical games and get that $P_F=\Phi(\mu_{n}-c)$ or that $Z_D=\mu_{s}-c$ and $Z_{CR}=c-\mu_{n}$ (this one is a little trickier ...).
Now on to your questions

(1) As in the plot above, d' is always depicted as the difference of the means of the two distributions (of signal and noise, for instance). Say however that I find in my data that the Hit rate (or Hit probability) is 0.8 - I would think that now, I would need to find z(Hit = 0.8), would this not be to the right of the mean:

This depends on what the means are. If the signal distribution has a mean of $-100\sigma$, then $Z_{hit}$ will likely be to the right of the mean, but if the signal distribution mean is $100\sigma$ it will likely be to the left.

In addition, I am am uncertain about the arrows associated with Z(CR) and Z(H) on panel A above.
For one, in my opinion, CR includes the entire area before the criterion. The arrow, however, associates Z(CR) with only the distance mean-criterion - why?

This is a direct result of the magic of the math above.


Does STDP make the Hebbian learning rule redundant? On Scholarpedia they introduce STDP (spike timing dependent plasticity) as a temporally asymmetric form of Hebbian learning, making it sound as if the original Hebbian rule still has relevance in neuroscience. On the wiki page on Hebbian theory, however, it seems SDTP and Hebbian theory are pretty much synonyms.

Do all cases of neuron types that were previously thought to follow the Hebbian learning rule (fire together, wire together) actually follow the STDP rule? If not, are there statistics about how often each learning rule occurs in the brain?

Short answer
Just like Mendel's ideas have been proven by the existence of DNA, Hebbian learning can be explained by STDP. That doesn't make Mendel's or Hebb's teachings obsolete.

Background
STDP is the long-term synaptic potentiation or depression governed by the timing of pre- and post synaptic cell firing. STDP depends on certain “critical windows” for spike timing. This critical window is on the order of tens of milliseconds (Dan & Poo, 2004). STDP is known for quite some time, but is by far a more novel idea than the idea of Hebbian learning posed in the 1940's (Markram et al., 2012). Hebbian learning has been popularly described as:

  ["C]ells that fire together, wire together.” In other words, if things keep happening more or less simultaneously, you may assume that there is a common cause for the firing. More importantly, if one of the cell is active systematically just slightly before another, the firing of the first one might have a causal link to the firing of the second one and this causal link could be remembered by increasing the wiring of connections, a notion we call synaptic plasticity. In short, timing matters because it may indicate causality.

In other words, Hebbian learning is mediated by STDP. Thus STDP may explain how Hebbian learning may come to exist.

But Markram et al. caution:

  ...this is not to say that STDP has been a panacea for all problems
  neuroscientific. Clearly cells that fire together wire together, there
  is no doubt about that, so the coming of STDP has not rendered the
  classical literature obsolete by any means.

In other words, Hebbian learning is more of a theoretical construct whereas STDP provides a neurophysiological explanation. Just like Mendel's ideas have been proven by the existence of DNA, and Darwin's ideas by a since buildup of fossil records, Hebbian learning has been explained by STDP, but that doesn't make Darwin nor Mendel's teachings obsolete.

References
- Dan & Poo, Neuron (2004); 44(1): 23-30
- Markram et al., Front Synaptic Neurosci (2012); 4: 2


Voltage Clamp Method I don't understand some points of the voltage clamp method. In the resting state, Command voltage and membrane potential are both -65mv. If the command voltage increases to 0mv, current is injected into an axon, so membrane potential become over than the threshold and sodium is going to flow into the axon.
I learned that current is the flow of electrons, so if the command voltage is changed into 0mv, electrons flow into an internal membrane. It implies that membrane becomes more negative, but it contradicts the fact that membrane potential becomes 0 mv.
Is there anything I misunderstood?

In voltage clamp, you measure current.

If you voltage clamp the cell near it's resting potential, you need little current to hold the cell.

If you want to voltage clamp the cell depolarized or hyperpolarized relative to rest, you need to inject current (positive or negative). How much current you need to inject depends on the membrane properties of the cell, and the leak conductance. Therefore, measuring the current as a function of the held voltage tells you about these membrane properties.

