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

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

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

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

# Answer
**Haldol** (haloperidol) is mainly known for its antipsychotic properties to treat schizophrenia. It's an aged antipsychotic with a lot of side effects. Because of this, haloperidol is nowadays mostly replaced by the atypical antipsychotics, such as clozapine as first-line treatment.

Haloperidol's primary mechanism of action is believed to be related to its antagonistic effects on the dopamine D2 receptor (Seeman, 2002). However, it indeed also finds use in controlling tics and vocal utterances that are part of **Tourette's syndrome** (Messiha *et al*., 1971).

Given that it may take several weeks before haloperidol's effects become apparent, it should be taken continuously. But perhaps even more importantly, sudden termination of taking haloperidol can lead to unpleasant **withdrawal symptoms**, including

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

In all, haloperidol looks like a medicine that should be taken regularly.

However, I couldn't find evidence that it is in any way *dangerous* to take it on an irregular regimen.

<sub>**References**
**-** Messiha *et al*., *Life Sciences* (1971); **10**(8-1): 449-57
**-** Seeman, *Can J Psychiatry* (2002); **47**(1): 27-38</sub>
> 8 votes

---
Tags: neuroscience, psychiatry, psychopharmacology, therapy, drugs
---


# Question
Title: How do congenitally deaf and mute people think?
If a person is born deaf and dumb, how can they think? In "what language" do these people think? Do they develop their own inner language?

Unfortunately I have not found an answer, and I actually doubt it has ever been elucidated.

# Answer
**Short answer**
The inner voice of congenitally (pre-lingually) deaf people who have not received treatment like cochlear implantation, is not sound-based. Instead, it is **mainly based on visual images**, such as sign-language or printed material.

**Background**
According to an anecdotal report published in the Independent of a congenitally deaf person, who deliberately refused cochlear implantation or other treatments, the inner voice is a **visual entity** taking the form of sign-language, or visual images, or sometimes printed words.

An interesting report from UCL investigated congenitally deaf people suffering from positive psychotic symptoms. In normal-hearing people, positive psychotic symptoms typically involve hearing voices (auditory hallucinations). In congenitally deaf folks, who obviously never had the chance to hear any voices in their lives, these auditory hallucinations were described as

> \[Not consisting of\] sounds, but \[...\] the gender and identity of the voice \[were recognized. They were\] image\[s\] of \[...\] voice\[s\] signing \[,\] or lips moving in their mind.

<sub>**Source**
**-** The Independent, December 21, 2013, UK</sub>
> 6 votes

---
Tags: cognitive-psychology, neuroscience, learning, hearing, speech
---


# Question
Title: The Art of Teaching: What are the most effective & proven methods for successfully imparting a concept/idea to another
I'm aware this is a bit of a general question & subjectively broad. It's that way on purpose. It felt like cogsci was the best place for this question and I couldn't find anything really like it anywhere on stackexchange.

I want to know in general, if I need to teach someone a concept and I really want them to understand it...what method, techniques, strategies are there out there which appear to have the biggest impact on the success of a teacher teaching the student a concept?

What other factors should one possibly consider when teaching something to someone else? (Bias, attention span...how do I deal with these?)

Research for backing up anything you suggest would be ideal, but I don't want that requirement to preclude someone from posting something that could potentially be very effective but just isn't cited somewhere for some reason...maybe they experienced it with a teacher they had. There can be value in those gems too.

---

I'd actually like for this post to be one that has **universal teaching ideas/strategy in it** and not just those applicable to my context below...as sometimes the only thing precluding the use of a teaching strategy in a different or more universal domain from where it came from is the ingenuity of the teacher.

Also, I tried finding a post on stackexchange anywhere containing this question in it's general sense with answers and couldn't....there is stuff on how to teach programming, but that's just programming....some of its ideas are partially applicable universally, but not all of them.

---

**Here is my specific context, although I don't want answers to get too wrapped up in it.**

I am teaching via Youtube video and already have planned out 1) Me drawing on a digital screen things while I'm talking 2) Using easy to relate to analogies 3) Obviously any other visuals 4) Pausing to quiz their knowledge on a previous section before they can move ahead 5) Wrapping this up in a hopefully entertaining package

To provide some context and the format/audience...what I'll practically be using this information for:

I am releasing a special documentary style video with the goal making users completely understand the entire path some special research recently published takes, its reasoning for every choice it makes, and the logic for it's sequencing and timing of element.

Thus, instead of me reciting a conclusion from some research paper, I take them through the journey so they understand it. It's a bit of an intense topic with a profound conclusion...one that most people would also brush off immediately without fully attempting to comprehend first.

It's also extremely technical and includes some involving several tricky concepts from many different domains all at the same time that must be put together all in synchronicity: overarching ideas within biology & evolution, micro & cellular biology, genetics, astronomy, astrobiology, space ethics, the nature of language, information theory & entropy, symbiotics (study of symbols), markings of culture, probabilities & combinations, and...statistics.

# Answer
> 5 votes
Your question is extremely broad so all I can do is give you an extremely broad answer. More specifically, I'll provide you a study done by John Hattie (2008), who meta-analyzed 800(!!) meta-analyses on effective teaching methods, used in primary education among others.

The linked document shows a "brief" overview of the different methods rated and sorted by their effect sizes. Some of the intervention may be more relevant to you compared to others. Providing feedback, for instance, is more difficult in indirect communications such as video's.

Hattie has also written much about providing feedback and how that affects students' learning ability (e.g. Hattie, 2007)

Hattie, J., & Timperley, H. (2007). The power of feedback. Review of educational research, 77(1), 81-112.

Hattie, J. (2008). Visible learning: A synthesis of over 800 meta-analyses relating to achievement. Routledge.

---
Tags: learning, educational-psychology, perceptual-learning
---


# Question
Title: Can we interconnect with other people mentally during dreaming?
In some of my dreams, I have seen people that I know, and I ask them about it the day after and they say that they saw me too. My older sister said that she had exactly the same dream as one of her male friends.

**Can we actually connect with other people mentally while sleeping?**

# Answer
**Short answer**
Telepathy is pseudoscience.

**Background**
I think you are referring to the phenomenon of **telepathy**, which can be defined as

> \[T\]he purported transmission of information from one person to another without using any of our known sensory channels or physical interaction

and you ask whether telepathy is a scientifically established phenomenon.

Telepathy in general is dismissed as being **pseudoscience** (Jogalekar, 2013) as it has been debunked in various scientific studies (*e.g.* Ayeroff & Abelson (1976)).

Likewise, **dream telepathy** is considered pseudoscience. It was reportedly first documented by Freud in the 1940s. Freud founded many other **pseudo-scientific** concepts, including psychoanalysis (Jupp, 1977). Ullman & Krippner from the dream laboratory in Maimonides Medical Center in New York City claimed they had proven the existence of dream telepathy in the 1960s and 70s (*e.g.* Krippner & Ullman (1970). However, the studies were rightfully challenged. For example, many of their studies were based on a few or even on single subjects (*e.g.* Ullman & Krippner (1966) and Krippner & Ullman (1970)). Indeed, more recent studies have failed to replicate their findings (*e.g.*., Belvedere & Foulkes, (1971) and Hearne (1989)).

<sub>**References**
**-** Ayeroff & Abelson, *Personality and Social Psychology* (1976); **34**(2): 240-7
**-** Belvedere & Foulkes, *Perceptual and Motor Skills* (1971); **33**(3)
**-** Hearne, J Soc Psychical Res (1989); **55**(814): 271-4
**-** Jogalekar, *Sci Am* (August 2013)
**-** Jupp, *Philosophy* (1977); **52**(202): 441-53
**-** Krippner & Ullman J Nervous & Mental Disease (1970)
**-** Ullman & Krippner *Int J Neuropsych*, **2**(5): 420-37</sub>
> 4 votes

---
Tags: sleep, dreams
---


# Question
Title: Spike-timing-dependent plasticity versus Homeostatic plasticity
How can spike-timing-dependent plasticity and homeostatic plasticity both be right? If spike-timing-dependent plasticity consistently tries to strengthen connections, but homeostatic plasticity consistently tries to weaken strong connections, wouldn't the two cancel each other out, causing no net plasticity to occur and consequently brains couldn't learn?

I have a pretty good understanding of spike-timing-dependent plasticity, but I just recently came across homeostatic plasticity and I'm trying to understand how both theories can be right. What am I misunderstanding? Can someone help me understand homeostatic plasticity better and how it applies to spike-timing-dependent plasticity?

# Answer
> 3 votes
Homoestatic plasticity can be used with spike-dependent plasticity given they have two different goals and aren't applied uniformly across neural population. To support this argument, I'm going to use a computation model taken from "Simultaneous unsupervised and supervised learning of cognitive functions in biologically plausible spiking neural networks" by Bekolay et al.

In the model, an ensemble of neurons with input and output weights \[1\], is trying to learn how to change their output weights to approximate a given function. PES (STDP rule) changes the output weights of the neurons to approximate. The BCM (homeostatic rule) increases the sparsity of the input weights. When used together as hPES, they allow for less parameter sensitivity of the ensemble and a lower overall spiking rate, allowing the group of neurons to conserve energy.

\[1\] For a visual explanation of what this means, see this blog post.

