# Question
Title: Memory game - short or long-term memory?
There is a game where "a suitcase is packed" and you have to remember all the words or objects that are packed into the suitcase.

Each participant adds a new word to the "chain of words" one after the other.

I wonder whether this information is stored in the "long-term memory" or whether it only remains in the "short-term memory".

# Answer
**Short answer**
The game you describe is a textbook example of one relying on working memory.

**Background**
The game you describe is an example of one that taxes **working memory**. Working memory can be conceptualized as (Chai *et al.*, 2018):

> a short-term storage component with a capacity limit that is heavily dependent on attention and other central executive processes that make use of stored information or that interact with long-term memory.

**Short term memory** being (Cowen, 2009):

> \[F\]aculties of the human mind that can hold a limited amount of information in a very accessible state temporarily.

The difference between working memory and short-term memory is confusing, and Cowen (2009) continues by disambiguating working memory and short term memory:

> \[W\]orking memory **includes short-term memory** and other processing mechanisms that help to make use of short-term memory.

However, Cowen (2009) points to another definition that is:

> the attention-related aspects of short-term memory. This, however, is not so much a debate about substance, but rather a slightly confusing discrepancy in the usage of terms.

Interestingly, when you look up the Wiki page on **memory span**, which describes the **digit span test**, a textbook example of a working-memory test, you can see that they also use the terms short-term memory and working memory interchangeably. So I reckon the exact differences between the two are indeed not always clear.

Now long-term memory is another matter altogether, and is, according to the current concepts about memory, not needed for your game, other than to associate and give meaning to the items added (remembering the attributes in the suitcase in a foreign language unbeknownst to you would certainly complicate matters!). Long-term memory being

> a vast store of knowledge and a record of prior events.

The difference with short-term storage is that it has a longer decay time and a larger capacity. However, the exact differences remain a matter of debate (Cowen, 2009).

Regardless the exact differences, conceptually, the game relies on working memory.

<sub>**References**
**-** Chai *et al*., *Front Psychol* (2018), **27**
**-** Cowen, *Prog Brain Res* (2008); **169**: 323-38.</sub>
> 1 votes

# Answer
Short-term memory capacity is very limited (How much can users hold in their short term memory), and that seems to be a fundamental property of short-term memory (Can working memory actually be improved?). So the longer this game progressed, the less likely it would be that players could keep the information in short-term memory. A few items would be fine. Ten items would be difficult, and items would start to drop out of short-term memory.

Memory experts use techniques like the method of loci to associate new information with an existing structure held in long-term memory. So they would have a significant advantage in this game.
> 1 votes

---
Tags: neuroscience, memory, terminology, working-memory, long-term-memory
---


# Question
Title: How are tactile pleasure and pain differentiated in the somatosensory cortex?
A recent question here asked about (mostly) how pain and pleasure are differentiated in pathways involving reward/aversion cues. But there was some confusion as to what the question really wanted to ask as it also mentioned "somatosensory mapping".

A reasonably different but also good question is how are pleasure and pain decoded before it gets to any feedback/reinforcement pathways, i.e. how are pain and pleasure distinguished in the somatosensory cortex. This discussion probably involves considering the way such stimuli are transmitted/encoded from the peripheral nervous system, (e.g. Lloyd, et al. 2015)

> The skin senses serve a discriminative function, allowing us to manipulate objects and detect touch and temperature, and an affective/emotional function, manifested as itch or pain when the skin is damaged. Two different classes of nerve fibre mediate these dissociable aspects of cutaneous somatosensation: (i) myelinated A-beta and A-delta afferents that provide rapid information about the location and physical characteristics of skin contact; and (ii) unmyelinated, slow-conducting C-fibre afferents that are typically associated with coding the emotional properties of pain and itch. However, recent research has identified a third class of C-fibre afferents that code for the pleasurable properties of touch - c-tactile afferents or CTs.

To keep answers to this question reasonably short, let's ask just how is tactile pleasure distinguished from (tactile) pain in the brain.

## References

Lloyd, D. M., McGlone, F. P., & Yosipovitch, G. (2015). Somatosensory pleasure circuit: from skin to brain and back. *Experimental dermatology*, 24(5), 321-324. doi: 10.1111/exd.12639
Free Full Text: https://onlinelibrary.wiley.com/doi/full/10.1111/exd.12639
Free PDF: https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.12639

# Answer
Obviously, pain and touch receptors are represented by entirely different receptors in the skin, *i.e.* nociceptors and mechanoreceptors, respectively. Each has physically different afferents that carry the signal to the brain. Pleasant touch is mediated by C-tactile afferents to the brain, represented by low-threshold non-myelinated C-fibers (Nees *et al*., 2019. Pain is mainly mediated via Aδ and C fibers (Beissner *et al*., 2010). Hence, different afferent pathways to the S1 exist from the periphery to the brain.

Once in the brain, there is no such thing as a single localized 'pain center', as proposed by Descartes in the early days (Ha, 2000). In fact, SI cannot be called the 'pain center', as ablation of this cortical region leads to an altered perception of pain, rather than its disappearance (Backonja, 1996). Pain perception involves many more brain centers, including S2, and those involved in higher cognitive and emotional-motivational processes, such as the orbitofrontal cortex (OFC), the anterior cingulate cortex (ACC), the ventral striatum (VS), and the insular cortex (Nees *et al*., 2019.

In the brain, pleasant touch seems mediated by a set of brain regions overlapping with that of pain, involving the insula, considered to be the primary somatovisceral cortex and connections to the striatum (Migliorini *et al*., 2013) and ACC. Interestingly, however, pleasant touch was also shown to activate the nucleus accumbens (Kreuder *et al*., 2017).

In all, to me it seems the pathways largely overlap centrally, barred the activation of the nucleus accumbens for pleasurable tactile stimuli, which is consistent with it being a pleasure center. I think there must be specific connections that are separated very early in the very periphery through a different set of skin receptors that signal to different neurons in brain regions that largely overlap between the two modalities.

**References**
**-** Backonja, *Pain Forum* (1996); **5**(3): 174-80
**-** Beissner *et al*., *Encyclopedia of the Neurological Sciences* 2nd ed., 2014
**-** Ha, MSc thesis, McGill University, Montreal, 2000
**-** Kreuder *et al*., *Human Brain Mapping* (2017); **38**(9): 4525-34
**-** Migliorini *et al*., *Drug and Alcohol Dependence* (2013); **133**(2): 661-8
**-** Nees *et al*., *Neurobiology of Pain* (2019); **5**: 100025
> 2 votes

---
Tags: neuroscience, perception, neurophysiology, brain, sensory-perception
---


# Question
Title: Is it possible to memorize the sound of a certain pitch?
Those how have an absolute pitch can name the note when they hear it. For those who don't have this ability is it possible to remember a pitch of at least one note?

# Answer
Yes, it seems like this ability can be acquired with practice.

In Identifying Notes without Perfect Pitch, the author picked twelve familiar songs, each of which started on one of the twelve pitches of the chromatic scale. Once he memorized the song-pitch association, he was able to recognize 10 out of of 12 pitches.

Some users of Music Stack Exchange mention similar results. For example, one person says they can remember the pitch of their tuning fork, and another suggests the song approach: "If hearing a note instantly reminds you of a song, then I think you *are* identifying that note, just by the song name, not the note name (that you may or may not happen to know)."
> 0 votes

---
Tags: memory
---


# Question
Title: How to take advantage of the withdrawal symptoms of antidopaminergics?
So this may be a stupid question as I am not trained in neuroscience or psychology at all, but I had an idea about a somewhat counterintuitive approach to psychotropics and was wondering whether if it was at all scientifically sound and feasible.

To distill my theory, it's basically that in the same way prolonged cocaine abuse can make you chronically unhappy and apathetic, could we encourage some sort of controlled antipsychotic abuse to make you chronically happy and energized? My thinking is this:

Since the mechanism of antipsychotic drugs in an oversimplified sense is just to decrease dopamine, naturally when you withdraw your brain would respond by having an increase of dopamine. More specifically, since your brain overreacts to the antipsychotics it starts dramatically over sensitizing your brain to dopamine. So it seems to me that the reverse effect of the withdrawal is way more powerful than the direct "purpose" of the drug (this is in a sense how I understand the condition of tardive dyskinesia). My thought is that this approach is particularly advantageous for the long-term use of physiatric drugs since in the long term the use of physiatric drugs has very little effect (and can sometimes even entrench mental illness further). Because of the fact that when dependence is developed the brain's structure and functioning in response to the ongoing presence of psychiatric medication is changing, it seems that developing drugs whose intended effects come from withdrawal would help resolve issues surrounding tolerance (as protracted withdrawal can sometimes last for years after the last dose of a drug was taken). Is it viable to use a drug originally meant to suppress dopamine transmission to induce tolerance and thus increase dopaminergic effects to treat another disease where more dopamine is needed? For instance, can we use the anti-dopaminergic compound haloperidol to induce tolerance to address lower concentrations of dopamine transporters in people with ADHD, as opposed to using amphetamines?

# Answer
> 2 votes
This is not an a totally absurd proposal if dosage and time-related issues weren't a factor, but it is rife with practical difficulties otherwise.

In schizophrenia patients, what you're talking about has been widely studied, under terms like "antipsychotic-evoked dopamine supersensitivity", "supersensitivity psychosis" (SP) etc. The latter is basically "a limbic equivalent of TD".

The problem is that TD and SP are pretty correlated, in terms of the dosage required to obtain them, and require "overdosing" the (schizophrenia) patient. Typically, in order to obtain the anti-psychotic effect, 65%-80% peak striatal D2 occupancy is needed. TD/SP most commonly occur at greater than 80% occupancy.

