title: A question on synapses

text:
# Question
Title: A question on synapses
we are looking into running simulations of the nervous system of C. Elegans. It is believed by most people that the worm's nervous system encodes information through graded potentials and/or plateau potentials rather than action potentials, as would be the case for example in many parts of the human nervous system.

We are planning on building upon a NEURON simulation created by the OpenWorm team. We want to see where we can get by including channel mechanisms and most importantly by making the transition from a spiking network model to a model reflecting the above belief that C. Elegans does not use action potentials. We then want to compare this with data collected at the University of Vienna.

Now, I am a student of mathematics and this is a project for university, so I am hopelessly confused by the neuroscience books I have been looking at. Instead, I hope that you guys can help me out with my question. To explain, consider the following scenario inside of C. Elegans:

Say I have neurons A and B, connected through some type of synapse. Neuron A is stimulated by a voltage clamp and generates a varying, graded potential lasting over a prolonged period (say 20 ms). Now what would a typical membrane potential of neuron B that one would expect in this situation look like? In pictures:

I realize this is a somewhat ill-posed question, but I am not asking for a detailed chemical or biological explanation of the process, but rather a heuristic that can serve as a starting point for a simulation. In case there is something already known in this respect, I would be thankful if you could point me to the references.

The next question would then be how one could implement this in NEURON, which has only NetCon to create networks. I figured I could use an artificial simulated synapse by drawing a small long cylinder with several compartments between neurons and then using a gap junction type connection, but I really don't know if this even makes sense.

# Answer
> 5 votes
According to this research paper by Lockary and Goodman, the resting membrane potential of C.Elegans is two fold because its a stepped resting potential of -70mV and -35mV. After an initial activation a resting potential of -35mV is held following a higher depolarisation, so on your graph the initial depolarisation would be a little higher, and then drops to -35mV for roughly 60+ secs. When terminated, or receiving a inhibitory signal this drops to -70mV. I don't see any reason why the receiving neuron would respond any differently so long as the activation strength was enough to create positive depolarisation. As mentioned by Izhaki in the comments, the strength of the synapse connections plays an important role. Here is a good thesis on transfer between neutrons in C.Elgans, it also explains the methods to investigates neutrons in the central nervous system of C.Elegans, and seems to see two patterns of activation depending on the method applied. Only a few of the neutrons have been fully recorded in C. Elegans so its possible that different potential patterns may occur, nervous systems are far from homogeneous, humans appear to use more than one type.

I can't respond anymore than this at the moment as I don't have time for the extra reading but I hope this is at least useful.

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Tags: theoretical-neuroscience, computational-modeling, neural-network
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# Question
Title: Can SSRI make things worse in the long term or cause delayed depression?
I found two articles that mention that taking SSRI for depression can actually make the depression worse.

Is this true? Can Tardive Dysphoria (delayed depression) be caused by SSRI?

They seem pretty convincing and I can't find anything against it but if it's true, it basically means that depression treatment is going back to the 60's before SSRI were invented.

# Answer
> 1 votes
Contrary to another post here, in my opinion and also that of an increasing majority of researchers studying this field, SSRIs and the so called 'antidepressant' drugs cause great harm.

Firstly here is a list of common side effects: Insomnia (which is common in depression anyway), increased anxiousness, feeling sick, indigestion, diarrhea or constipation, loss of appetite, fluctuations in weight, dizziness, blurred vision, dry mouth, excessive sweating, headaches, reduced sex drive, difficulty achieving orgasm, erectile dysfunction.

None of these are good effects which is why we don't give them to people who are 'healthy'. More importantly the devastating effect these side effects can have on a patients life could potentially be far more harmful than before the drug was taken, for example increased marital problems. According to Joanna Moncrieff these effects compound depression, and more importantly disturb the chemical balance in the the brain, and as a result compound or cause the very symptoms they are meant to cure. Central to this notion and the question presented here, the long-term use of SSRIs may causes what we call 'serotonin induced apathy', in other words, after initial positive effect of SSRIs (quiet possibly short-term placebo effect), patients become indifferent to their environments. Furthermore Long-term use of SSRIs leads to abnormal brain neurogenesis not seen in non-depressed samples, this is often taken to as proof of how SSRIs exert there action, or rather it was before 2008 (see below meta analysis). However it seems that this neurogenesis is less likely to be positive considering the negative effects and lack of efficacy SSRIs display.

The long-term use of SSRIs often leads to the development of apathy, which utimatley will lead many patients back into depression. The rate of relapse in people taking 'anti-depressants' is \>40% while patients with placebo is roughly 24%. If that isn't bad enough at a 12 month follow up only \<5% of patients are in remission for their depression. Why might this be? Well a 2008 meta-analysis by Kirsch et al found that all 'anti-depressants' are below clinical levels of acceptance, in other words no more effective than placebo. However it should be noted that in severe depression SSRIs are useful only!

The reason anti-depressants such as SSRIs are ineffective is because of the simplistic approach taken to treatment with these drugs. The brain is not some 'big bag of chemicals', neurons are not purely serotonergic in fact they often release multiple NTs. And crucially serotonin NT is used throughout the central nervous system, for more than mood regulation. The fact that SSRIs do not work over the long-term tells us the serotonin theory of depression is wrong. Perhaps more importantly roughly 10% of people in the UK are on 'anti-depressants', we can talk about over medicalisation of mental health, but the reality is large amounts of people are taking these drugs for large amounts of time (9-12 months recommend). This is not helped by the fact that governments are more interested in investing in cheap medical 'cures' than long-term methods with greater efficacy that cost more.

Sorry its so long, and I'm sorry its so short there is so much to say about how SSRIs don't work and how bad they are regarding people thinking they are getting effective cures, along with the neuroscience and discussions on publication bias. Its a fascinating topic, thanks for the question.

# Answer
> -2 votes
In general no SSRIs lasts long enough as an effective treatment for most patients to cause long term harm. Most of the time people are only on them for weeks or months before many of their symptoms are reduced. If someone remains on antidepressants for long term treatment for something like OCD intrusive thoughts or major depression it is possibility for the medicine to harm the nervous system. This is unlikely though because SSRIs are not that effective and most of the time they have to cycled to another kind of medicine for most diseases as the diseases adapt to the medication. The meds stop working and the doctor and patient must switch to another type.

Yes Tardive Dysphoria does really happen and its happened to me but no its not a big deal nor is it life altering. No we are not going back to the 60s. As there are other options in treatments. Doctors have known that inappropriate dosages or incorrect medications do cause depression. Sometimes more of the same SSRI will fix the problem. The antipsychotics and antidepressants have long since been known to sometimes have inverse effects on some patients. This is the reason why abilify though it be the latest and greatest antipsychotic is not necessarily the medicine of choice because of it high probability to induce psychosis. Thats because there are 8 genes responsible for the schizo type psychosis and how each person responds to medication varies based on their gene and biology. Likewise also for depression a much less understood condition the person's biology is going to determine their response to medication and final treatment.

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Tags: psychiatry, depression, psychopharmacology
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# Question
Title: Technical term for the displaying of 'bad' traits to seem more likeable
What is the technical name for the public display of personal traits that are unproductive or unhealthy as an attempt to make oneself seem more likeable or relatable? (e.g procrastination)

# Answer
> 1 votes
This may not fit exactly the scenario described, but some form of strategic affect display or 'appraisal theory', these relate to social theories of (& displays of) emotion, as oppose personality traits as such, but may be relevant nonetheless.

So for example, you might want to come across as being more aggressive & assertive, or alternately more compassionate & caring, in any given scenario, because you feel that is the appropriate thing to do, or you may gain some advantage from that - even though you may feel otherwise indifferent about whatever it is.

Having said that, the way the question is phrased - whether something is 'productive' or 'unproductive' in a social sense, as oppose to a personal level, is open to interpretation, i.e. if it makes you more 'likeable' then it is socially productive (at least in the short term), regardless of whether it it something that is generally regarded as being a negative trait.

Hope that's relevant.

# Answer
> 1 votes
There is a related concept to this in evolutionary biology called the Handicap Principle or Zahavi Principle \[1\]. It originally tried to explain why certain species evolved traits that are clearly not adaptive, but seemed to be favoured by sexual selection. For instance, the colourful plumage of the male peacock makes the male a target for predation, but may signal superior fitness to females. The logic behind is could be that the male is showing off that he can afford these non-adaptive nornaments and still get away with it. The kind of behaviour that you are describing may serve a similar purpose.

\[1\] Zahavi, Amotz (1975). "Mate selection—a selection for a handicap". Journal of Theoretical Biology 53 (1): 205–214. doi:10.1016/0022-5193(75)90111-3

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Tags: social-psychology, personality, terminology
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# Question
Title: What are the rules that govern neuron behavior?
This is what I know so far:
Neurons are nodes with a number called the threshold.
Neurons are connected to other neurons through directed axons.
Axons take the signals produced by neurons and deposit them on other neurons, these signals can be "negative" or "positive".
Once all the signals coming into a particular neuron are added up, if the sum is greater than the threshold, that neuron fires.
My question is: are these all the rules? And do all neurons have the same rules?

# Answer
> 7 votes
> My question is: are these all the rules?

## No.

Some things you left out:

## Plasticity (change)

* **Very-short-term *synaptic* "plasticity"** (changes in synaptic strength); at least a few different forms of this (post-tetanic potentiation, short term synaptic depression, synaptic facilitation).
* **Very-short-term *intrinsic* "plasticity"** (changes in spiking behavior): spiking accommodation, etc.
* **Medium to long-term synaptic plasticity**; several forms of this: classical Long Term Potentiation or Depression, Spike Timing Dependent Potentiation, synaptic underpinnings of habituation and sensitization in, e.g., Aplysia, synaptic scaling.
* **Medium to long-term plasticity of intrinsic properties**, like threshold, input resistance, firing properties.
* **Metaplasticity** (changing the changeability)

## Neuromodulation

* **Co-transmission** of classical neurotransmitters with a neuropeptides
* **Neuromodulation of ionic conductances** directly, postsynaptically
* **Neuromodulation of ionic conductances** directly, presynaptically
* **Neuromodulation via metabotropic receptors** and signaling to the nucleus
* Why there are **dozens of neuromodulators** just for controlling a **crab's digestion.** (ref)

## Odds n' Ends

* **Electrical "synapses"** ("gap junctions")
* **Refractory periods** preventing firing even if above threshold
* **Extrasynaptic and presynaptic** receptors
* **Retrograde transmission**
* **Axonal failures** and branch points
* **Non-traditional innervation** (dendro-axonic, dendro-dendritic, autapses, etc.)
* **Ephatic coupling** (ref) (through local electrical fields)
* **Wiggling dendritic** spines
* **Glial function** as a modifier of neuronal function.