As you depolarize the cell, yes, you will open voltage-gated conductances, but these conductances also often inactivate (sodium channels especially). That said, yes, if you depolarize a cell and channels open or close, you will record those changes in your voltage clamp. However, you will never get an action potential if you have a good clamp. The whole point of voltage clamp is that you hold the voltage constant. Action potentials are positive feedback increases in voltage. If you clamp a cell at -40mV, even if -40mV is normally above threshold in a current-clamped cell, the cell will stay at -40mV. It doesn't really make sense to think about action potential thresholds in voltage clamp, they don't exist because the threshold phenomenon (voltage positive feedback) is blocked by clamping the voltage.

One of the benefits of voltage clamp is that you can (somewhat indirectly) measure the flow of certain ions. If you set the voltage equal to the reversal potential for some ion, you know the current for that ion is exactly zero. This allows you to make inferences about how much current is flowing (and knowing voltage you can calculate conductance) at other voltages.


Has an upper-limit on the physical spacing represented by grid cells in Entorhinal cortex been probed? There is considerable research reporting activity of unit recordings from grid cells in the Entorhinal cortex (e.g. [1]) - typically of rats running around in enclosed spaces.

Is there any information on the upper-limits of the physical distance represented by the spacing between grid cells (and hence presumably an upper-limit of the distance between place cells) in a single 'space', in any species?

[1] Sargolini F et.al. Conjunctive representation of position, direction and velocity in entorhinal cortex (2006).  Science 312: 758-762.

There are a few factors which confound an effort to find such an upper bound for grid size.  Since these experiments normally require the rat to be attached to the recording apparatus to ensure the quality of the recorded data, the first obstacle would be perfecting the ability to record from the entorhinal cortex while the rat is untethered, through telemetry or bluetooth-enabled systems.  Systems with enough throughput for the task are just becoming available (see here and here).
While the recording technology may be getting there slowly, in order to establish the periodicity of the grid cells, the rats must be trained to run around their environment using cues.  In [1] the "polarity" of the bounded area was changed by rotating a white card in one corner.  The grid cell activity is thus dependent on "allothetic" cues from the environment.  Giving the rats carte blanche (forgive my pun) to roam around in a larger, less well defined area to test the scaling limits on grid cells might not provide enough constant visual cues to get a consistent grid map.
That's what we are not able know just yet, but what do we know?
In the rat it is known that the field spacing varies from 50 cm to 3 m depending on how far dorsal or ventral you are in the medial entorhinal cortex (within layer II).  The average of the distance varied from 39-73 cm across different cells, though the standard deviation remains small (3.2 cm) [1].  Spacing and field size got larger as you moved from the postrhinal border (from dorsal to ventral) [1],[2].  Stabilization of the measurements required at least some exposure to the experimental enclosure before measurements were taken.
In a rectangular area, the grid cells form a tiling of equilateral triangles, with the grid points at each mutual vertex.  In [2], the spatial periodicity of the grids was tested by placing the rats on a track, rather than in an enclosure, controlling for one of the dimensions.  This supports the above notion that to strengthen the knowledge about the grid cells, the focus has been on restricting the area of the experiment, rather than opening it up.  From this study, it has been learned that the smallest scales are represented at the dorsal level, with the largest number of cells.  Phase precession, a phenomenon in which spikes for a particular grid cell occurred later in the cycle of the theta wave at the center of the cell, and earlier upon entering the grid, was seen to decrease with the increasing field width.  All of this together adds up to the idea that multiple spatial scales can all be held within this one layer of the entorhinal cortex, and scaled up and down as necessary using the precession to code for the specified representation.
In terms of other species, there have been studies in humans [3] (but limited to transit through virtual worlds, for the sake of fMRI recordings), mice, and piglets (though electrophysiology was not done).  None of these studies have progressed beyond the initial stages.
So, much is known about the spacing characteristics of the grids themselves, but the upper limit of their spacing will have to wait for better experimental technology, and a clever design of a large experimental field that has consistent enough landmarks for the rats to incorporate into their grid representations.