Using 1st gen anti-psychotics (e.g. haloperidol) for this purpose in therapeutic is probably the worst idea, because achieving the desired super-sensitivity to striatal dopamine would mean giving the patient TD (tardive dyskinesia) with pretty high probability. TD is generally considered the worst side-effect of anti-psychotics (see previous link). You could say the cure (TD) is worse than the disease you'd want to treat (ADHD). On other hand, it may a little more plausible to do this with atypical (2nd gen) antipsychotics.

> For instance, quetiapine \[39\] and clozapine \[33,40\] can induce SP without producing overt or detectable drug-induced movement disorders.

But atypical anti-psychotics aren't totally free of the risk of TD, they just reduce it.

Even disregarding side-effects (which AliceD's answer covers aplenty), which would actually be exacerbated by the high dosage needed, the problem is that the SP phenomenon (which would be the basis of propose cure for ADHD) is variable in time:

> The persistence of the dopamine supersensitivity syndrome depends on the duration of the preceding blockade \[132\] and on the specific antipsychotics used (fluphenazine, perphenazine, clozapine, and quetiapine) \[1,41\].

So it would not be a cure for ADHD except possibly in small number of patients for whom the long-term effect comes out "just right". There's also the obvious risk of "overshooting" and inducing actual likelihood of psychosis in someone (with ADHD) who didn't have such a risk.

In general, giving a patient a drug and adjusting the dosage until the desired effect is observed is simpler than giving a drug hoping for permanent effect that only stabilizes some time after not taking the drug.

On top of these, there's the issue that the exact mechanism of ADHD isn't absolutely sure. And that basically all psychotropics act on more than one neurotransmitter, so the don't totally cancel each other out. For these reasons, there are even publications discussing co-medicating some/few patients with anti-psychotics and stimulants, even though these classes of drugs partially cancel each other out.

---

Now very interestingly, there is a 2014 paper (alas with only 6 citations) that does propose using very *low* doses of haloperidol as an adjuvant of L-Dopa in Parkisons precisely for this purpose of causing dopamine supersensitivity (and not for the common purpose of treating co-morbid psychosis that some Parkinson patients exhibit).

The trick that makes very low doses feasible for this purpose is that antipsychotics cause the D2 receptors to switch to a D2High (high-affinity) state. Apparently this switching happens even a low dosage of antipsychotics.

Unlike in your proposal though, although the effect apparently lasts for a while after haloperidol discontinuation, it begins on it.

>

The authors of this paper also emphasize a more substantial decline in "freezing" (a Parkinson symptom) that may coincide with the peak (and delayed) effect of D2High caused by haloperidol, but frankly the data is pretty weak in that regard and one can easily level "p-hacking" at this particular finding:

>

If it needs saying, even if this "trick" were to work better (e.g. with other doses), since Parkinson is neurodegenerative, there's only so much tweaking at the margin of the remaining neurons' sensitivity you can hope to do, before the loss of more/enough neurons overtakes that extra sensitivity.

Also, there actually many ways to trigger D2High states, stimulants themselves (e.g. amphetamine) do that.

# Answer
> 1 votes
**Short answer**
Taking dopamine antagonists leads to serious side effects, and stopping taking them leads to other, equally nasty side effects. None of them include happiness or feeling energized.

**Background**
So basically, based on our discussion in the comments, I think you are after the following:

> Is it viable to use a drug originally meant to suppress dopamine transmission to induce tolerance and thus increase dopaminergic effects to enhance dopaminergic transmission to enhance mood and happiness after stopping the drug to reap the benefits of long-term 'withdrawal' symptoms?

First off, drugs targeting the dopaminergic (DA) system are associated with serious negative side effects. To step into the class where you are after, the classical anti-psychotics that inhibit DA signaling are associated with the following side effects (taken from the page on haloperidol from WebMD):

* dizziness
* lightheadedness
* drowsiness
* difficulty urinating
* sleep disturbances
* headache
* anxiety
* in rare cases sometimes permanent tardive dyskinesia, a nasty side effect marked by stiff, jerky movements of the face and body, muscle twitches, eye blinking, tongue thrusting, uncontrollable shaking, or arm waving.
* rarely neuroleptic malignant syndrome occurs including: fever, muscle stiffness or muscle pain or muscle weakness, tiredness, confusion, sweating, fast/irregular heartbeat, dark urine, and kidney problems.
* And the list goes on, and on, and on (see also Drugs.com)
* Long term-use may lead to drug-induced Parkinsonism, which is actually the second most common cause of Pakinsonism in older people, after Parkinson's syndrome (Thanvi & Treadwell, 2009.

Now fast forward to your withdrawal state that should make you happy, as dopamine transmission may indeed be exacerbated. The tolerance to haloperidol comes, at least in part, because D2 transmission is enhanced in the striatum in the brain (Ginovart *et al*., 2009)0. This leads to the dreaded tardive dyskinesia.

Abrupt stopping haloperidol intake after chronic use results in side-effects on their own in psychotic patients (apart from re-inducing psychotic states), namely (Bronson, 1993):

* nausea and vomiting
* sweating
* as well as a relapse into psychosis characterized by anxiety, depression and internal chaos. Interestingly, the authors conclude that the so-called relapse into psychosis may actually be caused by withdrawal instead of the underlying disease state .

In all, happiness doesn't seem part of the deal of acute withdrawal from a well-investigated dopamine antagonist, unfortunately. Taking them is a pain, and stopping them abruptly is also not a pleasant thing to do either. When you slowly decrease dosage the withdrawal side effects will be less severe.

<sub>**References**
**-** Bronson, *Life Sci* (1993); **52**(16): PL129-33
**-** Ginovart *et al*., *Neuropsychopharmacology* (2009); **34**: 62–671
**-** Thanvi & Treadwell, *BMJ* (2009); **85**(1004): 322</sub>

---
Tags: neuroscience, psychopharmacology, drugs, medication
---


# Question
Title: What is the scientific term for the erroneous inversion of cause and effect?
What is the correct scientific term for the - erroneous - inversion of cause and effect?

# Answer
> 1 votes
According to a dictionary of psychology this is simply called "reverse causality"

> In attempting to understand the relationship between cause and effect, a tendency to attribute what is actually the cause to the effect. For example, does the ingestion of lead paint cause a lower intelligence quotient (IQ) or is it that children with lower IQs tend to eat lead paint?

# Answer
> 0 votes
Would the concept of contraposition from the world of mathematical logic work for you?

From the Wikipedia explanation of contraposition:

> The contrapositive of a statement has its antecedent and consequent inverted and flipped. For instance, the contrapositive of the conditional statement "If it is raining, then I wear my coat" is the statement "If I don't wear my coat, then it isn't raining."

# Answer
> 0 votes
Given your comment to the first answer...

> The logical error I am looking for, is "I am wearing my coat, therefore it is raining"

...I think you are referring to **deductive arguments**. A deductive argument (definition taken from Mark Storey, Bellevue College):

> ...claims (explicitly or implicitly) that if the premises all are true, then the conclusion must be true

Valid examples are (taken from the linked document from Mark Storey)

> * All bats are cute animals. No cute animals are mean. So, certainly, no bats are mean.
> * Joan is Lauren’s mother. Therefore, Joan must be older than Lauren.
> * Nobody knows Ned. Therefore, it must be that Ned does not know himself.
> * Some cats are pets. Thus, some pets must be cats.

A familiar invalid example is the following (taken from memory on my own Philosophy class, a long, long time ago):

> All cows have 4 legs. It has 4 legs, thus it must be a cow.

Your question proper states that it should be related to cause and effect. In terms of deductive reasoning, however, it is based on *premises* and *conclusions*. Quoting Mark Storey again:

> \[T\]he argument may fail in its aim; what makes the argument deductive is that it is the kind of argument that—if it were successful—would have the premises absolutely guarantee the conclusion to be true.

I think what you are after are examples where the *premises* do not guarantee the *conclusion* to be true. This is different from causes and effects, though.

---
Tags: cognitive-psychology, perception, terminology, cognition
---


# Question
Title: How do neurons know where to send transmitters?
If a single neuron can have thousands of synapses with other neurons, how do each neuron "knows" to which further neuron to send transmitters? i.e. selectivity

# Answer
When a neuron fires an action potential, it doesn't "select" a target. It releases neurotransmitter (somewhat probabilistically, as vesicle release has a probability \<1 at most synapses) to every cell it synapses on, all of the thousands you reference.

What is important for selectivity is the development of synapses, which are shaped by axon guidance cues and later by synaptic plasticity. All of this is laid down well before an action potential causes neurotransmitter release.

However, for almost all connections in the brain, a post-synaptic neuron won't fire due to the activity of a single pre-synaptic cell. Therefore, the selectivity in which neurons will fire an action potential is driven by the *population* of neurons that are previously active, not any one cell. Neurons that fire in the near future can be said to be determined by the *combination of all the neurons* firing in the recent past, including both excitatory and inhibitory neurons. This gives brains an incredible diversity of possible states. If we are to simplify neurons as "firing" or "not firing" in a given time window that would equal 2^(number of neurons) possible states, each leading to a different subsequent state.
> 1 votes

---
Tags: neuroscience, brain, neuro-transmitters
---


# Question
Title: Reaction when light is turning on and off
This question comes from a personal experience I've had over the last few days, 'experimenting' on my own.

I have a light bulb in a room that is turning on and off periodically, let's say per second. If I am standing in the room with my eyes open, after some time I get dizzy. Then I thought to check what will happen if I could close my eyes in sync with the light turning off; each time the light was gone I would close my eyes and then opened them again when it was on.

After some practice I managed to achieve this. What I noticed was that, although I was again moving between a period of light and a period of darkness, I was not getting dizzy anymore.