# Answer
> 2 votes
The key concept is that STDP is synapse specific, whereas homeostatic plasticity is more global. (As an aside, it is incorrect to say that STDP strengthens connections. STDP strengthens connections with pre-before-post spiking relationships, but weakens connections with post-before-pre spiking relationships. You man be thinking of Hebbian plasticity. The following explanation applies to either.) Let's say you have 100 synapses onto your neuron, all of which have a weight of 1. Let's say 10 of them undergo strengthening through Hebb's rule or STDP to achieve a weight of 10, so the total strength of all synapses into the neuron is now 190. Then, when homeostatic plasticity is applied so that the total input to the neuron returns to a value of 100, the 10 strengthened synapses will have a new weight of 10\*100/190 = 5.3, and the other 90 synapses will have a new weight of 1\*100/190 = 0.53. Therefore, even though the total input to the neuron is held constant, the distribution of those weights changes, so information gained through the initial Hebbian plasticity or STDP is retained.

---
Tags: neuroscience, theoretical-neuroscience, neurophysiology, plasticity
---


# Question
Title: Which is the most valid/validated scale for diagnosis of Major depression for an Indian population?
I am planning a study of an online intervention for depression in India. We were planning to use Patient Health Questionnaire-9 (PHQ-9) for assessing the depression symptom severity. One of our collaborators raised an important question in a recent meeting. He asked what is the validity of PHQ-9 in India and is there a possibility of using any other tool that is more valid?

I have searched the web and found some studies that have used PHQ-9 in adult (another study) as well as adolescent populations in India. I also found a paper that developed a slightly modified version of PHQ-9, called PHQ-12, for an Indian population.

I just wanted to know if there is any other tool that has been developed specifically for an Indian population or even any tool that has been well validated for an Indian population.

# Answer
> 3 votes
I am sharing my research here should anybody find it useful.

=========================================================================

Although PHQ-9 wasn’t developed for an Indian audience, it has been used by multiple studies in India \[1, 2, 3\]. It has also been validated for an adolescent population, and a score of was found to have high sensitivity (87.1%) and specificity (79.7%) \[4\]. A modified version of PHQ-9, the PHQ-12, was developed and validated on a South Indian population of 100 participants. PHQ-12 essentially tests the same symptoms as PHQ-9 but differs in number of questions, the specific wordings of the questions, and the marking scheme. PHQ-12 lets the patient mark every question in a ‘Yes’ or ‘No’. A ‘Yes’ is given a score of 1 and a ‘No’ a score of 0. A total score of \>4 according to this

marking scheme has shown the highest sensitivity (92.0%) and specificity (90.7%) when compared against PHQ-9 \[5\]. Other popular scales for diagnosis of depression - Hamilton Depression Rating Scale, Beck Depression Inventory, and Montogomery Asberg Depression Rating Scale - have been adapted for an Indian population \[6, 7, 8\]. Brief Patient Health Questionnaire has also been translated into 11 Indian languages and validated for an Indian population \[9\]. A novel scale, Amritsar Depressive Inventory (ADI), has been developed based on symptoms which are more prevalent in Indian populations \[10\].

1. Mehrotra, Seema, et al. "Profile of seekers of an internet-based self-help program for depression in India: observations and implications." International Journal Of Community Medicine And Public Health (2017).
2. Sidana, Surbhi, et al. "Prevalence of depression in students of a medical college in New Delhi: a cross-sectional study." The Australasian medical journal 5.5 (2012): 247.
3. Thour, Amit, et al. "Depression among patients with diabetes mellitus in North India evaluated using patient health questionnaire-9." Indian journal of endocrinology and metabolism 19.2 (2015): 252.
4. Ganguly, Samrat, et al. "Patient health questionnaire-9 as an effective tool for screening of depression among Indian adolescents." Journal of Adolescent Health 52.5 (2013): 546-551.
5. Poongothai, S., et al. "Reliability and validity of a modified PHQ-9 item inventory (PHQ-12) as a screening instrument for assessing depression in Asian Indians (CURES-65)." (2009).
6. Ajmany S, Nandi DN. Adaptation of A. T. Beck et al.'s "an inventory for measuring depression" Indian J Psychiatry 1973;15:386-90.
7. Ganguli M, Dube S, Johnston JM, Pandav R, Chandra V, Dodge HH. Depressive symptoms, cognitive impairment and functional impairment in a rural elderly population in India: A Hindi version of the geriatric depression scale (GDS-H). Int J Geriatr Psychiatry 1999;14:807-20.
8. Raguram R, Weiss MG, Channabasavanna SM, Devms GM. Stigma, depression, and somatization in south India. Am J Psychiatry 1996;1531043-9.
9. Kochhar, P. H., S. S. Rajadhyaksha, and V. R. Suvarna. "Translation and validation of brief patient health questionnaire against DSM IV as a tool to diagnose major depressive disorder in Indian patients." Journal of postgraduate medicine 53.2 (2007): 102.
10. Grover, Sandeep, Alakananda Dutt, and Ajit Avasthi. "An overview of Indian research in depression." Indian journal of psychiatry 52.Suppl1 (2010): S178.

---
Tags: measurement, depression, cross-cultural-psychology
---


# Question
Title: What are some credible conferences and journals in computational neuroscience?
I have a background in computer science, and I wish to introduce cognitive sciences to myself, particularly from a computational/mathematical perspective. My motivation for doing this artificial general intelligence research at a later stage.

So far I only know of a few conferences that accept papers in the area of computational neuroscience & machine learning, namely Cosyne, NIPS, ICML, and ICLR that accept papers in computational neuro. I guess that latter two (ICLR and ICML) accept papers which find some significance in ML. As for journals, I do not even know where to begin.

# Answer
> 4 votes
Adding to what was already mentioned, there are several "Frontiers" journals:

Then there are also several rather experimental journals that also sometimes publish computational papers, such as:

Another review journal would Annual Review of Neuroscience. I think Nature Neuroscience was also not mentioned yet but is very reputable. Some older (but classical) papers might even be in Physical Review Letters. Finally, there are many preprints to find on http://www.biorxiv.org/collection/neuroscience and https://arxiv.org/list/q-bio.NC/new.

I think it's worth mentioning that, as far as I know, conference papers are far less important in the field of Neuroscience than compared to Machine Learning.

# Answer
> 2 votes
I am not an expert on AI, but Cognitive Sciences at Indiana University lists the following journals that cover your topic. The journals look credible, as they are published by Elsevier and MIT, both reputable publishers of peer-reviewed journals:

# Answer
> 1 votes
You also will want to check out PLOS Computational Biology.

Most importantly, you want to read reviews in journals such as Nature Reviews Neuroscience, Trends in Cognitive Sciences, and Trends in Neurosciences, as well as the Current Opinion series such as Current Opinion in Neurobiology.

---
Tags: reference-request, theoretical-neuroscience, computational-modeling, artificial-intelligence
---


# Question
Title: Is a low Emotional Intelligence (EQ) pathological?
A sufficiently low cognitive intelligence is generally considered in society to be inherently pathological, or at least very nearly so. In fact, until recently, a diagnosis of Intellectual Disability (ID) could formally be made on the basis of a low (below a cutoff value) IQ test score alone, without any evidence that the person's low intelligence actually caused any significant practical problems (e.g. the "clinically significant distress or impairment" frequently mentioned in the DSM).

Is there a similar phenomenon with respect to *Emotional* Intelligence (EQ)? That is, is having a sufficiently low EQ very strongly correlated with or otherwise significantly indicative of a diagnosable medical or psychological disorder, or is there a significant population of people with low (or even abysmally low) EQ's who function well enough in society that they cannot be diagnosed with any disorder?

Please do not simply quip that "Low EQ==Autism" unless you have something to back that up!

# Answer
**Shortly** , a low EQ is not a sufficient condition to diagnose a mental psychiatric disorder.

This is the DSM-V Proposal for the Definition of Mental/Psychiatric Disorder

All these features have to be satisfied in order to diagnose a *Psychopathology*. Having said that, a low emotional intelligence is a risk factor to contract a Mental Disease. According to Eisenberg (1995), **our mind is influenced by biological and social factors** and we shouldn't embrace simplifying approaches.

Finally, a good psychiatrist has to consider four perspectives from which to view a psychopathology:

1) *The disease perspective*: in which patient is identified whith his illness

2) *The behavior perspective*: which looks at the behavior of the patient

3) *The dimensional perspective*: which looks at cognitive and emotional dimensions of the patient

4) *The life story perspective*: which looks at the life story of the patient

**References**
> 8 votes

---
Tags: emotion, measurement, abnormal-psychology, iq, emotional-intelligence
---


# Question
Title: Is it true that acting can affect one's behavior?
Is it true that acting can affect one's behaviour?

For example, if someone plays a protagonist, can this affect them to be a good person? Is there any solid evidence for this?

# Answer
> 23 votes
This is true. Mot *et al*. (1994) published scientific research about it. Also there are a lot of actors that claim they feel that their personality has changed since they played a role.

Also a similair practice can be used for insecure people. If they act confident it has been proven that after some time, they feel more confident as well.

---

**Edit:**

Since I'm new to stackexchange I did not know how much detail is desired. Therefore, let me expand upon my original comment.

The article states the following hypotheses:

> (1) the actor chosen to play a given character would have personality characteristics similar to that of his or her corresponding character

---

> (2) the actor′s self-perceived personality profile would become more similar to the character′s during the rehearsal and production period.

Later on the article states that:

> Support emerged for the second hypothesis, but not for the first. Observations regarding these findings and suggestions for future explorations are given.

The article expands upon this, but I can't access the paper, because it's pay-walled.

**Reference:**

---
Tags: social-psychology
---


# Question
Title: Does Emotional Intelligence (EQ) demonstrate the Flynn Effect?
The Flynn Effect is a well-known phenomenon whereby Intelligence Quotient (IQ) test scores among the general public seem to rise over time.

Does Emotional Intelligence (EQ) demonstrate the Flynn Effect or a similar effect? That is, is there any research indicating that people today are, are likely to be, or appear to be based on their scores more emotionally intelligent than people of the past?