And I'm sure I'm leaving out another 20 or so interesting ones. Arguably, everything I've listed here modifies or has causal relevance to the simple set of rules you provided above. And of course, I'm still leaving out an enormous amount of detail of neuroscience (cell types, architecture/circuit diagrams, molecular cascades, cytoskeletal aspects, development, etc.) that have relevance to "the rules" as well.

> And do all neurons have the same rules?

No. Any of the above may vary depending on cell type, part of the nervous system, individual differences, development, species, sex, time of day or other cycles, environmental factors, and possibly other factors.

# Answer
> 1 votes
Those are very simplified rules which are decent enough for simple neural networks but real neurons in the brain are a lot more complicated.

See this paper for some ways that an axon can play a role beyond the simplified rules you mentioned.

# Answer
> 0 votes
The rules that govern the behavior of neurons are described by the Nobel prize winning work of Hodgkin and Huxley. The model has seen a huge number of revisions and extension since its first publication, but remains the foundation by which we understand how neurons work. At its heart are a set of nonlinear differential equations that describe how ions flow across the cell membrane.

# Answer
> 0 votes
There's also Dale's law: in general, a given neuron releases only a single type of neurotransmitter. While that is not really true for neuromodulatory neurons, it is broadly true of neurons that receive glutamate and GABA, the primary excitatory and inhibitory neurotransmitters.

tl;dr Neurons are either inhibitory at all their output synapses or excitatory at all their output synapses but not both.

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Tags: neuroscience, neural-network
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# Question
Title: Is the ordering of Brodmann areas arbitrary?
A single Brodmann area is defined based off cellular composition. Are the Brodmann areas ordinal, and if so for what reason? (e.g. is there something that makes Brodmann area 1 the "first one", and area 2 the "second one"?)

# Answer
The place to find this answer is of course Brodmann's original 1909 manuscript *Vergleichende Lokalisationslehre der Großhirnrinde: in ihren Prinzipien dargestellt auf Grund des Zellenbaues* available here in German or here in English (*Brodmann's Localisation in the Cerebral Cortex: The Principles of Comparative Localisation in the Cerebral Cortex Based on Cytoarchitectonics*).

The English version is unfortunately not open access (and I don't have the inclination to pay US$90 for it) and the German version is a scanned copy of the original printing, so there's no easy way to search the text without reading all of it. However, skimming through it, I see that the description of the areas (which he calls *Felder*, lit. 'fields') begins in Kapitel IV (Chapter 4), page 130. He mentions that this work is largely an extension of his previous 1907 work, but beyond that there doesn't appear to be any mention of why he choose his numbering, at least not that I could find with a quick skim. It appears though that he choose a more or less arbitrary starting point and worked more or less counter clockwise from there, with a few small exceptions.

Elsewhere in the manuscript, Brodmann discusses the division of the cortex into larger homologous regions in both humans and other mammals (p. 129), and it's clear from the description of the areas that they are not divided up based on any study of homology. For example, he mentions that the *regio postcentralis* (lat. "post central region") is divided up into the cytoarchitectural areas 1, 2, 3 and 43 (pp. 130--132). The regions appear to correspond loosely with our modern notion of "lobes", but tend to be somewhat smaller (for example, there are additional subdivisions near the central sulcus).
> 3 votes

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Tags: neuroscience, neuroanatomy
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title: Modeling plateau potentials

text:
# Question
Title: Modeling plateau potentials
We are attempting to run simulations of the C. Elegans neuronal network by building upon work of the OpenWorm team. We are looking into implementing a neuron model that produces plateau potentials rather than action potentials, as suggested by this paper. Thanks to @Comte for pointing me to this paper (see this link for another question related to our project).

Here is my question: What are known-to-work mathematical models of neurons that produce plateau potentials, rather than action potentials? Ideally, the model should be formulated as a system of differential equations (as is for example the Hodgkin-Huxley model), hence easy to implement in NEURON.

(A note on my personal background: I am a student of mathematics, and this is a project for university.)

# Answer
> 1 votes
i once wrote a paper doing biophysical modeling of neurons that could create plateau potentials. While the paper itself is not exactly what you are looking for, there should be lots of good references in there:
http://www.jneurosci.org/content/33/2/424.short
Sanders H, Berends M, Major G, Goldman MS, Lisman JE. (2013) NMDA and GABAB (KIR) Conductances: The “Perfect Couple” for Bistability. J. Neurosci. 33, 424–429

also, check other articles that cited that paper: https://scholar.google.com/scholar?cites=2120401607202660739

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Tags: computational-modeling, model
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# Question
Title: In what ways do our brains use compression?
I am reading a book on information theory and one line in the book states that "Brains are the ultimate compression and communication systems." However, there is no further elaboration on the matter. I am curious to know what specifically this sentence may be referring to. In particular, how does the brain demonstrate compression?

# Answer
Say for example, you know what a particular type of flower looks like. You know it has purple petals and a white center. Now, unbeknownst to you, this flower has been slowly changing (evolving) to have a different shape, size, and even shade over the years since you first had seen one of these flowers. All the while, you have been around this flower your whole life. I mean, it grows in your current backyard, and it also grew in the backyard of the house you grew up in. In this scenario, you may have dreams about when you were a kid playing in the backyard. Instead of seeing what the flowers used to look like (when you actually *were* a kid), you will most likely see them as they appear to you today. Although your brain has memories of the *presence* of these flowers in the yard when you were a kid, their actual defining details have been rewritten over time with their current appearance. The hypothesis here is that your brain is trying to conserve capacity by linking all recorded encounters with this type of flower so that they all share the same "image file" in your brain. Witness testimonies have a similar problem -- where data received after the fact can change a person's memory of what happened and how things and people actually looked. I recommend you research the problems known about witness testimony.
> 2 votes

# Answer
Check out:

1.6. Bayesian Hierarchical predictive coding approach to explanation of the findings

from this thesis:

http://discovery.ucl.ac.uk/1435549/

There's a comparison between image compression algorithms and what the brain does.
> 2 votes

# Answer
Horace Barlow was probably the first to elaborate on the idea of compression in sensory systems:

Barlow, Possible principles underlying the transformation of sensory messages. Sensory Communication, 1961.

It is interesting to get his perspective 40 years later from:

Barlow, Redundancy reduction revisited., Network, 2001.

More recently, Bialek and colleagues have done a lot of research on this (again, primarily in sensory systems). For example, here is a recent study where they quantify the amount of predictive information (about the future state of a stimulus) compressed into retinal ganglion signalling (and downstream):

Palmer et al., Predictive information in a sensory population, PNAS, 2015.

In this case, they observe that the retina encodes predictive information about the future state of an external stimulus at a rate that approaches a theoretic limit (according to their model based on the Information Bottleneck principle) thus exhibiting (roughly) maximal compression.
> 1 votes

# Answer
The Semantic Pointer Architecture (SPA), which was used to built the biologically plausible cognitive-model Spaun, is a demonstration of the utility of compression in the brain.

In Spaun uses compression to relate concepts in a unified and grounded manner. For example, for number concepts in Spaun's "copying task", Spaun first gets the concept of the number by gradually extracting larger and larger features until from a visual hierarchy. This is analogous to the Deep Learning's Restricted Boltzmann Machines. This compressed representation can than be decompressed into individual motor actions and sent back down the motor hierarchy.

To summarize, the perception problem is the dual of the action problem and they are unified my compression, as visualised in the image below taken from the presentation found here.

This compression has also been used in terms of scalable knowledge representations.

For further information on the concepts behind SPA and Spaun, beyond the context of compression, see "How to Build a Brain" by Chris Eliasmith.
> 1 votes

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Tags: theoretical-neuroscience
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# Question
Title: Is semantic pointer architecture compatible with a predictive coding account of the brain?
Both SPA (Eliasmith et al.) and predictive coding (Friston, Clark, Rao, et al.) seem to have a lot of explanatory power.

My understanding of SPA is probably rudimentary, but Eliasmith and others seem to be able to explain and simulate higher-order psychological constructs (e.g., emotions, concepts) impressively well. Similarly, predictive coding (e.g., Clark, 2013)--if correct--is a very convincing account of the fundamental computations of the brain. And there's a lot of emerging evidence to support it.

**So I'm curious whether these frameworks can be integrated.** Would Spaun perform better by implementing some sort of predictive coding algorithm(s)? Or does SPA make this unnecessary? These questions may be poor due to my ignorance about the complexities of SPA and NEF, but any insight would be great.

# Answer
To begin to answer this question, we must first unpack the concepts in their current context.

The NEF makes no prediction about how error is propagated in the brain. It explains how to do computation using vectors in spiking neural networks. Also, it defines how error signals can be used to change how the signal is encoded (take in) and decoded (sent out) from the neural population, as well as perform probabilistic computations. For further information on this, see PES, BCM and VOja, as well as Chapter 9 of the NEF textbook.

The SPA also makes no claims how error is propagated throughout the brain. It only claims that compression must occur for scalable and grounded knowledge representation and defines some operations for accomplishing this.

Predictive coding appears to be (based off the paper you linked) about defining *how* the error is propagating. Specifically, errors go up with higher level impressions adjusting how errors go up the hierarchy based on predictions/impressions.