[1] Hafting, T., Fyhn, M., et al (2005).  Microstructure of a spatial map in the entorhinal cortex.  Nature, 436:801-806.
[2] Brun, V.H., Solstad, T., et al (2008) Progressive increase in grid scale from dorsal to ventral medial entorhinal cortex.  Hippocampus, 18:1200-1212.
[3] Doeller, C.F., Barry, C., Burgess, N. (2010).  Evidence for grid cells in a human memory network.  Nature, 463:657-661.


research based criteria domain and DSM5 Is there any major difference between the two classification systems ?
and why is there no awareness as of yet about research based domain for classifying mental disorders when it for the larger part focuses more on - neurobiological tests which indeed could tell us more about that disorder on various parameters .
thankyou

The Diagnostic and Statistical Manual of Mental Disorders (DSM) and the International Classification of Diseases (ICD) are clinical diagnostic and classification criteria for clinical work.
The Research Domain Criteria (RDoC) initiative is a research framework for investigating mental disorders. It integrates many levels of information (from genomics and circuits to behaviour and self-reports) in order to explore basic dimensions of functioning that span the full range of human behaviour from normal to abnormal. For more information, visit the About RDoC page.

In contrast to existing diagnostic guidelines, which are used for clinical purposes, RDoC is a research framework meant for supporting biobehavioral approaches for studying mental disorders. It is not for diagnosing mental disorders or for clinical practice. Studies that use the RDoC framework could lead to more knowledge of the mechanisms and processes in mental health and mental disorders. This information could help inform future diagnostic criteria (National Institute of Mental Health (NIMH)).

The concept behind the RDoC initiative can be seen as an extension to the debate over the level of real scientific research in psychology and psychiatry.
I have covered this extensively in my answer to a meta question on the subject.
On April 29, 2013, a few weeks before the publication of the latest version of the DSM (DSM-5), which is published by the American Psychiatric Association (APA), NIMH director Thomas Insel published a blog post critical of the methodology of the DSM and highlighting the improvement offered by the RDoC project (Insel, 2013).
It is good to debate things like this and I have no objection to debating the subject which in effect is what the NIMH is doing with this initiative (Insel & Lieberman 2013] emphasis below mine).

Thomas R. Insel, M.D., director, NIMH
Jeffrey A. Lieberman, M.D., president-elect, APA
NIMH and APA have a shared interest in ensuring that patients and health providers have the best available tools and information today to identify and treat mental health issues, while we continue to invest in improving and advancing mental disorder diagnostics for the future.
Today, the American Psychiatric Association’s (APA) Diagnostic and Statistical Manual of Mental Disorders (DSM), along with the International Classification of Diseases (ICD) represents the best information currently available for clinical diagnosis of mental disorders. Patients, families, and insurers can be confident that effective treatments are available and that the DSM is the key resource for delivering the best available care. The National Institute of Mental Health (NIMH) has not changed its position on DSM-5. As NIMH’s Research Domain Criteria (RDoC) project website states, “The diagnostic categories represented in the DSM-IV and the International Classification of Diseases-10 (ICD-10, containing virtually identical disorder codes) remain the contemporary consensus standard for how mental disorders are diagnosed and treated.”

The same applies now with DSM-5 and the International Classification of Diseases 11th Revision (ICD-11).  The DSM and RDoC could be used in combination, as the APA uses all research available to formulate their diagnostic criteria anyway.

The Diagnostic and Statistical Manual of Mental Disorders (DSM–5) is the product of more than 10 years of effort by hundreds of international experts in all aspects of mental health. Their dedication and hard work have yielded an authoritative volume that defines and classifies mental disorders in order to improve diagnoses, treatment, and research (APA, 2013).

References
APA. (2013). Diagnostic and statistical manual of mental disorders (DSM-5®). American Psychiatric Pub. https://www.psychiatry.org/psychiatrists/practice/dsm
Insel, T. R. (2013). Post by Former NIMH Director Thomas Insel: Transforming Diagnosis National Institute of Mental Health https://www.nimh.nih.gov/about/directors/thomas-insel/blog/2013/transforming-diagnosis.shtml
Insel, T. R. & Lieberman, J. A. (2013). DSM-5 and RDoC: Shared Interests (Press release). American Psychiatric Association. http://publichealthunited.org/pressreleases/DSM5andRDoCSharedInterests.pdf