Since the nature of the Flynn Effect in IQ is still controversial (whether it represents true gains in general cognitive ability or whether it represents a measurement error), an answer such as, "Johnson (2013) observed that average EQ scores rose by 20 points between 2000 and 2010, but he suspects that it was caused mostly by people being coached in the correct answers on EQ tests by reading pop psychology books and browsing online Question and Answer sites rather than a true gain in emotional processing and reasoning abilities." would be perfectly acceptable.

# Answer
The Flynn effect actually says that fluid intelligence is a function of modernization. This is shown as early as Luria's work during the introduction of formal education in rural Uzbekistan, and it can be still observed today in societies that for example do not allow women into formal education.

In such cases one sees that male IQ has increased during the past decades whereas female IQ has not. Thus an argument can be made, based upon cross-cultural comparisons and taking into account differences of various groups within the same culture.

For example between religious and not religious women in Israel -- the former do not serve in the military, the latter do, and this factor interacts with the male-female difference in IQ.

So, in order to find an emotional intelligence parallel to the Flynn effect, the question is whether there are cultural factors that are rapidly introduced to traditional societies and produce measurable differences in emotional intelligence between groups that have a different degree to exposure to these factors.
> -2 votes

---
Tags: emotion, intelligence, statistics, iq, emotional-intelligence
---


# Question
Title: Effects of aerobic vs. resistance training on cognition
The beneficial effects of exercise are well documented on cognitive ability (, ) and reducing cognitive decline (). However, has the type of exercise ever been analysed?

In healthy adults, is there a difference on the effects of aerobic (running) and resistance training (lifting weights) on cognitive ability?

# Answer
> 1 votes
According to "Exercise, brain, and cognition across the life span" which was cited in the original question, there are different effects that differ for various populations.

**Developing Brains**

There is no research on the effects resistance training in children. However, general exercise has significant benefits:

> a meta-analysis that aggregated results across 44 studies found an overall effect size of 0.32 for the association between childhood physical activity and fitness and cognition, with significant effects across a range of abilities, such as perceptual skills (0.49), creativity and concentration (0.40), academic readiness (0.39) and achievement (0.30), IQ (0.34), and math (0.20) and verbal (0.17) tests

Aerobic exercise has specifically been shown to increase the capabilities of relational memory and accuracy of cognitive performance.

**Adult Brains**

Since young brains are relatively stable, little research has been done on the effects of exercise on this population. All that has been determined behaviourly is:

> aerobic fitness effects on behavior may only emerge in this high-functioning group when the task is extremely difficult or that young adults have a greater range of compensatory strategies compared with children and older adults to achieve enhanced performance

**Ageing Brains**

Aerobic training has many positive effects on ageing across a broad range of intensities, however resistance training appears to only have benefits with higher resistance levels.

# Answer
> 3 votes
I tried to do a little research myself and like you observed, there is not much research being done on adults relating to this topic.

What I did find was research done by M.B. Pontifex *et al.* (2009). Although this research was done on healthy 21 year olds (Young Adults).

They researched the effects of aerobic exercise and resistance excercise on reaction time of tasks as well as accuracy of tasks amongst other things.

This data was collected via the following method:

> Twenty-one young adult participants completed a cardiorespiratory fitness test and maximal strength tests. On subsequent days, task performance measures of reaction time (RT) and accuracy were collected while participants completed a modified Sternberg working memory task before the start of, immediately after, and 30 min after an intervention consisting of 30 min of either resistance or aerobic exercise and a seated rest control.

Their observation was that after aerobic excercise their response time latency (reaction time) was decreased directly after or 30 minutes after the excercise. This was not observed after or 30 minutes after doing resistance excercise.

They stated:

> The current findings indicated shorter RT latency during a working memory task that was performed immediately and 30 min after an acute bout of aerobic exercise, relative to the pretest. Similar effects were not observed after acute resistance exercise or seated rest, indicating that different modes of exercise have differential effects on the executive control of working memory. Further, shorter RT latency was observed for task conditions requiring increased working memory capacity after aerobic exercise, relative to the pretest, providing support for the view that changes in cognitive function after acute exercise are disproportionately larger for tasks requiring greater amounts of executive control.

**References:** M.B. Pontifex, C.H.Hillman, B. Fernhall, K.M. Thompson and T.A. Valentini (2009) The Effect of Acute Aerobic and Resistance Exercise on Working Memory. *Med. Sci. Sports Exerc* 41(4):927–934

---
Tags: cognitive-psychology, exercise
---


# Question
Title: Empirical proof for social network models
I've recently encountered the domain of social network modelling while reading the papers on models of strategic voting (unpublished), opinion dynamics and influence spread.

All of these papers create complex computational models, usually modelling social networks as graphs and inferring that their behaviour match actual social behaviour.

However, I don't understand how these models can be empirically rigorous. It seems to me that the ways to validate a model is to match with empirical data, either via data matching or prediction. This doesn't seem to be done in any of those papers.

Consequently, how are these models validated?

# Answer
# Existing Papers

I found three papers in the same vein with considerably more empirical evidence.

## 1. Modeling the Size of Wars

In the paper, provinces and conflicts are modeled to justify Richardson's observation that the proportion of conflict severity in relation to their frequency is described by a power law. In other words, the more space there is between each conflict, the more casualties will result. The models uses a lot of detail. A geographical map is created and conflicts (down to technological advancement, political structural change and resource allocation) are simulated in models with dozens of parameters. More importantly, the level of detail in the paper allows parameters to be set to test historical scenarios to disprove or give further evidence to the model.

## 2. The Dynamics of Polarisation

The focus of the paper is modeling the change of public opinion in the United States as a way to provide explanation for two phenomenon:

1. Polarization of opinion is rare despite being perceived otherwise
2. Opinion homogeneity is rare, despite being perceive otherwise.

To model these phenomenon, a network similar to that of the Opinion Dynamics paper from the question is built, with imposed homophily. However, the paper grounds it's parameters in reality (for example, take-off issues that stimulate much discussion are considered rare). In contrast, the Opinion Dynamics paper creates parameters for skepticism and empathy, without giving much consideration for the mechanisms behind these attributes and how they might change over time.

## 3. A Psychologically-Motivated Model of Opinion Change with Applications to American Politics

This paper justifies modeling 2D distributed agents using the psychological parameters Influence, Susceptibility and Conformity and their interaction. The model is then validated on American political opinions as they shift over time.

# Conclusion

There are papers with empirical basis in the domain of social network models. Typically, this realism is achieved by basing parameters on empirical evidence, rather than simplification of cognitive phenomena.

# Reply from author of Social Network papers

The author of two of the papers I cited in the question, Alan Tsang, was kind enough to provide a rebuttal to my scepticism via personal correspondence:

> The premise behind both the papers was to examine the effects of a particular psychological phenomenon by examining it in isolation. We base our work on more conventional agent models from economics, which assume completely rational actors. We want to see what happens when the rational behavior is tweaked to incorporate a behavioral component. In particular, we are interested in the qualitative effects that are produced, and the mechanisms by which these are achieved. An agent based simulation is the ideal way of studying this, because it allows us to drill down and take measurements that would be impossible or very difficult to do in an actual community. So what we are doing is more mathematics and less science. The results of the papers provide qualitative insights on what are plausible effects of these behaviors on a larger system. The next step could certainly be to validate the model against real data, but the goal of the paper is not to perform "full stack" science. Rather, we hope it would prove useful component in a more detailed model to be used on data collect in the wild.
>
> That said, we are also interested in validating our model against real data as well, but they are difficult to come by. For instance, Facebook almost certainly has access to data that can be used to detect homophily in networks, and how they might affect opinions over time. But the data is very proprietary and, even if we were to get it, ethical concerns might limit how it can be used. As you've pointed out in the follow-up post, there are a few papers that examine political affiliation, and those could potentially be useful ground truth. But I don't have the background to properly assemble such a data set from scratch (as it would need both a time series of opinions, and the underlying network structure). Moreover, there are sure to be other effects at work as well, which may confound the analysis. We're giving some thought to gathering data for the last Canadian election, since strategic voting was so widespread and successful, but any data we collect will likely be disconnected from social network structure. Maybe some aggregate network properties could be inferred (ex: based on region), but it would be a multi-layered problem.
> 5 votes

# Answer
The paper "Can robots make good models of biological behaviour" by Barbara Webb comes from a slightly different area, i.e. modeling biological organisms with robotics, making artificial cockroaches for example.

It has a brilliant theoretical examination of modeling in terms of epistemology and philosophy of science. For your question it is possible that your skepticism is with regard dimensions 5 and 6 mentioned in the paper, i.e. structural accuracy and performance match.

In terms of structural accuracy for example, if a social network uses random graphs, like Erdős–Rényi, it makes an assumption that is not met by the actual degree distributions of human social networks.

In terms of performance match, the accuracy of the model's prediction can be assessed at various levels of precision. For example, the model may 'capture the trends' qualitatively, which may or may not be good enough for large scale simulations.

On the other extreme one would find precise numeric predictions and examine their fit to real data. I guess that most models fall somewhere in between.
> 2 votes

---
Tags: cognitive-modeling, social-networks, sociology
---


# Question
Title: The role of high-performance in neuropsychology
As far as I understand, neuropsychology gains most of its insights from the reconciliation of lesions of the brain and **cognitive impairments**. Normal functioning (both of the brain and the mind) plays a less important role in neuropsychology.

My question is:

> Which role does **cognitive high-performance** play in neuropsychology? Are there attempts to map cognitive high-performance processes to neurophysiological structures and processes? Some examples would be great.

Examples of cognitive high-performance:

The mere fact that for such high-performers there are possibly enlarged (and internally more strongly and probably more specifically connected) areas of the brain (and connections between them) is not what I am looking for. Especially for the more mathematical and intricate cases there must be more than that.