As hinted at previously, this is somewhat separate from the NEF/SPA, however this does not imply they can't be integrated, nor does it mean that there doesn't already exist some models that fulfill the predictive coding criteria other than simply unifying perception and action by using similar representations (I think the DeWolf's REACH control hierarchy might fall under this category). It just means that as of now, there have been no explicit relations between the two modelling philosophies. To create a stronger conclusion, I would need to understand the implementation details of Predictive Coding to see if they are biologically plausible or if they can't be formulated as vector based operations within the SPA. This seems to be the position that my colleagues share (they actually have an comment article appended to the one you linked called "God, the devil, and the details: Fleshing out the predictive processing framework") which is that more work needs to be done before a position can be taken.
> 2 votes

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Tags: theoretical-neuroscience, nef, spa
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# Question
Title: How are positions and counts of higher concepts encoded in sparse representations?
I understand that levels in the sensorimotor hierarchy of the brain learn recurring features of their input streams. The results are activation patterns with single neurons firing for the existence of specific higher level patterns. Those sparse representations are passed upward to the next higher layer.

For example, there is a neuron firing whenever there is a face in the scene. On this higher level, neurons are not restricted to a small window of our field of view anymore. My question is how those high level sparse representations still retain information about positions and counts of objects.

One bad explanation would be that there are neurons representing counts in general. If "three" and "face" are both active, there are three faces in the scene. But this doesn't hold for two kinds of objects at the same time since it's not clear which count is for which object. And what if both have the same count.

# Answer
> 1 votes
Two ideas on this so far:

* I think we have neurons representing multiple occurrences of a given feature, for example one neuron for "one face", one for "two faces", etc. At some number it doesn't really make a big difference anymore, so there is just a neuron for "group of faces". This would explain why we can recognize small number of objects in a glimpse but have to count for larger amount. Corrections and suggestions are welcome.
* In his 2014 talk at MIT, Prof. Hinton explains how the brain might find equivariant features instead of invariant features. Basically, in addition to existence of a feature, neurons in the same cortical cell might output the properties of this feature. In vision, those properties would be position and rotation, for example.

# Answer
> 1 votes
You are basically asking how to bind different concepts together based off their representation in neurons. The one way I know how to do this is using the Semantic Pointer Architecture (SPA).

To understand how lower level neural activities can be compressed as a concept, please see my answer on compression in the brain using the SPA. This answer explains how low-level features can be compressed into a higher level concept vector.

Once you've accepted, that concepts can be represented as high dimensional vectors and these vectors can be manipulated using neurons, we now have to define what types of manipulations can be used to represent counts.

A perfect example of this is Dan Rasmussen's neural system for solving Raven's Progressive Matrices. In the system, graphical cells in a matrice are represent using a neural symbols bound together using circular convolution. For example, the top-left cell in the below image could be represented as symbols bound together as `SHAPE*CIRCLE+COLOR*BLACK+NUMBER*ONE` where every word written in ALL CAPS is a symbol represented by a high dimensional vector and based on sensory input.

To relate numbers to each other, the number `ONE` is defined as a unitary vector which can be convolved with itself to represent new numbers. For example `TWO=ONE*ONE` and `THREE=ONE*ONE*ONE=TWO*ONE`.

For implementation details and to try out these concepts for yourself if a simulator, please see Nengo and "How to Build a Brain" by Chris Eliasmith.

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Tags: cognitive-neuroscience, cognitive-modeling, sensory-perception
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# Question
Title: Do gating mechanisms in the neocortex have individual degrees for all gated connections?
For example, the upward connection between layers in the neocortex flows through the thalamus which is assumed to have a gating function.

I wonder whether there is a single value per gate, determining the degree to which patterns can pass. Or can the gate be different for different synapses or signals at the same time? In this case, there would be more like a vector of degrees for all individual synapses of the gated nerve cord.

Is there anything known about this?

# Answer
A paper just came out last week in Neuron demonstrating dendrite-specific gating:
http://www.cell.com/neuron/fulltext/S0896-6273(16)00054-4?elsca1=etoc&elsca2=email&elsca3=0896-6273\_20160302\_89\_5\_&elsca4=Cell%20Press
Structured Dendritic Inhibition Supports Branch-Selective Integration in CA1 Pyramidal Cells Erik B. Bloss, Mark S. Cembrowski, Bill Karsh, Jennifer Colonell, Richard D. Fetter, Nelson Spruston
DOI: http://dx.doi.org/10.1016/j.neuron.2016.01.029
> 2 votes

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Tags: neuroscience, cognitive-neuroscience, computational-modeling
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# Question
Title: What correlation research has been done on MBTI vs Big5?
Big5 is probably the most used personality model in research, while MBTI has not gained status of being scientifically supported.

* What exact research has been done on correlating the two models?
* Could someone give me links to full research reports with correlations between the two models?
* Correlations between subfacets would be especially useful (i.e MBTI extroversion vs Big5 extroversion).

# Answer
The MBTI can be considered to be subsumed by the Big5/Five-Factor Model. McCrae and Costa examined this back in the late 1980’s. First of all, they showed that the types do not interact in a statistically meaningful way indicating that there isn’t a reason to interpret four type categories (e.g., ESTJ vs INFP). The categories (e.g., extraversion vs introversion) describe some meaningful amount of variance themselves but combining them into the types and interpreting the whole is not statistically warranted (McCrae & Costa Jr., 1989). Statistically, false dichotomization/median splits (here called types) reduces the predictive power of a measure in general.

To further examine the universality of the Five-Factor Model, they examined how the MBTI dimensional raw scores related to the FFM/Big5 scores. They showed that FFM-Extroversion was highly correlated to MBTI-Introversion (r = -.74), FFM-Neuroticism was weakly correlated to MBTI-Introversion (r = .16), FFM-Openness was correlated to MBTI-Intuition (r = .72), and to MBTI-Perception (r = .30), FFM-Agreeableness was correlated to MBTI-Feeling (r = .44), FFM-Contentiousness correlated to MBTI-Perception (r = .49). These correlations were for men only, but are reported to give as an example of how the FFM can account for MBTI measures. The MBTI does not capture trait Neuroticism which could be considered a fault because Neuroticism is strongly predictive of many negative outcomes (Barlow, Sauer-Zavala, Carl, Bullis, & Ellard, 2014). The other factors of the MBTI are accounted for in the FFM, but captures additional variance above and beyond the MBTI. Validity and universality of the Five-factor model is another question but, briefly, it is empirically derived from factor analysis of the entire English dictionary (lexical approach) a factor structure which has been replicated in over 40 languages (McCrae & Costa, 2008).

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                                **References**

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Barlow, D. H., Sauer-Zavala, S., Carl, J. R., Bullis, J. R., & Ellard, K. K. (2014). The Nature, Diagnosis, and Treatment of Neuroticism: Back to the Future . Clinical Psychological Science , 2 (3 ), 344–365.

McCrae, R. R., & Costa Jr., P. T. (1989). Reinterpreting the Myers-Briggs Type Indicator From the Perspective of the Five-Factor Model of Personality. Journal of Personality, 57(1), 17–40.(https://www.researchgate.net/profile/Paul\_Costa3/publication/20447534\_Reinterpreting\_the\_Myers-Briggs\_Type\_Indicator\_From\_the\_Perspective\_of\_the\_Five-Factor\_Model\_of\_Personality/links/00b49515b9ad847e86000000.pdf)

McCrae, R. R., & Costa, P. T. (2008). Empirical and Theoretical Status of the Five-Factor Model of Personality Traits. The SAGE Handbook of Personality Theory and Assessment: Volume 1 — Personality Theories and Models. SAGE Publications Ltd (pp. 273–295).
> 11 votes

# Answer
To quote my answer to another question:

> The IPIP website provides measures of the Big 5. The following table from Furnham (1996) summarises some correlations across a few studies between the NEO Big 5 and the MBTI.

> You can find a listing of some of the multi-construct measures including Big 5 measures on the ipip website.

### References

* Furnham, A. (1996). The big five versus the big four: the relationship between the Myers-Briggs Type Indicator (MBTI) and NEO-PI five factor model of personality. Personality and Individual Differences, 21, 303-307.
> 4 votes

# Answer
So far found these 2 sources:

The Myers-Briggs Type Indicator: A Critical Review and Practical Guide: Book by Rowan Bayne (1997). Google-book link here (Sorry I don't have the book), check on page 24-26.

Myers-Briggs and Four-Type Structure: A principal components and equimax study of the four dimensions of the Myers-Briggs Type Indicator. Research by Jamie Larson. Link here.

In short summary, I believe the above sources found that MBTI does correlate with BIG-5 Factor model.
> 3 votes

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Tags: personality, mbti, big-five
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title: Is something not worth remembering?

text:
# Question
Title: Is something not worth remembering?
Does it affect brain negatively if I remember unimportant things? In other words: Is the capacity of the brain (or just too much chaotic data densed together) sometimes a significant factor for an individual's inteligence? Is something practically not worth remembering?

# Answer
> 1 votes
There are capacity limitation, especially at the working memory, that makes it impossible and inefficient to process everything we experience in the past. Our brain creates abstractions of things i.e. we do not remember every dog we have seen, but we remember the dog category. We forget unimportant details, but we maintain episodic memory for things that are important or recent.

The dysfunctional aspect of remembering everything can be demonstrated through a Hyperthymesia patient called AJ.

> Hyperthymestic abilities can have a detrimental effect on cognitive capacity. The constant, irrepressible stream of memories has caused significant disruption to AJ's life. She described her recollection as "non-stop, uncontrollable and totally exhausting" and as "a burden".

...

> At school, AJ was an average student, clearly unable to apply her exceptional memory to her studies.

...

> Deficits in executive functioning and anomalous lateralisation were also identified in AJ. These cognitive deficiencies are characteristic of frontostriatal disorders.