It seems to me that somehow the brain is able to differentiate between an external source of change in light and when my eye-lids also participate ( so having so too say two stimuli, light and eye-lids).

I would like more information or thoughts on what exactly may happen in this situation, perhaps even with some reading recommendations on similar research. I admit that catching this "filter" on how the brain ( or the eyes??) understands and behaves when changes in the light happen, caught my interest.

# Answer
> 3 votes
In neurophysiology we refer to "efference copy". In short, efference copy is when the brain area that sends a signal to cause a movement also sends some "copy" of that signal to the sensory part of the brain. This copy signal helps the sensory brain areas predict what to expect from your own movements, and therefore lets your perception be driven by changes in the world rather than your own self-motion.

You can also frame this in predictive coding models of brain function, in which brains are said to create model of the world and respond primarily to violations of this model/relatively unexpected events (*for example, if a filing cabinet remains motionless in the corner, you don't notice it; your model is that filing cabinets are inanimate objects that stay still. If it moves forward a few centimeters, you will notice it quite quickly*). A light flashing on and off is a somewhat "unexpected" stimulus: ordinarily, lights stay either on or off. However, if you blink such that when your eyes are open only when the light is on, nothing unexpected is happening to the light: it's on when your eyes are open, and you expect to see nothing of the world when your eyes are shut so the absence of the light with eyes closed is expected.

For another example that's easy to test out, if you move your head side to side, you won't perceive other objects as "moving" (the vestibular system helps inform this perception of the world as stationary as well, by measuring rather than predicting your head movement). You may notice that your visual perspective changes, but you don't sense that objects are really moving *in the environment*. Same when you change your visual gaze from one target to another: you'll blink briefly and the image that lands on your retina will be *completely different* from the one you just saw, but you still perceive the world as having stayed the same, not as if everything in front of you has just jumped by a meter or more.

Other applications include understanding why it is difficult to "tickle yourself", and how an echolocating bat can differentiate between its own calls and the reflected echos.

The Wikipedia page I linked to at the start has a lot more to say about efference copy, and you can also use that phrase as a search term to find out more about the specific circumstance you're describing.

---
Tags: neuroscience, experimental-psychology, brain, stimulation
---


# Question
Title: How do I find the right psychologist for myself?
Many psychologists resist disclosing their opinions on school prior to making an appointment. I want to talk about my problems with being bullied in school, and I don't think that a therapist could help me unless they hated schools in general. I have had a bad experience with a liberal psychologist who had a regular set of opinions surrounding schools. How could I determine if a psychologist distrusts academia?

# Answer
> 0 votes
If you are lucky, you might be able to find a psychologist or a group practice who blogs specifically about bullying? That might a good way to find out the opinions and direction of how they would approach therapy with you. Unfortunately, there are no simple or easy ways to predict or decipher bias or the direction of the therapy. Usually it is worth visiting a couple of psychologists and decide after a couple of sessions?

---
Tags: social-psychology
---


# Question
Title: In principle, could a brain be rewired to experience more pleasure and/or pain?
I'm not sure if these are two separate questions, but I'm curious: in theory, could an existing adult mind/brain be modified to perceive pleasure/pain signals more intensely than otherwise? Without drastically changing the rest of the brain (i.e. while making sure that the brain is the same person; although this question is understandably complicated and potentially philosophical)?

As to the latter part of the question, the SCN9A gene might play a part. Maybe there exists a similar gene for pleasure?

(I made a post focusing on the genetic side on the biology SE. I *think* the questions are different enough for this to be acceptable, but it might be worth looking there to avoid duplicated effort.)

# Answer
> 1 votes
This is a difficult question to answer and likely can generate a variety of equally valid (or invalid) answers.

I thought to tackle this from a pathological vista - namely that of **sensory processing sensitivity** (SPS), which seemingly resembles your area of interest.

SPS can be defined as (Acevedo *et al*., 2018)

> \[A\] genetically based trait associated with greater sensitivity and responsivity to environmental and social stimuli. \[It\] is characterized by greater empathy, awareness, responsivity and depth of processing to salient stimuli.

In their article the authors review the structural underpinnings as observed by fMRI scanning of SPS, alongside the brains of Autism Spectrum Disorder, Schizophrenia and Post-Traumatic Stress Disorder who also exhibit SPS alongside their other symptoms.

Common activated regions in all disease types were shown in the **precentral gyrus**.

SPS was associated with activity in reward processing centers (ventral tegmental area (VTA) and substantia nigra (SN), centers for regulation of bodily physiology and pain (hypothalamus and periaqueductal gray (PAG); self versus non-self recognition and empathy (inferior frontal gyrus (IFG) and insula), awareness and self reflection (temporoparietal junction (TPJ)) and self-control (prefrontal cortex (PFC)).

In terms of Autism Spectrum Disorder, Schizophrenia and Post-Traumatic Stress Disorder the authors continue with multiple brain regions that are activated commonly and uniquely with respect to SPS proper. I refer to the review referenced below for details.

I reckon, but am unsure, that re-wiring of the pathways or altering the structures themselves with, *e.g.*, transcranial stimulation or with ablation techniques can emulate SPS symptoms, including pain and emotion processing. The practical ways to do this are difficult, given the complexity of the brain.

<sub>**References**
**-** Acevedo *et al*., *Philos Trans R Soc Lond B Biol Sci* (2018); **373**(1744): 20170161</sub>

# Answer
> 1 votes
> could an existing adult mind/brain be modified to perceive pleasure/pain signals more intensely than otherwise

It depends what you mean by "modified", but even without going to any genetic (or surgical, e.g. implants) modifications, the central mechanisms involved in pain can be sensitized merely by experience/exposure to a certain level of stimuli; see e.g. (fairly cited) review paper on central sensitization.

> The nociceptor-induced sensitization of the somatosensory system is adaptive in that it makes the system hyperalert in conditions in which a risk of further damage is high, for example, immediately after exposure to an intense or damaging stimulus. This sensitization is the expression of use-dependent synaptic plasticity triggered in the central nervous system (CNS) by the nociceptor input and was the first example of central sensitization, discovered \[in 1983\]. Since then, we have learned that a number of different forms of functional, chemical, and structural plasticity can sensitize the central nociceptive system to produce pain hypersensitivity under both normal and pathological circumstances, some of which are persistent.
>
> \[...\]
>
> To induce central sensitization, the noxious stimulus must be intense, repeated, and sustained. Input from many fibers is required over tens of seconds; a single stimulus, such as a pinch, is insufficient. Peripheral tissue injury is not necessary, although the degree of noxious stimulation that produces frank tissue injury almost always induces central sensitization, so that the phenomenon is very prominent after post-traumatic or surgical injury.

The mechanism\[s\] by which this happens are on one hand very diverse as far as initiation, but seem to converge in one final pathway (dorsal horn neurons):

> multiple different triggers can contribute to the establishment of this form of central sensitization: glutamate acting on NMDAR, but also on AMPAR and mGluR, the neuropeptides substance P and CGRP, the kinin bradykinin, as well as BDNF and NO. \[...\] The reason so many different transmitters, modulators, and their receptors are involved is that it is not their specific action that is important but rather that they are released directly from or induced in response to nociceptor afferent activity, and each can separately or together initiate the activation of those multiple intracellular signaling pathways that lead to the establishment of hyperexcitability in dorsal horn neurons \[...\]. In other words, there are many parallel inputs to dorsal horn neurons that can independently or cooperatively initiate central sensitization.

So that gives numerous potential \[malevolent\] pharmacological/genetic/physical interventions that could have the same (ultimate) effect of causing central sensitization to pain. And if you care about the practical details, you can read the experimental methods section of the papers cited in that review.

---

As far as "pleasure" is concerned, there have been numerous studies on sensitization to drugs that have addictive potential. But in that area, things are more muddy because "behavioral sensitization" doesn't really separate the "like" and "want" components, which have some common pathways in the brain (the famous dopamine mesolimbic/NAc) but also distinct for various "likes" (e.g. those for sweet taste have been fairly well identified) and it seems it is mainly other neurotransmitters are mainly involved in the latter (e.g. MOR-receptor agonists, like endorphins and also orexin for taste. Things are complicated in that regard because merely eating something that does not subjectively register as pleasant will also release pretty much the same neurotransmitters; there are apparently subtle differences to consider in what regions of the brain where they are released.) Behaviorally studied, preferences can have many confounders besides actual "like"; see e.g. \[amusing perhaps\] controversy on sugars vs cocaine, which was even the stuff of tabloids some years back (as "cupcakes vs cocaine" or thereabout).

While sensitization of D2 \[dopamine\] receptors involved in the feedback loop of addiction is fairly well understood (e.g. see all the D2High research), I'm not sure there's been comparable effort to understand if there is easily and *separately* triggerable sensitization in receptors involved in e.g. sweet tasting, although in general, mu opioid receptors can be sensitized as well.

---
Tags: neuroscience, perception, neurophysiology, brain, pain
---


# Question
Title: How much does money (or any desired good) influence a person on average?
I'd like to know if there's any study about that, I'm specially interested if it determines how much it influences a certain person behavior in a certain given percentage and the quantities from where a person wouldn't do a certain thing but for more money they end up doing them.

I'm not discovering anything new saying that there are tasks we wouldn't do if we don't earn money, that's basically what most jobs are about. But point is it does not end in that, most people can end up doing things that go against their morals if they are given enough money. I even believe that most people would do anything that goes extremely against their morals if very huge quantities of money were given to them.

Are there studies on how much that influences the behavior of a person on average?