The main difference between *neuropsycholgy by impairment* and *neuropsychology by high-performance* seems to be that in the former case you can more easily perform statistical studies (but also single-case studies), in the latter case you can only perform single-case studies.

# Answer
The short answer to your question is that, yes, you are correct. "Cognitive high performance" is a much smaller part of classic neuropsychology than the study of brain damage. There are studies of the topics that you mention from a cognitive neuroscience perspective (e.g., a study by Krawczyk et al. (2011) which does neuroimaging of chess experts). Some cases such as eidetic memory are disputed, so most of the science has focused on that. "The exceptional brain" is a classic book on "special talents" and neuropsychology, but it is pretty old now.

I don't completely agree with your final point. Extremely good and extremely poor performance can both be studied with single cases OR group studies, but for the latter you obviously need to find multiple people with similar behaviour which is hard for both classic neuropsychology (e.g., selective agnosias) and for special talents.

Some definitions of neuropsychology specifically refer to brain damage and deficits, so in that sense your point is trivially true. Some, or perhaps most, people studying patients are partly motivated by helping people who have problems, and so studying high achievers might be less useful. We have quite a good understanding of some syndromes because of their reasonably high frequency and many decades of research (e.g., Neglect, Balints, Ataxias, Aphasias). I think you could make the argument that the behaviour demonstrated in these cases is not just "less than" normal but qualitatively different. Most people can play chess, improve their memory and memorize long numbers, particularly with training. So it is easier to see those with "special talents" as just the extreme end of a continuum which could be studied with typical people.

Lastly, you might be interested in looking at work with autism which I think is a good example of something where people have looked at both the negative aspects and the (potential) advantages.

<sub> Krawczyk, D. C., Boggan, A. L., McClelland, M. M., & Bartlett, J. C. (2011). The neural organization of perception in chess experts. Neuroscience letters, 499(2), 64-69. \[PDF\]
Obler, L. K., & Fein, D. E. (1988). The exceptional brain: Neuropsychology of talent and special abilities. Guilford Press. </sub>
> 4 votes

---
Tags: neuroscience, cognitive-neuroscience, theoretical-neuroscience
---


# Question
Title: LSD and tryptamines harmless or neurotoxic?
It's commonly stated by numerous people that LSD and trytamines like DMT and psilocin are physically harmless and not neurotoxic. Is there evidence for this?

I recently read 5-meo-Dipt which is a tryptamine might be neurotoxic. Why would 5-meo-Dipt be neurotoxic but DMT and psilocin not be? From my understanding some people micro-dose with LSD and some tryptamines to feel sharper and increase felt intelligence.

Why would one tryptamine neurotoxic and others make someone feel more intelligent? Obviously "feel" is self reported and subjective, but I'm assuming there might be some truth to this if people aren't tripping when experiencing these micro dosing effects. LSD isn't a tryptamine, but I think some people do similar things with tryptamines. I'm hoping someone with a better understand of neurology can answer this.

To restate my question are typtamines and LSD generally neurotoxic and if not, could you please link to a study on it and what mechanism makes 5-meo-dipt possibly different, could other factors might have lead to a wrong conclusion, like for example harmful environment stress on rats or do you think all tryptamines are neurotoxic?

I'm trying to understand the possible reasons or lack there of for neurotoxicity in LSD and tryptamines but there seems to be lack of reliable sources.

# Answer
> 3 votes
**Short answer**
All neuropsychopharmaceuticals, including the tryptamines, are potentially neurotoxic depending on the dose at which they are ingested.

**Background**

Neurotoxicity is, arguaby, a broad definition. According to the NIH, neurotoxicity can be caused by processes ranging from radiation to transplants, and from chemical toxins to cosmetics. NIH defines neurotoxicity as:

> Neurotoxicity occurs when the exposure to natural or manmade toxic substances (neurotoxicants) alters the normal activity of the nervous system. This can eventually disrupt or even kill neurons, key cells that transmit and process signals in the brain and other parts of the nervous system. Neurotoxicity can result from exposure to substances used in chemotherapy, radiation treatment, drug therapies, and organ transplants, as well as exposure to heavy metals such as lead and mercury, certain foods and food additives, pesticides, industrial and/or cleaning solvents, cosmetics, and some naturally occurring substances.

LSD is a tryptamine (Shulgin, & Shulgin, 1997), see Fig. 1.

Fig. 1. LSD contains the tryptamine structure (in red). source: Shroomery

Secondly, every compound is toxic when taken in large quantities. For instance, water can kill, referred to as water intoxication, for example as seen in people tripping on MDMA and taking in too much water (Ballantyne, 2007). Oxygen, another key to life, is a deadly gas when taken in artificially high concentrations for too long. Likewise, neuropharmacologically active compounds will hence eventually become neurotoxins. This, because the definition of *neurotoxic* is indeed quite broad (source: NIH):

> Neurotoxicity occurs when the exposure to natural or manmade toxic substances (neurotoxicants) alters the normal activity of the nervous system. This can eventually disrupt or even kill neurons, key cells that transmit and process signals in the brain and other parts of the nervous system.

Thus when you ask

> are tryptamines, including LSD \[sic\] generally neurotoxic?

Then the answer is yes, depending on the dose.

Reversely, then, every neurotoxin becomes non-toxic once taken below a certain threshold dose. If this is what you refer to by 'microdosages', then yes, even the most potent toxin becomes harmless.

To specifically answer your question with regard to LSD and psilocin: LSD is suspected to be neurotoxic at clinically applied dosages (Larsen, 2014), and psilocin can result in convulsions and death follow massive overdose (Gold *et al*., 2003).

**References**
**-** Ballantyne, *Sci Am* 2007
**-** Gold *et al*., *Atlas of Clinical Neurology*, Springer. pp 503-24
**-** Larsen, *Hist Psychiatry* (2016); **27**(2):172-89
**-** Shulgin & Shulgin, Tihkal - The Continuation, pp. 490-99

---
Tags: neuroscience, psychopharmacology
---


# Question
Title: How does the brain encode order of information in sentences/stories?
When memorizing a sentence or a full story: then, how does the brain encode the order of the words of the sentence or the sentences in the story?

# Answer
> 1 votes
Similar to your other question, this one reduces to "what are the neural mechanisms behind language?", which is very much a work in progress.

The only neural model of language that I currently know of is the Semantic Pointer Architecture (SPA), which is largely theoretical and only has some super basic examples.

Basically, the SPA represents language as vector manipulation. The vectors are represented in neurons using the Neural Engineering Framework.

For more details on how this is done, check out "How to Build a Brain" by Chris Eliasmith and the work by Peter Blouw who is trying to solve part of this problem with his PhD thesis.

---
Tags: theoretical-neuroscience, cognitive-modeling, brain-development, linguistics
---


# Question
Title: Are There National Personality Archetypes?
I feel like in the U.S where I was born and raised there are definable personality archetypes which fall into obvious stereotypes such as a dry as dust country type accent and life-style, snob, ultra conservative old woman etc What I want to know is if these behaviors have been catalogued and defined. For instances, writers have alleged that there are 11 different "nations" in the United States.

What are their bases and why do people conform so rigidly to these types?

# Answer
News reporter Colin Woodard has published a book describing "11 nations" of North America, each with its unique personality, that also influences the individuals that live within their confines. For instance, Puritain northeasterners tend to well-educated, liberal "good government" types. Slightly to the south and west are the commercially oriented "New Netherlands" types that retain the early Dutch influence. The Midlanders and Appalachians are more fragmented and less pro-Government than others. The Tidewater and the South are more "traditional" areas that prefer state to Federal authority. The rugged western parts of the country value hard work and self-sufficiency and (mostly) have libertarian tendencies. "New France" and "First" (Indian) nations are unique subcultures within this group.

Each area was initially shaped by its historical experience, and later attracted the immigrants that were most like it.
> 2 votes

# Answer
David Fischer's Albion's Seed: Four British Folkways in America posits that there are four different "American" cultures - Puritans, Quakers, Cavaliers, and Hillbillies.
> 0 votes

---
Tags: personality
---


# Question
Title: Conceptual representations in brain by distributed groups of neurons
It seems generally agreed upon that semantic concepts are distributedly represented by groups and groups of groups of neurons spread over the cortex.

Disregarding the localizations, shapes and connectivity of these groups of neurons, I tried to consider them as sets (in the mathematical sense). Let $S(A)$ be the (probably fuzzy) set corresponding to concept $A$.

The only thing that I would take for granted is that for very similar semantic concepts $A$, $A'$ their corresponding sets of neurons $S(A), S(A')$ do overlap strongly. Otherwise the model of distributed representation would not make much sense to me.

Other answers aren't so obvious:

1. Does a more *general* concept $A$ use more neurons than a more specific concept $B \subset A$ - or less? Or does it depend (on what)?
2. How do the sets of neurons of two concepts $A, B$ with $B \subset A$ overlap? Is maybe one a (fuzzy) subset of the other? More generally: How are semantical or extensional relations between two concepts reflected by set theoretic relations between their corresponding sets of neurons? (My intuitive guess is: $S(A)$ is larger than $S(B)$, and $S(B)$ is contained in $S(A)$, i.e. $S(B)\subset S(A)$. But this may be simply wrong.)
3. Does a more *important* concept $A$ (being used more often) use more neurons than a more rarely used.

I wonder if there is any evidence (empircal or theoretical) that sheds some light on these questions.