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Tags: memory, brain-training
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# Question
Title: Why do Spiritual people try to sleep less?
In Monasteries and other spiritual contexts, there seems to be a "rule" that sleep is wasted time, and so the usual daily schedule only allows for about 4-5 hours of sleep. This might be enough for an 80-year-old, but anyone else will probably be sleep-deprived and not very functional, let alone be able to make any spiritual progress.

I asked about whether adults can get by with less sleep, and got no answers. Does anyone know *why* spiritual scenarios seem to try to reduce sleep hours? One thought is that people think it is associated with laziness, indolence, lethargy, unproductive time, idleness, sloth, etc. But no one tries to reduce food intake, or use of the toilet, so why is sleep the big bad guy?

# Answer
There's a difference between spiritual people and students trying to learn something. **Sleep deprivation is an effective tool of breaking old learned routines - you just cant remember them too well when sleep deprived** (Source). Once you learned what you need, sleep deprivation becomes very disruptive.

An example given is performing a novel task, like reciting the months of a calendar year backwards(December - November - October...). Old ingrained pattern of (January-February-March...) gets in the way, and people who are **sleep deprived are apparently doing better on a this task** than control subjects, because the old pattern is not remembered as well. (Same source)

There are a number of "programs" and "cults" like Landmark Forum, which attempt to teach/brainwash/indoctrinate you into learning some new outlook on life in a very short period of time. It has been proposed that sleep deprivation is a very big part of this "reprogramming".
> 3 votes

# Answer
Let's consider what happens when we sleep. Our body specially brain gets relaxed, you will see change in brain waves. During sleeping less cycles per second waves occur than awaken times. Blood circulation increases, your brain gets repaired from everyday workings. Now some spiritual activities may elevate these situations inside your brain, specially meditation. Almost all spiritual people meditate, one way or another. Research shows deep meditation for half an hour works like 2 hours of sleeping! What monks of course do.
> 0 votes

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Tags: sleep
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title: Good news or bad news first

text:
# Question
Title: Good news or bad news first
Is it true that people handle bad news better if they got told good news first, or do they 'forget' the good news if the bad news is told after?

Is it better to save the good news for last so the person who gets the news will have a better average feeling about the conversation?

# Answer
> 2 votes
My suggestion is to look to prospect theory here. In general, people feel losses 2.5x more than gains (Kahneman + Tversky). There's also an inversion curve: more good has diminishing returns, more bad has diminishing returns too. Basically we 'acclimate'

This is a very crude way to think about it.

Good news first: In this situation, we could go up the curve, then 2.5X down for the bad news, or the other way around.

Bad news first: In this situation, you go down the curve first, but coming back the curve you erase the curve of the bad news, which is 2.5x steeper, so you're actually net gaining in positive utility, because the same amount of good news brings you up the curve more.

This is called the silver lining effect in the literature.

So all in all, deliver the bad news first: you'll gain more 'upside' on reversing bad news than following up good news with bad (silver lining effect) + people will remember the good news at the end of the conversation (recency effect).

# Answer
> 0 votes
Micha, you've asked a question that promises divergent answers, but it gets to the heart of human relationships because it's a situation (telling news, sometimes good, sometimes bad, sometimes both) we all experience as tellers and as listeners. It would take some amazingly clever social scientists to devise experiments that might shed light on this question. The problem, however, is that there is no such thing as "good news" or "bad news," not in any scientific context. There may be bad news: "Your father died in an accident," or "I had a fender-bender in your car," or "The growth in your brain is malignant," or "You know your favorite vase? I accidentally broke it." Or good news: "The ABC company called and said you got the job," or "The growth in your brain is not malignant," or "Your little sister made an 'A' in her Chemistry class," or "Yes, I'd like to go to the concert with you." There is only specific news with a total range of degrees and kinds of bad things and good things. The point is, no one can answer your questions accurately using those general terms. But as I said, this is a vital question that we all deal with, in our personal and in our professional lives. You will find, in your research, that the variables are seemingly endless regarding factors in a person's response to good or bad news.

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Tags: social-psychology
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# Question
Title: How to efficiently use a statistical consultant?
I a fairly solid grasp of Statistics and have taught statistics to both undergraduate and graduate Psychology students. There are, however, sizable gaps in my knowledge and I have attempted to employ a statistical consultant a couple of times. The conversations generally devolved into the consultant suggesting experiments and analyses that did not answer the research questions I was interested in. I am beginning a retrospective epidemiological study which is far enough outside my experience that I want to try a statistical consultant again.

How do I prepare for talking to a statistical consultant such that our discussions can be productive. How much time will it take before I see progress being made on our mutual understanding of the issues (hours, days, weeks, months ...)?

# Answer
> 3 votes
This is a challenging question. As a bit of background, I am a cognitive scientist for the most part (by my highest graduate degree), but in addition to that, I have graduate degrees in both math and statistics and I have worked professionally as a consultant in those fields for many years. So I have some access to the problems on both sides of this question.

Statistical consulting is a point of training for some, but certainly *not* all, graduate students in statistics. What this means is that some people acting as consultants will be well trained in this activity, while others may be picking it up as they go. **So you want to talk to either a more senior consultant or work with a statistics consultancy that has more senior people there to make sure your consultant knows what he or she is doing.** That said, there is a *standard of care* in consulting these days, outlined in (among other examples) this ASA document, this 2010 conference paper, and this white paper by Flavia Jolliffe. Also Zahn and Isenberg is a classical paper on this. These may give you an idea of what the consultants who get trained are taught.

Consultants in statistics are well trained (usually!) in methodologies, but the main weakness in their training is usually exposure to the complexities of any given scientific field. In particular, unless they consult for people in your field regularly, the single hardest problem will be communicating in a concise way what it has taken you years to learn yourself: the specifics of your research problems. **A solution here is to find someone who specializes in problems related to your research area.** While not comprehensive, this page at ASA lets you search for statisticians by speciality, including some content areas (including epidemiology). Also remember that statisticians live in various academic departments (if you are using academic consultants) and these departments often are only vaguely aware of each other: as an example, I used to be at a university where the main campus statistical consultancy was in a school of social sciences, and the actual statistics department did not interact with them at all. Searching broadly is sometimes helpful.

**If you cannot find a specialist, then communication is the key, and it *will* take longer to get to results in your relationship with your consultant.** The paper by Jolliffe (above) has good advice that might be useful both to the consultant and to the client in terms of what to do and how to communicate (and there are some references there that go further). But this will be the central problem, so working closely on clarifying the research goals is probably the most important step.

**A good preparation is to think about the problem before meeting the consultant and imagine trying to explain it to a good student or colleague from another field.** Try to think through the particularly specialist parts of the problem before meeting the consultant; how would you explain these to someone new in your research lab? **Likewise, if the consultant is not clear in responding to you, be direct is asking for more clarity.** I believe this is covered by item E.2 of the ASA's ethical guidelines for consulting and collaborating for statisticians.

Not that any of this applies to your case, but from the point of view of the consultant, there are a number of things worth noting. First, clients, especially those with statistical knowledge, often come in with strong expectations of what the right answer is, and sometimes grow offended at questions from the consultant that try to get at the real questions being asked. As an example, I used to consult with psychologists who basically wanted me to tell them how to do an ANOVA on their data, even when that was the wrong analysis. So be open to analyses that you are not used to using. Also, a good consultant will ask a lot of questions to clarify the statistical question you want answered. Always assume good faith, and do try to answer the questions even if you don't fully understand them. But be willing to say (and *explain*) when you think the consultant's questions miss the point. Another issue is when people come into consulting so late that all there is for the statistician to do is conduct a *post mortem*. If you are serious about consulting, meet with them early on in the process. Finally, work out payments or collaboration rules up front. You would be amazed how often statisticians are asked to do *pro bono* work, either implicitly or explicitly.

**tl;dr Communication, and it may take some time.**

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Tags: statistics
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# Question
Title: Can habits be implemented by playing mental scenarios or playing things in your head?
A significant amount of people say that you need to do things over and over again to implement a habit into your subconscious mind where you no longer have to think to do it. If, let's say, I want to implement a habit of drinking water when I walk in my bathroom in the morning but fail to do it due to the fact that this is attempted in the morning 2 minutes after waking where I'm still tired and less awake, would it be possible for me to implement this habit or at least become much more conscious of it by playing the scenario in my head, maybe even acting it out mid-day, or just thinking about why I should do it, etc. ?

# Answer
The answer is yes and can be supported by a theory called implementation intention.

> An implementation intention is a self-regulatory strategy in the form of an "if-then plan" that can lead to better goal attainment, as well as help in habit and behavior modification. It is subordinate to goal intentions as it specifies the when, where and how portions of goal-directed behavior. The concept of implementation intentions was introduced in 1999 by psychologist Peter Gollwitzer. Studies conducted in 1997 and earlier showed that the use of implementation intentions can result in a higher probability of successful goal attainment, by predetermining a specific and desired goal-directed behavior in response to a particular future event or cue.
> 1 votes

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Tags: cognitive-psychology, cognitive-neuroscience, habituation
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# Question
Title: What is Joan suffering from in this example?
> Joan has seen several specialists and undergone numerous diagnostic tests to determine the cause of her recurring headaches and episodes of dizziness. The doctors are perplexed and can seem to find no physiological cause for Joan's symptoms.

My guess would be between 3 possible disorders:

1. If she's lying about the headaches and dizziness, then she is seeking attention which could point to Histrionic Personality Disorder (if she makes a big scene every time she goes to get tested).
2. If she's not lying and the doctors can't find a physiological symptom, then it could be Generalized Anxiety Disorder (she keeps going to get tested because she is having trouble identifying cause of stress).
3. If she is not lying, then she could just be imagining the headaches and suffering from schizophrenia, which is characterized by breaks from reality (as in, she imagines the headaches and dizziness but they don't really occur.

# Answer
> 5 votes
I don't think you can rule out that she really is suffering from headaches and dizziness. Just because the doctors can't find a physiological cause doesn't mean that there isn't one.