# Answer
> 1 votes
Here are two studies may be relevant to your question:

* Seeing green: Mere exposure to money triggers a business decision frame and unethical outcomes. The authors report that "individuals primed with money were more likely to demonstrate unethical intentions than those in the control group" and "money cues triggered a business decision frame, which led to a greater likelihood of unethical intentions and behavior." This article explains that the researchers "primed" the participants by showing them either "money-related" phrases or "neutral" phrases and measured how that affected their decisions in hypothetical scenarios or games. So even when there is no actual money involved, the study found that thinking about money can influence people's behavior.
* Social Class, Contextualism, and Empathic Accuracy. The authors report that "individuals of a lower social class are more empathically accurate in judging the emotions of other people." In this article, a study co-author points out that people with more modest financial resources need to depend on others more than people who are more able to solve their problems with money. This may give them more experience cooperating with people and developing empathy. So in this case it's the money that someone accumulates throughout their life that may prompt them to act in a less empathetic way.

---
Tags: behavior, behavioral-economics, sociology
---


# Question
Title: What is the difference between Cognitive Bias and Cognitive distortion?
I was asked by my professor to give a presentation on the topic ***"Cognitive biases and distortions"*** and during my prep I had this question. Could anyone please shed some light?

I tried finding more regarding the difference but I am yet to find "cognitive biases **vs** distortions" I have only found "cognitive biases **and** distortions". Going by definitions it seems to me that distortions might be a subset of biases but i'm not at all sure. The counter argument to this for me is maybe biases are more about ***what we see*** and distortions about ***how we interpret it*** .

Thanks

# Answer
> 4 votes
Wikipedia has articles on both of these terms, so that would be one place to start. Although you may not be able to cite Wikipedia as a source, both of these articles have good References sections.

Here are the Wikipedia definitions (emphasis added):

* Cognitive bias: "a systematic pattern of deviation from norm or rationality in judgment."
* Cognitive distortion: "an exaggerated or irrational thought pattern **involved in the onset or perpetuation of psychopathological states**, such as depression and anxiety."

So both of these terms apply to thought patterns that deviate from a theoretical rational standard. But cognitive distortions apply specifically to states considered psychologically abnormal, while cognitive biases refer to properties of human thinking that tend to affect everyone. The examples given in the articles seem to support this distinction.

As you mentioned, cognitive distortions could be seen as a subset of cognitive biases, specifically the subset that leads to psychopathological conditions.

---
Tags: cognitive-psychology, cognitive-neuroscience, cognitive-modeling, bias, cognitive-distortion
---


# Question
Title: Is short-term memory theoretically possible to with spiking neurons?
So I close my eyes, turn around, open them for just a blink and close again. I have observed a chair. I can't tell you how the chair looks like in detail, but I can more or less tell its shape and color. What's more, if I'm not disturbed, I can remember that shape and color for at least a minute.

What if I wanted to construct a device that could repeat this process. With digital hardware its not too hard - take a digital camera and a solid state memory device. For every bit of info in my solid state drive, I can call the operation "store" and my bit will be stored, or "erase" and it will be erased. Don't know how reliably each physical bit works with current technology, but given sufficient number of physical bits per logical bit I can theoretically make a device that will store my picture for as long as I want.

What about building a spiking neuronal network to do the same thing? I have tried some naive approaches, and I arrive at a fundamental problem: spiking neuronal networks seem to have almost no inertia on the fast timescale. A neuron only fires while there is sufficient input. When input is gone, it no longer fires (besides some resting state activity). I can construct a network with recurrently-connected neurons, in which case, in principle, the activity of the network could sustain itself after the input is gone. However, depending on the parameters of the network I observe a rapid switch between two very extreme behaviours. In one case, the feedback strength of the network is too weak, and the activity drops as soon as the input is gone. In the other, the feedback weight is too strong, and the activity of the network quickly reaches some maximal firing state independently of which exact input the network has received. These transitions happen exponentially fast. Theoretically, there are adaptive control mechanisms in neuronal networks, such as inhibition and synaptic plasticity. However, I am struggling to understand how such mechanisms can ever be fast enough to compensate for the sudden increase or drop of input.

**TL;DR**: Naively neuronal networks do not seem stable enough to implement robust short-term memory. What are the known mechanisms that nevertheless make it possible?

Note: I'm not asking how exactly short-term memory works. I am aware that nobody really knows. I'm asking for intuition to help disprove my argument that it should not work when implemented using neurons.

# Answer
> 1 votes
While we don't entirely know how all aspects of working memory operate, experiments show that a subset of cells in the brain exhibit *persistent activity* during working memory tasks.

Here's an example from a review by Curtis & D'Esposito:

This is a task in panel (a) where there is a cue presented briefly (marked by "C"), and then the monkey needs to remember the cue (during the time marked by "D"), and finally at time R the targets appear and the monkey can make a response.

We see in spiking recordings from monkeys that there are cells in dorsolateral prefrontal cortex that are activated not only by the cue and during the response, but they have persistent activity during the delay period. In human studies we can't ordinarily place electrodes but part (b) shows a similar study using fMRI, and the colored areas on the brain indicate brain areas that demonstrated more blood flow (marking metabolism) during the delay period, which includes areas of the same brain region as the monkey experiments.

The explanations are **recurrent network activity** and **bistability**: a population of cells that is excited can continue to excite each other and remain active until stopped (see for example attractor networks for a conceptual idea), as well as bistability in individual neurons where a neuron that reaches threshold *continues to fire tonically* rather than firing a single action potential, until firing is ceased via inhibition. Camperi and Wang 1998 is an excellent, clear review of these concepts with a straightforward mathematical approach to how you can model this *in silico*. It's probably more efficient to start from here rather than reinventing it on your own.

I also recommend other papers by XJ Wang who has done extensive work in this area. I also recommend you look at phase-space diagrams which can help conceptualize dynamic systems with stable properties (and which network parameters are necessary for stability), they come up a lot in theoretical neuroscience. Dayan and Abbott's Theoretical Neuroscience is also a good starting point if you can find a copy.

---

Camperi, M., & Wang, X. J. (1998). A model of visuospatial working memory in prefrontal cortex: recurrent network and cellular bistability. Journal of computational neuroscience, 5(4), 383-405.

Curtis, C. E., & D'Esposito, M. (2003). Persistent activity in the prefrontal cortex during working memory. Trends in cognitive sciences, 7(9), 415-423.

---
Tags: theoretical-neuroscience, working-memory, short-term-memory
---


title: Pomodoro Technique vs Flow

text:
# Question
Title: Pomodoro Technique vs Flow
Pomodoro technique and entering into flow states are two commonly mentioned productivity techniques used by people studying or doing creative work. I have used these two techniques and I feel more comfortable with the flow state is it feels like a hyperfocused state. Are there respectable scientific studies that support these techniques? Which technique is better?

# Answer
> 1 votes
Comparing the *Pomodoro Technique* and *flow state* is like comparing tomatoes and oranges. They are not two different techniques that you choose between. *Pomodoro* is a productivity / time management technique, and *flow* is a mental state. They are related in the sense that you could use Pomodoro to help get into a flow state, but you could also use some other technique for that purpose, which it sounds like you already do.

The canonical reference for flow is *Flow: The Psychology of Optimal Experience* by Mihály Csíkszentmihályi, who first used the term to refer to a mental state.

One thing to keep in mind about flow is that it's good for productivity, but not necessarily good for self-improvement. In a flow state, you tend to accomplish tasks without conscious thought, which accounts for the high productivity. But this also means that you aren't thinking about how you might get better. The process of *deliberate practice* could be seen as an anti-flow technique, where you consciously focus on each step of a task in order to improve. ()

I didn't find any rigorous scientific research about the effectiveness of the Pomodoro Technique. This HBR article has some informal results, and anecdotally it's a popular technique among knowledge workers.

---
Tags: performance, concentration
---


# Question
Title: Where can i find old archived patient records from 19th century psychiatric hospitals?
I do not have university access and do not want to spend money on protected documents. I am looking for free access. (Possibly I would spend money for original documents which should then be sent to me. ;) )

# Answer
A Google search for *patient records from 19th century psychiatric hospitals* (no quotes) turns up relevant results, though not for free access.

For example, here's a service from The National Archives (UK) that looks like exactly what you're talking about. And another one from New Zealand. I'm sure there are more.
> 1 votes

---
Tags: psychology
---


# Question
Title: "runs" or "sessions" in Structural MRI - Purpose and Implications for Quality Control
I am working on a graduate research project using the ABIDE I and II autism datasets.

MRIQC has been run on these data - and I now must remove participants marked as outliers on 3 specific quality metrics. However, I have run into an issue - there appear to be multiple "runs" per participant.

If, on one run, the participant fails QC stipulations, but not on another run, does this mean that the participant should be excluded from analyses? Or is the purpose of having multiple "runs" in structural MRI in order to have sufficient data that, if one run is "bad", another run can be used?

I have tried reading the MRIQC documentation; Googling; downloading and reading textbooks - for some reason, I find numerous resources on fMRI, but nothing for structural.

I would really appreciate any help anyone can offer - I am a bit desperate at this stage as my supervisors are on holiday.

Thank you for reading.

# Answer
It is common to remove especially motion-corrupted MRI runs without excluding the subject.

Without more knowledge about the project it's hard to know why exactly they have multiple runs present and whether there are differences between runs or just repeated scans. It may be that the operators made sure to collect more data when they suspected subjects had too much motion during the scan, they may have done so randomly or by convenience (such as according to patient comfort), or they may have had other reasons.

I would consult other papers published using the same data set (even the functional ones) for their inclusion criteria.
> 0 votes

---
Tags: neuroimaging
---


# Question
Title: What is the difference between "nudge theory" and "priming"?
I'm doing a minor in psychology and during my lesson in both psychological approaches and social psychology, this question popped into my head.