*\[If you think, this question is devoid of scientific meaning or otherwise ill-posed, please let me know why.\]*

# Answer
> 3 votes
You might want to take a look at the work about conceptual spaces by Peter Gärdenfors, e.g. https://www.amazon.com/Conceptual-Spaces-Geometry-Thought-Press/dp/0262572192

Also, the work about semantic pointers might be interesting here: https://www.ncbi.nlm.nih.gov/pubmed/26235459

My opinion with regard to this is, that using set theory to represent concepts is a fruitful approach, but there needs to be a precise definition of the "space" we are talking about as well as if and how it is possible to define some metric on this space or a higher structure, e.g. if it is a vector space. This metric must not only take into account set overlaps but also principal phenomena corresponding to what we know about neurobiology, e.g. classical/operant conditioning etc.

Let's try to build this up systematically (Note, that I do not use a fuzzy set definition here but it might provide some more flexibility and thanks for putting me on that track ;)): We could define the set of all neurons

```
N = {n_1,n_2,...,n_m}

```

and the set of all possible states of a neuron (avoiding, for now, a precise definition of what a state is. For example, a state could be a frequency or some pattern of action potentials, e.g. rate/temporal/population code or just a discrete value of the membrane potential)

```
S={s_1,s_2,...,s_l}

```

The Cartesian product set `N x S` will give us the set of all neurons in all possible states `C_0`:

```
C_0={n_1(s_1),n_1(s_2),n_2(s_1),n_2(s_2),...,n_m(s_l)}

```

Then let's define a *concept space* as a mapping `f1` from `C_0` to a new set `C_1`

```
C_1={{n_1(s_1),n_3(s_3),n_4(s_1),n_5(s_8)},{n_1(s_1),n_2(s_3),n_5(s_9)},...}={c1_1,c1_2,...,c1_x}

```

For example, an element (`c1_x`) of `C_1` could be a visual representation of a house or some sound or smell or just a point or a line. This is what Thagard & Steward (2014) defined as a semantic pointer and it shares some similarity with Tononi's (e.g. 2016) approach of a qualia space (although approached from a different (set theoretic) angle since Tononi uses information theory). This also is similar to Gardenförs' concept of a conceptual space, although he did not make his definitions mathematically precise. Because strictly, `C_1` still has no structure, i.e. is not a vector space or more generally a metric space. There still has to be defined some distance function, which is not easy to be found.

Now, it is possible to generate more and more sets representing more and more complex concepts by consecutive mappings `f1 to fn`. That is we can generate a new set `C_2` consisting of elements of `C_1`:

```
C_2={{c1_1,c1_3,c1_5,c1_9},{c1_7,c1_1,c1_8},...}={c2_1,c2_2,...,c2_x}

```

Imagine the element `c2_1` consisting of four lines with coordinates of length `l1 to l4` each of them in a specific angle `a1 to a4` such that they create a square. Or take `c2_2` as three lines with length `l1 to l3` and angles `a1 to a3` such that they create a triangle.

This process can be repeated to generate more and more abstract concepts. I think it is easy to understand it when considering how letters are combined to words and words form sentences and sentences form even more abstract meanings.

There are now many questions that arise, e.g. are the mappings injective, surjective or bijective? Do inverse mappings exist? What is a suitable metric that is in accord with neurobiological and experimental data? Can a higher structure e.g. vector space be defined?

Finally, I can try to answer your questions:

1. Based on the above definition one can assume that more general concept e.g. a cube is formed by a set of lines, i.e. a set of semantic pointers forms another set of semantic pointers. For example, a complex movement with the hand was initially learned by combining different simple movements. Or take learning to speak a word for example.
2. Also based on the definition above, there must not be an overlap between sets at all! Take two very different semantic pointers for example, like barking and the visual representation of a dog. Whereas one set of semantic pointers might represent the sound, the other may represent the visual aspect, but they might not share the same neurons. But all of them together create a concept of a dog. So here again, the definition of similarity seems to be not just a simple set overlap metric (e.g. Szymkiewicz-Simpson coefficient or Jaccard index).
3. This depends on the definition of important. If you define important as activated more often together, then one could just assume a simple (e.g. Hebbian or STDP) learning rule which strengthens the connection between neurons. But I doubt that more neurons will be included in the concept except when the concept is updated/broadened by new experiences.

Hope this helps a bit! I'm trying to build a more general understanding of conceptual spaced based on set theory for a while and I always welcome discussions, critique or collaborations :).

Sources:

-Thagard, Paul, and Terrence C. Stewart. "Two theories of consciousness: Semantic pointer competition vs. information integration." Consciousness and Cognition 30 (2014): 73-90.

-Tononi, Giulio. "Consciousness as integrated information: a provisional manifesto." The Biological Bulletin (2016).

---
Tags: neuroscience, cognitive-neuroscience, theoretical-neuroscience
---


title: Specification of SuperMemo 2

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

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

# Answer
> 2 votes
$EF$ is the "easiness factor". This means that the greater easiness you have, the longer will be the interval to next review ($I\_\text{new}$).

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

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

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

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

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

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

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

```

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

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

---
Tags: learning
---


title: How does speed listening work?

text:
# Question
Title: How does speed listening work?
I've recently gotten into listening to podcasts. Over time, as I get accustomed to the speaker's voice, I'm able to increase the speed of the podcast to as high as 3x speed. It still feels "normal" to me, as if the speaker is having a normal-speed conversation with me.

When I turn down the speed to 1x, it sounds unbearably slow. For non-speed-listeners, listen to something at 0.5x or 0.25x, and you'll know what 1x sounds like to speed listeners. It's as if speed listening shifts up a listener's range of acceptable speed, so that lower speeds are no longer in that range.

I know there are plenty of other speed listeners who do the same thing (just Google "speed listening" to see for yourself). Yet, others have told me that at this speed, podcasts are basically unintelligible.

Thus, I have a handful of related questions:

1. What occurs in the brain when a person speed listens?

a. Why does the podcast feel "normal" at such fast speeds?

b. Is there a fundamental/biological difference between those who can speed listen and those who can't, or is it a learned ability?
2. Is speed listening detrimental to listening comprehension?

# Answer
> 6 votes
Your question made me think of JAWS, a screen reader for the blind. I have worked with visually impaired people for a while and I have always wondered how on earth they can understand the speech produced by JAWS given the sheer high speech rates they apply on their gadgets.

Indeed, people with peripheral vision loss may learn to understand spoken language at rates of up to about 22 syllables per seconds, while the rate in normal listeners is about 8 syllables per sec (Dietrich *et al*., 2013). These numbers are based on speech *understanding*, as opposed to simply hearing it.

Hence in answer to your question

> Is speed listening detrimental to listening comprehension?

I would say no, at least not in above study, as speech understanding there was tested in a speech comprehension test, which is different than just *hearing* the speech.

Then your questions

> What occurs in the brain when a person speed listens?
> a. Why does the podcast feel "normal" at such fast speeds?
> b. Is there a fundamental/biological difference between those who can speed listen and those who can't, or is it a learned ability?

In case of blind people it has been shown that they activate their visual cortex when speed reading. This, because the deafferented area is recruited for other modalities, such as touch and hearing. This is probably not what you are after in your question though. In effect, I doubt gross effects on brain activity occurs in trained, normally sighted subjects and indeed a study where both sighted and blind individuals were trained on fast-speech understanding does not report on gross effects in the sighted group (Hertrich *et al*., 2006).

It feels normal because it is a **learned ability**; to continue with the example of these blind folks - they haven't been able to read for a long time and the only way they communicate through written materials is via screen readers. The spoken word is slower than reading so they crank up the speeds whenever possible, so they are slowly increasing their speech understanding skills.

<sub>**References**
**-** Dietrich *et al*., *Front Hum Neurosci* (2013); **7**: 701
**-** Hertrich *et al*. *Brain and Language* (2006); **124**(1): 9-21</sub>

# Answer
> 5 votes
1. There is probably not a large difference from what occurs during normal listening--and that is likely why speed listening is effective:

a. The reason it "feels" normal is the same that any other sensory stimuli feel normal after a while: your brain habituates to the patterns of your sensory experience. If you increased the pitch of the podcast without changing the speed, for example, eventually the chipmunk voices would sound normal.

b. It is almost certainly a learned ability, or, really, just a different comfort zone. The average rate of self-talk (i.e. verbal thoughts) is usually given as around 400 words-per-minute, and this is also the upper end of normal reading rates (200-400 WPM). According to the National Center for Voice and Speech, "The average rate of speech for English speakers in the United States is about 150 words per minute". Narrators for audiobooks and podcasts often speak somewhat slower than this to compensate for the lack of visual cues. So, at 3X speed, the typical audio track approaches the upper limits of typical verbal processing (by the way, reading, thinking, and listening ALL activate the same parts of auditory cortex associated with language). So, unlike with speed reading, it is entirely reasonable that a majority of people could learn to comprehend audio content at 3X the typical rate (but see caveat below). However, speed listening is going to require more *attention*. People who complain they cannot understand at higher listening rates likely should say they cannot do the simultaneous commentary/reflecting/daydreaming that they normally do simultaneously.
2. It depends on the content, but probably not for most podcasts. Let's assume that the baseline rate of the track is such that, at 3X, it doesn't go above 400 WPM. Most podcasts take care to provide narratives that are well-structured and easy to follow--that's why they're enjoyable to listen to. All the verbal reasoning necessary to comprehend the content is included in the track. But now imagine listening to a math or physics textbook at that speed. In this case, while sufficient information is provided for understanding, it requires quite a bit of cognitive "unpacking" (matching with context, relating concepts, generating cognitive models, etc.), a bit like a zip file. I remember my math professor saying even trained mathematicians can spend 30 min understanding a single page! Another caveat is memory. Even though you may comprehend every word of the track, you definitely won't remember it in every detail. And remember that commentary/reflecting/relating you gave up in focusing your attention? Studies show that's actually important to learning and memory (not so with daydreaming, of course). But as long as you pause when you come across an interesting point to really let it sink in, you'd probably solve that problem as well.

---
Tags: neuroscience, perception, hearing, speech, speech-comprehension
---


title: IQ, Intelligence and Critical Thinking

text:
# Question
Title: IQ, Intelligence and Critical Thinking
I consider myself to be a very critical and analytical thinker. I can't help obsess over every little detail, consider various perspectives, use-cases, etc. I've been programming since a young age (self-taught). At the same time, I have ADHD and a bad working memory.

If I master something, I find that I can think critically and outside the box much better than someone else. I can utilise it better, build upon it better, etc.

Because of my bad short term memory, I assume i will do generally bad in IQ tests and this is not surprising.

Because of my bad memory, it might take me longer to master something than someone else.

Do IQ tests measure critical thinking ability at all? Or just working memory? IQ and working memory are highly correlated.

# Answer
> 2 votes
There are a variety of "IQ" tests which attempt to achieve a particular goal (culture-fairness, isolating specialized aspects of cognition, etc.).

"Raven's Progressive Matrices" is a popular type of test that was originally developed in search of an IQ-metric that was "culture-fair" (that is, scoring well did not rely on any cultural background).

In the same vein, it's possible to find specialized IQ tests which selectively measure verbal reasoning, spatial reasoning, and/or memory in isolation. The following website is a battle-tested resource for these sorts of metrics: https://www.cambridgebrainsciences.com/

The results can be mapped back into "IQ" space by matching the percentiles (conveniently, with the aid of this table: https://www.iqcomparisonsite.com/iqtable.aspx ).

---
Tags: iq
---


# Question
Title: What are the differences between Asperger's Syndrome and Schizoid Personality Disorder?
They are specifically listed as two separate disorders in the ICD, but what are the differences between Asperger's Syndrome and Schizoid Personality Disorder?

Since both result in a withdrawal from social situations, the two can seem quite similar to an outside observer; is there any accurate method used to distinguish between the two in a subject?

# Answer
Schizoid personality disorder is characterized by a lack of interest in social relationships. However, with asperger syndrome, it's a limited empathy and understanding of other's situations. In other words, asperger syndrome deals with the inability to empathize while schizoid personality disorder deals with apathy toward other's emotions. Additionally, people with apserger syndrome tend to be less withdrawn than people with schizoid personality disorder. People who have asperger syndrome show repetitive behavior and interests, while schizoid personality disorder does not show this fixation toward repetitive behavior. Asperger syndrome is probably genetically linked somehow and is placed on the autism spectrum. However, schizoid personality disorder is not on the autism spectrum. I hope this response helped!
> 4 votes

# Answer
This is a very good question. It's true that there might be some problems to differentiate Asperger's Syndrome and Schizoid Personality Disorder, infact, according to DSM-5