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Tags: personality, schizophrenia, anxiety, personality-disorder
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# Question
Title: Models of a working (short-term) memory task that combine performance and reaction time?
I am looking for the advice regarding the modelling of the results of a working (short-term) memory test. In a typical case, performance in such tests can be characterized using the hit rate and false alarm rate, which can be nicely combined into d-prime, and the reaction time. My question is whether there are smart concepts how all these parameters may be fused together to generate some sort of the "working memory performance index"? (Toy example: d-prime that is weighted by the log-transformed reaction time.) Any references will be very much appreciated.

Upd: I am interesting in the specific application and possible specific pitfalls for the working memory research.

# Answer
This is a tough question, one that I have had to face in my own research. Your question has already been answered/addressed in How to analyze reaction times and accuracy together?

In short, there is no universal method. If you don't find the references or methods listed in that question useful, then I suggest you will require a computational model such as the Linear Ballistic Accumulator. The LBA is a (structurally and computationally) framework that informs process underling both RT and error data (drift rate vs response criterion).
> 1 votes

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Tags: working-memory
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# Question
Title: Why are so many people arachnophobes (afraid of spiders)?
Why are so many people *arachnophobes* (have an extreme fear of spiders)?

# Answer
> 1 votes
The answer can be found from evolutionary psychology. We are wired to feel fear when we encounter stimulus that look like spiders and snakes.

> Evolutionary psychologists argue that much of human behavior is the
> output of psychological adaptations that evolved to solve recurrent
> problems in human ancestral environments

Spiders and snakes were major threads in the early years of the evolutionary history of humans. Human ancestors that were more afraid of spiders/snakes had an evolutionary advantage over those who did not, because they were more cautious and survived more years.

> people nonetheless learn to fear spiders and snakes about as easily as they do a pointed gun, and more easily than an unpointed gun, rabbits or flowers. A potential explanation is that spiders and snakes were a threat to human ancestors throughout the Pleistocene, whereas guns (and rabbits and flowers) were not. There is thus a mismatch between humans' evolved fear-learning psychology and the modern environment.

# Answer
> 2 votes
Humans are most comfortable with those things that resemble themselves, both in terms of physical features and mentality. A dog, for example, may have an extra set of legs and a tail, but does not differ all that significantly from humans or other mammals—we can similarly see ourselves in the behavior and apparent emotions they exhibit.

Arachnids, on the other hand, are several orders of magnitude more alien. Beyond the gross physical dissimilarities, it is impossible to attribute anything resembling human emotion or motivation to them. Add to that their penchant for appearing unexpected in dark places and their inherently predatory nature, the very *idea* of spiders triggers in many people a primordial dread.

# Answer
> 2 votes
A quick lit scan suggests evolutionary advantage to being afraid of spiders and snakes. Unclear what causes this mechanism: http://news.nationalgeographic.com/news/2001/10/1004\_snakefears.html

Social conditioning also likely plays a huge role here. Spiders in our society are seen as evil / scary (via Halloween, movies, etc.). This unconscious bias makes people naturally afraid of bugs and spiders through social conditioning and social physics.

# Answer
> 0 votes
According to the American Psychiatric Association, phobias affect more than one in ten people in the US, and of those individuals, up to 40% of phobias are related to bugs (including spiders), mice, snake and bats.

There are clearly a lot of arachnophobes. But do they know why they fear spiders? Can they do something to control those fears?

Once bitten twice shy?

Psychologists believe that one reason why people fear spiders is because of some direct experience with the arachnids instilled that fear in them. This is known as the “conditioning” view of arachnophobia.

There was also an effect from family. Those people fearful of spiders reported having a family member with similar fears, but the study was unable to separate genetic factors from environmental ones.

Not surprisingly, if you give kids a list of things that might be scary for them, the vast majority check off things like not breathing, getting hit by a car, bombs, fire or burglars as quite important. Interestingly, if you give them a free option to tell researchers what sorts of things they fear the most, both boys and girls report “spiders” as their top fear (the second fear is being kidnapped, third is predators and fourth is the dark).

This is surprising. Of all the things kids might report, they list spiders as the number one fear. So in contrast to Davey’s work, Muris finds that the kids that were most fearful of spiders could relate that fear to specific events. Perhaps conditioning is the pathway to arachnophobia.

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Tags: cognitive-psychology, phobia
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# Question
Title: Which commodity technologies offer useful neuroimaging data?
Do any commodity technologies exist that offer useful neuroimaging data? By commodity I mean lowish cost and not requiring specialist technicians to run. By useful I mean able to reliably provide some signal at different times from the same subject, even if it is of a limited nature. If so, what are the capabilities of the technology?

For instance, do the cheap EEG machines provide useful data or not?

Are any such technologies likely to become available in the foreseeable future?

# Answer
The question is a little vague, but here is a partial answer.

There are a number of EEG systems available that are low-cost. Examples include Emotiv's EPOC System and the OpenBCI project. The former has been available in various models for some years now and it has been established that it records real EEG signals, as opposed to just recording signals generated in the muscles and other artifacts.

The first major validation document is by Ekanayake as a white paper, that has been updated (here). As I understand it, these are not peer reviewed, nor were they presented at a conference. But the work is quite good.

For the collection of ERP (Evoked Potentials) data, there are two substantial peer-reviewed papers by a research group: Validation of the Emotiv EPOC EEG system for research quality auditory event-related potentials in children by Badcock et al. (2015) and Validation of the Emotiv EPOC EEG gaming system for measuring research quality auditory ERPs, also by Badcock et al. (2013). While these papers are on ERP experiments, their results suggest that other collection styles, such as continuous collection, are likely to be ok as well.

Additionally, Liu et al. (2102), Implementation of SSVEP Based BCI with Emotiv EPOC, is suggestive but appears to be an unreviewed conference paper. As a *counterpoint* to this, there is Performance of the Emotiv Epoc headset for P300-based applications, by Duvinage et al. (2013). Searching Google Scholar for these topics, shows a trend that more recent papers are generally more positive, but I don't have time to work the statistics to show that is more than my quick opinion.

As an aside, our laboratory has been using the Emotiv system for approximately a year and a half, collecting data for approximately 6 months or so, and for continuous EEG collection (non-ERP) we are replicating the expected EEG phenomena. Hopefully we'll be added to the peer-reviewed literature above soon.
> 3 votes

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Tags: methodology, devices
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# Question
Title: Theories of Emotion: Schachter's Two Factor Theory Example
I'm currently in AP Psychology and studying for the exam using the College Board's course description, which contains sample psychology multiple choice questions. Here is one question, taken from the document:

> Lee is about to skydive for the first time. He interprets his racing heart to be the result of his eager anticipation and excitement. This best represents which theory of emotion?
>
> (a) Cannon-Bard
>
> (b) James-Lange
>
> (c) Drive reduction
>
> (d) Schachter’s two factor
>
> (e) Arousal

Immediately, I ruled out A, B, C, and E, leaving "D" as the choice. But per the definition of the Schachter two factor theory of emotion (alternatively known as the Schachter-Singer model), an emotion is felt only after there has been a physiological response and a cognitive appraisal of the situation. Here is one source that explains this, but our AP Psychology textbook also explains it in that way. I don't see how that matches the given scenario. Why is this correct?

# Answer
> 2 votes
I think it's because he interprets his emotion as anticipation and excitement because of the context - because he's about to go skydiving which is fun and exciting. If he was at home watching a boring TV show and had the same physiological experience, he might think he was having a symptom of some kind of heart disease. If he'd just tried a new drug and had the experience, he'd think it a side effect of the drug. If he'd just met a new person and had the racing heart, he might think he was in love. The physiological response (racing heart) is necessary, but it needs to be defined cognitively according to the context (skydiving), that's the two-factor theory.

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Tags: cognitive-psychology, emotion
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title: What would this dream mean?

text:
# Question
Title: What would this dream mean?
Alright, so last night I had a dream about someone being murdered in my apartment, basically the floor right above me, and there's this guy who always plays loud music and throws stuff out his window (I'm guessing he's distressed), what would this mean?

# Answer
> 1 votes
Dreams don't always make sense, nor do they always have to make sense, although founder of the psychoanalytic field Sigmund Freud believed in dream interpretation: that dreams have a manifest content (literally what goes on in the dream) and a latent content (symbolic, not-initially-apparent meaning of the dream). It's worth noting there's no scientific evidence to back this up, and it's just something Freud believed.

In the case of your dream, it could simply be that your mind associated your neighbor's aggression/distress with a display of aggression (homicide) and somehow connected the two in one dream. Freud would probably argue something along the lines of "Your repressed anger or frustration towards this individual manifests itself in the form of a dream in which he is murdered". Don't overthink this, and don't think your dream means anything bad. Dreams can be pretty bizarre.

# Answer
> 0 votes
**There's no external meaning to a dream. It's the dreamer who makes sense of it**, so they don't have a general meaning that could apply to everyone and they can't be "interpreted".

That been said, there are **hints to find our own sense out of a dream**: try to see it as it is speaking all about you (it is! as you are the dreamer). The house is you, the various floors are different aspects or levels of your personality (maybe mind, body, emotions... but that's just an example) or of your life (work, family, leisure... as another example), and the people involved just various aspects of your own personality, we can all see "different me's" inside ourselves (we are not the same "personality" when applying for a work than when we play with our kids... etc.)

So, and just as an example: maybe you have one of those auto-critical minds that never shuts up (the noisy distressed neighbour upstairs) that "kills" (murders) your spontaneity (another part of our personalities: the playful child we all also are). Or maybe vice-versa: you are very impulsive and the dream reflects your ignored fear of the consequences (that kills the much needed grown up we must also be).

Maybe these examples can help you gain an idea of a way to interpret your own dreams. After all, it's our own brain that produces images to balance our mind, so usually they reflect things that when we are awake we don't take into account or don't pay enough attention. In my examples, the "advice" that can be applied could be "don't be so hard on yourself, as you are "killing" your joy, spontaneity... etc" or "be more responsible, as you are "killing" your health or your future... etc".