For as far as I know nudge theory is about altering the choice-architecture, but without removing choice. This results in certain (wanted) behaviour. Examples of nudges are: a fly in a urinal; the piano stairs in train stations is way of nudging; stores putting certain brands on eye-level; etc. Where priming is receiving a certain stimulus which creates (temporary) schemes of behaviour.

Could someone help me understand the difference, or how they are connected?

Thanks in advance!

# Answer
> 1 votes
They are not necessarily related concepts, and I think. While nudge (in Thaler's sense) is a mechanism for fostering choice in a planned way, priming refers to a faster processing of new stimuli related to recently activated ones.

It seems like the nudge of might happen through several possible mental processes, including (possibly) priming - although I personally couldn't find any example of how priming could be used to nudge a decision, I'm certain it might. None of the cited examples work through priming, though. For instance, it seems to me that the fly in the urinal example might work through a salience effect (a salient bug in the urinal makes one direct their attention to the salient object).

An example of priming (unrelated to nudge) could be when you see the word "bee", and then see a related stimuli, like the word "honey", and you recognize it faster because there's a previously activated schema. Priming might happen through a lot of means, like words rhyming or starting with the same syllable, semantically related objects, recognition of one object in an abstract pattern, etc. However, in priming there's always at least one prime (a previous stimulus) and one target (a later stimulus) and the prime will make the activation/recognition of the target faster.

Hypothetically, one could use priming to nudge people into "better" decisions if one could offer a prime related to the "best" decision (our target). For instance, consider there is a (widely known) healthy meal and an unhealthy alternative as the options in a restaurant menu. You might put a text saying "Be Healthy" at the cover, which people will see before seeing the alternatives. This might enhance the activation of the healthy alternative, and it might influence the choice (or not). While it's uncertain on whether the healthy food will be chosen, theoretically its activation will be faster due to priming.

SUGGESTED REFERENCES:

Matlin, M. W. Cognition. Hoboken: Wiley, 2012, 8th edition.

Sternberg, R. J. Sternberg, K. Cognitive Psychology. Boston: 2017, 7th edition.

---
Tags: cognitive-psychology, social-psychology, behavioral-economics, priming
---


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

I have seen this paper referenced several times in other papers that track eye movements in mice, but it seems like the position of my cameras relative to the eye is different than what is shown in the paper and I worry this will affect the validity of the transformation.

I have the ability to track any feature of the eye that is useful. Right now I am tracking the center of the pupil, the corners of the eye, and the center of the top and bottom eyelid.

EDIT #1

Here is a description of the camera's position relative to the animal. The solid black object represents the animal (A=anterior, P=posterior, D=dorsal, V=ventral). The angle from each orientation represents the angle from the animal to the camera.

# Answer
In theory you can use the geometry of your setup to transform your data to the orientation reffered in the paper you mentioned using Scheimpflug Principle and then use the methods provided in it.

Practically, you can only approximate the geometry of your setup. If you have some idea about angles in something like this

please let me know, I might be able to do the math for you.

EDIT: The lens plane is parallel to image plane in cameras so now it is just the question of orientation of subject plane and lens plane(camera plane).
> 1 votes

---
Tags: eye-movement
---


# Question
Title: Why do psychologists often not use mathematical models to express their theories?
I come from an economics background where people often written explicit mathematical models for their theories. To be clear, the vast majority of economic models are not useful quantitatively — the functional forms, etc, tend to be way off. However, the models are useful in disciplining the qualitative predictions from the theory. Human intuition is faulty. If we just rely on intuition in building theories, we almost always miss something until we write them out using models.

When I read psychological theories, I find that most of them are not expressed in explicit models. This makes me worried that my understanding of the theories can be incomplete and different from what the original authors intended.

Why is this the common practice? Would we gain anything to make psychological theories mathematically explicit, or will that be a waste of time?

# Answer
> 2 votes
Come read some cognition! It's a wide open field with angles on all kinds of psychology stuff, and we're having a great time throwing greek letters around like confetti. I think you might like it!

One of my favorite recent pro-model rants is this one psyarxiv.com/rybh9/ Although, to be fair they do argue for 'computational' rather than 'mathematical'. I would argue these both mean 'explicit formalism', which is what you're after here?

There's a whole journal of mathematical psychology www.journals.elsevier.com/journal-of-mathematical-psychology

or Computational Brain and Behavior www.springer.com/journal/42113 is full of cool stuff on a surprisingly wide range of psych topics united by a common theme of awesome mathy-ness

Psych is very broad, but whatever corner of it you're interested in, there's almost certainly a math-y cognitive/computational version of it (as well). Those mathpsych folks definitely get around. Probably the most math-resistant corner of psych is social psych, emergent behavior of groups type stuff is absolutely vicious to model, as you would know, coming from econ... but see eg. cogsci.mindmodeling.org/2019/papers/0172/0172.pdf

Explicit formalism is the future of psych, and quite a lot of the future is here already

---
Tags: cognitive-modeling, computational-modeling, mathematical-psychology, model
---


# Question
Title: Why Do People Feel "Safe & Secure" with Their Emotional Distress?
I have noticed in some of my family members, who've been through struggles in life, to extremely "cling" into their sad emotions! They **don't **want**** let go of it. It almost feels like they feel safe and secure with their emotional "miseries". I have searched the net and found this is a common phenomena in many people. I was wondering if there is any scientific paper written on this subject. I don't know the proper terminology for this behavior. I was hoping someone can shed some light. Thanks,

# Answer
> 0 votes
You are right, and consolation often backfires. this is for 2 reasons.

1. We as human beings, want to be witnessed, heared. Few year ago a video based on research work of Megan Devine went viral over internet.

https://www.youtube.com/watch?v=l2zLCCRT-nE
https://refugeingrief.com/

2. Lot of positivity we say, is actually "toxic positivity". It make our pain invalidated, disbelieved, or may have a discriminatory "bad vibes unwelcome" approach. Toxic positivity may oppress people from telling their problem and finding a solution.

https://www.psychologytoday.com/us/blog/the-man-cave/201908/toxic-positivity-dont-always-look-the-bright-side

---
Tags: emotion
---


# Question
Title: Has the labelling and overshadowing effect from the Hannah Experiment been replicated?
"The Hannah Experiment" (Darley & Gross 1983) is cited as an example of labels biasing evaluation. This is described in "Drunk Tank Pink by Adam Alter" which I've paraphrased below:

> Princeton University students decided whether a young fourth-grader named Hannah was performing above, below, or precisely at the level expected of an average student in the fourth grade.

> During the first phase of the experiment, the students watched one of two brief videos:
>
> 1. Lucky Hannah is shown to come from a college-educated family and lives in a wealthy neighbourhood.
> 2. Unlucky Hannah is shown to come from a family with a high-school education and a poor neighbourhood.

> At this point, some of the students watched a second video, in which Hannah was asked to answer a series of twenty-five questions from an achievement test. The questions were designed to assess her mathematical, reading, science, and social science skills. Instead of presenting a clear image of her ability, the video was ambiguous: sometimes she was engaged, answering difficult questions correctly, and sometimes she seemed distracted and struggled with relatively easy questions.

> Hannah’s ability was difficult to discern from the video, but some of the students began watching with the labels “wealthy” and “college educated” in mind, whereas the others began watching with the labels “working class” and “high school educated” in mind. These labels functioned as tiebreakers when Hannah’s performance was neither flawless nor disastrous. The students who expected Hannah to succeed saw exactly that pattern of achievement in her responses (ignoring her missteps and distractibility), whereas those who expected less from Hannah saw exactly what the negative labels implied (ignoring her intermittent engagement and mastery of the difficult questions). In the end, the Lucky Hannah was judged to have performed above her fourth-grade level, whereas her Unlucky counterpart seemed to perform below fourth-grade level. The Hannah study showed that people are suggestible, willing to view the world with the guidance of labels when faced with an otherwise unbreakable tie.

Does this bias have a name? Has it been replicated/generalized?

## References

Darley, J. M., & Gross, P. H. (1983). A hypothesis-confirming bias in labeling effects. *Journal of Personality and Social Psychology, 44*(1), 20–33. https://doi.org/10.1037/0022-3514.44.1.20

# Answer
This is basically describing stereotyping. (Several biases overlap to form these, depending which theory you prefer the most.)

The most cited paper that cites Darley & Gross seem to be a 1995 review titled "Implicit social cognition: Attitudes, self-esteem, and stereotypes". It cites D & G for implicit stereotyping (research):

> Although research on stereotypes has often used direct or explicit measures (see Judd & Park, 1993), there are also substantial research programs on stereotypes that use indirect measures— ones in which a stigmatizing feature with which a stereotype is associated (e.g., weight, race, or gender) is peripheral to the respondent's judgment task (e.g., Darley & Gross, 1983) or in which the purpose of investigation is otherwise disguised (e.g., Hamilton & GifFord, 1976). Crosby, Bromley, and Saxe (1980) were able to locate enough research using indirect measures of prejudicial stereotypes to conclude that "anti-Black sentiments are much more prevalent among White Americans than the survey data \[i.e., direct or explicit measures of stereotypes\] lead one to expect." Although the use of indirect measures in these studies often reflects the researchers' intent to avoid intrusion of unwanted demand or impression-management artifacts (which would plausibly suppress accurate expressions of conscious stereotypes), some of the research that is summarized just below was designed specifically to investigate unconscious operation of stereotypes. These studies suggest that stereotypes are often expressed implicitly in the behavior of persons who explicitly disavow the stereotype. The next two sections focus attention on race and gender stereotypes because these, having been much more heavily investigated than other stereotypes, have provided the most persuasive evidence for implicit stereotyping.

Wikipedia also has a more specific article on implicit stereotype, although it seems someone was unhappy with it... The wiki article claims:

> Implicit stereotype was first defined by psychologists Mahzarin Banaji and Anthony Greenwald in 1995

which is probably referring to the above 1995 review, but I'm not sure how correct is the claim that Banaji & Greenwald were the first to define the notion. (They clearly were not the first to study it.)