```
Individuals with a Schizoid Personality Disorder shows a pattern of dethachment from social
relationships and a restricted range of emotional expression.

```

Moreover, the manual specifies the likeness of symptoms between Schizoid Personality Disorder and Autism Spectrum Disorder but *the latter records*

## **a more severely impaired social interaction and stereotyped behaviors and interests.**

According to DSM-5, A personality disorder is an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual's culture, **is pervasive and inflexible** and occur in two or more of these fields: 1- cognition 2- affectivity 3- interpersonal functioning 4- impulse control

The DSM-5 divided Personality disorders in three *Clusters*:

1. Cluster A includes paranoid, schizoid, and schizotypal personality disorders.
2. Cluster B includes antisocial, borderline, histrionic, and narcissistic personality disorders,
3. Cluster C includes avoidant, dependent, and obsessivecompulsive personality disorders.

**Cluster A** refers to "Individuals with these disorders often appear *odd or eccentric*." They show a bizzarre and strange behavior. The cognitive and perceptive dimension - dysfunctional in that disorders - has been correlated with an increased activity of dopaminergic system (Siever, Davis, 2004)

---

With regards to Aperger's Syndrome, DSM-5 folded it into the umbrella of autism spectrum disorders. To the diagnose is needed:

* Persistent deficits in social communication and social interaction across multiple contexts
* estricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following, currently or by history
* Symptoms must be present in the early developmental period (*Not essential for a diagnose of Schizoid Personality Disorder*)
* Symptoms cause clinically significant impairment in social, occupational, or other important areas of current functioning
* These disturbances are not better explained by intellectual disability

**References**

DSM-5 diagnostic criteria of Autism Spectrum Disorder

DSM - 5 (2013)

Siever LJ1, Davis KL. *The pathophysiology of schizophrenia disorders: perspectives from the spectrum*
> 2 votes

# Answer
Schizoid Personality Disorder has nothing to do with psychosis. A personality disorder is an enduring pattern of inner experience and behavior that deviates from the norm of the individual’s culture. The pattern is seen in two or more of the following areas: cognition; affect; interpersonal functioning; or impulse control. The enduring pattern is inflexible and pervasive across a broad range of personal and social situations. It typically leads to significant distress or impairment in social, work or other areas of functioning. The pattern is stable and of long duration and its onset can be traced back to early adulthood or adolescence.
> -1 votes

# Answer
It is difficult to distinguish between these two because tests and criteria are not perfect. Still, one is a form of autism, one is related to schizophrenia, so they should be different. I would look at autistic traits: tendency to see patterns, interest in numbers, inability to read emotions. If these are normal, then probably it is not asperger or any form of autism. As for schizoid personality disorder, there is a question if we are dealing with a disorder or a personality type. If it is not damaging to the quality of life of the person or others, it should not be evaluated as a disorder. There is an introvert personality type which resembles schizoid and is connected with many difficulties in life, but is still not a personality disorder. So make these three distinctions, separate autistic spectrum by its specific signs, then disorder by evaluating if is counts as a disorder (to be treated). If not, it is simply a possibly rare personality type.
> -1 votes

---
Tags: abnormal-psychology, aspergers
---


title: Implicit Learning vs. Latent Learning

text:
# Question
Title: Implicit Learning vs. Latent Learning
Sawyer (2005) defines "Implicit Learning" as:

> Implicit learning refers to situations in which complex information is acquired effortlessly (without a conscious effort), and the resulting knowledge is difficult to express verbally (e.g., Berry, 1997; Cleeremans, Destrebecqz, & Boyer, 1998; Reber, 1967 ). Although many types of implicit learning exist, a common process underlies most of them - the rapid, effortless, and untutored detection of patterns of covariation among events (Reber, 1993). (Page 19)

Also, this Wikipedia article provides a nice definition of it.

Soderstrom and Bjork (2015) have defined "Latent learning" as:

> Latent learning is defined as learning that occurs in the absence of any obvious reinforcement or noticeable behavioral changes. Learning is said to be “latent,” or hidden, because it is not exhibited unless a reinforcement of some kind is introduced to reveal it. Consider, for example, a person who recently moved to a new city and, apprehensive about driving, decides to ride the city bus each day to work. Riding the bus day after day, the route would be learned through observation, but such learning would only be evident if an incentive was present that required it—say, when it was necessary for the person to drive to work on his or her own. The early findings of latent learning were intriguing and controversial because they challenged the widely held assumption that learning could occur only in the presence of reinforcement. For a classic review of the early latent learning studies, we recommend Tolman (1948), in which the concept of “cognitive maps” was introduced, a term that refers to the mental representation of one’s spatial environment. (Page 177)

What is the difference between these two?

**References**

* Sawyer, R. K. (Ed.). (2005). *The Cambridge handbook of the learning sciences*. Cambridge University Press.
* Soderstrom, N. C., & Bjork, R. A. (2015). Learning versus
performance: An integrative review. Perspectives on Psychological
Science, 10(2), 176-199.

# Answer
> 1 votes
**Implicit Learning**

> Implicit learning refers to situations in which complex information is acquired effortlessly (*without a conscious effort*), and the resulting knowledge is *difficult to express verbally*. (Italics mine)

As discussed in the Wikipedia page, the exact definition is controversial, but all the paradigms (verbal reports, forced-choice tests, etc.) listed, the knowledge is gained *unintentionally* and *without awareness*.

Both these criteria relate to the learner's subjective relationship with the acquired knowledge. It says nothing about behavior and reinforcement, which may be readily apparent.

Consider social skills as an example. I may smile, gesture, and make eye-contact appropriately (behavior), and I experience positive social outcomes when I do so (reinforcement). However, I never explicitly set out to learn the number of milliseconds to maintain eye-contact, or what situations warrant a smile. Moreover, if someone offered to pay me to write instructions on how to engage socially, I would have a hard time articulating my knowledge. It is implicit.

**Latent Learning**

> Latent learning is defined as learning that occurs in the absence of any obvious *reinforcement* or noticeable *behavioral changes*. (Italics mine)

These criteria relate to the objective behavior and circumstances of the learner. It says nothing about the learner's subjective awareness of the knowledge.

Consider the bus ride example. I may be perfectly aware that I am gaining knowledge of the bus route through observation. But an objective observer would have no way of proving that I have learned the route: I behave the same as if I had not learned it, and I receive no clear reinforcement for doing so. However, if someone offered to pay me to give directions to my work place, I would be able to do so. My knowledge is explicit but hidden.

To sum it up very roughly:

*Implicit learning* is when the knowledge you gained isn't apparent to you. *Latent learning* is when the knowledge you gained isn't apparent to others.

---
Tags: cognitive-psychology, learning, definition
---


# Question
Title: Are chatbots based on deceased loved ones healthy?
I recently read an article about a journalist who created a chatbot to ensure that a conversational entity with elements of his dying father's personality would exist even after his father--terminally ill with cancer--passed away.

I am a software engineer experienced with creating chatbots and it has crossed my mind to create one for the parents of my best childhood friend who was killed 10 years ago in a car accident.

I speak to the parents a few times a year and we have a great relationship. Having been their son's best friend when we were growing up, I know his mannerisms and expressions almost as well as they do so I am confident that I could do a good job of training the chatbot.

That said, the parents have found their peace with my friend's passing and I don't want to do anything to jeopardize that. In any case, I would obviously discuss with them before creating such a chatbot. This leads to my ultimate question:

Would creating a chatbot based on a deceased loved one help or harm those of us left behind?

I really don't know the right answer to this. In my most generous thoughts of how this turns out, it could give his parents, siblings, and future family members a way to remember/meet his fun, goofy personality, but I could also see this opening old wounds.

# Answer
> 1 votes
In my opinion, it depends on whether they would like the AI to synthesize novel thoughts/opinions or to merely contextually quote a history of that individual's textual recordings.

Making a value judgement here, I would say than an AI saying "I forgive you." (from beyond the grave) is not healthy.

But if the chatbot acted as a way of indexing into the individual's actual history, then all potential errors become ones of context (and not content).
(This level of reproduction may not be totally necessary depending on the users' sensitivity to cognitive dissonance, but I would personally feel slimy if I tried to pass off a markov chain of scripts and data as my friend.)

If you're open to alternatives to chatbots, I would suggest that you frame the project as a tribute to your friend's life; even a simple collection of stories from your time together could have a powerful (healthy) impact on the grieving parents.

---
Tags: social-psychology, experimental-psychology
---


title: What is 'n-dynamics' mentioned by Poli?

text:
# Question
Title: What is 'n-dynamics' mentioned by Poli?