You can also find meaning in the emotion itself. Seems you are kind of an spectator in the dream, is your neighbour who is distressed and someone else is being killed. There are people that don't allow themselves to recognise they feel angry or they don't do something with their anger (anger is only destructive when it is not used to build), so they dream with things like "another one is distressed" "someone kills someone". Anger is much needed to survive and to live healthy. It tells us what hurts us and what things we want and don't want in our lives. So, if we "don't feel anger" we live sad and stressed lives. Anger is there but we don't listen and don't do anything constructive with it, so we dream with it. It's just like when we are thirsty, if we don't drink our brain constantly produces images and even sounds of water in our minds... isn't it? Well, dreaming is the same thing. In fact there's the saying: "I'm dreaming with a glass of water!" "I'm dreaming with my bed!" (when we are very tired) just because of that: don't forget and focus your attention on what you need.

In any case, it's only you who can tell you've come with the right meaning. You'll feel that something makes sense for you.

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Tags: dreams
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title: Why are dream so fast?

text:
# Question
Title: Why are dream so fast?
Psychology always tell us the brain is meant to relax during rest/sleep/unconsciousness, but why is it that when one sleep and have a dream, the dreams are so fast that you hardly remember 60% of the dream after you wake up.

1. Is it that the brain processes faster during sleep?
2. How can you remember at-least 60% of your dream, after you are awake, not after several days, month or years?

# Answer
> 2 votes
Sleeping is a usual, necessary process for memorization and brain rest. It is commonly known that there are two phases of sleeping: rapid eye movement sleep (REM) with high brain activity and non-rapid with low activity and usually without dreams. When you get tired and fall asleep, you enter directly into second, non-rapid phase, and your internal discourse stops. Obviously, this brain state doesn't differ faster processes.

During REM sleep there are some images, dreams in your head, combinations of ideas, memories and worries, which aren't useful, since brain erases most of it. But there is one interesting technic, lucid dream. Using that you can keep consciousness when falling asleep or get it while sleeping. You can control dreams, do whatever you want, even control memories, if you got high skill.

And what about speed of this REM condition? Despite the rapid eye-movements, this condition also doesn't provide high speed of thinking. Sometimes (e.g. during a nap or while awakening) you can have dreams and feel, hear things round you; and you can observe that your dreams and real world go at the same speed. However, when you awoke, thanks to special chemical mechanisms you forget dreams, it seems dim and far - that makes the illusion of fast feelings.

So, the answers are:

1. No, it is just another kind of brain work.
2. You can learn lucid dreaming. Also you may just try remember dreams every morning, e.g. I keep dreams diary for a few years and now can remember about 5 dreams per night, when I started from 1 dream per month.

I'd like to add, from mine and friends experience, there is nothing very interesting or useful about remembering or controlling dreams. It is a real trash for mind, although unusual trash.

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Tags: dreams
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# Question
Title: What is the word for: "I have to do" in CBT?
When people think "I must", "I have to", "I should", "he should", or "people have to" it can become a problem.

It's studied by Cognitive Behavioural Therapy but I don't know the name for this kind of problem.

This is the explanation in another language (translated in english): link

# Answer
I've found out that the name given by Albert Ellis is must-urbation

http://albertellis.org/musturbation-stop-rubbing-wrong-way/

https://en.wiktionary.org/wiki/musturbation

> The compulsive insistence that things ought to be a particular way.
> 0 votes

# Answer
You could be referring to two different things.

1) This is an example of an intermediate belief. Cognitions can be thought of as three levels: automatic thoughts (which are the first thoughts that pop into our heads), intermediate beliefs (which often take the form of rules, attitudes, and assumptions), and core beliefs (which reflect our deepest levels of thought and core values).

An example is:

* Situation: Not understanding part of a lecture
* Automatic thought: I'll never learn this! I'm an idiot! Why bother trying?
* Intermediate beliefs: (which can take the form of *should* or *must* statements)

\*Attitude: Failing at anything is terrible

\*Assumption: If I challenge myself, I'm sure to fail. If I do things that come easily, I'll succeed.

\*Rule: If I can't do this easily, I should just give up.
* Core belief: I'm incompetent

2) The statements you mention are also examples of dysfunctional thoughts (also called *cognitive distortions*), specifically all-or-nothing thinking (seeing things in black or white) or "imperatives" (should or must statements).

* These errors in thinking are our tendency to draw invalid conclusions or selectively pay attention to evidence to support our thinking.
* Example of all-or-nothing thinking: If I don't get a 100% on the test, I'm a failure. If she doesn't return my phone call immediately, she hates me. (That second example is also a bit of jumping to conclusions).
* Example of imperatives: Making any mistake is terrible; I should always do my best. If I ask for help, I am weak; I must be completely self-reliant.

Search these terms for more information: Intermediate beliefs, dysfunctional thoughts, cognitive distortions

Reference:

Beck, J.S. (2011). Cognitive Behavior Therapy. 2nd Edition. New York, NY: The Guilford Press.
> 7 votes

# Answer
In NLP (Neuro-Linguistic-Programming), these are called "modal operators" of necessity.
> 0 votes

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Tags: clinical-psychology
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# Question
Title: What is an interstitial personality trait?
The HEXACO and some other measures of personality describe certain traits as "interstitial". What does it mean for a personality trait to be "interstitial"?

# Answer
> 2 votes
Many personality measures are organised hierarchically where broad traits are defined as the combination of multiple narrow traits. Broad traits are often called domains and narrow traits are often called facets.

Two influential examples are the NEO-PI and the HEXACO models of personality. For example, the NEO-PI has five broad traits and each broad trait is composed of 6 narrow traits. The HEXACO model includes six broad traits and each broad trait is composed of four narrow traits.

However, some measures include narrow traits that do not fit so neatly within a particular hierarchical framework. For example, factor analytic research may indicate that the trait loads substantially on more than one broad trait.

**Interstitial traits are narrow traits that are meaningfully correlated with two or more broad traits.**

The terminology comes from the word "interstices" meaning "a small space that lies between things". Thus, such traits occupy a narrow unique space that overlaps with more than one broad trait.

I'm not sure whether the term "interstitial" could be used to describe traits that are relatively unrelated to any broad trait.

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Tags: personality
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# Question
Title: How / when does neurogenesis occur while learning?
I've heard that learning to Juggle (new things) helps increase neurogenesis. So, what does it depend on?

* Does it have to be a **physical skill** only?
* Or can I study / **read** about Economics(which is new to me) for that?
* Should I have new **emotional** experiences like death in family, first time love etc.?

Also, when we try memorize something, say a poem, **how is it decided that this has to be stored in the existing neurons or in the new neurons**.

I'm aware that while connecting the dots, new connections are formed.

# Answer
It has been discovered that neurogenesis takes place only on the hippocampus.

Quoting Leonard E. White:

> We now agree that the production of new neurons in the human brain is really limited to a special set of stem cells that seem to sit in the basal region of dentate gyrus of the hippocampus. So in this subgranular zone, we have a population of neural stem cells that can differentiate into interneurons that are found in the granule cell layer of the hippocampus.

Also as you said, this production could be modulated through some interventions (e.g. learning)

> This genesis of new neurons in the hippocampus can be modulated. By all kinds of different interventions including pharmacological agents such as antidepressant medications. As well as physical interventions, such as exercise.

Also, this has been mentioned in this ted talk:

https://www.ted.com/talks/sandrine\_thuret\_you\_can\_grow\_new\_brain\_cells\_here\_s\_how

In summary, the following activities impact **positively** on neurogenesis:

* Learning
* Sex
* Running
* Good diet

While these ones impact **negatively**:

* Stress
* Bad sleep
* Ageing

pd: Concerning how memory works, my knowledge there is limited.
> 1 votes

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Tags: neuroscience, learning
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title: Can CBT cure any kind of depression?

text:
# Question
Title: Can CBT cure any kind of depression?
CBT: Cognitive Behavioral Therapy, no doubt is far better than medications while having long terms goals in mind, but the question is: can it cure any kind of depression, like Seasonal Affective Disorder, Melancholic Depression etc? Or there are a few kinds of depression that can be cured only through medications?

# Answer
"Cure" is a very risky word here. If I stick to it, the answer is no, because no treatment is 100% successful; not in all cases. Let's talk about significant outcomes.

CBT is not the only therapy that science has proven to have aceptable outcomes in depression treatment. Also Interpersonal Therapy, CBASP or even electroshock therapy.

Also, the recent research in the field of antidepressants is surprisingly questioning their real outcomes.You can research the works of Irving Kirsch, who found that antidepressants weren't statistically better than placebo in the treatment of depression. He found out that the research that had been done till the moment was not completely double-blinded, as antidepressants have noticeable side effects and people "knew" when they were having the drug and not the placebo... the ones having side-effects improved. It seems that the more side effects, the more effective a substance was in major depression, either being an antidepressant, an opiate, synthetic thyroid hormone... etc. You may read further here.

This recent paper has also interesting results that apply to your question:

Driessen E, Hollon SD, Bockting CLH, Cuijpers P, Turner EH (2015) Does Publication Bias Inflate the Apparent Efficacy of Psychological Treatment for Major Depressive Disorder? A Systematic Review and Meta-Analysis of US National Institutes of Health-Funded Trials.

> "The efficacy of psychological interventions for depression has been overestimated in the published literature, just as it has been for pharmacotherapy. Both are efficacious but not to the extent that the published literature would suggest."

Then, first of all, CBT can *alleviate* any kind of depression, but not only CBT.

Second, it can be the case that someone has great results only with medication but usually they're not long term ones (there is also research that seem to point out that antidepressants worsen the long-term course of depression).