Greenwald has actually co-authored a more recent (2019) review titled just "Implicit Social Cognition", which (I guess) could be useful to check for research progress on implicit stereotyping. Most of the later research seems to have involved (the veritable explosion of) IAT studies. Greenwald (2019) summarizes several meta-analyses and does some moderator analysis.

For a broader theoretical perspective (and to clarify what Greenwald and Banaji actually introduced--it's actually the term "implicit cognition", with a specific def), Hahn & Gawronski (2015) write contrasting Greenwald's conception with De Houwer et al.'s:

> Drawing on the notion of implicit memory, Greenwald and Banaji (1995) defined implicit cognition as “introspectively unidentified (or inaccurately identified) trace of past experience that mediates responses” (p. 5). Although this definition was meant to imply unawareness of the sources of mental contents, it has often been interpreted to imply unawareness of the mental contents themselves (e.g., unawareness of the source of an attitude vs. unawareness of the attitude itself). However, the latter interpretation conflicts with a considerable body of evidence, suggesting that the psychological constructs captured by nonreactive, computerized measures are consciously accessible and thus not unconscious (e.g., Hahn et al., 2014).
>
> More recently, De Houwer et al. (2009) proposed an alternative conceptualization to overcome the common confusion regarding the meaning of the term implicit. \[...\] Measurement procedures \[...\] may be described as direct if their measurement outcomes are based on participants’ self-assessment of the to-be-measured attribute (e.g., when participants’ racial attitudes are inferred from their self-reported liking of Black people). Conversely, measurement procedures may be described as indirect if their outcomes are not based on a self-assessment (e.g., when participants’ racial attitudes are inferred from their reaction times to positive and negative words after being primed with Black faces) or when it is based on a self-assessment of attributes other than the to-be-measured attribute (e.g., when participants’ racial attitudes are inferred from their self-reported liking of a neutral object after being primed with Black faces).

Applying the latter categorization to D & G (1983) study, they clearly used an indirect measure in De Houwer's categorization. Thus from this methodological perspective (after glancing over De Houwer et al.) D & G (1983) is an affect priming study.
> 2 votes

---
Tags: social-psychology, reference-request
---


# Question
Title: is it possible to be severely autistic yet not being "visibly autistic"?
It is common problem for many "mild" (ASD level-1) autistics to be criticized as "***you do not look autistic***" *or some of its variants*. Also sometimes seen in social media that moderate autistics (level-2) (claimingly) facing similar issues to disclose their diagnosis.

By "visible" I mean the publicly considered easily observable disabilities, such as extreme intellectual disabilities, visibly heavily motor nonfunction or totally unable to move, saliva dripping from mouth, complete nonverbality or observably distorted voice and language, disfigurement or birth-defects, inability to hold urine or stool, etc. Usually the known to be severe (level-3) autistics have at least one of these "publicly perceived as disability" symptoms.

Incidentally, autism is not itself a visible condition at all, and the intellectual disability is not itself autism, its sometimes a co-morbid condition with autism but it is not identical to autism, rather autism is basically the impairment in social cognition. Also some of the symptoms of autism may be actually visible or easily observable **but these are commonly mistaken as intentional inappropriate behaviour or lack of morality or as some mental illness instead of cognitive difficulties or social disablilities**.

Now my question is; Is it possible that someone has level-3 (severe) autism yet on superficial look or talk the disability does not appear?

Theoretically it seems to be very possible that a severely autistic person may lack all of the publicly believed stereotype on disability, also can lack intellectual disability, moreover can apply sharp observations and observation to mask and fit-in, yet can have tremendous problem in social aspects. In such case a level-3 autistic too may face "you don't look autistic" situations. And probably all the observable symptoms will be imsinterpreted as mood or behaviour issue.

But does that happen in reality? or all of the severe (level-3) ASD have also some publicly believed stereotype of disability?

> Note: See also **Autism "severity" levels**
>
> Screenshot:

# Answer
What you propose

> Is it possible that someone has level-3 (severe) autism yet on superficial look or talk the disability does not appear?

is a contradiction in terms by the usual (DSM) definition of autism, which is based on several criteria which are behaviorally defined, i.e. from an observer's standpoint, to start with

> a child must have persistent deficits in each of three areas of social **communication** and **interaction** (see A.1. through A.3. below) plus at least two of four types of restricted, repetitive **behaviors**

Nowhere in there is that presupposed to be just "basically the impairment in social cognition" that may not even be manifested.

(Somewhat of an aside here; DSM-5 has tried to be less "atheoretical" than its III/IV predecessors, but in the end the differences in that regard are minor.)

---

Now if you want a bit of a deep\[er\] dive here, the DSM-5 acknowledges that some compensatory behaviors exist and should even be considered in assessing the (actual) severity of the diagnosis.

And a bit of digging through recent research finds a controversy in (re)defining (of sorts) "true" autism to mean Theory-of-Mind-deficits instead of \[DSM\] behavioral-autism... or at least (thus) identifying "camouflaged" or "highly compensated" autism (understood as ToM-deficits). This is quite a complicated discussion because ToM is multidimensional (or at least its measures are--and some correlate better than others with DSM-autism), and so (varied) are compensatory mechanisms for its deficits. The latter are surprisingly used by "normal" people as well, with perhaps only "shallow" compensation strategies specific to autism.

In the realm of personalities, you have prominent researchers on both sides of this dispute, e.g. Happé (responding to) Fombonne's (editorial). (h-index \> 100 for both.)

I'm guessing you've read & bought the ToM-deficits view of autism when you say "autism is not itself a visible condition at all" and "is basically the impairment in social cognition". Frankly if you look at Happé's last piece I linked, she (and her group) are cautious not to take that extreme position, although I'm sure it came off like that in some popsci article (the BBC at least has an article on people discovering their "hidden autism" thanks \[or at least in relation\] to Happé's research.)

As a final (recommended) reading here, which may help put this in context, some piece from Allen Frances who was quite involved with the previous editions of the DSM on the conflicting views on mental illness diagnosis standards in general (e.g. is clinical impairment needed) is also relevant here.
> 2 votes

---
Tags: measurement, autism, aspergers
---


# Question
Title: How to distinguish mental illness and neurodevelopmental disorders?
It looks like mental illness and neurodevelopmental disorders may look absolutely same if we superficially observe the behaviour.

Example:

1. Anger, destructive behaviour can be either due to a mental illness (anxiety, panic disorder, mood disorders, etc) and also can be a meltdown that is seen in neurodevelopmental conditions (Autism, Aspergers, ADHD, SPD etc).
2. Stereotypy and stimming behaviour can occur due to either mental illness like OCD and severe anxiety or it may have a neurodevelopmental origin.
3. Anxiety itself, can be either of a psychological origin (such as either fear of something irrational, or just a state of fear), or it may have a neurodevelopmental origin such as the patient of ADHD or Aspergers or SPD can not handle a overstimulated state and may feel anxious if they have to wait for uncertain period.

There are a lot of other similarities between neurodevelopmental and psychological conditions.

Now suppose the scene a patient comes in the chamber of a General Physician/ Psychiatrist with complaints of restlessness, anxiety, depression, psychosomatic illness (nausea, headache, numbness), forgetfulness, lack of concentration etc. The general symptoms signal either a primarily psychological condition, or may have a neurodevelopmental origin. How the General Physician / psychiatrist should distinguish it?

# Answer
As @BryanKrause said; mental illness and neurodevelopmental conditions are not distinctively separable.

Example: Neurodevelopmental hypothesis of schizophrenia, Obsessions and compulsions in Asperger syndrome and high-functioning autism Etc.
> 1 votes

---
Tags: neurology, diagnosis
---


# Question
Title: What do psychologists call the ability to quickly revise and remember things that a person had previously learnt
I am someone very far away from psychology, actually an engineering student, but I came up with this curiosity a few days ago.

To be specific, let's assume someone is learning physics. He previously took statistical mechanics course, and studied hard. About six months passed, and he still believes that his deep understanding of statistical mechanics is maintained.

But when he tries to remember the specific derivations of formulae, he encounters many obstacles. He doesn't remember the key ideas of individual derivations, but he definitely remembers how they roughly looked.

Then at a glance it looks like someone who studied statistical mechanics really hard and didn't revise for a long time doesn't have an advantage over someone who is in the middle of process of learning statistical mechanics yet isn't studying hard. They both share the fact that they don't know the details. The only difference, I would say, is that the former has enough confidence based on his experience of understanding the subject and performing well in the exams but the latter doesn't.

But it becomes a completely different story when the former starts to revise statistical mechanics. He can somehow pull out the "ancient" memories of the ways through which he made understanding possible, and without going through the entire textbooks, but by nearly skimming through them, can combine all the pieces into, and recover, one single piece of solid understanding. And it doesn't take long - the length of time needed varies, depending on the amount he has to revise, from a day to a few weeks. However it shouldn't definitely be more than a month.

Under what mechanism of psychology and neuroscience does this happen and what do psychologists call this?

# Answer
> 1 votes
Looks like when your friend was freshly learning the equations, he was using more of his episodic memory but as he went "used-to" with the equations, he tapped into more of semantic memory.

Lets use familiar example. When we recite something, we usually apply the episodic memory. It works much like how we searched a song "along" a tape of a cassette recorder. We had to forward/ rewind repeatedly to find the song.

We use semantic memory when we use language (or anything we learn at a depth and develop some experiene in it). Such as while reading, we instantly recognise the letter L (a shape) is linked with sound ELL or the word "CAT" indicates a mental image of a furry carnivorous animal. We do not scroll through the entire alphabet. If we compare episodic memory as a cassette system, then semantic memory is more like a modern digital file folder system, which is just "browse, click and play" type.