In a seminar abstract titled "THE UNREASONABLE INEFFECTIVENESS OF MATHEMATICS IN COGNITIVE SCIENCES" by Roberto Poli, he mentions

> I will consider some conceptual issues that might prove important for framing the problem of cognitive mathematics (= mathematics for the cognitive sciences), namely **the problem of n-dynamics**, of identity, of timing, and of the specious present.

What is **n-dynamics**?

# Answer
> 2 votes
I contacted the author. He's now in University of Trento.

He says it refers to the theory of multiple levels of reality, the dynamics of each level, and the interaction among them.

---
Tags: dynamic-systems
---


# Question
Title: Name of the bias towards not seeing small harm of many as important?
I observe this kind of thinking especially in politics, for instance when someone brings up that "It is fine to take a few dollars from a lot of people if it helps the country". I think the reason we see things like this is that we can better imagine the value of one thing with awesome qualities than million things of a small quality because we are more used to compare the quality, not the amount, in our daily lives. Is there a name for a similar cognitive bias/fallacy?

# Answer
Yes. This is a special case of the **identifiable victim effect**: the cognitive bias implicated in the quote, "A single death is a tragedy; a million deaths is a statistic."

The identifiable victim effect might be paraphrased as the tendency to view harm of many as unimportant. A direct corollary is the tendency to view *small* harm of many as unimportant. Going off AliceD's example, we might expect taking \\$1 from a million to sound preferable even to taking just \\$100k from 1 person.

**A potential objection** might be, "sure, but in this case, 'one person' isn't really an identifiable victim. It's really about the *small amount* of harm since both victims are just 'statistics'." Fair point, but even if you wanted to classify this as a bias distinct from the identifiable victim effect, they both result from the same cognitive heuristic: experiential thinking.

**Experiential thinking**, in this context, is evaluating a scenario by imagining yourself in it and judging what that experience would be like. For example, when I imagine losing \\$10, it is far preferable to losing \\$100k, but the fact that it is taken from a million people has little emotional relevance. You can't imagine experiencing the loss of $10 as more than one person at a time. Similarly, an identifiable victim makes my experiential thinking more vivid because I have a concrete situation in which to imagine myself. I can imagine what it's like being mugged at 11pm in an alley near 130th Street, but "1,000 muggings in the past month" is not something I can relate to experientially.
> 5 votes

# Answer
This comes under the heading of the theory of organized interests.The idea is that there are a few parties that stand to make large gains from a situation, and therefore have an incentive to organize and capture these gains. Meanwhile, there is a large number of people that stand to receive small losses. Because these losses are individually "small," the latter group of people do *not* have an incentive to organize to defend their interests against the first group.

The doctrine of Pareto efficiency suggests that the action should be undertaken if the aggregate gains outweigh the aggregate losses (because the winners can compensate the losers and still come out ahead; otherwise not.
> 2 votes

# Answer
I don't know if a "cognitive bias/fallacy exist", however you could find some answers to your question looking at the defense mechanisms that each one of us use.

**Defense mechanisms** were first described in 1874 by *Sigmund Freud* as strategies developed by the ego when under pressure by superego, unconscious and external reality.

First of all, they rise from conflicts and their nature depends on the quality of conflicts (Anna Freud, 1936). In this case we would talk about:

> **Denial:** A primitive defense mechanism which triggers an exclusion of an unpleasant and unbearable part of the reality from the conscious field. This exclusion occur by fantasy and by behaviour.

---

*An aspect of reality has been refused and unknown, splitting from the coscience* (White and Gilliland, 1975).

To sum up, denial allows these individuals to hide from a reality that is too hard to cope with.

I wish to have been helpful.

**References**

1. Anna Freud (1936) *"The Ego and the Mechanisms of Defence"*
2. White and Gilliland (1975) *"Elements of Psychopathology: Mechanisms of Defense"*
> 0 votes

---
Tags: cognitive-psychology, terminology, bias, economics, political-psychology
---


# Question
Title: Does dream recall interfere with "reverse learning"? (Crick and Mitchison's theory of REM sleep)
I've recently became aware of the idea of "reverse learning" that might happen during REM sleep - the brain's attempt to eliminate pathological attractors that might appear in neural networks. The idea was originally expressed by **Crick and Mitchison in their 1983 paper on "The function of dream sleep".**

I'm interested if there has any recent work that has supported that idea. I'm aware of this wikipedia article on reverse learning. More specifically, **I'm interested in how dream recall (writing down or recalling dreams upon awakening) affects the process of "reverse learning"?**

# Answer
**Recent supporting work**

In a paper published in the Jan 2017 issue of *Nature Neuroscience*, Wei Li and colleagues propose a mechanism that supports the "reverse learning" process based on dendritic calcium spikes that regulate spine formation.

However, as the authors discuss, the implications of their findings are more nuanced. They support the idea of reverse learning but show that it is not the only thing going on in REM sleep:

> REM sleep is not simply a substitute for wakefulness to stimulate plasticity, for pruning synapses during development or for persevering genetic identities of neuronal circuits. Instead, REM sleep is important for selectively incorporating new synapses into the existing circuits. It could be viewed as a “selection committee” for building and maintaining the synaptic network.

**Dream recall**

If we accept that reverse learning functions by the proposed mechanism, I would guess it would not be perturbed significantly by dream recall. This is because the calcium spikes in their experiments occurred on the order of seconds, and only during REM sleep. Dream recall, on the other hand, is is a high-level mental process that is probably restricted to humans.

This is just my best intuitive guess. For all we know, any neural event anywhere in the brain can potentially influence a subsequent event anywhere else in the brain, so really all bets are still on the table.
> 1 votes

---
Tags: learning, cognitive-modeling, sleep, dreams
---


# Question
Title: Is it possible for a human to feel no emotion?
I have heard that there are some people who don't feel emotions. Is that really true? Is it really possible for someone to feel no emotions?

# Answer
> 3 votes
It is a physical possibility but you need, at the bare minimum, to feel for your self to survive; like the need to eat. If you don't want to call hunger and similar things for feelings it would be a problem anyway because discus is what make you avoiding eating bad or toxic food and fear to avid getting eaten etc.

scorce: http://atlasofemotions.org/#continents/disgust

What you most likely have heard is that psychopaths don't feel anything and that is not true. They do care abut them self and others in self interest but would not start crying for anyone from feeling empathy. (I don't have a source for the later part but you can test it with a mind experiment with a psychopath and a smaller guy that tries to piss of the psychopath. Per definition the psychopath don't care if he kills the other dude but if he do he will end up in jail) http://www.dictionary.com/browse/psychopath

(Sorry for the horrible English, was a while since I last wrote anything)

---
Tags: emotion
---


title: Effect of plateau in BTSP

text:
# Question
Title: Effect of plateau in BTSP
In "Behavioral time scale synaptic plasticity underlies CA1 place fields" by Bittner et al. an alternative to Hebbian plasticity is proposed called Behavioral Time-scale Synaptic Plasticity (BTSP). Basically, instead of depending on Hebbian plasticity, a calcium-ion plateau can be used to create associations. From the paper:

> BTSP can rapidly store the entire sequence of events that occurred for several seconds before and after plateau-potential initiation within the synaptic weights of area CA1.

However, despite reading the paper, I'm still confused about the mechanism they think performs this. Does the "plateau" cause all spiking neurons to strengthen their connections or does the "plateau" use some other mechanism to influence neurons? Is excitation or potentiation even the correct way to understand this?

# Answer
> 1 votes
According to the Supplementary Materials the synaptic plasticity rule can be inferred from the data to be:

$$W(z) = W\_0(z) + \alpha \sum\_{t,t'=0}^{T} R\_{CA1}(t')K(t'-t)R\_{CA3}(z-x\_A(t))$$

Where:

* $z$ is the preferred location of the place cell
* $W\_0$ is the initial synaptic weight
* $\alpha$ is a learning-rate constant
* $T$ is the total running time of the experiment with $t'$ being when the plateau starts, although I'm not sure about $t'$ and it's significance
* $R\_{CA1}$ is a binary function which is 1 in the presence of the plateau
* $K(t'-t)$ is an unknown kernel that determines **synaptic weights change depending on the activity of the cells** at time $t'=t$
* $R\_{CA3}(z-x\_A(t))$ is a model of the firing rate of the place-cell given the preferred location and the current location of the animal

Given that the formula for weight change depends on both:

1. The firing rate of the place cell
2. A kernel which takes the firing rate of the place cell into account

I can say that the plateau selects for firing place cells. However, I'm still not clear on what they mean by storing "entire sequence of events that occurred for several seconds before and after plateau-potential initiation".

---
Tags: cognitive-neuroscience, neurophysiology, plasticity
---


# Question
Title: Are the receptive fields of bipolar and retinal ganglion cells directly stimulated by light?