And third, different kind of depressions have greater outcomes with different approaches. For example, it's well known that antidepressants don't work with dysthymia but learning social skills is usually very useful and leads to good results; that light therapy can alleviate a Seasonal Affective Disorder to the same extent as CBT, or that the best treatment for psychotic depression is electroshock therapy.
> 5 votes

# Answer
There are different levels of depression and some antidepressants work well than others as a variances in individuals mind may counteract against the meds. This is supposedly the key to upkeep the emotions in order to stabilize while going through CBT. It has helped me and I think it is critical if you want to get healthy faster. In other words psychological dependencies such as abusing substances can cause unhealthy changes to your overall health as it is cycled with mental and physical health. Not all depression can be "cured" through pharmaceutical medicines. It just helps like putting a bandaid on a fresh wound. But if CBT is involved then that would be like putting neosporin or antibiotic ointment on the wound to heal up with a rather cleaner scar than it is untreated. Not all scars can go away but proper psychological diagnosis with the insights can make a speedier process in the meantime for healing into good shape.
> 0 votes

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Tags: cognitive-psychology, depression
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title: Disprove that Humans are selfish

text:
# Question
Title: Disprove that Humans are selfish
Psychological egoism, can anyone provide an everyday action which a healthy human mind would carry out which doesn't have the motive of preservation of the individuals own life at heart?

For example, some may provide the example of forming friendships or falling in love. However this is ultimately because forming relationships with these people is mutually benefit since they will both have someone to rely on, crucial to Humans, who are social creatures which would struggle to survive by themselves.

Interested to see if anyone can dissuade me from this dark outlook of Humanity.

# Answer
> 4 votes
Giving a dollar to homeless people on the street serves no aid to the donor, since the only difference is who has that dollar, and clearly to have the dollar is better than not. This action is therefore entirely altruistic.

# Answer
> 2 votes
I encourage you to read what **evolutionary psychology** has to say about what you're talking about. This science is maybe the origin of your "dark" vision but it is due to a common oversimplification. As my explanation could be no way better than **Steven Pinker**'s one about this issue, I extract here this paragraphs that contain a clarification about your question (full text here):

> The attempt to dissect our moral intuitions can look like an attempt to debunk them. Evolutionary psychologists seem to want to unmask our noblest motives as ultimately self-interested — to show that our love for children, compassion for the unfortunate and sense of justice are just tactics in a Darwinian struggle to perpetuate our genes.\[...\]
>
> In reality, none of these fears are warranted, and it’s important to see why not. \[...\]
>
> Unfortunately, the meme of the selfish gene escaped from popular biology books and mutated into the idea that organisms (including people) are ruthlessly self-serving. And this doesn’t follow. Genes are not a reservoir of our dark unconscious wishes. **“Selfish” genes are perfectly compatible with selfless organisms, because a gene’s metaphorical goal of selfishly replicating itself can be implemented by wiring up the brain of the organism to do unselfish things**, like being nice to relatives or doing good deeds for needy strangers. **When a mother stays up all night comforting a sick child, the genes that endowed her with that tenderness were “selfish” in a metaphorical sense, but by no stretch of the imagination is she being selfish.**
>
> Nor does reciprocal altruism — the evolutionary rationale behind fairness — imply that people do good deeds in the cynical expectation of repayment down the line. We all know of unrequited good deeds, like tipping a waitress in a city you will never visit again and falling on a grenade to save platoonmates. These bursts of goodness are not as anomalous to a biologist as they might appear.
>
> In his classic 1971 article, Trivers, the biologist, showed how natural selection could push in the direction of true selflessness. \[...\]

Trivers' article is also clarifying to answer your question. If you read the full text of the article you'll also find an explanation about how true selflessness can perfectly be a product of natural selection.

The word "dark" in your question attracted my attention. Why should it be "dark" to profit from doing good? Is like saying that the pleasure of drinking water when one is thirsty is not a real pleasure because the "real intention" of thirst is to preserve one's own life (usually nobody drinks motivated by not dying but for pleasure, although avoiding death is what we are "really" doing). Why should be there any contradiction? does the "real" (functional) explanation of what we drink for make it less pleasant? Does any explanation about doing good to others make those things less good?

# Answer
> 0 votes
Depends on what you mean by "selfish"

Selfishness itself is generally defined as being concerned, sometimes excessively or exclusively, for oneself or one's own advantage, pleasure, or welfare, regardless of others.

If that's what you mean by being selfish, then a simple act of helping others at the cost of your own pleasure, benefits, or welfare already disapproves that deep-down humans are all selfish. You can argue that such acts may ultimately caused by expectations of a perceived benefit, conscious or not. But consider these examples:

* A mother/father jumping in to save their child from a speeding car, saving the child but killing them in the process.
* A soldier throwing him/herself to a grenade to save his/her fellow soldiers.
* Someone who attempt to stop a school-shooting, and got killed in the process

Acts such as those, which resulted in ending of one's life, most likely don't stem from expectations of future benefits (I mean, they would be dead afterwards, what benefits could they be possibly expecting?). And they surely don't have the motive of preservation of the individuals own life at heart.

Yes, you can still argue that "heaven" or similar religion's concepts may be the main motive. But I'm pretty sure that even people who doesn't believe such concepts would still likely to do the first example (at least).

Taking it further, such acts may indeed be explained by needs of preservation of human as a species (sacrificing one live in order to save more lives or future generation). If this still classifies as "selfish" to you, then I can't find other example. However, I would argue that what human behavior can't be ultimately traced back to "human species preservation" motive, with or without personal benefits? I believe that there's nothing wrong with that, and thus it's not a "dark outlook" at all.

---
Tags: motivation, philosophy-of-mind, behaviorism, self
---


# Question
Title: what is the "trial-averaged neural response function"?
i'am currently reading " theoretical neuroscience by dayan abbott" and it says

" If we ignore the brief duration of an action potential (about 1 ms), an action potential sequence can be characterized simply by a list of the times when spikes occurred. For n spikes, we denote these times by $ti$ with i = 1, 2,... , n. The trial during which the spikes are recorded is taken to start at time zero and end at time T, so 0 ≤ $ti$ ≤ T for all i. The spike sequence can also be represented as a sum of infinitesimally narrow, idealized spikes in the form of Dirac δ functions . "

then it says we average ρ(t) s that we get during the trials .

" We use angle brackets, \<\> , to denote averages over trials that use the same stimulus, so that for any quantity z is the sum of the values of z obtained from many trials involving the same stimulus, divided by the number of trials. The trial-averaged neural response function is thus denoted by \<ρ(t)\> "

how can we average ρ(t) . it consists of many infinity long spikes . so summing them and then dividing them by number of trials . is just like summing them . and does not give us the sense of average spikes .

the book further explains :

" In any integral expression, the neural response function generates a contribution whenever a spike occurs. If instead, we use the trial-average response function this generates contributions proportional to the fraction of trials on which a spike occurred. "

the materials I'm referring to are from pages 7 and 8 .

# Answer
ρ(t) in Equation 1.1 cannot be summed and averaged because the idealized spikes are infinitesimally narrow and the chance of two spikes from different trials occurring at the same time t is zero.

In Equation 1.2, the idea of convolving each idealized spike with a "well behaved function" h(t). If you use a rectangular function around zero as h(t), with a reasonable width (say 1ms), then Equation 1.2 will give you a timeseries that can be averaged. This is because the chances of two nonzero values from different trials occurring at the same t will become a more reasonable (nonzero) value.

If you have enough trials, then your trial-averaged neural response function using this more reasonable representation of spikes will give you a good sense of the average spike density.
> 3 votes

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Tags: theoretical-neuroscience, computational-modeling
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title: Does color constancy overestimate?

text:
# Question
Title: Does color constancy overestimate?
Consider I have a few references from white to yellowish, and I look at them in 2 different lights: a cool-coloured light (white/~6500k) and a warm-coloured light (yellow/~3500k). Firstly, intuitively, I thought that I will perceive the whiter ones to be yellower in yellow light, but I don't -- in fact, it's the opposite: I see the yellower ones whiter in yellow light.

What does it mean? Does it mean that the colour constancy mechanisms of humans notices there's a yellow light and tries to adjust the brain such that I perceive yellowish stuff as white? If so, how come the ones that are intrinsically yellowish are still perceived as white? Does the colour constancy mechanism overestimates how much to correct?

# Answer
> *Color constancy works only if the incident illumination contains a range of wavelengths. The different cone cells of the eye register different but overlapping ranges of wavelengths of the light reflected by every object in the scene. From this information, the visual system attempts to determine the approximate composition of the illuminating light. This illumination is then discounted in order to obtain the object's "true color" or reflectance: the wavelengths of light the object reflects. This reflectance then largely determines the perceived color.*

Source

It is also known that the color constancy of humans is subject to individual differences. The perception of painters like Claude Monet but also landscape photographs illustrate that attention and learning processes play a role while performing color constancy.

Anya Hurlbert: Colour vision: Is colour constancy real? Curr Biol. 9(15): 1999: R558-561, Review Article
> 1 votes

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Tags: perception, color, psychophysics
---


# Question
Title: How to random assign subjects to a group without any equipment?
I am working with a clinician and need her to randomly assign patients into one of two groups with the goal of having roughly equal numbers in both groups. The clinician does not have access to a random number generator and it would be inappropriate for her to flip a coin before the allocation. We initially decided upon using the second hand on a clock and splitting on the top/bottom half of the minute, but the exam room does not have a clock and she does not wear a watch.

We are thinking of splitting on the first letter of the first name which is on the patient's chart. We would then flip every couple of weeks whether the first half of the alphabet was in group A or group B. Is this a reasonable approach? Is there a better one? If we go this way, what letter do we split on to give roughly equal sizes?

# Answer
If the patient has given you some kind of ID number (soc#, drivers license, patient number, birthday month... most any number) just split by even/odd.

If we assume that such numbers are sequential or randomly assigned, then there should be no large bias, or association with any patient characteristics.

If you have two or more numbers available, you could add the last digits and see if that is even or odd.
> 2 votes

# Answer
**Disclaimer: I do not suggest using this solution for any real-world applications. This is simply a demonstration.**

---

I'm not sure what your background is, but this is really easy to do in code. You could simply run a random number generator and print off the results for the clinician.