---
Tags: memory, working-memory, long-term-memory, semantic-memory, procedural-memory
---


# Question
Title: What happens inside the brain when we concentrate?
What happens inside the brain when we concentrate (meditate), and why does a person find it difficult to continuously concentrate for a long time? That is, why does one need a break after working or studying for a given time, or why do we lose our concentration after a certain time?

# Answer
> -2 votes
The Neurons become refractory which means that they can't fire again until time has passed. Look up Action Potential and the limits of firing rating. There is also a competition for different circuits to become conscious so when one becomes tried the other takes over. This is why it is hard to continue to think about one thing, without soon considering something else.

---
Tags: cognitive-psychology, cognitive-neuroscience, brain, philosophy-of-mind, concentration
---


# Question
Title: What's the most appropriate statistical analysis to run for a correlational study?
I am designing a correlational study experiment to test children on their performance on a task at $t\_1$ and then at $t\_2$ a year later, specifically using the balance-scale paradigm (Siegler, 1981). I'm not sure which statistical tests will be appropriate to run.

I want to find out if the early use of a sophisticated decision rule at $t\_1$ is predictive of children using even more sophisticated rules in $t\_2$. Namely, is a child who can deploy a complex decision rule quicker than most of her peers at $t\_1$ more likely to use even more complex decision rules at $t\_2$? I will compare these results with the $t\_1$ vs $t\_2$ results of children who failed to deploy that more complicated decision rule at $t\_1$. These two decision rules will be operationalised as non-continuous binary variables.

What kind of statistical testing would be most appropriate here?

---

**References**

Siegler, R. S. (1981). Developmental sequences within and between concepts. Monographs of the Society for Research in Child Development, 46(2), 84

# Answer
> 3 votes
Although you have two times of testing, you really just have two binary variables and you'd like to know if they are associated, there are no repeated measures here. You'd like to know if the value of one binary variable depends on the value of the other binary variable. I'll call them A,B and X,Y.

If there is no relationship between A,B and X,Y, then you expect the ratio of X:Y to be the same for A as it is for B (this is your null hypothesis). You can examine your data by building a 2x2 contingency table with cells AX, AY, BX, and BY.

You can test the null hypothesis described with a chi-square test for independence, or Fisher's exact test if the sample size is fairly small.

---
Tags: developmental-psychology, statistics
---


# Question
Title: When and how did the concept of psychological trauma begin to be extended and expanded to include more mundane and less severe experiences?
I'm in my first semester studying mental health counseling at a master's level and I have heard several of my professors make comments to the effect that over the past 20-30 years they have seen the definition of trauma shift dramatically to include things of lesser and lesser severity. I was wondering where this trend started and whether there were any particular researchers or organizations that spearheaded this movement of thought within the field? Is it the result of any particular philosophical, political, or social movements that have affected the field as a whole? or have there been any landmark works that have pushed the field of trauma research in this direction?

I've already read *The Trauma Spectrum* by Robert Scaer, but it seems like things were already headed in the direction of expanding the definition of trauma already.

# Answer
One can't be certain what that kind of allusion refers to, but there has been a level of controversy stemming from the changes to the trauma criterion in DSM-IV (it was changed again in DSM-5). The change in DSM-IV--which does correspond with the time frame you mention--was seriously lambasted in some corners, e.g.:

> Criterion A1, certifies three groups of people as potentially eligible for the diagnosis of PTSD: direct recipients of serious threat or harm, such as rape victims or combat veterans; those experiencing vicarious exposure to the trauma experienced by others, such as bystanders at a drive-by shooting; and those experiencing ‘informational exposure’. This third group is new in DSM-IV. It consists of people who are ‘confronted with’ information about threats to others, such as horrified television viewers of the 9/11 terrorist attacks (Marshall et al., 2007). Although the authors of the original PTSD diagnosis surely would not have envisioned these viewers as trauma victims (McNally & Breslau, 2008), our current DSM concept of trauma certifies them as trauma survivors just as much as it does those who escaped the World Trade Center before its collapse. In fact, one survey indicated that about 4 per cent of American adults living far from the scenes of the terrorist attacks developed apparent PTSD (Schlenger et al., 2002), presumably while watching coverage of the attacks from the comfort of their living rooms. These people developed what Young (2007) wryly calls ‘posttraumatic stress disorder of the virtual kind’ (p.21).
>
> Because of this bracket creep in the definition of trauma (McNally, 2003a), most people today qualify as trauma survivors. For example, in one epidemiological survey, 89.6 per cent of adults in southeastern Michigan were trauma survivors by DSM-IV criteria (Breslau & Kessler, 2001). \[...\]

On the other hand, there are studies which point to a limited practical impact of that textual change between DSM-III and IV, in terms of actual PTSD diagnoses:

> We used data from the 2009 PTSD diagnostic subsample (N=3,013) of the Nurses Health Study II. We asked respondents about exposure to stressful events qualifying under 1) DSM-III, 2) DSM-IV, or 3) not qualifying under DSM Criterion A1. Respondents selected the event they considered worst and reported subsequent PTSD symptoms. Among participants who met all other DSM-IV PTSD criteria, we compared distress, symptom severity, duration, impairment, receipt of professional help, and nine physical, behavioral, and psychiatric sequelae (e.g. physical functioning, unemployment, depression) by precipitating event group. Various assessment tools were used to determine fulfillment of PTSD Criteria B through F and to assess these 14 outcomes.
>
> Participants with PTSD from DSM-III events reported on average 1 more symptom (DSM-III mean=11.8 symptoms, DSM-IV=10.7, non-DSM=10.9) and more often reported symptoms lasted one year or longer compared to participants with PTSD from other groups. However, sequelae of PTSD did not vary systematically with precipitating event type.

In other words, the expanded definition could have possibly been abused, but in practice that didn't happen much.
> 3 votes

---
Tags: ptsd, definition, trauma
---


title: research based criteria domain and DSM5

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

# Answer
> 2 votes
The Diagnostic and Statistical Manual of Mental Disorders (DSM) and the International Classification of Diseases (ICD) are clinical diagnostic and classification criteria for clinical work.

The Research Domain Criteria (RDoC) initiative is a research framework for investigating mental disorders. It integrates many levels of information (from genomics and circuits to behaviour and self-reports) in order to explore basic dimensions of functioning that span the full range of human behaviour from normal to abnormal. For more information, visit the About RDoC page.

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

The concept behind the RDoC initiative can be seen as an extension to the debate over the level of **real** scientific research in psychology and psychiatry.

I have covered this extensively in my answer to a meta question on the subject.

On April 29, 2013, a few weeks before the publication of the latest version of the DSM (DSM-5), which is published by the American Psychiatric Association (APA), NIMH director Thomas Insel published a blog post critical of the methodology of the DSM and highlighting the improvement offered by the RDoC project (Insel, 2013).

It is good to debate things like this and I have no objection to debating the subject which in effect is what the NIMH is doing with this initiative (Insel & Lieberman 2013\] **emphasis below mine**).

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

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

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

## References

APA. (2013). Diagnostic and statistical manual of mental disorders (DSM-5®). *American Psychiatric Pub*. https://www.psychiatry.org/psychiatrists/practice/dsm

Insel, T. R. (2013). Post by Former NIMH Director Thomas Insel: Transforming Diagnosis *National Institute of Mental Health* https://www.nimh.nih.gov/about/directors/thomas-insel/blog/2013/transforming-diagnosis.shtml

Insel, T. R. & Lieberman, J. A. (2013). DSM-5 and RDoC: Shared Interests (Press release). *American Psychiatric Association*. http://publichealthunited.org/pressreleases/DSM5andRDoCSharedInterests.pdf

---
Tags: neuroscience, clinical-psychology, dsm
---


# Question
Title: Why does autism sometimes only visibly appear later in life?
From what I know about the autism spectrum, a lot of people who were diagnosed later in life (not during childhood) didn't "seem autistic" until adolescence or young adulthood. Of courses, they had symptoms all this time but it didn't become obvious until later.

Why is that? Do you have some articles/youtube videos that I could read/watch to learn more about this (English or French)?

# Answer
It is important to remember when reading this question and answer is that Autism Spectrum Disorder (ASD) does not develop in adulthood, but symptoms can change for individuals over time because learning occurs.

Symptoms of ASD come in all shapes and forms because this is a spectrum disorder and therefore people present somewhere on a spectrum, often referred to as from low functioning to high functioning.

To answer the question directly, people who present symptoms later in life, as you say, often do present those symptoms in childhood but they aren't noticed by the adults in the child's life until it becomes a real problem for the individual.

*As an example, interpersonal skills are learned during childhood. It is perfectly acceptable for children to be at slightly different stages during development with regard to interpersonal skills. Some children will be more advanced then others. Interpersonal skills can be difficult for people with ASD to grasp and so someone with high functioning Autism can take longer to develop these skills, if they are developed at all. So that would potentially not show up until later when the other kids have developed these skills and the child with undiagnosed ASD has not.*

Often, 30+ years ago, before we had more advanced treatments and assessments children would 'fall through the cracks' and be labeled as gifted, rather then as having high functioning ASD. This would explain why some people who are highly successful in adulthood are diagnosed in adulthood rather then childhood. People with high functioning ASD often have a savant type qualities, meaning they are very skilled in some specific area. The diagnostic criteria (DSM) has been amended over the years which would account for some adults being diagnosed now, as they may not have qualified before the DSM changed the criteria.

This would be an interesting study to read to understand social interaction among children with high functioning ASD: Bauminger, N., Solomon, M., Aviezer, A. et al. J Abnorm Child Psychol (2008) 36: 135. https://doi.org/10.1007/s10802-007-9156-x

This article discusses changing symptoms (Behavioural) in youth and adults with ASD.