I know this is a basic question, but I can't find the answer anywhere. How can a cell that is not photoreceptive (eg LGN and retinal gangion cells) have a receptive field that is stimulated by "light" (as most textbooks explain it). Isn't it truer to say that they are stimulated by incoming neuronal inputs - in which case, how can they have a "circular surround"? Clearly I'm lost here, so all help appreciated! Thanks!

# Answer
> 1 votes
The (visual) receptive field of a neuron is the relation between the light that falls on the retina and the change in activity of that neuron, regardless of what happens in between the light and the neuron. Therefore, RGC, LGN, V1, or even higher order visual cortical neurons all have some sort of receptive fields. Not because they respond directly to patterns of light, but through cascade of signals that originate from the photoreceptors. So, yes, many LGN neurons would have center-surround receptive fields.

---
Tags: vision
---


# Question
Title: Voltage-dependent ion channels as operators
Does it make sense (or is even the standard approach) to model mathematically a voltage-dependent ion channel not as a *function*, that maps a voltage to a conductance ($f:\mathbb{R}\rightarrow \mathbb{R}$), but as an *operator* (in the sense of functional analysis), that maps a voltage profile (= function of time = element of a vector space) to a conductance profile (= function of time = element of another vector space)?

Are there references to the literature?

\[Considered as operators it would be interesting to know in which ranges (of the vector space of voltage profiles) the channels behave linearly (in mathematical terms: *are* linear) - so we were done with knowing their behaviour for only a couple of base vectors (= profiles), i.e. square signals of equal height, but different widths. We would learn about rise times and time delays. In other ranges of course they behave quite non-linearily, esp. when the voltage profile crosses the threshold.\]

# Answer
Yes, they are nonlinear filters, which are operators on temporal signals. I have not seen a single ion channel analyzed as nonlinear filter though. Most of the time, a system containing ion channels (such as some neuron's membrane) is analyzed as such. Papers describing the biophysics of neurons and their function as filtering devices has been one of the topics in computational neuroscience.

* Gerstner, W. and Kistler, W. M. (2002). Spiking Neuron Models. Cambridge University Press
* Marmarelis, V. Z. (2004). Nonlinear dynamic modeling of physiological systems.
> 3 votes

---
Tags: reference-request, theoretical-neuroscience, neurophysiology
---


# Question
Title: are serotonin levels higher or lower in dominant vs. non-dominant primates and humans?
On page 242 of The Moral Animal, Robert Wright states that

> In vervet monkey societies, dominant males have more of the neurotransmitter serotonin than do their subordinates. And one study found that in college fraternities, officers, on average, have more serotonin than do their less powerful fraternity brothers.

However, on page 82 of a different book, Scattered: How ADD Originates and What You Can Do About It, Gabor Maté states that

> In troops of monkeys, the dominant, most successfully aggressive males have been found to have less serotonin than others. This would seem to prove that low serotonin levels cause aggression. However, the serotonin levels drop only *after* these males achieve dominant status. So while the relative lack of serotonin may help to *maintain* the dominant male's aggressive capacities, it could not have *caused* them.

It seems that Wright (a journalist) is making the complete opposite interpretation of the primate research that Maté (a physician) is, and there doesn't seem to be any subtlety in the context that alleviates the seemingly glaring contradiction, so I'm assuming that one of these two simply misunderstood the research. Who is correct?

(to be clear, both of these people are citing research that others have done, not making claims based on their own research)

# Answer
> 1 votes
It seems Maté simply misread the research that he cited. The study on this, from 1984, says that

> Dominant male adult vervet monkeys have whole-blood serotonin concentrations approximately twice those of subordinate adult males.

---
Tags: neuroscience, aggression, serotonin
---


# Question
Title: How to specify the quickest movement a human can do based on MTM standards?
I am looking for a benchmark as a reference regarding the human Kinesiology that specifies the quickest movement a human can do on basic everyday movements like computer mouse clicking. As far as I know, there is an standard called MTM (Measurement Time Methods) in the field of industrial engineering and ergonomics which specifies the required time for each basic movement to be done by human. This MTM standard time is provided on the basis of not putting the human (worker) in an overload or underload working situation. So I assume MTM cannot provide me with the shortest possible duration (time) a basic movement can be performed. I am not sure whether we have such a benchmark based on human physiology, Do you have any suggestion in this regard? I recorded response times and have a distribution of these response times for many subjects, however, I would like to estimate the minimum possible response time a human can do in my experiment

# Answer
> 3 votes
I don't know about any MTM standards or benchmarks, but motor response latencies have been assessed in many studies. Importantly, auditory response latencies are smallest, then tactile followed by visual response times. This, because the auditory system is swift, while the visual system is sluggish by comparison (source: Packman & Packman).

For example, Jain *et al*. (2015) report a mean visual response latency of **247 ms** and an auditory response latency of **228 ms**. Another study reports approximately **144** and **133 ms**, respectively. The lower values are probably because the authors chose the lowest reading as their final measurement Gavkare *et al*, 2013). Other technical differences may also have yielded deviations. Importantly, stimulus intensity affects reaction time (*e.g.*, louder auditory stimuli decrease reaction time) and other stimulus parameters do so as well (source: Packman & Packman). Importantly, age is positively correlated with reaction time (Ng & Chan, 2012).

A large data set where the authors stratified their subject pool in age groups as well as other parameters can be found in Ng & Chan, 2012.

<sub>**References**
**-** Gavkare *et al*,, Indian Medical Gazette, June 2013
**-** Jain *et al*., *Int J Appl Basic Med Res* (2015); **5**(2)
**-** Ng & Chan, IMECS (2012)</sub>

# Answer
> -3 votes
Theoretically visual stimuli would be faster than auditory stimuli because of the given speed of light vs sound. Therefore I ***personally believe*** the time from stimuli to recognition would depend on the individual and furthermore the time from recognition to the time of response (ex. Clicking a mouse immediately upon recognition of a sound or sight, followed by \[roughly\] identifying said object) With all those variables, in ***MY OPINION*** there are absolute's: 1) light travels faster than sound; 2)visual contains more data than audio

---
Tags: motor, psychophysics, human-factors
---


# Question
Title: Simultaneous extracellular recording from different distant sites (in rodents)
I wonder whether it is technically possible today to have simultaneous extracellular recording in awake rodents (e.g., mice) from different non-proximate sites (e.g., V1 and frontal cortex). I mean to have two or more different electrode penetrations at the same time. Using multi-array / grid / tetrode it is possible record from many locations, but they are spatially proximate. Any references are appreciated.

# Answer
> 3 votes
I wouldn't know why multi-site cortical extracellular recordings would not be feasible? What would the practical experimental or technical limitation be in your opinion?

As long as you have a multichannel amplifier suitable for extracellular recording and you consider the choice between using a common reference, *i.e.*, monopolar recordings (Ludwig *et al*., 2009), or using paired recording-reference electrodes for bipolar measurements (Boatman-Reich *et al*., 2010) you should be fine.

<sub>**References**
**-** Boatman-Reich *et al*., *Front Comput Neurosci* (2010)
**-** Ludwig *et al*., *J Neurophysiol* (2009); **101**(3): 1679–89</sub>

---
Tags: neuroscience, electrophysiology, experimental-neuroscience
---


title: To what extent is maths talent innate?

text:
# Question
Title: To what extent is maths talent innate?
My dad always talks vaguely about how 'only 20% (or some other small figure) of the population has the kind of brain equipped with the machinery to process \[insert high-level mathematical process, e.g. sophisticated engineering technique or something of the like\].' This also applies to people's struggles with probability (e.g. neglecting base rates), et cetera. I was wondering how much of math's talent is just there or not there from birth, vs capable to be learned. Thanks.

In particular, is the majority of the population actually unequipped with the mental machinery (like, say, a frog) to process high-level (say, advanced high school and beyond) maths? Prediction: no.

# Answer
> 0 votes
While most people can master basic math, your dad is probably correct that perhaps "20%" of the population is capable of understanding math at the advanced level you are talking about.

One study on education concluded the following about "A.P." level high school courses (not just in math): \[These require students\] "to think in abstractions, to synthesize ideas, to grasp complicated interrelationships, to absorb and apply a large amount of academic knowledge. In no country is this ability possessed by more than a minority of children."

Source: Admiral Hyman Rickover, "American Education: A National Failure."

# Answer
> 2 votes
Intelignece is a combination of nature and nurture, like most human attributes. The exact percentage is not possible to measure, at least with todays knowledge.

Extract from the article by Neill, J.T. (2004). "Nature vs Nurture in Intelligence" :

> In the overfocus on nature vs. nurture issues, the attempts to estimate the relative contribution rests on the somewhat naive notion that there is a constant, true value. In reality, "gene expression is environment dependent" and it impossible to obtain pure estimates of genetic vs. environmental contribution - one could not exist without the other.

---
Tags: mathematical-ability
---