Here is an example solution in R:

```
ngen <- function(patients, weeks){
  df <- data.frame( t( replicate(patients, sample(c("A","B"), weeks, replace=T)) ) )
  colnames(df) <- paste(replicate(ncol(df), "Week"), as.character(1:ncol(df)))
  rownames(df) <- paste(replicate(nrow(df), "Patient"), as.character(1:nrow(df)))
  print(df)
}

```

---

*Example Usage*:

ngen(patients = 10, weeks = 5)

```
           Week 1 Week 2 Week 3 Week 4 Week 5
Patient 1       A      B      A      B      A
Patient 2       B      B      A      B      A
Patient 3       A      B      A      A      B
Patient 4       A      A      A      A      A
Patient 5       A      B      A      A      A
Patient 6       B      B      B      A      B
Patient 7       A      A      A      B      A
Patient 8       A      B      A      B      B
Patient 9       B      A      A      B      B
Patient 10      B      A      B      A      B

```

---

**Check by simulating 10,000 weeks:**

```
m <- ngen(patients = 10, weeks = 10000)

# look at patient 1:
mean(as.numeric(m[1,]) - 1)

```

The mean condition for patient 1 is 0.5, i.e., even chance of being in condition A or condition B as n weeks goes to infinity.
> 1 votes

# Answer
You could generate a random 0-1 sequence at the start of the study and allocate participants as they come in based on that sequence.

You can use this simple online tool to generate the sequence ( https://www.randomizer.org/ ), if you want to avoid doing some basic programming.

You'll need to have a system for allocating IDs to participants, so I imagine that just preparing the sequence of random allocation ahead of time should be okay.
> 1 votes

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Tags: statistics, experiment-design
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# Question
Title: What is the test-retest correlation for HEXACO personality?
I am wanting to get estimates of the test-retest correlation for the six HEXACO domains. I'm curious to obtain estimates of test-retest correlation over various time frames (e.g., 1 month, 1 years, 2 years, etc.).

# Answer
> 1 votes
I have not yet found HEXACO domain estimates. I've had a lock through the main articles listed as references on http://hexaco.org/references but they seem to focus more on internal structure.

However, the HEXACO-PI is quite similar to the the NEO-PI in terms of number of items per domain and the general approach to trait measurement. Thus, I would expect that NEO-PI stability would provide a ballpark of what to expect. The following is a summary of few studies from the Wikipedia article on the NEO-PI.

> * The test retest reliability of an early version of the NEO after 3 months was: N = .87, E = .91, O = .86.\[14\]
> * The test retest reliability reported in the manual of the NEO PI-R over 6 years was: N = .83, E = .82, O = .83, A = .63, C = .79.
> * A 2001 study by Kurtz and Parrish\[15\] on the short-term test-retest reliability yielded coefficients of α = .91–.93 for domains and α =.70–.91 for facets after a one-week interval. ...
> * A 2006 study by Terracciano et al.\[16\] on the long-term test-retest reliability yielded coefficients of α = .78–.85 for domains and α = .57–.82 for facets after a 10-year interval.

SOURCE

### References

* McCrae, R. R.; Costa, P. T. (1983). "Joint factors in self-reports and ratings: Neuroticism, extraversion and openness to experience". Personality and Individual Differences 4 (3): 245–255. doi:10.1016/0191-8869(83)90146-0.
* Kurtz J. E., Parrish C. L. (2001). "Semantic response consistency and protocol validity in structured personality assessment: The case of the NEO PI-R". Journal of Personality Assessment 76 (2): 315–332. doi:10.1207/S15327752JPA7602\_12. PMID 11393463.
* Terracciano, A.; Abdel-Khalek,et al (2005). "National Character Does Not Reflect Mean Personality Trait Levels in 49 Cultures". Science 310 (5745): 96–100. doi:10.1126/science.1117199. PMC 2775052. PMID 16210536.

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Tags: measurement, personality, correlation
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title: Biases in subjective survey

text:
# Question
Title: Biases in subjective survey
What are the commonly observed biases in survey and are there any statistical or non-statistical methods to avoid it?

I am conducting a survey for automobile seat comfort, I think my current methodology may have following issues :

Subjects may give average rating when they are unsure

Subjective rating may be anchored on the first vehicle subject sits in

# Answer
> 1 votes
There are lots of commonly observed biases in surveys, and a whole field of survey methodology and statistics which investigates them. To get an idea of this, take a look at the table of contents of these journals: http://poq.oxfordjournals.org/content/current http://jssam.oxfordjournals.org/content/current

Many people in this field are dealing with large data-sets (e.g., national censuses with many thousands of respondents), and they concentrate on things like estimating non-responses statistically (to take into account that some people with some opinions are less likely to complete the survey in the first place). Other widely investigated biases include "social desirability", which is the issue that people often respond with what is most social acceptable, even if it is not necessarily accurate.

However, your question suggests you are looking on a smaller scale. Although it is a bit old, this is a nice review of cross-overs between psychology and survey statistics. Not sure if the full article is stuck behind a paywall. This covers some similar ground.

**RE: Your first identified issue**, I assume that by "average" rating, you mean that people tend to choose the middle scale point if they are unsure (obviously they don't normally know the true average/mean response from their peers). There is evidence of this (see the Schwarz article above). From the abstract of Schwarz et al., 1985:

> These results indicate that subjects inferred the average amount of television watching from the response alternatives provided them and used it as a standard of comparison in evaluating their behavior and its implications.

What this means is that you should be a bit careful about choosing your scale (people will use the end points to evaluate what the average rating is). However, normally you are interested in relative deviations from this (which seats are rated higher or lower than average *relative to other seats*), so this is an issue only if you are seeking a "real number" answer (such as the number of hours people watch TV). One way to counteract the "centering" bias is to use a 4 or 6-point scale rather than an odd number (so that there is no exact centre option) A related issue is that people are often reluctant to choose the most extreme options ("endpoint bias"). The wiki on Likert scales has some information about this, assuming you are using such a scale.

**RE: Your second issue**, yes, question order matters. People often spend less time and respond differently on later questions (e.g., this paper). The specific issues of anchoring responses are discussed here. However, In your case this should be easy to control for by randomising the order in which they sit in the vehicles.

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Tags: bias, survey
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# Question
Title: Are superhero masks effective at concealing your identity?
In modern comic book fiction, a superhero wears a partial mask to obscure their identity. This mask is properly known as a "Domino Mask"

Now obviously these masks are not the most effective masks in the world. However, is there any cog sci evidence that they provide any protection at all? I highly doubt there's any evidence to show they prevent someone from identifying you, but is there any evidence to suggest they even slow identification down or increase errors?

# Answer
> 1 votes
I don't know of any proper identity recognition experiments using such a mask, and obviously it depends on how difficult the recognition test is. However, here is a paper where they found that sunglasses (and facemasks) impeded accuracy in an *emotion* recognition task. I would guess that often identity recognition is just as difficult as emotion recognition, so I would assume glasses or a mask would make people (slightly) worse. In general, this is a question about what features are necessary/useful for face recognition. There is lots of research about this, and studies such as this show that the eyes are particularly important. So disrupting this part of the face, and potentially the relationships between them, is actually not a bad way to disguise yourself (though obviously a full-on balaclava would be better!).

# Answer
> 0 votes
> *However, is there any cog sci evidence that they provide any protection at all? I highly doubt there's any evidence to show they prevent someone from identifying you, but is there any evidence to suggest they even slow identification down or increase errors?*

No and yes. As far as I know there's no evidence that **masks** in particular provide a special protection that differs from other physical objects that disrupt the face/bodyparts like when you cover your face with your own hands.

However I think it is helpful to explain (concisely) how identification and visual recognition in the process of perceptual organization works:

**Stage 1** When we see something in our environment (face of a person) our organ of perception (eyes in this case) receives a stimulus (light) that causes the creation of an neural impulse that is send to the brain (image of a face).

**Stage 2** Now our brain combines the information (the image of the face that we just saw) with a-priori-knowledge from our brain (a cocktail of experiences, expectations, language knowledge...). By doing so it identifies the object (face of my friend) **and** recognizes it. Recognizing means you are aware of the object's function (it's a friend, not a foe -\> no danger).

**Stage 3** The result is a mental re-creation of the object we just saw – a so called *percept*.

So to sum it up, if a mask or any other physical object is in the line of sight, it alters the information we receive about the covered object. And if our brain cannot *fill in the blanks*, the stage of identification is slowed down or the object cannot be identified at all. So it depends on what part of the face is covered and to what extend *and* how much information about the object we try to identify is already available in our brains.

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Tags: perception
---


# Question
Title: Can a person be hypnotized to act drunk?
I was wondering if a person could be hypnotized to act drunk? That is, can a person totally lose all his inhibitions while in hypnosis (similar to being drunk)?

# Answer
**Yes** (video example of Derren Brown making a man drunk) with caveats:

1. Not for every person being drunk means loosing his inhibitions
2. You can't force people to do something they don't want to do (example by Anthony Galie)
> -2 votes

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Tags: cognitive-psychology, social-psychology, hypnosis
---


# Question
Title: Is there anything called genetic anxiety?
We inherit a lot from our ancestors, but how much of the term **genetic anxiety** is real?

And if it is real, can it be cured similarly to how anxiety is treated (CBT, Exposure Therapy) or it requires medication? Put differently, can only medication cure genetic anxiety?

# Answer
Predisposition to anxiety can be inherited:

> Genetics and family history (e.g., parental anxiety) may predispose an individual for an increased risk of an anxiety disorder, but generally external stimuli will trigger its onset or exacerbation. Genetics accounts for about 43% variance in panic disorder and 28% in generalized anxiety disorder.

Treatment for anxiety disorders is not generally modified for genetic component, so therapies such as conditioning or CBT may be used regardless. All anxiety disorders are assumed to involve an environment (non-genetic) trigger that can be addressed through therapy.

Research by Dias & Ressler (2014) suggests that this is not necessarily the case in mice, where epigenetics alone (with no environmental trigger) can cause a purely genetic anxiety. (Layperson version)
> 3 votes

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Tags: cognitive-psychology, genetics, anxiety
---