This might be a good book for you to read together a good understanding of ASD in development, which might give you a better understanding as to why people can go undiagnosed until adulthood. Handbook of autism and pervasive developmental disorders, 2nd ed.

In conclusion, There are many reasons that someone might not be diagnosed until later in life, and autism is a spectrum which means people have many different symptoms that range on a vast scale.

---

References

Bauminger, N., Solomon, M., Aviezer, A. et al. J Abnorm Child Psychol (2008) 36: 135. https://doi.org/10.1007/s10802-007-9156-x

Shattuck, P.T., Seltzer, M.M., Greenberg, J.S. et al. J Autism Dev Disord (2007) 37: 1735. https://doi.org/10.1007/s10803-006-0307-7
> 4 votes

# Answer
More of an opinion based answer- the symptoms become more distinguishable from kids and adolescent behaviour when you age.

Restless behaviour, stimming behaviour, echolalia etc. can be confusing with typical childish behaviour.

Failing to organise things, fine motor skill problems, making clutters, forgetfulness etc. can be easily confused with adolescent and early adult behaviour.

But when the patient is adult, say 20 or 30 years old, yet having unusually childish behaviour, lack of social understanding, various skill deficits (and given that the patient fail to 'mask' hard enough); the neurodevelopmental anomalous pattern gets some more visibility.
> 0 votes

---
Tags: autism
---


# Question
Title: What makes it necessary to define autism beyond perceptual dysfunction?
One would think perceptual dysfunctions would be sufficient to define the condition since the inability to discern or perceive phenomena and failure to execute or adjust behavior due to lack of proper feedback could explain most if not all characteristic behavior

Unusual gestures and speech, improper social behavior would be explained by the inability to fully discern speech and gestures and learning them in a partial manner while repetitive behavior and rigid thinking would be explained by a limited range of feedback causing a failure to diverge. Even the stereotypes like lining up cars by color, spending hours watching washing machines spin, being really obsessed by specific sorts of machinery etc. can be explained by low-level patterns like color gradients, mechanical movement etc. registering much more dominantly than higher-level patterns with a larger number of elements and chaoticity.

I don't see how Occam's Razor would not apply here. What makes it necessary to define autism in such a nebulous way then? Is it the history behind it, or is it more nuanced than I think?

---

Edit: I should clarify, by 'perceptual dysfunction' I am speculating about a more general form of sensory processing disorder. There is no reason the mechanism behind sensory processing disorders would not affect perception of higher order emergent phenomena in the same manner.

For example, think about a chain of emergence like

`points -> curves -> shapes -> faces -> expressions -> nonverbal messages`

With sensory processing disorder in my example shapes might fail to register or dominate and disturb perception at a noticeably higher rate than without. I believe the same can also apply for a 'perceptional dysfunction' where faces, expressions etc. have a higher chance failing to register with or without disturbance in perception of lower level patterns.

# Answer
> 1 votes
There are several other aspects that I think are not just "perceptions" but something more complicated.

1. Having an weak or a different theory of mind; that hinders processing in general how other people may perceive or interpret something.
2. Having difficulty with cognitive empathy; that hinders understanding others' motives and intentions.
3. Having difficulty with consequences of something especially in social situations.
4. Problems with planning.
5. Problems with working memory.

---
Tags: autism
---


# Question
Title: Are the incidents of autism spectrum disorder on the rise, or is there an increase due to better definition of diagnostic criteria?
Statistics offered by the CDC indicate that the prevalance of autism spectrum disorder in the U.S. went from 1-in-150 children in 2002, up to 1-in-88 by 2008:

A new report released in 2013 shows that this number has risen to 1-in-50.

The most recent study concludes that it is likely that the changes in prevalence are due to an improved awareness/survey techniques:

> While it is not possible to definitively determine the underlying reason for this trend, several previous studies that also examined changes over time in ASD prevalence estimates within selected birth cohorts suggest that increasing recognition of children with ASD has had an important impact. Evidence from epidemiologic, genetic, and neuroscience research points to the prenatal period as the key exposure window for ASD risk factors. If the causes of ASD are related to factors that exist prior to or occur just after birth, it is unlikely that changes in ASD prevalence within the cohorts of children aged 6–13 in 2011–2012 reflect ‘‘true’’ increases in susceptibility to the condition at these ages. Rather, changes in prevalence of parent-reported ASD within these birth cohorts (children born in 1998–2005) likely reflect either changes in the recognition of ASD by health professionals or survey-based measurement changes over time

However, there also seems to be a significant support for the idea that ASD is rising to epidemic proportions, and that anything from changes in how many older couples are having children to various environmental factors may be increasing the rate of ASD incidents.

> These rising rates inspired Bob Wright, co-founder of Autism Speaks, to say, "We have an epidemic on our hands.... It is imperative that the U.S. government steps up its commitment to helping people living with autism today." Last November, the first congressional hearing on autism in 10 years was held to determine what the federal response should be. (It didn't exactly make front-page news: It aired on CSPAN-3.)

...and...

> "Now we know there's a host of genetic and environmental factors that are likely involved," says Dr. Susan Hyman, professor of pediatrics at the University of Rochester Medical Center and chair of the American Academy of Pediatrics subcommittee on autism.
>
> One possible contributor to autism's rise is that people are having babies later. The chance for gene glitches increases as parents -- especially dads -- age, explains Irva Hertz-Picciotto, an environmental epidemiologist at the MIND Institute at the University of California, Davis.
>
> But delayed childbearing explains only a very small fraction of the rise in autism rates. Environmental factors may turn many autism genes "on" or "off," says Hyman.
>
> "The best studies we have now point to things that babies are exposed to in the womb, when the brain is forming," says Hertz-Picciotto. Living in areas with high levels of air pollution (such as near a freeway), having low levels of folic acid, being overweight or diabetic, and having a high fever during pregnancy all seem to up a woman's risk of having a child with autism.

What studies or evidence support an actual increase in the rate of children with ASD? Presumably there are stronger connections to environmental factors than the infamous Wakefield study, given the comments by Dr. Hyman?

Are there studies that show a strong correlation with increased rates with changes in the diagnostic criteria, which would support the hypothesis that a significant portion of the increased prevalence is due to improvements in identifying individuals on the spectrum?

# Answer
Sociologists King and Bearman have been looking into this (see King & Bearman, 2009a; King & Bearman, 2009b; King & Bearman, 2011; King et al., 2009). They estimate that some of the increases in ASD identification are due to the following:

1. 25% attributed to diagnostic accretion - particularly children with mental retardation now being concurrently diagnosed with ASD.
2. 15% attributed to improved awareness of ASD.
3. 10% attributed to the increase in the age of mothers choosing to have children.
4. 4% to geographic clustering - that is, families might move to an area where services are available, leading to increased diagnoses in specific areas.

This leaves a significant proportion of the increase in ASD identification unexplained, and in need of further investigations.
> 13 votes

# Answer
What seems most intuitively to me; people did not knew about autism. With time, the awareness and diagnosis increased. Many of us know weird people who often stay alone, have communication problems, have unsuccessful life, is often pitied, bullied, called with derogatory terms. Now we know all these conditions have names.

One more factor almost nobody mentions; it has been got harder to "blend in" to a mainstream society. We are living in an age which is fast changing, unpredictable, competitive, always-connected. Social "cunningness" also got to be an important survival skill. The scenario was not such only a 20 years ago... if an adult behaved like a 12 year kid, it wont significantly impacted life, but now it does.

> “I have often thought that people on the mild end of the Asperger spectrum may have fit in better years ago than they do today. An eccentric stone mason who designed a cathedral would be admired for his work. A brilliant scientist who preferred the company of mice to humans might have been considered eccentric, but not necessarily labeled socially dysfunctional. In many ways, today’s “always connected” society has put more social demands on people, and a lack of social ability may be seen as more of a handicap than in the past.” — Temple Grandin (The way I see it)

Clearly, it is way more harder to just blend in.
> 1 votes

---
Tags: autism
---


# Question
Title: Is there a word that differentiate between image rotation and image translation?
For an image with an object (e.g., a cat) and its slightly tranlsated image (or its flipped image), an average person can instantly recognize that the objects in the both images are the same (i.e., a cat).

However, for an image with an object and its 90 or 180 degree rotated one, one cannot instantly recognize the objects in the images are the same especially when the object is quite a complacted or unfamiliar one.

In this context, is there a technical terminology (in neuroscience) that differentiate between image rotation and image translation?

# Answer
I believe you are talking about recognition part that say if the image is transformed to be flipped one is able to righaway recognize the object, however if the transformation is say 90 degrees then its hard. I believe the word is transformation-invariance.
> 4 votes

---
Tags: vision
---


# Question
Title: Which area of psychology studies false beliefs?
Imagine a person has some false beliefs, which are also reflected then in his actions:

* I don't want to interact with people because I don't trust them and 90% of time they will betray me
* If I form close relationship with people then I will not be able to move to different country because I will miss them
* ....

We can bring similar beliefs. I am interested **which direction in psychology** studies this situation when person has such beliefs? And tries to correct them

# Answer
These are typically called cognitive distortions and are a mainstay of CBT, but are equally likely to be addressed by any cognitive psychotherapist. This is usually done by building skills to identify and challenge such thoughts.

In the much older (and largely outdated) school of psychoanalysis, these are typically referred to as a defense mechanism called rationalizations.

In contrast, behavioral therapies are less likely to directly address such thoughts. With this paradigm, distortions typically subside once the underlying behavior pattern is addressed (eg, by improving social skills, and actually making friends).
> 1 votes

---
Tags: cognitive-psychology, rationality, cbt, human-error, belief
---